کد مقاله | کد نشریه | سال انتشار | مقاله انگلیسی | نسخه تمام متن |
---|---|---|---|---|
5810909 | 1114998 | 2014 | 4 صفحه PDF | دانلود رایگان |
عنوان انگلیسی مقاله ISI
Insulin-associated neuroinflammatory pathways as therapeutic targets for traumatic brain injury
ترجمه فارسی عنوان
سرطان های عصبی مصنوعی مرتبط با انسولین به عنوان اهداف درمانی برای آسیب مغزی آسیب دیده است
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موضوعات مرتبط
علوم زیستی و بیوفناوری
بیوشیمی، ژنتیک و زیست شناسی مولکولی
زیست شناسی تکاملی
چکیده انگلیسی
Traumatic brain injury (TBI) is characterized by an abrupt blow or exchange of force against the head and can be categorized as mild, moderate, and severe. The secondary cell death after TBI displays ischemic-like patterns including neuroinflammation. The scavenger receptor cluster of differentiation (CD) 36 is a lipid-associated protein capable of transducing intracellular signals to promote inflammatory mechanisms within different cell types. Expression and activation of CD36 is closely related to dyslipidemia secondary to diabetes. Diabetes mellitus (DM) has been documented as a co-morbidity factor in TBI, in that patients with a history of diabetes present with more severe brain damage and slower recovery from TBI than non-diabetic patients. Indeed, a strict regulation of blood serum glucose by the use of insulin promotes a better outcome for TBI patients. Based on these recent findings, we now advance the hypothesis that CD36 via DM insulin-associated pathways is closely involved in TBI chronic pathology.
ناشر
Database: Elsevier - ScienceDirect (ساینس دایرکت)
Journal: Medical Hypotheses - Volume 82, Issue 2, February 2014, Pages 171-174
Journal: Medical Hypotheses - Volume 82, Issue 2, February 2014, Pages 171-174
نویسندگان
Christian D. Cerecedo-López, Jennifer H. Kim-Lee, Diana Hernandez, Sandra A. Acosta, Cesar V. Borlongan,