DNA Methylation ; Helicobacter Infections ; complications ; Helicobacter pylori ; Humans ; Stomach Neoplasms ; etiology ; genetics ; Telomerase ; physiology

Inflammatory bowel disease(IBD)is an autoimmune disease and its etiology has not yet been clarified. Dysregulated immune responses resulted from complex interactions among genetic factors,intestinal flora and environmental cues have been considered as the etiology of IBD. Recently,the relationship between Th17 cells and IBD has become a hotspot of study,and more and more studies showed that Th17 cells and their related cytokines regulated by intestinal flora contributed to the pathogenesis of IBD. This article reviewed the role of Th17 cells and intestinal flora in the pathogenesis of IBD.

Inflammatory bowel disease (IBD)includes Crohn’s disease (CD)and ulcerative colitis (UC).The differential diagnosis between CD and UC mainly depends on clinical symptoms,endoscopy,pathological biopsy,laboratory and imaging examinations.In recent years,studies with a variety of IBD-related biomarkers develop rapidly because of its non-invasiveness,simple and easily acceptable.With the development of genome-wide association study (GWAS),great progress has been achieved in studies of gene mutations and susceptibility genes related with CD and UC,which provides new approach for diagnosis of the disease.This article reviewed the advances in studies on serum biomarkers and susceptibility genes in differential diagnosis of IBD.

As a new therapy in past twenty years,biological agents have been approved for the treatment of inflammatory bowel disease (IBD). However,biological agents currently used for IBD treatment require intravenous or subcutaneous injections,and some require infusion under close observation. Therefore,it is of positive clinical significance to find a safe and effective oral biological agent. This article reviewed recent advances in study on novel oral biological agents in the treatment of IBD.

Objective To explore the antineoplastic parvovirus H-1 induced cell death signaling pathways and their possible mechanisms in gastric carcinoma cells. Methods By using RT-PCR method, the mRNA expressional changes of mitogen-activated protein kinase (MAPK) signaling transduction pathway related genes were measured in gastric adenocarcinoma HGC27 cells infected by H-1 virus. Results The RT-PCR amplification results displayed that 48 h after HGC-27 cells were infected by H-1 virus, the expression of CREB was increased, the expression of ERK1, STAT2, p38-?, MEK2, ?-RAF and MTK1 were remarkably decreased, however, the expression of JNK2, ETS and ERK2 had no apparently change. Conclusions The cytotoxic effects of parvovirus H-1 might affect the gene expression involved in MAPK signal transduction pathway in gastric carcinoma HGC27 cells. It indicates that H-1 virus might interfere with specific cellular signal transduction pathways of gastric carcinoma cell to induce cell death. In conclusion, it was considered that modified and reconstructed parvovirus H-1 would be a very valuable tool in the anti-tumor study.

Objective To investigate the sensitivities of distinct gastric cancer cells to parvovirus H-1 induced cytotoxicity and its possible mechanisms. Methods Six distinct differentiated gastric cancer cell lines were employed in this study, including HGC27 (undifferentiated), BGC823(undifferentiated), MKN45(poor differentiated), AGS (poor differentiated), SGC7901(moderate differentiated) and MKN28 (well differentiated). The cell cycle distributions were measured by flow cytometry. The differential sensitivities of six distinct gastric cancer cells after H-1 virus infection were detected by MTT analysis. The RT-PCR was employed to detect viral NS-1 gene expression in all six gastric cancer cell lines. Results The S phase ratios of HGC27, BGC823, MKN45, AGS, SGC7901 and MKN28 were 24.72%, 30.15%, 27.10%, 29.03%, 31.82% and 33.73% respectively. HGC27 cells were sensitive to H-1 virus induced cytotoxicity followed by SGC7901 cells. MKN45 and AGS cells were moderately sensitive. MKN28 cells were insensitive. However, BGC823 cells were resistant to H-1 virus induced cytotoxicity. The expressions of viral NS-1 were higher in HGC27, BGC823, MKN45 and SGC7901 cells, whilst NS-1 gene expressions were lower in AGS and MKN28 cells. Conclusions The sensitivities of distinct gastric cancer cells to H-1 virus induced cytotoxicity could be markedly different. In general, the poorly differentiated cells showed an enhanced sensitivity to H-1 virus attack as compared to well differentiated ones. The enhanced sensitivity of poorly-versus well-differentiated gastric cancer cells to H-1 virus is due to at least in part, to the enhanced capacity of the former cells for NS-1 protein production and accumulation. The undifferentiated BGC823 cells were resistant to H-1 virus triggered cytotoxicity. It may further verify that not all the tumor cells were sensitive to H-1 virus lytic effects.

