OTSC assisted EFTR for the treatment of GIST: 40 cases analysis.

BACKGROUND AND AIMS: To verify the safety and efficacy of over-the-scope clip (OTSC)-assisted endoscopic full-thickness resection (EFTR) for the excision of stromal tumors. MATERIAL AND METHODS: Forty patients with gastric stromal tumors treated in the Department of Gastroenterology, Binzhou Medical University Hospital from December 2015 to March 2017 were included in this study. The surgical procedures included marking the lesion boundaries, cutting open the top surface of the lesion, installing an OTS, sucking the lesion into the transparent cap of the anatomical clip which was then released, application of an endoloop for EFTR, and confirming the complete resection and pathological examination of the lesion. Statistical analysis of the tumor site and size, operation time, success rates, complications, pathological examination results, and follow-up status was performed. RESULTS: The average operation duration was 38.40 ± 24.9 min. Three cases had an incomplete resection, but the lesion was later found to have fallen off together with the OTSC. Therefore, the treatment success rate was 100%. Postoperative pathological examination revealed leiomyomas in four cases and stromal tumors in the remaining 36 cases. CONCLUSIONS: OTSC-assisted EFTR is safe and effective for resection of gastrointestinal stromal tumors, especially for those <20 mm in size.

Probiotics in the treatment of peptic ulcer infected by helicobacter pylory and its safety.

This paper aimed to study the curative effect of probiotics in the treatment of peptic ulcer (PU) infected with Helicobacter Pylory (H. Pylory). A total of 132 cases of patients with PU infected by H. Pylory who were received and treated by department of gastroenterology from Binjiang Hospital, Guangxi from May 2013 to 2014 were recruited in the study. They were divided into observation group and control group based on random number table, 66 cases in each group. Patients in observation group were given probiotics combined with triple therapy while patients in control group were treated by traditional triple therapy. After one-month treatment, all the patients were examined by (14)C urea breath test for checking the treatment condition of H. Pylory and reviewed by gastroscope for checking union of ulcer. In addition, clinical effect and improvement of digestive tract symptom were compared between two groups. It was found that, the content of (14)C urea detected by breath test was 95.15 dpm/mmol ± 8.34 dpm/mmol in observation group after treatment; eradication rate of H. Pylory was 87.9%; symptom remission rate was 97%; adverse reaction rate was 4.5%; total effective rate of clinical treatment was 97%; while in control group, the content of (14)C urea was 100.3 dpm/mmol ± 10.34 dpm/mmol, eradication rate was 63.6%, symptom remission rate was 93.9%, adverse reaction rate was 18.2%, and total effective rate was 83.3%. These results demonstrated that, the symptom remission rate of the observation group and the control group was not obvious, but the content of (14)C urine, eradication rate of H. Pylory, incidence of adverse reaction and total effective rate were of significant significance in two groups (P<0.05). In conclusion, probiotics combined with triple therapy for treating PU infected by H. Pylory can greatly improve the eradication rate of H. Pylory and increase recovery rate of patients, with less adverse reaction. Therefore, the method is worth for promotion.

Obesity and the risk of cholangiocarcinoma: a meta-analysis.

A number of studies have shown that obesity is implicated in the susceptibility to several cancers. However, the association between obesity and cholangiocarcinoma remains unclear. This meta-analysis aimed to quantitatively assess the association between overweight or obesity and the incidence of cholangiocarcinoma. A literature search was performed for cohort and case-control studies published from 1996 to 2013 using PubMed, Cochrane, and EMBASE databases. Studies were included if they reported odds ratios (ORs) and corresponding 95 % confidence intervals (CIs) of cholangiocarcinoma with respect to obesity or overweight. Normal weight, overweight, and obesity were defined when the body mass index (BMI) was 18.5-24.9, 25-29.9, and ≥ 30 kg/m(2), respectively. Excess body weight was defined as BMI ≥ 25 kg/m(2). Ten studies met the inclusion criteria, which included five cohort and five case-control studies. Compared with normal weight, being overweight (pooled OR 1.30, 95 % CI 1.13-1.49), obesity (pooled OR 1.52, 95 % CI 1.13-1.89), and excess body weight (pooled OR 1.37, 95 %CI 1.22-1.55) were significantly associated with cholangiocarcinoma. The funnel plot revealed no evidence for publication bias. Obesity is associated with the increased risk of cholangiocarcinoma, which needs to be confirmed by long-term cohort studies.

