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恶性疟原虫疟疾后小脑功能障碍期间的免疫激活。

Immune activation during cerebellar dysfunction following Plasmodium falciparum malaria.

作者信息

de Silva H J, Hoang P, Dalton H, de Silva N R, Jewell D P, Peiris J B

机构信息

John Radcliffe Hospital, Oxford, UK.

出版信息

Trans R Soc Trop Med Hyg. 1992 Mar-Apr;86(2):129-31. doi: 10.1016/0035-9203(92)90536-l.

Abstract

Evidence for immune activation was investigated in 12 patients with a rare syndrome of self-limiting, delayed onset cerebellar dysfunction following an attack of falciparum malaria which occurred 18-26 d previously. Concentrations of tumour necrosis factor, interleukin 6 and interleukin 2 were all significantly higher in serum samples of patients during cerebellar ataxia than in recovery sera and in the sera of 8 patients who did not develop delayed cerebellar dysfunction following an attack of falciparum malaria. Cytokine concentrations in the cerebrospinal fluid were also significantly higher in ataxic patients than in controls. These findings suggest that immunological mechanisms may play a role in delayed cerebellar dysfunction following falciparum malaria.

摘要

对12例患有一种罕见综合征的患者进行了免疫激活证据的调查,这些患者在18 - 26天前发生恶性疟原虫感染后出现自限性、延迟发作的小脑功能障碍。在小脑共济失调患者的血清样本中,肿瘤坏死因子、白细胞介素6和白细胞介素2的浓度均显著高于康复期血清以及8例在恶性疟原虫感染后未发生延迟性小脑功能障碍患者的血清。共济失调患者脑脊液中的细胞因子浓度也显著高于对照组。这些发现表明,免疫机制可能在恶性疟原虫感染后的延迟性小脑功能障碍中起作用。

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