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12 th Congress of the European Hematology Association topenia model, the human platelet count was fully recovered. Interestingly, the numbers of CD34 + CD41 + human megakaryoblasts and 4N to 128N human megakaryocytes in xenografted mice were not significantly changed compared to the control mice after treatment with IFN for 7 weeks. We also analyzed the inhibitory effects of IFN on megakaryocytes in vitro. Although IFN slightly reduced the number of CFU-MKs [146±13 colonies/5000 cells (control), 130±13 colonies/5000 cells (10 ng/mL of IFN)], the percentage of megakaryocytes bearing PPT was significantly reduced by IFN [20.4±3.0%(control), 12.5±3.6% (10 ng/mL of IFN)]. Currently, we are investigating the inhibitory mechanisms of IFN for PPT. Conclusion. These results indicated that NIP-004 is effective for preventing IFN-induced thrombocytopenia in vivo. IFN might inhibit the PPT formation rather than the proliferation of human megakaryocytopoiesis. We expect that the small thrombopoietin molecule, NIP-004, can be applied for the treatment of IFN-induced thrombocytopenia in the patients with chronic hepatitis C. 0388 IN VITRO AND IN VIVO MICROPARTICLE-ASSOCIATED ENDOTHELIAL PROTEIN C RECEP- TOR CAN REVERSE PRO-INFLAMMATORY AND APOPTOTIC CELL SIGNALS AND EFFECTS T. Dutt, M. Perez-Casal, C.H. Toh University of Liverpool, LIVERPOOL, United Kingdom Background. We have described a novel mechanism of endothelial protein C receptor (EPCR) release from cell surfaces in vitro and in vivo. Induced by Activated Protein C (APC), EPCR is released in microparticulate (MP) form. Unlike APC bound to truncated soluble EPCR, APC on MP-EPCR retains proteolytic anticoagulant activity. We now hypothesise that the MP EPCR-APC complex can also cleave endothelial protease activated receptor-1 (PAR1) to modulate inflammation and cytoprotection. Aims. 1. To compare the efficacy of MP EPCR-APC versus free- APC, using two different pools of endothelial cells, following exposure to a pro-inflammatory stimulus. 2. To determine if circulating MP EPCR- APC from patients can regulate gene expression in a PAR1-dependent manner. Methods. Using an in vitro system of human umbilical vein endothelial cells (HUVECs) or human coronary artery endothelial cells (HCAECs), TNFα, 10 ng/mL, was added to represent a cell model of sepsis. After 4 hours the cells were treated with an equal concentration of either free or MP-bound APC and left for a total of 24 hours. RNA was extracted from the cells and used to make probes for hybridization of GEArray Human Endothelial Cell Biology Gene Array (SuperArray). Using untreated cells as a baseline, the specificity of APC and the role of PAR1 were assessed by using the appropriate blocking antibodies and antagonist. Circulating MPs were isolated from plasma of APC treated patients by standard methods and platelet-derived MPs depleted using a CD41a antibody and magnetic beads. MP-associated APC was estimated from a standard curve and 17nM used for gene profiling. PAR1mediated signalling was examined as above. Results. In TNFα stimulated cells, APC, selectively induced anti-inflammatory and suppressed pro-apoptotic gene regulation. In over 90% of these genes, MP-APC had a 2-7 fold greater effect in relation to free-APC. These observations were confirmed by Q-PCR for e-selectin, ICAM1, Bax, A20, caspase 10, GM-CSF and IL8. This translated into increased GM-CSF and interleukin 8 secretion, and cytoprotection against staurosporine-induced apoptosis. Protein C or PAR1 antagonism reversed these results to demonstrate that the induced effects by MPs were APC specific and PAR1-dependent. Further analysis using MP-associated EPCR from septic patients during APC treatment also demonstrated PAR1-mediated anti-inflammatory gene induction and anti-apoptotic function. Conclusions. APC on MP-associated EPCR can ameliorate TNF induced inflammatory changes and