Objective To investigate the effects of chronic pain on spatial learning ability and the expression of neuronal cell adhesion molecules (NCAM) in hippocampus in neonatal rats.Methods Sixty newborn SD rats of both sexes were randomly divided into pain group ( n = 30) and control group ( n= 30). In pain group complete Freund' s adjuvant (CFA) 20 ?l was injected subcutaneously in the plantar surface of left hindpaw on the 2nd day after birth, whereas in control group normal saline 20 ?l was injected instead of CFA. The animals were weighed on the 3rd, 11th and 22nd day after birth. Ten animals in each group were anesthetized with intraperitoneal pentobarbital and killed on the 11th and 22nd day after birth respectively. The brains were immediately removed for determination of NCAM expression in CA3 and dentate gyms of hippocampus using immuno-histochemical staining technique. Morris water maze test was performed starting from the 21st day after birth for 8 consecutive days to assess the spatial learning ability ( n = 10 in each group) .Results The latent period before finding the hidden-plateform was significantly longer on the 1st and 4th day of the test (22nd and 25th day after birth) in pain group than in control group (P

Objective To investigate the effects of chronic inflammatory pain induced by injection of complete Freund' s adjuvant (CFA) into the plantar surface of hindpaw on the development of learning and memory and proenkephalin mRNA expression in hippocampus of neonatal rats. Methods sixty neonatal SD rats (6 rats from each of 10 litters) were randomly divided into control and chronic pain group ( n = 30; 3 rats from each of the 10 litters). In chronic pain group CFA 20 ? l was injected subcutaneously into plantar surface of left hindpaw on the 2nd day after birth whereas in control group normal saline 20 ? l was injected instead of CFA. Ten animals (1 rat from each of the 10 litters) in each group were killed on the 10th and 21st day after birth respectively. Hippocampi were removed for determination of proenkephalin mRNA expression by RT-PCR. Ten animals (1 rat from each of the 10 litters) in each group underwent Morris water maze test 3 times a day for 8 days starting from the 21st day after birth. Results The mean latent period before the rats found the hidden platform was significantly longer in chronic pain group than in control group. When the platform was removed the swimming time and distance of the rats in chronic pain group were significantly shorter than those in control group. There was no significant difference in the latent period before the rats found the visible platform between the two groups. The proenkephalin mRNA expression in hippocampus on the 10th and 21st day after birth was significantly lower in chronic pain group than in control group ( P

0.05).The sera levels of sCD40L in CHD were significantly and positively correlated with Jenkins score(r=0.524,P

