Objective To research the spatiotemporal pattern of N-cadherin expression during development of rat cardiomyocytes and age-related changes of N-cadherin expression. Methods Using immunohistochemical method,myocardial N-cadherins distribution was investigated in fetal rat and postnatal development(1 postnatal day to old rat),and quantitied by HIPAS-1000 computerized image analytical instrument. Results The expression of N-cadherin was located in myocardium of atrial and ventricule and septum interventriculare and papillary muscles.The N-cadherin immunolabeling was found in myocyte membranes and within cytoplasm in fetal rat heart.From neonatal to infant rat,the pattern of N-cadherin immunolabeling changed progressively,from being dispersed over the entire cell surface as in the fetal to the transverse terminals of the myocytes,toward the distribution within the intercalated disk.From young to old rat heart,the typical N-cadherin was located in transversely orientated intercalated disk.The percentage of N-cadherin immune postive area in rat ventricular myocardium showed a progressively changement with age.Conclusion The present paper demonstrated that the N-cadherin expression exists progressively with ages and the changing pattern of N-cadherin is closely related with development of the intercalated disk in rat myocardium.The mechanical coupling provided by adherens junctions is essential for the stable cell-cell contact.

Objective To investigate the relationship between nutritional risk and cognitive score in pa-tients with acute stroke .Methods From January 2015 to December 2015, 160 inpatients with acute stroke were observed and divided into two groups according to Nutritional Risk Screening 2002 (NRS 2002) scores.All the patients were on natural diets and did not receive enteral or parenteral nutrition support .Cognitive functions were evaluated using the Mini-Mental State Examination ( MMSE) within 24 hours and 6 months after the acute cere-bral artery diseases .Logistic regression analysis was performed to investigate the effects of nutritional risks on the cognition.Results Totally 145 patients entered the final analysis , among whom 72 had nutritional risks and 73 had no nutritional risks .The average ages of patients with nutritional risks were significantly older than those without nutritional risks [ (67.04 ±8.95) years vs.(63.10 ±9.12) years, P=0.027], along with significantly higher incidence of diabetes (75.0%vs.49.3%, P=0.001).The lesion locations showed no statistically signif-icant difference between two groups ( frontal lobe 24.5%vs.17.5%, P=0.670;parietal lobe and occipital lobe 40.8%vs.26.3%, P=0.398;basal ganglia region 51.0%vs.49.1%, P=0.490;brain stem and cerebellum 53.0%vs.42.1%, P=0.777).Compared to the patients without nutritional risks , the MMSE scores of the pa-tients with nutritional risks were lower within 24 hours, but without statistical significance (27.45 ±2.21 vs. 28.09 ±1.27, P=0.209);however, six-month follow-up showed that the MMSE scores were significantly differ-ent between two groups (24.70 ±2.16 vs.27.43 ±2.32, P=0.036).Univariate Logistic regression analysis was used to evaluate factors associated with cognitive impairment (MMSE<27).NRS 2002, ages, diabetes mellitus history, and body mass index entered in the Logistic regression analysis .In all patients, ages and NRS 2002 had a positive correlation with cognitive impairment (P=0.000, OR=1.156;P=0.004, OR=2.341).Conclusion The cognitive function in stroke patients with nutritional risks is worse than in patients without nutritional risks .

Objective To study the effects of tumor necrosis factor-?(TNF-?) on hypermetabolism of skeletal muscle protein in rats with chronic obstructive pulmonary disease(COPD) and explore the mechanisms. Methods Forty-five SD rats were randomly divided into normal control group,COPD group and COPD +TNF-? group(n=15).Rat COPD models were established by passive cigarette smoking in COPD group and COPD +TNF-? group.After dissecting and isolating the extensor digitorium longus(EDL) muscles,the EDL muscles were either cultured with media containing 10 ug/L recombinant rat TNF-? or without TNF-?.The subsequent changes in ubiquitin mRNA and protein levels were determined by real-time quantitative PCR and Western blot,respectively. Results The expressions of ubiquitin mRNA and protein of COPD group and COPD+TNF-? group were higher than those of normal contro1 group(P

Objective To investigate the correlation between the combination of smoking with CYP2E1-RsaⅠ and GSTT1 genes polymorphisms and pancreatic cancer. Methods The genetic polymorphisms of CYP2E1-RsaⅠ and GSTT1 were analyzed by polymorphism-polymerase chain reaction (PCR) technique in peripheral blood leukocytes of 150 pancreatic cancer cases and 150 non-cancer controls. Results The frequency of CYP2E1-RsaⅠ(c1/c1) and GSTT1(-) was 38.7% and 69.3% in pancreatic cancer cases and 20.7% and 44.7% in healthy controls, respectively. Statistical tests showed significant differences in the frequencies between the two groups (χ~2=15.75, P<0.01; χ~2=18.62, P<0.01). The risk of pancreatic cancer patients with CYP2E1-RsaⅠ(c1/c1) was significantly higher than that of controls (OR=3.19, 95% CI=2.53-4.26). The individuals who carried with GSTT1(-) had a higher risk of pancreatic cancer (OR=2.85, 95% CI=1.92-4.64). Combined analysis of the polymorphisms showed that the percentage of CYP2E1-RsaⅠ(c1/c1)/GSTT1(-) in pancreatic cancer and control groups was 30.7% and 6.7%, respectively (χ~2= 42.39, P<0.01). People who carried with CYP2E1-RsaⅠ(c1/c1)/GSTT1(-) had a higher risk of pancreatic cancer (OR=16.63, 95% CI=8.94-22.01). The smoking ratewas significantly higher in the case group than in the control group (OR=2.74, 95% CI=1.32-4.58, P<0.01), and statistical analysis suggested an interaction between smoking and CYP2E1-RsaⅠ(c1/c1) or GSTT1(-) genotypes polymorphisms which increased the risk of pancreatic cancer (OR=8.84, 95% CI=5. 51-11.62; OR=20.40, 95% CI=4.98-29.53). Conclusion CYP2E1-RsaⅠ(c1/c1) and GSTT1(-) are the risk factors in pancreatic cancer. Smoking is also related to the susceptibility to pancreatic cancer. There may be a synergetic interaction among CYP2E1-RsaⅠ(c1/c1) and GSTT1(-) and smoking on the elevated susceptibility of pancreatic cancer.