staurosporine induced apoptosis in both HUVECs and HCAECs. As these effects are reproducible with MPs isolated from patients' plasma, this may have clinical relevance in the septic patient treated with APC. 142 | haematologica/the hematology journal | 2007; 92(s1) 0389 ENDOTHELIAL COLONY FORMING CELLS FROM PATIENTS WITH CML, POLYCYTEMIA VERA AND ESSENTIAL THROMBOCYTHEMIA, DERIVE FROM A STEM CELL LACKING THE DISEASE SPECIFIC MARKER F. Frassoni, 1 G. Piaggio, 2 M. Corselli, 1 F. Bertolotti, 1 S. Pozzi, 1 A. Parodi, 1 B. Chiavarina, 1 M. Sessarego, 3 G. Fugazza, 3 A. Garuti, 4 A. Ibatici, 1 A. Bacigalupo, 5 F. Frassoni1 1 Centro Cellule Staminali, GENOA; 2 Lab Diagnostica Emato e Colture in vitro, GENOVA; 3 Laboratorio Citogenetica DIMI, GENOVA; 4 Terapie Cellulari DIMI, GENOVA; 5 Ematologia e Trapianto AO S Martino, GENOVA, Italy Background. the persistence of a common progenitor to haematopoietic and vascular endothelial lineage in the adult haematopoietic tissue appeared to be validated when Bcr/Abl fusion gene was found in a variable proportion of endothelial like cells generated in vitro from the bone marrow and the peripheral blood of CML patients. However, the different colture conditions used to isolate and to expand endothelial cells (EC) in vitro have generated some confusion. Only recently, the existence of two EC populations has been clearly settled: early EPC, i.e. colony forming unit-endothelial cells (CFU-EC), are haematopoietic derived progeny committed to the myeloid lineage while late EPC, namely ECFCs, are vessel-forming progenitors. Aims. we have reconsidered the issue of endothelial cell origin (status) in CML and other MPDs to verify whether circulating EPCs, isolated and expanded from the peripheral blood of patients, bear the disease specific genetic marker of the leukaemia clone or this is restricted to the haematopoietic lineage. Methods. Forty-three patients and 12 normal controls were included in this study. Twenty-four samples were Philadelphia and Bcr/Abl positive CML, 19 were Philadelphia and Bcr/Abl negative MPDs, PV and ET with JAK2-V617F mutation. Peripheral blood mononuclear cells were cultured in vitro and expanded cells were searched for Bcr/Abl fusion gene by RQ-PCR and FISH, and for JAK2-V617F mutation by nested PCR. Flow cytometry and capillary formation assay in Matrigel were also performed. Results. due to the low frequency of late EPCs in the peripheral blood of patients, only 7/24 CML and 6/19 MPD samples gave rise in vitro to a progeny of EC. None of them carried the disease specific genetic marker. The expanded cells showed a complete outfit of endothelial associated antigens and were able to form capillary like structures in vitro. Conclusions. differently from previous reports and based on a clear distinction between early and late EPCs, this study shows for the first time that endothelial cells, derived in culture from Ph-positive, Bcr/Abl positive CML patients, lack the disease marker in the late EPC. In addition late EPCs from patients with PV or ET lack the JAK2-V617F mutation. Thus it appears that in CML , PV and ET the cell able to give rise to endothelial progenitors do not derive from the malignant clone. This finding, per se, does not exclude the possibility of a common ancestor cell for haematopoietic and endothelial lineage, and multiple explanations could be hypothesized: the leukemogenetic event that starts the CML involves a stem cells below the common ancestor cells. Indeed, most T cells in CML do not belong to the leukemic clone. Alternatively, since in the majority of newly diagnosed patients with CML, the bone marrow contains a high number of normal Ph-negative early progenitor cells (LTC-IC), one could argue that Ph-negative stem cells still give rise to EPC therefore diluting those deriving from Ph-positive ones. The same apply to MPD where it is now evident that part of haematopoietic progenitors do not carry the JAK2-V617F mutation.
