MicroRNAs (miRNAs)are a class of small non-coding RNA that regulate gene expression at the posttranscrip-tional level and play important roles in cell proliferation,differentiation,apoptosis and metabolism.Moreover,specific miR-NAs can be secreted or released from tissues and cells in different physiological or pathological statusand enteredinto blood circulation,and secreted miRNAs can be delivered into recipient cells and emerged as powerful regulatorsof a wide range of biological processes.Many recent studieshave shown that miRNAswere involved in the development and progression of type 2 diabetes (T2DM).Due to the widely source,highly stability,and specific expression patternunder different physiological or pathological conditions,circulating miRNAs may serve as a novelbiomarker for T2DM and may also participate in the devel-opment of type 2 diabetes.

To investigatethe relationship between p38 MAPK pathway and multidrug resistance of stomach cancer. The activity of p38 MAP kinase in stomach cancer cell SGC7901 and multidrug resistant cell SGC7901/VCR were examined by immunoprecipition after adriamycin treatment SGC7901 for 0, 2, 15, 30 and SGC7901/VCR for 0, 2, 15, 30, 60 minutes,respectively. The results indicated that adriamycin could activate the activity of p38 MAP kinase in gastric cancer cell SGC7901 with time dependency, but could decrease remarkably the activity of p38 MAP kinase in gastric cancer multidrug resistant cell SGC7901/VCR after adriamycin treatment it for 15 minutes. It suggested that adriamycin could affect the activity of p38 MAPK in gastric cancer cell SGC7901 and multidrug resistant cell SGC7901/VCR.

Objective To study the relation between p38 MAPK pathway and multidrug resistance of stomach cancer. Methods The activity of p38 MAPK in gastric cancer cell SGC7901 and multidrug resistant cell SGC7901/VCR was examined by immunoprecipitation after treating with vincristine for 0,2,15,30,60 minutes. Results Vincristine could activate the activity of p38 MAPK in gastric cancer cell SGC7901 and multidrug resistant cell SGC7901/VCR. The difference between them was that in cell SGC7901 vincristine activate the p38 MAPK rapidly whereas in cell SGC7901/VCR slowly. Conclusion Vincristine could affect the activity of p38 MAPK in gastric cancer cell SGC7901 and multidrug resistant cell SGC7901/VCR.

To ascertain whether heat shock gene expression could protect pulmonaryendothelial cell from hydrogen peroxide(H2O2)一indueed injury,the protective effect of HSPgene expression induced by pretreatment of bovine pulmonary endothelial eells(BPAECs)by heat shock (42 ℃, 2h)against lethal dose(lmmol?L(-1),45min) of H2O2一induced cyt-otoxieity was observed in vitro.It was found that BPAECs heat一shocked prior to exposureto H2O2(Immol?L(-1) 45min)showed significant decrease in H2O2一mediated incrementof LDH rdlease and TBARS production and had an obvious alleviation of H2O2一induccddecreased activities of catalase and superoxide dismutase. Further study showed thatcycloheximide, a protein synthesis inhibitor and Actinomycin D,a mRNA transcriptioninhibitor blocked the expression of HSP 70 and HSP 70 mRNA respectively.Both agentsprevented the cytoprotective effect of heat shock pretreatment against H2O2一mediatedBPAECs injury. The results suggested that HSP70 gene selectively translated after heat shockwas invoived in enhancement of eellular antioxidant mechanism and protected BPAECsagainst H2O2一induced injury

