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第117回日本解剖学会総会・全国学術集会 講演プログラム・抄録集 PDF ...

第117回日本解剖学会総会・全国学術集会 講演プログラム・抄録集 PDF ...

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<br />

1 2 2 3 1 1 1<br />

1 2 M2 3 M4


40<br />

117 <br />

<br />

<br />

E L C LC<br />

::OEPM I<br />

<br />

<br />

1OEPMI1 Singleneuron tracing study of thalamocortical projections arising from the rat mediodorsal<br />

nucleus<br />

1OEPMI2 V <br />

1OEPMI3 <br />

1OEPMI4 GABA <br />

<br />

::OEPM II<br />

<br />

<br />

1OEPMII1 BAF dpf1 GFP <br />

<br />

1OEPMII2 mRNA <br />

1OEPMII3 Immunocytochemical and proteomic analysis of the γsecretase complex using the<br />

conformationspecific antiNicastrin antibody<br />

F L C LC<br />

::OFPM I<br />

1<br />

<br />

1OFPMI1 Rho ROCK1, ROCK2<br />

1OFPMI2 Photoactivatable Rac1 <br />

1OFPMI3 GaAsP LIVE <br />

<br />

1OFPMI4 229E CD13<br />

<br />

::OFPM II<br />

<br />

<br />

1OFPMII1 Nphp3 <br />

1OFPMII2 <br />

1OFPMII3 PACAP 5 <br />

G L C LC<br />

::OGPM I<br />

<br />

<br />

1OGPMI1 microCTmicroMRI


117 41<br />

1OGPMI2<br />

<br />

1OGPMI3 HyperDry <br />

1OGPMI4 <br />

::OGPM II<br />

<br />

<br />

1OGPMII1 <br />

1OGPMII2 Muse iPS <br />

1OGPMII3 Monitoring DNA damage levels using γH2AX detection in vivo<br />

H L C LC<br />

::OHPM<br />

<br />

<br />

1OHPM1 <br />

1OHPM2 MS5 <br />

1OHPM3 <br />

1OHPM4 Two immunogenic passenger DC subsets in the rat liver with a distinct trafficking pattern and<br />

radiosensitivity<br />

::OHPM<br />

<br />

<br />

1OHPM5 <br />

1OHPM6 <br />

1OHPM7 <br />

I L C LC<br />

::OIPM<br />

<br />

<br />

1OIPM1 α 4 <br />

1OIPM2 L LFABP <br />

1OIPM3 EDA <br />

::OIPM<br />

<br />

<br />

1OIPM4 Kiyotaka Toshimori Fertilization analyzed by live imaging in the mouse<br />

1OIPM5 <br />

1OIPM6 microRNA


42<br />

117 <br />

<br />

E L C LC<br />

::OEAM III<br />

<br />

<br />

2OEAMIII1 <br />

2OEAMIII2 NPY <br />

2OEAMIII3 <br />

<br />

2OEAMIII4 gastrinreleasing<br />

peptide <br />

::OEAM IV<br />

<br />

<br />

2OEAMIV1 TRPV4 <br />

2OEAMIV2 Hh <br />

2OEAMIV3 AP1 Notch <br />

::OEAM V<br />

<br />

<br />

2OEAMV1 MAP1A supports NMDAreceptor transport for synaptic plasticity<br />

2OEAMV2 Homer1a regulates the activityinduced remodeling of synaptic structures in cultured<br />

hippocampal neurons<br />

2OEAMV3 PIPKα regulates neuronal microtubule depolymerase KIF2A and suppresses elongation of<br />

axon branches<br />

F L C LC<br />

::OFAM III<br />

<br />

<br />

2OFAMIII1 SNAP23 <br />

2OFAMIII2 <br />

2OFAMIII3 <br />

2OFAMIII4 Input pathway and target cell typedependent regulation of synaptic AMPAR subunits in<br />

hippocampal CA1 region<br />

::OFAM IV<br />

<br />

<br />

2OFAMIV1 <br />

2OFAMIV2 <br />

2OFAMIV3 <br />

::OFAM V<br />

<br />

<br />

2OFAMV1 BMP2 dexamethasone


117 43<br />

2OFAMV2 <br />

2OFAMV3 <br />

G L C LC<br />

::OGAM I<br />

<br />

<br />

2OGAMI1 <br />

<br />

2OGAMI2 <br />

2OGAMI3 <br />

2OGAMI4 <br />

::OGAM II<br />

<br />

<br />

2OGAMII1 Angela QuispeSalcedo<br />

The application of antimicrobials or glycogen accelerates the pulpal regeneration of replanted<br />

molars in mice<br />

2OGAMII2 <br />

2OGAMII3 BrdU <br />

::OGAM III<br />

<br />

<br />

2OGAMIII1 Cx45 NFATc <br />

2OGAMIII2 FGF <br />

2OGAMIII3 An attempt to identify novel ciliary genes by database comparison<br />

H L C LC<br />

::OHAM I<br />

<br />

<br />

2OHAMI1 <br />

2OHAMI2 On the phylogeny of the zygomatic arch, and its relationships among foramina and the bony<br />

wall of the orbit<br />

2OHAMI3 <br />

2OHAMI4 <br />

::OHAM II<br />

<br />

<br />

2OHAMII1 Nabil Eid Persistent median artery: Relationships to palmar arches and median nerve branches<br />

2OHAMII2 <br />

2OHAMII3 Thiel <br />

::OHAM III<br />

<br />

<br />

2OHAMIII1


44<br />

117 <br />

2OHAMIII2 <br />

2OHAMIII3 <br />

1 <br />

<br />

I L C LC<br />

::OIAM I<br />

<br />

<br />

2OIAMI1 CT <br />

<br />

2OIAMI2 <br />

2OIAMI3 klotho/ <br />

2OIAMI4 <br />

::OIAM II<br />

HBS <br />

<br />

2OIAMII1 Osteogenic culture <br />

<br />

2OIAMII2 PKR <br />

2OIAMII3 WT1 RNA <br />

::OIAM III<br />

<br />

<br />

2OIAMIII1 septoclast EFABP <br />

<br />

2OIAMIII2 <br />

<br />

2OIAMIII3


117 45<br />

<br />

D K LC<br />

::ODPM I<br />

<br />

<br />

3ODPMI1 Large Maf <br />

3ODPMI2 <br />

<br />

3ODPMI3 Notch <br />

3ODPMI4 <br />

::ODPM II<br />

<br />

<br />

3ODPMII1 Dini Ramadhani Expression of laminin isoforms during anterior pituitary development in the rat<br />

3ODPMII2<br />

<br />

3ODPMII3<br />

<br />

E L C LC<br />

::OEPM VI<br />

<br />

<br />

3OEPMVI1 <br />

3OEPMVI2 Developmental Origins of Health and Disease DOHaD <br />

<br />

3OEPMVI3 <br />

3OEPMVI4 15q1113 E/I <br />

::OEPM VII<br />

<br />

<br />

3OEPMVII1 <br />

3OEPMVII2 <br />

3OEPMVII3 RAGE<br />

<br />

::OEPM VIII<br />

<br />

<br />

3OEPMVIII1 Fasting and highfat diet alter histone deacetylase expression in the medial hypothalamus<br />

3OEPMVIII2 <br />

3OEPMVIII3 PAM


46<br />

117 <br />

F L C LC<br />

::OFPM VI<br />

<br />

<br />

3OFPMVI1 <br />

2 <br />

3OFPMVI2 Haruki Senoo Biodiversity and hepatic stellate cells<br />

3OFPMVI3 A <br />

3OFPMVI4 IEL DNA <br />

::OFPM VII<br />

<br />

<br />

3OFPMVII1 SU6656 p53 <br />

3OFPMVII2 <br />

3OFPMVII3 HORMAD2 <br />

::OFPM VIII<br />

<br />

<br />

3OFPMVIII1 α1 <br />

<br />

3OFPMVIII2 E3 HRD1 <br />

3OFPMVIII3 <br />

G L C LC<br />

::OGPM IV<br />

<br />

<br />

3OGPMIV1 NEX <br />

3OGPMIV2 FLRT Unc5 <br />

3OGPMIV3 Kyoji Ohyama Implications for cooperative versus noncooperative actions of the subunits of NatB, Mdm20<br />

and Nat5 in mouse embryonic brain<br />

3OGPMIV4 <br />

::OGPM V<br />

<br />

<br />

3OGPMV1 Hes1 <br />

3OGPMV2 M. iliotibialis cranialis<br />

3OGPMV3 <br />

<br />

::OGPM VI<br />

<br />

<br />

3OGPMVI1 Yoshiro Takano Differential effect of aberrant expression of ectodysplasinA receptor edar on scales and jaw<br />

and pharyngeal dentition of medaka<br />

3OGPMVI2 DNA TGFβ3


117 47<br />

H L C LC<br />

::OHPM IV<br />

<br />

<br />

3OHPMIV1 <br />

3OHPMIV2 3D <br />

3OHPMIV3 <br />

3OHPMIV4 <br />

3OHPMIV5 Takamitsu Arakawa Threedimensional modeling of the architecture of the plantar muscles of the great toe<br />

::OHPM I<br />

<br />

<br />

3OHPMI1 ShineOd Dalkhsuren<br />

The characteristic of the filiform and fungiform papillae of human tongue<br />

3OHPMI2 <br />

3OHPMI3 <br />

::OHPM II<br />

<br />

<br />

3OHPMII1 CRF <br />

3OHPMII2 <br />

I L C LC<br />

::OIPM IV<br />

<br />

<br />

3OIPMIV1 tendon gel <br />

3OIPMIV2 <br />

3OIPMIV3 <br />

::OIPM<br />

<br />

<br />

3OIPM1 <br />

<br />

3OIPM2 CT3 1 <br />

3OIPM3 <br />

::OIPM<br />

<br />

<br />

3OIPM4 Mari Hiraoka Organization of the lens elasticity associating with accommodation in monkey eyes<br />

3OIPM5 CCP1 <br />

3OIPM6


48<br />

117 <br />

<br />

<br />

::<br />

I<br />

1P001 S100A6 <br />

1P002 Yumiko Matsusue Distribution of corticosteroid receptors in oligodendrocytes of mice<br />

1P003 4F2<br />

<br />

1P004 Jiaorong Chen Immunohistochemical Analyses of Protein 4.1G in Enteric Peripheral Nervous Tissues by “in vivo<br />

Cryotechnique”<br />

1P005 in vivo in vitro<br />

1P006 <br />

1P007 <br />

1P008 <br />

1P009 <br />

1P010 <br />

1P011 1 DCC <br />

<br />

1P012 Spock3 null <br />

1P013 4 5 γ <br />

1P014 <br />

1P015 <br />

1P016 <br />

1P017 <br />

1P018 WNPW <br />

1P019 Kinya Kubo Chewing under restraint stress inhibits the stressinduced suppression of cell proliferation in the<br />

hippocampal dentate gyrus<br />

1P020 Kouko Tatsumi Voluntary exercise promotes astrogliogenesis from Olig2 cells in some nuclei of the basal ganglia of<br />

adult mouse<br />

1P021 GDNF mRNA <br />

1P022 II <br />

1P023 <br />

1P024 cfos <br />

1P025 cFos <br />

1P026 <br />

1P027 <br />

1P028 / <br />

2 <br />

1P029 n3 <br />

1P030 Shinji Tanaka Altered dynamics of the cortical neuronal circuit in a mouse model of autism<br />

1P031 Miwako MasugiTokita<br />

Mechanism of deficit in aggressive behavior of metabotropic glutamate receptor subtype 7 knockout<br />

mice<br />

1P032 PTPRA<br />

1P033 Kisspeptin


117 49<br />

1P034 <br />

1P035 <br />

1P036 TGFβ1 <br />

1P037 Hiroaki Okuda Identification of CSPG constituting DACS, a novel brain extracellular matrix<br />

1P038 <br />

1P039 Mutations in POLR3A and POLR3B encoding RNA polymerase III subunits cause an<br />

hypomyelinating leukoencephalopathy<br />

1P040 <br />

1P041 Zitter rat <br />

1P042 <br />

1P043 Stigmoid body <br />

1P044 <br />

1P045 <br />

I<br />

1P046 Eusthenopteron foodi<br />

1P047 <br />

1P048 <br />

1P049 NOS <br />

1P050 1 <br />

1P051 TNFα/RANKL microRNA <br />

1P052 hemokinin1 <br />

1P053 DGKζ Retinoblastoma <br />

1P054 <br />

1P055 PACAP VIP PACAP <br />

VIP <br />

1P056 5 <br />

1P057 gustducin <br />

1P058 <br />

1P059 <br />

1P060 APC Min/+ <br />

1P061 DPEP1 <br />

1P062 Md Moksed Ali Placenta specific miR-517a modulates gene expression in Jurkat cells<br />

1P063 microRNA CpG <br />

1P064 IgG IIb Fc FcRIIb<br />

<br />

1P065 Yoshiya Asano Agerelated accumulation of nonheme ferric and ferrous iron in mouse ovarian stroma visualized by<br />

sensitive iron histochemistries<br />

1P066 <br />

1P067 <br />

<br />

1P068 TG <br />

1P069 <br />

<br />

1P070 <br />

1P071 2 <br />

1P072


50<br />

117 <br />

1P073 Makoto Naganuma Activities of human upper limb muscles during a combined movement of elbow flexion/extension and<br />

forearm pronation/supination<br />

1P074 <br />

1P075<br />

<br />

1P076 <br />

1P077 <br />

1P078 <br />

1P079 <br />

1P080 <br />

1P081 <br />

1P082 <br />

1P083 <br />

1P084 <br />

1P085 <br />

1P086 <br />

1P087 Persistent left hepatic venous directly opening into the right atrium<br />

1P088 <br />

1P089 <br />

1P090 <br />

<br />

1P091 <br />

1P092 <br />

1P093 <br />

1P094 LEH<br />

1P095 <br />

1P096 <br />

1P097 Nacholapithecus kerioi <br />

<br />

1P098 Involvement of Olig2 in the formation of reciprocal connection between the thalamus and cortex<br />

1P099 Studying nascent daughter cells’ neighborship to understand the mechanism of cell fate choices in the<br />

neocortical neurogenesis<br />

1P100 GABAA <br />

1P101 <br />

1P102 kirrel3 <br />

1P103 Characterization of the RNAbinding protein Musashi1 in zebrafish<br />

1P104 PSANCAM <br />

1P105 mRNA <br />

1P106 CNTF <br />

1P107 <br />

1P108 <br />

1P109 kirrel3 <br />

1P110 <br />

1P111 / Sprouty4<br />

1P112 <br />

1P113 <br />

1P114 Dlg1 <br />

1P115 sox9


117 51<br />

1P116 Protocadherin 10a <br />

1P117 Developmental Origins of Health and Disease DOHaD <br />

<br />

1P118 α <br />

1P119 Occludin p63 <br />

1P120 <br />

1P121 <br />

1P122 <br />

1P123 <br />

1P124 LEF1 SP6 <br />

1P125 <br />

1P126 TTF1 <br />

1P127 Keishi Otsu The role of Rho signaling pathway in dental epithelial stem cells<br />

1P128 Ji Youn Kim Localization of osteopontin and osterix in periodontal tissue during orthodontic tooth movement in rats<br />

1P129 Esrat Jahan Fetal jaw movement affects molecular cascade in the development of mandibular condylar cartilage<br />

1P130 <br />

1P131 <br />

<br />

1P132 <br />

1P133 FIB/SEM <br />

<br />

::<br />

II<br />

2P001 Mohammad Rabiul Karim<br />

Molecular sequence and distribution of the NMDA receptor subunit NR1 mRNA in the central nervous<br />

system of pigeons Columba livia<br />

2P002 2 <br />

2P003 SULT2B1a<br />

2P004 <br />

2P005 Jahan Mir Rubayet<br />

Androgen receptor expression in the preoptic and anterior hypothalamic areas of the adult male rats<br />

and mice<br />

2P006 GABA parvalbumin <br />

2P007 SNARE <br />

2P008 GABA <br />

2P009 Expression of AMPA type glutamate receptor in developing chick vestibulocochlear ganglia<br />

2P010 <br />

<br />

2P011 C <br />

2P012 <br />

2P013 <br />

2P014 <br />

2P015 <br />

2P016 CART <br />

2P017 GABA


52<br />

117 <br />

2P018 Conserved properties of dendritic trees in four cortical interneuron subtypes<br />

2P019 Majid Ebrahimi FABP7 in astrocytes is involved in control of neuronal dendritic formation<br />

2P020 FILIP <br />

2P021 CA1 <br />

2P022 In vivo analysis of postsynaptic molecular dynamics in the developing mouse cortex<br />

2P023 Ayako Hayashi Direct monitoring of AMPA receptor recycling and trafficking<br />

2P024 Motor protein KIF1A is essential for hippocampal synaptogenesis and learning enhancement in an<br />

enriched environment<br />

2P025 Zheng Huang Activationspecific Changes of Angiotensin II Receptors in Mouse Cerebellum and Adrenal Glands<br />

with In Vivo Cryotechnique<br />

2P026 Toshiko Tsumori Nodose ganglion cells expressing melanocortin4 receptor send their fibers to the pancreatic islets in<br />

the mouse<br />

2P027 Runx1 <br />

2P028 A <br />

2P029 Features of boutons distribution along axons of neurons in the caudal nucleus of tractus solitarius of<br />

the rat<br />

2P030 Calbindin <br />

2P031 GALP <br />

2P032 Hitoshi Kawano Origins of nitric oxide pathways to the median preoptic nucleus<br />

2P033 Kisspeptin Tuberoinfundibular dopamine TIDA <br />

2P034 <br />

2P035 CA1 <br />

2P036 <br />

2P037 Classification of rat pallidofugal projection systems revealed by singleneuron tracing study with a<br />

viral vector<br />

2P038 A Morphological Analysis of Thalamocortical Axon Fibers of Rat Posterior Nuclei: A Single Neuron<br />

Tracing Study with Viral Vectors<br />

2P039 Morphological analysis of axon collaterals derived from single corticospinal neurons in subcortical<br />

structures<br />

2P040 <br />

2P041 Projections from the amygdaloid anterior basomedial and anterior cortical nuclei to MCHcontaining<br />

hypothalamic neurons of the rat<br />

2P042 Inhibitory inputs of CCKpositive neurons to PVexpressing neurons in mouse neocortex<br />

2P043 Elimination of somatic climbing fiber synapses proceeds with the differentiation of cerebellar<br />

interneurons<br />

2P044 Tectothalamic inhibitory neurons in the inferior colliculus receive converged axosomatic excitatory<br />

inputs from multiple sources<br />

2P045 Axon terminals of the corticocollicular projection in the rat auditory system<br />

2P046 Afferent projection to amygdaloid subnuclei and intrinsic connection of each subnuclei<br />

II<br />

2P047 <br />

2P048 <br />

2P049 Toshiyuki Oda Communication between Flagellar Outer and Inner Dynein Arms<br />

2P050 Toshiki Yagi A novel protein complex required for the formation of microtubule square lattice in green tree frog<br />

sperm<br />

2P051


117 53<br />

2P052<br />

Tomonori Naguro Mitochondria form continuous intracellular networkstructures: a study visualized by highresolution<br />

scanning electron microscopy<br />

2P053 <br />

2P054 <br />

2P055 <br />

<br />

2P056 VAMP5 <br />

2P057 <br />

<br />

2P058 Involvement of Rab35 in phagosome formation through regulating ARF6 activity by ACAP2<br />

2P059 Atg9AmRNA HeLa / A study on Atg9AmRNAknockdown<br />

HeLa cells<br />

2P060 mAtg9AAcGFP mDFCP1mCherry <br />

2P061<br />

Hironobu Nakane Histological analysis of adipose tissues in Xpg null mice<br />

2P062 mdx <br />

2P063 McARH 7777 ALP <br />

<br />

2P064 <br />

2P065 lamin A/C <br />

2P066 ABCG2 <br />

2P067<br />

<br />

2P068 DGKε <br />

2P069 DGKζ NAP DGKζ <br />

2P070 Cellular localization of ERα and their apoptotic effects<br />

2P071 <br />

2P072 αMangostin <br />

2P073 Sevoflurane rat Per2 <br />

<br />

2P074<br />

Khairani Astrid Feinisa<br />

Transverse anchoring system of myofibril to sarcolemma: the morphological study<br />

2P075 <br />

2P076 Prosaposin expression in cardiac muscle of mdx mice in early period of disease<br />

2P077 <br />

2P078 <br />

2P079 <br />

2P080 Thiel <br />

<br />

2P081 ATDC5 Notch14 PCNA <br />

2P082 Nox <br />

2P083 <br />

2P084 <br />

2P085 <br />

2P086 CT CT <br />

<br />

2P087 <br />

2P088 <br />

2P089


54<br />

117 <br />

2P090 <br />

2P091 <br />

2P092 Klotho <br />

2P093 FAM20A <br />

2P094 GABA GABA <br />

2P095 Polypterus senegalus Oxydoras niger <br />

<br />

2P096 planar cell polarity <br />

<br />

2P097 Miyuki Yamamoto 5 <br />

2P098 Kannika Adthapanyawanich<br />

Studies on the submandibular gland of androgen receptordeficient mice<br />

2P099 <br />

2P100 <br />

2P101 3A 3AB <br />

2P102 <br />

2P103 M Epidermal type FABP EFABP/FABP5 <br />

<br />

2P104 A <br />

2P105 cKIT <br />

2P106 ICCSP <br />

2P107 CCK1 <br />

2P108 Mayako Morii The metabolism of cholesterol after bile duct degeneration in lamprey<br />

2P109 NAFLD<br />

<br />

2P110 Deltalike3 <br />

2P111 <br />

<br />

2P112 CEACAM1 <br />

2P113 Masahiro Miura The role of peritoneal lymphatic system on the human peritoneal dissemination<br />

2P114 <br />

2P115 <br />

2P116 Masataka Sunohara The role of hematopoietic factors and Wnt signaling during tooth development<br />

2P117 <br />

2P118 podoplanin <br />

2P119 <br />

2P120 <br />

2P121 <br />

2P122 <br />

2P123 <br />

2P124 Nkx2.5 <br />

2P125 Hideyuki Tanaka Morphological analysis of effects with arachidonic acid in smooth muscle cells<br />

<br />

2P126 FABP7<br />

2P127


117 55<br />

2P128 Functional Analysis of Nucleoprotein diet from salmon testis, Shirako via Intestinal IgA secretion and<br />

TLR9 stimulation<br />

2P129 Musha Muhetaerjiang<br />

The effects of adjuvants on autoimmune responses against testicular antigens in mice<br />

2P130 <br />

2P131 Kuerban Maimaiti Germ cell death in testicular autoimmunity<br />

2P132 <br />

2P133 <br />

2P134 trafficking<br />

<br />

::<br />

III<br />

3P001 Tomiko Yakura Alterations of synaptic transcytosis induced by ethanol exposure: apocrinelike structure in the rat<br />

3P002 LAMP2 <br />

3P003 Souichi Oe Synergistic interaction between Golgi outposts and RNA granules in postlocal translational secretory<br />

pathway<br />

3P004 ARF6 BRAG2/IQSEC1 <br />

3P005 Arf6 EFA6A <br />

3P006 Roles of BMP signaling in synapse development<br />

3P007 Roles of ACF7, a large linker protein interacting with both microtubules and Factin, in the<br />

postsynaptic functions<br />

3P008 Imaging dynamics of axonal mitochondria<br />

3P009 ERRγR <br />

3P010 Agerelated changes in estrogen receptorβ mRNA expression in male rat brain<br />

3P011 PRLR<br />

<br />

3P012 <br />

3P013 Md. Nabiul Islam Sporadically lurking HAP1immunoreactive cells in the hippocampus and their morphological relation<br />

with steroid receptors<br />

3P014 GR<br />

3P015 <br />

3P016 GALP<br />

3P017 CGRP <br />

<br />

3P018 SSRI<br />

3P019 <br />

<br />

3P020 <br />

3P021 <br />

3P022 PACAP <br />

3P023<br />

Takehiko Sunabori Protective effects of hyaluronan tetrasaccharide on hippocampal pyramidal neurons in neonatal mouse<br />

after hypoxicischemic injury<br />

3P024 <br />

3P025 The Effects of an 18mer Peptide of Prosaposin in the Attenuation of MPP+/MPTP Toxicity in Vitro<br />

and in Vivo<br />

3P026 GABAA JM1232


56<br />

117 <br />

3P027 <br />

3P028 ABC <br />

3P029 <br />

3P030 PACAP <br />

3P031 PMES2 <br />

3P032 Müller <br />

3P033 <br />

3P034 <br />

3P035 <br />

<br />

3P036 2 15 <br />

3P037 Masako Nakanishi Involvement of acidic microenvironment on the cancerinduced bone pain<br />

3P038 Mineo Watanabe IL1β in trigeminal nucleus caudalis contributes to extraterritorial allodynia/hyperalgesia following a<br />

trigeminal nerve injury<br />

3P039 cFos <br />

3P040 Minocycline <br />

3P041 ITAM KO <br />

3P042 Zitter <br />

3P043 <br />

<br />

3P044 Scaffold attachment factor B SAFB1 and SAFB2 synergistically inhibit intranuclear mobility and<br />

function of ERα<br />

3P045 Estrogen αfetoprotein <br />

3P046 <br />

3P047 <br />

3P048 <br />

<br />

3P049 manserin <br />

<br />

3P050 5βreductase <br />

3P051 <br />

3P052 PACAP <br />

3P053 <br />

3P054 Mash1 AADC GAD67 <br />

3P055 P <br />

3P056 3A3B <br />

3P057 <br />

3P058 <br />

3P059 <br />

<br />

3P060 <br />

3P061 <br />

3P062 LPS<br />

3P063 <br />

3P064 Kenji Yamatoya Separatration of early stage acrosome reacted sperm and analyses of the proteins<br />

3P065 Cell adhesion molecule1 Nectin3 <br />

3P066 SF1


117 57<br />

3P067 Autoimmune responses induced by immunization with xenogenic testicular germ cells alone<br />

3P068 Di2ethylhexyl phthalate <br />

3P069 Yuki Ogawa The effect of cadmium on immunoenvironment in the testis<br />

3P070 TIRF <br />

3P071 PACAP TAC1 <br />

3P072 3 in vitro <br />

3P073 Ariful Islam Localization of fatty acid binding protein in mouse placenta and its possible role of fatty acid transport<br />

through trophoblasts<br />

<br />

3P074 Kardasewitsch Verocay <br />

<br />

3P075 MAP <br />

3P076 <br />

3P077 Masahiko Kawagishi<br />

In vivo labeling of halogenated volatile anesthetics via intrinsic molecular vibrations using nonlinear<br />

Raman spectroscopy<br />

3P078 Fluorescence Immunohistochemistry by Confocal LSM for Studies of SemiUltrathin Specimens of<br />

Epoxy ResinEmbedded Samples<br />

3P079 / <br />

<br />

3P080 <br />

<br />

3P081 GP<br />

3P082 <br />

3P083 iPad<br />

3P084 eLearning <br />

3P085 <br />

3P086 <br />

3P087 <br />

3P088 <br />

3P089 <br />

3P090 <br />

3P091 <br />

3P092 MRI<br />

3P093 4 <br />

3P094 <br />

3P095 <br />

<br />

3P096 <br />

3P097 Fossa <br />

3P098 <br />

3P099 <br />

3P100 Thiel <br />

3P101


58<br />

117 <br />

<br />

<br />

::<br />

3P102 <br />

3P103 <br />

3P104 Kenji Ohata Tubulin polyglutamylation regulates cytoskeletal distribution in brain<br />

3P105 KCC2 <br />

3P106 <br />

3P107 <br />

3P108 neuroligin1 <br />

3P109 <br />

3P110 1 <br />

3P111 <br />

3P112 <br />

3P113 <br />

3P114 <br />

3P115 <br />

3P116 1 <br />

3P117 <br />

3P118 <br />

3P119 2 <br />

3P120 1 <br />

3P121 <br />

3P122 <br />

3P123 1 5 <br />

3P124 1 <br />

3P125 2 <br />

3P126 KUHWrat <br />

3P127 9 <br />

3P128 <br />

3P129 <br />

3P130 2 <br />

3P131 myosinIIA <br />

3P132 FABP5


117


117 59<br />

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[1] R. Danev and K. Nagayama, “Transmission Electron Microscopy with Zernike Phase Plate”, Ultramicroscopy 88 (2001)<br />

243-252.<br />

[2] Rochat R H, Liu X, Murata K, Nagayama K, Rixon F and Chiu W, “Seeing the Genome Packaging Apparatus in Herpes<br />

Simplex Virus type I (HSV-1) B-capsids”, J. Virology, 85 (2011) 1871-1874.


60<br />

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<br />

GlialAxon Interactions in Health and Disease<br />

Bruce D. TrappDepartment of Neurosciences, Lerner Research Institute, Cleveland Clinic, USA<br />

The interaction between myelin forming cells and axons is one of the best described examples of cellcell<br />

interactions in mammals. Myelin plays multiple roles essential for normal nervous system function. Best<br />

known is the insulation of axons to permit rapid propagation of nerve impulses by saltatory conduction. By<br />

concentrating voltage gated sodium channels at nodal axoplasm myelin also saves energy. To attain similar<br />

conduction speeds of myelinated axons, unmyelinated axons would have to have diameters 100 times larger<br />

than myelinated axons. Myelin, therefore, also conserves space. One of the most clinically relevant functions<br />

of myelin is provide trophic support essential for axonal survival. This function reflects the fact that axons<br />

can be meters away from the neuronal cell body and has to rely on glia support rather than on neuronal gene<br />

transcription to respond to many local changes in environment. Since axonal degeneration is the major cause<br />

of neurological disability in primary diseases of myelin, we have been investigating the mechanisms by which<br />

myelin provides trophic support to axons. The purpose of this presentation is to summarize these studies with<br />

an emphasis on morphological studies of normal and abnormal myelin-axon interactions. Myelin is essential<br />

for long-time axonal survival. This is best illustrated by the primary axonal degeneration that develops in<br />

mice null for the myelin proteins MAG, PLP or CNP. The precise mechanisms by which myelin stabilizes the<br />

axon is poorly understood. Two general features are common to the axonal pathologies that precede axonal<br />

degeneration: the axonal cytoskeleton is abnormal and the pathologies dominate in paranodal regions. We<br />

have compared paranodal axoplasm in myelinated, demyelinated and dysmyelinated axons using time lapse<br />

imaging and 3-dimensional electron microscopy. We detect alterations in transport and distribution of axonal<br />

mitochondria and smooth endoplasmic reticulum following demyelination and dysmyelination. These data<br />

suggest that altered ATP production and calcium homeostasis precede axonal degeneration. In addition the<br />

stability, length and orientation of microtubules which contain increased phospho tau epitopes were detected.<br />

Alterations in microtubules inhibit axonal transport and result in paranodal axonal swellings due to organelle<br />

accumulation. We are also investigating molecular mechanisms responsible for mitochondria fission and fusion<br />

in normal, demyelinated and dysmyelinated axons. These studies are unraveling the cascade of molecular and<br />

morphological changes that eventually result in axonal degeneration so we can identify therapeutic targets that<br />

may delay or stop axonal degeneration in primary diseases of myelin.


117 61<br />

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Biomed. Rev., 15: 1192004<br />

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117 65<br />

S<br />

Physiological roles of cell death signaling in mouse<br />

neural development<br />

Masayuki Miura 1,2<br />

1<br />

2 CREST, JST<br />

Caspases function as regulatory molecules not only in cell death,<br />

but also in non-apoptotic functions. Live-imaging analysis with the<br />

mouse embryos expressing SCAT3, a fluorescent indicator protein to<br />

monitor caspase-3 activation in living cells, revealed that preventing<br />

apoptosis by inhibition of caspases disturbed smooth morphological<br />

changes of developing neural plates and also reduced the speed of the<br />

cranial neural tube closure.<br />

A considerable number of olfactory sensory neurons (OSNs) in<br />

the developing olfactory epithelium exhibited caspase-3 activity<br />

without the apoptotic changes of nuclei. This prompts us to assess<br />

whether caspases exert non-apoptotic functions in OSNs during<br />

olfactory development. Apaf-1/caspase-9-mediated signaling causes<br />

the cleavage of a membrane-anchored member of the semaphorin<br />

family of guidance proteins, Sema7A, in the axons of OSNs<br />

during development. Analysis of mutant mice deficient for apaf-<br />

1 or caspase-9 revealed that this Apaf-1/caspase-9-mediated nonapoptotic<br />

caspase signaling is important for the development of OSNs<br />

by affecting axonal pathfinding, synapse formation and maturation<br />

status.<br />

S<br />

Characterization of Early Pathogenesis in the<br />

SODGA Mouse Model of ALS.<br />

Carol Milligan, Sherry Vinsant, Carol Mansfield,<br />

Masaaki Yoshikawa, Ramon Moreno, David Prevette<br />

Ronald Oppenheim<br />

Department of Neurobiology and Anatomy, and the ALS Center,<br />

Wake Forest School of Medicine, WinstonSalem, NC 27157, US<br />

Charcot first described Amyotrophic Lateral Sclerosis in 1869<br />

yet, effective, long-term treatment strategies are not available. A<br />

mouse model was developed after the identification of mutations<br />

in the SOD1 gene approximately 17 years ago, and most of our<br />

knowledge of the etiology and pathogenesis of the disease is from<br />

studies using this model. Although numerous preclinical trials have<br />

been conducted, results have been disappointing in that they did not<br />

positively translate in clinical trials. Characterization of the early<br />

pathological events may provide insight into disease onset, help in the<br />

discovery of presymptomatic diagnostic disease markers, and identify<br />

novel therapeutic targets. Many previous studies have identified<br />

pathological events in the mutant SOD1 models involving spinal<br />

cord, peripheral axons, neuromuscular junctions or muscle; however,<br />

few have systematically examined pathogenesis at multiple sites. In<br />

this study, we examine both central and peripheral components of<br />

the neuromuscular system in the SOD1G93A mouse model of ALS<br />

and relate these alterations to early muscle denervation. Our results<br />

provide insight into the earliest pathological events in this model.<br />

S<br />

Nerve injury induced motor neuron death with<br />

reference to neuronglia interaction<br />

Hiroshi Kiyama<br />

Dept. Functional Anatomy & Neurosci., Nagoya Univ. Grad. Sch.<br />

Med.<br />

The peripheral nerve injury induces changes not only in the injured<br />

neurons but also in surrounding glial cells. An interaction between<br />

neurons and glial cells might be critical in proper regeneration and<br />

functional recovery. One of the prominent glial behaviors seen after<br />

motor nerve injury was the microglial migration, proliferation and<br />

adhesion to the surfaces of injured motor neurons in response to<br />

nerve injury. Although the consequence of this adhesion between the<br />

nerve injured motor neurons and microglia seen during the first two<br />

weeks is not clear, nerve injured motor neurons, which lacked the<br />

initial tight adhesion with microglia, showed degenerative feature.<br />

In addition the knockout of a chemokine receptor CCR5, which<br />

specifically expressed by microglia in response to nerve injury,<br />

accelerated the motor neuron death. These evidences suggest that the<br />

microglial behavior seems important perhaps to provide neurons with<br />

a signal for survival and regeneration. In this symposium I would like<br />

to address morphological characteristics observed in the nerve injury<br />

induced motor neuron death and the interactions among injured motor<br />

neuron and surrounding glial cells.<br />

S<br />

Autophagy in the neural network and its impairment<br />

Yasuo Uchiyama<br />

Dept of Cell Biol & Neurosci, Juntendo Univ Grad Sch of Med<br />

Cathepsin D (CD) is distributed in various mammalian cells. We have<br />

shown that CNS neurons in CD-deficient mouse brains present a new<br />

form of lysosomal accumulation disease with a phenotype resembling<br />

neuronal ceroid lipofuscinosis (NCL). The most striking feature of the<br />

CD-/- CNS neurons is storage of autophagosomes, autolysosomes,<br />

granular osmiophilic deposits (GRODs), and fingerprint profiles,<br />

morphological hallmarks of NCLs. Moreover, GRODs are found<br />

within nascent autophagosomes, indicating that the GROD is a potent<br />

inducer of autophagy in neuronal cells. Autophagosomes, but not<br />

GRODs or lysosomes, frequently accumulate in the axon, indicating<br />

that subsets required for autophagosome formation are present in<br />

the axon. Until recently, it has been reported that impairment of<br />

autophagy due to Atg7 or Atg5 deficiency in the axon terminal of<br />

Purkinje cells induces neurodegeneration. These results indicate that<br />

not only in autophagy-unable neurons but also in neurons with excess<br />

of autophagy impairment of autophagy in the axon and its terminal<br />

induces neurodegeneration. However, the molecular mechanism of<br />

autophagosome formation in the axon and its terminal largely remains<br />

unknown.


66<br />

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117 67<br />

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68<br />

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PLoS ONE , e21531, 2011<br />

<br />

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Tight junctions prevent the leakage of solutes through the paracellular<br />

pathway of epithelial cells and are indispensable in establishing the<br />

various compositionally distinct fluid compartments within the body<br />

of multicellular organisms.<br />

Based on morphological observations, two models about the tight<br />

junction have been proposed. The protein model proposes that a<br />

linear array of membrane protein particles polymerize to form a tight<br />

junction strand and that a network of these strands adhere with paired<br />

strands from apposing cells to obliterate the intercellular space. On<br />

the other hand, the lipid model, which originates from the observation<br />

of exoplasmic lipid leaflet fusion, proposes that the fusion of these<br />

lipid leaflets is associated with a transformation of the lamellar phase<br />

of the lipid bilayers into a non-lamellar, inverted micelle structure at<br />

tight junctions.<br />

Much has been learned about the membrane proteins at tight junctions<br />

over the last decade. However, how these membrane proteins function<br />

as the barriers in the paracellular space remains to be elucidated.<br />

Here, I will present recent progress toward a better understanding of<br />

supra-molecular complex at tight junctions.


117 69<br />

S<br />

The role of autophagyrelated proteins on lipid<br />

metabolism in the ER membrane<br />

Taki Nishimura 1 , Anoop Kumar Velikkakath 1 ,<br />

Naotada Ishihara 1,2 , Eiko Oita 1 , Noboru Mizushima 1<br />

1<br />

Dept. Physiol. Cell Biol., Tokyo Med. Dent. Univ., 2 Dept. Protein<br />

Biochem., Inst. Life Sci., Kurume Univ.<br />

Autophagy is an intracellular degradation system accompanied by<br />

dynamic membrane organization. Dynamic membrane remodeling is<br />

achieved by the interplay between lipids and proteins and modulated<br />

by changes in lipid composition. However, the role of autophagyrelated<br />

genes in the lipid metabolism remains elusive. Here we<br />

show that endogenous Atg2A localizes on the autophagic isolation<br />

membranes and LDs. Atg2A and Atg2B are essential for autophagy<br />

because autophagic flux is blocked in cells treated with siRNA against<br />

both Atg2A and Atg2B, although LC3-II is generated. Morphological<br />

and biochemical analyses of Atg2-depleted cells reveal accumulation<br />

of aberrant membrane structures, which contained other Atg proteins<br />

such as LC3 and Atg9. These structures may represent intermediate<br />

structures of autophagosome formation. In addition, LD turnover<br />

is also affected in Atg2-depleted cells. These data suggest that<br />

mammalian Atg2 homologues are required for autophagosome<br />

formation and have an additional role in LD turnover, both of which<br />

take place on the endoplasmic reticulum. Now we are analyzing the<br />

effect of other autophagy-related genes RNAi on the LDs turnover.<br />

S<br />

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Long chain fatty acids are important nutrients for brain development<br />

and function. However, the molecular basis of their actions in<br />

the brain is still unkown. Fatty acid-binding proteins (FABPs),<br />

intracellular chaperons of fatty acids, are involved in the promotion<br />

of cellular uptake and transport of fatty acids, the targeting of fatty<br />

acids to specific metabolic pathways, and the regulation of gene<br />

expression. We have so far revealed that FABP7, a strong binder<br />

of omega-3 PUFA, is involved in controlling fatty acid metabolism<br />

in the brain astrocytes and that its deficiency in mice results in the<br />

alteration of emotional behavioral responses. In this talk, I would<br />

introduce the possible mechanism by which FABP7 controls neuronal<br />

plasticity through regulating lipid metabolism in the astrocytes, and<br />

discuss the link of FABP- and/or PUFA-deficiency to the human<br />

psychosis including schizophrenia.


70<br />

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72<br />

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Flk1 VEGFR2Flt1 VEGFR1 <br />

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<br />

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<br />

2


74<br />

117 <br />

S<br />

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<br />

Brant Weinstein<br />

National Institutes of Health, NICHD<br />

The cranial vasculature is essential for the survival and development<br />

of the central nervous system, and is important in brain pathologies.<br />

Cranial vessels form in a reproducible and evolutionarily conserved<br />

manner, but the formation process remains unclear. We are using<br />

zebrafish to better understand the mechanisms underlying hindbrain<br />

vascular development by (i) carrying out a precise anatomical<br />

description of the formation process, (ii) investigating the molecular<br />

mechanisms guiding vascular patterning in the brain, and (iii) using<br />

genetic screens to identify new genes important for brain vessel<br />

formation. We found that the basilar artery is formed by a novel<br />

process of medial sprouting and migration of endothelial cells from a<br />

bilateral pair of veins, the primordial hindbrain channels. Subsequent<br />

second wave of dorsal sprouting from the primordial hindbrain<br />

channels give rise to angiogenic central arteries that penetrate into<br />

the hindbrain. We have also discovered that chemokine signaling<br />

is required to direct basilar artery assembly. I will report on these<br />

and other novel molecular processes involved in the assembly of<br />

hindbrain vascular networks.<br />

S<br />

Coordinated branching morphogenesis of coronary<br />

vessels and peripheral sympathetic nerves in the<br />

developing heart<br />

Yosuke Mukoyama 1,2<br />

1<br />

National Institutes of Health, 2 National Heart, Lung, and Blood<br />

Institute<br />

Anatomical proximity and close patterning of peripheral nerves<br />

and blood vessels suggest that there is interdependence between<br />

the two networks. The first such indication of this interplay is the<br />

responsiveness of vascular development to signals secreted by<br />

peripheral sensory nerves in the developing skin. Interestingly, we<br />

discovered a reciprocal guidance event in the patterning of peripheral<br />

sympathetic nerves in the developing heart. Our whole-mount<br />

imaging approaches revealed that sympathetic axons branch alongside<br />

large-diameter coronary veins in the surface layer of the dorsal<br />

ventricular wall prior to innervating final targets such as coronary<br />

arteries and cardiomyocytes in the deeper myocardial layer. Further<br />

genetic studies and in vitro organ culture experiments demonstrated<br />

that coronary veins serve as an intermediate template that guides<br />

distal sympathetic axon projection via local secretion of NGF by<br />

coronary vascular smooth muscle cells. Our results suggest that target<br />

organs possess unique and stereotypical patterns of innervation,<br />

mediated by tissue sub-structures, such as coronary veins in the heart,<br />

which adapt to complex organ structure and physiology.<br />

S<br />

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76<br />

117 <br />

S<br />

Underlying mechanism that generates a phase wave<br />

in the mammalian circadian center<br />

1 1 1 1 2<br />

1<br />

2 <br />

S<br />

<br />

<br />

1,2<br />

1<br />

2 <br />

The suprachiasmatic nucleus (SCN) is the center of the mammalian<br />

circadian rhythm. Individual oscillating neurons have diverse<br />

endogenous circadian periods but usually they are synchronized by<br />

intercellular coupling mechanism. In the present study, we artificially<br />

disrupted the intercellular coupling among oscillating neurons in<br />

the SCN and observed the regional differences of the period of the<br />

oscillating small-latticed regions on the SCN by using a transgenic<br />

rat bearing a luciferase reporter gene driven by regulatory elements<br />

from a per2 clock gene (Per2::dluc rat). The analysis divided the<br />

SCN into two regions; one region showing periods less than 24h (SPR)<br />

and another region showing periods longer than 24 hours (LPR).<br />

The SPR lies in the medial smaller region of the dorsal SCN and the<br />

LPR occupied the remaining larger region. Interestingly, the SPR<br />

corresponds well with the region in which the phase wave in the SCN<br />

is launched. Further, we introduced a mathematical model in order to<br />

investigate the kinetics of the oscillators and the function of the short<br />

period region in the SCN.<br />

<br />

<br />

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in vivo Multiunit nueral<br />

activityin vivo MUA <br />

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2 JST, <br />

We spend almost one third of our life time just to sleep. Sleep/<br />

wakefulness cycle is a very intriguing physiological phenomenon.<br />

However, the mechanism regulating sleep/wakefulness cycle has<br />

not been completely understood so far. Although orexin neurons in<br />

the hypothalamus have a crucial role in the regulation of sleep and<br />

wakefulness, how orexin neuronal activity promotes wakefulness<br />

is incompletely understood. To further examine the role of orexin<br />

neuronal activity in sleep/wakefulness regulation, we generated<br />

transgenic mice in which orexin neurons expressed halorhodopsin,<br />

an orange light-activated chloride ion pump. Slice patch clamp<br />

recordings of orexin neurons demonstrated that photic illumination<br />

hyperpolarized and reduced the discharge rate of orexin neurons<br />

in a wavelength- and intensity-dependent manner. Acute silencing<br />

of orexin neurons in vivo by orange light illumination decreased<br />

electromyography power and increased the delta frequency in the<br />

electroencephalogram, indicative of slow wave sleep, and was timeof-day<br />

dependent. These findings suggest that activation of orexin<br />

neurons is necessary to keep animals awake during the light period.


117 77<br />

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mtDNA <br />

<br />

HG D Lancet 1998HG<br />

D4a Hum Genet 2007; PLoS One<br />

2009mtDNA <br />

HG N9a 2 Am J Hum Genet 2007<br />

Diabetes 2007<br />

HG N9b <br />

Hum Genet 2007HG A <br />

Mitochondrion 2007<br />

HG A HG M7a <br />

J Atheroscler Thromb 2010<br />

HG G1 <br />

HG F Br J Sports<br />

Med 2010mtDNA


78<br />

117 <br />

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2010<br />

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2010


117 79<br />

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117 83<br />

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<br />

<br />

<br />

By means of retrograde transneuronal transport of rabies virus,<br />

ascending multisynaptic pathways from the trigeminal ganglion (TG)<br />

to the anterior cingulate cortex (ACC) were identified in the rat. After<br />

rabies injection into an electrophysiologically-defined trigeminal<br />

projection region of the ACC, transsynaptic labeling of secondorder<br />

neurons via the medial thalamus (including the parafascicular<br />

nucleus) was located in the spinal trigeminal nucleus pars caudalis.<br />

Third-order neuron labeling occurred in the TG. Most of these TG<br />

neurons were medium-sized or large cells giving rise to myelinated<br />

Aδ or Aβ afferent fibers, respectively. Furthermore, the TG neurons<br />

retrogradely labeled with fluorogold injected into the mental nerve<br />

were smaller in their sizes compared to those labeled with rabies. Our<br />

extracellular unit recordings revealed that a majority of ACC neurons<br />

responded to trigeminal nerve stimulation with latencies of shorter<br />

than 20 ms. Thus, somatosensory information conveyed to the ACC<br />

by multisynaptic ascending pathways derived predominantly from<br />

myelinated primary afferents and may be used to subserve affectivemotivational<br />

aspects of pain.<br />

S<br />

<br />

<br />

<br />

<br />

TSNC<br />

Vmo<br />

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FG<br />

BDA<br />

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TSNC S1<br />

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Vmo <br />

Vmo <br />

Vmo <br />

Vmo <br />

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ACeRFp<br />

Vm ACe Vm<br />

RFp 2<br />

ACe RRF RFp <br />

GABA ACe RFp <br />

RRF 3<br />

PLH RFp Vm <br />

PLH Vm <br />

RFp <br />

ACe PLH PLH GABA<br />

<br />

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<br />

S<br />

ES <br />

1 2 2 2 2 <br />

1,2<br />

1<br />

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2<br />

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MSCs <br />

<br />

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MSCs ES<br />

MSCs <br />

<br />

Differentiation 2011ES MSCs<br />

<br />

ES MSCs <br />

<br />

<br />

24 ES MSCs <br />

<br />

CatWalkNoldus <br />

ES MSCs <br />

MSCs <br />

<br />

<br />

1


84<br />

117 <br />

S<br />

BFI FIB/SEM <br />

<br />

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1 1 1<br />

1<br />

2 <br />

<br />

/ <br />

<br />

iPS <br />

Muse PDGFRα <br />

<br />

SEM BFI<br />

FIB/SEM <br />

BFI <br />

SEM <br />

<br />

<br />

FIB/SEM SEM <br />

FIB BFI <br />

<br />

<br />

<br />

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3 <br />

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S<br />

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1 2 1 2 1<br />

1<br />

2 2 1 <br />

Mesenchymal stem cell, MSC<br />

<br />

MSC DSS <br />

<br />

MSC <br />

MSC <br />

MSC <br />

conditioned medium, MSCCM<br />

DSS <br />

IEC6 <br />

MALDITOFMS MSCCM <br />

MSCCM DSS <br />

IEC6 PI3KAkt <br />

<br />

<br />

T MSCCM<br />

VEGF, IL13, TIMP <br />

<br />

MSC gut trophic factor <br />

<br />

S<br />

Motile and immune functions of intestinal<br />

subepithelial myofibroblasts<br />

Islam Md Shafiqul, Hiroshi Ozaki<br />

Department of Veterinary Pharmacology, Graduate School of<br />

Agriculture and Life Sciences, The university of Tokyo<br />

Intestinal subepithelial myofibroblasts (ISMF) are a syncytium of<br />

α-SMA-positive, mesenchymal cells, which reside subjacent to the<br />

basement membrane of the small and large intestines. ISMFs are<br />

considered to mediate the movement of intestinal villi, regulation of<br />

epithelial cell proliferation and differentiation, and mucosal protection<br />

under physiological condition. ISMFs secrete many proinflammatory<br />

cytokines, growth factors, chemokines and other inflammatory<br />

mediators, as well as extracellular matrix proteins. This allows ISMF<br />

cells to act in a paracrine and autocrine fashion to mediate immune<br />

functions under pathological conditions. Extracellular matrices, such<br />

as collagen, fibronectins and tenascin C (TnC), secreted by ISMFs<br />

are important in tissue remodeling and tissue repair. Our laboratory<br />

findings have been demonstrated that TnC and α-SMA densely<br />

expressed in DSS-induced colitis model mice particularly at the sites<br />

of inflammation, as well as in SAMP1/Yit spontaneous ileitis model<br />

mice. We have also identified ISMF as one of the TnC producing<br />

cells in the intestine. In this symposium, I shall describe the recent<br />

development of ISMF research, especially focusing TnC.<br />

S<br />

<br />

<br />

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fibroblastlike<br />

cells PDGF α SK3 <br />

<br />

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<br />

<br />

CD34 1 <br />

<br />

<br />

ATP NO <br />

<br />

<br />

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PDGF <br />

α CD34 PDGF α <br />

NG2 <br />

ATP P


117 85<br />

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PBL<br />

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PBL<br />

14 10 400 <br />

120 1 <br />

PBL <br />

<br />

Cadaver Seminar <br />

<br />

S<br />

<br />

<br />

<br />

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23 <br />

<br />

1 <br />

30 <br />

<br />

55 35 <br />

<br />

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<br />

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S<br />

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<br />

2 <br />

<br />

2004 <br />

<br />

3 <br />

<br />

<br />

CT MRI<br />

<br />

<br />

<br />

<br />

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<br />

7080 34


86<br />

117 <br />

S<br />

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nonIT <br />

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15 WebCT<br />

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30 <br />

IT <br />

<br />

<br />

S<br />

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Arp2/3


117 87<br />

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1,2,3<br />

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CREST, JST 3 SENTAN, JST<br />

