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本文引用的文献

1
Cerebral malaria pathogenesis: revisiting parasite and host contributions.脑型疟疾发病机制:重新审视寄生虫和宿主的作用。
Future Microbiol. 2012 Feb;7(2):291-302. doi: 10.2217/fmb.11.155.
2
Defibrotide interferes with several steps of the coagulation-inflammation cycle and exhibits therapeutic potential to treat severe malaria.地塞米松干扰凝血-炎症周期的几个步骤,并表现出治疗严重疟疾的治疗潜力。
Arterioscler Thromb Vasc Biol. 2012 Mar;32(3):786-98. doi: 10.1161/ATVBAHA.111.240291. Epub 2011 Nov 23.
3
Thrombocytopenia in malaria: who cares?疟疾相关性血小板减少症:谁在乎?
Mem Inst Oswaldo Cruz. 2011 Aug;106 Suppl 1:52-63. doi: 10.1590/s0074-02762011000900007.
4
Thrombocytopenia in childhood malaria with special reference to P. vivax monoinfection: A study from Bikaner (Northwestern India).儿童疟疾伴血小板减少症,特别提及间日疟原虫单感染:来自印度西北部比卡内尔的研究。
Platelets. 2012;23(3):211-6. doi: 10.3109/09537104.2011.607520. Epub 2011 Aug 24.
5
The role of platelets in defence against pathogens.血小板在防御病原体中的作用。
Hamostaseologie. 2011 Nov;31(4):264-8. doi: 10.5482/ha-1152. Epub 2011 Jun 28.
6
Plasma circulating nucleic acids levels increase according to the morbidity of Plasmodium vivax malaria.血浆循环核酸水平随着间日疟原虫疟疾的发病率而增加。
PLoS One. 2011;6(5):e19842. doi: 10.1371/journal.pone.0019842. Epub 2011 May 17.
7
Augmented plasma microparticles during acute Plasmodium vivax infection.急性间日疟原虫感染期间增强的血浆微颗粒。
Malar J. 2010 Nov 16;9:327. doi: 10.1186/1475-2875-9-327.
8
Molecular insight into human platelet antigens: structural and evolutionary conservation analyses offer new perspective to immunogenic disorders.深入了解人类血小板抗原:结构和进化保守性分析为免疫性疾病提供新视角。
Transfusion. 2011 Mar;51(3):558-69. doi: 10.1111/j.1537-2995.2010.02862.x. Epub 2010 Aug 30.
9
On the cytoadhesion of Plasmodium vivax-infected erythrocytes.关于感染疟原虫 vivax 的红细胞的细胞黏附。
J Infect Dis. 2010 Aug 15;202(4):638-47. doi: 10.1086/654815.
10
Greater endothelial activation, Weibel-Palade body release and host inflammatory response to Plasmodium vivax, compared with Plasmodium falciparum: a prospective study in Papua, Indonesia.与恶性疟原虫相比,间日疟原虫引起更大的内皮细胞激活、血小板 - 内皮细胞颗粒释放和宿主炎症反应:印度尼西亚巴布亚的一项前瞻性研究。
J Infect Dis. 2010 Jul 1;202(1):109-12. doi: 10.1086/653211.

血小板整合素 α2β1 密度的遗传变异性:可能是导致间日疟原虫引起严重血小板减少症的原因之一。

Genetic variability in platelet integrin α2β1 density: possible contributor to Plasmodium vivax-induced severe thrombocytopenia.

机构信息

Centro de Pesquisas René Rachou, Fundação Oswaldo Cruz, Belo Horizonte, Minas Gerais, Brazil.

出版信息

Am J Trop Med Hyg. 2013 Feb;88(2):325-8. doi: 10.4269/ajtmh.2012.12-0297. Epub 2012 Dec 18.

DOI:10.4269/ajtmh.2012.12-0297
PMID:23249684
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC3583325/
Abstract

Understanding the pathogenesis of Plasmodium vivax malaria is challenging. We hypothesized that susceptibility to P. vivax-induced thrombocytopenia could be associated with polymorphisms on relevant platelet membrane integrins: integrin α2 (C807T), and integrin β3 (T1565C). Although β3 polymorphism was not related with P. vivax malaria, α2 807T carriers, which show high levels of integrin α2β1, had a higher probability for severe thrombocytopenia than wild-type carriers. This evidence of the association of integrin polymorphism and P. vivax morbidity was further demonstrated by a moderate but significant correlation between clinical disease and surface levels of the integrin α2β1.

摘要

理解间日疟原虫疟疾的发病机制具有挑战性。我们假设对间日疟原虫诱导的血小板减少症的易感性可能与相关血小板膜整合素的多态性有关:整合素 α2(C807T)和整合素 β3(T1565C)。尽管 β3 多态性与间日疟原虫疟疾无关,但高表达整合素 α2β1 的 α2 807T 携带者发生严重血小板减少症的可能性高于野生型携带者。整合素多态性与间日疟原虫发病率之间的关联的证据进一步通过整合素 α2β1 的临床疾病与表面水平之间的中度但显著的相关性得到证明。