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Molecular studies related to the pathogenesis of cerebral malaria.

作者信息

Howard R J, Gilladoga A D

机构信息

Laboratory of Infectious Diseases, DNAX Research Institute of Molecular and Cellular Biology, Palo Alto, CA 94304-1104.

出版信息

Blood. 1989 Dec;74(8):2603-18.

PMID:2479423
Abstract
摘要

相似文献

1
Molecular studies related to the pathogenesis of cerebral malaria.
Blood. 1989 Dec;74(8):2603-18.
2
Host receptors for malaria-infected erythrocytes.疟原虫感染红细胞的宿主受体。
Am J Trop Med Hyg. 1990 Aug;43(2 Pt 2):6-14. doi: 10.4269/ajtmh.1990.43.6.
3
The molecular basis of pathogenesis of cerebral malaria.脑型疟疾发病机制的分子基础。
Microb Pathog. 1996 Feb;20(2):63-72. doi: 10.1006/mpat.1996.0006.
4
Rolling and stationary cytoadhesion of red blood cells parasitized by Plasmodium falciparum: separate roles for ICAM-1, CD36 and thrombospondin.恶性疟原虫感染的红细胞的滚动和固定细胞黏附:细胞间黏附分子-1、CD36和血小板反应蛋白的不同作用
Br J Haematol. 1994 May;87(1):162-70. doi: 10.1111/j.1365-2141.1994.tb04887.x.
5
CD36 directly mediates cytoadherence of Plasmodium falciparum parasitized erythrocytes.CD36直接介导恶性疟原虫寄生红细胞的细胞黏附。
Cell. 1989 Jul 14;58(1):95-101. doi: 10.1016/0092-8674(89)90406-6.
6
Plasmodium falciparum erythrocyte membrane protein 1 is a parasitized erythrocyte receptor for adherence to CD36, thrombospondin, and intercellular adhesion molecule 1.恶性疟原虫红细胞膜蛋白1是一种寄生红细胞与CD36、血小板反应蛋白和细胞间黏附分子1结合的受体。
Proc Natl Acad Sci U S A. 1996 Apr 16;93(8):3497-502. doi: 10.1073/pnas.93.8.3497.
7
Knob-independent cytoadherence of Plasmodium falciparum to the leukocyte differentiation antigen CD36.恶性疟原虫不依赖结节的细胞粘附至白细胞分化抗原CD36
J Exp Med. 1990 Jun 1;171(6):1883-92. doi: 10.1084/jem.171.6.1883.
8
Molecular basis of sequestration in severe and uncomplicated Plasmodium falciparum malaria: differential adhesion of infected erythrocytes to CD36 and ICAM-1.重症和非重症恶性疟原虫疟疾中隔离的分子基础:感染红细胞与CD36和细胞间黏附分子-1的差异黏附
J Infect Dis. 1991 Jul;164(1):163-9. doi: 10.1093/infdis/164.1.163.
9
Sequestrin, a CD36 recognition protein on Plasmodium falciparum malaria-infected erythrocytes identified by anti-idiotype antibodies.疟原虫素,一种通过抗独特型抗体鉴定出的、存在于恶性疟原虫感染红细胞上的CD36识别蛋白。
Proc Natl Acad Sci U S A. 1991 Apr 15;88(8):3175-9. doi: 10.1073/pnas.88.8.3175.
10
Plasmodium falciparum: soluble thrombospondin increases cytoadherence of parasitized erythrocytes to human microvascular endothelium under shear flow conditions.恶性疟原虫:可溶性血小板反应蛋白在剪切流条件下增加被寄生红细胞与人类微血管内皮的细胞黏附。
Exp Parasitol. 1997 Sep;87(1):69-72. doi: 10.1006/expr.1997.4186.

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Sticking for a Cause: The Falciparum Malaria Parasites Cytoadherence Paradigm.坚持一个事业:恶性疟原虫寄生虫细胞黏附范式。
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Liver accumulation of Plasmodium chabaudi-infected red blood cells and modulation of regulatory T cell and dendritic cell responses.恰氏疟原虫感染的红细胞在肝脏中的蓄积以及调节性T细胞和树突状细胞反应的调节
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Differential gene expression mediated by 15-hydroxyeicosatetraenoic acid in LPS-stimulated RAW 264.7 cells.15-羟基二十碳四烯酸介导的脂多糖刺激的RAW 264.7细胞中的差异基因表达
Malar J. 2009 Aug 11;8:195. doi: 10.1186/1475-2875-8-195.
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Pathogenic role of P-selectin in experimental cerebral malaria: importance of the endothelial compartment.P-选择素在实验性脑型疟疾中的致病作用:内皮细胞区室的重要性
Am J Pathol. 2004 Mar;164(3):781-6. doi: 10.1016/S0002-9440(10)63166-5.
7
The surface variant antigens of Plasmodium falciparum contain cross-reactive epitopes.恶性疟原虫的表面变异抗原含有交叉反应表位。
Proc Natl Acad Sci U S A. 2001 Feb 27;98(5):2664-9. doi: 10.1073/pnas.041602598. Epub 2001 Feb 13.
8
Molecular aspects of severe malaria.重症疟疾的分子层面
Clin Microbiol Rev. 2000 Jul;13(3):439-50. doi: 10.1128/CMR.13.3.439.
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Plasmodium chabaudi-infected erythrocytes adhere to CD36 and bind to microvascular endothelial cells in an organ-specific way.感染查巴迪疟原虫的红细胞会黏附于CD36,并以器官特异性方式与微血管内皮细胞结合。
Infect Immun. 2000 Jul;68(7):4135-44. doi: 10.1128/IAI.68.7.4135-4144.2000.
10
Virulence and transmission success of the malarial parasite Plasmodium falciparum.恶性疟原虫的毒力与传播成功
Proc Natl Acad Sci U S A. 1999 Apr 13;96(8):4563-8. doi: 10.1073/pnas.96.8.4563.