Objective To investigate the role of NF-kB in cytokines (IL-1?, TNF-? and IFN-r) -induced impairment of INS-1 cell, a pancreatic islet ?-cell line. Methods Retrovirus expressing IkB??N with mutant IkB?(inhibitor of NF-kB ) was constructed. Immunoblot analysis, fluorescence analysis using a kB-1uc reporter gene and thiazolyl blue viability assay were applied in this study. Results IL-1?-induced IkB? degradation and NF-kB activation were found in INS-1 cells but not in INS-1/IkB??N cells infected with IkB??N retrovirus. The viability of INS-1 cells incubated with the combination of IL-1? and IFN-r or TNF-? and IFN-r was decreased but INS-1/IkB??N cells could resist these cytokines-induced decrease of cell viability. Conclusion IL-1?, TNF-?can decrease the viability of? cells, while IFN-r may have some enhancing role. Inhibition of NF-kB activation can protect ? cells from the cytotoxicity of the cytokines.

OBJECTIVE:To discuss problems concerning the current sampling test of drugs in China.METHODS:The rationality of the current drug sampling test method was analyzed empirically according to the theory of sampling test.RESULTS&CONCLUSION:The current drug sampling test method is far from perfect and by which the quality of drugs was unable to be effectively controlled.It is recommended that drug monitoring institutions should work out more scientific sampling test scheme so as to ensure the quality of drugs.

Objective To observe the protective effect of high expression of mouse proxisome proliferator activated receptor γ1（PPARγ1）on free fatty acid （FFA）-induced βTC3 cell impairment. Methods The recombinant plasmid pcDNA3.1/PPARγ1 was generated with cloning and was stably transfected into pancreatic β TC3 cells. The expression was detected with semi-quantitative RT-PCR. Then the cell viability of wild βTC3 cells was compared with that of the βTC3 cells with high expressed PPARγ1 by MTT viability assay after they were exposed to high-level FFA for 48 hours. Results The sequencing results for amplified target gene showed that the sequence of PPARγ1 from Chinese Kunming mouse is similar to that of mouse PPARγ1 in Genebank, only the codon coding Asp at the site of 421 amino acid changed from AAU to AAC. PPARγ1 was efficiently expressed in βTC3 cells in vitro. The cell viability of wild βTC3 cells reduced after being exposed to high-level FFA for 48 hours（P< 0.01）. Higher the level of FFA was, more obvious the reduction of the cell viability was （r=-0.962, P<0.01）. However, at the same condition, the cell viability of the βTC3 cells high expressing PPARγ1 had no significant change（P>0.05）. Conclusion The high expression of PPARγ1 could protect βTC3 cells from FFA-induced impairment

Diabetes could damage the peripheral and central nervous system,and was the risk factor of cognitive impairment in the elderly.The pathogenesis of cognitive dysfunction caused by diabetes was complex.At present,hyperinsulinemia and/or insulin deficiency,glycemic control,glycation end-products,inflammatorv mediators,hypothalamic-pituitary-adrenal axis dysfunction,blood-brain barrier dysfunction and other factors were considered to be the major causes of cognitive impairment in elderly patients with diabetes.Good metabolic control may help prevent its occurrence and/or progression.

Objective To investigate the effects of melatonin on oxidative stress and metabolisms of glucose and lipid of diabetic patients.Methods By means of random,single-blind,placebo-parallel control clinical trial,91 of diabetic patients were randomly divided into melatonin group and placebo group.The parameters of Glutathione Peroxidase (GSH-Px),Superoxide Dismutase(SOD)and Malondialdehyde(MDA),as well as the profiles of glycemia and lipidemia were observed before and after 8 weeks treatments,respectively.Results Before treatment,both the serum levels of GSH-Px and SOD of diabetic patients were decreased significantly,whereas the serum level of MDA increased significantly.After 8 weeks consecutive melatonin treatment,the serum levels of GSH-Px and SOD increased significantly,whereas the serum level of MDA decreased significantly compared with pre-treatment in the melatonin group.There were no significant variations of serum levels of GSH,SOD and MDA observed before and after treatment in the placebo group.There were significan benefit on FBG and HbA1c after 8 weeks treatment compared with pre-treatment.The other profile of glycemia and lipidemia such as PBG,TG,TC,LDL-C and HDL-C hed no significant variations compared with pre-treatment.There were no significant variations of the profiles of glycemia and lipidemia compared with pre-treatment in the placebo group.Conclusion Melatonin significantly inhibits oxidative stress provoked by hyperglycemia and has beneficial effects on the glucose homeostasis of diabetic patients.

