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Carol Milligan, Sherry Vinsant, Carol Mansfield, Masaaki Yoshikawa, Ramon Moreno, David Prevette,<br />
Ronald OppenheimDepartment of Neurobiology and Anatomy, and the ALS Center, Wake Forest School of Medicine,<br />
WinstonSalem, NC 27157, US<br />
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Hiroshi KiyamaDept. Functional Anatomy & Neurosci., Nagoya Univ. Grad. Sch. Med.<br />
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1 Dept. Physiol. Cell Biol., Tokyo Med. Dent. Univ., 2 Dept. Protein Biochem., Inst. Life Sci., Kurume Univ.<br />
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1 2 <br />
<br />
1 2 1 2 <br />
<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 />
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3P080 <br />
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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 />
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3P096 <br />
3P097 Fossa <br />
3P098 <br />
3P099 <br />
3P100 Thiel <br />
3P101
58<br />
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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 />
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3P119 2 <br />
3P120 1 <br />
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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
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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.
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1981 1983 NIHFogarty International Fellow, NINCDS<br />
QFDE1984 1992 <br />
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1992 <br />
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Virchows Arch., 427:5195271996<br />
Biomed. Rev., 15: 1192004<br />
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J. Electron Microsc., 59:<br />
395408201021 <br />
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117 65<br />
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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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Rab GTP <br />
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evectin2 evectin2 <br />
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REs evectin2 PH domain <br />
in vitro phosphoinositides <br />
phosphatidylserine PS <br />
PS in vivo evectin2 PH<br />
domain PS PS <br />
lactadherin C2 domain <br />
REs PS <br />
REs <br />
PS evectin2 <br />
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117 67<br />
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Nature Cell Biol 2006; EMBO J 2003<br />
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Nature Methods , 227<br />
230, 2007<br />
<br />
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PNAS , 1347513480, 2009<br />
<br />
PLoS ONE , e21531, 2011<br />
<br />
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S<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 />
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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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Huh7 <br />
UBXD2UBXD8p97 <br />
UBXD2 UBXD8 p97 <br />
UBXD8 ApoB <br />
UBXD8 knockdown ApoBcrescent <br />
ApoB UBXD8/p97 <br />
UBXD8 <br />
Derlin1 <br />
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Derlin1 knockdown UBXD8 ApoB <br />
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ApoB Derlin1/UBXD8/p97 <br />
<br />
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DGKζ <br />
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DGKζ <br />
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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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2010 Science<br />
in vivo<br />
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II<br />
III<br />
shh <br />
AME <br />
AME <br />
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AME <br />
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AME <br />
AME <br />
AME <br />
shh <br />
AME Gli3<br />
shh K.O. GnRH <br />
LHβ <br />
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AME <br />
S<br />
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5 <br />
FS <br />
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ECMECM<br />
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ECM <br />
living ECM <br />
ECM FS <br />
<br />
ECM <br />
FS <br />
ECM <br />
<br />
S<br />
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1 2 3 2 <br />
1<br />
1<br />
2 <br />
3 <br />
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LH/FSH <br />
<br />
<br />
GnRH Leuprorelin <br />
LH/FSH <br />
<br />
<br />
<br />
GnRH <br />
<br />
<br />
Leuprorelin <br />
LH/FSH <br />
<br />
<br />
LH/FSH leuprorelin
72<br />
117 <br />
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5 <br />
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GH<br />
<br />
<br />
GH <br />
mRNA GH GHRH<br />
mRNA GHRH <br />
GH <br />
GHRH <br />
GH <br />
<br />
GHRH <br />
<br />
S<br />
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3D 3DTV<br />
2D <br />
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2D <br />
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2007 <br />
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3D <br />
