کد مقاله | کد نشریه | سال انتشار | مقاله انگلیسی | نسخه تمام متن |
---|---|---|---|---|
3065110 | 1580468 | 2008 | 4 صفحه PDF | دانلود رایگان |
عنوان انگلیسی مقاله ISI
Complement inhibitor prevents disruption of sodium channel clusters in a rabbit model of Guillain–Barré syndrome
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کلمات کلیدی
موضوعات مرتبط
علوم زیستی و بیوفناوری
ایمنی شناسی و میکروب شناسی
ایمونولوژی
پیش نمایش صفحه اول مقاله
چکیده انگلیسی
Complement-mediated disruption of voltage-gated sodium channels at the nodes of Ranvier acts in the development of acute motor axonal neuropathy. Nafamostat mesilate, a synthetic serine protease inhibitor, used in clinical practice for more than 20 years, has anti-complement activity. Acute motor axonal neuropathy rabbits obtained by GM1 ganglioside sensitization were or were not given nafamostat mesilate intravenously. Complement deposition and sodium channel disruption in the spinal anterior roots were significantly less frequent in the treated rabbits than in the controls. Nafamostat mesilate inhibited complement deposition and prevented sodium channel disruption. This provided the rationale for a clinical trial.
ناشر
Database: Elsevier - ScienceDirect (ساینس دایرکت)
Journal: Journal of Neuroimmunology - Volume 205, Issues 1–2, 15 December 2008, Pages 101–104
Journal: Journal of Neuroimmunology - Volume 205, Issues 1–2, 15 December 2008, Pages 101–104
نویسندگان
Vongsavanh Phongsisay, Keiichiro Susuki, Kenjiro Matsuno, Takuyu Yamahashi, Saori Okamoto, Kei Funakoshi, Koichi Hirata, Motoo Shinoda, Nobuhiro Yuki,