Clinical observation of valsartan on chronic pulmonary heart disease with heart failure / 中国生化药物杂志

Objective To study and analyze the clinical effect of valsartan on chronic pulmonary heart disease. Methods 100 cases of heart failure patients with pulmonary heart disease treated in our hospital from January 2015 to October 2016 were selected and randomly divided into the control group and the experimental group,50 cases in each group.Two groups of patients were given the basic treatment of diuretics,low salt diet, digitalis and nitrates,so as to ensure that the patients had enough rest.Patients in the control group were treated with benazepril,and the patients in the experimental group were treated with valsartan.The clinical indexes of the experimental group and the control group were compared and analyzed. Results After corresponding treatment,the number of effective treatment was 48 cases.In the control group,the total effective number was 41 cases. The effective rate of the control group (82.0％) was significantly lower than the experimental group(96.0％) (P<0.05).The incidence of adverse reactions in the experimental group was 8.0％, and the fatality rate was 10.0％. The incidence of adverse reactions in the control group was 10.0％, and the fatality rate was 12.0％.There was no significant difference between two groups.After treatment,the indexes of LVEDD and LVESD in the experimental group were better than those in the control group,with statistical significance(P<0.05).Conclusion Valsartan was effective in the treatment of chronic pulmonary heart disease with heart failure.It can improve the treatment efficiency and security in a certain extent,and has the significance of further popularization and application.

Expression of interferon-induced protein with tetratricopetide repeats 1 and liver cell apoptosis in mice with severe burns / 中南大学学报(医学版)

OBJECTIVE@#To explore the relationship between the expression of interferon-induced protein with tetratricopetide repeats 1 (IFIT1) and liver cell apoptosis in the acute stress period after severe burns.
@*METHODS@#A total of 25 C57/129 adult mice were randomly divided into the normal control group (0 h) and the groups at 1, 6, 12 or 24 after severe burns (n=5 per group). A model with third degree (20% of the total body surface area) burn injury was established and then liver tissues were taken. IFIT1 expression was examined by Western blot. The expression of caspase-3 and -8 was measured by immunohistochemistry. Liver cell apoptosis was detected by terminal deoxynucleotidyl transferase mediated nick end labeling (TUNEL).
@*RESULTS@#After burns, IFIT1 expression was increased at 1 h, which reached the highest level at 
6 h followed by a decrease at 12 h, which reached minimum level at 24 h. The differences between groups were significant (P<0.01). The caspase-3 and -8 levels significantly increased after burns in a time-dependent manner (P<0.01). Although at 0 h and 1 h there was no significant increase in liver cell apoptosis, the increase reached significance from 6 h to 24 h (P<0.01).
@*CONCLUSION@#The increase in IFIT1 expression after severe burns promotes liver cell apoptosis.

Effect of ropivacaine on proliferation and migration of rat bone marrow mesenchymal stem cells / 中南大学学报(医学版)

OBJECTIVE@#To observe the influence of ropivacaine on the proliferation and migration of rat bone marrow mesenchymal stem cells (BMSCs) and provide basis for the clinical application of BMSCs.@*METHODS@#Rat BMSCs were isolated and cultured by adherence method. Surface markers of BMSCs were examined by flow cytometry. Multipotent differentiation of BMSCs was detected by induced adipogenesis, osteogenesis and muscular differentiation. Proliferation of BMSCs was examined by CCK-8 and Brdu incorporation after ropivacaine treatment at different concentrations. Migration of BMSCs was tested by cell scratch assay and Millicell experiment.@*RESULTS@#Cultured cells had representative appearance and surface markers of BMSC, and they had potential multiple differentiation. Ropivacaine treatment at 50 and 100 μmol/L significantly reduced the proliferation rate of BMSCs and Brdu incorporation rate. There was significant difference compared with the control group (P<0.05). Cellular scratch assay and migration experiment indicated that ropivacaine significantly reduced the migration of BMSCs. There was significant difference compared with the control group (P<0.05). All these mentioned effects of ropivacaine on BMSCs were dose-dependent. There was significant difference between groups (P<0.05).@*CONCLUSION@#Ropivacaine can significantly reduce the proliferation and migration of rat BMSCs, suggesting that the influence of local anesthetics on BMSCs has to be taken into account when BMSCs are used in clinical practice.

Organochlorines, Glutathione S-transferase M1 Genetic Polymorphisms and Risk of Breast Cancer / 环境与健康杂志

Objective To study the potential effect of gene-environment interaction between glutathione S-transferase M1 (GSTM1) and serum organochlorines residues on the risk of breast cancer in women, in China. Methods Seventy newly pathologically diagnosed female patients with breast cancer from September 2006 to October 2007 were selected as the cases from five large hospitals in Tangshan. The controls were identified at the same hospital as cases. 1∶1 matched case-control study. Between the cases and controls, the difference of age was not over two years and the residence was similar. The organochlorine residues levels in the serum were measured by gas chromatography (GC). Genotypes of GSTM1 polymorphisms were analyzed by multiplex allele-specific polymerase chain reaction (PCR). Interaction indexes (?) were calculated to determine the type of gene-environment interaction. Results After confounding factors adjusted, the result showed that interaction existed in genetic polymorphisms of GSTM1 and DDT, HCH residues, and interaction indexes (?) value were 1.237 and 1.379. Conclusion GSTM1 genetic polymorphisms and DDT, HCH may present an interaction in the development of breast cancer.

Relationship between Environmental Endocrine Disruptors, Genetic Polymorphism of Related Metabolic Enzymes and Breast Cancer / 环境与健康杂志

Breast cancer is one of reproduction-endocrine related tumors, so the risk factors including environmental and genetic factors which can disrupt anabolism and function of estradiol may increase the risk of breast cancer. Persistent environmental endocrine disruptor chemical (EDCs) can disrupt anabolism and function of endogenous hormone and the degree of disruption may depend on genetic polymorphism. EDCs and metabolic enzyme genetic polymorphism were discussed in this paper. To study the risk factors of breast cancer, both of the environmental factors and the genetic factors should be included.