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3D <br />
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3D <br />
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3D 3D <br />
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TV <br />
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3D <br />
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S<br />
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X <br />
AFM <br />
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STORMDSLM <br />
X CTMRI <br />
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3D <br />
3D 3D <br />
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S<br />
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VEGF <br />
Flk1 VEGFR2Flt1 VEGFR1 <br />
ES Flk1<br />
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<br />
Flk1 Flk1Cre BAC <br />
<br />
8 <br />
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Flk1 <br />
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180 <br />
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Tie1:H2B::EYFP <br />
EYFP <br />
Sato et al., PloS One, 2010<br />
<br />
<br />
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Tie1:H2B::YFP <br />
<br />
2
74<br />
117 <br />
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Evans <br />
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Danio rerio<br />
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PICA <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 />
CT <br />
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CT <br />
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23 4 <br />
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<br />
CT <br />
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CT <br />
3 <br />
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117 75<br />
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2 2<br />
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PACS <br />
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5 8 12 4<br />
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CT <br />
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2 <br />
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CT <br />
CT <br />
CT <br />
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CTComputed Tomography<br />
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CT <br />
<br />
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CT <br />
CT <br />
CT <br />
<br />
CT <br />
<br />
CT <br />
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CT <br />
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21 23 <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 />
<br />
<br />
<br />
<br />
<br />
<br />
<br />
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<br />
<br />
in vivo Multiunit nueral<br />
activityin vivo MUA <br />
<br />
Clock MUA <br />
-<br />
<br />
S<br />
<br />
<br />
<br />
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1 <br />
<br />
<br />
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<br />
1997 <br />
<br />
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<br />
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<br />
<br />
<br />
1988 <br />
<br />
<br />
<br />
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S<br />
<br />
<br />
1,2<br />
1<br />
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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<br />
GSK3β<br />
glycogen synthase kinase 3β<br />
GSK3β <br />
REVERBαBmaL1 <br />
<br />
<br />
Polg DNA <br />
<br />
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S<br />
<br />
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II<br />
<br />
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19 <br />
1950 <br />
<br />
1980 <br />
cytochrome C oxidase <br />
targeting signal <br />
<br />
<br />
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21 <br />
<br />
<br />
S<br />
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1,2 1 2<br />
1<br />
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<br />
Cyanidioschyzon merolae<br />
12 μm <br />
<br />
100% <br />
<br />
MD/PD <br />
ER <br />
<br />
<br />
VIG1 <br />
<br />
<br />
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<br />
S<br />
<br />
<br />
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<br />
mtDNA <br />
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 />
S<br />
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1,2<br />
1<br />
II 2 <br />
<br />
ATP <br />
<br />
<br />
CoA TCA ATP<br />
β <br />
CoA 2 <br />
β <br />
20 1950-70 <br />
70 <br />
β 90<br />
β <br />
2 β <br />
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2 β 2 <br />
<br />
ATP <br />
<br />
β <br />
<br />
β <br />
<br />
S<br />
<br />
<br />
<br />
TCA β <br />
<br />
β <br />
<br />
<br />
GC/MS <br />
ESIMS/MS<br />
<br />
<br />
<br />
<br />
β <br />
in vitro probe assay β <br />
<br />
<br />
<br />
β <br />
β <br />
β <br />
<br />
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<br />
S<br />
<br />
<br />
<br />
II<br />
β<br />
<br />
β <br />
<br />
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PAG <br />
DNA <br />
<br />
β Leydig <br />
<br />
Sertoli <br />
<br />
<br />
β <br />
1/10 <br />
<br />
