Objective To investigate the effect of miRNA-1 on the cardiomyocyte apoptosis in rats. Methods MicroRNA-1 mimics was transfected into the cultured H9c2 cell line (miRNA-1 group). Cells transfected with random miR-NA fragment was used as negative control group. The cell apoptosis was evaluated by FCM assay. MTT assay was used to de-tect the cell viability. The expression level of miRNA-1 was detected by real-time PCR. The expression levels of Bcl-2 mRNA and protein were detected by real-time PCR and Western blot assay. Results Compared with normal and negative control groups, the expression level of miRNA-1 was significantly higher in H9c2 cardiomyocytes, the apoptosis rate was in-creased, the cell vitality and Bcl-2 expression level were significantly decreased after transfection of miRNA-1 mimics. Conclusion miRNA-1 mimics can up-regulate miRNA-1 level, inhibit proliferation and induce cardiomyocyte apoptosis.

Objective To investigate the relationship between homocysteine(Hcy)and blood uric acid(UA)in the patients with type 2 diabetes mellitus(T2DM)complicating hypertension.Methods 85 patients with T2DM complicating hypertension were se-lected as the groupⅠ,78 patients with simple T2DM as the group Ⅱ and 74 individuals with healthy physical examination as the group Ⅲ.Hcy,UA,TC,TG and HDL-C were measured in all the subjects.Results Compared with group Ⅲ(control),the levels of Hcy,UA,TC and TG in the group Ⅰand groupⅡwere significantly increased(P <0.05),but the level of HDL-C was significantly decreased(P <0.05).Compared with the group Ⅱ(T2DM),the levels of Hcy,UA,TC and TG in the group Ⅰwere significantly in-creased(P <0.05 ),but the level of HDL-C was obviously decreased,the difference had statistical significance (P <0.05 ).There was good positive correlation between the Hcy level and the UA level in the patients with T2DM complicating hypertension (r =0.658,P <0.05).Conclusion The levels of Hcy and UA are significantly increased in the patients with T2DM especially complica-ting hypertension.High Hcy and high UA are the important risk factors of T2DM complicating cardiocerebrovascular diseases.

Objective To study the relationships between sperm morphology and sperm vitality,sperm viability.Methods The sperm morphology and the sperm vitality were analyzed by automated sperm morphology analyzer(ASMA) and the sperm viability was analyzed using eosin staining.Results The normal morphology sperm rate of abnormal vitality group was lower than that of normal vitality group(P

Objective: To explore whether relieving effect of Ginsenosides-Rb1 (Gs-Rb1) on chronic heart failure (CHF) induced by adriamycin is related to improving levels of tumor necrosis factor (TNF) receptor (TNFR) and ligand TNF-α or not. Methods: Adriamycin-induced CHF model rats were randomly divided into adriamycin group (n=15, received adriamycin 1 μmol/L) and Gs-Rb1 group (n=17, received Gs-Rb1 70 mg•kg-1•d-1 based on adriamycin group), another 10 healthy Wistar rats were selected as normal control group. Meanwhile, cultured cardiomyocytes of neonatal rats were accordingly divided into normal control group, adriamycin group and adriamycin+Gs-Rb1 group. After intervention, echocardiography, levels of TNFR/TNF-α mRNA and protein were measured and compared among three groups. Results: 1. In vivo: Compared with normal control group TNFR-1 [protein（0.13±0.02）kDa, mRNA（0.19±0.05）bp]，TNFR-2[protein（0.24±0.01）kDa, mRNA（0.13±0.02）bp]，TNF-α [protein（0.11±0.01）kDa, mRNA（0.26±0.05）bp], the levels of TNFR-1 [protein（0.67±0.04）kDa,（0.51±0.04）kDa；mRNA（0.81±0.03）bp，（0.49±0.05）bp]，TNFR-2 [protein（0.61±0.05）kDa, （0.47±0.03）kDa，mRNA（0.28±0.03）bp，（0.18±0.04）bp] and TNF-α [protein（0.28±0.04）kDa, （0.20±0.03）kDa， mRNA（0.67±0.05）bp，（0.45±0.04）bp] significantly rose（P<0.05 or <0.01） in adriamycin group and Gs-Rb1 group; and those levels of TNFR-1, TNFR-2, TNF-α protein and mRNA of Gs-Rbl group were significant reduction than those of adriamycin group; 2. In vitro: The results were similar, those of adriamycin group and Gs-Rb1 group were also significant rise than those of normal control group（P<0.05 or <0.01），those of Gs-Rbl group were significant reduction than those of adriamycin group（P<0.05 or <0.01）. Conclusion: TNFR/TNF-α expression may play a certain role in the process of adriamycin-induced CHF; improving effect of Gs-Rb1 on adriamycin-induced CHF may be related to regulation of TNFR/TNF-α.