<br />

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3 <br />

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SN <br />

<br />

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Eos <br />

<br />

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<br />

Eos <br />

<br />

S<br />

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1,2 2<br />

1<br />

2 <br />

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<br />

<br />

20nm <br />

<br />

<br />

<br />

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II <br />

<br />

WASP, VASP, IQGAP1 <br />

<br />

<br />

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<br />

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<br />

S<br />

CEMOVIS <br />

<br />

1,2 1,2 1,3<br />

1<br />

2 CREST,JST 3 <br />

<br />

<br />

<br />

<br />

<br />

<br />

CEMOVISCryoElectron Microscopy of Vitreous<br />

Sections<br />

<br />

<br />

<br />

<br />

<br />

<br />

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<br />

<br />

CEMOVIS <br />

<br />

<br />

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S<br />

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SDS SDSFRL <br />

<br />

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SDSFRL


88<br />

117 <br />

S<br />

<br />

<br />

<br />

<br />

<br />

<br />

<br />

<br />

G1 <br />

DNA S <br />

G2 <br />

<br />

<br />

<br />

<br />

<br />

<br />

G2 <br />

<br />

G1 <br />

<br />

<br />

<br />

<br />

<br />

S<br />

<br />

<br />

<br />

<br />

Microtubule (MT) organization plays a key role in neuronal migration<br />

and axon/dendrite formation. Here we monitored the dynamics of<br />

centrosome and MT plus ends in neocortical neurons. In multipolar<br />

migrating neurons, newly emerging processes formed irrespective<br />

of the centrosome localization. The centrosome tended to move<br />

toward the dominant growing process. In locomoting neurons, which<br />

have a bipolar shape, the centrosome was targeted toward the piadirected<br />

leading process. However, the centrosome at the base of the<br />

leading process, in front of the nucleus, was occasionally overtaken<br />

by the translocating nucleus. When a locomoting neuron formed an<br />

axon-like trailing process opposite the direction of migration, the<br />

centrosome was located on the other side of the cell. MT growth in<br />

the leading processes of bipolar neurons was mostly directed toward<br />

the distal tip, while few bidirectional MT plus-end movements were<br />

detected in the trailing process. Depletion of gamma-tubulin in these<br />

neurons resulted in stacking of migration-defected neurons in the<br />

intermediate zone. Interestingly, neurons that managed to migrate into<br />

the cortical plate showed striking abnormalities in orientation.<br />

S<br />

<br />

<br />

1,2,3<br />

1<br />

<br />

2 <br />

3 <br />

<br />

<br />

<br />

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<br />

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<br />

<br />

<br />

<br />

<br />

<br />

S<br />

stathmin <br />

1 1,2,3 4 4 5 <br />

2 1,2,3<br />

1<br />

<br />

2 3 <br />

4 <br />

5 <br />

<br />

<br />

<br />

PACAP <br />

<br />

PACAP <br />

PACAP KO PACAP <br />

<br />

α/β tubulin <br />

stathmin1 Stathmin1 <br />

subgranular zone PACAP KO <br />

stathmin1 axon <br />

stathmin1 axon <br />

stathmin1 <br />

axon <br />

<br />

PACAP stathmin1 axon<br />

abnormal arborization <br />

<br />

stathmin1 adult neurogenesis <br />

stathmin1


117 89<br />

S<br />

C <br />

1 1 2<br />

1<br />

2 <br />

<br />

1 <br />

<br />

<br />

DA 5HT <br />

5HT 2C 5HT 2C R <br />

5HT 2C R <br />

5HT 2C R <br />

5HT 2C R 2 5AE <br />

RNA <br />

<br />

2 <br />

<br />

C57BL/6J RNA<br />

VXV 1.5 <br />

C3H/HeJ RNA <br />

5HT 2C R RNA <br />

ADAR1/2 <br />

5HT 2C R C57BL/6J <br />

<br />

5HT 2C R RNA <br />

<br />

S<br />

<br />

1,2 1 1<br />

1<br />

2 <br />

<br />

G GPCR <br />

<br />

GPCR <br />

<br />

<br />

<br />

<br />

GALP WNPW<br />

<br />

GALP NPW <br />

<br />

<br />

GALP NPW <br />

<br />

<br />

GALP <br />

<br />

GALP <br />

NPW <br />

<br />

<br />

S<br />

kisspeptin <br />

<br />

<br />

<br />

puberty<br />

<br />

<br />

<br />

<br />

GPR54 kisspeptin <br />

kisspeptin GnRH <br />

<br />

HPG<br />

axis kisspeptin kisspeptinHPG axis<br />

<br />

<br />

<br />

<br />

<br />

Kisspeptin<br />

<br />

<br />

<br />

Kisspeptin <br />

S<br />

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POMC


90<br />

117 <br />

S<br />

<br />

<br />

<br />

<br />

<br />

<br />

<br />

<br />

<br />

<br />

<br />

ER<br />

ER <br />

<br />

<br />

ERERαERβ<br />

<br />

ER <br />

2 ER <br />

<br />

<br />

<br />

<br />

<br />

S<br />

<br />

<br />

Fumiyo Aoyama, Nobuyasu Takahashi, Soyuki Ide,<br />

Akira Sawaguchi<br />

<br />

<br />

<br />

2 <br />

<br />

<br />

<br />

<br />

<br />

<br />

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H2 <br />

<br />

<br />

<br />

<br />

<br />

S<br />

<br />

<br />

1,2 1 1<br />

1<br />

2 <br />

IVCT <br />

in situ IVCT <br />

1 <br />

a BSA<br />

IVCT <br />

<br />

T BSA IgG <br />

b IVCT <br />

IgG <br />

<br />

2 IVCT <br />

focal adhesion kinase FAK <br />

FAK <br />

3 3 <br />

horseradish peroxidase<br />

/ <br />

IVCT <br />

IVCT <br />

<br />

<br />

S<br />

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<br />

<br />

<br />

<br />

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<br />

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FIBSEM <br />

<br />

<br />

Palade


117 91<br />

S<br />

Focused Ion BeamScanning Electron Microscopy<br />

FIBSEM Live imaging <br />

<br />

1,2<br />

1<br />

<br />

2<br />

Department of Neurosciences, Lerner Research Institute, Cleveland<br />

Clinic<br />

<br />

<br />

<br />

<br />

FIBSEM <br />

<br />

Na+ <br />

Ranvier NR Na+ <br />

NR <br />

<br />

NR Internode NR <br />

Slice <br />

Live imaging Na+K+ ATPase Internode <br />

NR <br />

<br />

FIBSEM Live imaging <br />

<br />

<br />

<br />

<br />

<br />

<br />

S<br />

CEACAM<br />

<br />

<br />

<br />

mRNA Differential Display<br />

5 Ceacam6 <br />

Ceacam6 isoform, Ceacam6L <br />

<br />

CEACAM6L <br />

<br />

apical Ectoplasmic Specialization <br />

<br />

CEACAM6L CEACAM6L<br />

<br />

CEACAM6L <br />

<br />

<br />

CEACAM CEACAM2 <br />

<br />

<br />

<br />

S<br />

<br />

<br />

<br />

<br />

3 <br />

<br />

<br />

<br />

<br />

<br />

Cell adhesion molecule1 Cadm1 <br />

Poliovirus receptor Pvr <br />

Nectin3 Nectin2 <br />

<br />

<br />

<br />

<br />

<br />

<br />

S<br />

<br />

<br />

<br />

<br />

<br />

<br />

<br />

immune priviliged organ


92<br />

117 <br />

S<br />

Implications of histone modification and DNA<br />

methylation during mouse spermatogenesis<br />

Ning Song, Takehiko Koji<br />

Department of Histology and Cell Biology, Nagasaki University<br />

Graduate School of Biomedical Sciences<br />

Epigenetic factors such as histone modification and DNA methylation<br />

have been implicated in the regulation of gene expression. However,<br />

the association of those factors with a specific stage of germ cells<br />

during spermatogenesis has not been fully understood. In the present<br />

study, we analysed DNA methylation states quantitatively in each<br />

germ cell by a novel method, HELMET. Histone H3 modifications<br />

were examined by immunohistochemistry. The methylation ratio<br />

of CCGG sequence gradually increased to a maximum in the<br />

stage from pachytene spermatocytes to round spermatids, and then<br />

declined. The increase in DNA methylation seemed to be correlated<br />

with deacetylation of histone H3, indicating genes are generally<br />

inactivated transcriptionally. We also found the promotion of histone<br />

H3 acetylation in parallel with DNA demethylation in elongating<br />

spermatids, may facilitate histone-protamine exchange. Interestingly,<br />

in vivo treatment of mice with 5-azadC reduced DNA methylation,<br />

but also induced H3K4me3 in spermatogonia accompanying with<br />

frequent apoptosis. These results indicate coordinate changes in the<br />

modifications of DNA and histone, and their close association with<br />

spermatogenesis.<br />

S<br />

Unique integration of fertilizationrelated protein<br />

Equatorin EQT into the acrosomal membrane<br />

during spermatogenesis<br />

Chizuru Ito, Kenji Yamatoya, Kiyotaka Toshimori<br />

Dept. Anatomy and Developmental Biology, Grad. Sch. Med., Univ.<br />

Chiba<br />

EQT is a widely distributed fertilization-related acrosomal protein in<br />

mammalian sperm. During the acrosome reaction some quantity of<br />

EQT is translocated on the plasma membrane covering the equatorial<br />

segment (ES) where sperm fuses with an oolemma, while the<br />

majority remains on the inner acrosomal membrane (IAM) until male<br />

pronucleus is formed. To analyze the nature of the EQT it is important<br />

to investigate its origin and expression during spermatogenesis. In<br />

this study we show the integration process of EQT in wild and EQT-<br />

EGFP transgenic mice using immunoelectron microscopy and highresolution<br />

light microscopy including STED nanoscopy. EQT mRNA<br />

was first detected in stage I-VII pachytene spermatocytes and then<br />

in step1-7 round spermatids. EQT protein was initially detected on<br />

the nascent outer acrosomal membrane of step 2 round spermatids<br />

and then gradually accumulated mainly on the IAM of the ES in<br />

elongating spermatids. EQT was not found acrosomal granules. We<br />

also found EQT forms complex with acrosomal matrices and the<br />

perinuclear theca (PT) by MS/MS analysis after immunoprecipitation.<br />

This evidence suggests EQT co-translocates associating with<br />

acrosomal matrices and PT.<br />

S<br />

<br />

<br />

<br />

<br />

<br />

<br />

<br />

<br />

<br />

<br />

3 4 <br />

<br />

<br />

<br />

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5 3 <br />

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<br />

Hox <br />

<br />

<br />

<br />

<br />

<br />

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S<br />

<br />

<br />

<br />

<br />

1996


117 93<br />

S<br />

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S<br />

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2 <br />

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Sabin 1902<br />

<br />

Huntington 1908<br />

Prox1 <br />

<br />

<br />

Sabin <br />

<br />

<br />

<br />

<br />

Isogai 2010


94<br />

117 <br />

S<br />

MRI <br />

MRTD <br />

1,2 2 1 3 4 <br />

4<br />

1<br />

2 <br />

3 4 <br />

<br />

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<br />

<br />

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99mTcphytat <br />

<br />

<br />

<br />

<br />

<br />

MRI MRM <br />

MRCP <br />

Magnetic<br />

ResonanceThoracic Ductography MRTD <br />

<br />

<br />

<br />

MRTD <br />

<br />

<br />

<br />

S<br />

Aspp <br />

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p53 Aspp1 <br />

Aspp1 <br />

Aspp1 / Aspp1 /<br />

<br />

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Aspp1 / <br />

<br />

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S<br />

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1,4 2 3 1 <br />

Brant Weinstein 4<br />

1<br />

2 <br />

3 <br />

4 Section on Vertebrate<br />

Organogenesis, NICHD, NIH<br />

<br />

<br />

<br />

<br />

<br />

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<br />

<br />

<br />

<br />

shear stress<br />

<br />

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<br />

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<br />

Huntington <br />

Kampmeier


117 95<br />

S<br />

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aPKCPAR <br />

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2<br />

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<br />

S<br />

<br />

<br />

<br />

<br />

<br />

<br />

<br />

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<br />

<br />

<br />

<br />

<br />

<br />

<br />

<br />

<br />

<br />

<br />

<br />

S<br />

<br />

<br />

<br />

axon initial segment, AIS Na <br />

<br />

AIS <br />

<br />

<br />

<br />

<br />

nucleus magnocellularis, NMAIS <br />

<br />

NM <br />

NM <br />

AIS <br />

NM <br />

<br />

NM AIS <br />

1.5 <br />

NM <br />

<br />

AIS


96<br />

117 <br />

S<br />

<br />

1,2 1,2 1 1,3 <br />

4 - 1 1,5 1 <br />

1 1,6 1<br />

1<br />

2 <br />

3<br />

JST, CREST 4 5 <br />

6 MRC <br />

<br />

Corticothalamic projection neurons (CTNs) in the cerebral cortex<br />

constitute an important component of the thalamocortical reciprocal<br />

circuit, an essential input/output organization for cortical information<br />

processing. However, the spatial organization of local excitatory<br />

connections to CTNs is only partially understood. Here, applying a<br />

newly developed adenoviral vector, we retrogradely visualized almost<br />

all layer (L) 6 CTNs from their cell bodies to fine dendritic spines in<br />

the rat barrel cortex. In cortical slices containing visualized L6 CTNs,<br />

we intracellularly stained single L2/3, L4, L5, and L6 pyramidal/<br />

spiny neurons and morphologically examined their local connections<br />

to CTNs. The CTNs received strong and focused connections from<br />

the L4 neurons just above them, and the most numerous nearby and<br />

distant sources of local excitatory connections to CTNs were CTNs<br />

themselves and L6 putative corticocortical neurons, respectively. The<br />

present results suggest that, through CTNs, L4 neurons together with<br />

L6 neurons may serve to modulate thalamic activity.<br />

S<br />

<br />

Recurrent connection selectivity of layer V pyramidal<br />

cells in frontal cortex<br />

1,2 1,2<br />

1<br />

2 <br />

Pyramidal cells in the neocortex are differentiated into several<br />

subgroups based on their extracortical projection targets. However,<br />

little is known regarding the relative intracortical connectivity<br />

of pyramidal cells specialized for their targets. We used paired<br />

recordings and quantitative morphological analysis to reveal<br />

distinct synaptic transmission properties, connection patterns, and<br />

morphological differentiation of rat frontal cortex. Retrograde<br />

tracers were used to label two projection subtypes in L5: crossedcorticostriatal<br />

(CCS) cells projecting to both sides of the striatum,<br />

and corticopontine (CPn) cells projecting to the ipsilateral pons.<br />

Although CPn/CPn and CCS/CCS pairs had similar connection<br />

probabilities, CPn/CPn pairs exhibited greater reciprocal connectivity,<br />

stronger unitary synaptic transmission, and more facilitation of<br />

paired-pulse responses. These synaptic characteristics were strongly<br />

correlated to the projection subtypes. CPn and CCS cells were further<br />

differentiated in their dendritic/ axonal arborization. Together, our<br />

data demonstrate that the pyramidal projection system is segregated<br />

according to subcortical target.<br />

S<br />

A Hz Oscillation Synchronizes Prefrontal, VTA, and<br />

Hippocampal Activities during Working memory<br />

Gyorgy Buzsaki<br />

Rutgers University<br />

Network oscillations support transient communication across brain<br />

structures. We show here, in rats, that task-related neuronal activity<br />

in the medial prefrontal cortex (PFC), hippocampus and ventral<br />

tegmental area (VTA), regions critical for working memory, is<br />

coordinated by a 4-Hz oscillation. A prominent increase of power<br />

and coherence of the 4-Hz oscillation in the PFC and VTA and its<br />

phase-modulation of gamma power in both structures was present<br />

during working memory. Subsets of both the PFC and hippocampal<br />

neurons predicted the turn choices of the rat. The goal-predicting<br />

PFC pyramidal neurons were more strongly phase-locked to both<br />

4-Hz and hippocampal theta oscillations than non-predicting cells.<br />

The 4-Hz and theta oscillations were phase-coupled and jointly<br />

modulated both gamma waves and neuronal spikes in the PFC, VTA<br />

and hippocampus. Thus, multiplexed timing mechanisms in the PFC-<br />

VTA-hippocampus axis may support processing of information,<br />

including working memory.<br />

S<br />

Development of orientation and direction selectivity<br />

in the mouse visual cortex<br />

1,2 Nathalie Rochefort 2 Christine Grienberger 2 <br />

Nima Marandi 2 Daniel Hill 2 Arthur Konnerth 2<br />

1<br />

2 Inst. Neuroscience, Technical<br />

Univ. Munich<br />

Functional features of the cortical neurons such as direction<br />

selectivity (DS) in the visual cortex are established during<br />

development. Previous studies of the ferret visual cortex implied<br />

that experience-dependent plasticity of local circuits in the cortex<br />

contributed to the development of DS. In spite of their usefulness, it<br />

has been less understood that how the rodent visual system develops.<br />

Here we used two-photon Ca 2+ imaging to study the development of<br />

DS in layer 2/3 neurons of the mouse visual cortex in vivo. At eyeopening,<br />

nearly all orientation-selective neurons were also directionselective.<br />

DS developed normally in dark-reared mice, indicating that<br />

the early development of DS is independent of vision. Furthermore,<br />

remarkable functional similarities existed between the development<br />

of DS in cortical neurons and the previously reported development<br />

of DS in the mouse retina. Together, these findings suggest a new<br />

experience-independent circuit mechanism for the development of DS<br />

in the mammalian brain. Since rodents lack columnar organization<br />

in the visual cortex, difference in the local connectivity may explain<br />

different developmental profile between species.


117 97<br />

W<br />

WG <br />

1,2<br />

1<br />

2 <br />

<br />

<br />

<br />

WG <br />

<br />

<br />

<br />

<br />

<br />

<br />

MDPhD <br />

<br />

<br />

3 MD<br />

PhD <br />

<br />

<br />

<br />

<br />

<br />

<br />

<br />

<br />

W<br />

<br />

<br />

1 1,2<br />

1<br />

<br />

2 <br />

<br />

<br />

<br />

<br />

<br />

<br />

4 <br />

<br />

<br />

2006 <br />

<br />

<br />

17 30 <br />

<br />

<br />

4 <br />

2010 2 <br />

<br />

<br />

<br />

<br />

<br />

W<br />

<br />

<br />

1 2<br />

1<br />

2 <br />

<br />

<br />

<br />

<br />

<br />

<br />

<br />

14 PhDMD <br />

20 MD <br />

23 <br />

<br />

<br />

<br />

<br />

<br />

<br />

<br />

<br />

<br />

MD <br />

<br />

<br />

<br />

W<br />

<br />

1 2 2 3 <br />

1 1 1<br />

1<br />

2 M2 3 M4 <br />

<br />

<br />

<br />

<br />

<br />

<br />

<br />

<br />

<br />

<br />

<br />

<br />

<br />

<br />

<br />

1


98<br />

117 <br />

W<br />

<br />

<br />

<br />

<br />

<br />

<br />

<br />

<br />

<br />

<br />

CBT <br />

<br />

<br />

<br />

<br />

<br />

<br />

<br />

<br />

<br />

<br />

<br />

<br />

<br />

<br />

W<br />

<br />

<br />

<br />

<br />

23 MDPhD <br />

2-4 <br />

3 <br />

1 <br />

<br />

<br />

<br />

19 <br />

<br />

<br />

<br />

MDPhD 8


117 99<br />

OEPMI<br />

Singleneuron tracing study of thalamocortical projections arising<br />

from the rat mediodorsal nucleus<br />

<br />

<br />

The mediodorsal thalamic nucleus (MD) receives inputs from a wide variety of<br />

subcortical structures, such as the amygdala, basal forebrain and brain stem, and<br />

projects its axons to the prefrontal cortex. The MD have been considered to play<br />

important roles in learning, working memory, emotion, and behavioral control.<br />

In the present study, we investigated dendritic and axonal arborizations of single<br />

MD neurons in rats using Sindbis viral vectors expressing membrane-targeted<br />

green or monomeric red fluorescent protein. Single MD neurons infected with<br />

the viral vectors were completely visualized by immunoperoxidase staining for<br />

fluorescent protein, and reconstructed. When the axons exited from the thalamus,<br />

the reconstructed MD neurons always emitted axon collaterals to the thalamic<br />

reticular nucleus. Two of the 6 reconstructed MD neurons formed abundant axon<br />

bush in the neostriatum. In the cerebral cortex, the MD neurons sent axon fibers<br />

mainly to middle layers of the orbital, prelimbic, cingulate and frontal association<br />

areas. Thus, MD neurons would be classified into core thalamic neurons according<br />

to Jones (1998, 2001).<br />

OEPMI<br />

V <br />

Stefan Trifonov <br />

<br />

Calbindin D28K<br />

Calbindinpoor compartment <br />

Calbindinpoor compartment <br />

<br />

Calbindinpoor compartment <br />

GAD1 mRNA Cannabinoid type 1 receptor<br />

CB1 mRNA in situ hybridization <br />

1 Calbindinpoor<br />

compartment Anterior, Middle, Posterior 3 <br />

2 GAD1 mRNA Middle region 3 CB1<br />

mRNA 3 4 Anterior region Posterior region<br />

<br />

Middle region V <br />

OEPMI<br />

<br />

<br />

<br />

<br />

D1 D2 D1RD2R<br />

<br />

D1R D2R in situ <br />

<br />

D1R<br />

mRNA D2R mRNA <br />

D1R D2R <br />

<br />

D2R <br />

<br />

<br />

<br />

<br />

D1R D2R <br />

<br />

<br />

<br />

<br />

OEPMI<br />

GABA <br />

<br />

<br />

<br />

PV GABA<br />

<br />

<br />

Correlated CLSMEM <br />

<br />

4 PV <br />

<br />

vGLuT2 <br />

driving input <br />

4 PV PV <br />

4 PV <br />

2/3 <br />

PV <br />

<br />

CA1 <br />

<br />

<br />

<br />

OEPMII<br />

BAF dpf GFP <br />

<br />

<br />

<br />

BAF 10 <br />

DNA <br />

BAF <br />

esBAFnpBAF<br />

nBAF ES <br />

<br />

<br />

zinc Dpf1 nBAF <br />

BAF45b <br />

Dpf1 <br />

<br />

tTAEGFP <br />

dpf1 <br />

dpf1tTAGFP 24 <br />

GFP 48 <br />

<br />

dpf1 GFP <br />

Dpf1 <br />

Dpf1 <br />

OEPMII<br />

mRNA <br />

1 2 2 1<br />

1<br />

2 <br />

<br />

<br />

<br />

<br />

<br />

<br />

mRNA <br />

<br />

<br />

<br />

<br />

mRNA <br />

<br />

<br />

RNA <br />

<br />

RNA <br />

mRNA


100<br />

117 <br />

OEPMII<br />

Immunocytochemical and proteomic analysis of the γsecretase<br />

complex using the conformationspecific antiNicastrin antibody<br />

1,2 2 4 3 4 5 <br />

2<br />

1<br />

2 3 <br />

4 5 <br />

<br />

γSecretase is a membranespanning, multimeric protease that cleaves APP and<br />

is responsible for generating the Aβ peptides. Although the intracellular traffic is<br />

implicated in the regulation of the Aβ production, exact subcellular location where<br />

the enzyme functions remains controversial. Here we established a monoclonal<br />

antibody A5226A against Nicastrin, one of the γsecretase components, and found<br />

that A5226A specifically recognizes the active γsecretase. Immunocytochemistry<br />

using A5226A revealed that γsecretase localizes at the cell surface and late<br />

endosome. Moreover, we applied A5226A for the targeted proteomics of the<br />

γsecretase complex. We identified about 30 interacting proteins including<br />

tetraspanin family members such as CD81, which are known to form membrane<br />

microdomains. We found that knockdown of CD81 reduced the secretion of Aβ.<br />

Furthermore, the internalization rate of both the enzyme and APP was reduced<br />

by knockdown. These results suggest that CD81 affects the Aβ generation via<br />

regulating the traffic of the enzyme and the substrate from the cell surface.<br />

OFPMI<br />

Rho ROCK, ROCK<br />

1,2 2 2 1 1 <br />

1 2<br />

1<br />

2 <br />

GTP Rho <br />

Rho <br />

Rho Rho <br />

Rho <br />

Rho ROCK1, ROCK2<br />

<br />

Rho <br />

ROCK1 ROCK2 <br />

ROCK1 <br />

ROCK2 <br />

ROCK1 <br />

ROCK2 <br />

ROCK2 <br />

<br />

<br />

Rho <br />

<br />

OFPMI<br />

Photoactivatable Rac <br />

<br />

<br />

GTPase Rac1 <br />

<br />

<br />

phototropin LOV2 GTP Rac1 photo<br />

activatable PARac1 <br />

PARac1 <br />

RAW Rac1<br />

photo<br />

manipulation<br />

mCherry PARac1 <br />

<br />

<br />

<br />

<br />

<br />

<br />

<br />

Rac1 <br />

<br />

OFPMI<br />

GaAsP LIVE <br />

<br />

1 2 1 1 3 <br />

1<br />

1<br />

2 3 <br />

<br />

<br />

<br />

<br />

<br />

A1, A2, A5LIVE <br />

GaAsP<br />

<br />

<br />

<br />

GaAsP <br />

GFP <br />

BSC1<br />

LIVE <br />

GaAsP <br />

A1, A2, A4, A5 A7 <br />

<br />

<br />

OFPMI<br />

E <br />

CD<br />

<br />

1<br />

229EHCoV229E CD13 <br />

<br />

<br />

HCoV229E <br />

CD13 <br />

<br />

HCoV229E CD13 <br />

CD13 <br />

1 CD13 <br />

2<br />

mCherryβactin<br />

EGFPlifeact CD13 Factin <br />

CD13 Factin <br />

cytochalasin Blatrunculin A actin<br />

CD13 Factin <br />

<br />

CD13 Factin <br />

OFPMII<br />

Nphp <br />

<br />

<br />

<br />

650 <br />

<br />

Nphp3 Nphp3 1325 <br />

coiledcoilCC<br />

Nphp3 <br />

<br />

<br />

Nphp3GFP <br />

<br />

<br />

Nphp3 N 200 <br />

N N <br />

CC 2 Nphp3 <br />

Nphp3 <br />

Kif7, Tctn2, Arl6 <br />

Nphp3


117 101<br />

OFPMII<br />

<br />

1 2 3 2 3 2 <br />

3 1<br />

1<br />

2 <br />

3 <br />

<br />

Cilia show variations in axonemal structure, motility, and the number per<br />

cell, and are classified into subtypes. Depending on the tissue origin and<br />

differentiation status, one cell type appears to adopt a certain ciliary subtype. We<br />

are characterizing unique, multiple 9+0 cilia in choroid plexus epithelial cells<br />

CPECs to elucidate the mechanism of ciliary diversification. Proteomic analysis<br />

of CPEC cilia identified 868 proteins, including several molecules implicated in<br />

ciliary motility such as Rsph9. Immunostaining for Rsph9 demonstrated that the<br />

molecule localized to a subpopulation of CPEC cilia. Live imaging of choroid<br />

plexus tissue exhibited that some CPEC cilia could beat vigorously at the neonatal<br />

stage, whereas others were nonmotile. The beating pattern, frequency, amplitude,<br />

and orientation were also variable and different from those of typical 9+2 cilia of<br />

ependyma. Transmission electron microscopy revealed the coexistence of 9+0 and<br />

9+2 configuration in neonatal CPEC. Overall, our results demonstrated striking<br />

molecular, functional, and ultrastructural heterogeneities in neonatal CPEC cilia,<br />

providing substantial novel insight on ciliary diversification.<br />

OFPMII<br />

PACAP <br />

1,2 1 1 1 1 <br />

1 1 2 3 3 3 <br />

1<br />

1<br />

2 3 <br />

<br />

<br />

PACAPKO<br />

PACAP <br />

PACAP <br />

PACAP <br />

PACAP <br />

PACAP cAMP<br />

PKA 30 <br />

PACAP AC<br />

<br />

AQP5 <br />

PACAPKO AQP5 <br />

PACAP 30 AQP5 <br />

AQP5 <br />

PACAP AC <br />

PACAP AC/cAMP/PKA <br />

AQP5 <br />

<br />

OGPMI<br />

microCTmicroMRI <br />

<br />

1,2 3 4 5 6 7<br />

1<br />

JST 2 3 <br />

4<br />

5 6 <br />

7 <br />

<br />

<br />

microCT microMRI <br />

<br />

<br />

microCTmicroMRI <br />

<br />

<br />

microCT CTmicroMRI <br />

<br />

<br />

CTMRI <br />

<br />

CT <br />

0.1<br />

mm <br />

<br />

<br />

OGPMI<br />

<br />

OGPMI<br />

HyperDry <br />

1 1 1 1 2<br />

1<br />

2 <br />

3<br />

<br />

HyperDry HD<br />

HD FD <br />

<br />

φ25 mm <br />

Swinnex, SX0002500, <br />

50 ml <br />

<br />

1 ml<br />

50ml 1 ml <br />

185 mmAq730 mmAq<br />

133 mmAq <br />

<br />

730 mmAq FD=3.7 ul/min, HD=1.5 ul/min FDHD <br />

FD <br />

HD FD <br />

<br />

<br />

OGPMI<br />

<br />

1 2 2 2 2 <br />

2 2 2 2 2 2 <br />

1 1 1 1<br />

1<br />

2 <br />

<br />

<br />

<br />

<br />

8 BALB/c <br />

4 mm <br />

<br />

3 0.1 mL <br />

Scion image <br />

6 <br />

1.71 14 0.38 <br />

3 <br />

0.49 0.65 0.81 <br />

7 0.80 6 0.86 <br />

9 1.19 14 <br />

3 14


102<br />

117 <br />

OGPMII<br />

<br />

<br />

<br />

<br />

<br />

<br />

<br />

<br />

<br />

<br />

MMC 3T3Feader Fibrin <br />

SHEM DMEMF12 10% FBS<br />

<br />

<br />

<br />

<br />

<br />

<br />

<br />

<br />

Collagen Type <br />

<br />

<br />

OGPMII<br />

Muse iPS <br />

<br />

<br />

<br />

Muse Multilineagedifferentiating Stress Enduring <br />

SSEA3 <br />

CD105 <br />

<br />

Muse <br />

<br />

iPS <br />

iPS <br />

iPS <br />

Muse <br />

<br />

iPS <br />

Muse iPS <br />

Muse iPS <br />

<br />

<br />

Muse iPS <br />

<br />

OGPMII<br />

Monitoring DNA damage levels using γHAX detection in vivo<br />

1,2 Christophe Redon 2 William Bonner 2 1<br />

1<br />

2 National Institutes of<br />

Health<br />

DNA double strand break DSB is one major initial cause of genomic instability<br />

leading to cancer. The creation of a DNA DSB in eukaryotic cells is generally<br />

accompanied by the formation of hundreds of phosphorylated H2AX γH2AX<br />

molecules in the chromatin flanking the DSB site. Antibodies to γH2AX allow<br />

the visualization of a “focus” at the DSB site. Since it has been demonstrated that<br />

the numbers of γH2AX foci correlate directly to the numbers of DNA DSB, the<br />

detection of γH2AX is an attractive candidate for monitoring DNA DSB levels.<br />

For medical purpose, the ability to quantify DNA damage levels in cancer patients<br />

during ongoing drugs/radiation therapy is a useful tool for optimizing treatment.<br />

Recently, we evaluated γH2AX biodosimetry in a study using nonhuman<br />

primates subjected to totalbody irradiation. We successfully applied γH2AX<br />

assay to monitor DNA damage in vivo and assessed γH2AX as a biodosimeter of<br />

radiation exposure. In addition, we performed preliminary experiments to detect<br />

γH2AX in cancer patients during chemotherapy. Being able to routinely monitor<br />

DSB levels in individuals could provide useful tools for improving human health.<br />

OHPM<br />

<br />

<br />

<br />

<br />

<br />

116 <br />

<br />

<br />

<br />

PHZ<br />

NBP<br />

<br />

TER119 <br />

CD71 PCNA <br />

<br />

TER119 <br />

<br />

RTPCR GATA1 <br />

GATA2 <br />

<br />

<br />

<br />

definitive <br />

<br />

OHPM<br />

MS <br />

<br />

<br />

<br />

<br />

<br />

<br />

<br />

Pentaerythritol triacrylate Ethyleneglycol dimethacrylate <br />

Methacrylic acidglycidyl methacrylate <br />

G02 <br />

MS5 <br />

CD34 CD34+ <br />

G02 MS5 MS5 <br />

CD34+ <br />

12 <br />

<br />

<br />

MS5 <br />

CD34+ <br />

<br />

<br />

OHPM<br />

<br />

1 1 1 2 3 <br />

Richard Wong 1<br />

1<br />

2 3 <br />

<br />

RNA <br />

30 <br />

<br />

AML<br />

NUP98 <br />

HOXA9 <br />

RAE1 <br />

<br />

NUP98 <br />

RAE1 <br />

NUP98 RAE1 <br />

NUP98 NUP98<br />

HOXA9 NUP98HOXA9 <br />

NUP98HOXA9 RAE1 <br />

AML <br />

RAE1NUP98 RAE1<br />

NUP98


117 103<br />

OHPM<br />

Two immunogenic passenger DC subsets in the rat liver with a<br />

distinct trafficking pattern and radiosensitivity<br />

<br />

<br />

To examine the phenotype, radiation sensitivity, trafficking pattern, and<br />

allosensitizing capabilities of conventional dendritic cell cDC subsets in<br />

liver graft rejection in rats, liver cDCs were examined by FACS or multicolor<br />

immunohistochemistry.<br />

We demonstrate two distinct immunogenic DC subsets. One is a CD172a+CD11b<br />

subset we previously reported that readily undergoes bloodborne migration<br />

to the recipient’s secondary lymphoid organs inducing systemic CD8+ Tcell<br />

responses. Another is a CD172a+CD11b+ subset that steadily appear in hepatic<br />

lymph. After transplantation, this subset further migrates to the parathymic lymph<br />

nodes, regional peritoneal cavity nodes, or partly persist in the graft and induces<br />

CD8+ Tcell responses there. Irradiation completely eliminated the migration and<br />

immunogenicity of the first subset, but only partly suppressed the migration of the<br />

second one. In this situation the grafts were acutely rejected and intragraft CD8+<br />

Tcell and regulatory Tcell responses were unchanged.<br />

In conclusion rat liver cDCs contain at least two distinct immunogenic passenger<br />

subsets; a radiosensitive bloodborne migrant and relatively radioresistant lymph<br />

borne migrant.<br />

OHPM<br />

<br />

1,3 1,2 3 1<br />

1<br />

2 3 <br />

<br />

<br />

CT SMA<br />

30 <br />

2 <br />

2 <br />

<br />

<br />

CT -SMA <br />

Image J Photoshop Elements9 <br />

CTSMA 5° <br />

20 <br />

20.12.9 mm CT Th12 12 L1 8 <br />

CT 1.610.41/ 0.350.17SMA <br />

0.840.38/ 0.480.14CTSMA 0.780.17/ 0.130.10 <br />

CT 0.370.12/ 0.400.15SMA 0.380.12/ 0.37<br />

0.12 CTSMA 10.8°8.6° <br />

CT SMA 3 15% CT SMA <br />

1 5% 20% <br />

<br />

OHPM<br />

<br />

1 2<br />

1<br />

2 <br />

10 nm <br />

Z <br />

<br />

<br />

<br />

<br />

<br />

<br />

<br />

<br />

<br />

<br />

<br />

<br />

<br />

<br />

<br />

OHPM<br />

<br />

<br />

<br />

<br />

pericyte<br />

Hashitani et al. 2011<br />

<br />

<br />

<br />

α <br />

<br />

cKit <br />

P <br />

ChAT <br />

<br />

<br />

<br />

<br />

<br />

<br />

<br />

<br />

OIPM<br />

α <br />

1 2 2 Gerald W Hart 3 2 <br />

1<br />

1<br />

2 3 Dept. Biol.<br />

Chem., Johns Hopkins Univ. Sch. Med<br />

O<br />

N OGlcNAc <br />

<br />

<br />

<br />

GK OGlcNAc <br />

OGlcNAc <br />

α 4<br />

ATP synthase OGlcNAc <br />

115 <br />

α 4 GK <br />

<br />

α 4 <br />

<br />

OGlcNAc 4 in situ Proximity<br />

Ligation Assay <br />

OIPM<br />

L LFABP <br />

1 2 2 1 <br />

1 2 1<br />

1<br />

2 <br />

<br />

L <br />

LFABP <br />

LFABP <br />

LFABP <br />

LFABP Tg II<br />

AngII Ang II <br />

4 <br />

<br />

<br />

LFABP <br />

LFABP LFABP <br />

LFABP <br />

LFABP


104<br />

117 <br />

OIPM<br />

EDA <br />

<br />

<br />

<br />

<br />

<br />

TGFβ1 <br />

<br />

TGFβ1 <br />

TGFβ1 24 <br />

FN EDA 48 α<br />

αSMA<br />

<br />

EDA 48 <br />

αSMA <br />

TGFβ1 <br />

FN EDA TGFβ1 <br />

<br />

EDA <br />

<br />

OIPM<br />

Fertilization analyzed by live imaging in the mouse<br />

Kiyotaka Toshimori, Chizuru Ito, Kenji Yamatoya, Mamiko Maekawa,<br />

Yoshiro Toyama<br />

Dept. Anatomy and Developmental Biology, Grad. Sch. Med., Univ. Chiba<br />

In order to analyze the fertilization process, it is important to visualize the events<br />

continuously induced during spermegg interaction. We analyzed the fertilization<br />

process by live imaging in the mouse, focusing on the relationship between<br />

pronucleus formation and fate of inner acrosomal membrane protein Equatorin<br />

EQT.<br />

Eggs interacting with fertilizing sperm in vivo were removed from oviduct<br />

and analyzed by live images, including immunofluorescence microscopy with<br />

antibodies against various sperm components and EQTEGFPtransgenic mice,<br />

under Olympus IX71 microscope equipped with high resolution Roper and<br />

CSU razor system Yokogawa. Sperm head was internalized and completely<br />

decondensed, releasing EQT in the ooplasm; it was before the initiation of<br />

the tail entry. Female pronucleus formation, in which a second polar body is<br />

released into the perivitelline space, started a bit faster than the male pronucleus<br />

formation, which was induced in the fertilization cone. It took about 90min to<br />

start the fertilization cone formation after spermegg fusion. Other live images<br />

and corresponding structural changes at early spermegg interaction stage will be<br />

presented.<br />

OIPM<br />

<br />

<br />

1 3 1,2 1 1 <br />

1 1,2<br />

1<br />

2 3 Dept. Pharmacology,<br />

Physiology and Toxicology, Marshall Univ. Joan C. Edwards School of Med. USA<br />

DecaBDE<br />

DecaBDE <br />

<br />

<br />

<br />

DecaBDE <br />

DecaBDE <br />

<br />

CTTN ERK 1/2SRC <br />

DecaBDE <br />

DecaBDE <br />

ICR 1-5 <br />

12 <br />

<br />

<br />

DecaBDE <br />

<br />

OIPM<br />

microRNA <br />

<br />

1 1 2 3 4 3 <br />

2 3<br />

1<br />

2 3 <br />

4<br />

<br />

microRNAmiRNA <br />

PE miRNA <br />

<br />

PE <br />

RNA GAIIx TaqManq<br />

Array in silico <br />

laser microdissection [LMD]realtime PCRWestern<br />

blot BeWo miRNA <br />

3’UTR<br />

1,000 <br />

667 PE 22 <br />

PE miRNA In silico 5 PE miRNA<br />

<br />

HSD17B1 PE HSD17B1 <br />

mRNA <br />

PE miRNA miR210 miR518c <br />

LMD miRNA <br />

<br />

miR210 miR518c HSD17B1 <br />

PE miRNA <br />

<br />

OEAMIII<br />

<br />

<br />

<br />

C3<br />

<br />

<br />

Lenhossék <br />

86, p9, 2011<br />

<br />

<br />

C1, 2 <br />

Isl1 <br />

Nkx2.2 <br />

C3 Lenhossék <br />

<br />

2 <br />

Phox2b <br />

<br />

<br />

<br />

<br />

OEAMIII<br />

NPY <br />

<br />

<br />

Y<br />

NPY NPY <br />

<br />

NPY<br />

<br />

<br />

NPY <br />

NPY <br />

80% NOS NPY <br />

40% 90% <br />

NOS NPY <br />

NOS TH <br />

NPY NOS ChAT<br />

NPY TH <br />

NPY <br />

ChAT/NPY NOS/NPY <br />

NOS/NPY


117 105<br />

OEAMIII<br />

<br />

<br />

<br />

<br />

<br />

<br />

<br />

<br />

PHAL<br />

<br />

<br />

SD T910 <br />

2.5%PHAL 30 μm <br />

<br />

<br />

700 μm2.3 mm <br />

<br />

<br />

<br />

<br />

<br />

<br />

<br />

<br />

OEAMIII<br />

gastrin<br />

releasing peptide <br />

1 1 Andrew Dobberfuhl 2 Lesley Marson 2<br />

1<br />

2 Division of Urologic<br />

Surgery, School of Medicine, The University of North Carolina at Chapel Hill,<br />

NC, USA<br />

gastrinreleasing peptide<br />

GRP<br />

<br />

PRV<br />

SNB<br />

<br />

<br />

GRP <br />

PRV <br />

GRP <br />

PRV 2 <br />

PRV/GRP <br />

GRP PRV SNB<br />

GRP <br />

SNB <br />

GRP <br />

<br />

OEAMIV<br />

TRPV <br />

<br />

<br />

<br />

<br />

CPECs <br />

<br />

TRPV4 <br />

<br />

CPECs TRPV4 mRNA <br />

CPECs <br />

TRPV4 <br />

TRPV4 CPECs <br />

<br />

TRPV4 GSK101670A <br />

CPECs <br />

CPECs <br />

CPECs <br />

TRPV4 <br />

<br />

OEAMIV<br />

Hh <br />

<br />

<br />

<br />

Hh <br />

Hh Patched Ptc<br />

Smoothened Smo <br />

<br />

Hh <br />

<br />

Schwann SC Hh <br />

/SC <br />

<br />

SC SC Ptc Smo<br />

<br />

SC Hh <br />

Hh <br />

<br />

<br />

SC Hh <br />

<br />

OEAMIV<br />

AP Notch <br />

1 2 3 4 1<br />

1<br />

2 3 <br />

4 <br />

<br />

AP1 <br />

<br />

<br />

<br />

<br />

<br />

AP1 <br />

<br />

AP1 Notch <br />

Notch <br />

AP1 RNAi <br />

AP1 <br />

CG8538 CG8538 AP1 <br />

Aftiphilin dAP1 <br />

CG8538p/dAftiphilin dAP1 <br />

Notch <br />

<br />

OEAMV<br />

MAPA supports NMDAreceptor transport for synaptic plasticity<br />

1 1 2 2 <br />

1<br />

1<br />

2 BSI<br />

Microtubuleassociated protein 1A MAP1A is one of the major components of<br />

the neuronal cytoskeleton. To examine the role of MAP1A, we generated mutant<br />

mice lacking MAP1A. Through analysis of their phenotypes, we found that<br />

MAP1A knockout mice exhibited severe memory disturbances. The MAP1A<br />

knockout neurons revealed reduced surface expression of NMDAreceptors<br />

concomitant with a decrease in NMDAdependent postsynaptic current and long<br />

term potentiation LTP. Reduced NMDA receptor transport underlay the altered<br />

receptor function. These results suggest that MAP1A supports the transport of<br />

NMDAreceptors and synaptic plasticity in neuronal dendrites.


106<br />

117 <br />

OEAMV<br />

Homera regulates the activityinduced remodeling of synaptic<br />

structures in cultured hippocampal neurons<br />

1 2 1 1 1 <br />

1 1 1 1<br />

1<br />

2 <br />

<br />

Homer1a LTP seizure <br />

PSD95 Homer1cFactin <br />

<br />

1h <br />

<br />

4h8hshRNA Homer1a <br />

knock down <br />

Homer1a <br />

OEAMV<br />

PIPKα regulates neuronal microtubule depolymerase KIFA and<br />

suppresses elongation of axon branches<br />

1,2,3 1,2 1 4 4 <br />

1<br />

1<br />

2 3 <br />

4 <br />

Neuronal morphology is regulated by the cytoskeleton. Kinesin superfamily<br />

protein 2A KIF2A depolymerizes microtubules MTs at growth cones and<br />

regulates axon pathfinding. The factors regulating KIF2A in neurite development<br />

remain elusive. Here, using immunoprecipitation with an antibody specific to<br />

KIF2A, we identified phosphatidylinositol 4phosphate 5kinase PIPK as a<br />

candidate membrane protein that regulates the activity of KIF2A. Yeast two<br />

hybrid and biochemical assays demonstrated direct binding between KIF2A and<br />

PIPKα. Partial colocalization of the clusters of punctate signals for these two<br />

molecules was detected by confocal microscopy and photoactivated localization<br />

microscopy. Additionally, the MTdepolymerizing activity of KIF2A was<br />

enhanced in the presence of PIPKα in vitro and in vivo, suggesting a novel PIPK<br />

mediated mechanism controlling MT dynamics in neurite remodeling.<br />

OFAMIII<br />

SNAP <br />

<br />

<br />

<br />

<br />

<br />

<br />

SNARE SNARE <br />

SNAP23 SNAP23 tSNARE<br />

<br />

<br />

<br />

SNAP23 SNAP23<br />

<br />

SNAP23 <br />

<br />

CreloxP <br />

NestinCre <br />

2<br />

<br />

SNAP23 <br />

<br />

OFAMIII<br />

<br />

<br />

<br />

<br />

<br />

<br />

<br />

<br />

GM130 <br />

GBF1 <br />

<br />

810 <br />

<br />

<br />

<br />

GM130 GBF1 <br />

GM130 GBF1 <br />

<br />

<br />

<br />

<br />

OFAMIII<br />

<br />

1 1 2<br />

1<br />

2 <br />

<br />

<br />

<br />

7 30 <br />

15 <br />

20 <br />

<br />

15 <br />

δ2 <br />

15 <br />

δ2 20 <br />

δ2 <br />

<br />

α2 15 <br />

20 <br />

<br />

<br />

OFAMIII<br />

Input pathway and target cell typedependent regulation of synaptic<br />

AMPAR subunits in hippocampal CA region<br />

1 2 3 3 3 <br />

1<br />

1<br />

Department of Anatomy, Hokkaido University Graduate School of Medicine,<br />

2<br />

Department of Anatomy, Kitasato University School of Medicine, 3 Department of<br />

Cellular Neurobiology, Brain Research Institute, Niigata University<br />

The AMPAtype glutamate receptor AMPAR is a tetramer of GluA subunits<br />

GluA1A4. Subunit combinations and contents of synaptic AMPAR are the<br />

major determinants of physiological properties of glutamatergic synapses. In<br />

the present study, the composition of synaptic AMPAR was investigated using<br />

subunitspecific antibodies and riboprobes in the mouse hippocampal CA1.<br />

Multiplelabeling in situ hybridization revealed that the subunit combination<br />

in pyramidal cells was GluA1, GluA2, and GluA3. Interneurons were high for<br />

GluA1, GluA3, and GluA4, and almost negative for GluA2. Exceptionally,<br />

parvalbumin PVpositive cells expressed all four subunits at high levels.<br />

Quantitative immunogold analyses revealed that labeling densities in Schaffer<br />

collateralCA1 pyramidal cell synapses were much higher than those in perforant<br />

path synapses, showing input pathwaydependent distribution. Synapses on PV<br />

positive cells displayed 23 times higher labeling densities for all four subunits<br />

than those on PVnegative interneurons. These results indicate that the subunit<br />

combinations and content of synaptic AMPAR are differently regulated by input<br />

pathway and target cell typedependent manners.


117 107<br />

OFAMIV<br />

<br />

<br />

1 1 1 2 3 <br />

4 3 1 1<br />

1<br />

2 3 <br />

4 <br />

1 Muse<br />

<br />

Muse <br />

<br />

Muse <br />

neoblast 5 <br />

<br />

Muse <br />

<br />

Muse <br />

<br />

<br />

3 <br />

2 <br />

Muse <br />

<br />

<br />

Muse <br />

<br />

<br />

OFAMIV<br />

<br />

<br />

<br />

<br />

<br />

<br />

<br />

<br />

<br />

<br />

Pax7 <br />

<br />

Pax7 <br />

in vitro <br />

<br />

<br />

<br />

<br />

<br />

<br />

<br />

OFAMIV<br />

<br />

1,2 3 1,2 1,2 3 <br />

1,2<br />

1<br />

II 2 <br />

3<br />

<br />

Shi <br />

<br />

2004, 2009<br />

<br />

<br />

<br />

CD146 fluorescent activate cell sorter <br />

in vitro <br />

<br />

<br />

<br />

CD146 <br />

<br />

CD146 <br />

CD146 <br />

CD146 <br />

2 <br />

CD146 <br />

<br />

OFAMV<br />

BMP dexamethasone <br />

1,2 1,2 1,2<br />

1<br />

1 2 <br />

<br />

dexamethasone Dex <br />

Dex <br />

<br />

Dex <br />

<br />

ROBC26 C26 BMP2<br />

<br />

C26 BMP2 Dex <br />

<br />

Dex C26 <br />

<br />

BMP2 <br />

OsterixOSX Dex <br />

BMP2 OSX OSX <br />

Dex <br />

Dex C26 <br />

BMP2 Dex <br />

<br />

OFAMV<br />

<br />

<br />

1 1 2 3 4 5 <br />

6 1 4 7<br />

1<br />

2 <br />

3 4 <br />

5 JAXA ISS 6 <br />

7 <br />

<br />

<br />

<br />

<br />

<br />

2010 5 ISS<br />

<br />

<br />

STS132ISS <br />

86 <br />

<br />

Flight μG, FμGFlight 1G, F1G<br />

Ground 1G 3 FμG F1G <br />

<br />

FμG <br />

<br />

<br />

<br />

OFAMV<br />

<br />

<br />

<br />

basolateral ventral <br />

ventral RB <br />

AR 2 <br />

ventral <br />

AP <br />

Unroofing ventral <br />

AP <br />

TEM <br />

AR RB <br />

AR ventral <br />

AR <br />

<br />

RB <br />

ventral <br />

AP <br />

RB AR <br />

RB AP <br />

<br />

AR integrin endocytosis


108<br />

117 <br />

OGAMI<br />

<br />

<br />

1,2 1 Takako Kondo 2 Eri Hashino 2<br />

1<br />

2 Dept. OtolaryngologyHNS, Indiana<br />

Univ. Sch. Med.<br />

95<br />

<br />

<br />

Wnt <br />

<br />

<br />

in vivo Tlx3<br />

<br />

<br />

Tlx3 <br />

<br />

Tlx3 <br />

Tlx3 Wnt <br />

<br />

<br />

Tlx3 <br />

Tlx3 <br />

<br />

OGAMI<br />

<br />

1 1 1 2 1 2 <br />

1 1 2 1<br />

1<br />

2 <br />

<br />

ES iPS <br />

<br />

<br />

<br />

<br />

<br />

Multilineage differentiating stress enduring Muse cell<br />

<br />

Muse ES <br />

Cluster Cluster <br />

3 <br />

<br />

3 <br />

<br />

SSEA3<br />

<br />

Muse <br />

<br />

<br />

OGAMI<br />

<br />

1 2 1 1 3 1<br />

1<br />

2 3 <br />

<br />

ES inner cell mass<br />

<br />

<br />

<br />

<br />

<br />

<br />

3 <br />

<br />

<br />

Oct3/4, OctA, Klf4, Nanog, cMyc, BCRP,<br />

Sox2, CK5, vimentin <br />

vimentin <br />

<br />

vimentin Oct3/4 <br />

23 ALP <br />

<br />

<br />

<br />

OGAMI<br />

<br />

1 2 1<br />

1<br />

2 <br />

<br />

<br />

<br />

<br />

<br />

<br />

<br />

<br />

<br />

6 <br />

9 <br />

10 μl <br />

<br />

10 <br />

<br />

<br />

2 mm <br />

5 mm <br />

2010 mm <br />

<br />

OGAMII<br />

The application of antimicrobials or glycogen accelerates the pulpal<br />

regeneration of replanted molars in mice<br />

Angela QuispeSalcedo, Hiroko IdaYonemochi, Hayato Ohshima<br />

Div. of Anatomy and Cell Biology of the Hard Tissue, Dept. of Tissue<br />

Regeneration and Reconstruction, Niigata Univ. Grad. Sch. of Med. and Dent. Sci.<br />

The intentionally prolonged time for the completion of tooth replantation<br />

induces bone formation, expanded inflammatory reaction, or fibrous tissue<br />

formation in pulp tissue. This study aims to clarify the effect of a combination<br />

of metronidazole, ciprofloxacine, and minocycline 3Mix or enzymatically<br />

synthesized glycogen ESG solution on the pulpal healing of replanted teeth.<br />

After extraction of the upper first molars of mice, the teeth were immersed in<br />

3Mix solution at four different concentrations standard, 50%, 75%, and 90%<br />

during 5 to 60 minutes with or without the use of a transfer solution PBS; and for<br />

60 min in ESG solution in addition to PBS alone control. Immunohistochemistry<br />

for nestin verified tertiary dentin formation 1 week after operation in the 3Mix<br />

groups and at 2 weeks in the ESG group. In contrast, no tertiary dentin formation<br />

was observed at 2 weeks in the control. Standard concentration of 3Mix induced<br />

severe ankylosis of the replanted tooth, in spite of the accelerated dentinogenesis.<br />

In conclusion, the application of 3Mix or ESG promotes the pulpal regeneration of<br />

replanted teeth, although the 3Mix may induce severe damage to the periodontal<br />

tissue.<br />

OGAMII<br />

<br />

1 2 1<br />

1<br />

<br />

2<br />

<br />

<br />

<br />

ESG <br />

ESG <br />

ESG <br />

<br />

<br />

ICR ESG 2 mg/mLESG<br />

3 <br />

3714 <br />

<br />

ESG <br />

<br />

ESG <br />

14 ESG 3 <br />

<br />

ESG DSPP <br />

ESG


117 109<br />

OGAMII<br />

BrdU <br />

<br />

<br />

<br />

Labelretaining cells<br />

LRCs <br />

ICR 3 BrdU 5 <br />

<br />

1 2 EDTA Nestin<br />

OPN BrdU TUNEL in situ <br />

Dsp <br />

1 TUNEL <br />

<br />

LRCs 35 <br />

Nestin LRCs <br />

Nestin 7 <br />

OPN <br />

DspmRNA <br />

LRCs <br />

<br />

OPN <br />

<br />

OGAMIII<br />

Cx NFATc <br />

1 2 1 3<br />

1<br />

2 3 <br />

Cx45 <br />

Cx45 <br />

Cx45 <br />

<br />

<br />

Cx45 <br />

<br />

Cx45 <br />

Cx45 <br />

Cx45 <br />

<br />

NFATc <br />

NFATc VEGF <br />

Cx45 <br />

NFATc <br />

<br />

<br />

OGAMIII<br />

FGF <br />

1 2<br />

1<br />

2 <br />

GDNF <br />

<br />

FGF <br />

1213 <br />

FGFcanonical, 15 FGF 7 <br />

FGF 3 <br />

GDNF Ret, GFRα1<br />

FGF5, FGF9,<br />

FGF17, FGF18, FGF22 FGF9 <br />

10 FGF9 <br />

Ret, GFRα1 GDNF <br />

<br />

FGF9 FGF9 <br />

FGF <br />

FGF9 <br />

FGF9 <br />

<br />

<br />

OGAMIII<br />

An attempt to identify novel ciliary genes by database comparison<br />

<br />

<br />

Cilia and flagella are hairlike organelles that project from the cell surface and<br />

have been implicated in a diversity of cell functions. Although a number of<br />

putative ciliary genes have been identified by several global analyses, little is<br />

known about the functions of these genes. To gain a better understanding of ciliary<br />

biology, we selected ciliary candidate genes from comprehensive ciliary protein<br />

data sets, named ciliome, and analyzed their antisenseknockdown phenotypes<br />

in medaka embryos. To maximize quality hits, we selected genes expressing<br />

in ciliary organs based on the zebrafish expression database. Comparing the<br />

expression among 5 ciliary organs, we found that 18 genes are commonly<br />

expressed in more than 4 organs out of the above 5. Comparing these genes with<br />

ciliome database, 5 out of the 18 genes were recorded in ciliome database. We<br />

therefore preliminary examined the medaka antisenseknockdown phenotypes of<br />

2 of the 5 genes. One revealed hydrocephalous and the other showed cystic kidney<br />

phenotype: both of which are ciliadefective phenotypes. This data suggests that<br />

our strategy is a promising approach to understanding various roles for ciliome<br />

proteins.<br />

OHAMI<br />

<br />

1 1 2 1<br />

1<br />

2 <br />

<br />

<br />

<br />

<br />

<br />

<br />

<br />

<br />

58 <br />

Rmax <br />

10 mm <br />

<br />

<br />

<br />

<br />

27 <br />

<br />

<br />

<br />

<br />

OHAMI<br />

On the phylogeny of the zygomatic arch, and its relationships among<br />

foramina and the bony wall of the orbit<br />

1,3 1 2 2 3 <br />

3 4 4 4 4<br />

1<br />

Kanagawa Dental College, 2 Edogawa Hospital, 3 Dept. Radiology, Yokohama City<br />

Univ. Sch. Med., 4 Dept. Neurosurgery, Yokohama City Univ. Sch. Med.<br />

The existence of the arcus zygomaticus is a characteristic of mammalian skulls.<br />

The arches provide surface for the masseter muscle to attach, and the canalis<br />

zygomaticus stores the passage of the zygomatic nerve. Romer & Parsons<br />

surmised that the arches are a last remnant of the former lateral walls of the<br />

reptilian skull. Only Simiiformes Catarrhini and Platyrrhini has the perfect bony<br />

orbital wall, whereas the Prosimii, Perissodactyla, and Artiodactyla lost the rear<br />

wall and floorbord of the bony orbit, and the Carnivora lost the lateral posterior<br />

bony wall of the orbit. However Hystricomorpha has another pair of arches on<br />

the lateral walls of the greatly enlarged infraorbital foramen. This structure seems<br />

to us a new frontal and rear expansion and reinforcement of the zygomatic arch.<br />

In the Simiiformes, the Fossa temporalis has a relatively large volume so that the<br />

brain case has become a high structure. Therefore it was not necessary for the<br />

zygomatic arch to enlarge in front and behind.