Sertoli β <br />
<br />
Sertoli <br />
Sertoli <br />
<br />
Fukasawa M et al. J Histochem Cytochem 58: 195–206,<br />
2010<br />
S<br />
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<br />
<br />
II<br />
<br />
glucoseonly dogma<br />
β <br />
dogma <br />
<br />
Müller <br />
PAG <br />
<br />
DNA <br />
<br />
β Müller <br />
<br />
β <br />
<br />
1/10 Müller 1/2 <br />
4 Müller 3 <br />
β <br />
Müller <br />
<br />
β <br />
<br />
Atsuzawa K et al. Histochem Cell Biol 134: 565–579,<br />
2010
117 79<br />
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niche<br />
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Angiopoietin1 Thrombopoietin <br />
<br />
<br />
ATM <br />
ROS p38MAPK <br />
<br />
ROS<br />
<br />
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HIF1α VHL <br />
<br />
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S<br />
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GFAP <br />
GFAPGFP GFAPCre <br />
<br />
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GFAP <br />
GFAP / <br />
<br />
S<br />
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MSCs<br />
<br />
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MSCs <br />
<br />
MSCs <br />
<br />
MSCs<br />
hMSCs<br />
PACAP <br />
hMSCs 10 <br />
PACAP <br />
PACAP <br />
hMSCs <br />
PACAP hMSCs<br />
PACAP hMSCs <br />
<br />
S<br />
<br />
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2<br />
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GFP <br />
GFP <br />
C57BL/6 5 <br />
<br />
<br />
mRNA CCR2 high /<br />
CX 3 CR1 low /CXCR4 high CCR2 <br />
/ CX 3 CR1 high /CXCR4 low <br />
MCP1 SDF1 <br />
GFP + /CXCR4 high β 3
80<br />
S<br />
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2 <br />
117 <br />
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proinsulin TNFα <br />
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In vivo <br />
in vitro <br />
<br />
Y Y <br />
TNFα <br />
<br />
<br />
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<br />
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polycomb group repressor complex PcG <br />
<br />
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S<br />
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<br />
bHLH Hes1 <br />
Hes1 <br />
Neurogenin2 Ngn2 <br />
Ngn2 <br />
Ngn2 <br />
<br />
<br />
Ngn2 <br />
Ngn2 <br />
Ngn2 <br />
Ngn2 <br />
Ngn2 <br />
Ngn2 <br />
Ngn2 <br />
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Ngn2 <br />
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S<br />
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6 <br />
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117 81<br />
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GABA<br />
<br />
<br />
GABA <br />
Cl KCC2ClNKCC1Cl <br />
NKCC1 Cl [Cl]i<br />
<br />
<br />
<br />
<br />
GABA <br />
GABA <br />
<br />
GABA <br />
<br />
GABAa Ca2+ <br />
<br />
GABA NKCC1 [Cl]i<br />
GABA <br />
KCC2 GABA <br />
<br />
Cl GABA <br />
<br />
GABA <br />
GABAa <br />
<br />
S<br />
Ai <br />
<br />
1 2 2 1 1 <br />
2 2 1<br />
1<br />
2 <br />
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1 23 6 <br />
Ai <br />
X CT Autopsy Imaging<br />
Ai <br />
3 <br />
3D <br />
<br />
ipad<br />
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OB <br />
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117 <br />
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Mes5 <br />
<br />
<br />
Mes5 <br />
brain<br />
derived neurotrophic factor BDNF<br />
dystonin Brn3a Mes5<br />
<br />
3 <br />
Mes5 <br />
BDNF Mes5 <br />
<br />
dystonin <br />
Mes5 wild<br />
type Brn3a <br />
<br />
<br />
Brn3a <br />
Mes5 <br />
<br />
BDNF Brn3a <br />
S
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 />
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Vmo<br />
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BDA<br />
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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 />
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1,2<br />
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MSCs <br />
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MSCs ES<br />
MSCs <br />
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Differentiation 2011ES MSCs<br />
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ES MSCs <br />
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24 ES MSCs <br />
<br />
CatWalkNoldus <br />
ES MSCs <br />
MSCs <br />
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1<br />
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iPS <br />
Muse PDGFRα <br />
<br />
SEM BFI<br />
FIB/SEM <br />
BFI <br />
SEM <br />
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FIB/SEM SEM <br />
FIB BFI <br />
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Mesenchymal stem cell, MSC<br />
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MSC DSS <br />
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MSC <br />
MSC <br />
MSC <br />
conditioned medium, MSCCM<br />
DSS <br />
IEC6 <br />
MALDITOFMS MSCCM <br />
MSCCM DSS <br />
IEC6 PI3KAkt <br />
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T MSCCM<br />
VEGF, IL13, TIMP <br />
<br />
MSC gut trophic factor <br />
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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 />
