Objective To investigate the relationship between hepatitis B virus (HBV) infection and hepatic metastasis from colorectal cancer.Methods Published literatures and unpublished conference papers from January 1990 to December 2011 were searched in PubMed,Cochrane library,Wanfang Database and CNKI.Data of the literatures were extracted by a table.All the patients with colorectal cancer were divided into the infected group and the control group according to the patients whether infected by HBV or not.The hepatic metastatic rate was analyzed.The Meta analysis was carried out by using the Review Manager 5.0 software,and the heterogeneity between studies was analyzed using the I2.Random effect regression model or fixed effects regression model was used according to the P value.The funnel plot was drawn to assess the potential for publication bias.The count data were presented by odds ratio (OR) and 95％ confidence intervals (95％ CI).Results Fifty-six articles were retrieved,and 11 of which met the criteria.The number of patients with colorectal cancer was 5622,and 924 were in the infected group,4698 in the control group.There was no statistical difference in the heterogeneity between all the articles (I2 =0,df=10,P ＞ 0.05).The hepatic metastatic rate was 10.61％ (98/924) in the infected group,which was significantly lower than 23.84％ (1120/4698) of the control group (OR =0.35,P ＜ 0.05).The funnel plot showed that there was no obvious publication bias in these studies.Conclusion Patients with colorectal cancer and infected by HBV have lower incidence of hepatic metastasis.

Objective To investigate the improvement role of aspirin combined with statins on carotid plaque of patients with cerebral thrombosis.Methods80 cases of patients with cerebral thrombosis in our hospital from May 2014 to May 2016 were selected, these patients were divided into aspirin combined with statins treatment group (combined treatment group, 40 cases) and single aspirin treatment group (single treatment group, 40 cases) two groups according to the treatment methods, the NIHSS scores, Barthel indexes, clinical curative effects, IMT, plaque areas of the two groups were statistically analyzed.ResultsThe NIHSS score of the combined treatment group was significantly lower (P<0.05), the Barthel index was significantly higher (P<0.05), the total treatment efficiency 95.0% (38/40) was significantly higher than the single treatment group 80.0% (32/40) (P<0.05), the IMT was significantly shorter (P<0.05), the plaque area was significantly smaller than the single treatment group (P<0.05).ConclusionAspirin combined with statins can more effectively improve the carotid plaque of patients with cerebral thrombosis than aspirin alone, so is worthy of promotion and use in the clinical.

Connective tissue growth factor (CTGF) has recently received much attention as a possible key determinant of progressive fibrosis. It promotes tissue fibrosis through different pathways, such as cell proliferation, extracellular matrix accumulation and cell transdifferentiation. A number of regulators of CTGF expression have been identified, including transforming growth factor ?, vascular endothelial growth factor, tumor necrosis factor ?, etc. The mechanism of profibrotic effect by CTGF was reviewed. [

Objective To evaluate the rationale of lowering the cutoff value of impaired fasting glucose(IFG)by studying the extent and severity of angiographic coronary artery disease(CAD)and the cardiovascular risk factors in subjects with different fasting plasma glucose(FPG)levels. Methods A total of 911 consecutive patients who had undergone coronary angiography were selected according to inclusion criteria. The subjects were studied in view of the extent and severity of angiographic CAD and the cardiovascular risk factors with different FPG levels. Results (1) Compared with the group of FPG<5.6mmol/L, the numbers of diseased vessels in the group with FPG 5.6-6.0mmol/L were significantly increased(P<0.05)after adjustment of age, sex and other influencing factors; the group with FPG 6.1-6.9mmol/L had both raised number of diseased vessels and the CAD Gensini cumulative index(P<0.01). (2) The prevalences of overweight, hypertension, hypertriglyceridemia, metabolic syndrome were progressively increasing with graded FPG levels. The prevalence of hypertriglyceridemia was significantly increased with FPG level at 5.0-5.6mmol/L(P<0.05),and the prevalences of metabolic syndrome and other components were significantly elevated with FPG level at 5.6-6.0mmol/L(P<0.05). Conclusion (1) The extent and severity of angiographic CAD were increased with increased FPG even in prediabetic period. The risk of angiographic CAD became increased significantly with FPG at 5.6-6.0mmol/L level. (2) The cardiovascular disease(CVD)risk was also increased with increasing FPG even in prediabetic period. The phenomenon of clustering of CVD risk factors was found at FPG 5.6mmol/L.

Objective: To investigate the role of Smads signaling pathway in the transdifferentiation of airway epithelial cells into myofibroblasts induced by rhTGF-?1 in vitro.Methods: We exposed cultured 16HBE cells to rhTGF-?1(10?g/L),detected the levels of Phosphorylated Smad2 and Smad3 in nucleus proteins by Western blot at different time points,treated with rhTGF-?1 the 16HBE cells pre-transfected with either the expression plasmid of Smad7(pCDNA3.0/Smad7) or the blank vector(pCDNA3.0),and determined the expression of ?-SMA by immunofluorescent staining and RT-PCR and that of E-cadherin by RT-PCR.Results: The expression of Phosphorylated Smad2 was observed and that of Smad3 increased in the TGF-?1-treated group,with the levels of Phosphorylated Smad2 and Smad3 elevated in a time-dependent manner.The level of ?-SMA was significantly decreased while that of E-cadherin markedly increased in the Smad7 transfection group as compared with the blank vector transfection group 24 h after TGF-?1 stimulation,and no differences were found between the two groups at 36 h.Correspondingly,the number of ?-SMA-positive cells was reduced in the Smad7 group compared with the blank vector group(P