110<br />

117 <br />

OHAMI<br />

<br />

<br />

<br />

<br />

<br />

<br />

<br />

5 10 <br />

<br />

<br />

<br />

<br />

<br />

<br />

<br />

<br />

<br />

<br />

<br />

<br />

<br />

<br />

OHAMI<br />

<br />

1 2 2 3<br />

1<br />

2 <br />

3 <br />

3 <br />

<br />

<br />

<br />

<br />

<br />

<br />

<br />

CT <br />

CG <br />

CT <br />

CG3dsMAX CT <br />

CG <br />

<br />

CG <br />

CG <br />

<br />

<br />

CG <br />

<br />

<br />

OHAMII<br />

Persistent median artery: Relationships to palmar arches and median<br />

nerve branches<br />

Nabil Eid, Yuko Ito, Yoshinori Otsuki<br />

Osaka medical college<br />

Two cases of unilateral persistent median artery PMA were detected during the<br />

dissection of 25 cadavers. The first case was a 75yearold man. A dissection of<br />

his left upper limb revealed a PMA piercing both the median nerve MN and<br />

the anterior interosseous nerve. The PMA coursed distally, deep to the transverse<br />

carpal ligament TCL, forming a medianulnar pattern of complete superficial<br />

palmar arch SPA. The PMA was superficial to two nerves at the distal edge of<br />

the TCL; the extraligamentous recurrent thenar RT branch of MN and the third<br />

common digital nerve TCDN. The other case was an 80 yearoldfemale. Her<br />

left forearm showed a high origin of the radial artery from the brachial artery with<br />

trifurcation of the latter into PMA, common interosseous and ulnar arteries. The<br />

PMA passed deep to the TCL forming radialmedian ulnar pattern of SPA. Both<br />

the transligamentous RT branch of MN and the TCDN passed deep to the PMA<br />

inside the carpal tunnel, before the crossing of the latter nerve ventral to the SPA<br />

on its way to the digits. The relationships of the PMA to MN branches may have<br />

important implications regarding the diagnosis and treatment of MN compressive<br />

syndromes.<br />

OHAMII<br />

<br />

<br />

<br />

<br />

<br />

<br />

<br />

<br />

<br />

10 20 <br />

<br />

<br />

<br />

<br />

<br />

<br />

<br />

<br />

<br />

<br />

<br />

<br />

<br />

OHAMII<br />

Thiel <br />

1 2 2 2 3 <br />

2<br />

1<br />

2 2 3 <br />

<br />

<br />

<br />

Thiel 5 9 <br />

<br />

12<br />

<br />

3 4 7 2 :<br />

4<br />

<br />

5<br />

<br />

67<br />

<br />

TFCC<br />

Thiel Graz Thiel <br />

<br />

variation <br />

<br />

<br />

OHAMIII<br />

<br />

<br />

<br />

<br />

<br />

<br />

<br />

11 20 <br />

<br />

<br />

3 <br />

<br />

<br />

<br />

<br />

<br />

<br />

<br />

<br />

variation


117 111<br />

OHAMIII<br />

<br />

1 2 2 2 2 <br />

2 2 2 2 1<br />

1<br />

2 <br />

2011 <br />

39 <br />

<br />

VSD<br />

15 12 mm<br />

<br />

7 cm <br />

<br />

<br />

<br />

<br />

<br />

64 mm <br />

1 <br />

<br />

<br />

5 mm 4 E <br />

7 <br />

6 <br />

<br />

OHAMIII<br />

<br />

<br />

<br />

deep circumflex iliac vein DCIV <br />

DCIV <br />

external iliac<br />

artery EIA <br />

<br />

EIA DCIV <br />

<br />

20092011 38 72 <br />

DCIV EIA 65<br />

242 8 DCIV <br />

3DCIV EIA <br />

<br />

63% <br />

<br />

Edwards and Robuck 1947 lateral<br />

femoroiliac circle LFIC <br />

DCIV 2 <br />

LFIC <br />

OIAMI<br />

CT <br />

<br />

1 2 1<br />

1<br />

2 <br />

<br />

<br />

<br />

<br />

5 <br />

CT <br />

48 5798<br />

24 4 <br />

2 CT <br />

<br />

5 <br />

<br />

> <br />

14 2 <br />

560 90 4 <br />

20 2 <br />

9<br />

<br />

<br />

<br />

OIAMI<br />

<br />

<br />

<br />

<br />

P6 SAMP6 <br />

<br />

SAMP6 <br />

<br />

SAMP6 <br />

18 SAMP6 8 18<br />

R1 SAMR1 8 <br />

CT RmCT, RIGAKU, Japan <br />

18 <br />

TRI/3DBON RATOC, Japan <br />

<br />

BV/TV Tb.N SAMP6 SAMR1 <br />

Tb.Th <br />

BV/TVTb.NTb.Th <br />

SAMP6 <br />

<br />

<br />

<br />

OIAMI<br />

klotho/ <br />

1,2 1 1 1 3,4 <br />

1 2 1<br />

1<br />

2 <br />

3 <br />

4 <br />

klotho klotho/ Ca/P <br />

<br />

klotho/ <br />

<br />

5 klotho/ <br />

von Kossa ALP,<br />

DMP1, MGP, osteocalcin DMP1 <br />

<br />

<br />

klotho/ ALP <br />

klotho/ <br />

DMP1 osteocalcin MGP <br />

DMP1 <br />

klotho/ <br />

klotho/ <br />

DMP1 osteocalcin <br />

<br />

OIAMI<br />

<br />

1,2 1 1 1 2 <br />

1<br />

1<br />

2 <br />

1960 Bélanger PTH <br />

osteocytic osteolysis<br />

<br />

FGF23 <br />

PTH <br />

<br />

12 ICR human PTH 134; 80 mg/<br />

kg 6 <br />

von Kossa , a3,d2 <br />

FGF23 <br />

PTH <br />

von Kossa <br />

FGF23 d2 <br />

a3 <br />

<br />

PTH


112<br />

117 <br />

OIAMII<br />

Osteogenic culture <br />

<br />

<br />

<br />

<br />

<br />

<br />

<br />

in vitro <br />

<br />

hMSC12 <br />

2<br />

<br />

<br />

<br />

<br />

<br />

in vitro <br />

<br />

<br />

in vitro <br />

<br />

OIAMII<br />

PKR <br />

1 1 1 2<br />

1<br />

2 <br />

PKR <br />

<br />

PKR PKR <br />

PKR <br />

2 2AP RAW264.7<br />

RAW RANKL TRAP <br />

<br />

mRNA RTPCR Real time PCR <br />

PKR RAW K296S <br />

2AP RAW RANKL TRAP<br />

RANKL pc<br />

TRAP PKR <br />

TRAP <br />

MFRDCSTAMP, Cathepsin K, CTR <br />

2AP PKR NFκB NFATc1<br />

2AP PKR STAT1 <br />

PKR <br />

NFκB STAT1 <br />

OIAMII<br />

WT RNA <br />

1 2 1<br />

1<br />

2 <br />

WT1 Wilms’ <br />

Zinc finger <br />

<br />

<br />

WT1 <br />

RNA <br />

in situ hybridization <br />

WT1 RNA <br />

WT1mRNA <br />

WT1 RNA <br />

RAWD <br />

WT1 <br />

WT1 WT1<br />

RNA RAWD WT1 <br />

WT1 <br />

RNA <br />

RNA WT1 <br />

<br />

<br />

OIAMIII<br />

septoclast <br />

EFABP <br />

1 1 1 1 2 <br />

1<br />

1<br />

2 <br />

FABPs <br />

FABPEFABP<br />

septoclast <br />

<br />

4% paraformaldehyde EDTA <br />

<br />

<br />

EFABP septoclast <br />

<br />

EFABP <br />

EFABP septoclast <br />

EFABP <br />

<br />

<br />

septoclast <br />

EFABP <br />

EFABP <br />

<br />

OIAMIII<br />

<br />

<br />

1 2 2 2<br />

1<br />

2 <br />

<br />

10<br />

<br />

<br />

HCl <br />

<br />

JXA8900 EPMA<br />

<br />

<br />

CaP <br />

<br />

ONa CaP<br />

CaP <br />

<br />

<br />

<br />

<br />

<br />

OIAMIII<br />

<br />

1,2 1 1 1 4,5 <br />

1 2 3 1<br />

1<br />

2 <br />

3<br />

4 5 <br />

<br />

periostin/<br />

periostin/ <br />

<br />

periostin/ <br />

<br />

MMP1,2, F4/80 <br />

<br />

<br />

shear zone MMP1 F4/80 <br />

<br />

periostin/ MMP1MMP2F4/80 <br />

shear zone <br />

<br />

<br />

periostin/ <br />

<br />

shear zone


117 113<br />

ODPMI<br />

Large Maf <br />

<br />

<br />

Large Maf <br />

MafAMafBcMafNRL<br />

4 Maf<br />

MafAMafB<br />

cMaf MafA <br />

β <br />

<br />

MafA <br />

MafA <br />

MafB <br />

MafB <br />

<br />

α β <br />

Large Maf <br />

ODPMI<br />

<br />

<br />

Mohamad Reza <br />

<br />

5 <br />

FS FS <br />

<br />

<br />

<br />

<br />

FS <br />

FS GFP S100bGFP TG <br />

FS DNA <br />

<br />

GFP FS<br />

S100b protein, bFGF, Vime<br />

<br />

MKMidkine <br />

PCR MK GFP <br />

in situ hybridization FS MK mRNA <br />

MK FS <br />

<br />

ODPMI<br />

Notch <br />

1 1 1 2<br />

1<br />

2 <br />

<br />

Juxtacrine Notch <br />

<br />

Hoechst 33342 <br />

Notch <br />

Notch <br />

<br />

Notch <br />

In situ hybridization<br />

4 Notch <br />

2 marginal layer <br />

Notch <br />

<br />

Notch <br />

Notch marginal layer<br />

<br />

<br />

ODPMI<br />

<br />

Dini RamadhaniDepicha Jindatip <br />

<br />

FS<br />

<br />

FS ECM <br />

gap junction <br />

<br />

FS <br />

FS FS FS FS<br />

3 realtime PCRin<br />

situ hybridization ISHFS 5 <br />

FS<br />

ECM I III <br />

FS<br />

FS<br />

ISH <br />

RGS5 FS<br />

FS <br />

<br />

ODPMII<br />

Expression of laminin isoforms during anterior pituitary development<br />

in the rat<br />

Dini Ramadhani <br />

<br />

Laminin isoforms LMs are major basement membrane components in anterior<br />

pituitary. Currently 19 LMs have been identified in vivo, and they have multiple<br />

functions, not only as a scaffold but also as induction of cell differentiation<br />

and cell signalling. However, LM function in anterior pituitary development<br />

has not been studied. The purpose of this study is to determine the laminin<br />

isoform expression during the anterior pituitary development. RTPCR, in situ<br />

hybridization ISH, and immunohistochemistry IHC were used. RTPCR and<br />

ISH analysis showed the laminin alpha 1, 3, and 4 gene expressions in adult<br />

anterior pituitary, while only laminin alpha 5 mRNA was expressed in early stage.<br />

Correlating with ISH data, IHC showed that laminin protein was first expressed<br />

around the pituitary in early stage and it was gradually expressed within the<br />

pituitary as vasculatures are formed in the gland. The results indicate that the<br />

expression of laminin isoforms varies during anterior pituitary development in<br />

the rat. This study may provide basic knowledge for further study on analysis of<br />

laminin functions in the anterior pituitary gland.<br />

ODPMII


114<br />

117 <br />

ODPMII<br />

<br />

OEPMVI<br />

<br />

<br />

1,2 1,2 1,2 1,2 1,2<br />

1<br />

2 <br />

<br />

<br />

<br />

<br />

<br />

<br />

<br />

<br />

<br />

IdaEto et al., Neurosci. Lett., in press 9 <br />

Wistar 15 <br />

<br />

<br />

2 <br />

<br />

<br />

OEPMVI<br />

Developmental Origins of Health and Disease DOHaD <br />

<br />

Randeep Rakwal <br />

<br />

<br />

DOHaDDevelopmental Origins of Health and Disease<br />

<br />

<br />

ADHD <br />

<br />

50% <br />

1018 17 <br />

18 mRNA <br />

DyeSwap DNA <br />

250 1300 <br />

140 <br />

GABA A neuromedin BStat1<br />

<br />

<br />

T <br />

<br />

<br />

OEPMVI<br />

<br />

1 - 1 1 1,2 1<br />

1<br />

2 <br />

<br />

PTSD <br />

<br />

<br />

maternal separation: MS <br />

<br />

<br />

cFos <br />

MS 2 3 / <br />

MS repeated MS: RMS 2 MS <br />

single MS:SMS cFos <br />

RMS SMS cFos <br />

RMS <br />

SMS MS <br />

<br />

<br />

MS <br />

OEPMVI<br />

q E/I <br />

1,2 1,4 1 1 1 <br />

3 3 5 1,2,6<br />

1<br />

2 <br />

3 <br />

4 Heidelberg University, Germany 5 <br />

6<br />

JST,CREST<br />

<br />

<br />

<br />

15q11q13 <br />

20 <br />

<br />

<br />

<br />

<br />

/ Excitation/Inhibition, E/I <br />

<br />

E/I <br />

<br />

E/I VGLUT1 Vesicular glutamate transporter 1 <br />

VGAT Vesicular GABA Transporter <br />

VGAT VGLUT1<br />

<br />

E/I <br />

OEPMVII<br />

<br />

<br />

<br />

<br />

DNA <br />

BromodeoxyuridineBrdU<br />

2 <br />

<br />

BrdU 2 <br />

<br />

<br />

<br />

1 2 <br />

<br />

Notch1 <br />

Notch1 <br />

<br />

Notch1


117 115<br />

OEPMVII<br />

<br />

1 1 2 2 1<br />

1<br />

2 <br />

<br />

<br />

<br />

<br />

experimental<br />

autoimmune encephalomyelitis: EAE EAE <br />

<br />

C57BL/6 Myelin oligodendrocyte<br />

glycoprotein 3555 MOG3555 <br />

EAE <br />

<br />

<br />

<br />

<br />

EAE <br />

<br />

<br />

<br />

EAE <br />

OEPMVII<br />

RAGE<br />

<br />

<br />

<br />

Receptor for advanced glycation end productsRAGE<br />

<br />

RAGE <br />

RAGE<br />

<br />

BCCAORAGE <br />

RAGE esRAGERAGE <br />

3 BCCAO <br />

<br />

BCCAO 12 <br />

3-7 RAGE <br />

RAGE esRAGE <br />

24 7 <br />

12 <br />

<br />

RAGE <br />

<br />

<br />

OEPMVIII<br />

Fasting and highfat diet alter histone deacetylase expression in the<br />

medial hypothalamus<br />

<br />

<br />

Increasing attention is now being given to the epigenetic regulation of animal<br />

and human behaviors including the stress response and drug addiction. Histone<br />

deacetylases HDACs are involved in the epigenetic control of gene expression<br />

and alter behavior in response to a variety of environmental factors. In response<br />

to fasting and highfat diets, the expression of both orexigenic and anorexigenic<br />

neuropeptides change in the medial hypothalamus, a crucial region for feeding<br />

behavior and body weight homeostasis. However, the mechanism by which gene<br />

expression is modulated in the medial hypothalamus remains to be clarified.<br />

Here, we examined the expression of HDAC family members in the medial<br />

hypothalamus of mice in response to either fasting or a highfat diet. In response<br />

to fasting, HDAC3 and 4 expression levels increased while HDAC10 and<br />

11 levels decreased. Four weeks on a highfat diet resulted in the increased<br />

expression of HDAC5 and 8. Therefore, HDACs may be implicated in altered<br />

gene expression profiles in the medial hypothalamus under different metabolic<br />

states.<br />

OEPMVIII<br />

<br />

1 2 3 1<br />

1<br />

2 3 <br />

<br />

<br />

<br />

<br />

1 2 <br />

3 <br />

1<br />

2 <br />

PGP9.5 <br />

CGRP <br />

1/3 <br />

Aδ <br />

C <br />

1/21/3 <br />

<br />

CGRP C <br />

<br />

<br />

<br />

OEPMVIII<br />

PAM <br />

1,2 1 1<br />

1<br />

2 <br />

PAMPressure Application Measurement<br />

Randall Selitto<br />

<br />

<br />

PAM <br />

5 <br />

6 <br />

<br />

NSAIDs 10 1 2 <br />

3 <br />

NSAIDs PAM<br />

<br />

<br />

cFos <br />

<br />

OFPMVI<br />

<br />

<br />

1 Watson Eileen 2 1<br />

1<br />

2 Dept. Oral Health Sciences, University of<br />

Washington<br />

Proteaseactivated receptor PAR <br />

G 7 PAR <br />

<br />

PAR <br />

PAR RTPCR PAR2 <br />

PAR2 SLIGRLNH 2 <br />

[Ca 2+ ] i Ca 2+ [Ca 2+ ] i<br />

<br />

Ca 2+ noncapacitative calcium entry NCCE <br />

<br />

Ca 2+ NOS <br />

LNAME <br />

ADP <br />

calmodulin kinase II CAMK II <br />

calmodulin [Ca 2+ ] i <br />

PAR2 [Ca 2+ ] i <br />

NOS <br />

Calmodulin CAMK II


116<br />

117 <br />

OFPMVI<br />

Biodiversity and hepatic stellate cells<br />

Haruki Senoo 1 , Yoshihiro Mezaki 1 , Mitsutaka Miura 1 , Katsuyuki Imai 1 ,<br />

Kiwamu Yoshikawa 1 , Mayako Morii 1 , Mutsunori Fujiwara 2 , Rune Blomhofff<br />

3<br />

1<br />

Dept. Cell Biology and Morphology, Akita Uni. Grad. Sch. Med., 2 Divis. Clinical<br />

Pathol, Japanese Red Cross Med. Center, 3 Dept. Nutrition, Inst. Basic Med. Sci,<br />

Fac. Med., Univ. Oslo<br />

Hepatic stellate cells HSCs exist in the space between hepatocytes and<br />

sinusoidal endothelial cells, and store 5080% of vitamin A in the whole body<br />

as retinyl palmitate in lipid droplets in the cytoplasm. We have performed a<br />

systematic characterization of the hepatic vitamin A storage in animals of the<br />

Svalbard archipelago and Greenland, and compared that in polar bears kept in<br />

zoos. The top predators contained about 1020 times more vitamin A than all other<br />

arctic animals studied as well as their genetically related continental top predators.<br />

This massive amount of hepatic vitamin A was located in large lipid droplets in<br />

HSCs. The contents of retinyl esters in the liver for polar bear kept in zoos were<br />

dependent on vitamin A content in the diet. The development of such an efficient<br />

vitamin Astoring mechanism in HSCs may have contributed to the survival of<br />

top predators in the extreme environment of the arctic. HSC that has capacity<br />

of taking up and storing of a large amount of vitamin A plays pivotal roles in<br />

maintenance of food web, food chain, biodiversity, and eventually ecology of the<br />

arctic.<br />

OFPMVI<br />

A <br />

1 1 1 1,2 1 <br />

1 1<br />

1<br />

2 <br />

<br />

A A <br />

A perilipin 2/ADRPperilipin 3/TIP47 <br />

ADRP TIP47 A <br />

A TIP47<br />

<br />

A A <br />

ADRPTIP47 <br />

A <br />

ADRPTIP47 <br />

A 24 A TIP47 <br />

7 A <br />

TIP47 A A <br />

<br />

A TIP47 <br />

A A <br />

24 7 TIP47 A <br />

A TIP47 <br />

ADRP A <br />

OFPMVI<br />

IEL DNA <br />

<br />

<br />

CD3 IEL<br />

30 IEC DNA 2 <br />

IEC <br />

IEC DNA DNA <br />

DNA IEL IEC <br />

DNA IEL <br />

BGrB IEL GrB <br />

IEC DNA GrB <br />

IEC DNA Pfn/GrB <br />

DNA <br />

IEL Pfn GrB <br />

IEL Pfn <br />

DNA <br />

GrB DNA 3<br />

IEL IEC DNA <br />

Pfn/GrB Pfn GrB <br />

DNA<br />

<br />

OFPMVII<br />

SU p <br />

<br />

<br />

<br />

Src SU6656 <br />

5F9A <br />

<br />

DNA BrdU DNA<br />

<br />

BrdU <br />

S <br />

<br />

<br />

2 2<br />

SU6656 <br />

<br />

p53 siRNA p53 <br />

SU6656 p53 <br />

Nutlin SU6656 <br />

SU6656 p53 <br />

p53 <br />

<br />

OFPMVII<br />

<br />

1 1 1 1 2<br />

1<br />

2 <br />

<br />

<br />

<br />

<br />

2 <br />

<br />

<br />

<br />

1 <br />

A single <br />

cKit <br />

A single A aligned cKit <br />

A1 A single A paired<br />

<br />

<br />

Np95 <br />

<br />

<br />

OFPMVII<br />

HORMAD <br />

<br />

<br />

HORMAD1HORMAD2 <br />

Hop1 HORMA<br />

<br />

HORMAD1 HORMAD1 <br />

HORMAD2 <br />

HORMAD2 <br />

HORMAD2 <br />

<br />

XYbody <br />

HORMAD2 <br />

SPO11 HORMAD2 <br />

SPO11 <br />

HORMAD2 <br />

HORMAD1 HORMAD2 <br />

HORMAD2 HORMAD1 <br />

<br />

<br />

<br />

HORMAD2


117 117<br />

OFPMVIII<br />

α <br />

<br />

<br />

<br />

<br />

<br />

<br />

<br />

<br />

NPC1L1 <br />

<br />

LC3II <br />

NPC1L1<br />

<br />

Lamp1 Ragulator <br />

p18 Lamp1 mTOR <br />

<br />

<br />

<br />

α1 ATZ <br />

<br />

α1<br />

<br />

OFPMVIII<br />

E HRD <br />

<br />

<br />

<br />

<br />

ERassociated<br />

degradation; ERAD unfolded<br />

protein response; UPR E3 <br />

HRD1 ERAD UPR <br />

<br />

ERAD UPR <br />

HRD1 <br />

<br />

ICR 6 4% <br />

HRD1 Abgent1.25 μg/ml<br />

<br />

HRD1 <br />

<br />

<br />

<br />

HRD1 <br />

<br />

OFPMVIII<br />

<br />

1 2 2<br />

1<br />

2 <br />

<br />

[Aim] We investigated the influence of the adrenal glands over the preservation<br />

of gap junctions between folliculostellate cells in the anterior pituitary glands of<br />

rats. [Maerials and Methods] 60 dayold WistarImamichi strain male rats were<br />

prepared. The animals were divided into six groups: untreated control, untreated<br />

but given 0.9 % NaCl drinking water, castrated, adrenalectomized, castrated and<br />

adrenalectomized, and castrated and adrenalectomized with the administration<br />

of testosterone. Five rats from each group were killed 1, 2, 3, 4, 5, 6 and 7<br />

days after the operation, and prepared for observation by transmission electron<br />

microscopy. [Results] The simultaneous removal of adrenal glands with castration<br />

resulted in the significantly decreasing effects of gap junctions, and the additional<br />

administration of testosterone to these rats could compensate for the decreasing<br />

effects of gap junctions, while few mitotic hormoneproducing granular cells<br />

were found. [Conclusion] These observations indicate that the preservation of gap<br />

junctions between folliculostellate cells is mainly dependent on the testosterone<br />

from both testes and adrenal glands in adult male rats.<br />

OGPMIV<br />

NEX <br />

<br />

<br />

<br />

<br />

<br />

<br />

<br />

<br />

<br />

<br />

<br />

NEX Math2 bHLHtype transcriptional factor <br />

Cre <br />

<br />

NEX <br />

<br />

OGPMIV<br />

FLRT Unc <br />

1,2 Falko Hampel 2 3 Daniel del Toro 2 <br />

Manuela Schwark 4 Elena Kvachnina 4 Martin Bastmeyer 5 3 <br />

Victor Tarabykin 4 Joaquim Egea 2 Ruediger Klein 2<br />

1<br />

2 MaxPlanck Institute of<br />

Neurobiology 3 4 MaxPlanck<br />

Institute for Experimental Medicine 5 Karlsruher Institute fuer Technologie<br />

<br />

<br />

<br />

FLRT <br />

Unc5 <br />

FLRT2 Unc5D UL2<br />

<br />

Unc5D UL2 <br />

RNA <br />

FLRT2 VVI UL2 <br />

IV Unc5D <br />

FLRT2/ UL2 <br />

FLRT2 UL2 <br />

<br />

OGPMIV<br />

Implications for cooperative versus noncooperative actions of the<br />

subunits of NatB, Mdm and Nat in mouse embryonic brain<br />

Kyoji Ohyama 1 , Kunihiko Yasuda 1 , Kazuko Onga 1 , Akira Kakizuka 2 ,<br />

Nozomu Mori 1<br />

1<br />

Dept. of Anatomy and Neurobiology, Grad. Sch. Biomedical Sciences, Nagasaki<br />

Univ., 1124 Sakamoto, Nagasaki 8528523, Japan, 2 Lab. of Functional Biology,<br />

Kyoto Univ. Grad. Sch.Biostudies, Kyoto 6068501, Japan<br />

The NatB complex, Nat5/Mdm20 acetyltransferase mediates Nacetylation to<br />

control cell cycle progression and actin dynamics in yeast. As yet, little is known<br />

about their expression patterns in multicellular organisms. Here we show that<br />

Mdm20 is highly expressed in mouse embryonic brain. At E11.5, Mdm20 was<br />

widely expressed in both neural progenitors and early differentiating neurons,<br />

whereas Nat5 was expressed in Sox1/3+/Mdm20+ neural progenitors. By E14.5,<br />

both Mdm20 and Nat5 were downregulated in ventricular zone neural progenitors,<br />

whereas both protein expression were found in differentiating neurons and<br />

maintained at E18.5 in derivatives of these cells, such as midbrain dopaminergic<br />

DA neurons. Intriguingly, our data also showed that Mdm20 is not always co<br />

expressed with Nat5 in all differentiated neurons, for example deep cerebellar<br />

neurons. Moreover, Mdm20 is also not necessarily colocalised with Nat5 within<br />

Nat5+/Mdm20+ midbrain DA neurons. Given that Nat5 is only a known member<br />

of Nat family protein that interacts with Mdm20, our data imply that Mdm20 may<br />

function either with an unidentified Nat protein partners or possibly in a Nat<br />

independent manner.


118<br />

117 <br />

OGPMIV<br />

<br />

<br />

1 1 1,2 1,3 1,4<br />

1<br />

2 3 <br />

4 <br />

CS<br />

<br />

<br />

CS <br />

<br />

IgG <br />

IgM<br />

CS <br />

IgM<br />

IgM Hierck 1994<br />

CS IgM<br />

CS<br />

ABC <br />

CS <br />

CSA CSD CS56 <br />

<br />

IgM <br />

<br />

OGPMV<br />

Hes <br />

<br />

1 2 3 3<br />

1<br />

2 3 <br />

<br />

NotchHes <br />

Hes1 /<br />

Hes1/ <br />

SCG <br />

12.5 E12.5 E13.5 SCG <br />

E14.5 C1C3 <br />

Hes1/ E13.5 SCG <br />

E17.5 SCG <br />

26.3% <br />

SCG E13.0 3 <br />

SCG E13.5 SCG <br />

Hes/ <br />

E17.5 <br />

52.5% H3 SCG <br />

Hes1/ <br />

Hes1 SCG <br />

<br />

OGPMV<br />

M. iliotibialis cranialis<br />

<br />

<br />

<br />

<br />

<br />

<br />

<br />

M.iliotibialis cranialis<br />

<br />

E5 <br />

<br />

E6 E7 <br />

E8 <br />

E9 L1<br />

L2 <br />

E5 <br />

<br />

<br />

<br />

OGPMV<br />

<br />

<br />

1 2 2 2<br />

1<br />

2 <br />

<br />

<br />

<br />

<br />

<br />

<br />

<br />

CL57BL/68 <br />

50 mm 500 mm 0 45 90 <br />

<br />

BrdU 1 mg/ml 2 <br />

BrdU <br />

BrdU <br />

<br />

<br />

<br />

<br />

OGPMVI<br />

Differential effect of aberrant expression of ectodysplasinA receptor<br />

edar on scales and jaw and pharyngeal dentition of medaka<br />

Otto Baba 1 , ADSL Atukorala 1 , Keiji Inohara 2 , Makoto Tabata 1 , Kiyoshi Mitani 3 ,<br />

Yoshiro Takano 1<br />

1<br />

Biostructural Science, Graduate School, Tokyo Medical & Dental University,<br />

2<br />

Biological Information, Tokyo Institute of Technology, 3 Biological Science,<br />

Graduate School of Frontier Science, University of Tokyo<br />

To find out the role of ectodermal cell signaling in scale and tooth formation in<br />

teleosts and thereby to gain insights in evolutionary origin of teeth, we analyzed<br />

scales and teeth in rs3 medaka mutant characterized by reduced scale numbers<br />

due to aberrant splicing of ectodysplasinA receptor edar. Results: In normal<br />

medaka, we confirmed edar signals in the enamel epithelium at early tooth<br />

development in both jaw and pharyngeal dentition. The signal was gone once<br />

mineralized matrix had deposited. In adult rs3, drastic loss of scales 83 %<br />

and teeth occurred in both oral 43.5 % and pharyngeal 73.5 % dentition.<br />

Remaining scales were irregular and much larger in size relative to those of wild<br />

type. In contrast, there was no abnormality in size and shape in the remaining<br />

teeth of rs3. ThreeD analyses of embryonic development of pharyngeal regions<br />

indicated that pharyngeal tooth formation preceded gill slit opening and showed<br />

no sign of ectodermal cell migration in pharyngeal endoderm and hence no direct<br />

evidence of ectodermal contribution to pharyngeal odontogenesis. Conclusion:<br />

These data support intrinsic odontogenic competence of rostral endoderm in<br />

medaka.<br />

OGPMVI<br />

DNA TGFβ <br />

<br />

1 1 2 3<br />

1<br />

2 3 <br />

DNA <br />

RG108 MEE <br />

TGFβ3 KO <br />

<br />

RG108 ICR C57BL/6J MEE<br />

<br />

100 C57BL/6J <br />

TGFβ3KO RG108 <br />

<br />

in vitro ICR C57BL/6J <br />

MEE RG108 <br />

C57BL/6J MEE ICR <br />

C57BL6J TGFβ3KO <br />

RG108 <br />

ICR TGFβ3KO <br />

15.8<br />

<br />

DNA


117 119<br />

OHPMIV<br />

<br />

<br />

<br />

<br />

<br />

<br />

<br />

<br />

<br />

<br />

<br />

<br />

1 MAL <br />

<br />

2 <br />

<br />

MAL <br />

<br />

<br />

<br />

<br />

OHPMIV<br />

D <br />

<br />

<br />

<br />

<br />

Saito et al., 2006, Steinke H et al., 2009<br />

<br />

3D <br />

<br />

5 <br />

<br />

<br />

MRI LaserErgo Scanner <br />

<br />

3D <br />

<br />

<br />

3D 3 <br />

<br />

Saito et al, Surg Radiol Anat 28, 228234, 2006<br />

Steinke H et al. Ann Anat 191, 408416, 2009<br />

OHPMIV<br />

<br />

1 2 3 3 4 3<br />

1<br />

2 3 4 <br />

<br />

2 <br />

19%<br />

<br />

<br />

1 <br />

<br />

Gray’s Anatomy <br />

Gottshalk 1989<br />

3 <br />

Akita 1993<br />

<br />

3 <br />

<br />

<br />

<br />

1 0.8 <br />

<br />

<br />

OHPMIV<br />

<br />

1 2 2,3<br />

1<br />

2 3 <br />

<br />

<br />

7<br />

12 <br />

3 <br />

<br />

<br />

<br />

<br />

67<br />

33<br />

1/31/6 50<br />

50<br />

<br />

<br />

<br />

<br />

<br />

<br />

<br />

OHPMIV<br />

Threedimensional modeling of the architecture of the plantar<br />

muscles of the great toe<br />

Takamitsu Arakawa 1,2 , Anne Agur 1<br />

1<br />

Division of Anatomy, Department of Surgery, Faculty of Medicine, University of<br />

Toronto, 2 Kobe University Graduate School of Health Sciences<br />

The plantar muscles of the great toe are involved in many foot pathologies,<br />

including hallux valgus. Forces acting along their tendons are important<br />

considerations in analyzing gait patterns and arch stability. Muscle models have<br />

not been constructed at the fiber bundle level, but rather using a series of single<br />

or multiple line segments to represent a muscle. The purpose of this study is to<br />

construct, at fiber bundle level, a volumetric 3D model of the plantar muscle of<br />

the great toe. In situ digitization with a Microscribe TM G2DX digitizer of one<br />

formalin embalmed cadaveric specimen was used to develop a 3D prototype<br />

model of abductor, adductor, and flexor hallucis muscles. Autodesk ® Maya ® , with<br />

additional plugins developed in this laboratory, were used to create a model the<br />

digitized data. Using this technique, a detailed model at the fiber bundle level was<br />

constructed and used to visualize and quantify the musculotendinous architecture<br />

of the plantar great toe muscles. This prototype may be further developed into<br />

a contractile model that enables functional analysis in normal and pathologic<br />

scenarios.<br />

OHPMI<br />

The characteristic of the filiform and fungiform papillae of human<br />

tongue<br />

ShineOd Dalkhsuren, Kikuji Yamashita, Dolgorsuren Aldartsogt,<br />

Kaori Sumida, Shinichiro Seki, Seiichiro Kitamura<br />

<br />

Objective: We aimed to clarify whether there are the structurally differences of the<br />

filiform and the fungiform papillae of human tongue depending on their position<br />

and function.<br />

Methods: The tissue specimens were separated to the significant parts: the tip, the<br />

body and the root of tongue and processed with the scanning electron microscopy<br />

SEM JCM5700, Jeol, Tokyo, Japan and the light microscopy.<br />

Results and discussions: The tip of tongue is the first sensing place for taste<br />

stimuli and the most active moving side. Consequently, the free longbased<br />

fungiform papillae distributed equable densely and a few filiform papillae<br />

containing the less and strong hairs placed along the margin of the fungiform<br />

papillae. The body of human tongue is the main mastication area. And it contained<br />

the numerous filiform papillae which are composed of a lot of hairs for making<br />

the soft sponge structure and holding the tongue plaque. In the root, the both of<br />

filiform and fungiform papillae were changed responding to the frictional stress as<br />

the swallowing.<br />

Conclusion: The structural variations of filiform and fungiform papillae might be<br />

depended on their positional role.


120<br />

117 <br />

OHPMI<br />

<br />

<br />

1 2 3 3 4 <br />

4 1,3<br />

1<br />

2 2 3 <br />

4 <br />

<br />

<br />

Wistar 2 <br />

2 <br />

HRP<br />

FcRn IgG EEA1 <br />

<br />

<br />

HRP <br />

<br />

<br />

<br />

FcRn IgG <br />

FcRn IgG FcRn<br />

<br />

<br />

<br />

<br />

OHPMI<br />

<br />

1,2<br />

1<br />

2 <br />

<br />

19 24<br />

10 30 1 3 30 90 ddY 3 <br />

3 Hthymidine, 3 Huridine, 3 Hleucine 1 <br />

<br />

400 kV <br />

<br />

10 <br />

1 8 <br />

1-2 15 2 <br />

DNA 7-14 <br />

<br />

1 24RNA <br />

2-6 <br />

2<br />

24<br />

<br />

<br />

<br />

<br />

OHPMII<br />

CRF <br />

1 1,2 1 1 1 1 <br />

1 1<br />

1<br />

2 <br />

<br />

<br />

FD<br />

IBS<br />

<br />

<br />

CRF <br />

<br />

<br />

1 2 Water avoidance WAS 7 <br />

<br />

CRF <br />

WAS <br />

WAS CRF <br />

alphahelical CRFWAS <br />

CRF <br />

<br />

WAS FD <br />

WAS CRF FD <br />

<br />

OHPMII<br />

<br />

1 2 3 4 5<br />

1<br />

2 3 <br />

4 5 <br />

<br />

<br />

<br />

αmangostin 7585γmangostin 515<br />

F344 200<br />

mg/kg 1 2 <br />

2000 4000 ppm <br />

500 ppm <br />

3 <br />

8 <br />

S GSTP <br />

2000<br />

4000 ppm GSTP <br />

<br />

GSTP <br />

<br />

<br />

OIPMIV<br />

tendon gel <br />

1 1,2 2 3 3 <br />

4 5<br />

1<br />

2 3 <br />

4<br />

5 <br />

<br />

<br />

1 mm <br />

2 <br />

40 <br />

1 <br />

10 tendon gel, TG <br />

TG <br />

<br />

TG 2 <br />

2 11 62 nm n=550<br />

3 <br />

12 40 <br />

6314 nm n=166 6820 nm n=161 <br />

2 TG<br />

TG <br />

TG 17.02 MPa <br />

TG TG <br />

327 nm n=214 <br />

OIPMIV<br />

<br />

<br />

<br />

desminvimentin <br />

<br />

<br />

<br />

desminvimentin <br />

<br />

<br />

desminvimentin <br />

1216 ICR <br />

HE<br />

desminvimentin <br />

desmin 12 <br />

vimentin 12 <br />

12 <br />

<br />

desminvimentin


117 121<br />

OIPMIV<br />

<br />

1 2 1 1 3 3<br />

1<br />

2 <br />

3 <br />

<br />

<br />

<br />

<br />

<br />

<br />

<br />

<br />

2 <br />

<br />

<br />

OIPM<br />

<br />

<br />

<br />

<br />

<br />

<br />

2007 <br />

SA<br />

<br />

SA <br />

<br />

<br />

<br />

<br />

SA 2 SA <br />

2 <br />

<br />

SA 2 SA <br />

SA <br />

<br />

<br />

<br />

OIPM<br />

CT <br />

1 2 2 3 4<br />

1<br />

2 3 <br />

4 <br />

21 X CT <br />

22 <br />

1 mm CT <br />

3 <br />

<br />

<br />

<br />

10 CT<br />

<br />

<br />

<br />

3 <br />

<br />

<br />

CT <br />

<br />

<br />

CT 3D <br />

<br />

OIPM<br />

<br />

1 2 2 2 2 <br />

2 3 1 1 1 1<br />

1<br />

2 <br />

3 <br />

2008 <br />

2009 <br />

2010 <br />

<br />

[ <br />

86: 3337 2011]1. 2. <br />

3. 4. <br />

3. 3 <br />

<br />

<br />

<br />

<br />

<br />

<br />

<br />

<br />

<br />

OIPM<br />

Organization of the lens elasticity associating with accommodation<br />

in monkey eyes<br />

Mari Hiraoka 1,2,3 , Haruki Senoo 3 , Masahiko Takada 4<br />

1<br />

Koganei Eye Clinic, 2 Lab. Brain Develop, Tokyo Metropolitan Inst. Med. Sci.,<br />

3<br />

Dept. Cell Biol. Morphol, Akita Univ. Grad. Sch. Med., 4 System Neurosci. Sect,<br />

Primate Res. Inst, Kyoto Univ.<br />

To understand the mechanism of accommodation, our dynamic connective tissue<br />

theory revealed the zonule inside of capsule may work for traction of capsule<br />

itself. And present study is conducted to analyze the comprehensive structure of<br />

lens fiber configuration to induce increase of central thickness and decrease of<br />

vertical diameter in primate eyes.<br />

Morphology of zonule, capsule and lens fiber arrangement and tracer uptake<br />

through capsule were examined.<br />

Premature lens had horizontally aligned fiber and vascular net. The most<br />

distinctive feature in mature lens was intracapsular zonular branching in equatorial<br />

and anterior apical regions. Adult lens showed subepithelial elastic lamellae<br />

localized in superficial equatorial and anterior region. In aged lens major internal<br />

structure was horizontally arranged, tightly packed nonelastic fibers.<br />

Lifelong growth of lens fiber causes degenerative deterioration on fiber flexibility<br />

and also capsular responsibility to the zonular active traction. These finding may<br />

support our theory.<br />

OIPM<br />

CCP <br />

<br />

<br />

<br />

50<br />

<br />

<br />

connecting cilium<br />

CCP1 <br />

<br />

<br />

<br />

CCP1 <br />

3 <br />

<br />

TTLL1 <br />

CCP1 TTLL1 <br />

CCP1 <br />

CCP1 <br />

CCP1


122<br />

117 <br />

OIPM<br />

<br />

<br />

<br />

<br />

TRPtransient receptor<br />

potential<br />

<br />

<br />

<br />

TRPV <br />

ruthenium red TRPV4 <br />

RN1734 ATP <br />

<br />

<br />

TRPV4


117 123<br />

P<br />

SA <br />

1 2<br />

1<br />

2 <br />

Glial fibrillary acidic protein GFAP S100β <br />

<br />

<br />

<br />

S100 <br />

S100A6 <br />

<br />

<br />

S100A6 <br />

CA1 S100A6 <br />

CA1 <br />

CA1 S100A6<br />

GFAPS100β <br />

S100A6 brain lipid binding protein BLBP <br />

S100A6 <br />

<br />

<br />

P<br />

Distribution of corticosteroid receptors in oligodendrocytes of mice<br />

Yumiko Matsusue 1,2 , Noriko HoriiHayashi 2 , Takayo Sasagawa 2 ,<br />

Wataru Matsunaga 2 , Katsuhiko Ono 3 , Mayumi Nishi 2<br />

1<br />

Dept. Oral. Maxillofac. Surg. Nara. Med. Univ., Nara, Japan, 2 Dept. Anat. & Cell<br />

Biol. Nara. Med. Univ., Nara, Japan, 3 Dept. Biol. Kyoto. Pref. Univ. Med., Kyoto,<br />

Japan<br />

Glucocorticoids are the mainstay in treating patients with diseases affecting the<br />

white matter, including multiple sclerosis in which the myelin sheaths around the<br />

axons of the brain, thereby leading to demyelination. In contrast, glucocorticoids<br />

are ineffective in gray matter injuries, such as head trauma. Many studies have<br />

reported glucocorticoid receptor GR is expressed in cultured oligodendrocytes.<br />

But very little study has revealed the expression of GR in oligodendrocytes<br />

in vivo. We investigated whether the oligodendorocytes were positive for GR<br />

by using two different oligodendorocyte markers, carbonic anhydrase CA<br />

II, a mature oligodendrocyte marker, and NG2, an oligodendrocyte progenitor<br />

marker. We focused on the gray matter regions including the cortex, hippocampus<br />

CA1, CA3, dentate gyrus, and amygdala, and the white matter regions<br />

including the external capsule, colpus callosum and fimbria hippocampus by<br />

using immunohistochemistry. We found over 80% of mature oligodendrocytes<br />

and oligodendrocyte progenitors express GR in various brain region. In<br />

contrast, neither oligodendrocytes nor oligodendrocyte progenitors express<br />

mineralocorticoid receptor MR.<br />

P<br />

F<br />

<br />

1 1 1 1 1 <br />

2 2 3<br />

1<br />

2 3 <br />

<br />

<br />

<br />

<br />

<br />

4F2 <br />

9 <br />

<br />

4F2 <br />

4F2 <br />

DEAD box RNA <br />

Ddx54 MBP 21.5 kDa <br />

<br />

<br />

P<br />

Immunohistochemical Analyses of Protein .G in Enteric Peripheral<br />

Nervous Tissues by in vivo Cryotechnique<br />

Jiaorong Chen, Nobuo Terada, Nobuhiko Ohno, Sei Saitoh, Yurika Saitoh,<br />

Shinichi Ohno<br />

Department of Anatomy and Molecular Histology, Interdisciplinary Graduate<br />

School of Medicine and Engineering, University of Yamanashi<br />

We have examined immunolocalization of protein 4.1G in peripheral nervous<br />

tissues of mouse large intestines with “in vivo cryotechnique” followed by freeze<br />

substitution. The 4.1G was mostly immunolocalized in Auerbach’s myenteric<br />

plexus. By immunofluorescence staining of 4.1G, GFAP and cKit, it was<br />

similarly immunolocalized with GFAP, but not with cKit. By preembedding<br />

immunoelectron microscopy, it was detected along glial cell membranes and their<br />

cytoplasmic processes around axon bundles. These findings indicate that 4.1G<br />

has some roles as adhesion and/or signal transduction in enteric glial cells of<br />

unmylinated nerve fibers in addition to myelination in the myelinated nerve ones.<br />

P<br />

<br />

in vivo in vitro<br />

1 1 2 1<br />

1<br />

1 2 2 <br />

<br />

TJ<br />

TJ <br />

mesaxon, paranode, SchmidtLanterman<br />

autotypic tight junction<br />

TJ tricellulin TRIC, claudin19 cldn19,<br />

junctional adhesion moleculeC JAMC <br />

in vivo in vitro <br />

Myelin Protein Zero 13 P13<br />

TJ TRICCldn19 JAMC 714 P714<br />

Cldn19 JAMC 14 <br />

TRIC 21 TRIC <br />

2 TJ <br />

4 Cldn19 JAMC <br />

mesaxonparanode SchmidtLanterman <br />

TRIC mesaxon paranode SchmidtLanterman <br />

TJ Cldn19 JAMC<br />

TRIC <br />

<br />

P<br />

<br />

<br />

1 2 2 1 2 <br />

1<br />

1<br />

2 <br />

<br />

10 <br />

<br />

14 <br />

<br />

MBP <br />

Calbindin <br />

<br />

<br />

Caspase3 <br />

<br />

Cux1 <br />

II/III, IV <br />

WGAHRP <br />

<br />

<br />

Laggard


124<br />

117 <br />

P<br />

<br />

<br />

<br />

<br />

<br />

<br />

<br />

NeuN, PGP 9.5<br />

nestin, vimentin, S100, GFAP <br />

E15<br />

5 vCo5P0 3 vS32 <br />

5 vL58 4 vL4<br />

3 <br />

E15 vCo5 , P0 vCo4 2 <br />

8 vCo2 <br />

E15 vCo6 ,P0 <br />

vCo8 2 8 vCo3 <br />

<br />

<br />

<br />

P<br />

<br />

1 2<br />

1<br />

2 <br />

<br />

490 <br />

42 <br />

21 <br />

42 <br />

<br />

<br />

4 10 <br />

<br />

10 21 <br />

21 <br />

<br />

<br />

<br />

JSPS 23590223 <br />

P<br />

<br />

<br />

<br />

<br />

<br />

<br />

<br />

<br />

<br />

<br />

<br />

Wistar <br />

Olfactory Marker Protein OMP <br />

<br />

OMP <br />

OMP <br />

<br />

<br />

<br />

<br />

<br />

<br />

P<br />

<br />

1 2 2 2 2 <br />

2 2<br />

1<br />

2 <br />

<br />

4-8 <br />

<br />

<br />

<br />

<br />

<br />

<br />

8-12 <br />

<br />

FG<br />

FG + FG <br />

DAB <br />

3D <br />

<br />

P<br />

<br />

DCC <br />

<br />

<br />

1 <br />

<br />

1 <br />

<br />

<br />

1 DCC deleted in<br />

colorectal cancer <br />

1 4 <br />

DCC <br />

1 <br />

DCC <br />

<br />

1 <br />

DCC <br />

1 DCC <br />

* <br />

23590225 <br />

P<br />

Spock3 null <br />

1 1 2 2 2<br />

1<br />

2 <br />

<br />

Spock3 BM40/SPARC/osteonectin <br />

Spock3 <br />

<br />

<br />

Spock3 <br />

<br />

<br />

<br />

<br />

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117 125<br />

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4 5 PIP5Kγ<br />

PIP5KγK γ636γ661γ687 <br />

RTPCR γ661 γ687<br />

<br />

PIP5Kγ<br />

<br />

PIP5Kγ<br />

<br />

<br />

KD<br />

PIP5Kγ<br />

636γ661γ687 KD<br />

PIP5Kγ<br />

661 <br />

PIP5KγK 661 PIP2 <br />

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DNA <br />

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in situ hybridization <br />

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P<br />

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1,2 1,4 1,2,3<br />

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DiI <br />

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RTPCR in situ<br />

hybridization <br />

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P<br />

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DNA cDNA <br />

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2 <br />

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DIO <br />

NPW NPW <br />

cFos <br />

NPW 1


126<br />

117 <br />

P<br />

Chewing under restraint stress inhibits the stressinduced<br />

suppression of cell proliferation in the hippocampal dentate gyrus<br />

Kinya Kubo 1 , Nobuyuki Karasawa 1 , Kazuhiko Satoh 2 , Yasutoku Kogaya 2 ,<br />

Sadakazu Ejiri 2 , Huayue Chen 3<br />

1<br />

Seijoh Univ Grad Sch Health Care Studies, 2 Dept Oral Anat, Asahi Univ Sch<br />

Dent, 3 Dept Anat, Gifu Univ Grad Sch Med<br />

Stress reduces new cell birth in the hippocampus dentate gyrus DG. Chewing<br />

under stress suppresses stressinduced responses. We examined whether chewing<br />

under restraint stress prevents the stressinduced suppression of cell proliferation.<br />

Male SAMP8 mice were used and divided into three groups as follows: control,<br />

restraint stress group, and restraint/chewing group. Mice in the restraint stress<br />

and restraint/chewing groups were placed in a ventilated plastic restraint tube,<br />

and then the tube containing the mouse was placed under a bright light for 45<br />

min, once a day for 14 days. Mice in the restraint/chewing group were allowed<br />

to chew on a wooden stick during this period. Plasma corticosterone levels were<br />

significantly higher in the restraint stress group than in the control and restraint/<br />

chewing groups in association with decreased cell proliferation in the hippocampal<br />

DG. The increase in plasma corticosterone levels induced by restraint stress was<br />

inhibited in the restraint/chewing group, and the reduction in cell proliferation was<br />

attenuated. These findings suggest that chewing under restraint stress prevents the<br />

stressinduced suppression of cell birth in the hippocampal DG.<br />

P<br />

Voluntary exercise promotes astrogliogenesis from Olig cells in<br />

some nuclei of the basal ganglia of adult mouse<br />

Kouko Tatsumi 1 , Hiroaki Okuda 1 , Mariko Yamano 2 , Akio Wanaka 1<br />

1<br />

Department of Anatomy and Neuroscience, Nara Medical University,<br />

2<br />

Department of Comprehensive Rehabilitation, Osaka Prefectural University<br />

We have previouly reported that astrocytes derived from Olig2 cells dramatically<br />

increased in the subthalamic nucleus STN after voluntary exercise in adult mice.<br />

Recently we comfirmed that astrogliogenesis is promoted in not only STN but also<br />

another nuclei of basal ganglia, e.g., the globus pallidus GP, substantial nigra<br />

SN, by voluntary excercise. Additionally, we observed that cfos expression<br />

significantly increased in neuron of these nuclei. It is well known that tha basal<br />

ganglia regurate motor activity by processing descending information from<br />

cortical regions. These findings implied the neuronastrocyte relationship based on<br />

glutamate metabolism in response to exercisestimuli. To confirm this relationship,<br />

we used fluorocitrate FC to metabolically inhibit astrocyte functions. As would<br />

be expected, mice regionally deficient of astrocytes in the STN exhibited reduction<br />

of spontaneous activities. On the other hand, FCmicroinjection into other but<br />

neighboring regions had little influence on motor activities. These findings suggest<br />

that astrocytic activities of the STN are closely related to neuronal outputs of the<br />

STN, possibly through the glutamate metabolism.<br />

P<br />

GDNF mRNA <br />

1 2 1 3 1<br />

1<br />

2 3 <br />

Glial cell linederived neurotrophic factor GDNF<br />

<br />

Wistar 2 <br />

12 10 10 4 <br />

17 m/min, 1 <br />

PCR GDNFGfra1Gfra2mRNA <br />

GDNFmRNAGfra2mRNA <br />

Gfra1mRNA <br />

<br />

<br />

P<br />

II <br />

<br />

<br />

<br />

<br />

IGFVEGF<br />

<br />

<br />

IIAngII<br />

<br />

AngII <br />

<br />

AngII ELISA <br />

2 <br />

AngII<br />

1 1 8 Bromodeoxiuridin<br />

BrdUVehicle BrdU 1.5 <br />

I <br />

AngII VEGF <br />

ELISA AngII <br />

<br />

P<br />

<br />

1 1 2 3 1 2 <br />

2 1 2<br />

1<br />

2 3 <br />

<br />

<br />

<br />

<br />

<br />

<br />

<br />

Watson <br />

2 Exercise<br />

EX Control CNT <br />

246810 Rotarod test <br />

HPLC <br />

<br />

Rotarod test EX <br />

6 CNT <br />

2 <br />

DA 1.7 10 EX <br />

DA CNT <br />

CNT TH <br />

<br />

P<br />

cfos <br />

<br />

1 2 1 1 1 3 <br />

3 4<br />

1<br />

2 <br />

3 <br />

4 <br />

<br />

<br />

<br />

<br />

cfos C57BL <br />

4 , <br />

20 12 m/min5<br />

5 / 4 <br />

<br />

cfos <br />

cfos <br />

34 cfos <br />

22cfos <br />

<br />

<br />

cfos


117 127<br />

P<br />

cFos <br />

<br />

1 2 1 1 1 3 <br />

3 4<br />

1<br />

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4 <br />

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cFos 5 <br />

C57BL High fat diet 32 4 <br />

2 <br />

5 12 m 20 <br />

5 4 <br />

5 μm ABC <br />

cFos <br />

cFos <br />

<br />

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<br />

cFos<br />

<br />

<br />

P<br />

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1 1 1 2 1<br />

1<br />

2 <br />

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<br />

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<br />

GFP <br />

E14 <br />

GFP 24h <br />

Tbr2 <br />

<br />

<br />

Tbr2 <br />

radial glia <br />

<br />

P<br />

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SD <br />

2-20 6 / <br />

5HT <br />

5HT <br />

Egr1 <br />

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Egr1 <br />

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1620 30 60 <br />

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P<br />

Altered dynamics of the cortical neuronal circuit in a mouse model of<br />

autism<br />

Shinji Tanaka 1 , Toru Takumi 2 , Shigeo Okabe 1<br />

1<br />

Department of Cellular Neurobiology, Graduate School of Medicine, University<br />

of Tokyo, 2 Laboratory of Integrative Bioscience, Graduate School of Biomedical<br />

Sciences, Hiroshima University<br />

Autism spectral disorder ASD is an early onset mental disease with impairments<br />

in higher cognitive functions. ASD symptoms may originate from altered<br />

connectivity of the neocortical neurons. This possibility can be tested by<br />

combining techniques of synapse imaging with reliable animal models of ASD.<br />

Genetically engineered mice that mimic the most frequent copy number variation<br />

in ASD human 15q1113 show multiple deficits in social behaviors. The<br />

postnatal synapse formation in the neocortex of this ASD model was studied by<br />

using twophoton in vivo imaging of pyramidal neurons expressing fluorescent<br />

proteins. Pyramidal neurons showed excess formation of nascent spines and<br />

their balanced elimination. Unexpectedly, analysis of PSD size changes in<br />

established spines, estimated from PSD95 clustering, revealed reduced PSD<br />

remodeling. Enhanced gain and loss of spines during network formation may<br />

increase mismatched connectivity, leading to altered pattern of neuronal activity<br />

that secondarily suppresses PSD remodeling. Negative correlation between<br />

spinogenesis and PSD remodeling may be a unique feature of this mouse model<br />

and its relevance to the etiology of ASD should be clarified.