0390 ELTROMBOPAG RAISES PLATELET COUNT AND REDUCES BLEEDING COMPARED WITH PLACEBO DURING SHORT-TERM TREATMENT IN CHRONIC IDIOPATHIC THROMBOCYTOPENIC PURPURA: A PHASE III STUDY J. Bussel, 1 A. Provan, 2 T. Shamsi, 3 G. Cheng, 4 L. Kovaleva, 5 N. Stone, 6 B. Mayer, 6 R. Poulin, 6 M. Arning 6 1 Weill Medical College Cornell University, NEW YORK, USA; 2 Southampton General Hospital, SOUTHAMPTON, United Kingdom; 3 Bismallah Taquee Inst. Health Sciences, KARACHI, Pakistan; 4 Chinese University of Hong Kong, SHATIN, Hongkong (China); 5 Hematology Research Center, MOSCOW, Russian Federation; 6 GlaxoSmithKline, COLLEGEVILLE, USA Background. Chronic idiopathic thrombocytopenic purpura (ITP) is a disease characterized by increased platelet destruction and impaired platelet production. In a previous, large phase II study, eltrombopag, a novel, non-peptide, oral platelet growth factor, increased platelet counts in adults with chronic ITP. Aims. In this global, randomized, doubleblind, placebo-controlled, phase III trial, the safety and efficacy of eltrombopag was studied in adults with chronic ITP and platelet counts
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haematologica the hematology journa
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Information for readers, authors an
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EHA Executive Board E. Hellström-L
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Poster session I POSTER SESSION POS
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12 th Congress of the European Hema
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dasatinib. Methods. We studied Ikar
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Expression of the oncogene H-Ras an
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is the gene for the erythropoietin
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safety of a slow-release liposomal
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0029 OUTCOME OF THE TREATMENT OF AD
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drug-induced apoptotic response of
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41% in the PI3K- group (p=0.001). I
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Acute myeloid leukemia - Clinical I
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to 60 years (n=116, or 72%) receive
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0056 PROGNOSTIC SIGNIFICANCE OF FLT
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Anemia and Bone marrow failure 0061
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tified with the current protocol. S
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new cases of lead poisoning due to
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icance, from baseline to week 6 (p
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0086 THROMBELASTOGRAPHIC CHART RELI
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trials. The aim of this retrospecti
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tant function in this disease, nega
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ed to a favorable outcome. Bialleli
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stronger levels of p21 in the cell
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hematological centers in one countr
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ure 1). Conclusions. Results for re
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patients. After a median follow-up
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Cytogenetics and Molecular diagnost
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0135 ROUTINE DETECTION OF CYTOGENET
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(MMolR, defined as a BCR-ABL x 100
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0146 ARSENIC TRIOXIDE INDUCES ACCUM
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tinguish between genotypic B-cell l
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Genomics and proteomics 0158 PLASMA
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0164 EVALUATION OF MULTIPLEX LIGATI
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each patient’s replicate conditio
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0174 RELATION BETWEEN LOW PML-RARα
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0179 ESHAP VS GIN AS SALVAGE AND MO
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Immunology and gene therapy 0184 EA
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Cell viability was not affected by
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month is not relevant to chronic Gv
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Infection and supportive care I 020
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0206 POTENTIAL ROLE OF CMV IN THE O
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3H-thymidine uptake in cell culture
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0217 TUBERCULOSIS AMONG A COHORT OF
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0222 COMPARISON OF IWG 2006 AND IWG
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tem (IPSS) to h-MDS was also invest
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PCH97-19) were studied. Conventiona
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of erythroid colonies was reduced i
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0245 POTENT AND SELECTIVE INHIBITIO
Page 99 and 100: 0250 INACTIVATION OF SUPPRESSOR OF
Page 101 and 102: Bortezomib 1.3 mg/m 2 days 1,4,8,11
Page 103 and 104: Response was defined according to E
Page 105 and 106: G-CSF can be used in neutropenic pa
Page 107 and 108: ence and functional activity of CD8
Page 109 and 110: itating tumor development, or engag
Page 111 and 112: phoma and SNT-13, -15 were establis
Page 113 and 114: usage (2/20 ie 10%) were observed.
