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通过(新西兰白兔×布氏小鼠)F1代与正常小鼠之间的血小板转移实验分析特发性血小板减少性紫癜易感小鼠的血小板减少症。

Analyses of thrombocytopenia in idiopathic thrombocytopenic purpura-prone mice by platelet transfer experiments between (NZW x BXSB)F1 and normal mice.

作者信息

Mizutani H, Furubayashi T, Kuriu A, Take H, Tomiyama Y, Yoshida H, Nakamura Y, Inaba M, Kurata Y, Yonezawa T

机构信息

Second Department of Internal Medicine, Osaka University Medical School, Japan.

出版信息

Blood. 1990 May 1;75(9):1809-12.

PMID:2331522
Abstract

Male (NZW x BXSB) F1 (W/B F1) mice, which develop lupus nephritis, myocardial infarction, and thrombocytopenia, showed reduced platelet lifespan (PLS) and increased platelet-associated antibody (PAA) values. There were statistically significant correlations between the increase in PAA values and either the reduction in PLS or the decrease in platelet counts. This and the results of platelet transfer experiments between old male W/B F1 mice and either female W/B F1 or normal BALB/c mice indicate that PAAs on the platelet surface play a crucial role in the destruction of platelets in W/B F1 mice. The mechanism of thrombocytopenia observed here appears similar to that of human idiopathic thrombocytopenic purpura (ITP). Therefore, we think that W/B F1 mice are a potentially useful animal model for investigating the effectiveness and mode of action of therapeutic agents in human ITP, and that they may provide additional information on the basic mechanisms of this autoimmune phenomenon.

摘要

雄性(NZW×BXSB)F1(W/B F1)小鼠会发展为狼疮性肾炎、心肌梗死和血小板减少症,其血小板寿命(PLS)缩短,血小板相关抗体(PAA)值升高。PAA值的增加与PLS的降低或血小板计数的减少之间存在统计学上的显著相关性。这以及老年雄性W/B F1小鼠与雌性W/B F1或正常BALB/c小鼠之间的血小板转移实验结果表明,血小板表面的PAA在W/B F1小鼠血小板的破坏中起关键作用。此处观察到的血小板减少症机制似乎与人类特发性血小板减少性紫癜(ITP)相似。因此,我们认为W/B F1小鼠是研究治疗药物对人类ITP有效性和作用方式的潜在有用动物模型,并且它们可能为这种自身免疫现象的基本机制提供更多信息。

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Analyses of thrombocytopenia in idiopathic thrombocytopenic purpura-prone mice by platelet transfer experiments between (NZW x BXSB)F1 and normal mice.通过(新西兰白兔×布氏小鼠)F1代与正常小鼠之间的血小板转移实验分析特发性血小板减少性紫癜易感小鼠的血小板减少症。
Blood. 1990 May 1;75(9):1809-12.
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Reduced microvascular thrombosis and improved outcome in acute murine stroke by inhibiting GP IIb/IIIa receptor-mediated platelet aggregation.
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