128<br />

117 <br />

P<br />

Mechanism of deficit in aggressive behavior of metabotropic<br />

glutamate receptor subtype knockout mice<br />

Miwako MasugiTokita 1 , Peter Josef Flor 2 , Mitsuhiro Kawata 1<br />

1<br />

Dept. of Anatomy and Neurobiology, Kyoto Pref. Univ. of Med.,<br />

2<br />

Univ. of Regensburg, Regensburg, Germany<br />

Metabotropic glutamate receptors mGluRs consist of eight different subtypes<br />

and exert their effects on second messengers and ion channels via Gproteins.<br />

The function of individual mGluR subtypes in the CNS, however, largely remains<br />

to be clarified. We examined the aggressive behavior in male wildtype and<br />

mGluR7 knockout littermates, using a residentintruder paradigm. Wildtype<br />

mice displayed intense aggression against olfactory bulbectomized intruders.<br />

In comparison, mGluR7 knockout mice showed significantly reduced levels<br />

of aggression. We also found that mGluR7 knockout mice showed grooming<br />

behavior against intruders.<br />

Olfaction is known to be the essential components of aggressive behavior.<br />

Although mGluR7 is widely distributed in the brain, intense expression is found in<br />

olfactory system. To investigate the mechanism of altered aggression, we further<br />

assessed urine preference of mGluR7 knockout mice. Two cotton pads wetted<br />

with different odorant sources were presented simultaneously to the mice. Wild<br />

type mice spent longer time to sniff male urine than saline, but mGluR7 knockout<br />

did not show such preference.<br />

P<br />

PTPRA<br />

<br />

<br />

PTPRA <br />

<br />

PTPRA <br />

<br />

PTPRA <br />

<br />

PTPRA <br />

9 <br />

<br />

<br />

PTPRA <br />

<br />

<br />

P<br />

Kisspeptin <br />

<br />

<br />

Kisspeptin <br />

<br />

kisspeptin <br />

<br />

kisspeptin <br />

kisspeptin in situ hybridization<br />

7 kisspeptin <br />

<br />

kisspeptin <br />

18 kisspeptin <br />

kisspeptin <br />

<br />

9 <br />

kisspeptin <br />

kisspeptin <br />

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GnRH <br />

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30 42 60 Wistar Rat GFAP <br />

GFAP <br />

<br />

GFAP 21 <br />

30 <br />

GFAP <br />

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GFAP <br />

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GnRH <br />

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GFAP <br />

Gi PAG GFAP <br />

Gi α GiA GFAP<br />

<br />

α Gi PAG <br />

GiA <br />

GFAP <br />

GiA <br />

<br />

P<br />

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<br />

<br />

<br />

<br />

TGFβ1 <br />

transforming growth factorβ1 TGFβ1 Komuta<br />

et al., Cell. Mol. Neurobiol. 30: 101111, 2010 10<br />

<br />

<br />

<br />

<br />

14 <br />

TGFβ1 <br />

<br />

0 <br />

TGFβ1 <br />

<br />

TGFβ1


117 129<br />

P<br />

Identification of CSPG constituting DACS, a novel brain extracellular<br />

matrix<br />

Hiroaki Okuda 1 , Yukinao Shibukawa 2 , Hiroaki Korekane 3,4 ,<br />

Noriko HoriiHayashi 5 , Kouko Tatsumi 1 , Yoshinao Wada 2 ,<br />

Naoyuki Taniguchi 3,4 , Akio Wanaka 1<br />

1<br />

Dept. Anatomy and Neuroscience, Nara Med. Univ., 2 Dept. Molecular Medicine,<br />

Osaka Med. Center and Research Institute for Maternal and Child Health,<br />

3<br />

Dept. Disease Glycomics, RIKENISIR, Osaka Univ. Alliance Lab., 4 Systems<br />

Glycobiology Research Group, Chemical Biology Dept., Advanced Science<br />

Institute, RIKEN, 5 Dept. Anatomy and Cell Biology, Nara Med. Univ.<br />

An antichondroitin sulfate antibody CS56 delineated a structure with a<br />

unique morphology like a dandelion clock. We named it DAndelion Clock<br />

like Structure DACS BBRC; 364: 4105, 2008. DACSs surrounded a group<br />

of NeuNpositive/GABAnegative neurons. At an ultrastructural level, CS56<br />

immunoreactivities were localized in the cytoplasm and on the membrane of<br />

astrocytes. As the postnatal cerebral cortex matured, DACSs became visible<br />

from the end of the critical period. Furthermore, DACSs is conserved among<br />

species. In this study, we have identified the core protein of DACSconstituting<br />

CSPG. We purified core proteins from the mouse cerebral cortex by anion<br />

charge, charge transfer and size exclusion chromatographies and identified one<br />

of them as TenascinR TNR using mass spectrophotometry. TNR is thought to<br />

constitute socalled perineuronal net that modulates plasticity of interneurons. In<br />

situ hybridization analysis revealed that TNR mRNA was selectively localized<br />

at CS56positive astrocytes, but not WFApositive GABAergic interneurons<br />

in the adult mouse brain. These results suggest that TNR may play previously<br />

unexpected roles in a subpopulation of cortical astrocytes.<br />

P<br />

<br />

1 2 1<br />

1<br />

2 <br />

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1980 <br />

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barrel <br />

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<br />

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<br />

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<br />

<br />

<br />

P<br />

Mutations in POLRA and POLRB encoding RNA polymerase III<br />

subunits cause an hypomyelinating leukoencephalopathy<br />

1 2 3 4 5 <br />

4 1 1<br />

1<br />

2 3 <br />

4 5 <br />

<br />

We have recently reported a hypomyelinating syndrome characterized by diffuse<br />

cerebral hypomyelination with cerebellar atrophy and hypoplasia of the corpus<br />

callosum HCAHC. We performed whole exome sequencing of three unrelated<br />

individuals with HCAHC, and identified compound heterozygous mutations in<br />

POLR3B in two individuals. The mutations include a nonsense mutation, a splice<br />

site mutation and two missense mutations at evolutionally conserved amino acids.<br />

Using reverse transcriptionPCR and sequencing, we demonstrated that the splice<br />

site mutation caused deletion of exon 18 from POLR3B mRNA, and that the<br />

transcript harboring the nonsense mutation underwent nonsensemediated mRNA<br />

decay. We also identified compound heterozygous missense mutations in POLR3A<br />

in the remaining individual. POLR3A and POLR3B encode the largest and second<br />

largest subunits of RNA Polymerase III Pol III, RPC1 and RPC2, respectively.<br />

Pol III is involved in the transcription of small noncoding RNAs, such as 5S<br />

ribosomal RNA and all transfer RNAs tRNA. Perturbation of Pol III target<br />

transcription could be a common pathological mechanism underlying POLR3A<br />

and POLR3B mutations.<br />

P<br />

<br />

1 1 1 1 1 2 <br />

2<br />

1<br />

2 <br />

polyQ <br />

CAG <br />

<br />

polyQ <br />

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<br />

polyQ <br />

ataxin3 polyQ Q77trAT3<br />

polyQ ubiquitin <br />

polyQ <br />

islet1 <br />

<br />

PolyQ <br />

1TUNEL <br />

caspase3 2 Bclxl <br />

<br />

<br />

P<br />

Zitter rat <br />

<br />

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Zitter attractin <br />

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Zitter <br />

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Zitter <br />

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Weigert Luxol<br />

fast blue<br />

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20 5 <br />

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<br />

100


130<br />

117 <br />

P<br />

Stigmoid body <br />

Islam Md. NabiulJahan Mir Rubayet <br />

<br />

<br />

Stigmoid body STB <br />

HAP1huntigtin associated protein 1 <br />

STB HAP1<br />

<br />

<br />

HeLa wistar PCM1 pericentriol<br />

material 1 <br />

<br />

PCM1 <br />

diffuse <br />

inclusion 3 2 PCM1 <br />

PCM1 inclusion STB <br />

HAP1 <br />

PCM1 HAP1/STB STB <br />

STB HAP1 PCM1 90% <br />

PCM1 inclusion STB <br />

in vitro HAP1 <br />

HeLa STB PCM1 <br />

HeLa STB PCM1 <br />

<br />

P<br />

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1 1 2 1<br />

1<br />

2 <br />

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<br />

Holmes <br />

<br />

PTAH<br />

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<br />

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ddY 20 g<br />

6 μm<br />

PTAH<br />

<br />

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PTAH <br />

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Holmes <br />

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celloidin Kultschitzky <br />

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90 1 1 <br />

celloidin <br />

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P<br />

Eusthenopteron foodi<br />

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1 2 3 4<br />

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4 <br />

Eusthenopteron foodi <br />

Eusthenopteron foodi<br />

TEM<br />

SEMEPMA X <br />

<br />

TEM <br />

<br />

2 <br />

<br />

TEM <br />

X <br />

fluoraptite EPMA <br />

Ca/P 1.96 Ca/P <br />

1.87 F 1.87-5.11Wt<br />

2.10-4.55 Wt 965-<br />

967cm 1 <br />

<br />

P<br />

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Palaeoniscus <br />

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3 <br />

Palaeoniscus <br />

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117 131<br />

P<br />

NOS <br />

1 2 4 4 4 <br />

3 4<br />

1<br />

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NO <br />

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NO<br />

NO <br />

<br />

NOS <br />

0371014 C57BL/6J <br />

4 PA <br />

10%EDTA <br />

nNOSiNOSeNOS <br />

<br />

NOS <br />

07 nNOS i<br />

eNOS 1014 nNOS <br />

<br />

ieNOS <br />

10 NOS <br />

<br />

<br />

P<br />

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1 1,2 1 1 1 <br />

1<br />

1<br />

2 <br />

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AQP1 <br />

<br />

AQP1 <br />

2 <br />

AQP1 <br />

<br />

-<br />

----<br />

--<br />

in situ AQP1mRNA <br />

<br />

<br />

AQP1 <br />

<br />

AQP1 <br />

<br />

P<br />

TNFα/RANKL microRNA <br />

<br />

<br />

microRNA 21 nt noncoding RNA mRNA <br />

3’UTR <br />

<br />

RANKL microRNA <br />

<br />

TNFα <br />

microRNA <br />

<br />

RAW264.7 <br />

TNFα TNFα RANKL<br />

RANKL 10 ng/ml <br />

TNFα/RANKL <br />

0, 24, 82 total RNA <br />

microRNA qRTPCR<br />

<br />

TNFα/RANKL 2 microRNA<br />

44 miR1224 <br />

miR223 <br />

microRNA TNFα/RANKL <br />

<br />

P<br />

hemokinin <br />

1 2 1 1 1 <br />

1 2<br />

1<br />

2 <br />

1HK1<br />

1 NK1 P SP SP <br />

HK1 <br />

<br />

in vivo 5 <br />

HK1 <br />

in vitro RANKL<br />

MCSF 7 RTPCR <br />

HK1 NK1 <br />

SP HK1 TRAP <br />

<br />

in vivo HK1 <br />

<br />

in vitro HK1 NK1 <br />

TRAP <br />

SP HK1 <br />

SP HK1 SP <br />

SP <br />

HK1 <br />

HK1 NK1 SP <br />

<br />

P<br />

DGKζ Retinoblastoma <br />

1,2 2 1<br />

1<br />

2 <br />

DGK <br />

<br />

Retinoblastoma Rb E2F <br />

DGK <br />

DGKζ Rb C2C12<br />

DGKζ Rb <br />

<br />

DGKζ <br />

DGKζ<br />

Rb <br />

ATDC5 <br />

DGKζ DGKζ<br />

Rb <br />

DGKζ mRNA <br />

<br />

P<br />

<br />

1 1 1 1 2 <br />

1<br />

1<br />

2 <br />

<br />

SSEA3 <br />

Multilineagedifferentiating<br />

Stress Enduring Muse Muse <br />

<br />

<br />

<br />

<br />

<br />

<br />

Muse<br />

FACS SSEA3 <br />

<br />

1 <br />

6<br />

<br />

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132<br />

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P<br />

Placenta specific miR-517a modulates gene expression in Jurkat<br />

cells<br />

Md Moksed Ali 1 , Xiaohui Song 1,2 , Osamu Ishibashi 1 , Kunio Kikuchi 1 ,<br />

Tomoko Ishikawa 1 , Takami Takizawa 1 , Toshihiro Takizawa 1<br />

1<br />

Dept Mol Med & Anat, Nippon Medical School 2 Dept Pharm, Harbin Medical<br />

University<br />

[Objective] MicroRNAs miRNAs are noncoding RNAs that repress gene<br />

expression posttranscriptionally. Recently we have found that human placenta<br />

specific miRNAs are transferable to Jurkat cells human T cell lymphoblast<br />

like cell line via exosomes manuscript in preparation. In this study, we<br />

overexpressed placenta specific miR-517a in Jurkat cells and did microarray<br />

analysis MA to identify its target mRNAs.<br />

[Methods] MA was performed on Jurkat cells overexpressing miR-517a.<br />

Validation of genes downregulated by miR-517a was carried out by realtime<br />

PCR, Western blot, and 3'UTRluciferase reporter assay.<br />

[Results] We found that cyclic GMP dependent protein kinase 1 (PRKG1), one<br />

of 8 downregulated genes identified in MA, is a target of miR-517a in silico. MiR-<br />

517a significantly downregulated the expression of PRKG1 at both the mRNA and<br />

protein levels. Furthermore, miR-517a significantly decreased luciferase reporter<br />

activity.<br />

[Conclusion] We identified that PRKG1 is indeed a target of miR-517a in Jurkat<br />

cells. These findings provide a mechanistic insight on the posttranscriptional<br />

regulation by miRNAs of placentaderived exosomes in T cells.<br />

P<br />

microRNA CpG <br />

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microRNA miRNA 22 RNA<br />

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19 miRNAs C19MC; miR-517a <br />

Luo<br />

et al. Biol Reprod 81: 717729, 2009 18<br />

kb CG DNA <br />

C19MC NoguerDance et al.<br />

Hum Mol Genet 19: 35663582, 2010<br />

BeWo JEG3<br />

HTR8/SVneo C19MC <br />

miRNA PCR <br />

DNA PCR <br />

CG <br />

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FcRIIb RAB GTPasesRAB1B RAB3D<br />

FcRIIb in vitro FcRIIb<br />

GFP FcRIIb <br />

pFCGR2B-GFP HUVEC<br />

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P<br />

Agerelated accumulation of nonheme ferric and ferrous iron in<br />

mouse ovarian stroma visualized by sensitive iron histochemistries<br />

Yoshiya Asano<br />

Department of Neuroanatomy, Cell Biology and Histology, Hirosaki University<br />

Graduate School of Medicine<br />

Sensitive nonheme iron histochemistries, namely perfusionPerls and Turnbull<br />

method, were applied to study the distribution and agerelated accumulation of<br />

nonheme iron in mouse ovary. Microscopic studies revealed that nonheme ferric<br />

iron is distributed predominantly in stromal tissue, especially in macrophages. By<br />

contrast, the distribution of nonheme ferrous iron was restricted to a few ovoid<br />

macrophages. Aged ovaries exhibited remarkable nonheme iron accumulation in<br />

all stromal cells. Particularly, nonheme ferrous iron level was increased in stroma,<br />

suggestive of increased levels of redoxactive iron, which can promote oxidative<br />

stress. Moreover, intense localization of both nonheme ferric and ferrous iron was<br />

observed in aggregated large stromal cells that were then characterized as ceroid<br />

laden enlarged macrophages. Iron overload in adult mice resulted in nonheme<br />

iron deposition in the stroma and generation of enlarged macrophages, suggesting<br />

that iron accumulation induced morphological changes. Our data indicated that<br />

nonheme iron accumulation in stromal tissue may be related to aging of the ovary<br />

which due to the increasing of oxidative stress.<br />

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Activities of human upper limb muscles during a combined<br />

movement of elbow flexion/extension and forearm pronation/<br />

supination<br />

Makoto Naganuma 1 , Wataru Hashizume 1 , Katsuhiko Suzuki 2 , Toshiaki Sato 3 ,<br />

Hiromi Fujii 3 , Akira Naito 1<br />

1<br />

Dept Anat, Yamagata Univ Sch Med, 2 Dept PT, Yamagata Pref Univ Health Sci,<br />

3<br />

Dept OT, Yamagata Pref Univ Health Sci<br />

Facilitation and inhibition mediated by group I afferents among human upper<br />

limb muscles have been studied. The former and latter must be active during,<br />

respectively, cocontraction and reciprocal contraction of the muscles. This study<br />

examined activities of the biceps brachii BB, pronator teres PT, extensor carpi<br />

radialis ECR and ulnaris ECU, and flexor carpi radialis FCR and ulnaris<br />

FCU during a combined movement of elbow flexion/extension EF/EE and<br />

forearm pronation/supination FP/FS in ten normal men with electromyography.<br />

During movements of EFFP/EEFS and EFFS/EEFP, BB and FCU group<br />

BB showed parallel activities cocontraction increasing and decreasing and<br />

PT, ECR, and ECU group PT those decreasing and increasing at the EEFS and<br />

EFFS, and EFFP and EEFP phases, respectively. These fluctuations resulted<br />

in reciprocal contraction between group BB and PT. The results suggest that the<br />

facilitation between PT and ECR and the inhibition between BB and PT are active<br />

during the movements. Findings of the contractions may indicate existence of<br />

facilitation between PT and ECU, and ECR and ECU, and inhibition between PT<br />

and FCU, ECR and FCU, and ECU and FCU.<br />

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Persistent left hepatic venous directly opening into the right atrium<br />

1 2 2 1<br />

1<br />

2 Department of Anatomy, Faculty of<br />

Medicine, Chiang Mai University<br />

An anomalous left hepatic vein opening independently of the coronary sinus into<br />

the right atrium was found in the cadaver of an 88yearold Japanese man. This<br />

vein originated from the left lobe of the liver, perforated the diaphragm at the left<br />

side of the vena caval foramen and opened into the right atrium. The left hepatic<br />

vein anastomosed mutually with the middle hepatic vein at the level of venule.<br />

The ligamentum venosum originated from the left branch of the portal vein and<br />

was connected directly to the left hepatic vein. The development of the central<br />

systemic venous system and a possible explanation for the morphogenesis of this<br />

anomaly were reviewed. As a result, the occurrence of this anomalous vein was<br />

explained as being due to the persistence of the left vitelline connection with the<br />

left sinus horn and the ductus venosus.<br />

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117 139<br />

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Nacholapithecus kerioi <br />

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Nacholapithecus kerioi 1500 <br />

1999 2002 <br />

Nacholapithecus <br />

Papio cynocephalus<br />

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Nacholapithecus <br />

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MacLarnon1995intermembral<br />

index<br />

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Nacholapithecus <br />

#20247033 <br />

P<br />

Involvement of Olig in the formation of reciprocal connection<br />

between the thalamus and cortex<br />

1,6 C Parras 2 Q Zhang 3 4,6 5 <br />

6<br />

1<br />

2 Institute of the Brain and Spinal Cord ICM, Inserm<br />

UPMC 3 BSI 4 5 <br />

6 <br />

Olig2 is a transcription factor essential for oligodendrocyte and motor neuron<br />

generation in the spinal cord. Although Olig2 is expressed throughout the<br />

embryonic central nervous system, the role of Olig2 in the brain development<br />

has not been uncovered well yet. To explore new function of Olig2, we first<br />

analyzed axonal architecture in Olig2 deficient mice. Immunohistochemistry<br />

against neurofilamentM showed abnormal course and fasciculation of axons<br />

in the mutant thalamus. Expression analysis of NetrinG confirmed that both<br />

thalamocortical and corticothalamic fibers are impaired in the mutant. We next<br />

performed microarray analysis of Olig2 deficient basal forebrain, and identified<br />

that several axon guidance molecules were up or downregulated in the Olig2<br />

mutant. To examine spatiotemporal expression patterns of these genes, we carried<br />

out in situ hybridization, and revealed that the expression of EphA3, Robo1 and<br />

Slit2 were altered in the mutant diencephalon. Our results suggest that Olig2 plays<br />

an essential role in the formation of reciprocal connection between the thalamus<br />

and cortex via regulating the expression of several axon guidance molecules.<br />

P<br />

Studying nascent daughter cells’ neighborship to understand the<br />

mechanism of cell fate choices in the neocortical neurogenesis<br />

<br />

<br />

Cellcell interactions are very important for developmental events that construct<br />

the central nervous system. However, we still cannot tell exactly when and<br />

where these interactions occur for nascent daughter cells born at the apical/<br />

ventricular surface of the neuroepithelium NE or ventricular zone VZ. NE/VZ<br />

is heterogeneous with cells differing in differentiation state and cell cycle phase,<br />

allowing cells to “neighbor” make contacts to a variety of types of cells. It is<br />

possible that such “neighborship” dynamically changes for each cell, because<br />

cell movements are an active. To ask whether/how the history of neighborship<br />

for each daughter cell might affect its subsequent fate determination, we are<br />

comprehensively monitoring the composition of cells that surround a given<br />

nascent 3hrold daughter cell. Confocal microscopy to obtain optical slices<br />

parallel to the apical/ventricular surface using brain/retinal primordia prepared<br />

from ROSA26 Lynvenus mice allows us to observe outlines of all cells in the<br />

periventricular area. Our live observations suggest that daughter cells born<br />

almost simultaneously within a limited area can be different as to how they are<br />

surrounded.<br />

P<br />

GABAA <br />

1 2 1 1<br />

1<br />

2 <br />

Student Lab<br />

GABAA <br />

<br />

Tochitani et al., 2010 GABAA <br />

<br />

10 E10<br />

GABAA alpha4 <br />

E10 E12 GABA <br />

E14 <br />

GABA <br />

GABA GAD65/67 <br />

GABA GABAA<br />

Taurine E10 <br />

preplate E12 E14 subplate marginal zone <br />

GABAA <br />

<br />

intermediate progenitor <br />

GABAA <br />

intermediate progenitor <br />

P<br />

<br />

<br />

<br />

<br />

<br />

<br />

6 <br />

<br />

<br />

transplantation <br />

<br />

<br />

<br />

transplantation <br />

14 <br />

<br />

<br />

<br />

<br />

P<br />

kirrel <br />

1 1 1 2 1 <br />

1<br />

1<br />

2 <br />

<br />

A member of the immunoglobulin superfamily, kirrel3 is widely expressed in<br />

the developing and adult central nervous system CNS. In the present study,<br />

we investigated spatiotemporal expression of kirrel3 in the CNS using kirrel3<br />

lacZ knockin mice. The expression of βgalactosidase βgal was found in<br />

the various regions of developing and adult CNS, including the olfactory bulb,<br />

striatum, cerebral cortex, hippocampus, and cerebellum. In the adult olfactory<br />

bulb, the expression of βgal was observed in the calbindin or carlretininpositive<br />

periglomerular neurons, subpopulation of Reelinpositive external tufted cells<br />

and mitral cells, and GAD67positive granule cells. In the adult striatum, βgal<br />

positive cells were mainly observed in the ventral striatum. In the developing<br />

olfactory bulb and striatum, βgal was expressed in the differentiating zone, but<br />

not in the ventricular zone. These results suggest that kirrel3 may be involved in<br />

development of several neural circuits, including the olfactory system and limbic<br />

system.<br />

This work was supported by a GrantinAid for Scientific Research B from<br />

Japan Society for the Promotion of Science 22390036.


140<br />

117 <br />

P<br />

Characterization of the RNAbinding protein Musashi in zebrafish<br />

<br />

<br />

Musashi Msi is an evolutionarily conserved gene family of RNAbinding<br />

proteins RBPs that is preferentially expressed in the nervous system. The first<br />

member of the Msi family was identified in Drosophila. Drosophila Msi plays<br />

an important role in regulating asymmetric cell division of the sensory organ<br />

precursor cells. The mammalian orthologs, including human and mouse Msi1, are<br />

neural RBPs that are strongly expressed in neural stem cells NSCs. Mammalian<br />

Msi1 contributes to self renewal of NSCs through translational regulation of<br />

several target mRNAs. In this study, the zebrafish Msi ortholog zMsi1 was<br />

identified and characterized. The normal spatial and temporal expression profiles<br />

for both protein and mRNA were determined. Overall, zMsi1 was strongly<br />

expressed in neural tissue in early stages of development and exhibited similarity<br />

to mammalian Msi1 expression patterns. To reveal the in vivo function of zMsi1,<br />

morpholinos against Msi1 were introduced into onecell stage zebrafish embryos.<br />

Knock down of zmsi1 frequently resulted in aberrant formation of the CNS. These<br />

results suggest that Msi1 plays roles in CNS development in vertebrates.<br />

P<br />

PSANCAM <br />

1 2 1<br />

1<br />

2 <br />

<br />

PSANCAMpolysialic acidneural cell adhesion molecule <br />

<br />

PSANCAM 57 E5E7 <br />

PSANCAM <br />

<br />

PSANCAM <br />

BrdU E5E7 BrdU <br />

FITC <br />

PSANCAM <br />

BrdU 10 E6 <br />

BrdU <br />

E5 BrdU E6 E7 <br />

BrdU PSANCAM <br />

E5E7 PSANCAM <br />

<br />

<br />

P<br />

mRNA <br />

1 2 1<br />

1<br />

2 <br />

<br />

<br />

GnRH <br />

mRNA <br />

mRNA 2.5 3.5 <br />

3.5 <br />

4 GnRH <br />

mRNA <br />

mRNA <br />

<br />

Tol2GFP 2.5 <br />

1619 GFP <br />

GnRH GFP <br />

mRNA <br />

mRNA <br />

mRNA GnRH <br />

GnRH <br />

<br />

P<br />

CNTF <br />

<br />

<br />

<br />

<br />

<br />

cuprizone <br />

MBPCNPase <br />

<br />

<br />

<br />

<br />

cuprizone<br />

<br />

<br />

MBPCNPase <br />

<br />

CNTF <br />

<br />

CNTF <br />

P<br />

<br />

<br />

<br />

<br />

<br />

<br />

<br />

E1313.5 E11.5<br />

<br />

Islet1Lim3Lhx3 MNR2 <br />

MMCl Lim3 <br />

<br />

Islet1Lim3Foxp1<br />

E11.5 <br />

Islet1 Lim3 <br />

<br />

Foxp1 <br />

<br />

P<br />

<br />

<br />

<br />

<br />

<br />

<br />

<br />

<br />

6


117 141<br />

P<br />

kirrel <br />

<br />

1 1 1 1 2 <br />

1<br />

1<br />

2 <br />

<br />

A member of the immunoglobulin superfamily, kirrel3, is expressed in the dorsal<br />

root ganglia DRGs. In the previous report, we have suggested that kirrel3<br />

may play a role in the development of tyrosine kinase receptor Trk Cpositive<br />

neurons. To get further insights into the function of kirrel3 in the DRG neurons,<br />

we characterized kirrel3expressing neurons in the DRGs of kirrel3lacZ Z knockin<br />

mice. In the lumber DRG neurons, the expression of βgalactosidase βgal<br />

was first observed at embryonic day 12.5, gradually increased, and reached<br />

the maximum level at postnatal day P 7. During embryonic stages, βgal was<br />

predominantly expressed in TrkA and TrkCpositive neurons, while some βgal<br />

positive neurons contained TrkB or Ret. The expression of Ret was increased in<br />

βgalpositive neurons between P7 and P14, and was observed in approximately<br />

43% of βgalpositive neurons of the adult DRGs. These results suggest that<br />

kirrel3 may be involved in the development of nociceptive and mechanoceptive<br />

neurons in addition to proprioceptive neurons.<br />

This work was supported by a GrantinAid for Scientific Research B from<br />

Japan Society for the Promotion of Science 22390036.<br />

P<br />

<br />

<br />

<br />

<br />

<br />

<br />

<br />

<br />

<br />

<br />

<br />

BMP4 FGF2 <br />

<br />

Dlx5Six1Eya2 PCR Dlx5 <br />

10 <br />

GATA3/keratin19 Slug <br />

Sox2 FGF2<br />

FGF8 <br />

BMP4 FGF2 <br />

<br />

P<br />

/ <br />

Sprouty<br />

1,2 2 3 2<br />

1<br />

2 <br />

3 <br />

<br />

<br />

in vitro <br />

bFGF <br />

Receptor tyrosine kinase RTK <br />

Sprouty 4 Sprouty<br />

in situ hybridization <br />

<br />

Sprouty4 Sprouty4 <br />

<br />

Sprouty4 <br />

<br />

Sprouty4 <br />

Sprouty4 <br />

<br />

<br />

P<br />

<br />

<br />

<br />

4 Oct3/4Sox2Klf4cMyc <br />

induced pluripotent stem cell<br />

iPS <br />

<br />

<br />

<br />

<br />

<br />

<br />

<br />

iPS <br />

<br />

P<br />

<br />

1 2 3 2<br />

1<br />

2 3 <br />

P<br />

Dlg <br />

1 1 2<br />

1<br />

2 <br />

<br />

<br />

<br />

<br />

<br />

<br />

3 16 Hox11Tcf21<br />

WT1Barx1Nkx3.2<br />

mesothelium<br />

<br />

<br />

Fgf16 FGF receptor12 <br />

mesothelium<br />

Fgf16 FGF receptor12 <br />

<br />

<br />

<br />

Dlg1 MAGUK <br />

Dlg1 Dlg1 -/- <br />

<br />

Dlg1 <br />

Dlg1 -/- <br />

Dlg1 <br />

2010 Wnt Fzd1 <br />

2 Dlg1 -/- <br />

Fzd1 -/- Fzd2 -/- <br />

Dlg1 -/- <br />

<br />

Fzd1 -/- Fzd2 -/- <br />

Dlg1 -/- <br />

Notch <br />

Notch <br />

<br />

Dlg1 -/- <br />

Dlg1 Notch


142<br />

117 <br />

P<br />

<br />

sox <br />

<br />

<br />

<br />

-<br />

<br />

<br />

200 sox <br />

sox9 sox9 <br />

sox9 <br />

<br />

in vitro siRNA sox9 <br />

sox9 <br />

<br />

<br />

sox9 <br />

α<br />

<br />

sox9 -<br />

<br />

P<br />

Protocadherin a <br />

<br />

<br />

Pcdh<br />

Pcdh10a <br />

Pcdh10b Pcdh <br />

<br />

<br />

<br />

Pcdh10a <br />

Pcdh10a <br />

<br />

Pcdh10a <br />

<br />

P<br />

Developmental Origins of Health and Disease DOHaD <br />

<br />

Randeep Rakwal <br />

<br />

<br />

<br />

<br />

DOHaDDevelopmental Origins of Health and Disease<br />

<br />

<br />

50% <br />

1018 18 <br />

mRNA <br />

DyeSwap DNA <br />

5500 4000 <br />

200<br />

<br />

Trib1 <br />

<br />

H1 H3 G Gpr88<br />

<br />

<br />

P<br />

α <br />

1 2 1<br />

1<br />

2 <br />

<br />

<br />

β α<br />

<br />

α <br />

Ca CADM1 SynCAM<br />

α <br />

α <br />

SynCAM <br />

<br />

SynCAM KO α <br />

α <br />

<br />

P<br />

Occludin p <br />

<br />

1 2<br />

1<br />

2 1 <br />

OccludinOCLN<br />

p63 <br />

<br />

SMG 11E11 12 <br />

<br />

<br />

OCLN p63 <br />

E1213 ICR p63 <br />

OCLN SMG <br />

p63 OCLN 48<br />

TB p63 <br />

OCLN E13 p63 E14 <br />

p63 TB OCLN <br />

TB TB OCLN <br />

p63 E18 <br />

p63 OCLN <br />

TB OCLN <br />

<br />

P<br />

<br />

<br />

1 2 1 2 3 4,5 <br />

1<br />

1<br />

2 3 <br />

4<br />

5 <br />

<br />

<br />

Ca 2+ <br />

<br />

L Ca 2+ <br />

Ca 2+ <br />

TEM <br />

12 nm <br />

<br />

<br />

Ca 2+ induced Ca 2+ release CICR <br />

<br />

CICR <br />

<br />

CICR


117 143<br />

P<br />

<br />

<br />

<br />

<br />

prechordal chondrocranium<br />

trabeculae<br />

trabecula communis<br />

<br />

<br />

<br />

intertrabeculae<br />

intertrabeculae <br />

<br />

PNA PNA <br />

<br />

PNA <br />

PNA <br />

PNA <br />

<br />

<br />

P<br />

<br />

<br />

<br />

<br />

<br />

<br />

1 2 <br />

3 <br />

<br />

13 DiI <br />

15 DiO<br />

<br />

22 1 2 <br />

3 4 <br />

<br />

24 1 2 <br />

3 4 <br />

<br />

<br />

<br />

<br />

<br />

<br />

P<br />

<br />

<br />

<br />

<br />

<br />

<br />

<br />

2 <br />

2 <br />

PET <br />

<br />

Aoyama et al., 2005PET <br />

24 7 <br />

<br />

PET 24 <br />

<br />

<br />

<br />

/ <br />

<br />

<br />

P<br />

LEFSP <br />

1 2 1<br />

1<br />

2 <br />

LEF1 Wnt/ßcatenin <br />

<br />

SP6 Wnt/ßcatenin BMP <br />

LEF1 LEF1 <br />

SP6 in vivo <br />

LEF1 SP6 <br />

<br />

19 10 <br />

LEF1 SP6 <br />

19 SP6 <br />

LEF1 <br />

10 SP6 <br />

<br />

LEF1 SP6 <br />

LEF1 SP6 LEF1<br />

<br />

LEF1 <br />

<br />

P<br />

<br />

1 2 3 1<br />

1<br />

1 2 <br />

3 <br />

<br />

Cynops<br />

pyrrhogaster<br />

<br />

<br />

<br />

/ TH/THR <br />

<br />

insitu <br />

THR <br />

<br />

<br />

THR <br />

2324 <br />

B23792117<br />

P<br />

TTF <br />

1,2 1 1 1,2 2 1<br />

1<br />

2 <br />

<br />

<br />

<br />

<br />

<br />

TTF1 <br />

0 00 0 E0<br />

E10E12 ddy 6 10 μm<br />

1 TTF1 <br />

LSAB DAB <br />

TUNEL HistoGreen <br />

<br />

E10.0 <br />

E10.75 E11.0 <br />

E11.25 E10.25 TTF1<br />

E11 <br />

TTF1 <br />

E11.25


144<br />

117 <br />

P<br />

The role of Rho signaling pathway in dental epithelial stem cells<br />

Keishi Otsu 1 , Ryota Kishigami 1 , Ai OikawaSasaki 1 , Naoki Fujiwara 1 ,<br />

Kiyoto Ishizeki 1 , Hidemitsu Harada 1<br />

1<br />

Dept. Anatomy, Iwate Med. Univ., 2 Advanced Oral Health Science Research<br />

Center, Iwate Med. Univ.<br />

We have recently found that Rho signaling plays an important role in ameloblast<br />

differentiation through maintenance of the cell polarity Otsu et al. Journal of<br />

Cellular Physiology, 2010. Consequently, we next focused on the role of Rho<br />

signaling in dental epithelial stem cells. In this study, we examined the function of<br />

ROCK, downstream Rho effectors, in dental epithelial cells isolated from mouse<br />

incisor apical bud. After treatment of ROCK inhibitor and knocking down ROCK<br />

by siRNA, the shape of cells changed from epithelial phenotype to mesenchymal<br />

like cells, and cellcell adhesions were lost. Real time RTPCR showed that<br />

ROCK inhibitor decreased expression of epithelial cell markers, and increased<br />

mesenchymal and stem cell markers. In the treated cells, mRNA expressions<br />

of slug, which is epithelialmesenchymal transition markers, increased and the<br />

intense nuclear accumulation was observed. In mouse incisor, slug was strongly<br />

expressed in apical bud compared to differentiated ameloblasts. Based on the<br />

data, we consider that Rhoslug signaling pathway is closely involved with the<br />

maintenance of dental epithelial stem cells.<br />

P<br />

Localization of osteopontin and osterix in periodontal tissue during<br />

orthodontic tooth movement in rats<br />

Ji Youn Kim, Byung In Kim, Seong Suk Jue, Jae Hyun Park, Je Won Shin<br />

Department of Oral Anatomy, Graduate School of Dentistry, Kyung Hee<br />

University, Seoul, KOREA<br />

The aim of this study was to evaluate the localization of osteopontin OPN<br />

and osterix in periodontal tissue during experimental tooth movement with<br />

heavy force in rats. Nickeltitanium closedcoil springs were used to create a<br />

100g mesial force to the maxillary first molars. On days 3, 7, 10, and 14 after<br />

force application, histological changes in periodontal tissue were examined by<br />

immunohistochemistry using proliferating cell nuclear antigen PCNA, OPN, and<br />

osterix. PCNApositive cells were found close to the alveolar bone and cementum<br />

on both sides. OPNpositive cells were observed along the cementing line of the<br />

cementum and bone on both sides and also were visible along with newly formed<br />

fibers in the periodontal ligament on the tension side. Osterixpositive cells were<br />

strongly detected on the surface of the alveolar bone and cementum on both sides.<br />

During tooth movement, periodontal remodeling occurs on both sides. These<br />

results indicate that OPN and osterix may play an important role of differentiation<br />

and osteoblasts and cementoblasts matrix formation during periodontal tissue<br />

remodeling.<br />

P<br />

Fetal jaw movement affects molecular cascade in the development of<br />

mandibular condylar cartilage<br />

Esrat Jahan 1,2 3 1 Ashiq Mahmood Rafiq 1,2 <br />

2 1<br />

1<br />

2 <br />

3 <br />

Fetal jaw movement restriction has been shown to cause deformity of the<br />

mandibular condyle. We hypothesized that this treatment affects the expression<br />

of mechanosensitive molecules, namely Indian hedgehog Ihh and bone<br />

morphogenetic protein2 Bmp2 in the condyle. We restrained jaw movement<br />

by suturing the jaw of E15.5 mouse embryos and allowed them to develop<br />

until E18.5 using exo utero system. Morphological, histomorphometric and<br />

immunohistochemical study showed that the mandibular condylar cartilage<br />

was deformed, volume and total cell number were reduced, and number and/<br />

or distribution of 5bromo2′deoxyuridinepositive cells, Ihh and Bmp2<br />

positive cells in the mesenchymal and prehypertrophic zones were significantly<br />

and correspondingly decreased in the sutured group. Our results revealed that<br />

the mechanical stress induced by prenatal jaw movement restriction decreased<br />

proliferating cells, the amount of cartilage, and altered expression of the Ihh and<br />

Bmp2, suggesting that Ihh and Bmp2 act as mechanotransduction mediators in<br />

the development of mandibular condylar cartilage.<br />

P<br />

<br />

1 2<br />

1<br />

2 <br />

<br />

<br />

<br />

<br />

<br />

<br />

<br />

<br />

<br />

<br />

FGF18<br />

<br />

<br />

<br />

<br />

Phase Field <br />

<br />

<br />

P<br />

<br />

<br />

1 1 1 2 3 1<br />

1<br />

2 3 I<br />

<br />

Muscle<br />

tendon junction: MTJMTJ <br />

ArgGlyAsp<br />

RGD<br />

RGDserine S <br />

<br />

MTJ <br />

RGDS <br />

ECM <br />

RGDS <br />

<br />

RGDS <br />

RGDS <br />

<br />

RGDS <br />

MTJ <br />

P<br />

<br />

1 2 2 3 4 <br />

4 5 1 1<br />

1<br />

2 <br />

3 <br />

RI 4 5 <br />

<br />

<br />

<br />

<br />

19 4 <br />

<br />

<br />

<br />

<br />

<br />

ECM<br />

iTRAQQ<br />

NanoLC <br />

MALDITOF/TOF MS/MS <br />

<br />

core protein collagen GAG<br />

Type I & II collagen GAGType I collagen <br />

Type II collagen <br />

<br />

<br />

ECM


117 145<br />

P<br />

FIB/SEM <br />

1,3 1 2 2 3 <br />

1<br />

1<br />

2 <br />

3 <br />

<br />

<br />

<br />

<br />

FIB/SEM <br />

CT <br />

8 <br />

5%EDTA<br />

5 1 OsO 4 <br />

EPON812 H7650<br />

FIB/SEM <br />

en block EPON812 <br />

, FIB/SEM <br />

Quanta 3D FEGFEIFIB <br />

Ga 1 nA 80 nm/step<br />

80 μm <br />

<br />

P<br />

Molecular sequence and distribution of the NMDA receptor subunit<br />

NR mRNA in the central nervous system of pigeons Columba livia<br />

Mohammad Rabiul Karim 1,2 , Shouichiro Saito 1 , Yasuro Atoji 1<br />

1<br />

Gifu Univ, Fac Appl Biol Sci, 2 Bangladesh Agri Univ, Fac Vet Sci<br />

NR1 is a key subunit of the NmethylDaspartate type of glutamate receptors<br />

maintaining the glutamatergic system in the mammalian central nervous system<br />

CNS. In the present study, cDNA sequence and expression pattern of NR1<br />

mRNA in the pigeon CNS were examined. From cDNA sequence analysis, its<br />

predicted amino acid sequence was revealed to show 96%, 95% and 85% identity<br />

to that of the chicken, zebra finch and human NR1, respectively. By RTPCR,<br />

pigeon NR1 mRNA was revealed to be highlevel in the olfactory bulb, pallium<br />

and subpallium of the telencephalon and in the cerebellum, mediumlevel in the<br />

diencephalon and optic tectum, and lowlevel in the lower brainstem and spinal<br />

cord. By in situ hybridization, intense hybridization signal was observed in the<br />

olfactory bulb, pallium except entopallium, septal nuclei and striatum of the<br />

telencephalon, and the granular and Purkinje cell layers of the cerebellum, and<br />

weak signal in the thalamus, optic tectum, lower brain stem and gray matter of<br />

the spinal cord. This study revealed the similarity of NR1 expression between the<br />

pigeon and mammals, indicating the functional importance of the glutamatergic<br />

system in the avian CNS.<br />

P<br />

<br />

<br />

<br />

<br />

<br />

<br />

2 VGLUT2mRNA <br />

VGLUT2 <br />

<br />

<br />

0.1% 4<br />

50 μm VGLUT2 C <br />

<br />

<br />

<br />

HVC, RA, area X <br />

<br />

MC,<br />

An, NL , MC <br />

VGLUT2mRNA <br />

<br />

<br />

P<br />

SULTBa <br />

<br />

<br />

<br />

<br />

<br />

<br />

GABA A<br />

GABA <br />

<br />

SULT2A1 SULT2B1a <br />

mRNA<br />

<br />

<br />

SULT2B1a SULT2B1a <br />

SULT2B1a <br />

<br />

SULT2B1a <br />

<br />

P<br />

<br />

<br />

<br />

DGDGK<br />

C DG <br />

DGK DGK<br />

DGKε DG <br />

DGKε <br />

DGKε <br />

DGKε <br />

64 kDa <br />

<br />

DGKε <br />

DGKε 1 <br />

IP3R1<br />

DGKε <br />

IP3R1 <br />

P<br />

Androgen receptor expression in the preoptic and anterior<br />

hypothalamic areas of the adult male rats and mice<br />

Jahan Mir Rubayet, Keiji Kokubu, Chikahisa Matsuo, Islam Md. Nabiul,<br />

Akie Yanai, Ryutaro Fujinaga, Koh Shinoda<br />

Functional Neuroanatomy, Yamaguchi Univ. Grad. Sch. of Med.<br />

Species difference has been suggested on androgeninduced functions of the<br />

preoptic and anterior hypothalamic areas PO/AH. Using paraformaldehyde<br />

fixed completely serial frozen sections, expression of androgen receptor AR was<br />

immunohistochemically compared in the PO/AH between adult male rats Wistar,<br />

SD and mice C57BL/6, DBA/2j, Balb/c. In general, AR expression was stronger<br />

in mice than rats, particularly in the medial preoptic area MPO, posterodorsal<br />

preoptic nucleus, dorsal PO/AH junction DPAJ and suprachiasmatic nucleus<br />

SCN. Exceptionally, more ARimmunoreactive ARir cells were seen in the<br />

sexually dimorphic nucleus SDN of the MPO and periventricular zone of the AH<br />

in rats. In addition, we found a distinct mousespecific ARir neuronal cluster as<br />

the “tear drop nucleus (TDN)” dorsal to the SCN, which resembles the rat SDN or<br />

mouse putative SDN in calbindin immunoreactivity, and two distinct ratspecific<br />

small clusters as the “DPAJ island” and “paraventricular island”. The present data<br />

might explain distinct androgeninduced psychotic, behavioral and endocrinergic<br />

responses between the two rodents, warning that data cannot directly be applied<br />

each other.


146<br />

117 <br />

P<br />

GABA <br />

parvalbumin <br />

1 1 1 1 1 <br />

1 2 3 1<br />

1<br />

2 <br />

3 <br />

MG GABA <br />

parvalbuminPV <br />

<br />

ABC GABA <br />

PV ir GABAir MG<br />

MGd MGv MGm <br />

GABAir <br />

MGm GABAir MGv <br />

MGd MGv PVir calbindinir <br />

MGv MGd PVir <br />

MGv MGm MGm MGv PVir <br />

PVir PVir <br />

MGv MGm GABAir PVir <br />

MGd PVir <br />

GABAir <br />

<br />

<br />

<br />

P<br />

SNARE <br />

<br />

<br />

SNARE <br />

<br />

SNARE <br />

<br />

<br />

<br />

SNARE <br />

<br />

SNARE syntaxin1, SNAP25, VAMP2 <br />

<br />

<br />

<br />

SNARE <br />

<br />

<br />

SNARE <br />

SNARE <br />

<br />

P<br />

GABA <br />

1 2 3 4 2 1<br />

1<br />

2 <br />

3 4 <br />

, <br />

TGNC<br />

SC GABA GABA <br />

GABA NC <br />

GABA NC GABA <br />

DNDS GABA GAT<br />

SC DNDS <br />

NC <br />

GABA <br />

GABA free 24 TG <br />

NC GABA SC GABA <br />

100 μM GABA 24 NC <br />

SC GABA GABA GAD<br />

GABA GAT NC SC<br />

<br />

NC GAT GABA SC <br />

GABA <br />

GABA <br />

NC SC <br />

<br />

P<br />

Expression of AMPA type glutamate receptor in developing chick<br />

vestibulocochlear ganglia<br />

<br />

1<br />

Expression of AMPA type glutamate receptor GluR14 in the vestibular VG<br />

and cochlear ganglia CG in developing chick embryo was examined. VG and<br />

CG at the embryonic day 10 E10, E12, E14, E16, E18 and E20 were prepared<br />

for reverse transcriptasePCR RTPCR and immunohistochemistry IHC. In<br />

the RTPCR study, GluR1 mRNA was weakly expressed from E10 to E20 in both<br />

ganglia. Expression of GluR2 mRNA was intensive at E10 and E12 in VG and at<br />

E10E14 in CG, and then, it was gradually weakened from E14 in VG and from<br />

E16 in CG. Expression of GluR3 mRNA in both ganglia was weak at E12E18<br />

and it was extremely augmented at E20. GluR4 mRNA was moderately expressed<br />

at E10E14 in VG and at E10E16 in CG, and then, it was gradually increased<br />

from E16 in VG and from E18 in CG. In the IHC study, immunoreactivity of<br />

GluR2 was observed in the cytoplasm and process and that of GluR2/3 and<br />

GluR4 was in the cytoplasm of the VG and CG cells, while that of GluR1 was<br />

never detected. These results suggest that GluR2, GluR3 and GluR4 are the major<br />

subunits of AMPA receptor during the development of the chick embryo VG and<br />

CG cells. They would have different roles for the development.<br />

P<br />

<br />

<br />

1 Mohammad Rabiul Karim 1,2 1<br />

1<br />

2 Faculty of Veterinary Science,<br />

Bangladesh Agricultural University<br />

<br />

<br />

3 <br />

VGLUT 1 <br />

<br />

<br />

1 <br />

VGLUT <br />

<br />

<br />

RTPCR in situ hybridization RT<br />

PCR 2 3 VGLUT 3 VGLUT<br />

2 VGLUT mRNA <br />

in situ hybridization <br />

<br />

<br />

2 VGLUT <br />

P<br />

C <br />

<br />

<br />

N 2 <br />

C PapillonLefevre <br />

HaimMunk <br />

C <br />

<br />

D <br />

<br />

8 <br />

<br />

CA2fasciola cinereumindusium griseumtenia tecta<br />

<br />

<br />

<br />

<br />

25<br />

8


117 147<br />

P<br />

<br />

<br />

<br />

VIP <br />

12 <br />

<br />

VIP A, B <br />

2receptor <br />

12 <br />

<br />

<br />

<br />

<br />

VIP <br />

VIP VIP <br />

<br />

A,B 2receptor <br />

A, B <br />

2receptor <br />

<br />

<br />

P<br />

<br />

<br />

<br />

<br />

PGP9.5 <br />

<br />

<br />

1 <br />

3.25 TH CGRP <br />

CGRP <br />

<br />

<br />

<br />

1 μm <br />

<br />

<br />

<br />

2, 3 <br />

<br />

<br />

<br />

P<br />

<br />

1 2 3 1<br />

1<br />

2 3 <br />

<br />

<br />

<br />

<br />

<br />

<br />

<br />

Protein gene product 9.5 PGP9.5 <br />

56, 67, 72, 88 4 6 10 <br />

10 <br />

<br />

415<br />

30/PBS 24 20 μ <br />

6 <br />

<br />

<br />

<br />

<br />

<br />

P<br />

<br />

<br />

<br />

<br />

<br />

<br />

<br />

<br />

<br />

<br />

<br />

N-<br />

N<br />

N<br />

<br />

<br />

N<br />

<br />

N<br />

<br />

<br />

P<br />

CART <br />

<br />

<br />

CARTCocaine and AmphetamineRegulated Transcript<br />

<br />

<br />

<br />

CART <br />

Sauropsida<br />

CART <br />

<br />

<br />

CART <br />

<br />

CART <br />

CART <br />

<br />

CART <br />

<br />

-CART <br />

CART <br />

P<br />

GABA <br />

<br />

<br />

<br />

<br />

<br />

GABA <br />

<br />

GABA <br />

<br />

<br />

<br />

GABA <br />

<br />

GABAA <br />

α1 <br />

G <br />

2 <br />

GABA


148<br />

117 <br />

P<br />

Conserved properties of dendritic trees in four cortical interneuron<br />

subtypes<br />

1,2 1,2 2,3 1,2<br />

1<br />

2 CREST 3 <br />

<br />

Dendritic trees influence synaptic integration and neuronal excitability, yet<br />

appear to develop in rather arbitrary patterns. Using electron microscopy and<br />

serial reconstructions, we analyzed the dendritic trees of four morphologically<br />

distinct neocortical interneuron subtypes to reveal two underlying organizational<br />

principles common to all. First, crosssectional areas at any given point within<br />

a dendrite were proportional to the summed length of all dendritic segments<br />

distal to that point. Consistent with this observation, total crosssectional area<br />

was almost perfectly conserved at bifurcation points. Second, dendritic cross<br />

sections became progressively more elliptical atmore proximal, larger diameter,<br />

dendritic locations. Finally, computer simulations revealed that these conserved<br />

morphological features limit distance dependent filtering of somatic EPSPs and<br />

facilitate distribution of somatic depolarization into all dendritic compartments.<br />

Because these features were shared by all interneurons studied, they may represent<br />

common organizationalprinciples underlying the otherwise diverse morphology of<br />

dendritic trees.<br />

P<br />

FABP in astrocytes is involved in control of neuronal dendritic<br />

formation<br />

Majid Ebrahimi, Yshiteru Kagawa, Kazem Sharifi, Yasuhiro Adachi,<br />

Tomoo Sawada, Nobuko Tokuda, Yuji Owada<br />

Department of Organ Anatomy, Yamaguchi University Graduate School of<br />

Medicine<br />

Alteration of fatty acid homeostasis in brain is associated with human functional<br />

psychosis. We previously showed that FABP7 braintype fatty acid binding<br />

protein, a cellular fatty acid chaperon abundantly expressed in astrocytes, is<br />

involved in control of emotional behavior. However, mechanism by which FABP7<br />

in astrocytes modulates neuronal activity is still unknown.<br />

Mixed cortical culture and neuron/astrocyte coculture were established from<br />

wildtype WT and FABP7 KO KO mice, and morphology of pyramidal<br />

neurons was evaluated by NeuronMetrics. GolgiCox staining was performed to<br />

examine dendrite morphology of neurons in cerebral cortex of KO mice.<br />

In mixed cortical culture, pyramidal neurons of KO mice showed decrease in<br />

length and number of dendritic branches. In the WT neuron/KO astrocyte hybrid<br />

coculture WTn/KOa such changes in dendrite morphology were also detected<br />

compared to WTn/WTa coculture. Moreover, pyramidal neurons in prefrontal<br />

cortex of KO mice showed aberrant dendrite formation.<br />

FABP7 may regulate neuronal dendrite formation by modulation of lipid<br />

homeostasis metabolism/signal transduction in astrocytes.<br />

P<br />

FILIP <br />

1 1 1 1 1 1 <br />

1,2 1<br />

1<br />

<br />

2<br />

<br />

<br />

<br />

<br />

<br />

<br />

<br />

FILIP <br />

A <br />

<br />

FILIP <br />

FILIP <br />

<br />

<br />

P<br />

CA <br />

<br />

<br />

<br />

<br />

<br />

<br />

CA1 <br />

<br />

Thy1 GFP <br />

9 2 <br />

mushroom type stubby type thin type <br />

CA1 Western blot<br />

<br />

BDNF PSD95 <br />

BDNF PSD95<br />

<br />

<br />

<br />

BDNFPSD95 <br />

<br />

P<br />

In vivo analysis of postsynaptic molecular dynamics in the<br />

developing mouse cortex<br />

<br />

<br />

Dynamic behavior of postsynaptic molecules is thought to play important<br />

roles in synaptic transmission and plasticity. Postsynaptic densities PSDs and<br />

spines are key elements in the process of postsynaptic signal transduction. We<br />

previously reported differential dynamics of molecules present in PSDs and<br />

spines in cultured hippocampal neurons. Photobleaching of actin, the prominent<br />

cytoskeletal component in the spine cytoplasm, and PSD scaffolding proteins<br />

PSD95 and Homer1c showed distinct mobility in the postsynaptic cytoplasm,<br />

indicating independent regulation of molecular dynamics. To gain more insights in<br />

the protein mobility at the postsynaptic sites and its regulation, information from<br />

neurons in the native environment should be obtained. To monitor protein mobility<br />

in vivo, we applied twophoton photoactivation/bleaching to pyramidal neurons<br />

in the mouse cortex and monitored fluorescence decay/recovery in individual<br />

spines at different developmental stages. Lifetime of PSD/spine structure was<br />

much longer than resident times of individual protein molecules, indicating the<br />

importance of protein network in maintenance of the postsynaptic structural<br />

organization.<br />

P<br />

Direct monitoring of AMPA receptor recycling and trafficking<br />

Ayako Hayashi 1 , Daisuke Asanuma 2 , Mako Kamiya 3 , Yasuteru Urano 3 , Shigeo<br />

Okabe 1<br />

1<br />

Department of Cellular Neurobiology, Graduate School of Medicine, The<br />

university of Tokyo, 2 Department of Neurobiology, Graduate School of Medicine,<br />

The university of Tokyo, 3 Department of Chemical Biology and Molecular<br />

Imaging, Graduate School of Medicine, The university of Tokyo<br />

Longlasting change of synaptic efficacy, such as LTP, is known to be correlated<br />

with increase of postsynaptic response of AMPAtype glutamate receptors<br />

AMPARs. AMPAR targeting is regulated by surface mobility and exo/<br />

endocytosis. Although single particle tracking revealed contribution of AMPAR<br />

lateral mobility in their trapping at the synaptic sites, dynamic recycling of<br />

AMPARcontaining vesicles after plasticityinducing stimuli has not yet been<br />

clarified. We expressed AMPAR subunit GluR1 tagged with ZIPbinding cassette<br />

in primary hippocampal neurons and visualized cell surface AMPARs by labeling<br />

with ZIP peptides conjugated with pH sensitive dye RhPM. RhPMlabeled<br />

GluR1 increased its fluorescence after endocytosis, due to the acidification in<br />

the endosomal compartment. To visualize the intracellular transport of GluR1<br />

containing vesicles after endocytosis, we monitored both superecliptic pHluorin<br />

tagged GluR1 and RhPMlabeled GluR1 simultaneously. We identified that GluR1<br />

endocytosis occurred on dendritic shafts and also in larger spines. Reciprocal<br />

signal change of SEP/RhPMlabeled receptors facilitates the identification of exo/<br />

endocytotic events within dendritic spines.