Page 115 and 116: 0294 MYCOSIS FUNGOIDES. IMMUNOHYSTO
Page 117 and 118: (range, 1-6) and 11 treatment cycle
Page 119 and 120: 0306 RISK-ADAPTED IMMUNOCHEMOTHERAP
Page 121 and 122: functional activity was confirmed b
Page 123 and 124: No major toxicity, neither hematolo
Page 125 and 126: enewal potential of X-RAR-positive
Page 127 and 128: (50-99) respectively. Serial analys
Page 129 and 130: cell-interaction, adhesion and acti
Page 131 and 132: 0340 ALTERED FIBRIN CLOT STRUCTURE
Page 133 and 134: Conclusions. This study demonstrate
Page 135 and 136: 0354 FACTOR V LEIDEN HOMOZYGOUS GEN
Page 137 and 138: Results. From July 2005 through Mar
Page 139 and 140: 0364 CLINICAL EFFICACY OF OXALIPLAT
Page 141 and 142: one marrow and peripheral blood ste
Page 143 and 144: ecently suggested (Boissel et al.,
Page 145 and 146: 0378 SAFETY AND EFFICACY OF THE TER
Page 147 and 148: Cytogenetics and molecular diagnost
Page 149: 0385 CYTOPLASMIC MUTATED NUCLEOPHOS
Page 153 and 154: factor for the achievement of CR wa
Page 155 and 156: The cases of RAS showed two peaks o
Page 157 and 158: is 85%. Seven out of the 25 relapse
Page 159 and 160: 0409 FRACTIONATED RADIOIMMUNOTHERAP
Page 161 and 162: 0414 COMPARATIVE ANALYSIS OF THE CO
Page 163 and 164: successfully managed with GM-CSF di
Page 165 and 166: 49% for PCR positive patients (95%
Page 167 and 168: +8 (1 PR+1 HI) and 14/24 pts with c
Page 169 and 170: (e.g. bcr-abl leading to CML). CSC
Page 171 and 172: 0438 TERC MUTATIONS ANALYSIS IN PAT
Page 173 and 174: observed in all mice. Analysis of l
Page 175 and 176: ex-vivo expansion of HUCB-derived H
Page 177 and 178: ic kidney disease in univariate or
Page 179 and 180: One hundred eleven CN AML patients,
Page 181 and 182: to asses intestinal epithelial dama
Page 183 and 184: genesis of acute myeloid leukaemia
Page 185 and 186: polymorphism at nucleotide 4889 of
Page 187 and 188: expression along with a decreased C
Page 189 and 190: 0487 MUTATIONAL STATUS OF NUCLEOPHO
Page 191 and 192: previously reported, a single cours
Page 193 and 194: 0497 SINGLE AGENT CLORETAZINE (VNP4
Page 195 and 196: ly received melphalan-based chemoth
Page 197 and 198: were similar among the 3 groups. Ho
Page 199 and 200: Methods. Several read-out systems w
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0518 SERUM AND CELLULAR EXPRESSION
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0523 DNA REPAIR INHIBITION IN RESTO
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held true when BMI-1 expression was
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Ph + cells in the bone marrow). We
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derivative chromosome (4p16, 7p14,
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0545 STABILIZED BONE MARROW IS NOT
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obtained in low (Sokal) risk patien
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median dose intensity being 800 (21
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from pivotal clinical trials. Metho
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Cytogenetics and Molecular diagnost
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to set up and optimize a D-HPLC-bas
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0576 WESTERN BLOT IDENTIFICATION OF
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Basic disease was AML (n=5), ALL (n
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0588 EXTRACORPOREAL PHOTOPHORESIS F
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acquire a cytolytic capacity agains
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informed vignettes describing healt
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using CHOP-21 in the UK, pegfilgras
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0609 SOFT TISSUE COMPLICATIONS IN P
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inding lectin (MBL) gene by polymer
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all infection rate (p=0.12) as well
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Myelodysplastic syndromes II 0623 M
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formation (in total 28 samples). Ti
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sion. In addition, confocal analysi
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Myeloproliferative disorders - Clin
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open-label, multi-centre study enro
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iopsies after 6 and 12 months treat
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Myeloproliferative disorders Chroni
