陈方平
从事血液病临床和基础研究工作
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- 姓名:陈方平
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学术头衔:
博士生导师
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学科领域:
临床医学
- 研究兴趣:从事血液病临床和基础研究工作
陈方平,男,1958年12月出生,现任中南大学湘雅医院院长、血液科主任、教授、博士和博士后导师,湖南省血液学会主任委员,中国细胞生物学会常委、理事,中华血液学会委员,中国实验血液学会委员,湖南省内科学会委员,美国血液学会(ASH)会员、国际血栓与止血学会(ISTH)会员。《国际病理科学与临床杂志》副主编、《临床血液学杂志》常务编委、《中国感染控制杂志》常务编委、《中国实验血液学杂志》编委、《血栓与止血杂志》编委、《中国医师杂志》编委、《中南大学学报(医学版)》编委、《医学临床研究》 编委。《国际病理科学与临床杂志》副主编、《临床血液学杂志》常务编委、《中国感染控制杂志》常务编委、《中国实验血液学杂志》编委、《血栓与止血杂志》编委、《中国医师杂志》编委、《中南大学学报(医学版)》编委、《医学临床研究》 编委。享受国家政府特殊津贴。长期从事血液病临床和基础研究工作,1992 --1994曾赴美国纽约州立大学石溪分校客座副教授,1997.10--1998.01赴美国纽约西奈山医院任高级访问学者,2001.07—2001.08在法国巴黎Robert Debre医院任高级访问学者。先后承担国家自然科学基金重点项目、863计划、卫生部临床学科重点项目等课题16项。获省、部级以上成果和奖励9项/次。在国内外杂志发表论文181篇。主编教育部高教出版社“十一五”规划教材《临床检验血液学》、人民卫生出版社《血液学检验》。
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陈方平, By Christine M. Grimaldi, Fangping Chen, ChanghongWu, Harvey J.Weiss, Barry S. Coller, and Deborah L. French
Blood, Vol 91, No 5 (March 1), 1998: pp 1562-1571,-0001,():
-1年11月30日
Glanzmann thrombasthenia is an inherited bleeding disorder due to a functional reduction or absence of platelet GPIIb/IIIa (aIIbb3) integrin receptors. Based on a prolonged bleeding time and absence of platelet aggregation in response to physiologic agonists, a 55-year-old white man was diagnosed as having Glanzmann thrombasthenia. The patient's platelet fibrinogen level was <5% of normal. As judged by complex-dependent monoclonal antibody (MoAb) binding, surface expression of platelet GPIIb/IIIa receptors was less than 5.5% of normal, whereas the binding of an anti-GPIIIa specific MoAb (7H2) was <12% of normal. Immunoblot analysis of the patient's platelet lysates showed <35% of normal levels of GPIIIa, <30% of normal levels of GPIIb, and an abnormally migrating fragment of GPIIb. Biotinylation of the surface proteins on the patient's latelets followed by immunoprecipitation and sodium dodecyl sulfate-polyacrylamide gel electrophoresis (SDS-PAGE) analysis showed only GPIIb and GPIIIa subunits of normal size. Surface expression of platelet avb3 receptors was 192% of normal, suggesting that the patients' defect was in GPIIb. Sequence analysis of the patient's GPIIb cDNA identified a T to C transition at nucleotide 643, predicting a Leu214Pro substitution. Direct sequencing of GPIIb exon 6 indicated that the patient is homozygous for the mutation. The nature of the Leu214Pro mutation was analyzed by expression in Chinese hamster ovary (CHO) cells. As judged by subunitspecific MoAb binding, surface expression of mutant receptors was <60% of normal, but these receptors were not recognized by the complex-dependent monoclonal antibodies, 10E5 and 7E3. In addition, mutant receptors pretreated with the ligand-induced binding site MoAb AP5 were not recognized by the activation-dependent MoAb PAC-1 and mutant expressing CHO cells did not adhere to immobilized fibrinogen. These data suggest that the Leu214Pro mutation in GPIIb disrupts the structural conformation, and either directly or indirectly, the ligand binding properties of the heterodimeric complex. This is in accord with studies from other integrins that have implicated a b-turn in a homologous region as important in ligand binding. Thus, the Leu214Pro mutation appears to produce the Glanzmann thrombasthenia phenotype by both qualitative and quantitative abnormalities. In addition, the mutation appears to confer susceptibility of the GPIIb subunit to proteolysis.
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