Staring from the significance of traditional Chinese virtues,this paper proposes to carry forward education of traditional Chinese virtues in the teaching of physician-patient communication,cultivate harmonious personalities of medical students and promote their abilities of communication with patients by absorbing the essence from traditional Chinese virtues.

C and C 5457T (D1819D) were 11.1%, 5.2%, 28.2% and 31.8%, respectively. The minor allele frequency of SNPs was not same as study from Japanese or Chinese. Conclusion The distribution of SCN5A SNPs may vary between different ethnicities.

Objective To develop miniature pig model of coronary microembolization (CME) by easy and cost-effi-cient technique. Methods A total of 11 miniature pigs were divided into control group (n=5) and CME group (n=6). Femo-ral artery was punctured using 21 gauge needle that is normally used for transradial procedures. Microspheres were injected into the left anterior descending artery of the CME group by 5 F coronary radiography catheter and 1.8 F coronary micro-guide catheter. Serum concentrations of brain natriuretic peptide (BNP) and cardiac troponin I (cTnI) were evaluated just be-fore CME and 6 hours after CME. Apical myocardial pathological lesions were evaluated by optical microscope 6 hours after CME. Results All miniature pigs in control group survived, but one died in the CME group. 5 F coronary radiography cathe-ter and 1.8 F coronary micro-guide catheter reached designated location successfully. Before CME, serum BNP (ng/L:143.00 ± 13.51 vs 134.00 ± 15.57) and cTnI (μg/L:0.39 ± 0.09 vs 0.38 ± 0.10) showed no significant differences between these two groups (t values are 0.976 and 0.294 respectively,both P>0.05). By contrast, serum BNP (561.00 ± 80.65) and cTnI (2.75±0.58) were much higher in CME group than those (BNP 139.00±13.87;cTnI 0.54±0.14 ) in control group after CME (t values are 11.530 and 8.337 respectively,both P＜0.001). In CME group, microspheres, micro-infarction and inflammatory cell infiltration were seen under an optical microscope which are absent in control group. Conclusion Using new surgical consumables can successfully develop miniature pig model with CME. And the technique is simple, cost-efficient, practical so it is worth promoting.

AIM: To investigate the effects of heptanol preconditioning on the changes of structure, function and connexin 43 (Cx43) content in mitochondria in a rabbit model of myocardial isehemia-reperfusion (IR) injury. METHODS: In anesthetized open-chest rabbits, the left anterior descending artery (LAD) was occluded for 30 min and reperfused for 4 h. Sixty-four rabbits were randomly divided into 4 groups (n=16 in each group): sham operation group (sham group), ischemia-reperfusion group (IR group), ischemic preconditioning group (IP group) and heptanol preconditioning group (HT group). All rabbits in the 4 groups were killed 4 h after reperfusion. Myocardial infarct size was determined at the end of the experiment. Mitochondria was isolated by centrifugations. The ultrastructural changes of the mitochondria were observed under electronic microscope. The mitochondrial membrane potential, Ca~(2+) concentration, MDA content and SOD activity of myocardial mitochondria were also examined. The content of mitochondria Cx43 was detected by Western blotting. RESULTS: Compared to IR group, the myocardial infarct size was significantly reduced in IP (18.97%±2.80%) and HT (19.97%±3.80%) groups, the damage of mitoehondrial ultrastructure was milder (P<0.05), mitochondrial membrane potential was significantly higher and Ca~(2+) concentration was much lower (P<0.01) in IP group and HT group. No significant difference of MDA content and SOD activity in myocardial mitochondria between IR group and HT group was found. However, MDA content were much lower and SOD activity was significantly higher in IP group as compared to IR group (P<0.01). Compared to sham group, the mitochondria Cx43 expression was distinctly decreased compared to IR group (P<0.05) and no significant difference was found between IP group and HT group (P>0.05). CONCLUSION: Heptanol preconditioning protects myocardium from ischemia-reperfusion injury. The mechanism may be related to increasing in mitochondrial membrane potential, alleviating Ca~(2+) overload in myocardial mitochondria and attenuating the decrease in mitochondria Cx43 expression induced by isehemia-reperfusion.