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ash, muscolar cramps, diarrhoea, he
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induced significant apoptosis (mean
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Myeloma and other monoclonal gammop
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the therapy of choice for POEMS is
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er patient does not indicate such t
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Myeloma and other monoclonal gammop
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secutive patients with MM, referred
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whether gene expression values may
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0705 THE SHIFT OF TREATMENT FOR NAS
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0710 CLINICO-PATHOLOGICAL FEATURES,
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patients presented a stage IV disea
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plete remission or recurrent diseas
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known at NHL diagnosis, were includ
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0731 THE IMPACT OF HIV ON NON-HODGK
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patients had died of their underlyi
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scripts and proteins most affected
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modulated after 24 h (37 up- and 59
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0753 A SUSTAINED REMISSION OF IDIOP
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and treatment, has rarely been syst
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uncontrolled massive bleeding affec
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Results. A total of 396 patients we
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C30 questionnaire, and the correspo
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wave length of light of reflected r
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0783 PREVALENCE OF MEMBRANE PROTEIN
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erozygous mother has a more severe
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0794 CARDIAC MANIFESTATIONS IN A BR
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0799 INEFFECTIVE ERYTHROPOIESIS IN
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p=0.014 and p=0.003, respectively).
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0809 CURRENT APPROACH TO CHELATION
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Thrombosis II 0814 UNSUSPECTED PULM
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the 97.5th percentile (5.2 U/mL) ge
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symptoms of DVT, 3 (7.89%) previous
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Transfusion medicine and vascular b
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tions (most bacterial, 2 malaria, 6
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0844 INCREASED LEUKOCYTE-PLATELET I
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0851 CORD BLOOD DERIVED MESENCHYMAL
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SIMULTANEOUS SESSION II Chronic mye
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0862 COMPARISON OF DASATINIB TO HIG
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0867 COMPREHENSIVE GERIATRIC ASSESS
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0872 MN1 INDUCES LEUKEMIA IN MICE A
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0877 PAX5/TEL TRANSDUCED PRE-BI CEL
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0882 CISPLATIN INDUCES THROMBIN GEN
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have an early manifestation of typi
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0892 INTEGRATION OF GENOME WIDE SNP
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0897 THE PHENOTYPE OF JAK2V617F MUT
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gest diverse sequences of NPM mutan
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2004 to January, 2006. At enrollmen
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with a p value of ≥ 0.10. Sets of
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BRIC 126 and 4N1K) in cells lacking
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sclerosis[NS] and 12 Mixed cellular
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0927 MK-0457, A NOVEL MULTIKINASE I
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Publication Only 0933 CLINICAL FEAT
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HSCT from the available Asian as we
