Expressions of Tumor Necrosis Factor alpha-induced Protein 3 and Mammary Serine Protease Inhibitor in Radiotherapy of Nasopharyngeal Carcinoma.

OBJECTIVE: To study the expressions of tumor necrosis factor alpha-induced protein 3(TNFAIP3) and mammary serine protease inhibitor (Maspin) in the radiotherapy of nasopharyngeal carcinoma and explore the differences in radiosensitivity and radioresistance,the relation with the occurrence and development of radioresistance. METHODS: The TNFAIP3 and Maspin mRNA expressions were detected by using TNFAIP3 and Maspin multi-point labeled DIG probes in situ hybridization. RESULTS: In radiosensitivity and radioresistance of nasopharyngeal carcinoma,the moderately and strongly positive TNFAIP3 mRNA expression rates were 27.50% and 48.33% (P=0.037), and the moderately and strongly positive Maspin mRNA expression rates were 67.50% and 46.67% (P=0.040). In the radioresistance of nasopharyngeal carcinoma,TNFAIP3 mRNA moderately and strongly positive expressions were positively correlated with TNM stage (P=0.005). In distant metastasis and no distant metastasis (70.00% and 37.50%, P=0.018), the expression rates had statistical significance. The Maspin mRNA moderately and strongly positive expressions were positively correlated with TNM stage (P=0.039) and T stage (P=0.021). In distant metastasis and no distant metastasis (65.00% and 37.50%, P=0.044), the expression rates had statistical significance. CONCLUSION: TNFAIP3 may be involved in the development of radioresistant nasopharyngeal carcinoma,and Maspin may be related with the invasion and metastasis of radioresistant nasopharyngeal carcinoma.

[Study on abnormal glucose and lipid metabolism among 771 in-patients with ischemic stroke].

OBJECTIVE: To study the epidemiological characteristics of abnormal glucose and lipid metabolism in in-patients with ischemic stroke. METHODS: A total number of 771 in-patients with ischemic stroke, hospitalized in the Department of Neurology/Endocrinology from Changzhou No. 2 Hospital from April 2007 to April 2008 were enrolled in this study. After identifying the condition of glucose metabolism, all diagnosis-undetermined patients received oral glucose tolerance test. RESULTS: Among in-patients with ischemic stroke, 41.8% of the patients were finally diagnosed as diabetes, with 23.4% classified as 'impaired glucose tolerance'. The prevalence of 'abnormal glucose metabolism' was 65.2% in total. If diabetes in the in-patients with ischemic stroke was diagnosed only by fast plasma glucose instead of oral glucose tolerance test, 58.5% diabetic patients would have been misdiagnosed. Abnormal lipid metabolism existed in inpatients with cerebral ischemic stroke were noticed. These abnormalities of lipid metabolism were mainly consisting of increased triglyceride and decreased HDL-C cholesterol. CONCLUSION: The majority of in-patients with ischemic stroke appeared to have had abnormal glucose and lipid metabolism. It seemed necessary to promptly and correctly diagnose these patients with abnormal glucose metabolism by oral glucose tolerance test to reduce the chances of developing the recurrence of stroke.

[Effects of calorie restriction on SIRT1 expression in liver of nonalcoholic fatty liver disease: experiment with rats].