Aim To investigate the roles of Cx43 in mitochondria and mitochondrial ATP sensitive potassium channe1(mitoK_(ATP)~+)participating in the protection for heptanol preconditioning on myocardial ischemia/reperfusion injury of rabbits.Methods In anesthetized open-chest rabbits,the left anterior descending artery(LAD)was occluded for 30 min and reperfused for 4 hrs.All rabbits were randomly divided into five groups(n=16 in each group):sham operation group(Group Sham),ischemic reperfusion group(Group IR),ischemic preconditioning group(Group IP),heptanol preconditioning group(Group HT)and 5-HD plus heptanol preconditioning group(Group HT+5-HD),All rabbits in the five groups were killed 4h after reperfusion.Myocardial infarct size was determined at the end of the experiment.The heart rate and the mean arterial pressure(MAP)were recorded and plasma CK-MB and cTnI activity were measured at baseline,the end of ischemia,and after 2 hrs and 4 hrs of reperfusion respectively.Mitochondria was isolated with different centrifugations.Ultrastructural changes of mitochondria were observed under electron microscope.The content of the mitochondria Cx43 was detected with Western blot.Results The plasma CK-MB,cTnI activity and myocardial infarct size were significantly reduced in IP(18.97±2.8)% and HT(19.97±3.8)% groups as compared to IR groups (35.67±5.8)%,(P<0.01).Compared to group IR,the damage of mitochondria in group IP and group HT were milder(P<0.01).No significant difference was found between Group IP and Group HT.Compared to sham group, the mitochondria Cx43 expression was distinctly decreased in group IR and group HT+5-HD(P<0.01)and no significant difference was found between Group IP and Group HT.Conclusions Heptanol preconditioning can protect the heart from I/R injury by improving mitochondrial ultrastructure and by attenuating the decrease of mitochondria Cx43 expression induced by I/R.The mitochondrial Cx43 expression may be concerned with depending on mito K_(ATP)~+.

AIM:To investigate the changes of connexin 43 (Cx43) via establishing a model of sympathomi-metic atrial fibrillation ( AF) .METHODS:The mongrels ( n=15) were randomly divided into control group , rapid atrial pacing (RAP) group and isoprenaline (ISO) perfusion+RAP group (ISO+RAP group).All mongrels’ hearts were taken out rapidly by median sternotomy to establish the cardiac model with Langendorff perfusion in vitro.The atrial effective re-fractory period ( AERP) and AF inducability were tested .The expression and distribution of tyrosine hydroxylase ( TH) were analyzed by immunohistochemistry .Total protein level of Cx 43 and phosphorylation of Cx 43 were determined by West-ern blot.The distribution of Cx43 were also observed by immunofluorescence staining .The cell apoptosis was analyzed by TUNEL staining.The generation of reactive oxygen species ( ROS) in the mitochondria was measured by fluorescence spec-trophotometry .RESULTS:No significant change of AERP was found between control group and RAP group , while that in ISO+RAP group was significantly decreased (P<0.05) and induced AF.Compared with control group, the expression of TH, apoptotic index and the generation of ROS increased gradually (P<0.05), while the content of Cx43 decreased grad-ually both in the total protein and the phosphorylation levels in RAP group and ISO +RAP group (P<0.05).The fluores-cence intensity of Cx43 was also attenuated and Cx43 were lateralized apparently in RAP group , while Cx43 were character-ized as punctate distribution in ISO +RAP group.CONCLUSION:Sympathetic nerves may activate autophagosome at in-tercalated discs and trigger cell apoptosis , resulting in remodeling and downregulation of Cx 43 via oxidative stress , thus having effects on mediating and maintaining AF .

BACKGROUND:There are most single-center studies about bone marrow stem cels applied to treat decompensated cirrhosis, but the therapeutic results are not ideal. It is possibly related to aging, physical weakness, poor bone marrow hematopoietic function, less available number of stem cels and feeble ability of regeneration and proliferation in liver cirrhosis patients. Umbilical cord mesenchymal stem cels are characterized of easy to obtain, wide source and weak immunogenicity. Co-transplantation of bone marrow stem cels and umbilical cord mesenchymal stem cels may improve the therapeutic effects on decompensated cirrhosis patients. OBJECTIVE:To investigate the efficacy and safety of co-transplantation of umbilical cord mesenchymal stem cels and bone marrow stem cels on decompensated cirrhosis.METHODS:Thirty-two decompensated cirrhosis patients were randomly divided into two groups: in stem cel group, 13 patients received co-transplantation of umbilical cord mesenchymal stem cels and bone marrow stem cels based on regular medical treatment; in control group, 19 patients only underwent the regular medical treatment. Al the patients were folow-up for 1 year. Alanine aminotransferase, albumin, total bilirubin, prothrombin time, Child-Pugh score and Model for End-Stage Liver Disease score, 1-year survival rate, Quality of Life score and adverse reactions related to stem cel therapy were observed and recorded in the two groups at 4, 12, 52 weeks after treatment. RESULTS AND CONCLUSION:At 4, 12, 52 weeks after treatment, improvements in the liver function, prothrombin time, Child-Pugh score and Model for End-Stage Liver Disease score were found in the two groups, but there was no difference between the two groups (P > 0.05). At 4 weeks after transplantation, the clinical symptoms and Quality of Life score in the stem cel group were significantly improved, which were better than those in the control group (P < 0.05). But at 12 and 52 weeks after treatment, no difference was found between the two groups (P > 0.05). In addition, the 1-year survival rate showed no difference between the two groups, and no severe adverse reactions related to stem cel therapy occurred during the folow-up. Co-transplantation of umbilical cord mesenchymal stem cels and bone marrow stem cels is safe and effective to improve the clinical symptoms of decompensated cirrhosis patients. However, further studies with larger samples are warranted to better clarify the co-transplantation effects.

