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AIM: To investigate the effects of vitamins (A, C and E) on liver injury induced by ethanol administration during liver regeneration in rats. METHODS: Male Wistar rats subjected to 70% partial hepatectomy were divided into five groups (groups 1-5). During the experiment, animals of Group 1 drank only water. The other four groups (2-5) drank 30 mL of ethanol/L of water. Group 3 additionally received vitamin A, those of group 4 vitamin C and those of group 5 received vitamin E. Subsequently serum alanine aminotransferase (ALT), aspartate aminotransferase (AST), albumin and bilirubin were measured colorimetrically. Lipid peroxidation (thiobarbituric-acid reactive substances, TBARS) both in plasma and liver was measured, as well as liver mass gain assessment and total DNA. RESULTS: Compared with sham group, serum AST and ALT increased significantly under ethanol treatment (43% and 93%, respectively, with P 〈 0.05). Vitamin C and vitamin E treatment attenuated the ethanol-induced increases in ALT and AST activity. Ethanol treatment also decreased serum albumin concentration compared to sham group (3.1 ± 0.4 g/dL vs 4.5 ± 0.2 g/dL; P 〈 0.05). During liver regeneration vitamins C and E significantly ameliorated liver injury for ethanol administration in hepatic lipid peroxidation (4.92 nmol/mg and 4.25 nmol/mg vs 14.78 nmol/mg, respectively, with P 〈 0.05). In association with hepatic injury, ethanol administration caused a significant increase in both hepatic and plasma lipid peroxidation. Vitamins (C and E) treatment attenuated hepatic and plasma lipid peroxidation. CONCLUSION: Vitamins C and E protect against liver injury and dysfunction, attenuate lipid peroxidation, and thus appear to be significantly more effective than vitamin A against ethanol-mediated toxic effects during liver regeneration.  相似文献   
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目的探讨卵裂球损伤对于不同冷冻方法冻融胚胎移植临床结局的影响。方法回顾性分析2009年1月至2013年12月共821例在本中心进行冻融胚胎移植的患者资料。根据胚胎卵裂球损伤情况分为A组:移植的胚胎均为卵裂球完整胚胎;B组:移植的2枚胚胎有1枚有卵裂球损伤;C组:移植3枚胚胎中只有1枚有卵裂球损伤;D组:移植3枚胚胎中只有1枚卵裂球完整胚胎;E组:移植胚胎均为卵裂球受损胚胎。按照冷冻方法(慢速程序法、玻璃化法)分别比较各组的临床资料和妊娠结局。结果慢速程序法中B、C、D三组临床妊娠率和胚胎种植率与A组相比均无显著性差异(P0.05),而E组临床妊娠率和胚胎种植率显著低于A组(P0.05)。玻璃化法中A组临床妊娠率和胚胎种植率显著高于B、D、E三组(P0.05)。结论移植包含1~2枚卵裂球受损胚胎对于慢速程序化冻融胚胎移植临床结局无显著影响;对于玻璃化冻融胚胎移植,移植胚胎中卵裂球完整胚胎2枚时其临床妊娠率和胚胎种植率显著降低。  相似文献   
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目的:调查产科医生对妊娠期妇女的心理支持与产褥期妇女SCL-90为负相关因素。方法:采用王征宇修订的症状自评量表(SCL-90)对300名在霸州市第一医院及霸州市妇幼保健院孕检及分娩的妇女作为研究对象做产褥期(SCL-90)测查。结果:产科医生心理支持降低产褥期妇女中阳性症状者(大于43)出现率,占群体的45.33%。结论:产科医生心理支持降低产褥期妇女中阳性症状者的出现率,提高产褥期妇女心理健康水平。  相似文献   
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Objective To investigate the effect ofperoxisome proliferator-activated receptor-α (PPARα) and PPARγ activators on tumor necrosis factor-α (TNFα) expression in neonatal rat cardiac myocytes.Methods Primary cultures of cardiac myocytes from 1- to 3-day-old Wistar rats were prepared, and myocytes were exposed to lipopolysaccharide (LPS) and varying concentrations of PPARα or PPARγ activator (fenofibrate or pioglitazone).RT-PCR and ELISA were used to measure TNFα, PPARα, and PPARγexpression in cultured cardiac myocytes. Transient transfection of TNFα promoter with or without nuclear factor-kappaB (NF-κB) binding site to cardiac myocytes was performed.Results Pretreatment of cardiac myocytes with fenofibrate or pioglitazone inhibited LPS-induced TNFα mRNA and protein expression in a dose-dependent manner. However, no significant changes were observed on PPARα or PPARγ mRNA expression when cardiac myocytes were pretreated with fenofibrate or pioglitazone. Proportional suppression of TNFαpromoter activity was observed when myocytes was transiently transfected with whole length of TNFα promoter (-721/ 17) after being stimulated with LPS and fenofibrate or pioglitazone, whereas no change of promoter activity was observed with transfection of TNFα reporter construct in deletion of NF-κB binding site (-182/ 17).Conclusions PPARα and PPARγ activators may inhibit cardiac TNFα expression but not accompanied by change of PPARα or PPARγmRNA expression. Therefore PPARα and PPARγ activators appear to play a role in anti-inflammation.The mechanism may partly be involved in suppression of the NF-κB pathway.  相似文献   
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Objective:To investigate the apoptosis of dopaminergic neurons and the protective effect of nicotine in 1-methyl-4-phenyl- 1, 2,3,6-tetrahydropyridine (MPTP)-induced mouse model of Parkinson's disease. Methods:The mouse model of Parkinson's disease were formed by MPTP (30 mg/kg/d×7, i.p. ); and the loss and apoptosis of dopaminergic neurons was observed by Tyrosine Hydroxylase(TH) and TUNEL stains.In "Nicotime plus MPTP" group, mice were pretreated with nicotine before MPTP injection. The putative protective effect of nicotine was analyzed. Results:The number of TH-positive cells decreased during MPTP treatment. Apoptotic neurons began to appear after three injections of MPTP and peaked on the 8th day. In the MPTP-intoxicated mice treated with nicotine, the loss of TH-positive cells was significantly less than that of MPTP- treated group (30 mg/kg/d×7)(P 〈 0.05). Conclusion:The chronic treatment of MPTP can induce the apoptosis of dopaminergic neurons in substantia nigra, and nicotine might have a neuroprotecitve effect on dopaminergic neurons against MPTP toxicity.  相似文献   
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