Objective To investigate the incidence trends,clinical features and prognosis of ischemic colitis (IC) in China,and improve the level of diagnosis and treatment of IC.Methods China National Knowledge Infrastructure and VIP Chinese Science and Technology Periodical Database were searched.The ending date of search was May 15,2014.Results A total of 324 references were found,which were published from 1982 to 2013.There were 9202 cases reported,3973 cases of males and 5229 cases of females,with the male/female ratio of 1 ∶ 1.32 and mean age of (63.6±7.8)years.The amount of references and cases reported began to rise after 2002.Estimated ratio of cumulative incidence was higher in the north than in other areas of China (x2 =1097.95,P=0.000).The most common IC accompanying diseases were hypertension,heart diseases,diabetes,hyperlipidemia and constipation.There were statistically significant differences in the accompanying diseases between different regions and different times.Drugs,enteroscopy,surgery and low blood volume might be the precipitating factors.Patients commonly complained of abdominal pain,diarrhea/ desiring to defecate and hematochezia.Computed tomography was feasible in detecting lesions.Colonoscopy was the main method for diagnosis.The lesions were most common located in the left half colon including sigmoid colon,descending colon and splenic flexure,with typically in a segmental manner.Pan-colon involvement or rectum involvement rarely occurred.Type of transient lesion was the predominant subtype,which was generally managed non-operatively with good prognosis.Different from the type of transient lesion,pathological changes in gangrenous type were located in the right half colon including hepatic flexure of transverse colon,ascending colon and ileocecal junction.Gangrenous type required prompt surgical intervention but the mortality was much higher.Conclusions Incidence of CI has been increasing year by year.Patients who complain of abdominal pain,diarrhea/desiring to defecate and hematochezia should be considered as IC,particularly in the elderly women and patients with cardiovascular disease.Diseased regions are mainly located in sigmoid colon,descending colon and splenic flexure.Transient colitis is the predominant subtype,which have good prognosis.

AIM To investigate the roles of Cl- channels in Ca2+ influx induced by activaion of al- adrenoceptor subtypes in transfected-CHO cells. METHODS The effects of drugs on ?1A、?1B and ?1D- AR-induced Ca2+ influx were investigated with Fura2 fluorescence technique. RESULTS The ?1A-AR- induced Ca2+ influx was inhibited by furosemide(2 .5 ~ 10 M?mol?L- 1 )and SK&F96365(5- 15 ?mol?L- 1 ) in a concentration- dependent manner respectively; The ?1B-AR-induced Ca2+ influx could also be inhibit inhibited by NFA(2. 5 ~ 10 ?mol? L-1 ), whereas the alD AR-induced Ca2+ influx was only suppressed by NFA. In ?1B-CHO cells, Adr-triggered Ca2+ influx could be further inhibited by NFA or furosemide after the maximal inhibition by SK&F96365;SK&F96365 could further inhibit Ca2+ influx which had been inhibited by NFA or furosemide. In ?1A-CHO cells, Adr-triggered Ca2+ influx could be further inhibited by SK&F96365 after had been inhibited by furosemide; furosemide could not further inhibite Ca2+ influx which had been inhibited by S&F96365. CONCLUSION There are different characteristics of CI- channels related to ?1A、 ?1B and ?1D-AR-induced Ca2+ influx.

To comparatively investigate ultrastructural characteristics and expressions of AFP (alpha-fetoprotein) and Tn (Thomsen-Friedenreich-related antigen) protein in AFP negative (AFP-) and AFP positive (AFP+) primary hepatocellular carcinoma. Fourty-three cases of AFP- and AFP+ hepatocellular carcinoma (HCC) tissues and five cases of normal liver tissues were divided into three groups: control group (normal liver tissue, n=5); AFP+ HCC group (the serum AFP level was higher than 10 ng/ml, n = 22); AFP- HCC group (the serum AFP level was lower than 10 ng/ml, n=21). The ultrastructural morphology was studied by transmission electron microscopy, the expressions of AFP and Tn protein were detected by immunohistochemistry and cell image analysis. 1. The immunohistochemical study showed that (1) the expression intensity and positive rate of Tn protein in AFP- HCC group were markedly higher than that in AFP+ HCC group (P<0.01); (2) The expression intensity of AFP in AFP- HCC group was lower than that in AFP+ HCC group (P<0.01). 2. The transmission electron microscopy demonstrated that some AFP- HCC cells linked closely with each other, others dispersed loosely just as cultured cells, the remarkable morphologic features in AFP- HCC cells were simple organelles, but they were abundant in the free polyribosomes. In AFP+ HCC group, all the HCC cells linked closely together and were rich organelles in their cytoplasm, especially the rough endoplasmic reticula. In addition, mitochondria and Golgi complex were obviously observed. (1) The AFP and Tn protein had discrepancy distribution in AFP- and AFP+ HCC tissues, Tn protein may be one of the early diagnostic indicators in AFP- HCC; (2) The synthetic locations of the AFP and Tn protein were different in hepatocarcinoma cells by ultrastructural observation.