Objective To make comparisons of the three models of acute and chronic rheumatic carditis to find out an optimal animal model.Methods AntigenⅠwas a emulsifier mixed by complete freund’ s adjuvant( CFA) and Group A streptococcus(GAS).AntigenⅡwas mixed by incomplete freund’s adjuvant(IFA) and GAS.Female Lewis rats were randomly divided into four groups: A, B, C treatmeat groups were immuned with antigenⅠat the foot pad firstly. Subsequently, rats in group A、B、C were injected antigenⅠ, antigenⅡand activated GAS respectively to make the models of RHD.Rats in control group D were immunized with the same protocol outlined as treatment groups but without GAS. Respectively 7, 12, 24 weeks the rats were sacrificed 24 ( each group was 6).The blood biochemical item and Hematoxylin-eosin( HE) staining of hearts were detected.Results In group C the mortality was 25%.In group A, the incidence of carditis was the highest.Histopathological manifestations of group A, C was not only revealed acute damage such as inflammatory cell infiltrate as well as group B, but also the Aschofflike cells in the myocardial cells interstitial.But in group A and C there had a great degree of the inflammatory cells infiltration than group B.At 24th week rats in group A detected the rate and degree of valve fibrosis in chronic damage were higher than group B and C.None of rats in group D presented carditis or valvulitis.Conclusion In group A, giving the GAS with continuous stimulation after using the mixed emulsification of CFA and GAS to immune Lewis rats for five times was a appropriate method which could provide an optimal animal model for experimental study of acute and chronic rheumatic heart disease.

Objective To investigate the effects of ischemic postconditioning on apoptosis, structural and functional changes of mitochondria induced by myocardial isehemia/reperfusion (I/R) injury of rabbits and potential mechanism. Methods Eighty healthy rabbits were divided randomly into five groups: sham operation group ( Group Sham) , ischemic reperfusion group (Group IR) , ischemic preconditioning group (Group IP) , ischemic postconditioning group (Group PC) and 5-HD plus ischemic postconditioning group (Group PC +5-HD). All rabbits in the five groups were killed 4 h after reperfusion. The hearts were quickly collected for microscopy by TUNEL. We observed ultrastructural changes of myocardium under electron microscope and examined mitochondrial membrane potential and Ca~(2+) concentration, MDA content and SOD activity of myocardial mitochondria. Results Compared with group IR, the damage of mitoehondrial ultrastrueture was milder, the apoptosis rate decreased and Ca concentration and MDA content were much lower in group IP and group PC ( P < 0. 05 ). Mitochondrial membrane potential and SOD activity of myocardial mitochondria in group IP and group PC was significantly higher than that in group IR(P<0.05). The protective effect of PC against I/R injury was partially counteracted by 5-HD .Conclusion Ischemic posteonditioning can protect the heart from I/R injury, this is supported by improvement mitochondrial ultrastructure and by decreasing apoptosis, increasing mitochondrial membrane potential and SOD activity, alleviating Ca~(2+) overload and decreasing MDA content in myocardial mitochondria. The cardio protective effects may be explained by mitochondrial ATP sensitive potassium channel.

In our previous study, we identified a novel testis-specific expressed gene 2 (TSEG-2) from mouse testis. To further investigate its functions, 35 male Balb/c mice (8 weeks old) were divided into cryptorchidism group (n=20), sham group (n=10), and control group (n=5). In cryptorchidism group, the right testes were anchored to the inner lateral abdominal wall. In situ hybridization (ISH) was applied to measure the localization of TSEG-2 in mouse testis. Real-time quantitative PCR was performed to detect the expression of TSEG-2 gene. Meanwhile, under the mediation of polyethylenimine (PEI), the recombinant vector pEGFP-TSEG-2 (n=5) or empty vector (mock, n=5) was transfected into the testis of male mice. The transfection efficiencies were measured under a fluorescence microscope. The apoptosis of spermatogenic cells was detected by terminal deoxynuleotidyl-mediated nick end labeling (TUNEL). The results showed that TSEG-2 was expressed in convoluted seminiferous tubules, more precisely, in spermatogonia and spermatocytes. As compared with sham and control groups, the TSEG-2 transcription was significantly enhanced (P<0.05) and was correlated with apoptosis of spermatogenic cells in cryptorchid testes (P<0.05). PEI was efficient in mediating transfection of TSEG-2 into seminiferous tubules of testis. One week post-transfection, intratesticular injection of TSEG-2 resulted in increased apoptosis of spermatogenic cells in vivo (P<0.05). These results indicate that TSEG-2 may participate in the apoptosis of spermatogenic cells and the pathogenesis of cryptorchidism.