117 149<br />

P<br />

Motor protein KIFA is essential for hippocampal synaptogenesis<br />

and learning enhancement in an enriched environment<br />

<br />

<br />

Environmental enrichment causes a variety of effects on brain structure and<br />

function. Brainderived neurotrophic factor BDNF plays an important role<br />

in enrichmentinduced neuronal changes; however, the precise mechanism<br />

underlying these effects remains uncertain. In this study, a specific upregulation of<br />

kinesin superfamily motor protein 1A KIF1A was observed in the hippocampi<br />

of mice kept in an enriched environment and, in hippocampal neurons in vitro,<br />

BDNF increased the levels of KIF1A and of KIF1Amediated cargo transport.<br />

Analysis of Bdnf +/-<br />

and Kif1a +/- mice revealed that a lack of KIF1A upregulation<br />

resulted in a loss of enrichmentinduced hippocampal synaptogenesis and learning<br />

enhancement. Meanwhile, KIF1A overexpression promoted synaptogenesis via<br />

the formation of presynaptic boutons. These findings demonstrate that KIF1A<br />

is indispensable for BDNFmediated hippocampal synaptogenesis and learning<br />

enhancement induced by enrichment. This is a new molecular motormediated<br />

presynaptic mechanism underlying experiencedependent neuroplasticity.<br />

P<br />

Activationspecific Changes of Angiotensin II Receptors in Mouse<br />

Cerebellum and Adrenal Glands with In Vivo Cryotechnique<br />

Zheng Huang, Nobuo Terada, Yurika Saitoh, Jiaorong Chen, Shinichi Ohno<br />

Department of Anatomy and Molecular Histology, Interdisciplinary Graduate<br />

School of Medicine and Engineering, University of Yamanashi<br />

We have performed immunohistochemical analyses of AT1/2R with molecular<br />

activationspecific antibodies in living mouse cerebellum and adrenal glands under<br />

normal or hypoxic conditions with “in vivo cryotechnique” IVCT followed by<br />

freezesubstitution FS. In the cerebellum, outer molecular layers and some areas<br />

around Purkinje cells were immunostained as dotted patterns, which were closely<br />

related to Bergmann glia. At 5 and 10 min after hypoxia, the immunoreactivity<br />

was remarkably reduced, though it was still remained the same in the adrenal<br />

glands at 15min after hypoxia. This immunohistochemical approach with IVCT<br />

FS enabled us to perform their precise analyses.<br />

P<br />

Nodose ganglion cells expressing melanocortin receptor send their<br />

fibers to the pancreatic islets in the mouse<br />

Toshiko Tsumori, Tatsuro Oka, Jianguo Niu, Yukihiko Yasui<br />

Dept. Anat. & Morphol. Neurosci., Shimane Univ. Sch. Med.<br />

Melanocortin system including melanocortin4 receptor MC4R plays a<br />

crucial role in the control of feeding and energy expenditure. Using a transgenic<br />

mouse model in which green fluorescent protein GFP is produced under the<br />

control of the MC4R promoter, we recently reported that the dorsal motor<br />

nucleus of the vagus nerve contains many MC4Rexpressing neurons which<br />

project to the intrapancreatic ganglia. In this study, we examined whether or<br />

not MC4Rexpressing nodose ganglion cells send their fibers to the pancreas.<br />

Using retrograde tracing with chorela toxin B subunit in combination with<br />

immunohistochemistry for GFP, we demonstrated that some of the nodose<br />

ganglion cells sending their fibers to the pancreas showed GFP immunoreactivity.<br />

Using double immunofluorecence staining for insulin and GFP, we also showed<br />

that GFPimmunoreactive ir boutonlike varicosities were distributed within<br />

the pancreatic islets and some of them were in close apposition to insulinir cell<br />

bodies. The previous and present results suggest that both of the vagal afferent<br />

and efferent neurons expressing MC4R may be closely related to exocrine and<br />

endocrine pancreatic functions on energy expenditure.<br />

P<br />

Runx<br />

<br />

<br />

Runx runt Runx13 3 <br />

Runx1 Runx1 <br />

12.5 E12.5<br />

Runx1 <br />

Runx1 Runx1 -/- ::TgE12.5 <br />

Runx1 E17.5 <br />

Runx1 Runx1 <br />

Runx1 <br />

<br />

Runx1 <br />

NeurofilamentM <br />

VAChTRunx1 +/+ ::Tg Runx1 -/- ::Tg <br />

<br />

3 <br />

Runx1 -/- ::Tg VAChT <br />

Runx1 +/+ ::Tg <br />

Runx1 -/- ::Tg Runx1 <br />

<br />

P<br />

A <br />

<br />

1 2 1<br />

1<br />

2 <br />

A Cholecystokinin A receptor: CCKAR<br />

CCK CCKAR mRNA <br />

nodose ganglion: NGNG CCK<br />

binding site <br />

CCKAR CCKAR <br />

<br />

CCK<br />

AR CCKAR <br />

2 <br />

VGluT2<br />

CCKAR <br />

CCKAR NG <br />

<br />

B <br />

NG CCKAR/<br />

VGluT2 CCKAR <br />

CCKAR <br />

NG <br />

<br />

P<br />

Features of boutons distribution along axons of neurons in the<br />

caudal nucleus of tractus solitarius of the rat<br />

<br />

<br />

A large amount of the information processing that happens in the brain occurs<br />

in the microcircuitry. For comprehensive understanding of the mechanisms<br />

regulating connectivity among neurons within the microcircuitry, it is essential<br />

to elucidate how pre and postsynaptic components are connected. In this study,<br />

to understand the rules by which axons make synapses, we investigated the<br />

arrangement of synaptic boutons on axons of biocytinfilled neurons in the caudal<br />

nucleus of the tractus solitarius cNTS of medulla oblongata. We analyzed the<br />

length and distribution of interbouton intervals ibi under the light microscope.<br />

The overall average length of ibi was 4.7 μm and varied by neurons ranged<br />

from 2.8 to 8.1 μm. Although there was considerable variation in the average<br />

length of ibi among neurons, a general scaling relationship between the standard<br />

deviation and the average was found. In addition, the distribution of ibi was<br />

characteristically skewed and the tail of that was fitted well to an exponential<br />

distribution. These results suggest that the synaptic boutons along axons of cNTS<br />

neurons are distributed in a fundamentally similar manner, a random manner.


150<br />

117 <br />

P<br />

Calbindin <br />

<br />

<br />

<br />

mitral<br />

cellMCMC <br />

MC mitral cell layer<br />

MCL olfactory cortex <br />

granule cell GC <br />

GC MC reciprocal synapses <br />

<br />

<br />

MCL CB <br />

Neurolucida <br />

<br />

CB MCL <br />

2-4 <br />

GC <br />

<br />

<br />

<br />

P<br />

GALP <br />

1 2 2 1,3 1<br />

1<br />

2 3 <br />

<br />

GALP<br />

<br />

GALP<br />

mRNA <br />

GALP <br />

CreloxP GFP <br />

GFP β <br />

Tg Tg <br />

7 <br />

GFP <br />

β <br />

GALP <br />

<br />

GALP <br />

<br />

<br />

P<br />

Origins of nitric oxide pathways to the median preoptic nucleus<br />

Hitoshi Kawano, Sadahiko Masuko<br />

Saga University<br />

It has been revealed that many nerve fibers containing nitric oxide NO as a<br />

neurotransmitter are found in the median preoptic nucleus POMe by means of<br />

NADPHdiaphorase histochemistry. We investigated where the NO pathways<br />

terminating at the POMe come from, using retrograde tracing method and<br />

immunohistochemistry for NO synthase NOS, a marker for NO neurons. After<br />

injection of a retrograde tracer in the POMe, a larger number of retrogradely<br />

labeled neurons in the subfornical organ SFO showed NOS immunoreactivity. In<br />

addition, a few neurons were doublelabeled in the parvocellular paraventricular,<br />

the periventricular, and the ventromedial nuclei of the hypothalamus. The finding<br />

indicates that the principal NO pathway to the POMe comes from SFO.<br />

P<br />

Kisspeptin Tuberoinfundibular dopamine<br />

TIDA <br />

1 2 1 1 1<br />

1<br />

2 <br />

kisspeptin HPG axis <br />

kisspeptin <br />

kisspeptin GnRH <br />

kisspeptin GnRH <br />

<br />

kisspeptin <br />

kisspeptin <br />

<br />

Tuberoinfundibular dopamine neuronsTIDA<br />

neuronskisspeptin TIDA neuron <br />

kisspeptin <br />

TH synaptophysin <br />

kisspeptin <br />

TIDA neuron <br />

kisspeptin TIDA neuron <br />

in vitro kisspeptin <br />

kisspeptin <br />

TIDA neuron <br />

<br />

P<br />

<br />

1 2<br />

1<br />

2 <br />

P<br />

CA <br />

1 2<br />

1<br />

2 <br />

<br />

<br />

<br />

AD30 29 <br />

<br />

116 B <br />

CTb<br />

AD <br />

2.5 kg<br />

CTb 7 CTb <br />

AD <br />

30 CTb AD <br />

30 AD <br />

29 <br />

AD <br />

AD AD 30<br />

29 <br />

<br />

<br />

<br />

<br />

<br />

<br />

<br />

<br />

1 <br />

<br />

CTb <br />

CA1 <br />

CA1 BDA <br />

VVI <br />

CA1 <br />

<br />

CA1


117 151<br />

P<br />

<br />

<br />

<br />

<br />

<br />

<br />

<br />

<br />

<br />

<br />

<br />

<br />

parvicellular<br />

part of the ventral posterior nucleus of the thalamus VPPC<br />

retrouniens area central medial thalamic nucleusparafascicular<br />

thalamic nucleusparvicellular part of the subparafascicular thalamic nucleus<br />

oval paracentral thalamic nucleus paraventricular thalamic nuclei<br />

rhomboid thalamic nucleus <br />

VPPC<br />

<br />

<br />

P<br />

Classification of rat pallidofugal projection systems revealed by<br />

singleneuron tracing study with a viral vector<br />

1,2 1 1 1 1<br />

1<br />

2 JST, CREST<br />

The main striatofugal system is divided into two neural populations, the<br />

striatonigral neurons striatal direct pathway neurons and the striatopallidal<br />

neurons striatal indirect pathway neurons. However, the striatal direct pathway<br />

neurons also give collaterals in the globus pallidus GPe, which is a relay nucleus<br />

in the indirect pathway of the basal ganglia Kawaguchi et al., 1990; Fujiyama<br />

et al., 2011. We also found the targeted region in GPe were different between<br />

the striatal direct and indirect pathway neurons Fujiyama et al., 2011. Our next<br />

question is whether the GPe neurons located in the different regions targeted<br />

by striatal direct and indirect pathway neurons show the same axonal trajectory<br />

or not. To reveal it, the single GPe neurons in rat were labeled by recombinant<br />

Sindbis virus that is designed to express the membranetargeted green fluorescent<br />

protein. In the present study, we found two types of axonal trajectory of GPe<br />

neurons in the different regions and discuss the possibility that the GPe can be<br />

separated functionally to be involved in the different network of the basal ganglia.<br />

P<br />

A Morphological Analysis of Thalamocortical Axon Fibers of Rat<br />

Posterior Nuclei: A Single Neuron Tracing Study with Viral Vectors<br />

1,2 1 1 1 1 <br />

1,4 3 3 2 1<br />

1<br />

2 <br />

3 4 JST, CREST<br />

The posterior thalamic nuclei POm receives inputs from the spinal cord and<br />

trigeminal nuclei, and projects to the primary somatosensory S1 cortex and other<br />

cortical areas. Although thalamocortical axons of single ventral posterior nuclei<br />

neurons are well known to innervate layer L 4 of the S1 cortex with distinct<br />

columnar organization, those of POm neurons have not been elucidated yet. In<br />

the present study, we investigated complete axonal and dendritic arborizations<br />

of single POm neurons in rats using Sindbis viral vectors. When we divided the<br />

POm into anterior and posterior parts according to calbindin immunoreactivity,<br />

dendrites of posterior POm neurons were wider but less numerous than those<br />

of anterior neurons. More interestingly, axon fibers of anterior POm neurons<br />

were preferentially distributed in L5 of the S1 cortex, whereas those of posterior<br />

neurons were principally spread in L1 with wider and sparser arborization than<br />

those of anterior neurons. These results suggest that the POm is functionally<br />

segregated into anterior and posterior parts, and that the two parts may play<br />

different roles in somatosensory information processing.<br />

P<br />

Morphological analysis of axon collaterals derived from single<br />

corticospinal neurons in subcortical structures<br />

<br />

<br />

The corticospinal tract which conveys the final command for control of voluntary<br />

movement has been known to give axon collaterals to various cortical and<br />

subcortical regions. The target regions thus receive the same information with that<br />

gives rise to muscle actions. To assess the collaterals in the subcortical regions by<br />

a morphological approach, we visualized axons of single corticospinal neurons<br />

by injecting a recombinant sindbis virus expressing membranetargeted GFP into<br />

the pyramidal tract. The labeled cortical neurons were distributed in layer V of<br />

the motor cortex and motorsensory corticesareas FL and HL. The corticospinal<br />

neurons gave multiple axon collaterals to various subcortical structures and<br />

especially sent branches, with high frequency, to the striatum 71%, zona incerta<br />

67%, pontine and reticulotegmental nuclei 100%, which are known to play a<br />

role in control of voluntary movement or gating of peripheral inputs to thalamic<br />

nuclei. These abundant subcortical collaterals suggest that the "copy" of final<br />

motor command from the cortex plays an important role in motor and sensory<br />

processing of the subcortical structures.<br />

P<br />

<br />

<br />

1 2 2 2<br />

1<br />

2 <br />

<br />

MCH<br />

<br />

2VGLUT2<br />

MCH <br />

MCH VGLUT2 <br />

<br />

SD MCH <br />

VGLUT2 mRNA in situ hybridizationISH<br />

MCH <br />

VGLUT2 cRNA <br />

<br />

MCH <br />

VGLUT2 <br />

MCH <br />

MCH VGLUT2 <br />

VGLUT2 <br />

<br />

P<br />

Projections from the amygdaloid anterior basomedial and anterior<br />

cortical nuclei to MCHcontaining hypothalamic neurons of the rat<br />

<br />

Dept. Anat. & Morphol. Neurosci., Shimane Univ. Sch. Med., Izumo, Japan<br />

Melaninconcentrating hormone MCH is involve in the regulation of feeding<br />

behavior, and MCHcontaining neurons are distributed mainly in the lateral<br />

hypothalamus LH. The anterior bosomedial nucleus BMA and anterior cortical<br />

nucleus ACo of the amygdala have been known to project to the LH, and to<br />

form part of a circuit involved in processing olfactory, gustatory and visceral<br />

information related to feeding. However, it is still unknown whether or not MCH<br />

containing LH neurons are under the direct influence of the BMA and ACo. Here<br />

the organization of projections from the BMA and ACo to MCHcontaining LH<br />

neurons was examined and new data were provided as follows: 1 the prominent<br />

overlap of the distribution field of the BMA or ACo fibers and that of the MCH<br />

ir neurons is found in the ventrolateral LH; 2 the BMA and ACo axon terminals<br />

make asymmetrical synapses with MCHir neurons; and 3 most of the BMA and<br />

ACo neurons projecting to the ventrolateral LH are positive for VGLUT2 mRNA.<br />

These data suggest that the BMA and ACo of the amygdala may exert excitatory<br />

influence upon the MCHcontaining LH neurons for the regulation of feeding<br />

behavior.


152<br />

117 <br />

P<br />

Inhibitory inputs of CCKpositive neurons to PVexpressing neurons<br />

in mouse neocortex<br />

1 1 1 1 2 <br />

1 1,3 1<br />

1<br />

2 <br />

3 CREST<br />

Neocortical GABAergic interneurons are roughly classified into three subgroups<br />

by chemical markers, parvalbumin PV, somatostatin SS and others such<br />

as vasoactive intestinal polypeptide VIP and cholecystokinin CCK. PV<br />

expressing neurons, fastspiking neurons, are a major component of GABAergic<br />

interneurons in neocortex. We generated transgenic mice expressing dendritic<br />

membranetargeted GFP selectively in PVexpressing neurons, and succeeded in<br />

visualizing somata and dendrites in a Golgi stainlike fashion.<br />

We previously investigated inhibitory inputs to PVexpressing neurons from PV,<br />

SS or VIPexpressing neurons, by combining immunofluorescence labeling of<br />

presynaptic and postsynaptic sites with antibodies to presynaptic markers and<br />

gephyrin, respectively. PV or SSpositive axon terminals made close contacts<br />

to the dendrite, whereas axon terminals of VIPexpressing neurons preferred the<br />

soma.<br />

In the present study, we visualize axon terminals of CCKexpressing neurons by<br />

immunofluorescence staining in the transgenic mice, observe the close appositions<br />

to PVexpressing neurons under confocal laserscanning microscope, and analyze<br />

the inputs quantitatively.<br />

P<br />

Elimination of somatic climbing fiber synapses proceeds with the<br />

differentiation of cerebellar interneurons<br />

<br />

<br />

In the developing cerebellum, the soma of individual Purkinje cells PCs is<br />

innervated by multiple climbing fibers CFs. Through their competition, only<br />

a single winner CF translocates to dendrites and the remaining somatic CF<br />

synapses are eliminated, leading to the establishment of CF monoinnervation.<br />

Concomitantly, basket cell fibers BFs begin to form inhibitory synapses on<br />

PC somata. Here, we examined anatomical relationship between declining CFs<br />

and developing inhibitory neurons at PC soma by light and electron microscopic<br />

analysis. In the first postnatal week of murine life, CFs innervated the entire<br />

somatic surface. Thereafter, BFs expanded their innervation from the apical<br />

side of PC somata downwards in synchrony with the reduction of somatic CF<br />

synapses. Furthermore, CF terminals frequently detached from the basal side of<br />

PC somata and often formed synapses on the somatodendritic domain of Lugaro<br />

cells LCs, a cerebellar interneuron lying just below the PC layer. These findings<br />

suggest that elimination of somatic CFs proceeds with the differentiation of<br />

cerebellar interneurons, such as BFs expelling somatic CF synapses and LCs<br />

accommodating perisomatic CF terminals.<br />

P<br />

Tectothalamic inhibitory neurons in the inferior colliculus receive<br />

converged axosomatic excitatory inputs from multiple sources<br />

<br />

<br />

Tectothalamic inhibitory TTI cells in the inferior colliculus IC are encircled<br />

by dense excitatory terminals positive for vesicular glutamate transporter 2<br />

VGLUT2. Four auditory brainstem nuclei including IC itself were identified<br />

as possible sources by examining mRNA expression of VGLUT1 and VGLUT2<br />

in ICprojecting cells. In this study, Sindbis/palGFP virus was injected in these<br />

nuclei to elucidate whether neurons in the nuclei make axosomatic contacts on<br />

TTI cells or not. Labeled neurons in all four nuclei made axosomatic contacts<br />

on large GABAergic neurons with dense axosomatic terminals, presumable TTI<br />

PTTI cells. Furthermore, a single axon made one to six contacts on a PTTI cell.<br />

In 3 cases, single IC excitatory cell was successfully labeled, and analyzed for<br />

spatial relationship between the labeled axon and PTTI cells. Single IC excitatory<br />

cell made axosomatic contacts on 1030 PTTI cells in the ipsilateral IC. Finally,<br />

double injection of Sindbis/palGFP and Sindbis/palmRFP viruses in 2 nuclei<br />

revealed convergence of inputs from 2 nuclei on a single PTTI cell. The results<br />

imply both divergence and convergence of auditory information on the cell bodies<br />

of TTI cells.<br />

P<br />

Axon terminals of the corticocollicular projection in the rat auditory<br />

system<br />

<br />

<br />

<br />

The corticocollicular projection was visualized by Sidbis virus and studied<br />

morphologically. The axons visualized with Golgi method in the inferior colliculus<br />

IC have been classified into three types and studied electronmicroscopically, A.<br />

J. Rocket and E. G. Jones, 1972,1973 with their origins mentioned prooflessly.<br />

We successfully visualized corticocollicular projection exclusively by infection<br />

of a recombinant Sindbis virus into cortical projection neurons in the auditory<br />

area. The Sindbis virus which expresses palmitoilationsiteadded GFP as the<br />

reporter gene is a kind gift from Dr. Kaneko in Kyotouniversity. The cortico<br />

collicular axon terminal images in the inferior colliculus was morphologically<br />

studied and compared with intrinsic axons from IC neuron which are stained in the<br />

same way. We further observed cortical projections into the nucleus of brachium<br />

of IC, external nucleus of IC, central nucleus of IC and deep layer of the superior<br />

colliculus. It should be noted that different types of termination exist in the above<br />

mentioned auditory brainstem.<br />

P<br />

Afferent projection to amygdaloid subnuclei and intrinsic connection<br />

of each subnuclei<br />

<br />

<br />

The amygdala is structurally diverse and comprised of several subnuclei. Extra<br />

and intraamygdala inputs into these subnuclei were extensively investigated by<br />

injection of CTb into various amygdaloid subnucleri, respectively. Ce received<br />

moderate to heavy inputs from almost all amygdaloid subnuclei, and from limbic<br />

cortex and hippocampus APir and AI, thalamus PV and MGM, hypothalamus<br />

VMH and midbrain PB. Me received moderate to heavy inputs from BM, Co,<br />

and from limbic cortex and hippocampus Pir, AHi and CA1, thalamus PV and<br />

hypothalamus VMH. BM received moderate inputs from Me, Co and BL, and<br />

from limbic cortex AI and thalamus PV. BL received moderate inputs from<br />

Me, La, BM, Co, and from limbic cortex and hippocampus LEnt, APir and CA1,<br />

thalamus PV and midbrain PB. La received moderate to heavy inputs from<br />

Me, Co, BM and BL, and from limbic cortex Ect and PRh, thalamus MGM<br />

and hypothalamus VMH. Co received light to heavy inputs from La, Me, and<br />

from limbic cortex and hippocampus AI, Pir and DEn and thalamus PV, PT and<br />

MGM. These subnucleispecific afferent projections are involved in emotional<br />

process in a different manner.<br />

P<br />

<br />

<br />

<br />

<br />

<br />

<br />

<br />

<br />

<br />

HeLa <br />

<br />

αtubulin Hec1CENPA


117 153<br />

P<br />

<br />

<br />

<br />

<br />

SEM <br />

<br />

<br />

75 mM KCl <br />

<br />

<br />

SEM <br />

<br />

SEM <br />

<br />

<br />

<br />

<br />

SEM <br />

<br />

P<br />

Communication between Flagellar Outer and Inner Dynein Arms<br />

Toshiyuki Oda, Toshiki Yagi, Masahide Kikkawa<br />

Dept. Cell Biology, Univ. Tokyo, Grad. Sch. Medicine<br />

The beating motion of cilia and flagella is driven by two rows of dynein arms:<br />

the outer dynein arms ODA and the inner dynein arms IDA. The ODAs are<br />

required to generate the normal beat frequency and the IDAs are responsible for<br />

the amplitude of the waveform. Although structural connections between the ODA<br />

and the IDA have been observed by cryoelectron tomography, the functional<br />

communication between the two species of the dynein arms has not been<br />

elucidated. In this study, we investigated the roles of the two intermediate chains<br />

IC1 and IC2 of Chlamydomonas ODA. We located the positions of the termini<br />

of the ICs within the ODAmicrotubule complexes by biotinstreptavidin labeling<br />

and cryoelection microscopy. It is noteworthy that the location of the Nterminus<br />

of IC2 is close to the previously observed ODAIDA linker. The biotintag added<br />

to the Nterminus of IC2 reduced the amplitude of the beating by half while the<br />

beat frequency was not decreased. These results suggest the Nterminus of IC2<br />

mediates the communication between the ODA and the IDA.<br />

P<br />

A novel protein complex required for the formation of microtubule<br />

square lattice in green tree frog sperm<br />

Toshiki Yagi 1 , Hiroshi Kubota 2 , Masahide Kikkawa 1<br />

1<br />

Grad. Sch. Medicine, Univ. Tokyo, 2 Grad. Sch. Science, Kyoto Univ.<br />

Fertilization of the green tree frog occurs in the viscous environment of a foam<br />

nest laid on the vegetation. The sperm cell moves through viscous media by<br />

spinning of the spiral head with flagellar bending movements. Previous EM<br />

analysis showed that the flagellum is composed of a pair of axonemes surrounded<br />

by a regular square lattice of hundreds of satellite microtubules MTs. To<br />

understand how the unique MT lattice structure forms, here we purified MT<br />

bundling proteins from the flagella and examined the properties of the proteins.<br />

Sperm cells were fragmented and fractionated into heads and short flagella by<br />

sonication and centrifugation. Proteins with MT bundling activity was purified<br />

from high salt extract of demembranated flagella by gel filtration chromatography.<br />

This fraction contained six proteins with the molecular size of 3545 kDa. All the<br />

proteins were precipitated together by MTpelleting assay, suggesting that they<br />

form a complex with MT. EM analysis on salt extracted sperm showed that the<br />

flagella lost crosslink structures in the MT lattice. Taken together, we suggest that<br />

the protein complex constitutes the crosslink structure required for the MT lattice<br />

formation.<br />

P<br />

<br />

<br />

<br />

<br />

<br />

<br />

LH/FSH <br />

<br />

<br />

LH/FSH <br />

TGN38 trans γtubulin<br />

<br />

<br />

cistrans <br />

<br />

<br />

<br />

<br />

<br />

<br />

<br />

P<br />

Mitochondria form continuous intracellular networkstructures: a<br />

study visualized by highresolution scanning electron microscopy<br />

Tomonori Naguro, Hironobu Nakane, Sumire Inaga<br />

Division of Genome Morphology, Fac. Medicine, Tottori Univ.<br />

The mitochondria of rat olfactorybulb granule cells in vivo cells within the<br />

tissue formed a continuous network of various shapes in each cell. On the basis<br />

of the morphological characteristics, these mitochondrial networks were roughly<br />

classified into four groups: Type1: Mitochondrial networks are composed of<br />

a single branched tubule of almost uniform thickness, 250300 nm. Type2:<br />

Distinguished by thickness, mitochondrial networks have two kinds of tubules:<br />

about 250350 nm and 100 nm across, respectively. Type3: Mitochondrial<br />

networks are composed of two parts; a globular part around 1.0 μm in diameter<br />

and a filamentous part about 45100 nm across. Type4: Highly complex<br />

mitochondrial networks consisting of elements those vary in shape.<br />

The significance of this morphological diversity of mitochondrial networks<br />

is discussed referring to recent studies with other means, notably light and<br />

transmissionelectron microscopy while considering the advantages and<br />

disadvantages of scanning electron microscopy methods employed for this here.<br />

P<br />

<br />

<br />

<br />

<br />

<br />

Mt <br />

C57BL/6 <br />

1 5 <br />

2<br />

2.5<br />

<br />

<br />

<br />

Mt Mt <br />

1 <br />

Mt Mt <br />

5 Mt <br />

Mt <br />

<br />

Mt <br />

Mt <br />

Mt


154<br />

117 <br />

P<br />

<br />

1 2<br />

1<br />

2 <br />

<br />

<br />

<br />

<br />

<br />

<br />

<br />

<br />

<br />

<br />

<br />

<br />

<br />

<br />

<br />

<br />

P<br />

-<br />

<br />

<br />

• • <br />

EGFR<br />

EGF <br />

EGFR <br />

EGFR <br />

EGFR -<br />

-<br />

AP1 GGA <br />

EGFR <br />

AP1 GGA2 <br />

EGFR GGA1 <br />

GGA3 <br />

AP1 GGA2 <br />

EGFR <br />

D EGFR GGA2<br />

<br />

CIMPR EGFR <br />

AP1•GGA2 EGFR EGFR <br />

<br />

P<br />

VAMP <br />

Khairani Astrid Feinisa <br />

<br />

<br />

SNARE <br />

VAMP <br />

vSNARE VAMP5 mRNA <br />

<br />

VAMP5 <br />

VAMP5 <br />

VAMP5 <br />

<br />

<br />

<br />

<br />

VAMP5 <br />

<br />

P<br />

<br />

<br />

1 2 3 3<br />

1<br />

2 3 <br />

<br />

<br />

<br />

<br />

<br />

<br />

<br />

A23187: f6 μM Zymosan <br />

5 ms/frame <br />

AQUACOSMOS <br />

<br />

1 <br />

47 <br />

<br />

23 ms n=41<br />

18 ms n=21 <br />

<br />

<br />

<br />

P<br />

Involvement of Rab in phagosome formation through regulating<br />

ARF activity by ACAP<br />

1 2 1<br />

1<br />

2 <br />

Phagosome formation and subsequent maturation are complex sequences of<br />

events that involve actin cytoskeleton remodeling and membrane trafficking. In<br />

our livecell studies, we found that Rab35 accumulated markedly at the membrane<br />

where IgG opsonized erythrocytes IgGEs are bound. Rab35 silencing by RNA<br />

interference or the expression of GDP or GTPlocked Rab35 mutant drastically<br />

reduced the rate of phagocytosis of IgGEs. Actinmediated pseudopod extension<br />

to form phagocytic cups was disturbed by the Rab35 silencing or the expression<br />

of GDPRab35, although initial actin assembly at the IgGE binding sites was<br />

not inhibited. Furthermore, GTPRab35dependent recruitment of ACAP2, an<br />

ARF6 GAP, was shown in the phagocytic cup formation. The ARF6 activation<br />

during FcγRmediated phagocytosis was severely impaired by expressing GTP<br />

bound mutant of Rab35. Concomitantly, overexpression of ACAP2 along with<br />

GTPlocked Rab35 showed a synergistic inhibitory effect on phagocytosis. Taken<br />

together, it is likely that Rab35 regulates actindependent phagosome formation<br />

by recruiting ACAP2, which might control actin remodeling through ARF6.<br />

P<br />

AtgAmRNA HeLa /A study on<br />

AtgAmRNAknockdown HeLa cells<br />

<br />

<br />

<br />

Atg9 <br />

<br />

Atg9A 9B <br />

Atg9A <br />

HeLa <br />

Atg9AmRNA siRNA <br />

lamp1 <br />

<br />

<br />

EEA1 <br />

<br />

<br />

<br />

Atg9A


117 155<br />

P<br />

mAtgAAcGFP mDFCPmCherry <br />

<br />

1 1 2 1<br />

1<br />

2 <br />

<br />

Atg<br />

<br />

Atg9A <br />

Atg9A<br />

<br />

DFCP1<br />

Double FYVEdomain Containing Protein 1<br />

mAtg9A<br />

AcGFPmDFCP1mCherry <br />

mAtg9AAcGFP <br />

in vivo <br />

<br />

Atg9ADFCP1 <br />

<br />

P<br />

Histological analysis of adipose tissues in Xpg null mice<br />

Hironobu Nakane 1 , Tadahiro Shiomi 2 , Toshio Kameie 1 , Sumire Inaga 1 ,<br />

Tomonori Naguro 1<br />

1<br />

Div.Genome Morph., Fac. Med., Tottori Univ., 2 Rad. Safety Res. Center, Natl.<br />

Inst. Radiol. Sci.<br />

Some xeroderma pigmentosum group G XPG patients exhibit skin<br />

abnormalities, growth failure, lifeshortening and neurological dysfunctions,<br />

which are also characteristic features of Cockayne syndrome CS. The XPG<br />

gene XPG<br />

encodes a structurespecific DNA endonuclease that functions in<br />

nucleotide excision repair NER. The Xpg null mice showed postnatal growth<br />

failure, ataxia and premature death. We examined pathological changes of<br />

adipose tissues corresponding to clinical manifestations in the Xpg null mice,<br />

such as cachexia, joint contractures. Xpg null mice provide a good animal model<br />

for studying the mechanisms underlying clinical symptoms of XPG/CS, CS in<br />

humans. We will discuss the function of XPG protein in the adipose tissues of the<br />

Xpg null mice.<br />

P<br />

mdx <br />

1 1 2 1 <br />

Khairani Astrid Feinisa 1 1 1 1<br />

1<br />

2 <br />

<br />

<br />

<br />

<br />

<br />

<br />

<br />

<br />

<br />

<br />

mdx <br />

LC3p62 <br />

P<br />

McARH <br />

ALP <br />

<br />

<br />

McARH 7777 <br />

ALP <br />

ALP <br />

ALP<br />

1EEA1<br />

<br />

<br />

ALP ALP <br />

EEA1 ALP <br />

EEA1 ALP<br />

EEA1 EEA1 <br />

<br />

ALP ALP <br />

15 <br />

ALP <br />

McARH 7777 ALP<br />

EEA1 <br />

<br />

ALP <br />

<br />

P<br />

<br />

<br />

<br />

focal adhesion, FA<br />

FA <br />

ECM <br />

<br />

ECM <br />

<br />

Cytograph, DNP• 10, 15, 30 μm <br />

FA Rho <br />

cSrc <br />

<br />

FA <br />

<br />

FA <br />

cSrc pY 418 <br />

cSrc <br />

Rho <br />

<br />

cSrc Rho ECM <br />

<br />

P<br />

lamin A/C <br />

<br />

<br />

Type <br />

lamin A/C <br />

lamin A/C <br />

<br />

ROBC26 C26 lamin<br />

A/C <br />

C26 lamin A/C <br />

Dexamethasone, IBMX, insulin C26 <br />

lamin A/C <br />

lamin A/C<br />

lamin A/C short hairpin<br />

RNA shRNA lamin A/C <br />

C26 <br />

lamin A/C


156<br />

117 <br />

P<br />

ABCG <br />

1 2 1 1<br />

1<br />

2 <br />

<br />

5aminolevulinic acid ALA PDD <br />

PDT <br />

ALA protoporphyrin IX PpIX <br />

imatinib ATPbinding cassette ABC<br />

transporter G2 ABCG2 PpIX <br />

genistein ALA PpIX<br />

PDD PDT <br />

genistein ALA PpIX <br />

ABCG2 <br />

ABCG2 Ko143 <br />

genistein doxorubicin <br />

genistein <br />

PpIX <br />

PpIX ALAgenistein incubation <br />

<br />

genistein ALA PDD PDT <br />

<br />

P<br />

<br />

P<br />

DGKε <br />

<br />

<br />

DGK<br />

C DG <br />

DGKDGKε<br />

DGK / DG<br />

<br />

DGKε <br />

DGKε <br />

DGKε <br />

N DGKεNhalf <br />

DGKεKD <br />

DGKε ER tracker calreticulin <br />

DGKε <br />

DGKεNhalf<br />

DGKεKD <br />

DGKε N <br />

<br />

P<br />

DGKζ NAP DGKζ <br />

<br />

<br />

DGK C <br />

<br />

HeLa DNA <br />

Doxorubicin p53 <br />

DGKζ <br />

p53 <br />

<br />

MG132 p53 <br />

<br />

<br />

DGKζ Nucleosome<br />

assembly protein NAP 1 NAP2 DGKζ <br />

HeLa DNA p53 <br />

DGKζ <br />

NAP1/NAP2 p53 <br />

NAP DGKζ p53 <br />

<br />

P<br />

Cellular localization of ERα and their apoptotic effects<br />

<br />

<br />

The actions of estrogen have traditionally been thought to occur through binding<br />

estrogen receptors in nucleus. Recent data, however, support the idea that some<br />

of ERα in the cytoplasm of various target cells are localized in mitochondria.<br />

Moreover, ERα collaborates with a number of factors on cell membrane, in<br />

cytoplasm, and nucleus to effectively modulate transcription of distinctive<br />

groups of target genes. While some of these factors appear to regulate the<br />

chromatin configuration by controlling histone modifications at the promoter,<br />

others are members of various kinase cascades. In order to discern functions and<br />

interactions of ERα and its coregulators, we allocated ERα to different locations<br />

in ERαnegative Ishikawa cell, using permanent transfection technique. In this<br />

report the antiapoptotic effects were examined for ERα at different cellular<br />

locations in the presence of inhibitors for EGFR, PI3K, MEK, and p38MAPK.<br />

Cellular alterations in proliferation, membrane potential, and caspase activities<br />

were examined using immunohistochemistry, flow cytometry, and related<br />

techniques. The present results might shed light on different pathways of ERα<br />

signal transduction.<br />

P<br />

<br />

<br />

1,2 1 1 1,2 3 <br />

2 1<br />

1<br />

2 2 2 <br />

3<br />

<br />

<br />

<br />

<br />

<br />

<br />

<br />

<br />

<br />

PERKeIF2α Western blotting <br />

WST1 assay <br />

DNA ladder <br />

eIF2α <br />

eIF2α CHOP <br />

<br />

3% <br />

DNA


117 157<br />

P<br />

αMangostin <br />

1 2 3 1<br />

1<br />

2 <br />

3 <br />

HER2ER, PgR<br />

<br />

αMangostin <br />

<br />

MDAMB231 αMangostin<br />

Caspase <br />

c Realtime PCR <br />

<br />

<br />

Caspase389 <br />

Caspase4 <br />

c G1 S <br />

p21 Cip1 <br />

PCNACyclin D1cdc25ACdK2 Cdk6 <br />

Aktp38α ERK1/2 <br />

αMangostin Akt <br />

<br />

p21 Cip1 G1 G1 <br />

<br />

<br />

P<br />

Sevoflurane rat Per <br />

1,2 1 2 1<br />

1<br />

2 <br />

<br />

Per2 suprachiasmatic<br />

nucleus: SCN 24 <br />

mouse Per2 sevoflurane <br />

<br />

Ohe et al, 2010 SCN Per2 <br />

<br />

sevoflurane SCN <br />

Wister rat Per2 rPer2 mRNA <br />

RI in situ hybridizasion rPer2 <br />

Per2 <br />

<br />

rPer2 <br />

SCN rPer2<br />

25 rPer2<br />

sevofrurane <br />

SCN <br />

Per2 <br />

P<br />

Transverse anchoring system of myofibril to sarcolemma: the<br />

morphological study<br />

Khairani Astrid Feinisa, Yuki Tajika, Maiko Takahashi, Hitoshi Ueno,<br />

Tohru Murakami, Hiroshi Yorifuji<br />

Grad.Sch.of Medicine Gunma Univ.<br />

Transverse anchoring system of myofibril to sarcolemma is subplasmalemmal<br />

cytoskeleton network that is anchored into the sarcolemma and provides an<br />

overall diffuse protection system of skeletal muscle. Three types of filament have<br />

been indicated as the transverse anchoring system; γ actin, desmin, and keratin.<br />

We have examined these subsarcolemmal cytoskeletal components in diaphragm<br />

and lower limb muscles of adult wild type and mdx mice by electron microscopy<br />

EM and immunohistochemistry. Isolated single fibers as well as small blocks<br />

of the muscles are used for both methods. EM revealed that the intermediate<br />

filaments seemed to either connect between the sarcolemma and the Zdisc and<br />

Mline or run as a part of subsarcolemmal density. These filamentous networks<br />

apparently decrease in mdx mice. These data suggest a morphological model of<br />

transverse anchoring system and how it affects the functions of skeletal muscle.<br />

P<br />

<br />

Khairani Astrid Feinisa <br />

<br />

<br />

<br />

<br />

<br />

<br />

<br />

<br />

SNARE <br />

<br />

2 SNARE <br />

<br />

SNARE <br />

<br />

<br />

P<br />

Prosaposin expression in cardiac muscle of mdx mice in early period<br />

of disease<br />

1 1 1 1 1 2 <br />

1<br />

1<br />

2 <br />

<br />

This study investigated the expression of the trophic factor prosaposin in the<br />

cardiac muscles of mdx mice. Prosaposin is strongly expressed in adult rat<br />

cardiac and skeletal muscles and plays a myotrophic role in vitro. However, few<br />

studies have focused on the role of prosaposin during muscle regeneration in mdx<br />

mice, which do not express the dystrophin gene. Dystrophin deficiency leads to<br />

progressive cardiac and skeletal muscle pathology. We examined the expression<br />

of prosaposin in the cardiac muscle in mdx and C57BL mice using HE staining,<br />

immunohistochemistry, and in situ hybridization in 4weekold mice. HE staining<br />

showed no obvious change in morphology of mdx cardiac muscles compared<br />

with control mice. The results of in situ hybridization showed that the main form<br />

of prosaposin mRNA is PS+0 in the cardiac muscle of mdx mice, and the mRNA<br />

expression is obviously lower in the cardiac muscles of mdx mice. Prosaposin<br />

protein also decreased in mdx cardiac muscle. These results suggest that the<br />

change of prosaposin expression happened earlier than morphological change in<br />

cardiac muscle of mdx mice.<br />

P<br />

<br />

<br />

<br />

<br />

14 <br />

<br />

<br />

<br />

<br />

<br />

30%ST<br />

96 21<br />

34 56 58 42


158<br />

117 <br />

P<br />

<br />

<br />

<br />

<br />

<br />

<br />

<br />

<br />

12 <br />

Wistar n=18<br />

2 <br />

ATPase pH 4.5<br />

Western blot 1 2 <br />

<br />

<br />

1 <br />

2 <br />

<br />

2 <br />

<br />

<br />

<br />

P<br />

<br />

<br />

<br />

<br />

<br />

dbdbdbm<br />

dbm dbm NDdbm dbm<br />

HPDdbdb dbdb NDdbdb dbdb HPD <br />

MF <br />

50 3 <br />

dbm HPD dbdb HPD<br />

dbdb HPD <br />

dbm HPD <br />

dbm HPD 2 <br />

dbdb<br />

HPD type1 <br />

dbmND <br />

<br />

<br />

<br />

type <br />

P<br />

Thiel <br />

<br />

1 1 2 1,3 4 4 <br />

4 2 5 4<br />

1<br />

2 2 3 <br />

4 2 5 <br />

Thiel Graz Dr. Thiel <br />

<br />

Thiel<br />

<br />

<br />

<br />

<br />

<br />

Thiel 5 8 <br />

<br />

<br />

<br />

<br />

85.016.5<br />

mm81.712.3 mmThiel <br />

<br />

<br />

<br />

P<br />

ATDC Notch PCNA <br />

<br />

<br />

ATDC5 <br />

Notch14 <br />

<br />

<br />

Notch STK1 ATDC5 <br />

60 STK3 <br />

9 <br />

Notch14 <br />

PCNA 0 Notch14 <br />

PCNA 70<br />

Notch 3 30<br />

5 Notch2, 3 <br />

9 Notch <br />

<br />

Notch1 Notch4 PCNA <br />

Notch2 Notch3 <br />

Notch23 <br />

P<br />

Nox <br />

<br />

1 2 3 1 4 <br />

1<br />

1<br />

2 <br />

3 4 <br />

<br />

<br />

Nox<br />

<br />

<br />

<br />

340 op/op <br />

4<br />

10%EDTA <br />

<br />

op/op 3 Nox4 <br />

Nox1Noxa1Noxo1 <br />

18 Nox4 <br />

Nox1Noxa1Noxo1 3 <br />

40 Nox1Noxa1Noxo1 <br />

Nox4 <br />

<br />

op/op Nox <br />

<br />

<br />

P<br />

<br />

1 1 1 2<br />

1<br />

2 <br />

BFABP/FABP7<br />

<br />

4EDTA<br />

<br />

BFABP <br />

MAC2 <br />

BFABP <br />

<br />

<br />

BFABP <br />

MAC2 <br />

BFABP <br />

<br />

BFABP BFABP <br />

BFABP <br />

BFABP <br />

<br />

BFABP


117 159<br />

P<br />

<br />

1 1 1 1 2<br />

1<br />

2 <br />

P<br />

<br />

1 2<br />

1<br />

2 <br />

<br />

<br />

<br />

<br />

<br />

<br />

<br />

<br />

<br />

<br />

123 5 wistar <br />

<br />

<br />

<br />

<br />

1 <br />

3 <br />

<br />

<br />

<br />

<br />

<br />

7 <br />

<br />

<br />

<br />

<br />

<br />

<br />

<br />

<br />

<br />

<br />

<br />

<br />

<br />

<br />

<br />

<br />

P<br />

CT CT <br />

<br />

1 1 2 2 2 2<br />

1<br />

2 <br />

<br />

CT <br />

<br />

,CT , <br />

, , <br />

2123 <br />

35 CT CT DXA<br />

H CT N CT <br />

L CT 3 μX CT <br />

3<br />

μX CT H N L <br />

<br />

H <br />

99.55N 75.29L 50.34 <br />

H 0.67GPaN 0.63GPaL 0.58GPa<br />

CT <br />

<br />

<br />

<br />

P<br />

<br />

1 2 1 2 2 <br />

2<br />

1<br />

2 <br />

<br />

<br />

232 <br />

73 <br />

<br />

1975<br />

1983232 <br />

23 9.9<br />

70.3 58.3 <br />

30 70 9 <br />

1 <br />

grade 4 <br />

17.813 60.914 <br />

9 5 <br />

3 10 <br />

<br />

<br />

<br />

<br />

<br />

P<br />

<br />

1,2 2 2 1 2<br />

1<br />

2 <br />

P<br />

<br />

1 1 1 2 2<br />

1<br />

2 <br />

<br />

<br />

<br />

12 3,8mm <br />

1 2 4 4<br />

<br />

CT <br />

<br />

<br />

SEMEDX<br />

Ca, P, C CT<br />

1 <br />

2 4 <br />

SEMEDX 2 4 <br />

Ca P C <br />

<br />

<br />

<br />

<br />

<br />

<br />

<br />

<br />

<br />

<br />

<br />

5 wistar <br />

EX CO 4 7 <br />

14 3 1 <br />

<br />

<br />

<br />

<br />

7 14 <br />

4 <br />

7


160<br />

117 <br />

P<br />

<br />

1 1 1 2 1<br />

1<br />

2 <br />

<br />

<br />

<br />

<br />

<br />

<br />

<br />

<br />

/ +/+, +/,/+,/ 4 1 1<br />

30 10 <br />

CL TC <br />

<br />

+/+ /+ / <br />

2 <br />

<br />

<br />

<br />

<br />

P<br />

<br />

<br />

1 2 3 4<br />

1<br />

2 3 <br />

4 <br />

<br />

<br />

<br />

<br />

<br />

<br />

<br />

<br />

<br />

<br />

<br />

<br />

Softex <br />

<br />

<br />

<br />

90<br />

<br />

<br />

P<br />

Klotho <br />

1 1 1 2,3 4 <br />

1<br />

1<br />

2 <br />

3 4 <br />

<br />

<br />

klotho klotho/<br />

<br />

5 klotho/ <br />

von Kossa, van Geison I MGPαsmooth<br />

muscle actinα SMAALPENPP1 <br />

TEM MGP <br />

klotho/ α SMA <br />

MGP I <br />

<br />

ALP ENPP1 <br />

TEM <br />

MGP <br />

klotho/ <br />

<br />

<br />

<br />

P<br />

FAMA <br />

1 1 1 1 1 2 <br />

2 1<br />

1<br />

2 <br />

FAM20A is a member of family with sequence similarity 20 FAM20 which<br />

has three members FAM20A, FAM20B and FAM20C in mammals. We have<br />

reported a transgenic Tg mouse line the lineage 230 exhibiting growth disorder<br />

associated with a 58kb fragment deletion in chromosome 11E1 that encompasses<br />

part of the FAM20A gene. Recently, some studies have reported that patients<br />

with amelogenesis imperfecta caused by FAM20A mutation display several<br />

dental phenotypes including hypoplastic enamel, failure of tooth development<br />

and gingival hyperplasia. In the present study, we aimed to clarify how the loss of<br />

FAM20A protein influenced the development of mouse dental tissues. We have<br />

observed delayed tooth eruption in the homozygous mice of the lineage 230.<br />

Immunohistochemistry indicated that FAM20a protein was expressed in osteoid<br />

tissue and tooth germ of normal mice of the lineage 230, but was not expressed<br />

in homozygous mice of the lineage 230. The light microscopy demonstrated<br />

hypoplastic enamel and gingival hyperplasia in the homozygous mice of the<br />

lineage 230. In conclusion, this study revealed that the FAM20A protein played a<br />

critical role in enamel biomineralization.<br />

P<br />

GABA GABA <br />

1 2 2 2 3 <br />

3 4 1<br />

1<br />

2 <br />

3 4 <br />

<br />

<br />

<br />

GABA <br />

GAD <br />

GABA <br />

GABA GABA <br />

GABA <br />

<br />

OUMS27<br />

RTPCR GABA GABA <br />

<br />

RTPCR GABA GABAA <br />

α2α5β1 GABAB <br />

GABAB1 <br />

GABAB2 mRNA GABAB2 <br />

mRNA <br />

<br />

GABAB GABAB <br />

<br />

P<br />

Polypterus senegalus <br />

Oxydoras niger <br />

1 1 1 1 2 <br />

1<br />

1<br />

2 <br />

5 <br />

<br />

Polypterus senegalus Oxydoras niger <br />

<br />

SGCs <br />

<br />

<br />

<br />

SGCs <br />

SGCs <br />

<br />

50 μm <br />

100 μm <br />

SGCs <br />

<br />

SGCs <br />

SGCs <br />

SGCs


117 161<br />

P<br />

planar cell polarity <br />

<br />

1 2<br />

1<br />

2 RI <br />

<br />

2 <br />

<br />

<br />

planar cell polarity <br />

4-5 Wistar <br />

EDTA <br />

frizzled3 Vangl2 Alexa488 Alexa555 <br />

<br />

<br />

β N <br />

Vangl2 <br />

<br />

frizzled3 <br />

<br />

planar cell polarity <br />

<br />

P<br />

<br />

Miyuki Yamamoto, Shoichi Iseki<br />

<br />

<br />

<br />

SD GCT <br />

GCT SD ID <br />

stem or progenitor cell <br />

5 K5 <br />

progenitor cell basal<br />

epithelial cell K5 <br />

K5 <br />

progenitor cell <br />

C57BL/6 K5 <br />

stem cell <br />

<br />

<br />

ID ID <br />

lumen <br />

progenitor cell<br />

<br />

P<br />

Studies on the submandibular gland of androgen receptordeficient mice<br />

Kannika Adthapanyawanich, Hiroki Nakata, Tomohiko Wakayama,<br />

Shoichi Iseki<br />

Department of Histology and Embryology, Graduate School of Medical Science,<br />

Kanazawa University<br />

In the submandibular gland SG of mice, the duct portion called granular<br />

convoluted tubule GCT is developed preferentially in the male. To clarify if<br />

the androgendependent differentiation of GCT cells is mediated by the classical<br />

androgen receptor AR, we examined SG in the C57BL/6 strain mouse deficient<br />

for AR ARKO. The ARKO mouse was generated by the Cre/loxP recombination<br />

system using the floxedAR mouse provided by Dr. Shigeaki Kato. In male ARKO,<br />

GCT was not formed in the duct system during the postnatal development,<br />

resulting in the femaletype SG at adult age 8W. No abnormality was recognized<br />

in development of the acinar system. The levels of the expression of NGF and<br />

