Objective To investigate the relationship of peroxisome proliferator activated receptor gamma ( PPAR?)C161T gene polymorphism with related diseases of metabolic syndrome. To disscuss the mechanism of the elderly diseases from gene level and the relation between the gene polymorphism and lipid metabolism. Methods Three hundred seventy one non-sibship subjects of Han nationality were investigated in this study, including 69 old healthy subjects, 302 elderly cases diagnosed as metabolic syndrome. PPAR? C161T gene polymorphism was determined by polymerase chain reaction and restriction fragment length polymorphism, and radioimmunoassay was used to detect serum insulin. The insulin resistance was obtained from homeostasis model assessment (HOMA), and blood glucose, blood lipoprotein, height, weight and so on were tested. The frequencies of PPAR? C161T genotypes and the allele were compared with the clinical data. Results (1) In the groups of old normal health and metabolic syndrome, "T" allele frequency was 0.217,0.201, and "C" allele frequency was 0.783, 0.798 . There was no significant difference between the groups. (2)The triglyceride in CC genotypes of the metabolic syndrome was significantly higher than that in "T" allele carriers. Conclusions (1) The distributing trend of PPAR ? C161T gene polymorphism of the Han nationality in Wuhan in the elderly normal healthy group was in accord with that in the group of the elderly metabolic syndrome. (2) PPAR ? C161T substitution can influence metabolic syndrome, especially in liporprotain metabolism. "T" allele is associated with lower level of triglyceride.

AIM: To explore the effect and mechanism of endothelin receptor antagonist on local angiotensin system of hypertrophic myocardial tissue. METHODS: Twenty four rats were randomly divided into 3 groups, control group (CG), hypertrophy group (HG) and endothelin receptor antagonist group (EG). The ratios of left ventricle weight to body weight (LVW/BW) and left ventricle weight to heart weight (LVW/HW) were measured to reflect myocardial hypertrophy. Protein expression of AT1R was detected by immunohistochemistry. The concentration of Ang Ⅱ was determined by ria. Activity of ACE was examined by spectrophotometry. A piece of myocardial tissue was observed in light microscope after HE or VG dyeing. RESULTS:(1) In comparison to CG, LVW/BW, LVW/HW, ACE activity, the concentration of Ang Ⅱ and the expression of AT1R of HG were increased significantly (P

AIM: To evaluate the effects of interfer ?-2b (IFN ?-2b ) on atherosclerosis(AS).METHODS: Thirty normal male rabbits were randomly divided into five groups:normal control group(NC group, n= 6), atherosclerosis group(AS group, n =6),virus (herpesvirus Ⅰ,HSV-Ⅰ)infected atherosclerosis group(V group, n= 6), interferon (interferon ?-2b) intervented atherosclerosis group (IFN-Ⅰgroup, n= 6),interferon intervented and virus infected atherosclerosis group (IFN-Ⅱ group, n= 6). Serum lipids were measured and the thoracic aortas were sampled for histopathological, immunohistochemical and in situ hybridization study. RESULTS: The aorta atherosclerosis areas of NC, IFN-Ⅰ and IFN-Ⅱ groups were lower than that of AS group significantly, respectively, and the area of AS group was lower than that of V group ( P

BACKGROUND: Peroxisome proliferation-activated receptor-gamma (PPARγ) is the member of nuclear receptor superfamily, and closely related with the formation of atherosclerosis.OBJECTIVE: To investigate the relationship between PPARγ C161→T gene polymorphism and coronary atherosclerotic heart disease (CAHD).DESIGN: Randomized controlled experiment SETTING: Department of Cardiology, Tonai Hospital of Huazhong University of Science and Technology; Department of Cardiology, Zhongnan Hospital of Wuhan University; Center for Human Genome Research,Huazhong University of Science and Technology; Department of Internal Medicine, Affiliated Hospital of Hubei University of Traditional Chinese Medicine; Institute of Geriatrics, Dongzhimen Hospital, Beijing University of Chinese Medicine PARTICIPANTS: Totally 203 CAHD patients aged (65±11) years, including 129 males and 74 females, were the inpatients and outpatients of Zhongnan Hospital of Wuhan University and Tonai Hospital of Huazhong University of Science and Technology from June 2002 to December 2005.And 156 cases of them were diagnosed by coronary arteriongraphy, among which 43 patients without coronary artery affection or with coronary stricture ＜ 50%, and 113 patients with coronary stricture ＞ 50 %. While 89 healthy physical examinees of Han race and mean (59±9) years old were enrolled as control group, including 56 males and 33 females. There was no blood relationship between controls and patients.METHODS: The experiment was conducted at Tongji Hospital of Huazhong University of Science and Technology from June 2002 to December 2005. PPARγ C161→T gene polymorphism was determined by polymerase chain reaction and restriction endonuclease fragment length polymorphisms. The radio-immunity technique, coronary angiography and clinical routine biochemical index were applied to analyze the genotypic frequency and allele frequency distributions as well as the relation between clinical data, biochemical index and different genotypes. The risk factors of CAHD were estimated in the patients of different genotypes.MAIN OUTCOME MEASURES: The genotypic frequency and allele frequency distributions, the relation between clinical data, biochemical index and different genotypes, along with the blood lipid, blood glucose, fasting insulin and body mass index (BMI).RESULTS: Totally 103 CAHD patients and 89 controls were involved in the result analysis of gene polymorphism and yielded different gene distribution frequencies.① In control group, "T" allele frequency was 0.213 and "C" allele frequency was 0.787, and in CAHD group, "T" allele frequency was 0.192 and "C" allele frequency was 0.808. There was no significant difference in the genotypic frequency and C, T allele frequencies between two groups (P ＞ 0.05).② The CC genotype was dominant in CAHD patients with coronary artery lesions, and showed significant differences from "T"allele carriers (CT+TT) (P ＜ 0.05). The CAHD risk in the "T" allele carries (OR: 0.56, 95% CI: 0.24-0.63) was much lower than that in the CC homozygote (OR: 1.92, 95% CI: 1.09-2.54).③ Apolipoprotein B in patients with CC genotype was obviously higher than that in patients with "T" allele (CT+TT) (P ＜ 0.05), and there was insignificant difference in the insulin resistance index (P ＞ 0.05).CONCLUSION: There is an important correlation between the substitution of PPARγ C161→T and CAHD, and "T" allele carriers demonstrate a lower risk of CAHD.