Seawater,hyperosmotic and alkaline, is a complex wound factor. Specific pathophysiological changes appear when wounds are socked in seawater. and special treatments are needed for such injuries. This paper reviewed the pathophysiological changes and treatment of seawater-soaked soft tissue wound, cranioccrebral trauma, open chest trauma,open ahdom-inal trauma,sea water drowning and seawater immersion during shock.

Objective To investigate the clinical autopsy results of patients died of cardiovascular disease or other disease complicated with cardiac damage. Methods Complete autopsy was performed on 86 cases with uncertain cause of death. Through integrating clinical diagnosis and treatment with gross autopsy findings and microscopic observations, 86 autopsies were determined the major cause of death. Results In 86 autopsies, 69 cases were heart disease. Differences between pathological diagnosis and clinical diagnosis were compared. Twenty-seven cases were cardiac deaths, with diagnosis accrodance rate of 81. 5%. Fortytwo cases died of non-cardiac disease but complicated with heart disease or involving the heart which accelerated the death in patients, with accordance rate of 78.6%. Conclusion Scientific and correct performance of autopsy was important to determine the causes of death, to promote development of related disciplines and to improve the diagnosis and treatment of the diseases.

Objective:To explore whether the effect relieving chronic heart failure (CHF) induced by Adriamycin of Ginsenoside-Rbl (Gs-Rbl ) is related to inhibiting Toll-like receptor (TLR ) . Methods :Adriamycin-induced CHF model rats were randomly divided into Adriamycin group (n=15) and Gs-Rb1 group (70 mg/kg d ,n=17);another 10 normal rats were regard as control group .Neonate rat cardiomyocytes were also randomly divided into control group ,Adriamycin group (1 μmol/L) and Gs-Rb1 group (1 μmol/L Adriamycin + 200 μmol/L Gs-Rbl) .After the intervention being performed ,echocardiography and expressions of TLR2/TLR4 gene and protein were assessed in all groups .Results:(1) Both studies in vivo and in vitro indicated that expressions of TLR 2 protein and mRNA in Adriamycin group were significantly higher than those of control group ,compared with Adriamycin group ,there were significant reductions in expressions of TLR2 protein [ (0.975 ± 0.022/0.564 ± 0.031) vs .(0.593 ± 0.018/0.344 ± 0.024)] and mRNA [ (0.576 ± 0.029/0.853 ± 0.043) vs .(0.349 ± 0.015/0.401 ± 0.021)] in Gs-Rbl group ,P<0.01 both ;(2) No matter study in vivo or in vitro ,expressions of TLR4 protein and mRNA in Adriamy-cin group were significantly higher than those of control group ,compared with Adriamycin group ,there were signif-icant reductions in expressions of TRL4 protein [ (0.654 ± 0.032/0.519 ± 0.013 ) vs . (0.371 ± 0.013/0.254 ± 0.027)] and mRNA [ (1.602 ± 0.013/0.838 ± 0.021) vs .(1.140 ± 0.021/0.503 ± 0.022)] in Gs-Rbl group , P<0.01 both .Conclusion:Adriamycin may trigger the process of CHF through increasing TLR 2 and TLR4. The effect of Gs-Rbl improving adriamycin-induced CHF may be related to inhibition of TLR 2 and TLR4 .