AIM: To investigate the relationship between chloride channels and the Ca 2+influx induced by adrendine(Adr). METHODS: The effects of drugs on Adr-induced Ca 2+influx were investigated with Fura-2 fluorescence technique. RESULTS: Adr-induced Ca 2+influx was inhibited by nifedipine,SK&F96365,NFA and furosemide in a concentration manner respectively; Ca 2+influx could be further inhibited by NFA or furosemide after the maximal inhibition by SK&F96365;SK&F96365 also could further inhibit the Ca 2+influx which had been inhibited by NFA or furosemide. Genistein and vanadate could reduce or increase the Ca 2+influx respectively. CONCLUSION: Ca 2+influx induced by Adr is related to VDC and ROC, and chloride channels involves in the processes.The levels of tyrosine phosphoralation affect the Ca 2+influx.

Objective To evaluate the value of indirect hemagglutination test(IHA)in schistosomiasis diagnosis. Meth?ods The literature concerned schistosomiasis diagnosis with IHA in the databases of Medline,CNKI,VIP and Wanfang Data from 1982 to 2014 was collected and evaluated. Results Totally 21 articles which were satisfied with the research criteria were analyzed with the Meta?analysis method. The IHA method had high value in schistosomiasis diagnosis,the AUCSROC of IHA in laboratory evaluation was 0.990 6,while in filed evaluation was 0.832 9,and the difference between them was significant(Z=4.50,P<0.05). Conclusion The diagnosis value of IHA in field evaluation is less than that in laboratory. In the process of the elimination of schistosomiasis,developing a new and higher sensitive reagent in schistosomiasis diagnosis is needed.

Objective:This study aimed to investigate the effect of human lymphatic endothelial cells (HLECs) on proteins secreted by epithelial ovarian cancer (EOC) cells SKOV3-pm4 with highly directional lymphatic metastasis. Methods:The supernatants of the four groups of cultured cells (A, SKOV3;B, SKOV3+HLEC;C, SKOV3-PM4;and D, SKOV3-PM4+HLEC) were collected. The proteins of these cells were detected by antibody arrays and iTRAQ-2D-LC-MALDI-TOF/TOF/MS. The screened significantly differential proteins were further analyzed by bioinformatics and validated in the human serum and cell culture medium by ELISA. Results:Progranulin (GRN) and vascular endothelial growth factor A (VEGF-A) were upregulated between groups C and A. In addition, insulin-like growth factor binding protein-7 (IGFBP-7) and secreted protein acid rich in cysteine (SPARC) were downregulated between groups D and C. Comprehensive bioinformatics analysis revealed that IGFBP7 interacted with VEGFA. VEGF exhibited the highest expression in ovarian cancer and IGFBP7 exhibited the lowest expression compared with the serum of the normal control group. Statistically significant differences were observed between the two substances. Conclusion:The HLEC microenvironment is closely associated with directional metastasis in lymph nodes with differential proteins, including matricellular proteins and adhesion factors. In particular, the upregulation of VEGFA and GRN and the downregulation of SPARC and IGFBP7 were closely associated with the directional metastasis of EOC cells in lymph nodes.

The effects of drugs on intracellular calcium concentration(［Ca2+］i) were investigated with fura-2 fluorescence technique to investigate ATP and thrombin-induced Ca2+ entry in bovine aortic endothelial cells(BAEC). It was found that application of ATP and thrombin gave rise to biphasic ［Ca2+］i elevation. ATP or thrombin only triggered a fraction of cyclopiazonic acid(CPA)-sensitive Ca2+ store, which was enough to activate Ca2+ entry. The Ca2+ release induced by thrombin resulted from the activation of phospholipase C(PLC), whereas the PLC-independent mechanism was involved in ATP-induced Ca2+ release. Nifedipine had no effect on ATP and thrombin- induced Ca2+ entry. SK&F 96365 and ginsenoside-2A inhibited both ATP and CPA-induced Ca2+ entry, however no effect of them on thrombin-induced Ca2+ entry was found. The inhibitory effects of SK&F 96365 and ginsenoside-2A on CPA-induced Ca2+ entry were less than that on ATP-induced Ca2+ entry. The Ca2+ influx sensitive to SK&F 96365 was not the same as that to ginsenoside-2A. These observations suggest that both ATP and thrombin evoke Ca2+ release and Ca2+ influx by activation of different receptor. However their mechanisms appear different.