OBJECTIVE: To investigate the molecular mechanisms of calorie restriction (CR) in treatment of nonalcoholic fatty liver disease (NAFLD). METHODS: 25 male Wistar rats were randomly divided into 2 groups: normal control group (NC, n = 7) fed with regular diet and high fat diet-NAFLD model group (HFM, n = 18) fed with high-fat diet. Two months later, the rats in Group HFM were further divided into 2 subgroups: continuous high-fat feeding group (HF, n = 9) and normal diet feeding with 60% calorie restriction group (CR, n = 9). The rats were sacrificed after 1 month calorie restriction. By the end of experiment, body weight (BW), visceral fat mass (VF), fasting plasma glucose (FPG), fasting serum insulin (FINS), blood lipids (BL), including total cholesterol (TC) and triglyceride (TG), and hepatoultrastructure changes were examined to evaluate the effect of different feeding protocols on the experimental animals. The mRNA expression of the longevity gene SIRT1 in the liver was detected by RT-PCR. Western blot analysis was performed to determine the expression of SIRT1 protein in each group. RESULTS: Electron microscopy showed that the rats in group HF displayed obviously abnormal hepatoultrastructure, and the ultramicropathology changes of liver cell were improved obviously in Group CR. The VF, FINS, FPG, TC, and TG of the Group HF were 15.1 g +/- 4.1 g, 29.22 mU/L +/- 7.28 mU/L, 6.2 mmol/L +/- 1.46 mmol/L, 2.61 mmol/L +/- 0.29 mmol/L, and 1.35 mmol/L +/- 0.21 mmol/L respectively, all significantly higher than those in Group NC (9.0 g +/- 0.4 g, 13.09 mU/L +/- 1.18 mU/L, 4.4 mmol/L +/- 0.57 mmol/L, 1.41 mmol/L +/- 0.28 mmol/L, and 0.67 mmol/L +/- 0.10 mmol/L respectively, all P < 0.01). The mRNA expression of SIRT1 in the liver of Group HF was significantly lower than that of Group NC (P < 0.05), and the mRNA expression of SIRT1 in the liver of Group CR was significantly higher than those of Group HF and Group NC (both P < 0.01). The protein expression of SIRT1 of Group HF was significantly lower than that of Group NC (P < 0.01), and that of Group CR was significantly higher than that of Group HF, however, still significantly lower than that of Group NC (both P < 0.01). The BW and VF, FINS, FPG, TC, and TG of Group CR were all significantly lower than those of Group HF (all P < 0.01). CONCLUSION: CR can reverse NAFLD significantly. The increased expression of SIRT1 in liver induced by CR may be an important molecular mechanism involved in the improvement of NAFLD by CR.

The expression of SIRT1 in nonalcoholic fatty liver disease induced by high-fat diet in rats.

OBJECTIVE: SIRT1 is an NAD(+)-dependent deacetylase and its enzymatic activity may be regulated by cellular energy. SIRT1 overexpression reduces the level of oxygen consumption, which is correlative with nonalcoholic fatty liver disease (NAFLD). To elucidate the role of SIRT1 on the development of NAFLD, we investigated the expression of SIRT1 in NAFLD induced by high-fat diet in rats and the effects of calorie restriction. METHODS: Thirty-one male Wistar rats were divided at random into four groups. The rats in the normal control group NC (n=7) and in the NAFLD model group HF (n=9) were fed ad libitum with normal chow and high-fat diet, respectively, for 3 months, the rats in the calorie restriction (CR) group HCR (n=9) were fed with a high-fat diet for 2 months and then 60% CR with normal chow for 1 month, and the rats in group CRH (n=6) were firstly fed with 60% CR with normal chow for 1 month and then fed a high-fat diet for 2 months. At the end of the experiment, some parameters and expressions of SIRT1 were detected. RESULTS: The rats in group HF displayed NAFLD. Compared with group NC, the expression of SIRT1 protein was significantly decreased (P<0.01). However, the lower body weight and visceral fat mass of rats in group HCR were showed. Compared with group HF, CR increased the expression of SIRT1 in liver significantly (P<0.01). Consequently, the ultramicropathology changes of NAFLD prominently improved in this group. Meanwhile, the rats in group CRH displayed higher expression of SIRT1 protein and very gentle pathology changes of NAFLD. CONCLUSION: The expression of SIRT1 is reduced significantly in NAFLD induced by high-fat diet in rats. CR increase-SIRT1 protein expression may be an important mechanism by which CR improves NAFLD.