EGF, markers of GCT cells, in SG of ARKO male were even lower than those<br />

of wildtype female. When testosterone was administered to ARKO male and<br />

wildtype female, the duct system of wildtype female was converted to the male<br />

type both morphologically and in the levels of marker gene expression, whereas<br />

that of ARKO male remained in the female type. These results confirmed that<br />

the androgendependent cell differentiation in the duct system of mouse SG is<br />

mediated by the classical AR.<br />

P<br />

<br />

1 2 3<br />

1<br />

2 NPO <br />

3 <br />

<br />

<br />

Neovison vison <br />

<br />

<br />

HE 3.5NHCl <br />

S800 <br />

45 V <br />

<br />

1 <br />

<br />

<br />

<br />

1 <br />

1 <br />

<br />

<br />

<br />

<br />

<br />

P<br />

<br />

<br />

<br />

<br />

<br />

7 <br />

<br />

7 1 <br />

deoxycholate <br />

<br />

<br />

<br />

<br />

deoxycholate <br />

<br />

STIM stromal interaction molecule<br />

SOCEstoreoperated calcium entry<br />

SOCE <br />

<br />

P<br />

A AB <br />

<br />

<br />

<br />

3 <br />

<br />

3A <br />

3AB <br />

3A 3AB <br />

SN38 <br />

<br />

3A 3AB


162<br />

117 <br />

P<br />

<br />

<br />

<br />

IVCT FS <br />

IgA Ig <br />

<br />

-193 IVCT<br />

2% PFA <br />

FS <br />

2%PFA 2%PFA -<br />

- PFDH <br />

- HE IgA <br />

IgG1 Ig κ Lκ IgM IVCT<br />

HE <br />

IgA IgLκ <br />

IgG1 IgM <br />

IgG1 <br />

PFDH IgA <br />

IVCTFS <br />

<br />

P<br />

M Epidermal type FABP EFABP/FABP<br />

<br />

1 2 1<br />

1<br />

2 <br />

Fatty acid binding protein FABP <br />

<br />

Epidermal type FABP EFABP/FABP5 <br />

M <br />

Histochem Cell Biol. vol.1326, 2009 M <br />

17 18 <br />

116 M <br />

16, 17, 18, 19 <br />

IgA IgA <br />

EFABP <br />

M EFABP <br />

EFABP <br />

<br />

galectin4 <br />

M EFABP galectin4 <br />

<br />

P<br />

A <br />

1 2 1 1 1 <br />

1 2 1<br />

1<br />

2 <br />

<br />

Lampreys are ancestral representatives of vertebrates known as jawless fish. The<br />

Japanese lamprey, Lethenteron japonicum, is a parasitic member of the lampreys<br />

known to store large amounts of vitamin A within its body. How this storage is<br />

achieved, however, is wholly unknown. Within the body, the absorption, transfer<br />

and metabolism of vitamin A are regulated by a family of proteins called retinoid<br />

binding proteins. Here we have cloned a cDNA for cellular retinolbinding<br />

protein CRBP from the Japanese lamprey, and phylogenetic analysis suggests<br />

that lamprey CRBP is an ancestor of both CRBP I and II. The lamprey CRBP<br />

protein was expressed in bacteria and purified. Binding of the lamprey CRBP to<br />

retinol Kd of 13.2 nM was identified by fluorimetric titration. However, results<br />

obtained with the protein fluorescence quenching technique indicated that lamprey<br />

CRBP does not bind to retinal. Northern blot analysis showed that lamprey CRBP<br />

mRNA was ubiquitously expressed, although expression was most abundant in the<br />

intestine. Together, these results suggest that lamprey CRBP has an important role<br />

in absorbing vitamin A from the blood of host animals.<br />

P<br />

cKIT <br />

<br />

<br />

<br />

<br />

ICC<br />

ICC <br />

cKIT <br />

<br />

ICC <br />

αSMA cKIT <br />

αSMA E11.5 <br />

12 cKIT E11.5 <br />

E12.5 <br />

cKIT αSMA E13.5 cKIT<br />

αSMA E15.5 αSMA<br />

cKIT <br />

<br />

αSMA E18.5 <br />

E14.5 E16.5 αSMA <br />

cKIT <br />

αSMAcKIT <br />

<br />

P<br />

ICCSP <br />

<br />

<br />

<br />

Interstitial cells of Cajal: ICC <br />

<br />

Subserosa: SS ICC ICCSS <br />

Submucosal Plexus: SP ICC ICCSP <br />

ICCSP <br />

ICC <br />

<br />

<br />

<br />

<br />

<br />

ICCSP <br />

<br />

<br />

P<br />

CCK <br />

<br />

<br />

CCK<br />

CCK1<br />

CCK1 <br />

<br />

CCK1 <br />

in situ hybridization<br />

<br />

CCK1 <br />

<br />

CCK <br />

<br />

G <br />

<br />

<br />

CCK1 <br />

CCK


117 163<br />

P<br />

The metabolism of cholesterol after bile duct degeneration in lamprey<br />

Mayako Morii 1 , Yoshihiro Mezaki 2 , Noriko Yamaguchi 2 , Kiwamu Yoshikawa 2 ,<br />

Mitsutaka Miura 2 , Katsuyuki Imai 2 , Taku Hebiguchi 1 , Ryo Watanabe 1 ,<br />

Hiroaki Yoshino 1 , Haruki Senoo 2<br />

1<br />

Department of Pediatric Surgery, Akita University Graduate School of Medicine,<br />

2<br />

Department of Cell Biology and Morphology, Akita University Graduate School<br />

of Medicine<br />

Lampreys are unique vertebrates in that they lose biliary trees entirely during<br />

the metamorphosis. Despite the biliary atresia, lampreys do not develop neither<br />

biliary cirrhosis nor liver dysfunction. In other vertebrates, obstruction of bile<br />

ducts results in fatality because of the cytotoxicity of bile salts. It means that<br />

lampreys have evolved to use another metabolic pathway of bile juice in order<br />

to evade the cholestasis. However, molecular mechanism of this pathway is still<br />

unknown. The aim of this study is to investigate the way how the lamprey avoid<br />

the pathological consequence of cholestasis. We have cloned the cDNA sequences<br />

of two kinds of P450, which show high degree of homology with mammalian<br />

CYP7A1 and CYP27A1, respectively. We are now evaluating the expression<br />

levels of the mRNA for these genes in liver, gonad, gill, heart and intestine along<br />

with the temporal expression profiles from larva to adult. The present study<br />

suggests how and where bile acids are detoxified in adult lampreys. Understanding<br />

how lampreys avoid cholestasis could be valuable for progress in the treatment of<br />

human obstructive cholangiopathy.<br />

P<br />

NAFLD <br />

<br />

1 1 1 2 1<br />

1<br />

2 <br />

<br />

<br />

NAFLD NAFLD <br />

NASH NAFLD <br />

NASH <br />

9 C57BL/6 MCD <br />

30 M R MCD 8 16<br />

30 2 AST, ALT <br />

<br />

M 2 AST, ALT <br />

NAFLD <br />

10 <br />

M 16 CD68 <br />

CD68 <br />

R 3 <br />

R 16 <br />

MCD 16 CD68 <br />

30 <br />

CD68 <br />

<br />

P<br />

Deltalike <br />

<br />

<br />

<br />

<br />

Deltalike3 DLL3 <br />

DLL3 <br />

Huh2 DLL3 <br />

<br />

AnexinV TUNEL singlestrand DNA <br />

DLL3 Huh2 <br />

DLL3 binding<br />

assay DLL3 Small G Cdc42 <br />

CRIB <br />

DLL3 HuH2 Cdc42 <br />

PAK1 MAP kinase <br />

DLL3 <br />

<br />

DLL3 Cdc42 PAK1 MAP kinase <br />

<br />

P<br />

<br />

1 2 2 2 1<br />

1<br />

2 <br />

<br />

<br />

CLD<br />

<br />

<br />

<br />

<br />

ICR 85O 2 <br />

RA21Air 14 <br />

RA 7 RA14 Air14d<br />

14 O 2 14dRA 21 Air21dO 2 Air21d<br />

4%PFA<br />

<br />

O 2 14d <br />

O 2 <br />

Air21d <br />

<br />

<br />

CLD <br />

<br />

P<br />

CEACAM <br />

1 Nabil Eid 1 2 1 1<br />

1<br />

2 <br />

<br />

prox1 <br />

<br />

Carcinoembryonic cell adhesion molecule1 CEACAM1 <br />

CEACAM1 <br />

VEGFC <br />

BJMC338 VEGFC <br />

BJMC3879 <br />

2 CEACAM1, <br />

VEGFR3VEGFR3 <br />

phosphotyrosine <br />

VEGFA <br />

BJMC3879 <br />

CEACAM1 BJMC3879 <br />

CEACAM1 BJMC338<br />

BJMC3879 <br />

BJMC3879 VEGFR3 <br />

BJMC3879 CEACAM1 <br />

VEGFC <br />

<br />

P<br />

The role of peritoneal lymphatic system on the human peritoneal<br />

dissemination<br />

Masahiro Miura 1 , Yutaka Yonemura 2 , Yoshio Endou 3<br />

1<br />

Department of Human Anatomy, Faculty of Medicine, Oita University, 2 NPO<br />

organization to support peritoneal dissemination treatment, 3 Department of<br />

Molecular Targeting Therapy, Kanazawa University<br />

The role of lymphatic microenvironment on cancer metastasis was studied.<br />

VEGFCgene transfectants of the gastric cancer cell lines were inoculated into<br />

the peritoneal cavity of nude mice. The tissue samples from human disseminated<br />

peritoneum were stained with 5,NaseALPase double staining and aniti<br />

VEGFR3 immunostaining. Mouse VEGFR3 gene expression was induced after<br />

inoculation. In the early peritoneal dissemination PD stage, newly lymphatic<br />

networks LN were detected in the periphery of the primary tumor. The main<br />

source of lymphatic dissemination may originate from the peritumoral LN. In the<br />

PD, three patterns of tumor lymphangiogenesis, namely centrifugal, centripetaland<br />

combination growth patterns were found. Free cancer cells invaded the numerous<br />

blind endings that came from extended subperitoneal LN. In the late PD stage,<br />

the number of LN decreased due to the destruction of cancer cells. In SEM<br />

observation, Macula cribriformis were seen in the diaphragmatic subperitoneal<br />

tissue layer and Morrison pouch. Lymphangioginesis including newly formed LN,<br />

induced by VEGFC is closely associated in formation of PD and lymph node<br />

metastasis mainly via the prelymphatic channels.


164<br />

117 <br />

P<br />

<br />

<br />

<br />

<br />

<br />

<br />

<br />

α β 2<br />

α 18 β 8 24 <br />

<br />

<br />

3<br />

<br />

α <br />

β <br />

Zeiss LSM710 <br />

β18 <br />

β5 β5 2 <br />

αv <br />

<br />

P<br />

<br />

<br />

<br />

66 CD41 <br />

<br />

<br />

<br />

ICR <br />

<br />

CD41 <br />

12 22.96.6/mm 3 14<br />

38.410.0/mm 3 16 <br />

0 21.710.0/mm 3 6 3.62.0/mm 3 20 <br />

<br />

<br />

<br />

<br />

<br />

2 <br />

<br />

P<br />

The role of hematopoietic factors and Wnt signaling during tooth<br />

development<br />

Masataka Sunohara, Iwao Sato<br />

Department of Anatomy, School of Life Dentistry at Tokyo, The Nippon Dental<br />

University, Tokyo, Japan<br />

Purpose:It has been reported that Wnt signaling pathway is involved in the early<br />

tooth development and regulates haematopoietic stem cells HSCs. However<br />

the role of hematopoietic factors during tooth development remain unclear.<br />

Here we examine the role of hematopoietic factors and Wnt signaling during<br />

tooth development in mice. Methods:We performed in situ hybridization and<br />

immunohistochemically stained serial sections of dental tissues with antibodies<br />

against hematopoietic factors and Wnt.<br />

Results:We observed that hematopoietic factors were detected at the some stages<br />

of tooth development and Wnt was localized in mesenchymal layers at the late<br />

stage of tooth development. Conclusions:These data suggest that hematopoietic<br />

factors and Wnt were involved in tooth germ development in mice.<br />

*This study was was supported by a GrantinAid for Scientific Research C<br />

No.22592052.<br />

P<br />

<br />

1 2 2 2<br />

1<br />

2 <br />

<br />

<br />

Al V 64<br />

Ti6Al4V PMN <br />

PMN NADPH oxidase <br />

O2 H2O2 <br />

PMN <br />

OPZ OPZ H2O2<br />

Ce V <br />

PMN Al PMN <br />

PMN <br />

Ti6Al4V PMN H2O2<br />

<br />

PMN Ti6Al4V PMN <br />

3710 Ce H2O2 <br />

3720 GA <br />

<br />

PMN PMN H2O2 <br />

P<br />

podoplanin <br />

<br />

<br />

<br />

<br />

<br />

C57BL/6 4% <br />

<br />

podoplaninLYVE1 <br />

in situ hybridization<br />

CCL21 <br />

<br />

5 HE <br />

3 <br />

podoplanin <br />

LYVE1 podoplnanin <br />

3 5 CCL21 in<br />

situ hybridization <br />

CCL21 podoplanin podoplanin<br />

<br />

<br />

P<br />

<br />

<br />

<br />

<br />

<br />

<br />

<br />

<br />

VEGFA <br />

<br />

<br />

VEGFA <br />

<br />

PDGFRβ NG2 NG2 <br />

PDGFRβ NG2


117 165<br />

P<br />

<br />

1 1 2 2 1<br />

1<br />

2 <br />

<br />

<br />

DDS <br />

<br />

<br />

<br />

<br />

<br />

SCID 1 <br />

CDDP 3 <br />

<br />

<br />

<br />

<br />

CDDP 1 <br />

<br />

<br />

<br />

<br />

<br />

P<br />

<br />

1 1 2 3 3 1<br />

1<br />

2 3 <br />

<br />

<br />

<br />

5 8 <br />

<br />

<br />

<br />

10<br />

<br />

<br />

<br />

1 <br />

1 4-7 2 <br />

3-7 3 3-7 <br />

<br />

1 <br />

7-12 2 6-14 3 <br />

5-11 <br />

<br />

<br />

<br />

P<br />

<br />

<br />

<br />

64 128 <br />

<br />

124 97<br />

94 73<br />

46 36 27 <br />

21% 1 1%<br />

<br />

<br />

IVI 6 IIV <br />

N<br />

I II<br />

IIIIV III <br />

V <br />

VI <br />

<br />

<br />

<br />

<br />

<br />

P<br />

<br />

<br />

1 1 2 1 1 <br />

1 1<br />

1<br />

2 <br />

<br />

<br />

<br />

<br />

Wistar <br />

<br />

<br />

SDSPAGE <br />

50 nm <br />

<br />

<br />

<br />

<br />

<br />

<br />

SDSPAGE <br />

<br />

<br />

P<br />

Nkx. <br />

1 1 1 1 2 <br />

1<br />

1<br />

2 <br />

<br />

Nkx2.5 <br />

GATA4 TBX5 <br />

Nkx2.5 <br />

<br />

KONkx2.5+/−<br />

<br />

Nkx2.5+/− <br />

<br />

1020 C57BL/6JNkx2.5+/− <br />

4%PFA <br />

<br />

<br />

Nkx2.5+/− <br />

<br />

<br />

<br />

P<br />

Morphological analysis of effects with arachidonic acid in smooth<br />

muscle cells<br />

Hideyuki Tanaka 1 , Haruo Hagiwara 2 , Shinnichi Mitui 1<br />

1<br />

Labo.Sci, Gunma Univ. Grad. Sch. Health Sci., 2 Anatomy, Teikyo Univ. Sch. Med.<br />

We previously reported that arachidonic acid enhanced the ATPase activity<br />

of smooth muscle myosin of which 20 kDa myosin light chain MLC20 was<br />

phosphorylated to leave no room for the additional phosphorylation. We report<br />

here that configuration of smooth muscle myosin changes to activated form<br />

with arachidonic acid from inactiveted form under unphosphorytated condition.<br />

And, selfaseembly of each myosins was enhanced in vitro. Such a direct effect<br />

of arahidonic acid was confirmed by inducing superprecipitation, an invitro<br />

contraction, and contraction of TritonX skinned fiber of smooth muscle under<br />

conditions that the phosphorylation of MLC20 didi not proceed. An electron<br />

microscopic observation of superprecipitation, and of skinned fibers with<br />

arachidonic acid indicated an enhanced association of actin fibers with myosin<br />

filaments.


166<br />

117 <br />

P<br />

FABP<br />

<br />

<br />

<br />

<br />

FABP7 <br />

Kupffer KC<br />

KC FABP7 <br />

FABP7 KC <br />

FABP7 clodoronateliposome clo<br />

lipo KC FABP7 <br />

clolipo 7 F4/80+KC <br />

FABP7 <br />

clolipo 7 F4/80+KC 78% FABP7+ <br />

FABP7 J774 FABP7/J774LPS <br />

TNFα TNFα <br />

IκB <br />

FABP7 FABP7 <br />

KC <br />

<br />

P<br />

<br />

1,3 Randeep Rakwal 1 1 1 1 <br />

1 1 2 3 1<br />

1<br />

2 3 NPO <br />

<br />

<br />

<br />

<br />

<br />

<br />

<br />

1/3<br />

1.2% 5 / 1.2%NP 4 <br />

6 LPS 10 mg/<br />

kg mRNA DyeSwap <br />

DNA 1.2%NP 5000<br />

<br />

<br />

1000 <br />

<br />

<br />

<br />

<br />

P<br />

Functional Analysis of Nucleoprotein diet from salmon testis, Shirako<br />

via Intestinal IgA secretion and TLR stimulation<br />

1 Randeep Rakwal 1 1 1 1 <br />

1 1 2 3 1 1<br />

1<br />

2 3 NPO <br />

<br />

Salmon testis, Shirako contains in plenty nucleic acids and protamin protein,<br />

termed as Nucleoprotein NP. However, we know little about their functions in<br />

the human body, and molecular evidence for these potential beneficial effects.<br />

Therefore, the aim of this study was to elucidate the effects of dietary NP and<br />

know molecular evidence for these potential beneficial effects.<br />

First, we analyzed the innate immunity response in mice by measuring IgA<br />

secretion in feces. To do so, mice were fed high or low level NP diets for 4 weeks.<br />

Fecal IgA level was measured with an ELISA kit. Our results revealed that the<br />

fecal level of IgA was little higher in the highNP diets group than in the lowNP<br />

diets group.<br />

Next, we examined the human TLR9 stimulation and cytokine production<br />

by effect of NP. We added NP into HEK293 cells overexpressed human TLR<br />

9 to measure NFκB transcriptional activity and, PMA induced U937 cells to<br />

measure several cytokine expressions. The results show that NP affects on TLR9<br />

stimulation and some cytokine expressions.<br />

Here, we show some evidences and hypothesize that NP diet might affect on some<br />

cytokine expressions to increase mucosal immunity.<br />

P<br />

The effects of adjuvants on autoimmune responses against testicular<br />

antigens in mice<br />

Musha Muhetaerjiang, Shuichi Hirai, Munekazu Naito, Hayato Terayama,<br />

Qu Ning, Masahiro Itoh<br />

<br />

A subcutaneous injection with testicular homogenate TH can easily induce<br />

systemic immune responses against the autoantigens of germ cells. Experimental<br />

autoimmune orchitis EAO is pathologically characterized by lymphocytic<br />

inflammation accompanied by the spermatogenic disturbance. Classically, the<br />

murine EAO is induced by immunization with TH + Complete Freund’s Adjuvant<br />

+ Bordetella Pertussigens, and it has been considered that these adjuvants is<br />

needed to enhance the immune responses. However, there remains a possibility<br />

that adjuvants affect autoimmune responses against the autoantigens without<br />

TH. In the present study, we examined this possibility using real time RTPCR,<br />

Western Blotting and immunohistochemical staining. The results demonstrated<br />

that testicular histopathological state and expressions of intratesticular cytokines<br />

were normal in mice injected with adjuvants alone. However, various kinds of<br />

serum autoantibodies with not only germ cells but also Sertoli cells were detected<br />

in the adjuvant injected mice. These results indicate that adjuvants alone can<br />

evoke testicular autoimmune reactions against various autoantigens irrespective of<br />

no use of TH.<br />

P<br />

<br />

<br />

<br />

<br />

<br />

<br />

<br />

<br />

<br />

<br />

<br />

<br />

<br />

2<br />

<br />

<br />

<br />

<br />

P<br />

Germ cell death in testicular autoimmunity<br />

Kuerban Maimaiti, Shuichi Hirai, Hayato Terayama, Qu Ning, Yuki Ogawa,<br />

Musha Muhetaerjiang, Munekazu Naito, Masahiro Itoh<br />

<br />

Experimental autoimmune orchitis EAO is characterized by T celldependent<br />

lymphocytic inflammation and damage to seminiferous tubules, causing death of<br />

testicular germ cell TGC. The aim of the present study is to investigate the role<br />

of apoptosis systems in the TGC death in EAO in mice, using real time RTPCR<br />

and immunostaining. The results showed that the many Tdt mediated dUTP nick<br />

end labeling positive TGC were found at the active EAO stage and persistently<br />

observed in the seminiferous epithelium until the postactive EAO stage. Intra<br />

testicular mRNAs expression of both Fas and Bax increased at the active EAO<br />

stage and dramatically decreased at the postactive EAO stage. In contrast, intra<br />

testicular the mRNAs expression of both FasL and Bcl2 did not show significant<br />

changes at the active EAO stage but extremely increased at the postactive EAO<br />

stage. Immunohistochemically, some Fas or Baxpositive TGC were detected at<br />

the active EAO stage and hardly found at the postactive EAO stage. In contrast,<br />

some FasL or Bcl2 positive TGC were found at the active EAO stage but many<br />

of them were observed at the postactive EAO stage.


117 167<br />

P<br />

<br />

1 2 1 3 1<br />

1<br />

2 <br />

3<br />

<br />

<br />

A,B,C D <br />

<br />

<br />

<br />

<br />

<br />

B PNAS, Yuan et al. 2007<br />

<br />

<br />

152 <br />

<br />

<br />

<br />

CD68S100<br />

Fascin <br />

<br />

<br />

P<br />

<br />

<br />

<br />

1 <br />

<br />

<br />

conduit <br />

<br />

ICR <br />

2000 kDa<br />

10 kDa 310 4 PFA<br />

3 530<br />

OCT 10 μm <br />

Tris ER<br />

TR7 TypeIV <br />

5 nm<br />

54 nm<br />

<br />

<br />

<br />

<br />

<br />

P<br />

trafficking<br />

<br />

<br />

secondary lymphoid organ, SLO<br />

traffickingT <br />

SLO <br />

<br />

T DC<br />

DC <br />

<br />

T T <br />

trafficking molecule <br />

DC trafficking <br />

DC <br />

DC <br />

<br />

<br />

T DC trafficking SLO <br />

P<br />

Alterations of synaptic transcytosis induced by ethanol exposure:<br />

apocrinelike structure in the rat<br />

Tomiko Yakura 1 , Takanori Miki 1 , JunQian Liu 1 , Kenichi Ohta 1 ,<br />

Katsuhiko Warita 1 , Yoshiki Matsumoto 2 , Shingo Suzuki 1 , Motoki Tamai 1 ,<br />

Yoshiki Takeuchi 1<br />

1<br />

Department of Anatomy and Neurobiology, Faculty of Medicine, Kagawa<br />

University, 2 Laboratory of Animal Science, Faculty of Agriculture, Kagawa<br />

University<br />

Effects of alcohol exposure on synaptic structure were investigated in the NST<br />

in the rat. Ethanolfed animals were allowed free access to liquid diet containing<br />

ethanol for 3 weeks. A few terminals were characterized by deep indentation<br />

of axodendritic membranes into the postsynaptic neurons which was similar to<br />

the apocrine structure. Other animals of ethanol exposure received injection of<br />

WGAHRP into the vagus nerve and were prepared for electron microscopy.<br />

HRPreaction product RP was recognized easily as electron dense lysosomal<br />

substance when lead citrate staining was omitted. The terminals containing HRP<br />

RP also revealed quite similar structure to indentation of axodendritic membranes<br />

described above. The results are considered to confirm that terminals forming<br />

“apocrine-like structure” are originated from afferent fibers of the vagus nerve.<br />

The present study raised the possibility that remarkable alteration of the synaptic<br />

structure induced by ethanol exposure leads neuronal transcytosis of materials<br />

including proteins which is absolutely different from vesicular exocytosis involved<br />

in chemical synaptic transmission.<br />

P<br />

LAMP <br />

<br />

<br />

Lysosomeassociated membrane protein2 LAMP2<br />

LAMP2 <br />

X <br />

<br />

<br />

<br />

LAMP2 <br />

12 LAMP2 <br />

LAMP1 D <br />

<br />

A <br />

GM130 <br />

<br />

LC3 LAMP2 <br />

<br />

LAMP2 <br />

<br />

P<br />

Synergistic interaction between Golgi outposts and RNA granules in<br />

postlocal translational secretory pathway<br />

Souichi Oe, Yasuko Noda<br />

Jichi Med. Univ. Tochigi, Japan<br />

In the central nervous system, neurons have Golgi outposts in dendrites and<br />

it has been shown that its subcellular distribution and morphology are related<br />

with various aspects of cellular event. In this study, we analyzed the subcellular<br />

localization of Golgi outposts under the various stimulations in cultured<br />

hippocampal neurons. In normal conditions, Golgi outposts localized in basal<br />

dendrites and contained some Golgi matrix proteins including GM130, GRASP65<br />

and BicaudalD2. When the neurons were cultured with several stimulations, the<br />

distribution of Golgi outposts were enhanced towards the distal dendrites. This<br />

observation was similar to the dynamics of RNA granules, and in fact, Golgi<br />

outposts colocalized with CPEB which is the translational repressor and the<br />

component of the RNA granules. Furthermore, we constructed the GFP based<br />

reporter plasmid that has the signal sequence and the dendritic localization signal<br />

of CaMKII mRNA and observed the localization in dendrites with or without the<br />

stimulations. These results suggest that Golgi outposts act synergistically with<br />

RNA granules and contribute to the postlocal translational secretory pathway in<br />

dendrites.


168<br />

117 <br />

P<br />

ARF BRAG/IQSEC <br />

<br />

<br />

Brefeldin Aresistant ArfGEF 2 BRAG2/IQSEC1 <br />

ADP 6 Arf6 <br />

GEF <br />

BRAG2 AMPA <br />

<br />

BRAG2 <br />

BRAG2 <br />

BRAG2pan C <br />

BRAG2LC BRAG2 <br />

<br />

BRAG2LC <br />

PSD AMPA <br />

BRAG2pan PSD <br />

<br />

BRAG2 PSD <br />

<br />

BRAG2Arf6 AMPA <br />

<br />

P<br />

Arf EFAA <br />

<br />

<br />

GTP ADP 6 ARF6 <br />

<br />

<br />

ARF6 GEF <br />

EFA6A <br />

<br />

EFA6A <br />

<br />

EFA6A <br />

PSD95 <br />

<br />

<br />

EFA6A <br />

<br />

EFA6A PSD PSD <br />

EFA6A <br />

PSD PSD ARF6 <br />

<br />

P<br />

Roles of BMP signaling in synapse development<br />

<br />

<br />

Continual formation and elimination of synapses is required for refinement<br />

of the neuronal circuit. Synapse remodeling should be regulated by specific<br />

signaling mechanisms, but few molecules involved in synapse elimination have<br />

been identified, despite a large body of work on molecular cascades that initiate<br />

or enhance synapse formation. Here, we report that BMP4 negatively regulates<br />

hippocampal synapse formation in vitro. First, we confirmed that hippocampal<br />

neurons respond to BMP4 by measuring accumulation of activated Smad by<br />

immunocytochemistry. Next, we constructed BMP4EGFP and visualized its<br />

localization in living hippocampal neurons. Timelapse fluorescence imaging<br />

revealed that BMP4EGFP clusters showed bidirectional movements in the<br />

somatodendritic compartment. Finally, overexpression of BMP4 in neurons<br />

induced reduction of both density and immunoreactivity of VGluT1positive<br />

presynaptic puncta associated with BMP4expressing dendrites. These results<br />

indicate the presence of transsynaptic retrograde signaling in BMP4dependent<br />

suppression of synapse formation.<br />

P<br />

Roles of ACF, a large linker protein interacting with both<br />

microtubules and Factin, in the postsynaptic functions<br />

<br />

<br />

Two major components of the cytoskeletal system, Factin and microtubules MTs,<br />

have been shown to be involved in the postsynaptic functions. Actin network<br />

regulates the spine shape and motility. MTs invade into spines intermittently and<br />

help spine head expansion through the remodeling of actin network. Although<br />

these observations suggest importance of coordination between two cytoskeletal<br />

systems, there have been few reports on molecular mechanisms that regulate their<br />

interaction.<br />

ACF7/MACF1 is a member of spectraplakin family protein and links between<br />

Factin and MTs. By manipulating ACF7 content in cultured hippocampal<br />

neurons, we assessed the impact of ACF7dependent cytoskeletal reorganization<br />

on spine morphology. First, overexpression of ACF7GFP revealed accumulation<br />

of ACF7 in a subset of dendritic spines. This selective targeting may reflect<br />

specific functional states of spines. Second, downregulation of ACF7 by shRNA<br />

induced elongation of spines, which was rescued by expression of shRNA<br />

registant ACF7 cDNA. This phenotype may indicate that reduction of ACF7<br />

blocks MTdependent spine head expansion and reversibly enhances excess<br />

growth of thin spines.<br />

P<br />

Imaging dynamics of axonal mitochondria<br />

<br />

<br />

The complex geometry of neuron requires specialized mechanism to allocate<br />

sufficient number of organelle to neurites and synapses. Proper distribution<br />

of mitochondria is critical for multiple neuronal functions including energy<br />

production, calcium homeostasis, neuronal apoptosis, synaptic transmission and<br />

plasticity. However, mitochondrial dynamics underlying the maintenance of<br />

their proper distribution is largely unknown. To study mitochondrial dynamics in<br />

neurons, we established a live imaging system to visualize neuronal mitochondria<br />

in hippocampal dissociated culture. We are now investigating neuronal<br />

mitochondria distribution and trafficking by expressing mitochondrial outer<br />

membrane protein Omp25C tagged with fluorescent proteins and performing time<br />

lapse confocal imaging. The size, distribution and motility of mitochondria in the<br />

axon and synaptic contact sites are analyzed quantitatively and these data will be<br />

integrated to estimate the rate and extent of mitochondria replacement in specific<br />

neuronal compartments.<br />

P<br />

ERRγ <br />

<br />

<br />

estrogenrelated receptor: ERR<br />

<br />

estrogen receptor: ERαßγ 3 <br />

ERR <br />

DNA ER ERR <br />

ER <br />

ER ERR <br />

3 ERRγR <br />

10 ERRγR <br />

<br />

<br />

<br />

ER <br />

ERRγR <br />

ER <br />

ERRγR ER


117 169<br />

P<br />

Agerelated changes in estrogen receptorβ mRNA expression in<br />

male rat brain<br />

<br />

<br />

Estrogen plays important roles not only in reproductive function but also in other<br />

functions such as cognition and emotion. Estrogen acts mainly via its receptor<br />

ER, ERα and β, in target tissues. During aging, estrogenic actions are altered<br />

in both females and males, raising the possibility that expression level of ER may<br />

be altered with age. Agerelated changes in ER expression in female rat brain<br />

have been well demonstrated with regard to reproductive aging, while very little<br />

is known about the effects of age on the expression of ERs, especially ERβ, in<br />

males. In this study, to elucidate the effects of aging on ERβ expression in the<br />

male brain at the transcriptional level, we performed in situ hybridization using<br />

young, middleaged and old male rats. We revealed the number of ERβ mRNA<br />

positive cells was decreased with age in the cerebral cortex, hippocampus,<br />

dorsal endopiriform nucleus, medial septal nucleus, amygdala, anteroventral<br />

periventricular nucleus, substantia nigra, raphe and locus coeruleus. These<br />

results suggest that ERβ expression in male rat brain decreases with age at the<br />

transcriptional level and that these aging effects are regionspecific.<br />

P<br />

PRLR <br />

<br />

1,2 2 2 1 2<br />

1<br />

2 <br />

<br />

ARC <br />

PRLR PRLR<br />

<br />

<br />

TH<br />

PRLR <br />

<br />

PRLR <br />

ARC TH PRLR <br />

<br />

TH PRLR <br />

PRLR <br />

ARC <br />

PRL ARC <br />

PRLR PRL <br />

PRLR <br />

<br />

P<br />

<br />

<br />

<br />

<br />

<br />

<br />

<br />

RTPCR 2 Wistar <br />

OVX Sham 1 <br />

2 <br />

17β<br />

1 2 17α/C1720 <br />

1 <br />

OVX 2 OVX<br />

Sham <br />

1 2 <br />

<br />

<br />

<br />

P<br />

Sporadically lurking HAPimmunoreactive cells in the hippocampus<br />

and their morphological relation with steroid receptors<br />

Md. Nabiul Islam, Ryutaro Fujinaga, Akie Yanai, Mir Rubayet Jahan,<br />

Yukio Takeshita, Keiji Kokubu, Koh Shinoda<br />

Division of Neuroanatomy, Yamaguchi University Graduate School of Medicine<br />

Huntingtinassociated protein 1 HAP1 is a neural huntingtin interactor that is<br />

widely expressed in the limbic and hypothalamic regions. Although HAP1 has<br />

been reported to be associated with steroid receptors, HAP1immunoreactive<br />

HAP1ir cells remain to be identified in the hippocampus. We determined the<br />

distribution of hippocampal HAP1ir cells in light and fluorescence microscopy<br />

and characterized their morphological relationships with steroid receptors,<br />

markers of adult neurogenesis and the GABAergic system in adult Wistar rats<br />

of both sexes. HAP1ir cells that were sporadically distributed in the subgranular<br />

zone SGZ of the dentate gyrus and in the interface between the stratum<br />

lacunosummoleculare and stratum radiatum of Ammon’s horn, were identified as<br />

the “sporadically lurking HAP1-ir (SLH)” cells. The SLH cells showed no clear<br />

association with the markers of adult neurogenesis in the SGZ, while all the SLH<br />

cells expressed neuN. More than 90% of the SLH cells expressed nuclear ERα,<br />

while more than 65% of them exhibited GABA immunoreactivity. We conclude<br />

that SLH cells might be involved in estrogendependent hippocampal functions<br />

through ERα and GABAergic regulation.<br />

P<br />

GR<br />

<br />

<br />

<br />

<br />

GR<br />

GR <br />

<br />

GR <br />

vimentin GR<br />

GR GR<br />

coactivator p300 SRC1 <br />

ADX<br />

GR coactivator <br />

vimentin <br />

GR vimentin p300<br />

SRC1 ADX vimentin <br />

GR <br />

p300SRC1 <br />

GR <br />

GR<br />

<br />

P<br />

<br />

1 1 2 1<br />

1<br />

2 <br />

24 <br />

<br />

<br />

<br />

cfos, Per1 <br />

cfos, Per1 <br />

gate<br />

<br />

<br />

<br />

<br />

10 <br />

1 3 2 30 <br />

cfos Per1 <br />

in situ hybridization


170<br />

117 <br />

P<br />

GALP<br />

1 1 1,2 1<br />

1<br />

2 <br />

GALP<br />

GALP <br />

<br />

<br />

GALP GALP <br />

24 <br />

GALP <br />

GALP <br />

GALP <br />

GALP <br />

4510 1216<br />

<br />

GALP <br />

PEPCK SREBP1 <br />

GALP <br />

GALP <br />

GALP <br />

GALP <br />

P<br />

CGRP <br />

<br />

<br />

<br />

CGRP<br />

<br />

CGRP jugular ganglion <br />

<br />

Fluorogold <br />

<br />

nodose ganglion Fluorogold CGRP <br />

Fluorogold <br />

jugular ganglion Fluorogold 40% CGRP <br />

jugular ganglion nodose ganglion <br />

Fluorogold 20% <br />

Fluorogold CGRP <br />

2% <br />

CGRP <br />

<br />

CGRP <br />

<br />

P<br />

SSRI<br />

<br />

<br />

<br />

<br />

<br />

SSRI <br />

<br />

SSRI cAMP 1 transforming<br />

growth factor beta TGFβ <br />

2 cAMP <br />

cAMP response element binding protein CREB <br />

brainderived neurotrophic factor: BDNF <br />

<br />

<br />

<br />

SSRI 2 4 <br />

<br />

<br />

SSRI <br />

P<br />

<br />

<br />

1 1 1 1 2 3 <br />

2 1<br />

1<br />

2 3 <br />

<br />

MSCs<br />

1989 <br />

PACAP<br />

MSCs PACAP <br />

MSCshMSCs<br />

PACAP SCI<br />

<br />

C57/BL6 9/10 SCI <br />

10/11 50 /μLμ<br />

hMSCs<br />

SCI <br />

PACAP PCR <br />

SCI 7 hMSCs <br />

<br />

SCI PACAP 7 <br />

hMSCs <br />

PACAP PACAP <br />

hMSCs hMSCs <br />

<br />

hMSCs PACAP <br />

<br />

P<br />

<br />

1,2 1 1 3 1<br />

1<br />

2 3 NPO <br />

<br />

PD <br />

PD <br />

<br />

<br />

2 <br />

1.2% 7 <br />

20 mg/kg MPTP 2 4 <br />

MPTP 7 <br />

<br />

<br />

O2 in<br />

situ <br />

MPTP 7 <br />

<br />

TH <br />

MPTP O2<br />

<br />

O2 <br />

MPTP <br />

<br />

P<br />

<br />

<br />

1 2 1 3 4<br />

1<br />

2 <br />

3 4 <br />

ASIC2a <br />

<br />

ASIC2a degenerin<br />

<br />

degenerin 2 <br />

gain<br />

offunction <br />

ASIC2a 2 <br />

430 <br />

ASIC2a gainoffunction <br />

ASIC2a degenerin <br />

<br />

ASIC2aG430F ASIC2a <br />

TG<br />

TG <br />

TG


117 171<br />

P<br />

PACAP <br />

<br />

1,2 1,3 Randeep Rakwal 1 1 1 <br />

1 1 1 1 1 1 <br />

1 2 1<br />

1<br />

2 3 <br />

<br />

PACAP<br />

PACAP <br />

PMCAO<br />

PACAP <br />

PACAP <br />

PMCAO PACAP38 <br />

6, 24 RNA DNA <br />

PACAP <br />

1.7 <br />

6 34 <br />

24 Hedgehog 15 0.5<br />

6 <br />

1524 <br />

87<br />

PACAP <br />

PACAP <br />

<br />

P<br />

Protective effects of hyaluronan tetrasaccharide on hippocampal<br />

pyramidal neurons in neonatal mouse after hypoxicischemic injury<br />

Takehiko Sunabori, Masato Koike, Yasuo Uchiyama<br />

<br />

Hyaluronan HA is one of the major components of the extracellular matrix<br />

that contributes to a wide range of biological functions. The effects of HA differ<br />

mainly depending on the size of the polymers. Here we examined the effect<br />

of HA on hypoxicischemic HI brain injury against neonatal mice with a<br />

lowmolecularsize, HA tetrasaccharide HA4, and largemolecularsize HA<br />

800 kDa. Interestingly, only the HA4treated mice rescued the hippocampal<br />

pyramidal neurons 24hours after HI injury. To explore the underlining pathway,<br />

we focused on the contribution of the Tolllike receptor TLR /NFkB pathway,<br />

since the TLR2 and 4 are also known as receptors for HA. The TLR2 and TLR4<br />

null mice showed protective effects against HI injury, respectively. Moreover, the<br />

transient upregulation of the phosphorylation of p65/RelA, 1hour after HI injury<br />

was canceled when HA4 was administrated. Finally, the expression of the early<br />

inflammatory cytokine, IL1b was also inhibited by HA4 administration. These<br />

results suggest that the protective effect of neurons by HA4 is closely related to<br />

inactivation of the Tolllike receptor/NFkB pathway and reduced expression of<br />

inflammatory cytokines.<br />

P<br />

<br />

1 1 1 1 2 <br />

3 4 1<br />

1<br />

2 <br />

3 4 <br />

<br />

4 <br />

<br />

<br />

<br />

<br />

1 <br />

<br />

<br />

5 mg/kg <br />

CA1 CA3, CA4 <br />

<br />

mRNA <br />

<br />

Iba1 5 mg/kg<br />

<br />

<br />

<br />

<br />

P<br />

The Effects of an mer Peptide of Prosaposin in the Attenuation of<br />

MPP+/MPTP Toxicity in Vitro and in Vivo<br />

1 1 1 1 1 2 <br />

1<br />

1<br />

2 <br />

Parkinson’s disease PD is a chronic, progressive neurological disorder with<br />

increasing incidence in the aging population. In the present study, we used MPTP<br />

or 1methyl4phenylpyridnium ion MPP+induced dopaminergic neurotoxicity<br />

in C57BL/6J mice or SHSY5Y cells and explore the protective effect and<br />

mechanisms of an 18mer peptide of Prosaposin PS18 on dopaminergic<br />

neurons. PS18 2.0 mg/kg significantly improved behavioral deficits, and<br />

enhanced the survival of THpositive neurons and decreased the activity of<br />

astrocytes in the substantia nigra and striatum in MPTPinduced PD model<br />

mice. In vitro, the CCK8 assay and Hoechst 33258 staining clarified that PS<br />

18 300 ng/ml cotreated with 5mM MPP+ could protect the MMP+induced<br />

nuclear morphological changes and attenuated the cell death induced by MPP+.<br />

In addition, PS18 showed protection from MPP+/MPTPinduced apoptosis in the<br />

SHSY5Y cells and dopaminergic neurons in the PD model mouse via suppression<br />

of JNK/cJun pathway and up regulation of Bcl2 protein, down regulation of<br />

Bax, and inhibition of caspase3.<br />

P<br />

GABAA JM <br />

<br />

1 2 2 Raj Ladher 3 1<br />

1<br />

2 3 CDB<br />

<br />

JM1232 GABAA <br />

JM1232 <br />

oxygenglucose deprivationOGD<br />

GABAA <br />

GABAA <br />

JM1232 <br />

microarray system OGD <br />

OGD <br />

JM1232 <br />

JM1232 <br />

<br />

Real time RTPCR <br />

JM1232 <br />

7 6 <br />

GABAA <br />

<br />

<br />

<br />

P<br />

<br />

1 1 2 1 2 1<br />

1<br />

2 <br />

<br />

<br />

<br />

Ed<br />

<br />

Ed <br />

, <br />

3.0 mg/kg 24 <br />

1.22.4 mm , <br />

<br />

Nitrotyrosine NT <br />

24 <br />

<br />

, Ed NT <br />

,


172<br />

117 <br />

P<br />

ABC <br />

<br />

<br />

<br />

<br />

<br />

CSPG<br />

<br />

CSPG <br />

ABC <br />

<br />

<br />

ABC <br />

CSPG <br />

BDA<br />

<br />

<br />

CSPG <br />

ABC <br />

P<br />

<br />

<br />

<br />

<br />

<br />

<br />

8 SD 13 10 3 <br />

C7C8 <br />

234w 3 Little<br />

<br />

C1Th3Th4Th7Th8Th13L1 4<br />

5hydroxytryptamin5HT <br />

<br />

0.5 26 6 <br />

14 5HT 2w3w4w <br />

5HT <br />

5HT 5HT <br />

<br />

<br />

P<br />

PACAP <br />

1 1 1 1 1 1 <br />

1 1 2 1<br />

1<br />

2 <br />

<br />

PACAP<br />

<br />

PACAP <br />

PACAP <br />

WT PACAP<br />

PACAP/ PACAP <br />

<br />

Benchmark<br />

stereotaxic impactor 0.5 mm Basso Mouse<br />

ScaleBMS WT <br />

PACAP/<br />

3 <br />

7 PACAP/<br />

3 ssDNA PACAP<br />

/ ssDNA <br />

BMS <br />

PACAP <br />

<br />

P<br />

PMES <br />

<br />

Stefan Trifonov <br />

<br />

PMES2 <br />

PMES2 <br />

NeuN, GFAP, NG2, S100b,<br />

Iba1 single cell PCR <br />

<br />

PMES2 <br />

115 <br />

<br />

<br />

PMES2 <br />

<br />

GFAP <br />

in situ hybridization PCR<br />

PMES2 <br />

PMES2 <br />

P<br />

Müller <br />

1 2 1<br />

1<br />

2 / <br />

<br />

<br />

Müller <br />

Müller<br />

<br />

Müller <br />

MAPK<br />

PI3K/AKTJAK/STAT5 <br />

methylnitrosourea MNU <br />

Müller Erk1/2p38AKTStat3 <br />

MNU <br />

12 TUNEL 3 4 <br />

Müller Ki67MCM6BrdU <br />

MNU Müller Erk1/2p38AKT<br />

Stat3 3 <br />

4 <br />

Müller <br />

<br />

P


117 173<br />

P<br />

<br />

<br />

<br />

<br />

<br />

Vc <br />

Vc <br />

MAPK <br />

Wistar 7 <br />

10 μl 0.9% <br />

pH7.25% pH4.05 1 <br />

24 4% <br />

24 <br />

30 μmanti<br />

Iba1antipERK1/2antip38 <br />

Vc <br />

1 24 <br />

Vc <br />

1 24 Vc <br />

<br />

<br />

<br />

P<br />

<br />

<br />

<br />

<br />

Macrophages infiltrate in the peripheral nerve and dorsal root ganglia DRGs<br />

after the peripheral nerve injury. Although macrophages are mainly divided into<br />

M1 classically activated and M2 alternatively activated subtypes, it is unclear<br />

what subtypes of macrophages infiltrate in the injured nerve and DRGs after the<br />

peripheral nerve injury. Many macrophages infiltrated around the injured region<br />

of the sciatic nerve on day 1 after the nerve injury. All macrophages infiltrated in<br />

the injured nerve were inducible nitric oxide synthetase iNOS + /arginase1 Arg<br />

1 M1 type. In contrast to the injured nerve, significant increase in macrophages<br />

was observed in the ipsilateral side of DRGs on day 2 after the nerve injury and<br />

almost all macrophages in the DRGs were iNOS /Arg1 + M2 type. Double<br />

immunofluorescence staining revealed that the increased macrophages were<br />

positive for CD163 and CD206. However, CD86 + macrophages were not increased<br />

in the DRGs. These findings suggest that functional phenotypes of macrophages<br />

infiltrated in the DRGs are distinct from those infiltrated in the injured peripheral<br />

nerves.<br />

P<br />

<br />

<br />

1 2<br />

1<br />

2 <br />

2 15 CAP, 50 mg/kg<br />

CAP 20 <br />

γcarrageenan carr., 2%, 20 μl Carr Base<br />

24 Hargreaves NTS, von<br />

Frey <br />

2 CAP NTS <br />

Base 2.3 carr CAP carr<br />

NTS Base 3.2 <br />

6.2von Frey CAP carr <br />

15 CAP carr Base<br />

4.2 NTS 3.0CAP <br />

Base 7.5 CAP <br />

carr NTS Base 4.9<br />

von Frey CAP carr Base <br />

2 CAP NTS carr <br />

CAP TRPV1 <br />

15 CAP NTS carr TRPV1<br />

von Frey TRPV1 <br />

carr <br />

P<br />

Involvement of acidic microenvironment on the cancerinduced bone<br />

pain<br />

Masako Nakanishi 1,2 , Kenji Hata 2 , Toshiyuki Yoneda 2 , Yoshinori Otsuki 1<br />

1<br />

Dept. Anatomy, Osaka Medical College, 2 Dept. Biochem, Osaka Univ. Grad. Sch.<br />

Dent<br />

Microenvironments of bone metastasis are acidic due to the presence of cancer<br />

cells, inflammatory cells and boneresorbing osteoclasts. Since acid is a widely<br />

recognized algesic substance, we examined the effects of acid on the expression of<br />

calcitonin gene related peptide CGRP, which has been proposed to play a critical<br />

role in pain transmission. The expression of CGRP and transient receptor potential<br />

vanilloid subtype 1 TRPV1, an acidsensing nociceptor, was overlapped in<br />

dorsal root ganglion DRG. In organ culture of DRG, acid increased CGRP<br />

mRNA expression and this increase was significantly reduced by TRPV1<br />

antagonist IRTX. In addition, acid increased phosphorylation of CREB, a crucial<br />

transcription factor in neural functions. This was inhibited by IRTX. Knockdown<br />

of CREB expression or blockade of CREB signaling diminished acidinduced<br />

CGRP mRNA expression. Our results suggest that acidic microenvironments<br />

created in bone metastases activate TRPV1 in the sensory neurons, which<br />

in turn leads to upregulation of CGRP mRNA expression via activation of<br />

CREB transcriptional activity. These series of events may be involved in the<br />

pathophysiology of bone pain.<br />

P<br />

ILβ in trigeminal nucleus caudalis contributes to extraterritorial<br />

allodynia/hyperalgesia following a trigeminal nerve injury<br />

Mineo Watanabe, Shinji Hiyama, Takashi Uchida<br />

Department of Oral Biology, Division of Molecular Medical Science, Hiroshima<br />

University Graduate School of Biomedical Sciences<br />

The whisker pad WP area, which is innervated by the second branch of the<br />

trigeminal nerve, shows allodynia/hyperalgesia AH following transection of<br />

the mental nerve MN: the third branch of the trigeminal nerve. Glia is known<br />

to facilitate perception of noxious input, raising a possibility that these non<br />

neuronal cells are involved in the spread of AH at noninjured skin territory. After<br />

the MN transection, AH developed on the ipsilateral WP area. In response to<br />

MN transection, IL1β was upregulated in astrocytes in the trigeminal nucleus<br />

caudalis Vc. AH at WP area induced by MN transection was attenuated by IL1<br />

receptor antagonist IL1ra. Fos immunoreactive Fos+ neurons were observed in<br />

the Vc after nonnoxious mechanical stimulation of the WP area in the rats with<br />

MN transection. Administration of IL1ra also attenuated the number of Fos+<br />

neurons. Administration of a noncompetitive antagonist of NMDA receptors MK<br />

801 reversed AH. IL1 receptor type I was localized in Fos+ and phospho NR1<br />

immunoreactive neurons. IL1β in the Vc might play an important role in the<br />

development of extraterritorial AH after MN transection.<br />

P<br />

cFos <br />

1 1 1,2 1 1 1,2<br />

1<br />

2 <br />

<br />

<br />

<br />

<br />

<br />

<br />

cFos SD <br />

2 <br />

1 5 <br />

13 4 <br />

cFos cFos <br />

1 cFos <br />

<br />

5 13 <br />

1 <br />

cFos


174<br />

117 <br />

P<br />

Minocycline<br />

<br />

1 1,2 1 1,2 1 1<br />

1<br />

2 <br />

P<br />

ITAM KO <br />

1 1 2 1 1 1 <br />

2 1<br />

1<br />

2 <br />

<br />

<br />

<br />

<br />

<br />

SD 2 <br />

<br />

Minocycline 100 μg /day PBS 10 μl /day 8 <br />

1 8 Minocycline PBS <br />

von Frey<br />

test 2 1 <br />

1 <br />

OX42<br />

Minocycline PBS <br />

<br />

<br />

<br />

<br />

<br />

<br />

<br />

<br />

ITAM DAP12 CARD9 KO <br />

L4 1 <br />

<br />

Iba1 GFAP <br />

KO <br />

Iba1 <br />

KO <br />

Iba1 <br />

GFAP <br />

KO GFAP <br />

DAP12 CARD9 ITAM <br />

<br />

<br />

<br />

<br />

P<br />

Zitter <br />

<br />

<br />

<br />

<br />

Zitter <br />

Zi<br />

Zi <br />

<br />

Iba1 Ca2+ <br />

ED1<br />

3 <br />

1Iba1 <br />

ED1 <br />

2<br />

ED1 3<br />

1 2 Iba1 <br />

ED1 1 3<br />

2 <br />

<br />

qPCR <br />

<br />

P<br />

<br />

1 1 2 1,3 1<br />

1<br />

2 <br />

3 <br />

<br />

<br />

<br />

<br />

DRG<br />

ERα <br />

GPR30 <br />

<br />

OVX <br />

OVX+E 4 <br />

<br />

OVX+E <br />

OVX <br />

<br />

<br />

DRG <br />

CGRP <br />

OVX+E OVX CGRP <br />

<br />

P<br />

Scaffold attachment factor B SAFB and SAFB synergistically<br />

inhibit intranuclear mobility and function of ERα<br />

<br />

<br />

Estrogen receptor alpha ERα plays a key role in physiological processes as a<br />

transcriptional factor that is regulated by cofactors. ERαmediated transcriptional<br />

regulation is correlated with the mobility of ERα in the nucleus associating with<br />

the nuclear matrix, the framework for nuclear events including transcription.<br />

However, the relationship between ERα mobility and the cofactors is unclear.<br />

Scaffold attachment factor B1 SAFB1 and its paralog SAFB2 are nuclear matrix<br />

binding proteins that have been characterized as ERα corepressors. Here, using<br />

chimeric fluorescent proteins, we show that SAFB1 and SAFB2 colocalize and<br />

interact with ERα in the nucleus of living cells after 17βestradiol E2 treatment.<br />

Fluorescence recovery after photobleaching analysis revealed that SAFB1 and<br />

SAFB2 each decrease ERα mobility, and coexpression of SAFB1 and SAFB2<br />

causes a synergistic reduction in ERα dynamics under E2 treatment. In accordance<br />

with these changes, ERαmediated transcription and proliferation is cooperatively<br />

inhibited by SAFB1 and SAFB2. These results indicate that SAFB1 and SAFB2<br />

are crucial repressors for ERα dynamics and function in association with the<br />

nuclear matrix.<br />

P<br />

Estrogen αfetoprotein <br />

<br />

<br />

Estrogen Aromatase <br />

Estrogen 20 <br />

Estrogen <br />

Estrogen 20 <br />

Estrogen <br />

αfetoprotein AFP Estrogen<br />

AFP Estrogen <br />

5-40 <br />

Wistar AFP Western<br />

blotting Realtime PCR <br />

Estradiol17β EIA kit 1 AFP<br />

5 20 2 <br />

AFP 20 3 AFP <br />

20 4 <br />

Aromatase AFP 5 AFP<br />

Estrogen AFP <br />

Aromatase <br />

AFP Estrogen


117 175<br />

P<br />

<br />

<br />

<br />

C <br />

<br />

β ISL1<br />

NKX2.2 NKX2.2 NKX6.1 C <br />

<br />

β PDX1<br />

12 <br />

18 1 <br />

RTPCR β <br />

MafA Ngn3 <br />

PCR 14 1 <br />

MafA <br />

1 14 15 <br />

MafA 14 65 <br />

PDX1 10 β <br />

PDX1<br />

β PDX1 <br />

<br />

<br />

P<br />

<br />

<br />

<br />

<br />

<br />

<br />

<br />

RFamide <br />

<br />

<br />

<br />

C GlyLeuTrpNH2 <br />

GLWamide ArgPheNH2 RFamide <br />

Hym176 APFIFPGPKVamide <br />

CysGLWamide, CysRFamide, Cys<br />

Hym176 <br />

ELISA<br />

<br />

1 3 1 <br />

<br />

<br />

P<br />

<br />

<br />

1,2 2 2 1<br />

1<br />

2 <br />

kisspeptin GnRH <br />

<br />

NEDA <br />

GPR54 <br />

GnRH <br />

NEDA fos <br />

NEDA <br />

NEDA <br />

tyrosine hydroxylase TH <br />

TH <br />

<br />

NEDA TH <br />

TH <br />

<br />

TH <br />

NEDA TH <br />

<br />

<br />

P<br />

manserin <br />

<br />

<br />

<br />

manserin <br />

Neuroreport 15:<br />

17551759, 2004; Histochem Cell Biol. 134: 5357, 2010; Int J Pept Res Ther. 17:<br />