Objective: To study the mechanism of interleukin (IL)-17 in mice with non-alcoholic fatty liver disease for promoting M1-type macrophage polarization to exacerbate liver inflammation, and to provide references for the mechanism of NAFLD occurrence and development. Methods: A mouse model of NAFLD was constructed by high-fat diet. Mice were divided into control group, model group, IL-17 group, and anti IL-17 group. Histopathological changes of the liver were observed by HE staining. The serum levels of ALT and AST in peripheral blood of mice was detected by chemical colorimetry. Macrophages labeled with F4/80-PE, CD11C-FITC was designated as M1-type macrophages, those labeled with F4/80-PE, and CD206-APC was designated as M2-type macrophages. The proportion of M1 and M2 macrophages infiltrated into the liver tissues of mice were measured by flow cytometry. CD168 expression level of liver tissues was detected using immunohistochemistry. Protein and mRNA levels of the marker molecules (iNOS, TNF-alpha and IL-6) of M1 macrophages were detected using ELISA and RT-Q PCR. Western blot was used to detect the protein expression of JAK-STAT signal pathway and the expression level of MCP-1. Data were analyzed using one-way ANOVA and t-test. Results: High-fat diet NAFLD mice model was successfully constructed. IL-17 had increased the proportion of M1 macrophages in mice liver tissues and decreased the proportion of M2 macrophages (P < 0.05). The proportion of M1 and M2 macrophages in the liver tissues of normal mice was 7.9% ± 1.1% and 19.2% ± 1.8%. The proportion of M1 and M2 macrophages in the model group was 17.3% ± 2.5% and 15.0% ± 2.1. The proportion of M1 macrophages (33.8% ± 4.2%) in IL-17 group was higher than model group, while the proportion of M2 macrophages (7.8% + 1.0%) in IL-17 group was lower than model group. Protein and mRNA marker levels of M1 macrophage (iNOS, IL-12, TNFα and IL-6) in liver tissues were significantly higher than model group, control group, and anti-IL-17 group (P < 0.05). The expression levels of JAK1, STAT1, MCP-1, and CD168 in mice liver tissues of IL-17 group had increased (P < 0.05). The levels of aspartate and alanine aminotransferases in peripheral blood of mice in IL-17 group were significantly higher than other three groups (P < 0.05). Conclusion IL-17 can promote M1-type macrophage polarization, and exacerbates the liver inflammatory response to accelerate the progression of NAFLD in mice.

Objective To determine the effect of signal transducers and activators of transcription 3 (STAT3) gene silencing by shRNA mediated by lentiviral vector for the treatment of colorectal cancer. Methods The recombinant lentiviral vector pRNAT-shSTAT3, empty lentiviral vector pRNAT-GFP, and lentiviral packaging plasmids in supernatant were collected to transfect HT-29 cells for harvesting the HT-29-shSTAT3 cells and HT29-GFP cells. Fifteen male rats were divided into three groups (n = 5 ), and then they were inoculated with HT-29cells, HT-29-GFP cells and HT-29-shSTAT3 cells, respectively. Cell growth was assessed by MTT assay and the changes in cell cycle were detected by flow cytometry. The changes in microvessel density (MVD) of tumors were detected by immunohistochemistry. All data were analysed by one-way analysis of variance. Results The growth of HT-29-shSTAT3 cells was significantly suppressed compared with HT-29 and HT-29-GFP cells (F = 632.50,P ＜ 0. 05 ). The proportions of cells at the G0/G1 phase were 68.7% ± 2.9% in HT-29-shSTAT3 cells, 38.5% ±1.6% in HT-29-GFP cells and 38.7% ± 2.3% in HT-29 cells, with a significant difference among the three groups (F = 166.53, P ＜ 0.05 ). The MVDs of HT-29 cells, HT-29-GFP cells and HT-29-shSTAT3 cells were 29 ±5, 28 ±4 and 10 ±3, respectively, with a significant difference among the three groups (F=31.60, P ＜0.05). Conclusion STAT3 gene silencing by shRNA mediated by lentiviral vector can significantly inhibit the growth of colorectal cancer cells.

Objective:To observe the effect of low-expression or over-expression of NUP88 gene on the proliferation and invasion ability of breast cancer cell line BT-20.Methods: NUP88 recombinant adenovirus expression vector and NUP88 RNAi adenovirus vector were transfected into breast cancer BT-20 cells to obtain BT-20 cells over-expressing NUP88 and BT-20 cells lower-expressing NUP88 and then detected the expression of NUP88 mRNA and NUP88 protein.After that,the apoptosis of BT-20 cells was detected by flow cytometry and the invasion and metastasis of BT-20 cells were detected by Transwell invasion assay.The expression of apoptosis protein and invasion and metastasis proteins were detected by Western blot.Results: BT-20 cell with the over expression levels of NUP88 mRNA and NUP88 protein and BT-20 cell with the low expression levels of NUP88 mRNA and NUP88 protein were structured.The over-expression of NUP88 gene led to proliferation rate and the number of invasive cells were significantly higher than BT-20 cells,apoptosis cells were significantly lower than BT-20 cells(P<0.05).However,the low-expression of NUP88 gene led to proliferation rate and the number of invasive cells were significantly lower than BT-20 cells,apoptosis cells was significantly higher than BT-20 cells(P<0.05).The over-expression of NUP88 gene led to Bcl-2 and β-catenin level were significantly higher than that of BT-20 cells,and Bax and E-cadherin level were significantly lower than that of BT-20 cells(P<0.05).However,the low-expression of NUP88 gene led to Bcl-2 and β-catenin level were significantly lower than that of BT-20 cells,and Bax and E-cadherin level were significantly higher than that of BT-20 cells(P<0.05).Conclusion: NUP88 gene regulates the proliferation and invasion and migration ability of breast cancer cells by regulating the expression of Bax,Bcl-2,E-cadherin and β-catenin.It has an important significance in the target treatment of breast cancer.