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.

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.

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.

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

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