Objective To study the expression status of estrogen receptor-alpha36(ER-α36)in breast cancer tissue and its rela-tionships with the occurrence,development and clinical prognosis of breast cancer.Methods 653 cases of breast cancer tissues were selected in this study.The real-time reverse transcription polymerase chain reaction(RT-PCR)and immunohistochemistry were used to detect the expression of ER-α36,estrogen receptor-alpha66 (ER-α66),progesterone receptor(PR)and human epidermal growth factor receptor-2(Her-2).The relationships between the expression of ER-α36,ER-α66,PR and Her-2 and the pathological charac-ter were analyzed.Results The expression rate of ER-α36 in all cases was 40%.The expression rate of ER-α36 in Her-2 positive tissues(63%)was significantly higher than that in the Her-2 negative group(44%,P <0.05).The expression rate of ER-α36 in ER-α66/PR/Her-2 negative tissues(66%)was significantly higher than that in the non-three-negative group(35%,P <0.05).The differences of ER-α36 expression rate between ER-α66 positive samples and negative samples or between PR positive and negative samples showed no statistical significance(P >0.05).The expression rate of ER-α36 in stage Ⅲ+Ⅳ breast cancer tissues(54%) was significantly higher than that in stage Ⅰ+Ⅱ breast cancer tissues(28%,P <0.05).The expression rate of ER-α36 in breast cancer tissues with lymph node metastasis (55%)was significantly higher than that in breast cancer tissues without lymph node me-tastasis (23%,P <0.05).Conclusion The results indicate that ER-α36 may play a very important role in the occurrence,develop-ment and lymph node metastasis of breast cancer,and be associated with the expression of Her-2,breast cancer staging and lymph node metastasis.ER-α36 is expected to become a new tumor marker and clinical diagnosis and treatment target.

Objective: To evaluate the efficacy and safety of tirofiban infusion to infarct related vessels on patients with ST segment elevation myocardial infarction (STEMI) during emergency percutaneous coronary intervention (PCI). Methods: From Jan 2013 to Jun 2014, a total of 30 STEMI patients were enrolled as tirofiban group (tirofiban 500μg was infused to infarct related vessels during emergency PCI), and received intravenous drip of tirofiban 0.1 μg•kg-1•min-1 for 24h after stent implantation; another 31 STEMI patients were regarded as pure stenting group during the same period and they received direct stent implantation during emergency PCI. Computer-assisted Quantitative Blush Evaluator (QuBE) score, left ventricular ejection fraction (LVEF) during hospitalization and after six-month follow-up and incidence rate of major adverse cardiovascular events were compared and analyzed between two groups. Results: There were no significant difference in baseline data between two groups, P>0.05. Compared with pure stenting group, after six months, there were significant rise in QuBE score [(10.88±5.03) scores vs. (14.70±6.69) scores] and LVEF [(57.19±4.59)% vs. (59.80±5.34)%], and significant reduction in incidence rate of MACE (35.5% vs. 10.0%) in tirofiban group, P<0.05 all. Conclusion: Tirofiban application in infarct related vessels during emergency PCI in STEMI patients can effectively and safely improve myocardial microcirculation perfusion level and it is worth extending.

Objective To investigate the incidence of metabolic syndrome among obese children in clinics. Methods One hundred and thirteen obese children aged 7 to 14 years were selected from clinics of nutrition(case group),and another 366 healthy students aged 7 to 14 years were served as controls.Height,body weight,waist circumference,hip circumference,blood pressure and liver ultrasound were measured,related biochemical parameters such as fasting blood glucose,fasting insulin,serum total cholesterol,triglyceride(TG),hiSh density lipoprotein and low density lipoprotein were detected,and the incidences of metabolic syndrome were obtained in two groups.Insulin resistance(IR)was evaluated by homeostasis model assessment(HOMA). Results There was no significant difference in age and gender between case group and control group(P>0.05).Body weight,body mass index(BMI),waist circumference,hip circumference,waist to hip ratio,systolic blood pressure,diastolic blood pressure,fasting blood glucose,fasting insulin,HOMA index and TG in case group were significantly higher than those in control group(P<0.01).The 75th percentile of HOMA index in control group was 3.28,and IR subgroup and non-IR subgroup were divided according to this cutpoint.In case group,body weight,BMI,waist circumference and TG in non-IR subgroup were significantly higher than those in IR subgroup (P< 0.05).Metabolic syndrome occurred in 51 cases(45.1%) in case group.The incidence of metabolic syndrome was higher in IR subgroup than that in non-IR group(50.0% vs 21.1%)(P<0.05). Conclusion The prevalence of metabolic syndrome is higher in overweight and obese children.IR has a close relationship with metabolic syndrome.

