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1.
Chinese Journal of Medical Education Research ; (12): 501-503, 2011.
Artigo em Chinês | WPRIM | ID: wpr-416125

RESUMO

To better understand the current status of medical students in clinical medical ethics,we design the relevant questionnaire,with 468 medical students conducting a questionnaire survey.Findings in general are more satisfactory.but there are great differences on certain issues.Educational Strategies:medical education curriculum should open more humanities courses and post-clinical teachers should pay close attention to ethics education for medical students.

2.
Chinese Journal of Clinical Pharmacology and Therapeutics ; (12)2004.
Artigo em Chinês | WPRIM | ID: wpr-564405

RESUMO

AIM:To investigate the protection mechanisms of rosiglitazone on diabetic nephropathy.METHODS:Rat mesangial cells(MC) were incubated in media containing 5.5 mmol/L normal control glucose,25 mmol/L high concentration glucose,25 mmol/L glucose +20 ?mol/L rosiglitazone maleate.Cells proliferation were assessed by CCK-8.Synthesis of fibronectin(FN),type Ⅳ collagen(Col-Ⅳ),transforming growth factor-?1(TGF-?1) and matrix metalloproteinase inhibitor-1(TIMP-1) in supernatant were determined by ELISA method,the activities of matrix metalloproteinase-2,9(MMP-2,9) in supernatant were determined by gelatinase zymography.RESULTS:Compared with control group,MC cultured with high concentration glucose showed a high growth rate and increased synthesis of Col-Ⅳand FN,decreased the activities of MMP-2 and MMP-9,and increased secretion of TGF-?1 and TIMP-1.Compared with high glucose group,these changes could be reversed by rosiglitazone intervention.CONCLUSION:Rosiglitazone could inhibit high concentration glucose-induced proliferation of mesangial cells,decrease synthesis of extracellular matrix,and increase degradation of extracellular matrix.

3.
Chinese Journal of Clinical Pharmacology and Therapeutics ; (12)2002.
Artigo em Chinês | WPRIM | ID: wpr-565659

RESUMO

AIM: To investigate the effects of fenofibrate(FB) and rosiglitazone(RG) on the signal passway of p38 mitogen-activated protein kinases(p38 MAPK) in glomerular mesangial cells cultivated in high concentration of glucose.METHODS: Rat mesangial cells(MC) were incubated in 5.5 mmol/L normal control glucose,25 mmol/L high glucose(HG),HG+100 ?mol/L fenofibrate(FB+HG),HG+20 ?mol/L rosiglitazone maleate(RG+HG),respectively.The fibronectin(FN) and type Ⅳ collagen(Col-Ⅳ) in supernatant were determined by ELISA.The expressions of p38MAPK and phospho-p38MAPK proteins in cytoplasm and nuclei were detected by Phospho-ELISA.The mRNA expression of p38MAPK was detected by semi-quantitative reverse transcription polymerase chain reaction(RT-PCR).RESULTS: Compared with normal control,the Col-Ⅳand FN in supernatant in HG group were much higher,the expression of p-p38MAPK was increased in cytoplasms and nuclei.Col-Ⅳ and FN were obviously decreased with the treatment of FB or RG,and the expression of p-p38MAPK in nuclei was down-regulated,but the expression of p-p38MAPK in intracytoplasm had no changes.There were no significant differences of the expressions of total protein and mRNA of p38MAPK among four groups.CONCLUSION: FB,RG could inhibit the activation of p38MAPK in nuceli of MC cultivated in high concentration of glucose,and then reduce the synthesis of extracellular matrix.

4.
Chinese Journal of Clinical Pharmacology and Therapeutics ; (12)2000.
Artigo em Chinês | WPRIM | ID: wpr-558185

RESUMO

AIM: To investigate the effect of losartan on the mRNA expression of type 2 angiotensin II receptor and cytokines in diabetic rat kidney.METHODS: SD rats were randomly divided by following groups: control rats(group C),diabetic rats(group D) and diabetic rats treated with losartan (30(mg?kg~(-1)?d~(-1)),by gavage,group DT).At the end of 8-weeks study,mRNA expressions of the type 2 angiotensin II receptor(AT_2),transforming growth factor-?_1(TGF-?_1),platelet-derived growth factor-B(PDGF-B),tumor necrosis factor-?(TNF-?) and collagen Ⅳ in rats renal cortex were measured by RT-PCR,respectively.In addition,angiotensin Ⅱ level in renal cortex was determined by the radioimmunoassay.RESULTS: In group D,urine protein excretion(P

5.
Chinese Journal of Pathophysiology ; (12)1986.
Artigo em Chinês | WPRIM | ID: wpr-524445

RESUMO

AIM: To investigate the molecular mechanism of amylin in inducing apoptosis of human pancreatic islet ?-cells. METHODS: Human pancreatic islet cells were isolated and cultured. The cells were treated with amylin or amylin and aminoguanidine (AG group) for 24 h, respectively. Apoptosis of pancreatic islet ?-cells was studied by in situ TUNEL method combined with double staining for insulin and ELISA. The levels of insulin, NO 2 -/NO 3 - and glutathione (GSH), p53 mRNA and bcl-2 mRNA were also detected. RESULTS: (1) The enrichment factor and the apoptosis rate of pancreatic islet ?-cells in amylin group were markedly higher than that in control group and AG group ( P

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