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fibroblastlike<br />
cells PDGF α SK3 <br />
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α CD34 PDGF α <br />
NG2 <br />
ATP P
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PBL <br />
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Cadaver Seminar <br />
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2 <br />
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2 CREST,JST 3 <br />
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CEMOVISCryoElectron Microscopy of Vitreous<br />
Sections<br />
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CEMOVIS <br />
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<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 />
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stathmin <br />
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2 1,2,3<br />
1<br />
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2 3 <br />
4 <br />
5 <br />
<br />
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PACAP <br />
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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 />
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PACAP stathmin1 axon<br />
abnormal arborization <br />
<br />
stathmin1 adult neurogenesis <br />
stathmin1
117 89<br />
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C <br />
1 1 2<br />
1<br />
2 <br />
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1 <br />
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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 />
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5HT 2C R RNA <br />
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S<br />
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1<br />
2 <br />
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G GPCR <br />
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GALP <br />
NPW <br />
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kisspeptin <br />
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puberty<br />
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GPR54 kisspeptin <br />
kisspeptin GnRH <br />
<br />
HPG<br />
axis kisspeptin kisspeptinHPG axis<br />
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Kisspeptin<br />
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Kisspeptin <br />
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ER <br />
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ERERαERβ<br />
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ER <br />
2 ER <br />
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S<br />
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<br />
Fumiyo Aoyama, Nobuyasu Takahashi, Soyuki Ide,<br />
Akira Sawaguchi<br />
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2 <br />
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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 />
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FIBSEM <br />
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Palade
117 91<br />
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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 />
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S<br />
CEACAM<br />
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mRNA Differential Display<br />
5 Ceacam6 <br />
Ceacam6 isoform, Ceacam6L <br />
<br />
CEACAM6L <br />
<br />
apical Ectoplasmic Specialization <br />
<br />
CEACAM6L CEACAM6L<br />
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CEACAM6L <br />
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CEACAM CEACAM2 <br />
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S<br />
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3 <br />
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Cell adhesion molecule1 Cadm1 <br />
Poliovirus receptor Pvr <br />
Nectin3 Nectin2 <br />
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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 />
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1 2<br />
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2 <br />
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Sabin 1902<br />
<br />
Huntington 1908<br />
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<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 />
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99mTcphytat <br />
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MRI MRM <br />
MRCP <br />
Magnetic<br />
ResonanceThoracic Ductography MRTD <br />
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MRTD <br />
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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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Aspp1 <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 />
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shear stress<br />
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Huntington <br />
Kampmeier
117 95<br />
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S<br />
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axon initial segment, AIS Na <br />
<br />
AIS <br />
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nucleus magnocellularis, NMAIS <br />