Atherosclerosis ; complications ; pathology ; Humans ; Thrombosis ; complications ; pathology

During percutaneous coronary intervention,thrombotic storm which is mediated by hypercoagulable state,mechanical distension induced-plaque rupture,platelet activation and adhesion is still the main cause of cardiovascular adverse events.The mortality rate is extremely high if not treated properly.Thrombotic storm can be diagnosed quickly through coronary artery angiography and myocardial blush grades.Once coronary thrombosis occurs,medicine including platelet Ⅱ b/Ⅲ a receptor antagonist tirofiban or vasodilators can rapidly improve coronary flow and effectively treat it.

Objective To investigate the correlation between the combination of smoking with CYP2E1-RsaⅠ and GSTT1 genes polymorphisms and pancreatic cancer.Methods The genetic polymorphisms of CYP2E1-RsaⅠ and GSTT1 were analyzed by polymorphism-polymerase chain reaction(PCR) technique in peripheral blood leukocytes of 150 pancreatic cancer cases and 150 non-cancer controls.Results The frequency of CYP2E1-RsaⅠ(c1/c1) and GSTT1(-) was 38.7% and 69.3% in pancreatic cancer cases and 20.7% and 44.7% in healthy controls,respectively.Statistical tests showed significant differences in the frequencies between the two groups(?2=15.75,P

Objective To investigate the association between syncope and transient suppression of sinoatrial node in patients with preexcitation syndrome and paroxysmal supraventricular tachycardia (PSVT).Methods Twelve patients (male 8,female 4;age range:19-49 years) were enrolled due to WPW(Wolff-Parkinson-White) syndrome and syncope when the tachycardia terminated.The function of sinoatrial node was evaluated with clinical electrophysiologic study,and then radiofrequency catheter ablation (RFCA) or antitachycardia pacemaker were optimized for the patients with a follow-up of 2 to 5 years.Results Electrocardiographic features of the 12 patients were: ventricular preexcitation (type A in 7 and type B in 5) and long pause when tachycardias ended up.Electrophysiologic study revealed the function of sinoatrial node was normal.Four patients received antitachycardia pacing therapy,5 underwent RFCA,and 3 received both.The 2 to 5 years follow-up found no relapse of PSVT associated syncope.Conclusion Transient suppression of sinoatrial node might explain the mechanism of syncope with preexcitation and PSVT.However,the reason why such a small group of patients differ from the majority of preexcited cases in clinical course remains to be unsettled.The first choice of prevention and treatment for these patients should be eliminating PSVT.Conventional pacemaker implantation for preventing syncope seems to be unnecessary.

Objective TO study the effect of trimetazidine on patients with unstable angina pectoris. Methods The pa-tients with unstable anglna pectoris with routine treatment were divided randomly into trimetazidine group(T) and nitro-glycerin group(N). They were given such treatment two weeks. Results There is decreased incidence of angina pectorisand less amount of nitroglycerin consumption in both groups. compared with before. There was no significant difference be-tween the two groups. Conclusion There are no signficantly. Trimetazidine has a definite effect in treating unstable angi-na pectoris,and it is similar to nitroglycerin in effects.

Objective To approach the capacity of erythrocyte regulating IL-8 in patients with primary hepatocarcinoma (PHC) by a new experimental system of hemaimmune. Methods 0.2ml suspension of cancer cells (S180: 5?10~6/ml) or NS were added into 0.2ml anticoagulant suspension of whole blood cells or leukocytes and 0.3ml plasma, then incubated for 1 h at 37℃. The content of IL-8 was determined by ELISA. Results In the patients with PHC, the IL-8 levels (pg/ml) in experimental and control groups of whole blood cells, and in experimental and control groups of leukocytes were 376.35?243.96, 353.64?271.92, 461.27?277.11 and 424.97?278.93, respectively; while in the normal human, they were 11.36?6.93, 4.98?4.35, 29.41?30.66 and 20.77?24.20, respectively. In the patients with PHC, the activation rates of cancer cells in the experimental groups of both whole blood cell and leukocyte were 0.22?0.24 and 0.25?0.53, respectively; while in normal human, they were 2.49?2.33 and 0.75?0.21, respectively. In the patients with PHC, the IL-8 adsorption rate of erythrocyte in both experimental and control groups of whole blood cell were 0.22?0.18 and 0.17?0.33, respectively; while in normal human, they were 1.18?2.29 and 0.86?0.49, respectively. The IL-8 activated rates of erythrocyte in the patients with PHC was much lower than in the normal human (P