AIM: To investigate the regulatory effects of nuclear factor-κB ( NF-κB) and activator protein-1 (AP-1) on the expression of ectopic trypsin and proinflammatory cytokines in influenza A virus (IAV)-induced myocardi-tis.METHODS:Male BALB/c mice of 8 weeks old ( n=40) were randomly divided into 4 groups:normal control group ( NC) , infection control group ( IC) , NF-κB inhibitor group ( NI) and AP-1 inhibitor group ( AI) .The mice in NC group and IC group were instilled intranasally with 15μL saline and 40 plaque forming units ( PFU) IAV, respectively.The mice in NI group and AI group were infected intranasally with 40 PFU IAV and injected intraperitoneally with 10 mg/kg NF-κB inhibitor pyrrolidine dithiocarbamate ( PDTC) or 2.5 mg/kg AP-1 inhibitor nordihydroguaiaretic acid ( NDGA) once daily. The mice were euthanized at day 9 after instillation, and the hearts were removed for pathological and biochemical analysis. RESULTS:IAV infection induced significant up-regulation of ectopic trypsin, and proinflammatory cytokines interleukin 6 (IL-6), IL-1βand tumor necrosis factor-α(TNF-α) in the myocardium, and triggered acute myocarditis.PDTC signifi-cantly inhibited NF-κB activation and up-regulation of ectopic trypsin and proinflammatory cytokines, and effectively sup-pressed IAV replication and myocardial inflammatory response (P<0.01).NDGA effectively inhibited AP-1 activity (P<0.01) and mildly suppressed up-regulation of proinflammatory cytokines ( P<0.05) , but had no effects on the expression of ectopic trypsin, IAV replication and the extent of myocarditis ( P>0.05) .CONCLUSION:IAV infection induces up-regulation of ectopic trypsin and proinflammatory cytokines in myocardium predominantly by the activation of NF-κB.AP-1 signaling pathway might be only partially involved in the regulation of proinflammatory cytokines.

Objective In order to discuss the practicability and risk analysis of deep venous catheter in AIDS patients.Methods 112 patients who needed to keep the intravenous route between October in 2010 and February in 2012 in Yunnan AIDS care center were implemented deep venous catheter.Results Right Subclavian vein catheter 101 cases,right internal jugular vein catheter 10 cases,right femoral vein catheter in 1.Wound happened in 5 cases,catheter heterotopia 1 case.Conclusion Deep venous catheter in patients with HIV/AIDS clinical diagnosis and treatment work could not only relieve the patients' pain because of repeated puncture,reduce the nursing workload,ensure the smooth progress of the clinical diagnosis and treatment,but also the more important is to reduce the occupational exposure risk of medical staff.

Objective To estimate the biological effects of leptin on human HaCaT keratinocytes and explore their molecular mechanisms.Methods Cell counting kit-8 (CCK-8) was used to evaluate the proliferation of cultured HaCaT cells treated with different concentrations of leptin for 24 and 48 hours.Some HaCaT cells were classified into four groups to remain untreated,be treated with leptin (100 μg/L) and piceatannol (a specific inhibitor of STAT3 phosphorylation) alone or in combination for 24 hours,respectively,followed by the evaluation of cell proliferation using CCK-8 kit.Flow cytometry was performed to assess cell cycle of HaCaT cells treated with leptin of 100 μg/L,Western blot to determine the phosphorylation level of Erk1/2 and STAT3 in HaCaT cells treated with leptin of 100 μg/L for different durations.Statistical analysis was done by Student's t-test for unpaired data using GraphPad Prism 5 software.Results The proliferation of HaCaT cells was accelerated to different degrees after treatment with leptin of 50 and 100 μg/L for 24 and 48 hours,and the accelerating effect was in a dose-dependent manner within 24 hours (r =0.9989,P ＜ 0.05).Piceatannol apparently inhibited the promotive effect of leptin on the proliferation of HaCaT cells.There was an obvious elevation in the percentage of cells at S phase ((57.70 ± 5.88)％ vs.(42.50 ± 7.55)％,P ＞ 0.05),but a significant decrease in that at G0/G1 phase ((39.70 ± 1.57)％ vs.(45.20 ± 1.44)％,P ＜ 0.05),with a significant increase in proliferation index (0.603 ±0.0157 vs.0.564 ± 0.0144,P ＜ 0.05) in HaCaT cells treated with leptin of 100 μg/L for 24 hours compared with the untreated controls.Western blot showed that leptin of 100 μg/L markedly enhanced the phosphorylation level of STAT3 in HaCaT cells.Conclusion Leptin may upregulate the proliferation of HaCaT cells through activation of STAT3 pathway.

Objective To investigate the effect of remote ischemic preconditioning on myocardial infarction and the involved protective mechanisms. Methods Twenty-four male SD rats were randomly divided into four groups: ischemia-reperfusion (I/R) group, rote ischemic preconditioning (RIPC) group, remote ischemic preconditioning + ischemia-reperfusion (RIPC+I/R) group, and RIPC+AG490+I/R group. The blood samples and myocardial specimens were collected and prepared for tests. The related enzymes were detected and the size of myocardial infarction was measured. The cardiac cells were determined by electron microscopy and light microscopy. Results The size of myocardial infarct and myocardial enzymes were significantly reduced in RIPC+I/R group compared to those in I/R group (P < 0.05). The size of myocardial infarction and myocardial enzymes were significantly increased in AG490 group compared to those in RIPC+I/R group (P < 0.05), but were significantly reduced in AG490 group compared to those in I/R group (P < 0.05). Conclusions Remote ischemic preconditioning may be effective in cardioprotection. The JAK/STAT pathway is involved in the cardioprotection of remote ischemic preconditioning.