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红细胞缺陷与疟疾。

Red blood cell defects and malaria.

作者信息

Williams Thomas N

机构信息

Kemri/Wellcome Trust Collaborative Programme, P.O. Box 230, Kilifi, Kenya.

出版信息

Mol Biochem Parasitol. 2006 Oct;149(2):121-7. doi: 10.1016/j.molbiopara.2006.05.007. Epub 2006 Jun 9.

Abstract

Malaria is a major cause of childhood death throughout much of the tropical world. As a result, it has exerted a powerful force for the evolutionary selection of genes that confer a survival advantage. Identifying which genes are involved, and how they affect malaria risk, is a potentially useful way of exploring the host-parasite relationship. To date, some of the best-described malaria-protective polymorphisms relate to genes that affect the structure or function of red blood cells (RBC). Recent years have seen significant advances in our understanding of the importance of some of these genes, including glycophorin C (GYPC); complement receptor 1 (CR1); band 3 (SLC4A1); pyruvate kinase (Pklr); and the genes for alpha-(HBA) and beta-globin (HBB). The challenge for the future must be to convert these advances into fresh approaches to the prevention and treatment of malaria.

摘要

疟疾是热带世界大部分地区儿童死亡的主要原因。因此,它对赋予生存优势的基因进行进化选择施加了强大的力量。确定哪些基因参与其中以及它们如何影响疟疾风险,是探索宿主-寄生虫关系的一种潜在有用方法。迄今为止,一些描述得最为详尽的疟疾保护性多态性与影响红细胞(RBC)结构或功能的基因有关。近年来,我们对其中一些基因重要性的理解取得了重大进展,包括血型糖蛋白C(GYPC)、补体受体1(CR1)、带3蛋白(SLC4A1)、丙酮酸激酶(Pklr)以及α-珠蛋白(HBA)和β-珠蛋白(HBB)的基因。未来的挑战必然是将这些进展转化为预防和治疗疟疾的新方法。

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