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that the incidence of JAK2 mutation
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without type 2 diabetes. Methods. T
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pts (38.8%) that were isolated (abs
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y using the Miltenyi CD34 isolation
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0969 COMPARISON OF CD25 IMMUNOHISTO
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cytes was 24 days (range 8-32 days)
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a cytogenetic hallmark for M4/M5 su
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normal human BM B progenitor cells
Page 377 and 378:
0994 INCIDENCE OF INVASIVE ASPERGIL
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3 of disease relapse.TRM at day+100
Page 381 and 382:
survival of five years. This dismal
Page 383 and 384:
1011 FLOW CYTOMETRIC DNA INDEX AND
Page 385 and 386:
1018 THE EFFECT OF THE SUGARBAKER P
Page 387 and 388:
1024 KIR/HLA CLASS I MISMATCHING AN
Page 389 and 390:
ment details and thrombotic histori
Page 391 and 392:
1036 INCIDENCE AND SPECTRUM OF INFE
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tinely by our stem cell lab prior t
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tion to a translocation t(5;14)(q35
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ment of CML and induces a high rate
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due to reactivation and/or progress
Page 401 and 402:
1063 ABNORMAL METHYLATION STATUS OF
Page 403 and 404:
1069 CLINICAL RELEVANCE OF REGULATO
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1076 SERUM LEVELS OF SOLUBLE HLA CL
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patient is still undergoing intensi
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nificant MVD differences were detec
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dictor of OS (p=0.004). High dose t
Page 413 and 414:
1099 ALTERATIONS IN THE NATURAL KIL
Page 415 and 416:
1105 CYTOGENETIC ABNORMALITIES IN 3
Page 417 and 418:
1110 CONSTITUTIVE ACTIVATION OF STA
Page 419 and 420:
efficacy results with a well-tolera
Page 421 and 422:
unmutated VH genes, and high and lo
Page 423 and 424:
Aims. Aim of this study was to pred
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tested across a wide range of human
Page 427 and 428:
were incidentally diagnosed (52%).
Page 429 and 430:
ß2GP1 may be considered as determi
Page 431 and 432:
characterized in 198 β thalassaemi
Page 433 and 434:
1155 PLATELET AGGREGATION IN CHILDR
Page 435 and 436:
to-pelvic or perineal trauma. No me
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in age. High prevalence of LBM amon
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ecause some of the patients were or
Page 441 and 442:
of the drug is crucial to allow lon
Page 443 and 444:
egarding cost analysis of ASCT in G
Page 445 and 446:
ID Allo-BMT, 1 family one mismatche
Page 447 and 448:
admitted to ICU were discharged des
Page 449 and 450:
events -Postoperative states: 9,19%
Page 451 and 452:
efficacy and decreased atherosclero
Page 453 and 454:
1217 INCIDENCE OF EARLY STAGE IDIOP
Page 455 and 456:
1691GA and 1 homozygous 1691AA. The
Page 457 and 458:
1230 ASSOCIATION OF HEPARANASE GENE
Page 459 and 460:
posed, was: DF = (CD43%+FMC7%+CD79b
Page 461 and 462:
treatment of acute promyelocityc le
Page 463 and 464:
loaded group and 35 (70%) were non-
Page 465 and 466:
mild. Fas and soluble Fas ligand le
Page 467 and 468:
1265 POSACONAZOLE THERAPY IN REFRAC
Page 469 and 470:
ly express the cytoplasmic (inactiv
Page 471 and 472:
findings confirmed the significant
Page 473 and 474:
a less favorable prognosis. Interes
Page 475 and 476:
disease (HD), 4 patients (9%) with
Page 477 and 478:
1295 HEMOPHAGOCYTIC LYMPHOHYSTIOCYT
Page 479 and 480:
phamide 750 mg/m 2 on day 1, vincri
Page 481 and 482:
nomenon is unclear. It has been sug
Page 483 and 484:
oped mild thrombocytopenia (platele
Page 485 and 486:
gle dose of 54mg/m 2 rituximab furt
Page 487 and 488:
patients (pts), 36 male, with acute
Page 489 and 490:
esulting alterations of the endothe
Page 491 and 492:
(range 1-7) and 28,6% of patients h
Page 493 and 494:
three decades. In vivo, Ara-C is tr
Page 495 and 496:
statistical analysis. Results. Seve
Page 497 and 498:
Results. Though there was no recogn
Page 499 and 500:
2% and 19% of patients with or with
Page 501 and 502:
were older than 65 y) which can be
Page 503 and 504:
1376 RESVERATROL INDUCED P53 MEDIAT
Page 505 and 506:
median time of 21 days to reach >0.
