Myocardial fibrosis is the common results of the development of a variety of heart diseases which leads to extracellular matrix protein metabolic disorders and causes cardiac remodeling owing to cardiac fibroblasts proliferation, eventually results in malignant arrhythmia, heart failure, and even the occurrence of sudden cardiac death. Effective inhibition of myocardial remodeling could prevent the occurrence of sudden death. To know the protein kinase C (PKC) effective mechanism of regulation on myocardial fibrosis, a new therapeutic target for reversing myocardial remodeling might be provided.

Objective To study the relationship with internet addiction disorder(IAD)of the youth,the degree of IAD and home environment,attachment.To study the relationship with home environment and attachment.Methods 490 students were assessed with Internet Addiction Disorder Test,FES-CV,Attachment Questionnaire.Results 37 subjects can be defined as IAD according to Internet Addition Disorder test;IAD group have a higher score in contradictoriness(P＜0.05)of home environment and lack of maternal love,lack of fatherly love,father's rejection,parent's passive entangle,angry with parent[the average score of IAD group Was 13.16±4.62,14.18±5.42,14.41±5.44,19.10±4.59,18.89±4.42,12.37±4.80,11.35±4.17;the average score of normal group was 11.77±4.06,11.59±4.02,16.56±4.99,15.78±4.91,9.87±4.52,9.65±4.25,P＜0.05,0.01].Home environment were significantly correlated with all factors of attachment except independence(P＜0.05,0.01).There Was a significant negative correlation between the degree of IAD and lack of maternal love(r=-0.360).Conclusion Contradiction in home environment and passive attachment,that played an important role in internet addiction disorder of the youth.

Aim To investigate the effects of enalapril(Ena) on cardiac fibrosis induced by isoprenaline(Iso) and to explore its mechanism.Methods Effect of Ena and captopril(Cap) on collagen content,HW/BW,LVI,hydroxyprolnie(Hyp) level,and TGF-?1 protein expression was observed with IH and WB in rats induced by Iso subcutaneous injection.Results Different doses of Ena could decrease HW/BW,LVI and Hyp level dramatically,and decrease TGF-?1 protein expression which was closely related to myocardial fibrosis(MF).Conclusion Enalapril can inhibit TGF-?1 protein expression,by which inhibit myocardial fibrosis.

Objective To investigate the anti-proliferation effect of Ginseng Rh2(G-Rh2)on mouse MFC gastric cells and its mechanism.Methods MFC cells (1.0?109?L-1) were divided into four gourps:control group and G-Rh2(3,10,30 mg?L-1) groups.The cell viability was determined by MTT;the cell cycle was detected by flow cytometry;the protein expression of cyclin D1 and p27kip1 were observed respectively by qualitative and quantitative analysis.Results Compared with control group,the cell viabilities decreased gradually with the increasing of dose and time in G-Rh2(3,10,30 mg?L-1) groups at different time(1,2,4 h)(P

Aim To investigate the effects of angiotensin-converting enzyme inhibitor Ena on proliferation and cell cycle protein of cardiac fibroblasts and to explore the mechanism of Ena on cardiac fibrosis.Methods CFb was isolated by trypsin digestion method.MTT colorimetric assay was adopted to evaluate cell proliferation,collagen synthesis was observed by hydroxyproline concentration method,flow cytometry,immunofluorescenic and Western blot was used to measure cell cycle and CKI p27kip1 with Ena.Results Ena decreased MTT value and collagen synthesis dramatically;Ena increased phase G0/G1 and decreased phase S percentage ratio in cell cycle;Ena enhanced p27kip1 protein expression in a dose-dependent manner.Conclusion The antiproliferative effects of Ena on CFb can be attributed to upregulating CKI p27kip1 protein expression.

A dynamic model of disease can be used to quantitatively describe the pattern and characteristics of disease transmission, predict the disease status and evaluate the efficacy of control strategy.This review summarizes the basic transmission dynamic models of echinococcosis granulosus and their application.