Objective To investigate the effects of fluvastatin on expression of connective tissue growth factor (CTGF)in the myocardium of diabetic rats. Methods Thirty-two Sprague-Dawley rats were randomized into four groups: normal control, untreated and STZ-induced diabetic rats, and diabetic rats treated with low-dose and high-dose fluvastatin.After 12 weeks′ intervention, body weight as well as the weights of both whole heart and its left ventricle were measured to calculate the ratio of heart weight to body weight (H/B) and the left ventricle mass index (LVMI).The mRNA expression of CTGF, transforming growth factor β1 (TGF-β1), fibronectin (FN),collagen type Ⅲ (ColⅢ) in the myocardium were detected by RT-PCR. Results Compared with the normal control group, the untreated diabetic group showed the increased (all P<0.05) H/B, LVMI and mRNA expressions of CTGF, TGF-β1, FN, and Col Ⅲ in the myocardium. In addition to the effective regulation of lipid metabolism, fluvastatin treatment could obviously reduce the increment of H/B and LVMI(P<0.05～0.01), and suppress the mRNA expressions of CTGF, TGF-β1, FN, and Col Ⅲ in the myocardium of diabetic rats(P<0.01).The down-regulation of CTGF was more significant than that of TGF-β1.All these effects were in dose dependent way. Conclusions Fluvastatin inhibits extracellular matrix accumulation in the myocardium of diabetic rat.Down-regulating the overexpression of CTGF in diabetics is an underlying mechanism of fluvastatin in the cardiac protection.

Rosiglitazone was used for intervention of atherosclerosis in diabetic rabbits.The results showed that the intima/medium thickness ratio,cross section area of plaque,and the expressions of NADPH oxidase p22phox,gp91 phox were decreased;while the total anti-oxidative ability was increased after administration of rosiglitazone as compared with the non-intervention group(all P<0.05).Compared with rosiglitazone treatment group,serum hepatocuprein leveI in rosiglitazone prevention group was increased,while serum malonaldehyde level decreased(both P<0.05).This study suggests that rosiglitazone may have the effect of reducing the oxidative stress and the formation of atherosclerotic plaque in diabetics.

Detection of the possible role of ERp46,new endoplasmic reticulum protein,on palmitic acid-inducedendoplasmic reticulum stress-apoptosis pathway in βTC6 cells for the new treatment of type 2 diabetes.Results showed that ERp46 played a protective role in palnutic acid-induced cell apoptosis by decreasing the endoplasmic reticulum stress response through three pathway.

Through investigation on the cognition and status of the cultivation of innovative ability of the students,we found that the innovative ability of medical students was extremely weak.Their practical ability was out of joint to the cognition of innovative ability.We are trying to analyze the reasons and resolve the problem.

Objecfive To evaluate the effects of cilostazol on the prevention of microvascular complications in diabetic patients.Methods 60 diabetic patients with microvascular complications were orally given cilostazol for 1 month.Changes of Mean platelet volume (MPV),plateletcrit (PCT),platelet distribution width (PDW) and platelet count (PLT) were studied.Results With administration of cilostazol,MPV and PDW decreased significantly. Conclusion Cilostazol improves platelet parameters,suggesting that it could prevent the progression of microvascular diseases.