<br />
NM <br />
NM <br />
AIS <br />
NM <br />
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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 />
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WG <br />
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MDPhD <br />
<br />
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3 MD<br />
PhD <br />
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W<br />
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1 1,2<br />
1<br />
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2 <br />
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4 <br />
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2006 <br />
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17 30 <br />
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4 <br />
2010 2 <br />
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1 2<br />
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14 PhDMD <br />
20 MD <br />
23 <br />
<br />
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MD <br />
<br />
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W<br />
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1 2 2 3 <br />
1 1 1<br />
1<br />
2 M2 3 M4 <br />
<br />
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1
98<br />
117 <br />
W<br />
<br />
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<br />
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<br />
CBT <br />
<br />
<br />
<br />
<br />
<br />
<br />
<br />
<br />
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W<br />
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23 MDPhD <br />
2-4 <br />
3 <br />
1 <br />
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19 <br />
<br />
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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 />
<br />
<br />
<br />
<br />
<br />
Spock3
117 125<br />
P<br />
<br />
γ <br />
<br />
<br />
<br />
<br />
<br />
<br />
4,52 PIP2 <br />
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 />
<br />
P<br />
<br />
1,2 1,2,3<br />
1<br />
2 <br />
3 <br />
<br />
<br />
<br />
<br />
<br />
<br />
<br />
<br />
<br />
<br />
<br />
<br />
<br />
<br />
<br />
DNA <br />
<br />
in situ hybridization <br />
<br />
P<br />
<br />
1,2 1,3 1 1,2 1,2 <br />
1,2 1,4 1,2,3<br />
1<br />
2 3 <br />
4 <br />
V<br />
<br />
<br />
<br />
DiI <br />
<br />
<br />
<br />
<br />
<br />
<br />
<br />
<br />
<br />
RTPCR in situ<br />
hybridization <br />
<br />
P<br />
<br />
<br />
<br />
<br />
<br />
<br />
<br />
<br />
<br />
<br />
<br />
<br />
<br />
<br />
<br />
DNA cDNA <br />
<br />
<br />
P<br />
<br />
<br />
<br />
<br />
<br />
<br />
<br />
hPAP <br />
<br />
LS2 <br />
2 <br />
<br />
II-III <br />
<br />
LS2 <br />
hPAP T1 <br />
hPAP <br />
LS2 ephrinA2<br />
Sema3F<br />
<br />
<br />
P<br />
W NPW <br />
<br />
1 1 2 1<br />
1<br />
2 <br />
W G <br />
NPW <br />
<br />
<br />
NPW Y<br />
<br />
NPW <br />
DIO <br />
NPW <br />
NPW <br />
cFos NPW <br />
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 />
2 3 <br />
4 <br />
<br />
<br />
<br />
<br />
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 />
<br />
<br />
cFos<br />
<br />
<br />
P<br />
<br />
1 1 1 2 1<br />
1<br />
2 <br />
<br />
<br />
<br />
<br />
<br />
<br />
<br />
<br />
GFP <br />
E14 <br />
GFP 24h <br />
Tbr2 <br />
<br />
<br />
Tbr2 <br />
radial glia <br />
<br />
P<br />
<br />
<br />
<br />
<br />
<br />
<br />
<br />
<br />
<br />
SD <br />
2-20 6 / <br />
5HT <br />
5HT <br />
Egr1 <br />
<br />
<br />
Egr1 <br />
21<br />
<br />
<br />
<br />
<br />
<br />
P<br />
/ <br />
<br />
<br />
<br />
<br />
<br />
<br />
<br />
<br />
Wistar 1015 3 <br />
/ IGF1/IGF1R BDNF/TrkB <br />
1620 30 60 <br />
<br />
<br />
<br />
/ <br />
<br />
P<br />
n <br />
<br />
<br />
<br />
<br />
1 <br />
<br />
<br />
n3 <br />
<br />
21 <br />
<br />
<br />
<br />
<br />
<br />
<br />
<br />
<br />
<br />
<br />
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 />
<br />
<br />
P<br />
<br />
<br />
<br />
<br />
GnRH <br />
<br />
<br />
GnRH <br />
<br />
<br />
21<br />
30 42 60 Wistar Rat GFAP <br />
GFAP <br />
<br />
GFAP 21 <br />
30 <br />
GFAP <br />
<br />
GFAP <br />
<br />
GnRH <br />
<br />
<br />
P<br />
<br />
<br />
<br />
<br />
<br />
GiPAG<br />
<br />
<br />
<br />
<br />
Gi PAG <br />
<br />
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 />
TGFβ <br />
<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 />
<br />
<br />
<br />
<br />
<br />
1980 <br />
<br />
GABA<br />
<br />
barrel <br />
<br />
<br />
<br />
<br />
<br />
<br />
<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 />
<br />
<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 />
<br />
Zitter attractin <br />
<br />
<br />
Zitter <br />
<br />
<br />
<br />
<br />
Zitter <br />
<br />
<br />
<br />
2 <br />
<br />
<br />
<br />
<br />
<br />
P<br />
<br />
1 2 2,3 4 4 2<br />
1<br />
2 3 <br />
4 <br />
<br />
<br />
Marchi Nauta<br />
<br />
<br />
Weigert Luxol<br />
fast blue<br />
<br />
<br />
20 5 <br />
Goto 1987 LPH <br />
<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 />
<br />
1 1 2 1<br />
1<br />
2 <br />
<br />
<br />
Holmes <br />
<br />
PTAH<br />
<br />
<br />
<br />
<br />
ddY 20 g<br />