Objective To study the removal effect of Moringa seedprotein on turbidity water. Methods The protein of Moringaoleifera seed was extracted by salting out and salting out methodand the protein concentration of Moringa oleifera seed wasdetermined by Coomassie blue staining;The removal effect of Moringa seed protein on turbidity water was determined by coagulation test.The contents of COD, ammonia nitrogen and nitrate nitrogen in the water were determined to determine the effect of Moringa seed protein on water quality. Results The experimental results showed that Moringa oleifera seed protein has good removal effect on high and medium turbidity water, and its removal effect is in a dose - dependent manner.The removal rate of 7 mg/L of Moringa seed protein to high and medium turbidity water reached 92.25 ％ and 64.71 ％ respectively. But the removal efficiency of low turbidity water was less than 7 mg/L, the removal rate of low turbidity water was only 31.91％.The results of determination of COD, ammonia nitrogen and nitrate nitrogen showed that the Moringa seed protein did not increase the content of organic matter in the water while removing turbidity effectively. Conclusion Moringa oleifera seed protein has a certain removal effect on turbidity water, among which the removal effect of high and medium turbidity water is strong, and the removal effect of low turbidity water is poor.Moringa oleifera seed protein had little effect on water quality.

Objective To develop a high performance liquid chromatographic method (HPLC) for the analysis of of cholesterol in erythrocyte membranes.Methods The study included 167 consecutive chest pain patients who underwent coronary artery angiography in the Department of Cardiology,Nanjing General Hospital of Nanjing Command between September 2012 and February 2013.According to the clinical symptoms and t angiographic results,patients were divided into three groups:acute coronary syndrome (ACS) group (n =46),stable angina pectoris (SAP) group (n =76) and the control group (n =45).After the erythrocyte sample was hypotonically lysed and washed,saponification was carried out in a polassium hydroxide solution at 70 ℃.After extraction by Hexane/isopropanol mixture,the sample was separated on a Lichrospher column and detected by ultraviolet absorbance at 208 nm.A mobile phase composed of acetonitrile-isopropyl alcohol was found to be the most suitable for this separation.Concentrations of cholesterol in erythrocyte membranes were tested.Analysis of variance with covariates (ANOVA) was used to evaluate differences in CEM levels among groups.The relationship between continuous variables was evaluated by Spearman's correlation coefficient.Results Under the chromatographic conditions described,retention time of the cholesterol was approximately 6.1 min.Good separation and detectability of cholesterol in erythrocyte membranes were obtained.The method proved to be linear in the injection range of cholesterol from 0.05 g to 2.00 g.Cholesterol content in erythrocyte membranes were (87.0 μg/mg,75.4-98.9 μg/mg),(92.9 μg/mg,83.8-109.0 μg/mg) and (173.9 μg/mg,140.0-188.8 μ g/mg) in the control,SAP and ACS groups,respectively.Cholesterol content in erythrocyte membranes was significantly higher in ACS group than that in SAP and control groups (P ＜ 0.01).Conclusion We have successfully developed a method for the determination of cholesterol in erythrocyte membranes with good sensitivity,specificity and repeatability.

AIM:To investigate the effect of signal transducer and activator of transcription 1 ( STAT 1 ) on proliferation and interferon-β(IFN-β) sensitivity of human non-small-cell lung cancer H1299 cells.METHODS:STAT1 or EGFP gene was transfected into H1299 cells by the lentiviral vectors system.The cell number was counted under a mi-croscope and cell proliferation was tested by MTT assay.In addition, the cells transfected with STAT1 and EGFP were trea-ted with IFN-βand cell viability was measured by MTT assay.The protein levels of p-STAT1, ICAM-1 and PCNA were de-tected by Western blot.RESULTS: Over-expression of STAT1 inhibited H1299 cell proliferation (P<0.05).H1299 cells transfected with STAT1 gene had a higher sensitivity to IFN-βthan the control cells transfected with EGFP ( P <0.05).Overexpression of STAT1 increased the protein level of p-STAT1, and reduced IACM-1 expression in H1299 cells. Moreover, STAT1 enhanced STAT1 phosphorylation and downregulated the expression of PCNA in H1299 cells treated with IFN-β.CONCLUSION:STAT1 inhibits the proliferation and enhances the IFN-βsensitivity of non-small-cell lung cancer H1299 cells.