Objective To evaluate the killing effects of oxymatrine(OM) on human colon cancer cell line SW1116 and the mechanism of its anti-neoplastic effect. Methods Methyl thiazolyl tetrazolium analysis, flow cytometry , polymerase chain reaction(PCR)-enzyme linked immunosorbent assay (ELISA) and RT-PCR were used to detect the killing effects of OM and its influence on cell cycle dis- tribution , telomerase activity, expressions of human telomerase reverse transcriptase (hTERT), c-myc ,p53 and mad1 genes in SW1116 cells. Results OM exhibited dose-dependent killing effects on SW1116 cells and induced the increase of G1/G0-phase cells and decrease of S-phase cells. It was found that OM could supress the telomerase activity of SW1116 cells, and the effects were dose- and time-dependent. After OM administration, the expression of hTERT gene in SW1116 cells was decreased, those of p53 and mad1 genes were increased, and the expression of c-myc gene had no marked changes. Conclusions OM has dose-dependent killing effects on SW1116 cells.The anti-neoplastic activity of OM might be due to the inhibition of telomerase activity by means of its influence on hTERT and the up-stream regulation genes.

Objectives To observe the effect of inhibition of transforming growth factor (TGF)?1 on the growth and aggression of colon cancer cells by RNA interference. Methods HCT116 colon cancer cells were transfected with small interfering dsRNA (siRNA), the effect of the inhibition of TGF?1 was tested by semi-quantitative RT-PCR, and changes in cell cycle distribution were analyzed by flow cylometry, the ability of aggression was detected by soft agar colony assay. Results The inhibition of the expression of TGF?1 was significantly detected after the transfection of siRNA against TGF?1, which induced the increase of S phase by 59.0%-82. 5% and decrease in G2 phase, colony assay further demonstrated that siRNA against TGF?1 led to a significant reduction in colony formation as compared with the control group. Conclusions The present data suggested that the expression of TGF?1 was conveniently and rapidly blocked by siRNA transfection, and this may lead to the cell cycle arrest and inhibition of the growth and tumorigenesis of colon cells.

Objective To analyze the consistency of transcutaneous perianal ultrasonography (TPUS) and pelvic magnetic resonance imaging (MRI) in diagnosing perianal lesions of Crohn's disease (CD), and to evaluate the value of transcutaneous perianal ultrasonography in detecting perianal lesions of CD. Methods A cohort of 102 patients diagnosed as Corhn's disease were enrolled from August 2008 to August 2010. Perianal abscess and fistula of these CD patients was diagnosed by ultrasonography and MRI system. Statistics was performed with SPSS 11.5 software for X2 test. The consistency was analyzed with Kappa test. Results The mean onset time of perianal lesions in CD was -0.443 year (95％CI:-1.659～0.773 year) before typical symptoms showed up. There was no significant difference in detecting perianal lesions of CD between transcutaneous perianal ultrasonography and pelvic magnetic resonance imaging (P ＝ 0.706, Kappa ＝ 0.541). If pelvic magnetic resonance imaging was considered as the golden standard in detecting perianal lesions of CD,the sensitivity (Sen), specificity (Spe), Youden's index, positive predictive value (PPV) and negative predictive value (NPV) of TPUS were 72.73％, 82.61％, 0.55, 66.67％ and 86.36％ respectively.Furthermore, there was no significant difference between transcutaneous perianal ultrasonography and pelvic magnetic resonance imaging in detecting perianal abscess ( P ＝ 0.706, Kappa ＝ 0.496) and fistula (P＝0.655, Kappa＝0.546) of CD. Conclusions Perianal lesions occur in the entire course of CD. There was favorable consistency between transcutaneous perianal ultrasonography and pelvic magnetic resonance imaging in detecting perianal abscess and fistula of CD. Transcutaneous perianal ultrasonography can be used as an additional method in detecting and evaluting perianal lesions of CD.

Objective To investigate the role of cDNA microarray techniques in detection of the changes of gene expressional profiles in the gastric carcinoma cell line HGC27 induced by parvovirus H 1 infection. Methods The mRNA of gastric carcinoma cell line HGC27 was collected at the time before or 48 h after H 1 virus infection. Using cDNA microarray, we investigated the diversification of gene expression of HGC27 after H 1 virus infection. A part of genes whose expressions were changed in cDNA microarray analysis were further identified by RT PCR and Northern blot. Results The cDNA microarray analysis showed that the expressions of 920 genes were changed among total of 8000 genes, in which 363 genes showed decreased expressions whilst 557 gene expressions were increased. Among them, some of the genes, including ? raf, sarp1, creb, p38 ? and rad21, were further confirmed by RT PCR and Northern blot analysis. The results of RT PCR and Northern blot were coincided well with the cDNA microarray results. Conclusions The cDNA microarray is an effective method for the large scale comparison of multiple genes expressions in a single hybridization and for the studies on anti tumor mechanisms of parvovirus H 1.