Objective:To explore whether ginsenosides-Rb1 (Gs-Rb1)can relieve cardiomyocyte hypertrophy induced by endothelin-1 (ET-1)via protein kinase C (PKC)system.Methods:Cardiomyocytes of neonatal rat were random-ly divided into blank control group,Gs-Rb1 group,ET-1 group,Gs-Rb1+ET-1 group,ET-1+CHE (chelerythrine, PKC blocker)group and Gs-Rb1 +ET-1 +CHE group.After 96h intervention,cardiomyocyte surface area,total protein content,PKC activity,c-fos and p-c-jun expressions were measured.Results: (1)Cardiomyocyte surface area and total protein content in Gs-Rb1+ET-1 group were significantly lower than those of ET-1 group (P <0.05~<0.001),but not significant different with those of Gs-Rb1+ET-1+CHE group,P =0.569;(2)PKC activity in Gs-Rb1+ET-1 group was significantly lower than that of ET-1 group [(9.3±0.6)pmol·min-1 ·mg-1 vs.(14.1± 0.9)pmol·min-1 ·mg-1 ],but significantly higher than that of Gs-Rb1+ET-1+CHE group [(2.7±0.2)pmol· min-1 ·mg-1 ],P <0.001 all;(3)Expressions of c-fos and p-c-jun gene and protein in ET-1 group were significant-ly higher than those of blank control group (P <0.001 all);compared with ET-1 group,there were significant re-ductions in expressions of c-fos [mRNA/protein:(0.53±0.05/0.39±0.02)vs.(0.43±0.03/0.31±0.03)]and p-c-jun [mRNA/protein:(0.64±0.04/0.44±0.02)vs.(0.33±0.05/0.37±0.03)]in Gs-Rb1+ET-1 group and ex-pressions of c-fos [mRNA/protein:0.41 ± 0.05/0.31 ± 0.02]and p-c-jun [mRNA/protein:0.31 ± 0.05/0.36 ±0.03]in ET-1+CHE group (P <0.05 or <0.001),expressions of c-fos and p-c-jun gene and protein in Gs-Rb1+ET-1+CHE group were significantly lower than those of Gs-Rb1+ET-1 group and ET-1+CHE group (P <0.05 or<0.001).Conclusion:Gs-Rb1 can significantly inhibit cardiomyocyte hypertrophy induced by ET-1 and PKC system is one of pathways mediating this biological effect.

Clinician-scientists are doctors who perform laboratory-based or clinically oriented research and have direct patient contact.Not only do they play a critical role in the research and practice of translational medicine,but also they are the educators of the next generation of clinician-scientists.However,clinician-scientists are vanishing.It is urgent to train new clinician-scientists who can be engaged in clinic work,research,and also education.Thus,in order to correct understand the importance of the work of clinical scientists,from multi angle analysis of clinical scientists training problems that may be encountered in the process,the active improvement of the education system and condition,and sustained and efficient guidance to the outstanding seedlings are advocated.Besides,aspiring candidates are also encouraged to seek ideal guidance and support through their career,arrange their work reasonably,strengthen their cooperation and the management ability,and strive to grow into excellent clinician-scientists.

Objective To investigate the expression of TMS1/ASC gene induced by gemcitabine(GEM) in pancreatic carcinoma cell line PANC-1.To study the relationship between cysteine aspartase(caspase-1),nuclear factor-κB(NF-κB) and the expression of TMS1/ASC.Methods The pancreatic carcinoma cell line PANC-1 was cultured in Dnlbecco's modification of Eagle's medium(DMEM).Methyl thiazolyl tetrazolium (MTT)method was used to measure the effect of GEM at different time points(24,48 h)at different concentrations(1,2,4,8,16 μg/ml) on growth of PANC-l.RT-PCR was used to detect the expression of TMS1/ASC mRNA stimulated by medium alone and by GEM(4.27μg/ml)for 24 h and 48 h.Western blot analysis was performed with inhibitory protein of NF-κB multiclonal antibody,caspase-1 multiclonal antibody and β-actin monoclonal antibody to observe the expression of β-actin,caspase-1 and IκBα in GEM group and in the control group.The activation state of caspase-1 and NF-κB was examined.Results GEM inhibited the growth of PANC-1 cells in a concentrationand-time-dependent manners and its half maximal inhibitory concentration(IC50)was 4.27 μg/ml on 24 h.The expression of TMS1/ASC was 0.3 ±0.004 and 0.63 ±0.007 respectively in GEM group while it was 0.1 ±0.001 and 0.21 ± 0.006 in the control group on 24h and 48h.The difference between the 2 groups at the same time point had statistical significance (P ＜ 0.01).Western blot showed that GEM caused the activation of caspase-1.The expression of IκBα had no obvious differencebetween the 2 groups.GEM couldn't induce the activation of NF-κB.Conclusions GEM can inhibit proliferation of PANC-1 cells and induce their apoptosis.The drug sensitivity decreased with prolongation of exposure time.GEM might induce and increase the expression of TMS1/ASC,which might influence the apoptosis of the cells later.The apoptosis of PANC-1 cells induced by GEM is dependent of caspase-1 signaling pathway and independent of NF-κB signaling pathway.