Objective To observe the effects of ACE inhibitor enalaprilat(Ena) and protein kinase C(PKC) inhibitor chelerythrine(Chele)on proliferation,collagen Ⅰ,cell cycle,PKC and cyclinD1 protein expression of neonatal cardiac fibroblasts(CFb) and to probe its molecular mechanism.Methods CFb of neonatal Wistar rats were divided into control group,AngⅡ group,Chele+AngⅡ group,Chele+AngⅡ+Ena group and AngⅡ+Ena group.CFb were isolated by trypsin digestion method.MTT colorimetric assay was adopted to evaluate cell proliferation,immunocytochemical staining(IC) was used to measure collagen Ⅰ content,Western blotting and flow cytometry were used to detect PKC,cyclinD1 and cell cycle respectively.Results Compared with AngⅡ group,the MTT value decreased dramatically(P

AIM To investigate the effect of urapidil on NO, ET, ANF and AngⅡ of spontaneously hypertensive rats. METHODS The content of nitric oxide (NO), endothelin (ET), atrial natriuretic factor (ANF) and angiotensin Ⅱ (AngⅡ) were determined by spectrophotometry and radioimmunoassay of spontaneously hypertensive rat (SHR) during the process of decreasing blood pressure with urapidil. RESULTS\ They were as follows: compared with the same aged normal blood pressure WKY rats, in the SHR, the content of serum NO decreased, the level of ET and ANF in the plasma increased. Whereas the level of AngⅡ has no difference in any group. Compared with the control of SHR,urapidil can increase the contents of serum NO, decrease the level of ET and ANF in the plasma. CONCLUSION \ It is suggested that urapidil may adjust the imbalance of cardiovasco-active substances by increasing the release of endogenous vasodilators and reducing the release of endogenous vasocontrictors to antihypertention.

Objective To investigate the anti-fatigue effect of complex bear gall agent in mice.Methods Different dose of complex bear gall agent(4.4ml/kg、6.6ml/kg、13.2rml/kg)were given to mice by intragastric administration. The time of climbing-pole and loaded-swimming, hepatic glycogen content, serum urea nitrogen,lactic acid and lactate dehydrogenase of mice after swim were observed. Results The experiments indicated that complex bear gall agent could greatly increase the time of loaded-swimming and climbing Pole,increase the hepatic glycogen content and serum lactate dehydrogenase activity ,decrease serum urea nitrogen and blood lactic acid content in mice. Conclusion Complex bear gall agent had a significant anti-fatigue effect.

Aim To observe the protection effect of Tribulus terrestris saponin monomer B (TTSMB) on cadiocytes impaired by hypoxia-reoxygenation (H/R).Methods Cadiocytes of neonate rat were cultivated for 72 hours and divided into normal control group, H/R group,GSTT 100 mg·L~(-1) group and TTSMB 10,1,0.1 nmol·L~(-1) group.Morphocytology change of cadiocytes was observed after the treatment.Cadiocyte survival rate was detected with MTT colorimetric method.Levels of creatine kinase (CK), lactate dehydrogenase (LDH), aspartate aminotransferase (AST), malondialdehyde (MDA), and activity of superoxide dismutase (SOD) were determined. Apoptosis rate was detected with flow cytometry.Expression of caspase-3 was examined with western blot.Results Compared with the control group, the survival cell number in H/R group decreased obviously, content of CK,LDH, AST, MAD increased, and activity of SOD decreased (P<0.01).Compared with the model group, the survival cell population increased in TTSMB 10,1,0.1 nmol·L~(-1) group (P<0.05 and P<0.01).Contents of CK, LDH, AST, MAD decreased, whereas the activity of SOD increased (P<0.05 and P<0.01).Apoptosis rate and expression of caspase-3 also reduced in TTSMB 10,1,0.1 nmol·L~(-1) group.Conclusion TTSMB has significant cadiocytes protective effect against H/R and inhibits cadiocyte apoptosis,and the mechanism depends on the effect against oxygen free radical.