2.Spasmogens and cerebral vasospasm in cerebrospinal fluid after subarachnoid hemorrhage
Xi WU ; Bo HONG ; Jianmin LIU
International Journal of Cerebrovascular Diseases 2009;17(8):618-622
Cerebral vasospasm is the main reasons of cerebral infarction and delayed ischemic neurological deficit in patients with spontaneous subarachnoid hemorrhage. At present, the research of cerebral vasospasm is relatively focused on the spasmogens in bloody cerebro-spinal fluid. This article reviews the mechanisms of cerebral vasospasm induced by the major spasmogens in the bloody cerebrospinal fluid after subarachnoid hemorrhage.
6.Metabolomics used in the research of pediatrics.
Chinese Journal of Pediatrics 2010;48(6):442-445
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Humans
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Metabolomics
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Pediatrics
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methods
8.Intermedin ameliorates renal injury by inhibition of tubular epithelial cell apoptosis in a renal ischemia/reperfusion rat model
Xinyan LIU ; Xinghua LIU ; Xi QIAO ; Hong LI ; Rongshan LI
Chinese Journal of Nephrology 2011;27(1):29-33
Objective To investigate the effect of intermedin (IMD) on tubular cells apoptosis induced by renal ischemia/reperfusion (I/R) injury and its associated mechanism.Methods A total of twenty-four male Wistar rats were randomly divided into four groups (control group, I/R group, empty plasmid group and IMD group). One week after the removal of right kidney, ultrasound plasmid was used to transfect empty or IMD plasmid into the left kidney. Renal I/R model was made by clasping the left renal artery for 45 minutes. Tubular cell apoptosis was determined by TUNEL. Expression of Bax, Bcl-2, Fas was detected by semi-quantitative RT-PCR.Activity of caspase-8 and caspase-9 was evaluated with commercially available kits respectively.Protein level of caspase-3 was measured by Western blotting analysis. Results Compared with control group, apoptosis of tubular epithelial cells, expression of Bax and Fas, activities of caspase-8 and caspase-9, as well as protein level of caspase-3 were all significantly increased in I/R group (all P＜0.05). IMD pre-treatment significantly inhibited all these effects (all P＜0.05). There were no differences of above parameters between empty plasmid group and I/R group. Conclusion IMD pre-treatment protects against renal I/R injury by inhibion of tubular epithelial cell apoptosis.
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