193199, 2011 manserin SgII <br />

<br />

manserin <br />

manserin <br />

manserin <br />

manserin <br />

manserin TSH <br />

manserin TSH <br />

<br />

manserin SgII <br />

manserin 1/3 <br />

manserin <br />

<br />

manserin <br />

<br />

P<br />

βreductase <br />

<br />

1 <br />

<br />

<br />

<br />

<br />

3αhydroxysteroid dehydrogenase 3αHSD 3βHSD <br />

<br />

<br />

5βreductase <br />

<br />

5βreductase COS1 <br />

<br />

<br />

<br />

<br />

P<br />

<br />

<br />

<br />

V <br />

<br />

<br />

<br />

A, B1, B2, C 4 <br />

A C <br />

B1 B2 <br />

<br />

<br />

<br />

<br />

<br />

<br />

<br />

B1 B2 <br />

C <br />

A


176<br />

117 <br />

P<br />

PACAP <br />

<br />

1,2 1,3 1,2 1 1 <br />

1 1 1 Jozsef Farkas 1 1 <br />

1 1,2,4 2 1<br />

1<br />

2 3 <br />

4 <br />

<br />

PACAP NMDA <br />

RGC<br />

<br />

<br />

NMDA PACAP RGC <br />

MG/Mφ<br />

NMDA <br />

PACAP PACAP10 8 10 12 M NMDA <br />

<br />

Iba1 PACAP 10 10 M <br />

3 MG/Mφ NMDA <br />

MG/Mφ RGC RTPCR<br />

tgf-β<br />

1 PACAP 10 10 M<br />

TGFβ1 <br />

MG/Mφ TGFβ1 <br />

PACAP <br />

<br />

P<br />

<br />

1,2 Thomas Finger 2 3 3 3 <br />

1 1<br />

1<br />

2 Rocky Mountain Taste and Smell Ctr, Uni.<br />

Colorado Med Sch 3 <br />

ATP ATP <br />

P2X <br />

P2XP2Y ATP ATP <br />

NTPDase2 ATP NTPase2 <br />

ATP <br />

<br />

4 <br />

A1A2AA2BA3 <br />

<br />

RTPCRin situ hybridization<br />

A2B <br />

<br />

P<br />

Mash AADC GAD <br />

1 1 2 1<br />

1<br />

2 <br />

3 <br />

<br />

bHLH Mash1 3 Mash1 <br />

3 Mash1<br />

3 <br />

Mash1 <br />

<br />

Mash1 <br />

<br />

AADC GABA <br />

GAD67 Mash1 <br />

Mash1 3 AADC, GAD67 <br />

<br />

P<br />

P <br />

<br />

1 2 3 2 1<br />

1<br />

2 <br />

3<br />

<br />

substance P SP <br />

15 <br />

2 4%PFA <br />

SP <br />

1/4 <br />

3/4 <br />

SP <br />

<br />

<br />

SP <br />

<br />

SP <br />

3/4 <br />

1/4 <br />

SP <br />

3/4 SP <br />

<br />

<br />

P<br />

AB <br />

<br />

<br />

<br />

<br />

3 <br />

<br />

3 <br />

<br />

3 <br />

ATP <br />

P2X2 P2X3 <br />

P2X2 P2X3 <br />

ATP <br />

<br />

<br />

<br />

Double in situ hybridization <br />

3A B <br />

<br />

P<br />

<br />

1 2 1<br />

1<br />

2 <br />

<br />

<br />

Ca 2+ [Ca 2+ ] i Ca 2+<br />

imaging HPLC <br />

<br />

HPLC <br />

150 μm <br />

Ca 2+ indicatorfura2<br />

HEPESRinger buffer HPLC 1:10000[Ca 2+ ] i<br />

<br />

HPLC UV <br />

<br />

[Ca 2+ ] i


117 177<br />

P<br />

<br />

1 2 3 4,5 4 1<br />

1<br />

2 3 <br />

4 5 <br />

<br />

<br />

<br />

<br />

<br />

HE <br />

<br />

<br />

<br />

PAS<br />

PAS <br />

GolfNCAMvimentin TAAR2 <br />

<br />

G <br />

TAAR2 <br />

<br />

<br />

P<br />

<br />

1,2 2 1 2<br />

1<br />

2 <br />

<br />

<br />

<br />

Wistar <br />

<br />

2KOHcollagenase <br />

Ushiki & Ide, 1988 <br />

<br />

10% <br />

<br />

KOHcollagenase <br />

<br />

1 <br />

<br />

<br />

<br />

<br />

<br />

P<br />

<br />

<br />

<br />

<br />

ACh <br />

<br />

ACh mAChR <br />

NRK52E <br />

CarbacolCch 60 10 12 <br />

3 <br />

mRNA RTPCR mAChR <br />

NRK52E <br />

mAChR M1R M4R Cch <br />

10 M2R 3 M4R <br />

M2R M2R M4R <br />

<br />

ATP K + Kir6.1 30 M4R<br />

Kir6.1 M4R <br />

M4R Kir6.1 <br />

NRK52E in vivo<br />

<br />

P<br />

<br />

<br />

<br />

<br />

<br />

IR <br />

LC3 <br />

LC3I LC3II LC3 <br />

<br />

IR IR 4 24 <br />

LC3 <br />

LC3 24 <br />

LC3 <br />

LC3 <br />

IR LC3 <br />

D,L IR <br />

<br />

<br />

<br />

IR <br />

<br />

P<br />

LPS <br />

<br />

1 2 1 1 3 <br />

1<br />

1<br />

2 <br />

3 <br />

<br />

<br />

<br />

<br />

LPS <br />

<br />

12 9 3 1 <br />

2 LPS 3 LPS <br />

2 LPSErsherichia coli O157 5 mg/kg <br />

0 3 10 <br />

3 LPS 0 3 10 3 <br />

17 1 0 3 <br />

HE PAS <br />

LPS <br />

<br />

LPS <br />

<br />

<br />

P<br />

<br />

<br />

G1<br />

MCTs<br />

MCT <br />

<br />

CD147EMMPRIN<br />

MCT1MCT2MCT4 <br />

<br />

MCT1 <br />

MCT2 <br />

MCT4 Leydig <br />

MCT2 <br />

<br />

MCT2 <br />

<br />

MCT1 MCT4 MCT2 <br />

MCT2 <br />

MCT1MCT2<br />

MCT4


178<br />

117 <br />

P<br />

Separatration of early stage acrosome reacted sperm and analyses<br />

of the proteins<br />

Kenji Yamatoya, Chizuru Ito, Cheng Chen, Mamiko Maekawa,<br />

Yoshiro Toyama, Kiyotaka Toshimori<br />

Dept. Anatomy and Developmental Biology, Grad. Sch. Med., Univ. Chiba<br />

During the acrosome reaction, the contents of sperm acrosome are released from<br />

the original location to the final destination and working place. The molecular<br />

distribution and nature are posttranslationally modified. We reported that flow<br />

cytometric analyses using antiacrosomal membrane protein antibodies anti<br />

IZUMO1 and antiSPACA1 can discriminate the early stage of acrosome reaction,<br />

classifying into 7 populations.<br />

In this study, we analyzed the 7 populations and found that the populations<br />

number 4 and 5 contain acrosomeswelling sperm. Acrosomeswelling occurs at<br />

a very early stage of acrosome reaction which starts before the exposure of inner<br />

acrosomal membrane. One of the acrosomal membrane proteins, SPACA1, was<br />

cleaved during this swelling stage. Western blot showed that SPACA1 was 35 kDa<br />

before acrosome reaction and became 21 kDa in acrosomeswelling sperm.<br />

Thus, this flow cytometric method is useful to analyze the detailed acrosome<br />

reaction process and the molecular changes during the acrosome reaction which<br />

are the last preparatory process for the spermegg interaction.<br />

P<br />

Cell adhesion molecule Nectin <br />

<br />

Kannika Adthapanyawanich <br />

<br />

<br />

Cell adhesion molecule1 Cadm1 Nectin3 <br />

Cadm1 <br />

Poliovirus receptor <br />

Nectin3 Nectin2<br />

<br />

Cadm1 Nectin3 <br />

Cadm1 Nectin3 <br />

<br />

Cadm1//Nectin3/ Cadm1/ <br />

Nectin3/ <br />

<br />

<br />

Cadm1 Nectin3 <br />

<br />

P<br />

SF <br />

<br />

<br />

<br />

SF1 <br />

<br />

<br />

2 anti<br />

Müllerian hormone type 2 receptor Cre CreloxP <br />

SF1 <br />

0 21 SF1 <br />

7 <br />

14 21 <br />

<br />

14 21 SF1 <br />

AMH <br />

p27 <br />

WT1SOX9GATA4androgen receptor <br />

SF1 <br />

SF1 <br />

<br />

P<br />

Autoimmune responses induced by immunization with xenogenic<br />

testicular germ cells alone<br />

<br />

<br />

Experimental autoimmune orchitis EAO is one of the models of immunological<br />

male infertility. Classically, the immunization of mice with a testicular<br />

homogenate emulsified in complete Freund's adjuvant followed by intravenous<br />

injections of Bordetella pertussis is necessary for the induction of murine EAO.<br />

Later, we previously established a mouse EAO model that can be induced by two<br />

subcutaneous injections of viable syngeneic testicular germ cells TGC alone,<br />

and the autoantigens involved in the mouse EAO have been analyzed using two<br />

dimensional gel systems and western blotting. In the present study, to examine<br />

whether the xenogenic TGC can induce a mouse EAO, we immunized mice with<br />

viable TGC taken from the rat or the guinea pig. The results showed that mouse<br />

EAO was also inducible by the rat TGC but not the guinea pig TGC. Therefore,<br />

the results suggest that the autoantigens that induce the mouse EAO are present in<br />

not only the mouse TGC but also xenogenic TGC = the rat TGC. Analyses of the<br />

common autoantigens responsible for EAO induction are now in progress.<br />

P<br />

Diethylhexyl phthalate <br />

<br />

<br />

Di2ethylhexyl phthalate=DEHP <br />

<br />

<br />

DEHP <br />

A/J <br />

8 0%0.01%0.1%DEHP 8 <br />

<br />

0.01%DEHP 0.1%DEHP <br />

<br />

0.01%<br />

0.1%DEHP <br />

DEHP <br />

MHC Class RTPCR <br />

DEHP <br />

IL10IFNγ <br />

DEHP <br />

<br />

P<br />

The effect of cadmium on immunoenvironment in the testis<br />

Yuki Ogawa 1,2 , Masahiro Itoh 1 , Shuichi Hirai 1 , Munekazu Naito 1 ,<br />

Ning Qu 1 , Hayato Terayama 1 , Hidenobu Miyaso 2 , Yoshiharu Matsuno 2 ,<br />

Masatoshi Komiyama 2 , Chisato Mori 2<br />

1<br />

Dept. Anat., Tokyo Med. Univ., 2 Dept. Bioenv. Med., Grad. Sch. Med., Chiba Univ.<br />

Cadmium, one of various environmental toxicants, is known to suppress systemic<br />

immunity and to injure the testicular capillary endothelia with resultant necrosis of<br />

testicular tissues in mice and rats treated with high doses. Recently, it also became<br />

evident that cadmium can affect the integrity of the bloodtestis barrier BTB,<br />

the endocrine function of Leydig cells, apoptosis of germ cells and systemic<br />

immunity, even on treatment with a low dose that does not induce spermatogenic<br />

disturbance. Experimental autoimmune orchitis EAO, i.e., an organ<br />

specific autoimmunity of the testis, can be induced by repeated immunization<br />

with testicular antigens, and its pathology is characterized by lymphocytic<br />

inflammation and spermatogenic disturbance. In the present study, we investigated<br />

the morphological and functional changes of testes in mice treated with a low dose<br />

of cadmium chloride CdCl 2 and also examined its toxicity as to susceptibility to<br />

EAO.


117 179<br />

P<br />

TIRF <br />

<br />

<br />

<br />

ECM<br />

<br />

ECM <br />

<br />

1 I <br />

Col1FN2<br />

VI Col6fib3 IV<br />

Col4TIRF <br />

ECM <br />

ECM <br />

ECM <br />

Col1FN <br />

fib Col4 <br />

Col1FN Col6 fib Col4 Col6<br />

<br />

Col6 <br />

<br />

P<br />

PACAP TAC <br />

1 1 2 3 4<br />

1<br />

2 <br />

3 4 <br />

<br />

2 <br />

<br />

<br />

<br />

PACAP<br />

PACAP PAC1R <br />

PACAP <br />

<br />

PACAP <br />

<br />

PACAP 2 <br />

PACAP <br />

PACAP <br />

PACAP <br />

DNA <br />

3 40 <br />

P <br />

A TAC1 6 <br />

<br />

P<br />

in vitro <br />

1 2 2 3 <br />

3 2 2 3 1<br />

1<br />

2 3 <br />

<br />

<br />

10<br />

<br />

<br />

<br />

3 <br />

<br />

3 <br />

in vitro <br />

<br />

1 mm <br />

endometrial<br />

glands <br />

<br />

<br />

in vitro <br />

<br />

<br />

<br />

P<br />

Localization of fatty acid binding protein in mouse placenta and its<br />

possible role of fatty acid transport through trophoblasts<br />

Ariful Islam, Nobuko Tokuda, Yasuhiro Adachi, Tomoo Sawada, Yuji Owada<br />

Department of Organ Anatomy, Yamaguchi University Graduate School of<br />

Medicine<br />

Background: Malnutrition of mother during pregnancy is now thought to<br />

contribute to the etiology of various metabolic and/or neural disorders that<br />

manifest throughout life. Placenta is the key organ for regulating the transfer<br />

of nutrients including fatty acids from mother to embryo. In this study, we<br />

investigated the functional role of fatty acid binding protein 3 FABP3 after<br />

determining the localization of FABPs, cellular fatty acid chaperons, in the mouse<br />

placenta.<br />

Results: In RTPCR, gene expression of FABP3, 4 & 5 was detected. The protein<br />

expression of FABP 3, 4 & 5 was also confirmed by western blot analysis. In<br />

immunohistochemistry, FABP3 was highly expressed in the labyrinthine transport<br />

zone of mouse placenta; FABP4 was highly expressed in deciduas basalis zone;<br />

FABP5 was weakly and widely distributed in the labyrinthine, decidua and<br />

spongiotrophoblast zone.<br />

Discussion: FABPs were expressed in the mouse placenta with spatial<br />

differences. FABP3 and 5 were suggested to be involved in regulation of cellular<br />

transfer of fatty acids in trophoblasts of placenta. The functional significance of<br />

FABP expression in trophoblasts is now under investigation.<br />

P<br />

Kardasewitsch Verocay <br />

<br />

1,2 2,3 2,3 4 4 <br />

1<br />

1<br />

2 3 <br />

4 <br />

<br />

<br />

<br />

<br />

<br />

Kardasewitsch Verocay Kardasewitsch <br />

Verocay 2 HE <br />

<br />

<br />

Verocay Kardasewitsch <br />

<br />

<br />

<br />

<br />

P<br />

MAP <br />

1 2<br />

1<br />

2 <br />

MAP <br />

<br />

MAP in situ<br />

<br />

MAP <br />

<br />

<br />

<br />

<br />

13 17 <br />

ERK1/2 <br />

<br />

JNK1/2 <br />

ERK1/2 p38 ERK5 <br />

<br />

MAP <br />

ERK1/2 JNK1/2


180<br />

117 <br />

P<br />

<br />

<br />

<br />

<br />

<br />

<br />

QD <br />

<br />

193 2% <br />

HE <br />

QD AF <br />

Alb <br />

QD 1 <br />

QD 2 <br />

5 QD <br />

AF <br />

<br />

Alb <br />

<br />

QD <br />

<br />

P<br />

In vivo labeling of halogenated volatile anesthetics via intrinsic<br />

molecular vibrations using nonlinear Raman spectroscopy<br />

Masahiko Kawagishi 1 , Takayuki Suzuki 2 , Yu Nagashima 1,2 , Sumio Terada 1 ,<br />

Kazuhiko Misawa 2<br />

1<br />

Sect. Neuroanat. Cellular Neurobiol., Dept. Systems Neurosci., Tokyo Med.<br />

Dent. Univ., 2 Dept. Applied Physics, Tokyo Univ. Agriculture and Technology<br />

Halogenated volatile anesthetics are frequently used for inhaled anesthesia<br />

in clinical practice. No appropriate biological method has been available for<br />

visualizing their localization in action. Therefore, despite their frequent use, the<br />

mechanism of action of these drugs has not been fully investigated. We measured<br />

coherent antiStokes Raman scattering CARS spectra of sevoflurane and<br />

isoflurane, two of the most representative volatile anesthetics, and determined the<br />

lowfrequency vibrational modes without nonresonant background disturbance.<br />

Molecular dynamics calculations predict that these modes are associated with<br />

multiple halogen atoms. Because halogen atoms rarely appear in biological<br />

compounds, the entire spectral landscape of these modes is expected to be a<br />

good marker for investigating the spatial localization of these drugs within the<br />

intracellular environment. Using live squid giant axons, we could detect the<br />

unique CARS spectra of sevoflurane for the first time in a biological setting.<br />

P<br />

Fluorescence Immunohistochemistry by Confocal LSM for Studies of<br />

SemiUltrathin Specimens of Epoxy ResinEmbedded Samples<br />

1 2<br />

1<br />

2 <br />

<br />

We have developed a technique, using a combination of immunofluorescence<br />

staining of semiultrathin sections of epoxy resinembedded samples and the DIC<br />

images and images in transmission mode obtained by LSM, that provides detailed<br />

information about the immunolocalization of antigens and histological and cellular<br />

structures. To demonstrate the effectiveness of our method, we examined the<br />

immunofluorescence of immunostained K13 and K14 and that of immunostained<br />

CII and CIII and the corresponding DIC and transmission images during the<br />

morphogenesis of filiform papillae on the lingual epithelium of rat fetuses and<br />

juveniles. We demonstrated that our newly developed technique for localization of<br />

pairs of antigens should be useful for investigations of very small specimens, such<br />

as fetal tissues and organs.<br />

P<br />

/ <br />

<br />

1 2 2 3 1 1 <br />

2 1 2<br />

1<br />

2 <br />

3 <br />

Quantitative analysis of morphological synaptic connectivity depends on exact<br />

threedimensional reconstructions of synaptic ultrastructure using electron<br />

microscopy of serial ultrathin sections. However, reconstructions from serial<br />

section transmission electron microscope TEM are extremely timeconsuming<br />

and difficult. To overcome these problems, we have applied a new three<br />

dimensional reconstruction method that involves the combination of focused ion<br />

beam milling and scanning electron microscopy FIB/SEM. Dendrites of the rat<br />

neostriatum neurons were visualized by a recombinant virus vector, which labeled<br />

the infected neurons in a Golgi stainlike fashion. Axon terminals and dendritic<br />

spines in the rat neostriatum neurons were stained by the immunofluorescence<br />

method. The appostitions of dendrites to the inputs were detected three<br />

dimensionally with a confocal laserscanning microscope. Then, these sections<br />

were stained by peroxidase anti peroxidase method and observed three<br />

dimensionally with a focused ion beam milling and scanning electron microscopy<br />

FIB/SEM.<br />

P<br />

<br />

<br />

<br />

<br />

<br />

3 <br />

<br />

<br />

Atomic Force Microscopy; AFM<br />

<br />

<br />

DNaseI <br />

AraC 5 4<br />

AFM Alexa488 phalloidin <br />

<br />

<br />

AFM P C <br />

<br />

<br />

<br />

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P<br />

GP<br />

<br />

1 1 1 1 2 <br />

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GP <br />

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117 181<br />

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1 1 1 1 1 <br />

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23 4 SGL <br />

TBL SGL <br />

SGL <br />

SGL <br />

<br />

SGL <br />

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SGL <br />

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P<br />

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23 4<br />

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CT MR <br />

4 <br />

1 1 <br />

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4 <br />

DICOM Osirix CT MR <br />

2 3 <br />

<br />

23 <br />

Ai Autopsy imaging CT <br />

<br />

<br />

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P<br />

eLearning <br />

<br />

<br />

eLearning <br />

eLearning <br />

eLearning <br />

<br />

Moodle Moodle <br />

<br />

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P<br />

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1,3 1 1 1 2 <br />

2 2 2 2 2<br />

1<br />

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PT <br />

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16 <br />

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<br />

22 <br />

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PTOT <br />

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PTOT <br />

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P<br />

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4 1 1 1 1 1<br />

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182<br />

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1 2 3 3 4 5<br />

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<br />

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66 <br />

78 <br />

2 <br />

<br />

<br />

2005 <br />

138 <br />

<br />

<br />

77.5%107 <br />

62.3%86 25.4%35 <br />

14.5%20 <br />

<br />

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MRI<br />

1 2 2 3 1 1 <br />

4 4 5 6<br />

1<br />

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4 5 <br />

6 <br />

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<br />

MRI<br />

95 59 36 23.27.8 <br />

Hüter <br />

20 mm 40 mm 3 mm <br />

<br />

Hüter <br />

<br />

<br />

Hüter <br />

3.441.00 mm 4.041.18 mm<br />

3.450.88 mm BMI <br />

p


117 183<br />

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1 2 1 1 1<br />

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2 <br />

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DIP <br />

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MRI <br />

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Apple Osirix Realia <br />

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VoxBlast <br />

KY500 <br />

<br />

3 μm <br />

3 μm <br />

<br />

KY<br />

500 <br />

3 <br />

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<br />

P<br />

Fossa <br />

<br />

<br />

Terminologia Anatomica <br />

Fossa<br />

Fossa 1Fossa <br />

2Fossa 3Fossa <br />

4Fossa 5Fossa <br />

6Fossa 7Fossa <br />

8Fossa <br />

Fossa olecraniOlecranon<br />

olecrani <br />

Fossa canina<br />

Musculus levator<br />

anguli oris Musculus caninus<br />

<br />

Fossa radialis Radius<br />

radialis <br />

<br />

<br />

<br />

P<br />

<br />

<br />

<br />

FA<br />

2008 <br />

3<br />

2008 3 <br />

FA 0.1 ppm FA <br />

2009 <br />

FA 710 7 <br />

<br />

FA <br />

40 4 2 50<br />

3 5 2 <br />

FA 2 FP30<br />

00.4 ppm GASTEC 0.15 ppm<br />

FA <br />

FA <br />

<br />

P<br />

<br />

1,2 1 1 1 1<br />

1<br />

2 <br />

<br />

20082009 <br />

FA FA 2 <br />

5 0.1 ppm <br />

FA <br />

FA <br />

20102011 <br />

10% 3.5%FA100%<br />

3<br />

FA 4<br />

4/ FA <br />

10 cm <br />

30 FA 0.01<br />

ppm 2010 FA <br />

FA <br />

FA 2010 <br />

DNPHHPLC 11 <br />

0.0064 ppm 0.0039 ppm 1/10


184<br />

117 <br />

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Thiel <br />

1 1 2 2 2 <br />

3 2 1<br />

1<br />

2 2 3 <br />

<br />

Thiel Graz Dr. Thiel <br />

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<br />

<br />

Thiel <br />

<br />

<br />

<br />

16 <br />

8 Thiel 4 <br />

<br />

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Thiel <br />

<br />

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Thiel <br />

<br />

P<br />

<br />

<br />

1 1 2 2 1 <br />

1 1 1 1<br />

1<br />

2 <br />

2008 <br />

FA 0.1 ppm <br />

FA <br />

FA <br />

<br />

<br />

20 <br />

FA <br />

FA <br />

FA B <br />

0.1 ppm <br />

B FA <br />

<br />

FA 0.1 ppm <br />

FA 0.1 ppm <br />

FA <br />

<br />

<br />

P<br />

<br />

1 2,3 2,3,4<br />

1<br />

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3 4 <br />

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6 <br />

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Hedgehog<br />

<br />

Hedgehog SmoothenedSmo<br />

Smo 9 <br />

cKO<br />

<br />

SmocKO <br />

<br />

<br />

SmocKO <br />

<br />

P<br />

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1 1 2 2 2 <br />

3 3 3 3<br />

1<br />

4 2 3 <br />

3 <br />

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PF <br />

PF Cholera toxin b subunitCTb<br />

CTb cFos <br />

mapping CTb <br />

<br />

CA1<br />

C1 <br />

<br />

CTb cFos <br />

<br />

<br />

<br />

<br />

<br />

P<br />

Tubulin polyglutamylation regulates cytoskeletal distribution in brain<br />

Kenji Ohata 1 , Yoshiyuki Konishi 2 , Reiko Tsuchiya 3 , Koji Ikegami 1 ,<br />

Mitsutoshi Setou 1<br />

1<br />

Dept. of Cell Biology and Anatomy, Hamamatsu Univ. Sch. of Med., 2 Dept. of<br />

Human and artificial intelligent Systems, Univ. of Fukui, 3 MitsubishiKagaku<br />

Institute of Life Sciences<br />

Microtubules form the structural basis of neuronal morphology and partake in<br />

directing intracellular transport. Tubulins, components of microtubules, are known<br />

to be highly polyglutamylated in neurons, and we, along with another group,<br />

have recently shown that a part of tubulin tyrosine ligaselike Ttll proteins<br />

catalyzes polyglutamylation of tubulins though the subsequent function of this<br />

polyglutamylation remains unclear. Present study demonstrates that Ttll1 and Ttll7<br />

play major roles in adding glutamate chain to alpha and beta tubulin respectively<br />

in the brain. Ttll1 or Ttll7 singleknockout mice exhibited only a slight decrease<br />

in total polyglutamylation. To reveal the neuronal polyglutamylation function, we<br />

generated Ttll1Ttll7 doubleknockout mice which showed significant decrease<br />

in neuronal polyglutamylation. Immunohistochemical and electron microscopic<br />

analyses showed fewer neurofilaments in dendrites of cortical neurons in the<br />

doubleknockout mice compared to the wild type, while the neurofilament<br />

distribution in Ttll1 or Ttll7 singleknockout mice was similar to that of the<br />

wild type. These results suggest that polyglutamilation regulates neurofilament<br />