BACKGROUND: The emphasis for preventing and treating cardiovascular diseases is to detect correlated risk factors. Among those accepted risk factors, whether serum uric acid (SUA) plays an independent role in the development of diseases is unknown.OBJECTIVE: To study SUA distribution and the prevalence of hyperuricemia, in middle-aged and elderly residents from the conjoining area between city and countryside in Guangzhou, and its association with other cardiovascular disease risk factors.DESIGN: Cross-sectional study.SETTING: Department of Cardiovascular internal medicine, Prevention and Health department, the Third Affiliated Hospital of Sun Yat-sen University.PARTICIPANTS: An investigation on the risk factors of cardiovascular diseases was carriedout among total 890 residents living at the conjoining area between city and countryside in Guangzhou in December 2002. A total of 642 persons including 152 men and 490 women who were above 55years and had complete data were involved, and all of them understood and agreed to the investigation.the-spot investigation. Systolic pressure, diastolic pressure, body height and body mass were measured, and then body mass index [body mass (kg)/body height (m)2] was calculated. High-density lipoprotein cholesterol, low-density lipoprotein cholesterol, triglyceride and total cholesterol were measured by endpoint method; SUA was measured by uricolase turbidimetric method.were defined as hyperuricemia. Diagnosis of hypertension was made according to the WHO/ISH 1999 Prevention and Cure Guidelines of Hypertension. Various kinds of dyslipidemia were diagnosed based on Prevention and Cure suggestions of dyslipidemia for Chinese (1997). Obesity was defined, according to 2002 International Obesity Special Working Group'skewness distribution and described by Median ± quartile. Spearson correlation analysis was used to determine the dependability between SUA and other selected cardiovascular risk factors. Binary Logistic regression analysis was done for further analysis.SUA and other cardiovascular risk factors.terolemia and hypertriglyceridemia in men and women were 30.3%, 30.8%;were (357.30±66.77) and (299.80±59.64) μmol/L respectively. SUA level was positive correlated with age in women (r=0.18, P ＜ 0.01), but was not of SUA in men were 293.53, 357.30, 427.08 (μmol/L), and in women were 247.60, 299.80, 366.88 (μmol/L). Low-density lipoprotein cholesterol, total cholesterol, triglyceride, blood pressure and body mass index were positively associated with SUA, while high-density lipoprootein cholesteral was negtive correlated with SUA. In both men and women, triglyceride, total cholesterol, systolic blood pressure and body mass index were positively correlated with SUA significantly (r=0.09-0.35, P ＜ 0.05-0.01), but highdensity lipoprotein cholesterol was negatively correlated with SUA significantly (r=-0.21, -0.25, P ＜ 0.05, 0.01); diastolic blood pressure in men and low high-density lipoprotein cholesterol in women were positively correincluded to Logistic regression equation were age, body mass index and triglyceride [OR (95%CI): 1.048 (1.023-1.073), P=0.000; OR (95%CI): 1.156(1.096-1.219), P=0.000; OR (95%CI): 1.436 (1.224-1.684), P=0.000].uricemia is correlated with hypertension and various kinds of dyslipidemia.The elevation of SUA may be an important marker of cardiovascular dismay affect SUA mostly, and increase the risk for hyperuricemia.

AIM: To study the effects of metformin on the pressure overload-induced cardiac hypertrophy in rats. METHODS: Transverse aortic constriction (TAC) model of rat was made through laparotomy. One week after TAC surgery, the rats were randomly divided into 5 groups (n=8 in each group) and were administered with the corresponding drugs orally every day for 8 weeks: sham group (sham surgery, administered with 2 mL distilled water);TAC group (TAC rats, administered with 2 mL distilled water);metformin(MET) group (TAC rats, administered with MET at dose of 300 mg·kg~(-1)·d~(-1));MN group [TAC rats, administered with MET at dose of 300 mg·kg~(-1)·d~(-1) plus NOS inhibitor, NG-nitro-L-arginine methyl ester (L-NAME) 50 mg·kg~(-1)·d~(-1)] and L-NAME group (TAC rats, administered with L-NAME at dose of 50 mg·kg~(-1)·d~(-1)). After treated for 8 weeks, the echocardiography, hemodynamics, the ratio of heart weight to body weight (HW/BW) and histological examination of the heart were performed. The levels of myocardial AMP-activated protein kinase subunit α (AMPKα), p-AMPKα~(Thr172), endothelial nitric oxide synthase (eNOS) and p-eNOS~(Ser1177) were detected by Western blotting. Plasma and myocardial nitric oxide (NO) were detected biochemically. RESULTS: After 8 weeks treatment, the wall thickness of left ventricle, the heart weight/body weight ratio (HW/BW), and the left ventricular myocardial perivascular fibrosis and myocardial interstitial fibrosis of the animals in TAC group were significantly increased as compared to those in sham rats. Treatment with MET for 8 weeks significantly attenuated left ventricular hypertrophy and improved cardiac function in TAC rats. These effects of MET were mostly abolished by L-NAME. Molecular biology and biochemical testing revealed that the levels of left ventricular myocardial p-AMPKα~(Thr172) and p-eNOS~(Ser1177), as well as the levels of myocardial and serum NO were significantly increased in MET group. CONCLUSION: Long-term MET treatment significantly inhibits the cardiac hypertrophy and the myocardial fibrosis and improves the cardiac functions in pressure-overload rats. The anti-hypertrophic effects of MET may be mediated via activation of AMPK-eNOS signaling pathway.