6 μm<br />
PTAH<br />
<br />
<br />
PTAH <br />
<br />
<br />
<br />
Holmes <br />
<br />
P<br />
<br />
1,2 1,3 2 1<br />
1<br />
2 3 <br />
<br />
<br />
<br />
91 <br />
<br />
celloidin Kultschitzky <br />
<br />
<br />
90 1 1 <br />
celloidin <br />
<br />
<br />
2 <br />
<br />
P<br />
Eusthenopteron foodi<br />
<br />
1 2 3 4<br />
1<br />
2 3 <br />
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 />
<br />
<br />
<br />
<br />
<br />
<br />
<br />
<br />
<br />
<br />
<br />
Palaeoniscus <br />
<br />
3 <br />
Palaeoniscus <br />
<br />
<br />
<br />
<br />
P<br />
<br />
<br />
<br />
<br />
<br />
<br />
<br />
<br />
<br />
11 <br />
14 4 <br />
<br />
11 12 <br />
14 <br />
<br />
12 <br />
14 <br />
13 <br />
14
117 131<br />
P<br />
NOS <br />
1 2 4 4 4 <br />
3 4<br />
1<br />
2 <br />
3<br />
4 <br />
NO <br />
<br />
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 />
<br />
1 1,2 1 1 1 <br />
1<br />
1<br />
2 <br />
1AQP1<br />
<br />
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 />
Muse
132<br />
117 <br />
P<br />
PACAP VIP <br />
PACAP VIP <br />
1 2 2 1<br />
1<br />
2 1 <br />
<br />
PACAP <br />
<br />
VIP <br />
PACAP <br />
8 C57BL/6 <br />
PACAP PAC1R VIP <br />
VPAC1 PAC1R <br />
pillar<br />
cell <br />
VPAC1 <br />
pillar cell <br />
PAC1R<br />
VPAC1 <br />
PACAP VIP <br />
<br />
<br />
<br />
P<br />
<br />
<br />
1,2 2 2 1 2 <br />
2<br />
1<br />
2 <br />
5 AQP5 <br />
AQP5 <br />
AQP5 <br />
AQP5 <br />
<br />
9 Wistar <br />
AQP5 <br />
3 AQP5<br />
<br />
<br />
<br />
AQP5 <br />
<br />
AQP5 <br />
<br />
P<br />
gustducin <br />
<br />
2 <br />
116 <br />
gustducin G <br />
NSE <br />
<br />
<br />
4 Hartley 4%PFA <br />
<br />
calbindin gustducin <br />
ABC gustducin <br />
TEM<br />
0.5-1 μm <br />
ABC gustducin <br />
<br />
gustducin calbindin TEM <br />
<br />
<br />
gustducin <br />
<br />
P<br />
<br />
<br />
<br />
<br />
<br />
ZnT <br />
<br />
ZnT7 ZnT5<br />
ZnT2 ZnT5 Se Zn <br />
<br />
<br />
ZnSO45 mg/100 g ZnT <br />
<br />
<br />
<br />
H1250M<br />
<br />
<br />
<br />
<br />
<br />
P<br />
<br />
1 1 1 2 1 <br />
2 1<br />
1<br />
2 <br />
P<br />
APC Min/+ <br />
<br />
1 1 1 2<br />
1<br />
2 <br />
HSC <br />
<br />
E HSC <br />
δ<br />
HSC <br />
HSCT6 δ<br />
HepG2 <br />
α<br />
HepG2 <br />
<br />
4 δ<br />
FACS TUNEL δ<br />
HSC <br />
<br />
δ<br />
β1 <br />
<br />
<br />
APC Min/+ <br />
<br />
Interstitial cells of<br />
Cajal; ICCICC <br />
<br />
<br />
ICC <br />
7 APC Min/+ <br />
ICC <br />
ICCMPICCDMP<br />
cKit <br />
cKit ICCMP <br />
ICC <br />
<br />
<br />
ICC ICC
117 133<br />
P<br />
DPEP <br />
1 2 2 1 2<br />
1<br />
2 <br />
Dipeptidase1 DPEP1 dipeptideglutathioneleukotrieneD4 <br />
<br />
GPI <br />
DPEP1 <br />
HCC56 <br />
<br />
caveolin1 flotillin1 <br />
GPI CD59 <br />
<br />
DPEP1 <br />
GPI <br />
<br />
<br />
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 />
1 1,2 3 1<br />
1<br />
2 3 <br />
<br />
microRNA miRNA 22 RNA<br />
<br />
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 />
BeWoJEG3 C19MC HTR8/SVneo<br />
BeWo, JEG3 C19MC <br />
HTR8/SVneo <br />
<br />
P<br />
IgG IIb Fc <br />
FcRIIb<br />
1 2 1 3 1<br />
1<br />
2 3 <br />
<br />
HPEC <br />
IgG <br />
HPEC IIb Fc <br />
FcRIIb IgG <br />
J Immunol 175: 2331, 2005<br />
FcRIIb RAB GTPasesRAB1B RAB3D<br />
FcRIIb in vitro FcRIIb<br />
GFP FcRIIb <br />
pFCGR2B-GFP HUVEC<br />
FcRIIb RAB1BRAB3D siRNA <br />
FcRIIbsiRAB1B<br />
siRAB3D HUVEC pFCGR2B-GFP <br />
GFPFcRIIb GFPFcRIIb <br />
HUVEC siRNA GFPFcRIIb <br />
GFPFcRIIbHPEC <br />
RAB1B RAB3D FcRIIb <br />
<br />
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 />
P<br />
<br />
<br />
<br />
<br />
<br />
CD34 <br />
CD141 <br />
<br />
<br />
<br />
5 μm CD34 CD141 DAB <br />
CCD <br />
<br />
<br />
<br />
CD34 <br />
CD141 <br />
CD34 <br />
<br />
<br />
CD34
134<br />
117 <br />
P<br />
<br />
<br />
1 1 2 2 1<br />
1<br />
2 <br />
<br />
<br />
<br />
<br />
<br />
<br />
<br />
42.3<br />
M 1 μm <br />
<br />
<br />
10.1<br />
48 <br />
<br />
<br />
<br />
1 1 <br />
GTH <br />
<br />
P<br />
TG <br />
1 2 2 1 1 2<br />
1<br />
2 <br />
<br />
TG tdTomato <br />
tdTomato<br />
<br />
in vivo <br />
<br />
4%PFA <br />
10 μm filmtransfer <br />
<br />
<br />
<br />
<br />
<br />
<br />
<br />
<br />
<br />
P<br />
<br />
1 2 1 1 1 <br />
1 1 1 1 3 2 <br />
1 1<br />
1<br />
2 <br />
3 <br />
<br />
X CTMRI <br />
CT <br />
1 <br />
90 <br />
CT <br />
<br />
<br />
<br />
<br />
<br />
<br />
<br />
<br />
<br />
<br />
<br />
P<br />
<br />
Dolgorsuren AldartsogtShineOd Dalkhsuren<br />
<br />
<br />
<br />
<br />
<br />
<br />
31 49 <br />
3 <br />
<br />
HE <br />
21 <br />
26 2 <br />
<br />
21 5<br />
16 26 <br />
13 13 <br />
<br />
<br />
<br />
<br />
<br />
<br />
P<br />
<br />
1 1 1 1 2 <br />
1<br />
1<br />
2 <br />
<br />
<br />
Nikolai and Bramble, 1983<br />
<br />
2 <br />
Dipodomys merriami <br />
Jaculus orientalis <br />
Rattus rattus Satoh and Iwaku,<br />
2008<br />
<br />
13<br />
<br />
<br />
<br />
2 <br />
<br />
<br />
P<br />
<br />
1 1,2 1<br />
1<br />
2 <br />
2 <br />
<br />
<br />
80 <br />
<br />
<br />
<br />
<br />
12 Wistar 1
117 135<br />
P<br />
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 />
P<br />
<br />
1 3 2 2 2 <br />
2<br />