arrangement.<br />

P<br />

KCC <br />

1 2<br />

1<br />

2 <br />

3 KCC2 Cl – <br />

GABA <br />

<br />

KCC2 in situ hybridization <br />

in situ hybridization KCC2<br />

mRNA 5 P5 P7 <br />

P14 <br />

<br />

P7 <br />

VGluT2 <br />

P14 KCC2 <br />

P7 <br />

KCC2 <br />

<br />

2 KCC2 mRNA <br />

GABA <br />

KCC2


117 185<br />

P<br />

<br />

<br />

<br />

<br />

<br />

NMJ<br />

<br />

<br />

<br />

NMJ <br />

<br />

d <br />

NMJ <br />

<br />

<br />

NMJ <br />

P<br />

<br />

<br />

<br />

Hh <br />

<br />

<br />

<br />

Hh <br />

<br />

Hh <br />

SC <br />

Hh <br />

SC <br />

<br />

Hh <br />

SC<br />

<br />

<br />

Hh <br />

<br />

P<br />

neuroligin <br />

<br />

<br />

<br />

<br />

3 <br />

neuroligin <br />

neurexin <br />

Neuroligin <br />

<br />

Neuroligin family <br />

neuroligin <br />

<br />

neuroligin 1EGFP dsRed2 <br />

neuroligin1 <br />

Neuroligin1 <br />

neuroligin1 <br />

neuroligin <br />

<br />

P<br />

<br />

1 2 2 2 3 <br />

2<br />

1<br />

4 2 3 <br />

<br />

<br />

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<br />

<br />

<br />

<br />

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<br />

ABCD <br />

<br />

<br />

<br />

<br />

ABCD <br />

<br />

<br />

P<br />

<br />

1 1 1 1 2 2 <br />

2 2<br />

1<br />

3 2 <br />

<br />

4 3 <br />

<br />

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22 74 <br />

<br />

4 4<br />

2 <br />

<br />

<br />

<br />

1992IX1 0.8%<br />

<br />

P<br />

<br />

1 1 1,2 1 2 <br />

2 2<br />

1<br />

2 <br />

<br />

Gi F O<br />

Tr 3 Nf <br />

Gi 2 L5/S1 S1/S2 S1/S2<br />

S2/S2 S1/S1 S2/S2 Gi S1/S2 <br />

S2/S2 S2/S3 <br />

1Gi2 4 L5/S1 S1/S2 1 Nf L4L4<br />

3 Tr>F>O L4 Tr <br />

S1/S2 S2/S2 2 Nf <br />

L43 F>Tr>O S1/S1 <br />

S2/S2 1 Nf L4F>O>Tr <br />

<br />

2Gi1 5 S1/S2 1 L3 Tr Nf L3+L4<br />

S2/S2 2 Nf L4F>Tr>O <br />

1 F>O>Tr <br />

1 S2/S3 2 L4 L5 F, O, Tr 3 Nf<br />

L4+L5<br />

Gi


186<br />

117 <br />

P<br />

<br />

1 1,2 1 2 2 <br />

2<br />

1<br />

2 <br />

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Gs F O<br />

Tr 3 Nf<br />

<br />

Gs L4/L5 L5/S1 S1/S2 <br />

1L4/L5 5 Nf L3+L41 L44 <br />

Nf L3+L4 Nf L4 L4 3 <br />

Tr>F>O3 L4 Tr <br />

L4 3 F>Tr>O 1 <br />

<br />

2L5/S1 5 Nf L42 L4+L52 L51 <br />

L4 F>Tr>O 1<br />

F>O>Tr 1 <br />

L4+L5 L4 3 F>O>Tr L5 FTr 1<br />

L5 FOTr 1 Nf L5 L4 Tr <br />

L5 3 <br />

<br />

3S1/S2 1 Nf L4+L5 <br />

Gs <br />

<br />

P<br />

<br />

<br />

<br />

<br />

<br />

<br />

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3 <br />

70 90 4<br />

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50 <br />

PGP9.5 <br />

P<br />

CCD <br />

<br />

<br />

P <br />

<br />

<br />

P <br />

<br />

<br />

P<br />

<br />

1 2 2 2<br />

1<br />

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22 92 1 <br />

<br />

<br />

<br />

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<br />

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<br />

Humphry <br />

Miyauchi <br />

Humphry <br />

<br />

<br />

<br />

P<br />

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1 1,2 1 2 2 <br />

2<br />

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<br />

H23 A. mediana, M<br />

A. brachialis superficialis, BS BS <br />

Ax <br />

Ax BS <br />

A. radialis,<br />

R A. ulnaris, U BS <br />

A. antebrachii superficialis, AS AS <br />

<br />

M M <br />

U R <br />

R <br />

R M U <br />

M BS<br />

<br />

BS <br />

M <br />

<br />

P<br />

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1 1 1 1 2 3 <br />

3<br />

1<br />

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<br />

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75 <br />

<br />

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P<br />

<br />

1 2 3 4 4 <br />

4,5 2<br />

1<br />

2 <br />

3<br />

/ 4 <br />

5 <br />

5 DP <br />

DP 7 #1-7 DP <br />

#1 #2 #3 #1 <br />

#2 <br />

#3 DP <br />

DP <br />

#4 #5 #4 #5 <br />

#4 #5 <br />

DP #6 #7 #6<br />

<br />

#7 <br />

7<br />

<br />

#1367<br />

#245 <br />

cranial ventral dorsal <br />

caudal ventral


117 187<br />

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<br />

<br />

<br />

<br />

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2023 66 Ruge <br />

5 I <br />

2 3II <br />

1 10 15III 8 <br />

12IV <br />

40 61V 6 9<br />

<br />

<br />

4 <br />

6 <br />

9 <br />

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<br />

III <br />

IV <br />

<br />

<br />

P<br />

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2011 <br />

2 <br />

<br />

<br />

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<br />

• <br />

<br />

<br />

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<br />

1952 2011 2161 <br />

2 – <br />

<br />

2011 2 <br />

3 <br />

<br />

P<br />

<br />

1 1 1 1 1 <br />

2,3 3 3<br />

1<br />

2 2 <br />

3 <br />

2011 <br />

1 81 <br />

<br />

5 <br />

<br />

2 <br />

2 <br />

1 1 3 <br />

<br />

2 2 <br />

<br />

<br />

<br />

3 89<br />

<br />

5 <br />

<br />

<br />

P<br />

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1 1 2,3 2 2<br />

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36 <br />

<br />

14 6 5 <br />

1 <br />

2 2 <br />

3 <br />

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4 2<br />

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1 1 1 1 1 <br />

1 1 1 1 1 1 <br />

1 1 1 1 1 2<br />

1<br />

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<br />

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27 <br />

CTCBCT<br />

<br />

<br />

80 1 <br />

<br />

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P<br />

<br />

1 1 1 1 2 3 <br />

4 2<br />

1<br />

2 3 <br />

4 <br />

2011 77 <br />

<br />

<br />

<br />

5 <br />

<br />

1/3<br />

<br />

1 <br />

<br />

<br />

3.5 mm<br />

9 cm <br />

<br />

1 <br />

1 <br />

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188<br />

117 <br />

P<br />

<br />

1 1 1 1 1 <br />

2 2 2 2<br />

1<br />

3 2 <br />

<br />

<br />

0.15-0.48 22 <br />

70 <br />

12.5 cm<br />

12.5 cm<br />

<br />

328 g <br />

6 <br />

<br />

1 <br />

<br />

<br />

<br />

P<br />

<br />

1 1 2 2<br />

1<br />

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P<br />

KUHWrat <br />

<br />

<br />

KUHWrat <br />

1720 100% <br />

90 Wtype Stype <br />

Ntype <br />

<br />

742 Stype 178 13475.3<br />

4424.7<br />

Stype <br />

<br />

3823.4 1840.9<br />

2 <br />

96 53.9 26 14.6<br />

Ntype 38 <br />

8 21.1 3 7.9 11 39.3<br />

<br />

Ganzer, Maynert, Gudden <br />

<br />

Wtype <br />

R=0.875<br />

P<br />

<br />

<br />

1<br />

2 <br />

3 4 <br />

5 <br />

9 <br />

<br />

<br />

<br />

Z <br />

<br />

AI <br />

AI Z <br />

<br />

I 2 3 Z<br />

<br />

<br />

Z <br />

I 1.5 4 <br />

9 <br />

Z <br />

Z I Z <br />

I <br />

<br />

P<br />

<br />

<br />

<br />

<br />

<br />

P <br />

<br />

<br />

<br />

3 4<br />

<br />

50 <br />

<br />

PGP9.5 P CCD <br />

<br />

<br />

18 P <br />

<br />

<br />

3<br />

<br />

<br />

P <br />

P<br />

<br />

<br />

<br />

<br />

<br />

<br />

<br />

<br />

ICR 18 <br />

<br />

6 5 FITC <br />

4%PFA <br />

<br />

3 <br />

3 <br />

5 <br />

HIF1α


117 189<br />

P<br />

<br />

1 1 1 1 1 <br />

1,2 1 1 1 1<br />

1<br />

2 <br />

<br />

2AQP2<br />

VP <br />

VP <br />

VP <br />

VP AQP2 AQP2 <br />

AQP2 <br />

4 <br />

256 256S 269 269S<br />

AQP2 <br />

VP DDI/Ddia <br />

VP <br />

256S <br />

VP 256S <br />

256S VP <br />

VP 269S AQP2<br />

<br />

AQP2 <br />

269S <br />

P<br />

myosinIIA <br />

<br />

<br />

<br />

<br />

Epstein <br />

myosinIIA <br />

PLP 1 <br />

10%15% 20 sucrose OCT <br />

<br />

<br />

<br />

<br />

myosinIIA <br />

<br />

myosinIIA <br />

<br />

PAN myosinIIA <br />

myosinIIA <br />

myosinIIA <br />

<br />

P<br />

FABP<br />

1 1 1 1,2 1 1 <br />

1<br />

1<br />

2 <br />

<br />

<br />

<br />

<br />

<br />

FABP5<br />

FABP5 blimp1<br />

cmyc <br />

FABP5KO CRABP2 <br />

blimp1 cmyc <br />

FABP5KO <br />

30<br />

FABP5KO <br />

FABP5


190<br />

117 <br />

<br />

ATP <br />

<br />

<br />

ATP <br />

ATP P2X <br />

ATP G P2Y <br />

TRPV1 <br />

DRG P2XP2Y mRNA <br />

in situ hybridization ATP <br />

ATP <br />

ATP P2Y12 <br />

p38 MAPK <br />

<br />

ATP


117


117 191<br />

<br />

<br />

<br />

Adachi, Yasuhiro<br />

2P019<br />

Fujiwara, Mutsunori<br />

3OFPMVI2<br />

<br />

2P093<br />

3P073<br />

Fujiwara, Naoki<br />

1P127<br />

Jindatip, Depicha<br />

3ODPMI4<br />

Adthapanyawanich, Kannika<br />

2P098<br />

Grienberger, Christine<br />

S264<br />

Josef Flor, Peter<br />

1P031<br />

3P065<br />

Hagiwara, Haruo<br />

2P125<br />

Jue, Seong Suk<br />

1P128<br />

Agur, Anne<br />

3OHPMIV5<br />

Hampel, Falko<br />

3OGPMIV2<br />

Kagawa, Yshiteru<br />

2P019<br />

Aldartsogt, Dolgorsuren<br />

3OHPMI1<br />

<br />

1P096<br />

Kakizuka, Akira<br />

3OGPMIV3<br />

1P070<br />

Harada, Hidemitsu<br />

1P127<br />

Kameie, Toshio<br />

2P061<br />

Ali, Md Moksed<br />

1P062<br />

Hart, Gerald W<br />

1OIPM1<br />

Kamiya, Mako<br />

2P023<br />

<br />

2P093<br />

Hashino, Eri<br />

2OGAMI1<br />

Karasawa, Nobuyuki<br />

1P019<br />

Aoyama, Fumiyo<br />

S211<br />

Hashizume, Wataru<br />

1P073<br />

Karim, Mohammad Rabiul<br />

2P001<br />

Arakawa, Takamitsu<br />

3OHPMIV5<br />

Hata, Kenji<br />

3P037<br />

2P010<br />

Asano, Yoshiya<br />

1P065<br />

Hayashi, Ayako<br />

2P023<br />

Kawagishi, Masahiko<br />

3P077<br />

Asanuma, Daisuke<br />

2P023<br />

Hayato, Terayama<br />

2P129<br />

Kawano, Hitoshi<br />

2P032<br />

Astrid Feinisa, Khairani<br />

2P056<br />

2P131<br />

Kawata, Mitsuhiro<br />

1P031<br />

2P062<br />

Hebiguchi, Taku<br />

2P108<br />

Kikkawa, Masahide<br />

2P049<br />

2P074<br />

Hill, Daniel<br />

S264<br />

2P050<br />

2P075<br />

Hirai, Shuichi<br />

3P069<br />

Kikuchi, Kunio<br />

1P062<br />

Atoji, Yasuro<br />

2P001<br />

Hiraoka, Mari<br />

3OIPM4<br />

Kim, Byung In<br />

1P128<br />

Atukorala, ADSL<br />

3OGPMVI1<br />

Hiyama, Shinji<br />

3P038<br />

Kim, Ji Youn<br />

1P128<br />

Baba, Otto<br />

3OGPMVI1<br />

HoriiHayashi, Noriko<br />

1P002<br />

kishigami, Ryota<br />

1P127<br />

Bastmeyer, Martin<br />

3OGPMIV2<br />

1P037<br />

Kitamura, Seiichiro<br />

3OHPMI1<br />

Blomhoff, Rune<br />

3OFPMVI2<br />

Huang, Zheng<br />

2P025<br />

Kiyama, Hiroshi<br />

S13<br />

Bonner, William<br />

1OGPMII3<br />

IdaYonemochi, Hiroko<br />

2OGAMII1<br />

Klein, Ruediger<br />

3OGPMIV2<br />

Buzsaki, Gyorgy<br />

S263<br />

Ide, Soyuki<br />

S211<br />

Kogaya, Yasutoku<br />

1P019<br />

Chen, Cheng<br />

3P064<br />

Ikegami, Koji<br />

3P104<br />

Koike, Masato<br />

3P023<br />

Chen, Huayue<br />

1P019<br />

Imai, Katsuyuki<br />

3OFPMVI2<br />

Koji, Takehiko<br />

S224<br />

Chen, Jiaorong<br />

1P004<br />

2P108<br />

Kokubu, Keiji<br />

2P005<br />

2P025<br />

Inaga, Sumire<br />

2P052<br />

3P013<br />

<br />

S43<br />

2P061<br />

Komiyama, Masatoshi<br />

3P069<br />

3OFPMVIII1<br />

Inohara, Keiji<br />

3OGPMVI1<br />

Kondo, Takako<br />

2OGAMI1<br />

Dalkhsuren, ShineOd<br />

3OHPMI1<br />

Iseki, Shoichi<br />

2P097<br />

Konishi, Yoshiyuki<br />

3P104<br />

1P070<br />

2P098<br />

Konnerth, Arthur<br />

S264<br />

del Toro, Daniel<br />

3OGPMIV2<br />

Ishibashi, Osamu<br />

1P062<br />

Korekane, Hiroaki<br />

1P037<br />

Dobberfuhl, Andrew<br />

2OEAMIII4<br />

Ishihara, Naotada<br />

S42<br />

Kubo, Kinya<br />

1P019<br />

Ebrahimi, Majid<br />

2P019<br />

Ishikawa, Tomoko<br />

1P062<br />

Kubota, Hiroshi<br />

2P050<br />

Egea, Joaquim<br />

3OGPMIV2<br />

Ishizeki, Kiyoto<br />

1P127<br />

Kvachnina, Elena<br />

3OGPMIV2<br />

Eid, Nabil<br />

2OHAMII1<br />

Islam, Ariful<br />

3P073<br />

Ladher, Raj<br />

3P026<br />

2P112<br />

Islam, Md. Nabiul<br />

3P013<br />

<br />

3P041<br />

Eileen, Watson<br />

3OFPMVI1<br />

Islam Md, Shafiqul<br />

S164<br />

<br />

2OIAMI3<br />

Ejiri, Sadakazu<br />

1P019<br />

Ito, Chizuru<br />

S225<br />

Liu, JunQian<br />

3P001<br />

Endou, Yoshio<br />

2P113<br />

1OIPM4<br />

<br />

1P063<br />

Farkas, Jozsef<br />

3P052<br />

3P064<br />

Maekawa, Mamiko<br />

1OIPM4<br />

Finger, Thomas<br />

3P053<br />

Ito, Yuko<br />

2OHAMII1<br />

3P064<br />

Fujii, Hiromi<br />

1P073<br />

Itoh, Masahiro<br />

3P069<br />

Maimaiti, Kuerban<br />

2P131<br />

Fujinaga, Ryutaro<br />

2P005<br />

Jahan, Esrat<br />

1P129<br />

Mansfield, Carol<br />

S12<br />

3P013<br />

Jahan, Mir Rubayet<br />

3P013<br />

Marandi, Nima<br />

S264


192<br />

117 <br />

Marson, Lesley<br />

Masahiro, Itoh<br />

MasugiTokita, Miwako<br />

Masuko, Sadahiko<br />

Matsumoto, Yoshiki<br />

Matsunaga, Wataru<br />

Matsuno, Yoshiharu<br />

Matsuo, Chikahisa<br />

Matsusue, Yumiko<br />

Md. Nabiul, Islam<br />

Mezaki, Yoshihiro<br />

Miki, Takanori<br />

Milligan, Carol<br />

Mir Rubayet, Jahan<br />

Misawa, Kazuhiko<br />

Mitani, Kiyoshi<br />

Mitui, Shinnichi<br />

Miura, Masahiro<br />

Miura, Masayuki<br />

Miura, Mitsutaka<br />

Miyaso, Hidenobu<br />

Mizushima, Noboru<br />

Moreno, Ramon<br />

Mori, Chisato<br />

Mori, Nozomu<br />

Morii, Mayako<br />

Muhetaerjiang, Musha<br />

Mukoyama, Yosuke<br />

Munekazu, Naito<br />

Murakami, Tohru<br />

Naganuma, Makoto<br />

Nagashima, Yu<br />

Naguro, Tomonori<br />

Naito, Akira<br />

Naito, Munekazu<br />

Nakane, Hironobu<br />

Nakanishi, Masako<br />

Nakata, Hiroki<br />

Ning, Qu<br />

Nishi, Mayumi<br />

2OEAMIII4<br />

2P129<br />

2P131<br />

1P031<br />

2P032<br />

3P001<br />

1P002<br />

3P069<br />

2P005<br />

1P002<br />

1P043<br />

2P005<br />

3OFPMVI2<br />

2P108<br />

3P001<br />

S12<br />

1P043<br />

2P005<br />

3P077<br />

3OGPMVI1<br />

2P125<br />

2P113<br />

S11<br />

3OFPMVI2<br />

2P108<br />

3P069<br />

S42<br />

S12<br />

3P069<br />

3OGPMIV3<br />

3OFPMVI2<br />

2P108<br />

2P129<br />

2P131<br />

S85<br />

2P129<br />

2P131<br />

2P074<br />

1P073<br />

3P077<br />

2P052<br />

2P061<br />

1P073<br />

3P069<br />

2P052<br />

2P061<br />

3P037<br />

2P098<br />

2P129<br />

2P131<br />

1P002<br />

Nishimura, Taki<br />

Niu, Jianguo<br />

<br />

Noda, Yasuko<br />

Oda, Toshiyuki<br />

Oe, Souichi<br />

Ogawa, Yuki<br />

Ohata, Kenji<br />

Ohno, Nobuhiko<br />

Ohno, Shinichi<br />

Ohshima, Hayato<br />

Ohta, Kenichi<br />

Ohyama, Kyoji<br />

OikawaSasaki, Ai<br />

Oita, Eiko<br />

Oka, Tatsuro<br />

Okabe, Shigeo<br />

Okuda, Hiroaki<br />

Onga, Kazuko<br />

Ono, Katsuhiko<br />

Oppenheim, Ronald<br />

Otsu, Keishi<br />

Otsuki, Yoshinori<br />

Owada, Yuji<br />

Ozaki, Hiroshi<br />

<br />

Park, Jae Hyun<br />

Parras, C<br />

Prevette, David<br />

<br />

<br />

Qu, Ning<br />

QuispeSalcedo, Angela<br />

Rafiq, Ashiq Mahmood<br />

Rakwal, Randeep<br />

Ramadhani, Dini<br />

Redon, Christophe<br />

Reza, Mohamad<br />

Rochefort, Nathalie<br />

S42<br />

2P026<br />

2P041<br />

3P003<br />

2P049<br />

3P003<br />

3P069<br />

3P104<br />

1P004<br />

1P004<br />

2P025<br />

2OGAMII1<br />

3P001<br />

3OGPMIV3<br />

1P127<br />

S42<br />

2P026<br />

1P030<br />

2P023<br />

1P020<br />

1P037<br />

3OGPMIV3<br />

1P002<br />

S12<br />

1P127<br />

2OHAMII1<br />

3P037<br />

2P019<br />

3P073<br />

S164<br />

1OEPMI1<br />

1P128<br />

1P098<br />

S12<br />

1P063<br />

2P130<br />

3P067<br />

3P068<br />

3P069<br />

2OGAMII1<br />

1P129<br />

3OEPMVI2<br />

1P117<br />

2P127<br />

2P128<br />

3P022<br />

3ODPMI4<br />

3ODPMII1<br />

1OGPMII3<br />

3ODPMI2<br />

S264<br />

Saito, Shouichiro<br />

Saitoh, Sei<br />

Saitoh, Yurika<br />

Sasagawa, Takayo<br />

Sato, Iwao<br />

Sato, Toshiaki<br />

Satoh, Kazuhiko<br />

Sawada, Tomoo<br />

Sawaguchi, Akira<br />

Schwark, Manuela<br />

Seki, Shinichiro<br />

Senoo, Haruki<br />

Setou, Mitsutoshi<br />

Sharifi, Kazem<br />

Shibukawa, Yukinao<br />

Shin, Je Won<br />

Shinoda, Koh<br />

Shiomi, Tadahiro<br />

Shuichi, Hirai<br />

<br />

Song, Ning<br />

Song, Xiaohui<br />

Sumida, Kaori<br />

Sunabori, Takehiko<br />

Sunohara, Masataka<br />

Suzuki, Katsuhiko<br />

Suzuki, Shingo<br />

Suzuki, Takayuki<br />

Tabata, Makoto<br />

Tajika, Yuki<br />

Takada, Masahiko<br />

Takahashi, Maiko<br />

Takahashi, Nobuyasu<br />

Takano, Yoshiro<br />

Takeshita, Yukio<br />

Takeuchi, Yoshiki<br />

Takizawa, Takami<br />

Takizawa, Toshihiro<br />

Takumi, Toru<br />

Tamai, Motoki<br />

Tanaka, hideyuki<br />

Tanaka, Shinji<br />

Taniguchi, Naoyuki<br />

Tarabykin, Victor<br />

2P001<br />

1P004<br />

1P004<br />

2P025<br />

1P002<br />

2P116<br />

1P073<br />

1P019<br />

2P019<br />

3P073<br />

S211<br />

3OGPMIV2<br />

3OHPMI1<br />

3OFPMVI2<br />

3OIPM4<br />

2P108<br />

3P104<br />

2P019<br />

1P037<br />

1P128<br />

2P005<br />

3P013<br />

2P061<br />

2P129<br />

2P131<br />

2P042<br />

S224<br />

1P062<br />

3OHPMI1<br />

3P023<br />

2P116<br />

1P073<br />

3P001<br />

3P077<br />

3OGPMVI1<br />

2P074<br />

3OIPM4<br />

2P074<br />

S211<br />

3OGPMVI1<br />

3P013<br />

3P001<br />

1P062<br />

1P062<br />

1P030<br />

3P001<br />

2P125<br />

1P030<br />

1P037<br />

3OGPMIV2


117 193<br />

Tatsumi, Kouko<br />

Terada, Nobuo<br />

Terada, Sumio<br />

Terayama, Hayato<br />

Tokuda, Nobuko<br />

Toshimori, Kiyotaka<br />

Toyama, Yoshiro<br />

Trifonov, Stefan<br />

Tsuchiya, Reiko<br />

Tsumori, Toshiko<br />

Uchida, Takashi<br />

Uchiyama, Yasuo<br />

Ueno, Hitoshi<br />

Urano, Yasuteru<br />

Velikkakath, Anoop Kumar<br />

Vinsant, Sherry<br />

Wada, Yoshinao<br />

Wakayama, Tomohiko<br />

Wanaka, Akio<br />

<br />

<br />

Warita, Katsuhiko<br />

Watanabe, Mineo<br />

Watanabe, Ryo<br />

Weinstein, Brant<br />

Wong, Richard<br />

<br />

Yagi, Toshiki<br />

Yakura, Tomiko<br />

Yamaguchi, Noriko<br />

Yamamoto, Miyuki<br />

Yamano, Mariko<br />

Yamashita, Kikuji<br />

Yamatoya, Kenji<br />

Yanai, Akie<br />

<br />

1P020<br />

1P037<br />

1P004<br />

2P025<br />

3P077<br />

3P069<br />

2P019<br />

3P073<br />

S225<br />

1OIPM4<br />

3P064<br />

1OIPM4<br />

3P064<br />

1OEPMI2<br />

3P031<br />

3P104<br />

2P026<br />

3P038<br />

S14<br />

3P023<br />

2P074<br />

2P023<br />

S42<br />

S12<br />

1P037<br />

2P098<br />

1P020<br />

1P037<br />

3OIPM6<br />

1P015<br />

2P020<br />

3P001<br />

3P038<br />

2P108<br />

S84<br />

S245<br />

1OHPM3<br />

1P015<br />

2P049<br />

2P050<br />

3P001<br />

2P108<br />

2P097<br />

1P020<br />

3OHPMI1<br />

S225<br />

1OIPM4<br />

3P064<br />

2P005<br />

3P013<br />

1P034<br />

Yasuda, Kunihiko<br />

Yasui, Yukihiko<br />

Yoneda, Toshiyuki<br />

Yonemura, Yutaka<br />

Yorifuji, Hiroshi<br />

Yoshikawa, Kiwamu<br />

Yoshikawa, Masaaki<br />

Yoshino, Hiroaki<br />

<br />

<br />

Yuki, Ogawa<br />

<br />

<br />

Zhang, Q<br />

<br />

<br />

<br />

3P122<br />

1OHPM2<br />

3OGPMIV3<br />

2P026<br />

3P037<br />

2P113<br />

2P074<br />

3OFPMVI2<br />

2P108<br />

S12<br />

2P108<br />

1OHPM4<br />

2P121<br />

2P131<br />

3OIPM6<br />

1P078 3P111<br />

<br />

<br />

<br />

<br />

<br />

3P112<br />

3P117<br />

1OFPMII3<br />

3OIPM6<br />

S72<br />

3P128<br />

1P054<br />

2P121<br />

1P098<br />

3P115<br />

2P045 3P085<br />

<br />

3P088<br />

3P127<br />

3P089<br />

1P056 3P130<br />

<br />

<br />

<br />

3P078<br />

2OEAMV2<br />

1P132<br />

1P122 1P123<br />

<br />

<br />

<br />

<br />

<br />

<br />

<br />

<br />

<br />

<br />

<br />

2P012<br />

2P012<br />

1OGPMII2<br />

2OFAMIV1<br />

2OGAMI2<br />

2OFAMIV1<br />

1P072<br />

2OFAMV3<br />

3OGPMVI2<br />

2OHAMII2<br />

2OHAMII3<br />

2P080<br />

3P072<br />

3P113<br />

2P080<br />

1OIPM1<br />

3P100<br />

1P045<br />

3P057<br />

S101 3P015<br />

3P122<br />

1P120<br />

3P055<br />

2OEAMIII3<br />

3OHPMIV2<br />

1P077 3P039<br />

3P040 3P116<br />

3P120 3P121<br />

<br />

1P087<br />

2OHAMIII2<br />

2OFAMIII4<br />

1P003<br />

S124 S125<br />

S163<br />

2OHAMII3<br />

2P080<br />

3OIPM3<br />

3P100<br />

2P126 3P132<br />

<br />

2OEAMV1<br />

S117<br />

3P019 3P030<br />

2P002 2P010<br />

1P108 3P018<br />

3P111 3P112<br />

3P118<br />

1OGPMII1<br />

2OIAMI2<br />

3OIPMIV2<br />

1P048<br />

3P097<br />

2P103 3P118<br />

1P044<br />

2OFAMIII4<br />

1P093<br />

3P047<br />

2OIAMIII1<br />

1P126 2P083<br />

2P014<br />

1OFPMI1<br />

W15<br />

2OIAMI3<br />

2OIAMI4<br />

2OIAMIII3<br />

2P092<br />

1P017<br />

2P078 3P117


194<br />

117 <br />

<br />

<br />

<br />

<br />

<br />

<br />

1OFPMI2<br />

1OFPMI3<br />

2P058<br />

2P094<br />

1OFPMII3<br />

2P031<br />

3P071<br />

3P082<br />

3OHPMI2<br />

3P120 3P121<br />

<br />

3P094<br />

W12 3P107<br />

<br />

<br />

<br />

<br />

<br />

<br />

<br />

S163<br />

3P027<br />

2OGAMI4<br />

3P034<br />

3P125<br />

3P055<br />

1P009<br />

S243 1P068<br />

<br />

<br />

2P080<br />

S192<br />

1P049 2P082<br />

<br />

<br />

<br />

3OHPMII1<br />

3P101<br />

S103<br />

1P033 2P033<br />

<br />

<br />

<br />

<br />

<br />

<br />

2P073<br />

3P048<br />

3P128<br />

1P121<br />

2OIAMIII3<br />

S222<br />

1OFPMI1<br />

3OHPMII2<br />

2P072<br />

3P011<br />

S94 S165<br />

<br />

<br />

<br />

2P105<br />

1P053<br />

3OHPMIV3<br />

1P083<br />

3P122<br />

1P015 2P020<br />

<br />

<br />

<br />

<br />

<br />

<br />

3OIPM5<br />

2OFAMV2<br />

2P057<br />

3P066<br />

1P098<br />

S41<br />

1OIPM2<br />

1OIPM5<br />

3P111<br />

3P122<br />

1OIPM6<br />

1P064 3P082<br />

2OEAMV2<br />

2OHAMIII1<br />

2P006<br />

3P118<br />

1P097<br />

2P100 2P101<br />

3P056<br />

W16<br />

1OIPM6<br />

1P064 3P082<br />

3P072<br />

2P071<br />

3P012<br />

1P047<br />

3P092<br />

2P057<br />

1P050<br />

S221 3P065<br />

2OFAMV2<br />

S83 S241<br />

S245<br />

2OFAMIV3<br />

S161<br />

2OFAMIV1<br />

2OGAMII2<br />

2P109<br />

1OIPM2<br />

S151<br />

2OFAMIII3<br />

3OIPM3<br />

2P022<br />

1OGPMII1<br />

2OIAMI2<br />

3OIPMIV2<br />

1P048<br />

3P016<br />

1P040 1P112<br />

1P074<br />

1P003 2P003<br />

2P046 3P050<br />

3P103 3P110<br />

3P124<br />

3P063<br />

3OFPMVI4<br />

S94 2P044<br />

1OHPM5<br />

3P092<br />

3P120<br />

S71<br />

3P059<br />

S33<br />

S223<br />

1OHPM5<br />

1P089 2P130<br />

3P067 3P068<br />

3P098<br />

3P090<br />

1OEPMII2<br />

2P112<br />

2P027<br />

S92<br />

1OIPM3<br />

3OFPMVII3<br />

3P035<br />

1P093<br />

2P093<br />

3P034<br />

3P043<br />

S52<br />

2OIAMIII1<br />

1P126<br />

2P066<br />

1OFPMII2<br />

S141 1P131<br />

1OHPM2<br />

2OHAMI2<br />

2OIAMI3<br />

2OEAMV2<br />

2OHAMIII1<br />

2P006<br />

2P045 3P085<br />

3P088 3P089<br />

3P095<br />

3P120<br />

1P057<br />

1P017<br />

3OFPMVI3<br />

1P059 2P104<br />

3P022 3P030<br />

3P052<br />

S61<br />

3P062<br />

1P132<br />

S72<br />

2P087<br />

S112


117 195<br />

<br />

<br />

2P086<br />

S235<br />

2P036 3P079<br />

2P093 3P034<br />

<br />

<br />

<br />

<br />

2P017<br />

S185<br />

3P078<br />

3P108<br />

2P033 3P011<br />

<br />

3P014<br />

1OEPMII3<br />

2P028 2P107<br />

<br />

<br />

<br />

<br />

<br />

<br />

2P107<br />

1OGPMII1<br />

1P048<br />

3OGPMVI2<br />

1P003<br />

1OHPM4<br />

2P134<br />

2P093 3P034<br />

1P041 3P042<br />

<br />

<br />

<br />

<br />

3P021<br />

2P094<br />

2P094<br />

3P130<br />

S95 1P116<br />

<br />

<br />

<br />

2P056<br />

2P075<br />

1P078<br />

2P114<br />

1P040<br />

2P062<br />

S23 2P055<br />

S143 2P036<br />

<br />

2P038<br />

2P121<br />

3P079<br />

1P003 2P003<br />

<br />

<br />

2P046<br />

3P103<br />

3P124<br />

3P021<br />

1P076<br />

3P050<br />

3P110<br />

S63 S74<br />

<br />

<br />

1P066<br />

2P047<br />

3P059<br />

S184<br />

S111<br />

1P067<br />

2P048<br />

2P127 2P128<br />

S145 1P129<br />

<br />

<br />

<br />

<br />

<br />

<br />

1P131<br />

3P088<br />

1P132<br />

1OEPMI3<br />

2P017<br />

2P079<br />

3P072<br />

3OIPM3<br />

1P012<br />

3P085<br />

3P089<br />

1P104 1P105<br />

<br />

<br />

<br />

<br />

<br />

<br />

2P011<br />

2P060<br />

3P061<br />

2OIAMII1<br />

1P103<br />

3OHPMIV2<br />

3P079<br />

1OFPMI3<br />

2P058<br />

2P059<br />

3P002<br />

1P060 2P111<br />

2P119 2P120<br />

2P124<br />

3P129<br />

2P109 2P118<br />

1P071 2P095<br />

<br />

<br />

<br />

<br />

<br />

<br />

<br />

<br />

<br />

<br />

<br />

<br />

<br />

<br />

<br />

<br />

<br />

3OHPMIV4<br />

1P074<br />

S51<br />

3OEPMVI1<br />

3P049<br />

3P042<br />

S53<br />

S81<br />

1P069<br />

3P052<br />

1P018<br />

S95<br />

1OIPM1<br />

2P085<br />

2OFAMV2<br />

1P120<br />

1OFPMI1<br />

3P039 3P040<br />

<br />

<br />

<br />

3OFPMVII3<br />

3P122<br />

2P088<br />

3OEPMVI1<br />

3P049<br />

1OIPM6<br />

1OGPMI4<br />

3OIPMIV1<br />

3OIPM6<br />

S43<br />

3OFPMVIII1<br />

2P084 2P089<br />

3P039 3P040<br />

3P122<br />

2OGAMII2<br />

2OGAMII3<br />

1OHPM2<br />

2OEAMIII3<br />

S162 S213<br />

W14 1P133<br />

1P027 1P028<br />

S123<br />

1OFPMII3<br />

3P019 3P020<br />

3P027<br />

2P013 3P017<br />

3P060<br />

S141 1P129<br />

1P131<br />

S81<br />

2P123<br />

3OFPMVIII3<br />

S43<br />

1P074<br />

1OHPM1<br />

1OGPMII3<br />

2P008 2P070<br />

2P072 2P094<br />

2P110 2P112<br />

1P024 1P025<br />

1OEPMII2<br />

2P038<br />

S252<br />

S212 2P053<br />

2P102 3P076<br />

1P049<br />

S214<br />

2P117<br />

3OFPMVII2<br />

2OEAMV3<br />

3P039 3P040<br />

3P039 3P040<br />

2P085<br />

2OIAMII1


196<br />

117 <br />

3P042<br />

2OFAMV2<br />

3OEPMVI1<br />

3P049<br />

S45<br />

2OIAMIII1<br />

2P083 2P103<br />

2P126 3P132<br />

S141 2P041<br />

1P014 1P015<br />

2P020<br />

1P096<br />

1P024 1P025<br />

2OEAMIII1<br />

2P069<br />

3OFPMVI4<br />

1P103<br />

2P022 3P006<br />

3P007 3P008<br />

3P108<br />

1P110 1P118<br />

1OGPMI3<br />

2OGAMI3<br />

S91 1P092<br />

1P096 2P087<br />

3P083<br />

2P042<br />

1P040<br />

1P099<br />

3P122<br />

- S261<br />

3P124<br />

S205<br />

3OEPMVI2<br />

3OEPMVIII3<br />

1P117 2P127<br />

2P128<br />

3P022<br />

S64<br />

1P097<br />

2P084<br />

3P116<br />

S242<br />

3OHPMIV3<br />

1P083<br />

3P110<br />

3P026<br />

1P054<br />

1P039<br />

2P027<br />

<br />

3OHPMII1<br />

3P101<br />

S203 1P033<br />

1P034 2P033<br />

<br />

<br />

<br />

<br />

<br />

<br />

<br />

<br />

<br />

<br />

<br />

<br />

2P073<br />

3P014<br />

3P125<br />

1P081<br />

3P011<br />

3P048<br />

3OEPMVIII1<br />

2OEAMIII4<br />

2P086<br />

1OIPM5<br />

2P071<br />

S204<br />

1P098<br />

3P012<br />

3P070<br />

3P123<br />

3P008 3P108<br />

<br />

<br />

<br />

1P120<br />

1P081<br />

1OFPMII2<br />

1P092 1P094<br />

<br />

<br />

<br />

<br />

<br />

3P059<br />

1P115<br />

2P015<br />

1OFPMI1<br />

2P076 3P025<br />

<br />

<br />

1OFPMII3<br />

3P022<br />

3P052<br />

1P111<br />

3P030<br />

1P051 1P068<br />

<br />

3P122<br />

1P046 2P091<br />

1P009 1P010<br />

<br />

3P028<br />

3OHPMIV4<br />

1P078<br />

3P112<br />

3P117<br />

3P033<br />

3P111<br />

3P115<br />

S202 1P018<br />

2P031 3P016<br />

<br />

<br />

<br />

<br />

<br />

S132<br />

3P026<br />

3P072<br />

1P111<br />

3P007<br />

1P049 2P082<br />

1P080<br />

1OEPMI2<br />

3P031<br />

3P053 3P054<br />

3P114<br />

3P106<br />

1P064<br />

S185<br />

S194<br />

2P080<br />

1P113<br />

1P123<br />

2P064<br />

1P092 1P094<br />

1OFPMI1<br />

S51<br />

S105<br />

1P017<br />

3OGPMV1<br />

3P066<br />

3P125<br />

2OHAMI2<br />

1P044<br />

2P016<br />

2P007<br />

S35<br />

S162<br />

3P074<br />

S261<br />

1OEPMI1<br />

2P037 2P038<br />

2P039 2P042<br />

3P079<br />

S54<br />

2OEAMIII2<br />

1P021 1P080<br />

3P092<br />

2OGAMI1<br />

3OFPMVII2<br />

3OEPMVII3<br />

3P101<br />

S231<br />

2P015<br />

3P095<br />

S261 2P042<br />

3OGPMV1<br />

2OEAMIV3<br />

S23<br />

2OEAMIV3<br />

1P023<br />

2P018


117 197<br />

<br />

<br />

<br />

<br />

<br />

1P082<br />

2P117<br />

3P127<br />

2P029<br />

S25<br />

S142 1P072<br />

<br />

1OIPM1<br />

1P009 1P010<br />

<br />

3P028<br />

3P105<br />

3P033<br />

S262 2P018<br />

<br />

<br />

<br />

1P093<br />

2OEAMV2<br />

2OHAMIII1<br />

2P006<br />

2P012<br />

1P089 3P098<br />

1P035 2P021<br />

<br />

<br />

<br />

<br />

<br />

<br />

<br />

<br />

<br />

<br />

<br />

<br />

<br />

<br />

3P009<br />

3P044<br />

S112<br />

1P050<br />

3P043<br />

3OGPMIV4<br />

1P036<br />

1P050<br />

3P074<br />

S161<br />

3P055<br />

2OHAMI2<br />

1P103<br />

1OEPMII3<br />

2P040<br />

2P096<br />

2OHAMI2<br />

2P094<br />

<br />

1P119 2P133<br />

<br />

3OIPMIV2<br />

1P063 3P082<br />

<br />

<br />

<br />

<br />

<br />

<br />

<br />

3OIPM3<br />

1P005<br />

3P122<br />

3ODPMI3<br />

1P097<br />

3OIPMIV2<br />

3OEPMVII3<br />

3P068<br />

1P092 1P094<br />

1P096<br />

<br />

<br />

1OHPM4<br />

2P134<br />

1OGPMII2<br />

2OFAMIV1<br />

2OFAMIV2<br />

2OGAMI2<br />

3OEPMVII1<br />

1P054<br />

1P060 2P109<br />

<br />

2P111<br />

2P124<br />

2OHAMI4<br />

1P070<br />

2P120<br />

3P129<br />

1P102 1P109<br />

<br />

<br />

S92<br />

1OIPM3<br />

1OEPMII1<br />

S181 W13<br />

<br />

<br />

<br />

<br />

<br />

<br />

2OEAMV1<br />

S175<br />

3OIPM6<br />

1OGPMI4<br />

2OIAMI2<br />

2P094<br />

3P090<br />

1P080 2P006<br />

3P092<br />

W14 3P119<br />

<br />

<br />

<br />

<br />

S83<br />

1OFPMI1<br />

1OIPM2<br />

1P069<br />

2P045 3P085<br />

- <br />

<br />

3P088<br />

1P036<br />

S64<br />

3P089<br />

3OEPMVIII2<br />

3P021<br />

1P102 1P109<br />

<br />

2P030<br />

S223 1P089<br />

<br />

<br />

<br />

<br />

<br />

<br />

<br />

<br />

3P098<br />

1P072<br />

S92<br />

2P126<br />

3P020<br />

3OHPMIV3<br />

2OIAMII3<br />

2OIAMII3<br />

1P133<br />

2P111<br />

3OIPMIV1<br />

1P066 1P067<br />

2P094<br />

2OIAMIII3<br />

1P084<br />

S145 2P045<br />

3P085 3P088<br />

3P089<br />

S251<br />

2OFAMIII1<br />

1P097<br />

3P011<br />

S254<br />

2OIAMI1<br />

1P023 1P071<br />

2P095<br />

3P122<br />

3P122<br />

3P101<br />

2P018<br />

3OHPMI2<br />

3OHPMIV4<br />

1P078 3P111<br />

3P112 3P115<br />

3P117<br />

2P123<br />

3OHPMIV1<br />

3OIPM2<br />

2P093 3P034<br />

3P041<br />

1OIPM6<br />

1P052<br />

S235<br />

3OFPMVII3<br />

1OEPMI1<br />

2P037 2P038<br />

2P042<br />

2OEAMIII2<br />

3P131<br />

S34<br />

<br />

2P130<br />

3OGPMV3<br />

1P052<br />

S112<br />

1P006<br />

3P128<br />

3OHPMII2<br />

2P072


198<br />

117 <br />

1P015 2P020<br />

<br />

<br />

<br />

<br />

<br />

<br />

<br />

<br />

<br />

3OEPMVIII1<br />

1OGPMII2<br />

2OFAMIV1<br />

2OFAMIV2<br />

2OGAMI2<br />

1P054<br />

3OEPMVI2<br />

2P128<br />

1P068<br />

2P120<br />

1P052<br />

3P051<br />

1OGPMI3<br />

2OGAMI3<br />

3P028 3P033<br />

2P011 2P059<br />

<br />

<br />

<br />

<br />

<br />

<br />

3P061<br />

3P123<br />

3P047<br />

S55<br />

S233<br />

3P052<br />

S101<br />

S63 S74<br />

<br />

<br />

<br />

<br />

<br />

1P066<br />

2P048<br />

3ODPMI4<br />

1OFPMI4<br />

1P114<br />

1P067<br />

3P059<br />

3OFPMVII3<br />

2OGAMI2<br />

3P122<br />

3P086 3P087<br />

<br />

3OHPMI2<br />

1P071 2P095<br />

<br />

<br />

<br />

<br />

<br />

<br />

1P043<br />

2P123<br />

3OHPMII1<br />

S242<br />

1P005<br />

3P122<br />

2P077 3P093<br />

<br />

<br />

3P111<br />

3P115<br />

3OFPMVII2<br />

3P099<br />

3P112<br />

S191 1P101<br />

<br />

1OEPMII3<br />

S44 1P053<br />

2P004 2P068<br />

2P069<br />

2OEAMIV3<br />

1P042 1P045<br />

2OIAMIII2<br />

1P052 3P053<br />

3P114<br />

1P042 1P045<br />

S131<br />

3OHPMIV1<br />

1OHPM3<br />

1P069<br />

3OIPM2<br />

1P052 3P053<br />

3P114<br />

1OFPMII1<br />

2OGAMIII3<br />

1P090 2P076<br />

2P132 3P024<br />

3P025 3P081<br />

3P109<br />

3P020<br />

2OEAMIII1<br />

2P009 3P045<br />

1P048<br />

3P011<br />

S161<br />

2OGAMIII1<br />

3P026<br />

S31<br />

3OEPMVI4<br />

2P048<br />

1P120 3P095<br />

1P015 2P020<br />

3P102<br />

3P122<br />

3P113<br />

1P116<br />

3P122<br />

1P021 1P080<br />

2P006 3P092<br />

S95<br />

3P071<br />

1OIPM5<br />

3P086<br />

3OGPMIV4<br />

1P036<br />

1P060 2P106<br />

1P109 3P035<br />

3P103 3P124<br />

<br />

<br />

<br />

<br />

<br />

<br />

<br />

<br />

<br />

3P098<br />

1P022<br />

1P029<br />

3P055<br />

3P120<br />

1P100<br />

1OFPMII2<br />

2P024<br />

1P039<br />

2P028 2P107<br />

S261 2P042<br />

<br />

S91 1P092<br />

<br />

<br />

<br />

<br />

<br />

<br />

<br />

<br />

<br />

<br />

1P096<br />

3P122<br />

3OIPMIV3<br />

1P039<br />

2P080<br />

1P024<br />

1P025<br />

S83<br />

2OGAMII3<br />

1OGPMI3<br />

2OGAMI3<br />

3P083<br />

2P002 2P010<br />

2P053 2P102<br />

<br />

<br />

<br />

<br />

3P076<br />

3OGPMV1<br />

3OHPMIV2<br />

1P077<br />

3OEPMVI2<br />

1P117<br />

2P128<br />

2P127<br />

3P086 3P087<br />

<br />

1P076<br />

S212 2P053<br />

2P102 3P076<br />

<br />

<br />

<br />

<br />

<br />

2OFAMIV3<br />

1P121<br />

3OFPMVI1<br />

2P087<br />

1P121<br />

W14 3P119<br />

2P090 3P029<br />

3P062<br />

1P084 2P054<br />

<br />

<br />

<br />

3P131<br />

2OEAMV2<br />

1P093<br />

2P091


117 199<br />

2OFAMIII2<br />

1P013 3P004<br />

3P005<br />

S192<br />

3OHPMI2<br />

3P113<br />

2P086<br />

1P126<br />

1P100<br />

3P099<br />

2P073<br />

3P086 3P087<br />

2OHAMII2<br />

3P113 3P128<br />

2OEAMIII4<br />

3P043<br />

2OHAMI3<br />

2P118 2P119<br />

1P006<br />

1OEPMII1<br />

1P006<br />

2OFAMIII4<br />

2OIAMIII1<br />

1P126 2P083<br />

3OFPMVIII3<br />

3P021<br />

1P016<br />

3OHPMI2<br />

1P032<br />

2OGAMIII2<br />

1P099<br />

1P046 1P047<br />

3OEPMVI3<br />

2P115<br />

2OIAMII1<br />

2P066 2P082<br />

1P118<br />

3P074<br />

1P039<br />

2P059 2P060<br />

3P061<br />

W15<br />

2OIAMI3<br />

2OIAMI4<br />

2OIAMIII3<br />

2P092<br />

2OHAMIII2<br />

2P088<br />

2OEAMIV1<br />

3P019<br />

<br />

3OIPMIV3<br />

1P125 3P122<br />

2P128 3P027<br />

1P071 2P095<br />

<br />

<br />

<br />

<br />

<br />

<br />

<br />

<br />

3P123<br />

S24<br />

3P074<br />

1P026<br />

S192<br />

3OGPMV2<br />

1P040 1P112<br />

3P106<br />

1OHPM3<br />

2OEAMV2<br />

2OHAMIII1<br />

2P006 3P032<br />

3P092<br />

S193 1P014<br />

<br />

1P015 2P020<br />

3P102<br />

2OHAMI2<br />

1P024 1P025<br />

<br />

<br />

<br />

<br />

<br />

<br />

<br />

<br />

<br />

S24<br />

S82<br />

S173<br />

3OFPMVI1<br />

3P057<br />

2OHAMIII2<br />

3OIPMIV1<br />

2OHAMI4<br />

3P094<br />

3P113<br />

1P080<br />

3P128<br />

1P117 2P127<br />

2P128<br />

1P056 2P033<br />

<br />

<br />

<br />

3P048 3P130<br />

1P008<br />

2OIAMI2<br />

1P091<br />

2P126 3P132<br />

<br />

<br />

<br />

<br />

<br />

<br />

1P061<br />

3P070<br />

2P090<br />

2OHAMI2<br />

1OHPM4<br />

2P134<br />

S54<br />

<br />

<br />

<br />

<br />

2P006<br />

1P069<br />

3P090<br />

S61 S202<br />

1OFPMII3<br />

3OEPMVI2<br />

3OEPMVIII3<br />

1P018<br />

1P042<br />

1P055<br />

2P031<br />

2P128<br />

3P019<br />

3P022<br />

3P030<br />

1P026<br />

1P045<br />

1P117<br />

2P127<br />

3P016<br />

3P020<br />

3P027<br />

3P052<br />

1P024 1P025<br />

<br />

<br />

<br />

<br />

2P027<br />

3P097<br />

1P110<br />

1OGPMII2<br />

2OFAMIV2<br />

2OGAMI2<br />

S101 3P015<br />

<br />

<br />

<br />

<br />

2P123<br />

1P043<br />

1P026<br />

S163<br />

1P003 2P003<br />

<br />

<br />

<br />

<br />

3P050<br />

1OFPMII1<br />

2OGAMIII3<br />

3P097<br />

1P103<br />

2OFAMIV1<br />

2P034 2P035<br />

<br />

<br />

<br />

<br />

<br />

<br />

<br />

<br />

<br />

3OHPMII2<br />

2P072<br />

2P112<br />

3OHPMIV3<br />

1P042 1P074<br />

1P083<br />

1P112<br />

3OGPMV2<br />

1P040<br />

2OGAMIII1<br />

3OEPMVI2<br />

1P117<br />

3P022<br />

1P039<br />

2P086<br />

2P088<br />

3P106<br />

2P127


200<br />

117 <br />

<br />

<br />

2OHAMI1<br />

2OHAMIII3<br />

1P085<br />

2P014<br />

1P118<br />

1P125<br />

2P100 2P101<br />

<br />

<br />

3P021<br />

1OHPM6<br />

1P088<br />

3P056<br />

3P103 3P110<br />

<br />

<br />

<br />

<br />

<br />

1P088<br />

1P098<br />

2P118<br />

3P130<br />

1P097<br />

1P024 1P025<br />

<br />

<br />

<br />

2OFAMIV3<br />

2P102<br />

3P094<br />

1P090 2P076<br />

<br />

<br />

2P132<br />

3P025<br />

3P109<br />

2OIAMI4<br />

1P069<br />

3P024<br />

3P081<br />

S241 S245<br />

<br />

<br />

<br />

<br />

<br />

<br />

<br />

<br />

<br />

2OHAMIII3<br />

1P085<br />

1OFPMI4<br />

2OGAMI1<br />

2P020<br />

3P118<br />

2P040<br />

2OGAMIII2<br />

3OHPMII1<br />

3P101<br />

3OFPMVII2<br />

3P130<br />

2P009 3P045<br />

<br />

<br />

S194<br />

1OFPMII3<br />

2P099<br />

1P001 1P038<br />

<br />

<br />

1P023<br />

3OIPM3<br />

<br />

3P086 3P087<br />

<br />

<br />

<br />

3P058<br />

1OIPM2<br />

2OHAMI1<br />

<br />

<br />

<br />

<br />

<br />

<br />

<br />

<br />

<br />

<br />

<br />

<br />

<br />

3P058<br />

2OGAMI3<br />

1OEPMI2<br />

3P031<br />

S152<br />

S95<br />

2P038<br />

2P012<br />

2OEAMV2<br />

1P076<br />

1P056<br />

2P057<br />

3OEPMVII1<br />

W13<br />

1P027 1P028<br />

<br />

<br />

<br />

<br />

<br />

<br />

2OHAMII3<br />

3OIPM3<br />

2P080<br />

3P061<br />

2P089<br />

1P017<br />

3P074<br />

2OFAMV2<br />

3P100<br />

1P074 3P084<br />

3P086 3P087<br />

<br />

<br />

<br />

S43<br />

3OFPMVIII1<br />

1P086<br />

1P078<br />

2P103 3P118<br />

<br />

<br />

<br />

<br />

<br />

<br />

<br />

2OIAMI4<br />

S121<br />

2P115<br />

3P061<br />

2P062<br />

3OIPMIV3<br />

2OHAMI4<br />

1P070<br />

1P009 1P010<br />

<br />

<br />

<br />

<br />

<br />

<br />

3P028<br />

1OEPMII1<br />

3P099<br />

2P121<br />

2OGAMIII1<br />

1P070<br />

3P033<br />

S122 1P026<br />

<br />

1P104<br />

1OFPMII3<br />

3P052<br />

2P013 3P017<br />

<br />

<br />

<br />

<br />

<br />

<br />

<br />

<br />

<br />

<br />

<br />

<br />

<br />

<br />

<br />

3P060<br />

1P038<br />

S231<br />

3P099<br />

2OGAMI4<br />

1P129<br />

1P079<br />

3P053<br />

3P054<br />

1P006<br />

3OIPM5<br />

3OFPMVI3<br />

2P104<br />

1P084<br />

3P060<br />

2P027<br />

2OIAMI1<br />

1P114<br />

1P102 1P109<br />

<br />

<br />

<br />

<br />

<br />

3P035<br />

3P019<br />

2P008<br />

1P023<br />

2P115<br />

S143 S261<br />

2P036 2P038<br />

3P079<br />

2P009 3P045<br />

<br />

<br />

<br />

<br />

1P111<br />

3OGPMVI2<br />

3OIPM6<br />

S72 S73<br />

<br />

<br />

<br />

<br />

<br />

<br />

<br />

<br />

<br />

<br />

<br />

<br />

<br />

S75<br />

3P071<br />

2OHAMIII2<br />

3OEPMVIII1<br />

S81<br />

3P130<br />

S53<br />

2OGAMII2<br />

1P056<br />

S153<br />

3P100<br />

S73<br />

1OEPMII3<br />

1P039


117 201<br />

3P043<br />

1P120<br />

1P097<br />

2P086<br />

W14<br />

2P012<br />

S81<br />

3ODPMI1<br />

1P049 2P082<br />

2OHAMI2<br />

3OHPMIV3<br />

3OIPM2<br />

1P083<br />

1OHPM5<br />

3OEPMVI4<br />

2OFAMV1<br />

2P065<br />

3P119<br />

2P056 2P062<br />

2P075<br />

1P115<br />

2P086<br />

2OIAMIII2<br />

3P118<br />

2P117<br />

3P120<br />

3P051<br />

1P021<br />

2OEAMV2<br />

2OHAMIII1<br />

2P006 3P092<br />

S204<br />

2P045 3P085<br />

3P088 3P089<br />

3P058<br />

3OGPMVI2<br />

3P113<br />

3P018<br />

2OIAMIII1<br />

1P126<br />

3P082<br />

1OIPM6<br />

1P063 1P064<br />

3P082<br />

3OEPMVIII2<br />

S22<br />

2P063<br />

1P033 1P034<br />

3OEPMVI4<br />

2OEAMV1<br />

2P024<br />

<br />

<br />

<br />

1OEPMII2<br />

1OHPM5<br />

1P023<br />

1P027 1P028<br />

<br />

1OIPM6<br />

3P082<br />

1P108 3P018<br />

<br />

<br />

<br />

W12<br />

1OFPMII2<br />

2OEAMIV1<br />

2OEAMIV2<br />

3OIPM1<br />

3P107<br />

3P102<br />

1P061<br />

S202 1P018<br />

<br />

<br />

<br />

<br />

2P031 3P016<br />

2P132<br />

1P098<br />

2P121<br />

1OGPMI1<br />

S95 1P116<br />

<br />

<br />

<br />

<br />

<br />

<br />

<br />

<br />

<br />

<br />

<br />

<br />

2P056 2P062<br />

2P075<br />

1P079<br />

3OEPMVI1<br />

3P049<br />

2P060<br />

S171<br />

S92<br />

1OIPM3<br />

1P113<br />

2OFAMIII3<br />

3OIPM3<br />

1P005<br />

S231<br />

3P055<br />

3P099<br />

3P072<br />

2P013 3P017<br />

3P060<br />

1P069<br />

2OHAMI2<br />

1P106<br />

3P130<br />

2P069<br />

S201<br />

S113<br />

S261 2P038<br />

S261<br />

1P069<br />

<br />

<br />

1P132<br />

1P029<br />

1P081 1P086<br />

<br />

<br />

<br />

<br />

<br />

<br />

<br />

<br />

<br />

<br />

<br />

<br />

<br />

<br />

<br />

<br />

<br />

<br />

<br />

<br />

3P071<br />

3P124<br />

2P080<br />

3OIPMIV3<br />

3P009<br />

2OGAMI2<br />

S162<br />

1P133<br />

W15<br />

2OIAMI3<br />

2OIAMIII3<br />

2OFAMV2<br />

3P119<br />

2OHAMII3<br />

3P022<br />

2OFAMIII2<br />

3OEPMVI4<br />

2P106<br />

2OHAMI1<br />

2OHAMIII3<br />

1P085<br />

3OGPMIV1<br />

3P022<br />

S231<br />

2P059<br />

2P060 3P061<br />

<br />

<br />

<br />

<br />

<br />

<br />

<br />

<br />

<br />

<br />

<br />

<br />

<br />

<br />

<br />

<br />

2P071<br />

3ODPMI3<br />

2P063<br />

2OHAMIII2<br />

1P081<br />

3P123<br />

1P069<br />

2P122<br />

3OEPMVIII3<br />

1P023<br />

3P080<br />

2OIAMI1<br />

3P063<br />

3P091<br />

3ODPMI4<br />

3ODPMII1<br />

2OHAMI1<br />

3P058<br />

1P024 1P025


202<br />

117 <br />

<br />

<br />

<br />

<br />

S36<br />

1P097<br />

S95<br />

S52<br />

3P022 3P030<br />

3P052<br />

3P022 3P030<br />

<br />

<br />

<br />

<br />

<br />

<br />

<br />

<br />

<br />

3P052<br />

3OHPMIV3<br />

1P053<br />

1OGPMII2<br />

2P012<br />

3OFPMVII3<br />

1P078<br />

3P117<br />

2OHAMIII2<br />

1OHPM2<br />

3P019<br />

S141 2P041<br />

1P003 2P003<br />

<br />

<br />

2P046<br />

3P103<br />

3P124<br />

2OHAMIII2<br />

1OGPMI4<br />

3P050<br />

3P110<br />

S91 1P092<br />

<br />

<br />

<br />

<br />

<br />

<br />

<br />

<br />

1P096<br />

3P083<br />

1P064<br />

S245<br />

3P110<br />

1OGPMII2<br />

2OFAMIV1<br />

2OFAMIV2<br />

2OGAMI2<br />

3OEPMVII1<br />

1P054<br />

3P075<br />

3P097<br />

1OEPMII1<br />

1P006<br />

2P087<br />

3P117<br />

S212 2P053<br />

<br />

<br />

2P102<br />

1P050<br />

2OIAMII2<br />

3P076<br />

S223 1P089<br />

<br />

2P130<br />

3P068<br />

S152<br />

3P067<br />

3P098<br />

<br />

<br />

<br />

2P071<br />

3OEPMVI4<br />

1P101<br />

2P030<br />

1P090 2P076<br />

<br />

<br />

<br />

<br />

3P024<br />

3P081<br />

3OGPMIV4<br />

1P087<br />

1P087<br />

S194<br />

3P025<br />

3P109<br />

3P093 3P111<br />

3P112<br />

3P115<br />

2P126 3P132<br />

S162 1P133<br />

<br />

<br />

<br />

<br />

<br />

3OHPMII2<br />

3P063<br />

1P026<br />

1OIPM1<br />

1P100<br />

1P081 1P086<br />

<br />

<br />

<br />

<br />

3P027<br />

1OEPMII3<br />

3P090<br />

3P063<br />

3P053 3P054<br />

3P053 3P054<br />

<br />

<br />

<br />

2OFAMIV3<br />

3OIPMIV1<br />

S161<br />

<br />

2P009 3P045<br />

<br />

<br />

2P123<br />

2OFAMV1<br />

2P065<br />

S223 1P089<br />

<br />

<br />

<br />

2P130<br />

3P068<br />

3OEPMVI4<br />

1P061<br />

S53<br />

3P067<br />

S124 S125<br />

<br />

S163<br />

2OHAMII3<br />

3OIPM3<br />

2P080<br />

3P100<br />

1P093 1P095<br />

1P049 2P082<br />

<br />

3P036<br />

2OIAMII1<br />

2P066<br />

2OIAMII2<br />

S25 S133<br />

3OFPMVII2<br />

2P047 2P048<br />

S242<br />

1P115<br />

1OGPMI4<br />

S234<br />

3OGPMV2<br />

3P106<br />

1P101<br />

S144 1P011<br />

1P120 3P072<br />

1OFPMII1<br />

3P065<br />

2P109 2P118<br />

3OHPMI3<br />

1P041 3P042<br />

1OGPMI4<br />

2P093 3P034<br />

1P097<br />

1P044<br />

2P124<br />

2P111<br />

2P112<br />

3P130<br />

2OEAMIII3<br />

3OHPMIV2<br />

1P077 2P037<br />

3P039 3P040<br />

3P116 3P120<br />

3P121 3P125<br />

3P127<br />

1OGPMI4<br />

1P097<br />

S101 3P015<br />

1P096<br />

3P109<br />

2P123<br />

2P071<br />

1OFPMII3<br />

1P055 3P019<br />

3P022 3P030<br />

3P052<br />

1OGPMII3<br />

3P118<br />

S162 S213<br />

W14 1P133<br />

3P052


117 203<br />

<br />

<br />

<br />

<br />

<br />

S261<br />

1OHPM3<br />

3OHPMII1<br />

3P101<br />

1OIPM5<br />

1OFPMII2<br />

3P085 3P088<br />

3P089<br />

<br />

<br />

<br />

1OHPM1<br />

1P042 1P055<br />

2P088<br />

3P119<br />

2P100 2P101<br />

<br />

<br />

<br />

<br />

3P056<br />

S102<br />

1P051<br />

1P040<br />

2OHAMII2<br />

1P090 2P076<br />

<br />

<br />

<br />

<br />

3P024<br />

3P081<br />

S51<br />

S182<br />

3P025<br />

3P109<br />

1OFPMII2<br />

2OEAMIV1<br />

3P123<br />

1P081 1P086<br />

<br />

<br />

3P123<br />

3OEPMVI1<br />

3P049<br />

S264<br />

1P080 3P092<br />

<br />

<br />

<br />

<br />

<br />

<br />

<br />

3OHPMIV2<br />

1P077<br />

S242<br />

1OGPMI3<br />

2OGAMI3<br />

1P113<br />

3OEPMVI3<br />

1P087<br />

2P090 3P029<br />

<br />

<br />

<br />

<br />

<br />

<br />

<br />

3P062<br />

2OGAMIII1<br />

3P131<br />

2OGAMI2<br />

2P096<br />

1OGPMI4<br />

3P092<br />

3P046<br />

<br />

1P029<br />

2P045 3P085<br />

<br />

<br />

<br />

<br />

<br />

<br />

<br />

<br />

<br />

<br />

<br />

<br />

<br />

<br />

3P088<br />

1P107<br />

S34<br />

S161<br />

3OIPM3<br />

1P005<br />

2OHAMII2<br />

3P089<br />

2OEAMV3<br />

2P029<br />

3P132<br />

3OGPMV1<br />

2P040<br />

2OIAMI2<br />

1P078<br />

S192<br />

- 1P050<br />

<br />

<br />

<br />

1P058<br />

2OEAMV3<br />

2P064<br />

2P030<br />

3P058<br />

1P042 1P055<br />

<br />

<br />

<br />

<br />

<br />

<br />

<br />

<br />

<br />

<br />

<br />

<br />

1OFPMII2<br />

3P032<br />

3OEPMVII2<br />

S231<br />

2P018<br />

1OFPMI4<br />

2OHAMI2<br />

1OEPMII2<br />

2P073<br />

1OHPM7<br />

1OHPM3<br />

S114 3P044<br />

<br />

<br />

S194<br />

1OFPMII3<br />

3P127<br />

S141 1P131<br />

<br />

<br />

3P130<br />

W15<br />

2OIAMI3<br />

2OIAMI4<br />

2OIAMIII3<br />

2P092<br />

1P023<br />

3OGPMIV2<br />

1OFPMII2<br />

1P088 1P131<br />

2OFAMV2<br />

3OIPM5<br />

1P012<br />

2OIAMII2<br />

S194<br />

1OFPMII3<br />

2P094<br />

2OFAMV2<br />

3OHPMI2<br />

2P071<br />

1OEPMII3<br />

1P022<br />

1P105<br />

3P047<br />

1P039<br />

3P047<br />

3OEPMVII3<br />

3P026<br />

1OFPMI3<br />

2P013 3P017<br />

3P060<br />

1OGPMI1<br />

1P012<br />

2P008<br />

1OEPMII3<br />

3OHPMII1<br />

3P101<br />

3P116 3P120<br />

3P121<br />

1OGPMI4<br />

2P133<br />

1P021 1P080<br />

3P092<br />

1OFPMI3<br />

3P123<br />

3OIPMIV3<br />

S242<br />

3P041<br />

1OHPM2<br />

1P013 3P004<br />

S251<br />

2OFAMIII1<br />

1OHPM2<br />

2P126<br />

2OIAMIII1<br />

1P126 2P083


204<br />

117 <br />

<br />

<br />

<br />

<br />

<br />

<br />

<br />

<br />

<br />

3OEPMVII2<br />

1P106<br />

3P036<br />

3P124<br />

1P114<br />

S261<br />

1OEPMI1<br />

2P038<br />

2P012<br />

3P006<br />

1P088<br />

2P042<br />

S162 1P133<br />

<br />

<br />

1OGPMI1<br />

3P062<br />

1P102 1P109<br />

<br />

<br />

<br />

3P035<br />

S53<br />

2P040<br />

3OFPMVIII2<br />

1P077 2P090<br />

3P029<br />

S83 S245<br />

<br />

<br />

<br />

3P057<br />

3P126<br />

3OFPMVIII2<br />

2P062<br />

S223 1P089<br />

<br />

<br />

<br />

<br />

<br />

<br />

<br />

<br />

<br />

<br />

<br />

<br />

<br />

<br />

<br />

<br />

2P130<br />

3P068<br />

3P019<br />

3P058<br />

S244<br />

S53<br />

S242<br />

1OIPM2<br />

1P091<br />

1OGPMI4<br />

2OGAMI4<br />

1P112<br />

2P027<br />

3P051<br />

3P067<br />

1P010<br />

S161<br />

3P090<br />

2OEAMV1<br />

2OEAMV3<br />

2P024<br />

3P094<br />

3P067<br />

3P098<br />

1P095<br />

<br />

<br />

<br />

<br />

<br />

<br />

<br />

<br />

<br />

<br />

<br />

S253<br />

3P034<br />

1P076<br />

S116<br />

S186<br />

1P069<br />

2OFAMIII4<br />

3P004<br />

1P100<br />

2P099<br />

3P005<br />

3P005<br />

1P009 1P010<br />

3P028<br />

3P033<br />

S134 2P008<br />

<br />

<br />

<br />

<br />

<br />

<br />

<br />

<br />

<br />

1P052<br />

S176<br />

1OEPMI4<br />

2OEAMV3<br />

2P058<br />

3OEPMVI4<br />

2P120<br />

1OFPMI2<br />

2P053<br />

3P032<br />

2P084 2P089<br />

<br />

<br />

<br />

1P006<br />

S92<br />

1OIPM3<br />

S263<br />

W14 3P119<br />

<br />

<br />

<br />

<br />

<br />

<br />

<br />

<br />

<br />

3P072<br />

3P041<br />

2P078<br />

2P066<br />

2OIAMII1<br />

3OHPMI2<br />

S84<br />

1P132<br />

1P043<br />

S124 S125<br />

S163<br />

2OHAMII3<br />

3OIPM3<br />

2P080<br />

3P100<br />

S173 S243<br />

<br />

<br />

1P068<br />

1P102<br />

S43<br />

3OFPMVIII1<br />

S261 2P037<br />

2P038 2P042<br />

<br />

<br />

<br />

<br />

<br />

<br />

3P079<br />

2OFAMIV1<br />

2OGAMI2<br />

3ODPMI2<br />

2P057<br />

2P084<br />

3OIPM1<br />

2P089<br />

1P108 2P016<br />

<br />

<br />

3P018<br />

1OHPM3<br />

3OEPMVIII1<br />

<br />

<br />

<br />

<br />

<br />

<br />

<br />

<br />

<br />

<br />

<br />

<br />

<br />

<br />

<br />

<br />

<br />

<br />

<br />

<br />

<br />

<br />

<br />

<br />

<br />

<br />

<br />

<br />

3P072<br />

S101<br />

1P068<br />

1P022<br />

3P002<br />

S261<br />

1OEPMI1<br />

2P037 2P039<br />

3P079<br />

2P038<br />

2OHAMIII2<br />

1OGPMI4<br />

2OEAMV1<br />

2P088<br />

2P121<br />

3P103<br />

1OEPMI2<br />

S63<br />

3P080<br />

1OIPM2<br />

2P031<br />

3P086<br />

2P054<br />

S63<br />

3OEPMVII2<br />

1P067<br />

2P093<br />

2P004<br />

2P051<br />

3OEPMVII3<br />

3OHPMII1<br />

3P101<br />

3P132


117 205<br />

3P022 3P030<br />

- <br />

<br />

3P052<br />

3OEPMVI3<br />

S141<br />

S94 S165<br />

<br />

2P105<br />

S62<br />

S165 2P105<br />

<br />

<br />

W15<br />

2OIAMI3<br />

2OIAMI4<br />

2OIAMIII3<br />

2P092<br />

2OFAMIV3<br />

2P034 2P035<br />

<br />

3P085<br />

1P089 2P045<br />

<br />

<br />

<br />

<br />

<br />

3P088<br />

2P007<br />

2OEAMV3<br />

3P063<br />

2P087<br />

3P089<br />

2P013 3P017<br />

<br />

<br />

<br />

3P060<br />

1P050<br />

2P110<br />

S192<br />

<br />

2P021<br />

1P007 3P041<br />

<br />

<br />

<br />

<br />

<br />

<br />

<br />

<br />

<br />

<br />

<br />

<br />

1P016<br />

3P116<br />

3P015<br />

1P120<br />

2OIAMIII2<br />

2P068<br />

1P119<br />

1OGPMI1<br />

3P090<br />

1P083<br />

S194<br />

1P056<br />

3P048 3P130<br />

<br />

<br />

<br />

1P094<br />

3OEPMVI3<br />

3P088<br />

3P009 3P043<br />

<br />

3P044<br />

3P071<br />

1P090 2P076<br />

<br />

<br />

2P132<br />

3P025<br />

3P109<br />

1OFPMI3<br />

3OIPM5<br />

3P024<br />

3P081<br />

S145 3P079<br />

<br />

3P085<br />

2OIAMI2<br />

3P089<br />

2P127 2P128<br />

<br />

<br />

<br />

<br />

<br />

<br />

<br />

3P020<br />

3OEPMVI3<br />

S172<br />

1OHPM4<br />

2P134<br />

S93<br />

1OIPM5<br />

3P086<br />

1P069<br />

1OIPM6<br />

2P014<br />

3OIPM3<br />

S141 1P129<br />

<br />

<br />

<br />

<br />

<br />

<br />

<br />

<br />

<br />

<br />

<br />

<br />

<br />

<br />

1P131<br />

2P078<br />

2P033<br />

S81<br />

1P132<br />

3P072<br />

S92<br />

3P124<br />

1P039<br />

1P011<br />

3OEPMVI4<br />

3P127<br />

1P122<br />

3OHPMII2<br />

S232<br />

1P092 1P094<br />

<br />

<br />

<br />

<br />

<br />

<br />

<br />

<br />

<br />

3P116<br />

1OEPMI2<br />

3P031<br />

2OFAMV2<br />

1P046<br />

1P069<br />

3P075<br />

3P103<br />

S32<br />

1P130<br />

1P132<br />

1P068<br />

3P046<br />

1P132<br />

3OFPMVI3<br />

1P059 2P104<br />

1OIPM1<br />

2OHAMIII2<br />

1P047<br />

2OFAMV1<br />

2P065<br />

2P078 3P117<br />

1P027 1P028<br />

<br />

1OIPM2<br />

2OHAMIII2<br />

2P122 3P123<br />

S53<br />

1P069<br />

S53<br />

1P046 2P091<br />

3P108<br />

1P023<br />

3OEPMVIII2<br />

1OFPMI1<br />

2OHAMI4<br />

1OHPM7<br />

3P121<br />

3P094<br />

3P115<br />

S184<br />

2OHAMIII3<br />

1P085<br />

1P104<br />

3OHPMIV2<br />

1OFPMI3<br />

3OIPMIV1<br />

2P043<br />

S185<br />

2P126<br />

2OFAMV2<br />

1OIPM5<br />

3P086<br />

S174 S192<br />

1P099<br />

1OGPMI4<br />

S51<br />

3P027<br />

1P060<br />

3P024 3P081<br />

3OIPMIV3<br />

1P125


206<br />

117 <br />

<br />

<br />

1P022<br />

<br />

2P130<br />

<br />

<br />

<br />

<br />

<br />

<br />

<br />

3OEPMVI2<br />

1OGPMI4<br />

2OEAMV2<br />

2OHAMIII1<br />

2P006<br />

1P106<br />

1P105<br />

1OGPMI1<br />

1P086<br />

S95 1P116<br />

2P056<br />

2P075<br />

2P062<br />

3P103 3P110<br />

1P007 3P041<br />

<br />

<br />

<br />

<br />

<br />

<br />

<br />

<br />

<br />

<br />

<br />

<br />

<br />

3P128<br />

3OEPMVI2<br />

1P117<br />

2P128<br />

2P127<br />

3OFPMVI3<br />

1P059 2P104<br />

1OGPMI4<br />

2P123<br />

2OIAMIII2<br />

1OIPM5<br />

3P086<br />

3OGPMV3<br />

3P051<br />

S92<br />

2OEAMIII2<br />

3OFPMVI3<br />

1P059<br />

2P104<br />

1P009 1P010<br />

3P028<br />

3P033<br />

2P109 2P119<br />

2P120<br />

3P129<br />

2P124<br />

1P102 1P109<br />

<br />

<br />

<br />

<br />

3P035<br />

3P116<br />

2P117<br />

1P124<br />

2P008<br />

2P124 3P129<br />

<br />

<br />

S262<br />

3P108<br />

2P084 2P089<br />

1P093 1P095<br />

1P071 2P095<br />

<br />

<br />

<br />

<br />

<br />

<br />

2OIAMII2<br />

2P071<br />

1P021<br />

3OIPM2<br />

1P074<br />

1P049<br />

3P086<br />

2P014<br />

1P015 2P020<br />

<br />

<br />

W11<br />

2OEAMIII1<br />

1P016<br />

3P074<br />

1P107<br />

1P027 1P028<br />

<br />

<br />

<br />

3P041<br />

S62<br />

3ODPMI2<br />

3ODPMI3<br />

3ODPMI4<br />

3ODPMII1<br />

3OEPMVIII2<br />

S141 S155<br />

<br />

<br />

<br />

<br />

<br />

<br />

<br />

<br />

<br />

<br />

<br />

2P041<br />

1OGPMI4<br />

3OGPMV2<br />

1P040<br />

S183<br />

3ODPMI3<br />

1P043<br />

1P115<br />

1P124<br />

2P081<br />

1P083<br />

3P100<br />

3P100<br />

3P106<br />

W14 3P119<br />

<br />

<br />

<br />

<br />

<br />

<br />

<br />

3OGPMIV2<br />

1P115<br />

1P052<br />

2OHAMII2<br />

S115<br />

1P125<br />

1OHPM6<br />

3OHPMII1<br />

3P101<br />

<br />

<br />

<br />

<br />

3P010<br />

3OFPMVI3<br />

1P059 2P104<br />

1P132<br />

2OFAMIII4<br />

2P118 2P119<br />

<br />

<br />

<br />

<br />

1P070<br />

3OGPMIV2<br />

1OEPMI2<br />

3P031<br />

1P069<br />

1P023 1P044<br />

3P062<br />

2P090 3P029<br />

<br />

3P062<br />

S194<br />

1P001 1P038<br />

1P035 3P009<br />

2P100 2P101<br />

<br />

<br />

<br />

<br />

<br />

3P056<br />

1P079<br />

3OGPMV3<br />

3P051<br />

1P124<br />

3P063<br />

S104<br />

2P036 3P079<br />

<br />

<br />

<br />

<br />

<br />

3P114<br />

3P047<br />

3P132<br />

2P079<br />

3OFPMVIII1<br />

1P012 1P029<br />

<br />

3P024<br />

1P012 1P029<br />

<br />

<br />

<br />

<br />

<br />

<br />

<br />

2OIAMI3<br />

2OIAMIII3<br />

1P017<br />

3OEPMVII3<br />

3OIPMIV2<br />

1P003<br />

1P061<br />

3OEPMVII3<br />

1P003 2P003<br />

2P046 3P050<br />

<br />

<br />

<br />

3P103<br />

3P124<br />

2P134<br />

2OFAMIV3<br />

3P110


117 207<br />

<br />

<br />

<br />

3P010<br />

1OFPMII3<br />

1P117 2P127<br />

2P128<br />

1P009 1P010<br />

<br />

<br />

<br />

3P028<br />

1P113<br />

1P056<br />

1OGPMI4<br />

3P033<br />

1P047 1P057<br />

<br />

<br />

<br />

<br />

<br />

<br />

2P041<br />

3OEPMVIII1<br />

2P110<br />

2P092<br />

2OHAMI2<br />

1OFPMII1<br />

2OGAMIII3<br />

2P111 2P124<br />

<br />

<br />

<br />

3P129<br />

1P057<br />

3OGPMIV4<br />

1OGPMI1<br />

3P022 3P030<br />

<br />

<br />

<br />

<br />

<br />

<br />

<br />

3P052<br />

3OFPMVI3<br />

1P059 2P104<br />

3OIPM2<br />

2P027<br />

2P091<br />

S154<br />

3OIPMIV1<br />

3OFPMVII1<br />

2P009 3P045<br />

<br />

<br />

<br />

<br />

<br />

<br />

2P008<br />

3OEPMVII2<br />

1P106<br />

1OGPMI3<br />

2OGAMI3<br />

3OIPMIV1<br />

1P081<br />

3P041<br />

S204<br />

1P059 2P104<br />

<br />

<br />

<br />

<br />

1P111<br />

2P099<br />

1P130<br />

2OEAMIV2<br />

3P107<br />

S21 S251<br />

<br />

<br />

S201<br />

2OEAMIV3<br />

S95 1P116<br />

<br />

<br />

<br />

<br />

<br />

2P056<br />

2P075<br />

1OIPM6<br />

2OIAMII3<br />

3OGPMIV4<br />

2P062<br />

2P076 3P025<br />

<br />

<br />

<br />

<br />

<br />

2P070<br />

2P021<br />

2OIAMIII3<br />

2P092<br />

1P007<br />

S162<br />

1P027 1P028<br />

<br />

<br />

1OGPMII2<br />

2OFAMIV1<br />

2OFAMIV2<br />

2OGAMI2<br />

1P054<br />

1P024 1P025<br />

<br />

3OGPMV3<br />

3P051<br />

S221 3P065<br />

<br />

2P007<br />

2P132 3P024<br />

<br />

3P081<br />

3P131<br />

S23 W16<br />

2OEAMIV3<br />

1P061<br />

2P055<br />

S91 1P092<br />

<br />

<br />

<br />

<br />

<br />

<br />

1P096<br />

3P083<br />

2P087<br />

3OFPMVIII3<br />

1P121<br />

1OFPMII3<br />

3P022<br />

3P052<br />

1P017<br />

3P119<br />

3P096<br />

3P030<br />

1P081 1P086<br />

<br />

1P083<br />

S63<br />

3OEPMVII2<br />

1P067 2P051<br />

1P049 2P082<br />

1OEPMI3<br />

2OFAMIII3<br />

2OFAMIII4<br />

2P017 2P028<br />

2P043 2P107<br />

3P105<br />

1P008<br />

3OEPMVI4<br />

S201<br />

1P071 2P095<br />

1P028


117 209<br />

<br />

<br />

117 <br />

<br />

2012 2 22 <br />

<br />

<br />

<br />

<br />

<br />

<br />

<br />

EM <br />

<br />

<br />

<br />

<br />

<br />

<br />

<br />

<br />

<br />

<br />

<br />

<br />

<br />

<br />

<br />

<br />

<br />

<br />

<br />

22 <br />

<br />

<br />

<br />

<br />

<br />

<br />

<br />

<br />

<br />

<br />

50


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