Page 507 and 508:
ly. Conclusions. 1. Combined intens
Page 509 and 510:
to the presence of IVS1-6 mutation
Page 511 and 512:
fy predictive factors for these abn
Page 513 and 514:
acute leukemia. However, we cannot
Page 515 and 516:
agents. They involve primarily the
Page 517 and 518:
voriconazole for 2 months followed
Page 519 and 520:
typed using a commercially availabl
Page 521 and 522:
low up of ABL KD mutations’ level
Page 523 and 524:
with development of BC/AP. 2. EVI-1
Page 525 and 526:
1447 THE IMPACT OF DISPARITY IN SHO
Page 527 and 528:
three had visual field defects, two
Page 529 and 530:
acquired mutation most prone to cau
Page 531 and 532:
1466 ROS GENERATION AND APOPTOSIS I
Page 533 and 534:
1473 DIARRHEIC SYNDROME, A CLINICAL
Page 535 and 536:
gene fusion is an independent progn
Page 537 and 538:
1484 EPIDEMIOLOGY AND RESPONSE TO T
Page 539 and 540:
1492 FREQUENCY OF MEDITERRANEAN GLU
Page 541 and 542:
immune globulin was administered at
Page 543 and 544:
maintained on Imatinib 400 mg. Afte
Page 545 and 546:
Hodgkin’s disease is well known,
Page 547 and 548:
gram provided a unique chance to de
Page 549 and 550:
even when ADP-induced plt activatio
Page 551 and 552:
medullary involvement of multiple m
Page 553 and 554:
1540 ADMINISTRATION OF G-CSF AND CH
Page 555 and 556:
1548 QUALITY ANALYSIS OF THE MULTID
Page 557 and 558:
Index of authors A Aapro, M., 0377,
Page 559 and 560:
Bahr, J., 0148 Bai, M., 1551 Baia,
Page 561 and 562:
Bottini, P.V., 1181 Botto, B., 0408
Page 563 and 564:
Chaidos, A., 0456, 0498, 0599, 0686
Page 565 and 566:
De Keersmaecker, K., 0442, 0875 De
Page 567 and 568:
El-Sharkawy, N., 0016 Elwahidi, G.,
Page 569 and 570:
Garcia-Frade, J., 0346, 0680, 1105
Page 571 and 572:
H Haas, N., 0742 Haas, O.A., 0001,
Page 573 and 574:
Jaksic, B., 0127, 0446 Jaksic, O.,
Page 575 and 576:
Körmöczi, G., 0848 Kornblau, S.,
Page 577 and 578:
Lin, L.-I., 0030, 0484 Lin, T., 012
Page 579 and 580:
Massé, A., 0249 Massó, P., 1287,
Page 581 and 582:
Musto, P., 0254, 0401, 0422, 0569,
Page 583 and 584:
Papadavid, E., 1442 Papageorgiou, E
Page 585 and 586:
Probatova, N., 0704 Prochazka, V.,
Page 587 and 588:
Rykavicin, O., 0504 Ryningen, A., 0
Page 589 and 590:
Sirard, C., 0127, 0128 Sirigou, A.,
Page 591 and 592:
Thiebaut, A., 0454 Thieblemont, C.,
Page 593 and 594:
Vincenzi, C., 1060 Viniou, N.-A., 0
Page 595 and 596:
Zouabi, H., 0503, 0999 Zoumbos, N.C
Page 597 and 598:
Page 599 and 600:
Page 601 and 602:
Page 603:
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