1<br />
2 3 <br />
<br />
<br />
<br />
<br />
<br />
<br />
<br />
<br />
<br />
<br />
<br />
<br />
<br />
<br />
<br />
P<br />
<br />
P<br />
<br />
<br />
<br />
<br />
<br />
<br />
<br />
<br />
<br />
<br />
<br />
<br />
<br />
<br />
nerve point <br />
<br />
23 cm <br />
Erb’s point <br />
P<br />
<br />
1 2 3 2 2<br />
1<br />
2 3 <br />
<br />
<br />
31 <br />
<br />
<br />
<br />
<br />
<br />
<br />
<br />
<br />
<br />
<br />
<br />
<br />
<br />
<br />
<br />
P<br />
<br />
1 2 3 4 5 5 <br />
5<br />
1<br />
2 3 <br />
4 5 <br />
<br />
2010 8 4 <br />
82 <br />
<br />
5 cm 1 cm<br />
5 mm 1<br />
2C7C8 3C7 <br />
4 1 <br />
13C7 <br />
4 2 <br />
<br />
3 <br />
2 <br />
<br />
<br />
C6 1/3
136<br />
117 <br />
P<br />
<br />
1 2 2<br />
1<br />
2 <br />
3 1 C3T1<br />
201121:1<br />
<br />
<br />
<br />
C36C47<br />
C6T1 C57<br />
C5,6 C35C58<br />
<br />
M. coracohumeralis C5,6 <br />
<br />
M. coraco<br />
humeralis <br />
<br />
<br />
<br />
<br />
<br />
P<br />
<br />
1 2 2 3 4 <br />
4 4<br />
1<br />
2 3 4 <br />
<br />
<br />
<br />
<br />
20 50 25 15 10 <br />
2 cm <br />
100<br />
Prick painDull pain<br />
100<br />
25 <br />
<br />
<br />
<br />
<br />
<br />
<br />
<br />
<br />
<br />
P<br />
<br />
<br />
1,2 2 3 2 4 1 <br />
1 1<br />
1<br />
2 3 <br />
4 <br />
<br />
<br />
<br />
MP MP<br />
13 26 <br />
21 12 16 <br />
MP <br />
MP <br />
<br />
MP <br />
<br />
<br />
MP Levene 2 <br />
MP <br />
MP MP <br />
<br />
MP MP <br />
<br />
P<br />
<br />
<br />
<br />
<br />
<br />
<br />
<br />
<br />
22 <br />
582 1088 567 1125 <br />
<br />
723 584 <br />
584 <br />
440 118 <br />
26 <br />
139 74 <br />
64 <br />
<br />
<br />
<br />
<br />
<br />
P<br />
<br />
1 1 2 1 1 1 <br />
1<br />
1<br />
2 <br />
<br />
2011 <br />
<br />
84 <br />
<br />
<br />
<br />
2 <br />
<br />
<br />
6 <br />
<br />
<br />
<br />
<br />
<br />
Adachi G <br />
P<br />
<br />
1,2 2 2<br />
1<br />
2 <br />
<br />
6 7 <br />
7 <br />
SS 3 SS+BS <br />
2 N 2 1<br />
SpsCs<br />
SS SS+BS N Sps <br />
2 Cs SS 1<br />
SS+BS 2 Sps 3<br />
SpsCsTd 3 RmA<br />
RmS RmBN <br />
RmA RmS Td SS <br />
RmS SS+BS RmS Sps<br />
RmB 2 <br />
Sps Cs <br />
<br />
SS SS+Bs Sps Cs
117 137<br />
P<br />
<br />
<br />
<br />
2010 77 <br />
<br />
<br />
2 <br />
<br />
<br />
<br />
1<br />
<br />
<br />
2<br />
3<br />
<br />
4<br />
<br />
5<br />
<br />
P<br />
<br />
1 1,2 3 1 1 3<br />
1<br />
2 <br />
3 <br />
<br />
<br />
<br />
<br />
2006 <br />
<br />
<br />
<br />
2010 37 <br />
21.6837 <br />
<br />
<br />
5.4237<br />
<br />
<br />
2011 <br />
<br />
P<br />
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 />
P<br />
<br />
<br />
I<br />
G L H<br />
M 3 TC <br />
<br />
4 G, L, H, M <br />
4 <br />
1. TC H HA 2. <br />
AA HA 3. TC M HA<br />
4. M H HA 5. M H HA <br />
6. TC M AA <br />
H <br />
M 5 <br />
<br />
<br />
TC<br />
<br />
<br />
P<br />
<br />
1 1 1 1 1 2 <br />
1<br />
1<br />
2 <br />
30 2<br />
3 4 20 21<br />
<br />
7 8 <br />
1 1 1 85 <br />
5 3 <br />
hilar artery<br />
1 2 <br />
78 4 4 1 <br />
<br />
2 2 3 2 <br />
hilar artery 2 1 <br />
polar artery<br />
hilar artery polar artery <br />
<br />
rete arteriosum Felix<br />
<br />
P<br />
<br />
1 1 1 2 1<br />
1<br />
2 <br />
<br />
<br />
90 <br />
30 510<br />
mm
138<br />
117 <br />
P<br />
<br />
<br />
<br />
<br />
<br />
622 366 <br />
453 <br />
<br />
77.8%35/45<br />
71.2%37/52 70.3%71/101 87.7%71/81<br />
83.8%57/68 84.2%16/19<br />
89.5%51/57 94.3%66/70 85.3%<br />
145/170 95.8%68/71 93.5%58/62 91.3%<br />
21/23Fisher <br />
5% p=0.046<br />
<br />
<br />
<br />
<br />
P<br />
<br />
1 1 1 2 3 <br />
3 3 3<br />
1<br />
2 <br />
3 <br />
<br />
<br />
<br />
<br />
<br />
2,000 <br />
<br />
<br />
<br />
<br />
<br />
<br />
<br />
<br />
<br />
<br />
<br />
P<br />
<br />
1 2 3 4 5 <br />
6<br />
1<br />
2 <br />
3<br />
4 5 <br />
6 <br />
<br />
40 <br />
<br />
<br />
<br />
<br />
<br />
P<br />
LEH<br />
1 1 2 3 1<br />
1<br />
2 <br />
3<br />
<br />
<br />
<br />
1710 <br />
<br />
<br />
<br />
<br />
LEH<br />
LEH<br />
<br />
<br />
<br />
<br />
<br />
<br />
<br />
<br />
<br />
P<br />
<br />
1 2 1<br />
1<br />
2 <br />
<br />
Phenice <br />
<br />
Bruzek Murail <br />
Phenice Bruzek <br />
<br />
<br />
Phenice <br />
90Bruzek 9294Murail 7580Bruzek<br />
<br />
8994 8694<br />
PheniceBruzekMurail <br />
<br />
P<br />
<br />
<br />
1 1 1 1 2 <br />
3 4 5<br />
1<br />
2 3 <br />
4 5 <br />
<br />
205 83 <br />
35 <br />
<br />
P0.05 <br />
2 <br />
<br />
45.6% 40.3%<br />
12.9% 14.9% 1.2% 2.3%<br />
15 <br />
17 Smith <br />
<br />
<br />
<br />
<br />
Smith
117 139<br />
P<br />
Nacholapithecus kerioi <br />
<br />
1 2 3 3 4 5 <br />
6 4 7<br />
1<br />
2 3 4 <br />
5 6 7 <br />
Nacholapithecus kerioi 1500 <br />
1999 2002 <br />
Nacholapithecus <br />
Papio cynocephalus<br />
<br />
<br />
Nacholapithecus <br />
<br />
<br />
<br />
<br />
<br />
MacLarnon1995intermembral<br />
index<br />
<br />
<br />
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 />
<br />
<br />
P<br />
GP<br />
<br />
1 1 1 1 2 <br />
3 4<br />
1<br />
2 <br />
3 4 <br />
<br />
<br />
<br />
<br />
<br />
<br />
<br />
<br />
GP <br />
<br />
<br />
<br />
30<br />
<br />
PC <br />
<br />
524
117 181<br />
P<br />
<br />
1 1 1 1 1 <br />
2 1<br />
1<br />
2 <br />
SGL 11 4 <br />
23 4 SGL <br />
TBL SGL <br />
SGL <br />
SGL <br />
<br />
SGL <br />
<br />
<br />
<br />
<br />
<br />
<br />
<br />
<br />
<br />
<br />
SGL <br />
<br />
<br />
P<br />
iPad <br />
<br />
<br />
23 4<br />
iPad 30 <br />
CT MR <br />
4 <br />
1 1 <br />
2 <br />
3 <br />
4 <br />
DICOM Osirix CT MR <br />
2 3 <br />
<br />
23 <br />
Ai Autopsy imaging CT <br />
<br />
<br />
<br />
<br />
<br />
P<br />
eLearning <br />
<br />
<br />
eLearning <br />
eLearning <br />
eLearning <br />
<br />
Moodle Moodle <br />
<br />
<br />
P<br />
<br />
1,3 1 1 1 2 <br />
2 2 2 2 2<br />
1<br />
2 3 <br />
PT <br />
<br />
<br />
16 <br />
<br />
5 <br />
<br />
22 <br />
<br />
PTOT <br />
<br />
<br />
<br />
<br />
PTOT <br />
<br />
<br />
PTOT <br />
<br />
P<br />
<br />
1,2 3 3 3 2 <br />
4 1 1 1 1 1<br />
1<br />
2 3 <br />
4 <br />
<br />
<br />
<br />
<br />
<br />
<br />
<br />
<br />
P<br />
<br />
1 2 2 3 4<br />
1<br />
2 3 4 <br />
<br />
<br />
<br />
<br />
45
182<br />
117 <br />
P<br />
<br />
1,2 1 1 1 1 <br />
1 1 1 1 1<br />
1<br />
2 <br />
<br />
<br />
<br />
22 <br />
46<br />
<br />
<br />
1 3 <br />
<br />
<br />
<br />
<br />
<br />
<br />
P<br />
<br />
<br />
<br />
<br />
<br />
<br />
<br />
22 355 <br />
<br />
<br />
<br />
<br />
<br />
<br />
<br />
99<br />
76<br />
99<br />
<br />
<br />
P<br />
<br />
<br />
1 2 3 3 4 5<br />
1<br />
2 3 <br />
4 5 <br />
<br />
<br />
<br />
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 />
<br />
<br />
<br />
<br />
P<br />
<br />
<br />
<br />
<br />
<br />
<br />
4 1 <br />
<br />
<br />
<br />
<br />
<br />
2 83 <br />
<br />
<br />
<br />
10<br />
<br />
<br />
<br />
<br />
<br />
<br />
P<br />
MRI<br />
1 2 2 3 1 1 <br />
4 4 5 6<br />
1<br />
2 3 <br />
4 5 <br />
6 <br />
<br />
<br />
<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 />
P<br />
<br />
1 2 1 1 1<br />
1<br />
2 <br />
4 <br />
<br />
<br />
<br />
1 5 MP PIP<br />
DIP <br />
1 <br />
<br />
<br />
<br />
<br />
<br />
<br />
<br />
<br />
P<br />
<br />
<br />
<br />
<br />
<br />
<br />
<br />
<br />
<br />
MRI <br />
<br />
<br />
Apple Osirix Realia <br />
<br />
<br />
<br />
<br />
<br />
<br />
<br />
<br />
<br />
P<br />
<br />
<br />
<br />
<br />
<br />
1 <br />
<br />
<br />
<br />
<br />
VoxBlast <br />
KY500 <br />
<br />
3 μm <br />
3 μm <br />
<br />
KY<br />
500 <br />
3 <br />
<br />
<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 />
P<br />
Thiel <br />
1 1 2 2 2 <br />
3 2 1<br />
1<br />
2 2 3 <br />
<br />
Thiel Graz Dr. Thiel <br />
<br />
<br />
<br />
Thiel <br />
<br />
<br />
<br />
16 <br />
8 Thiel 4 <br />
<br />
<br />
Thiel <br />
<br />
<br />
<br />
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 />
4 2 <br />
3 4 <br />
<br />
<br />
<br />
<br />
<br />
<br />
<br />
6 <br />
<br />
Hedgehog<br />
<br />
Hedgehog SmoothenedSmo<br />
Smo 9 <br />
cKO<br />
<br />
SmocKO <br />
<br />
<br />
SmocKO <br />
<br />
P<br />
<br />
1 1 2 2 2 <br />
3 3 3 3<br />
1<br />
4 2 3 <br />
3 <br />
<br />
<br />
<br />
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 />
<br />
<br />
<br />
<br />
<br />
<br />
<br />
<br />
<br />
<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 />
<br />
<br />
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 />
<br />
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 />
<br />
3 <br />
70 90 4<br />
<br />
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 />
2 <br />
22 92 1 <br />
<br />
<br />
<br />
<br />
<br />
<br />
<br />
<br />
<br />
Humphry <br />
Miyauchi <br />
Humphry <br />
<br />
<br />
<br />
P<br />
<br />
1 1,2 1 2 2 <br />
2<br />
1<br />
2 <br />
<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 />
<br />
1 1 1 1 2 3 <br />
3<br />
1<br />
2 3 <br />
<br />
<br />
<br />
<br />
<br />
<br />
<br />
75 <br />
<br />
<br />
<br />
<br />
<br />
1 <br />
<br />
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<br />
<br />
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 />
P<br />
<br />
<br />
<br />
<br />
<br />
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 />
2 <br />
<br />
III <br />
IV <br />
<br />
<br />
P<br />
<br />
<br />
<br />
<br />
2011 <br />
2 <br />
<br />
<br />
<br />
<br />
• <br />
<br />
<br />
<br />
• • <br />
<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 />
<br />
1 1 2,3 2 2<br />
1<br />
2 3 <br />
<br />
<br />
<br />
<br />
36 <br />
<br />
14 6 5 <br />
1 <br />
2 2 <br />
3 <br />
2 <br />
4 2<br />
<br />
<br />
5 <br />
3 <br />
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<br />
<br />
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P<br />
<br />
1 1 1 1 1 <br />
1 1 1 1 1 1 <br />
1 1 1 1 1 2<br />
1<br />
3 2 <br />
<br />
<br />
<br />
27 <br />
CTCBCT<br />
<br />
<br />
80 1 <br />
<br />
<br />
<br />
<br />
<br />
<br />
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 />
2
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 />
3 2 <br />
<br />
<br />
<br />
<br />
<br />
<br />
<br />
<br />
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<br />
<br />
<br />
<br />
<br />
<br />
<br />
<br />
<br />
<br />
<br />
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 />
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