Silencing of Long Non-Coding RNA-HCG18 Inhibits the Tumorigenesis of Gastric Cancer Through Blocking PI3K/Akt Pathway.

PURPOSE: Long non-coding RNAs (lncRNAs) play critical regulatory roles in the tumorigenesis of GC. This study aimed to investigate the regulatory effect and mechanism of lncRNA-HCG18 on GC. METHODS: The expression of lncRNA-HCG18 was detected in GC tissues and cell lines by qRT-PCR. LncRNA-HCG18 was silenced in AGS and MGC803 cells by the transfection of lncRNA-HCG18 siRNA (si-HCG18). MTT, transwell and Annexin V-PI double staining assay were performed to assess the proliferation, migration, invasion and apoptosis of GC cells. The expression of PI3K/Akt pathway-, apoptosis-, and migration-related proteins were detected by Western blot. An activator of PI3K/Akt pathway 740 Y-P was used to activate the PI3K/Akt pathway in AGS cells. A human tumor xenograft model was established in mice to evaluate the effects of si-HCG18 in vivo. RESULTS: LncRNA-HCG18 was overexpressed in GC tissues and cells. Up-regulation of lncRNA-HCG18 was positively correlated with the stage of tumor node metastasis and invasion depth. Silencing of lncRNA-HCG18 suppressed the proliferation, migration and invasion, and induced the apoptosis of GC cells. Silencing of lncRNA-HCG18 blocked the PI3K/Akt pathway. The intervention of 740Y-P reversed the anti-tumor effect of lncRNA-HCG18 on GC cells. In addition, silencing of lncRNA-HCG18 suppressed the growth of GC xenografts in mice. CONCLUSION: Silencing of lncRNA-HCG18 inhibited the tumorigenesis of GC through blocking the PI3K/Akt pathway, suggesting a novel therapeutic target for GC.

Lactobacilli inhibit interleukin-8 production induced by Helicobacter pylori lipopolysaccharide-activated Toll-like receptor 4.

AIM: To investigate the effect of Lactobacillus bulgaricus (LBG) on the Toll-like receptor 4 (TLR4) pathway and interleukin-8 (IL-8) production in SGC-7901 cells treated with Helicobacter pyloriSydney strain 1 lipopolysaccharide (H pyloriSS1-LPS). METHODS: SGC-7901 cells were treated with H pyloriSS1-LPS in the presence or absence of pretreatment for 1 h with viable LBG or supernatant recovered from LBG culture MRS broth (LBG-(s)). Cellular lysates were prepared for Western blot with anti-TLR4, anti-transforming growth factor beta-activated kinase 1 (TAK1), anti-phospho-TAK1, anti-nuclear factor kappaB (NF-kappaB), anti-p38 mitogen-activated protein kinase (p38MAPK), and anti-phospho-p38MAPK antibodies. The amount of IL-8 in cell culture medium was measured by ELISA. RESULTS: H pyloriSS1-LPS up-regulated the expression of TLR4, stimulated the phosphorylation of TAK1, subsequently enhanced the activation of NF-kappaB and the phosphorylation of p38MAPK in a time-dependent manner, leading to augmentation of IL-8 production in SGC-7901 cells. Viable LBG or LBG-(s) pretreatment attenuated the expression of TLR4, inhibited the phosphorylation of TAK1 and p38MAPK, prevented the activation of NF-kappaB, and consequently blocked IL-8 production. CONCLUSION: H pyloriSS1-LPS induces IL-8 production through activating TLR4 signaling in SGC-7901 cells and viable LBG or LBG-(s) prevents H pyloriSS1-LPS-mediated IL-8 production via inhibition of the TLR4 pathway.

Notch signaling promotes serrated neoplasia pathway in colorectal cancer through epigenetic modification of EPHB2 and EPHB4.

BACKGROUND: Dysregulation of erythropoietin-producing hepatoma (Eph) proteins in human cancers is extensively documented but not clear in colorectal cancer (CRC). In this study, we aimed to investigate the role of Notch signaling pathway and epigenetic modification of EPHB2 and EPHB4 expression in serrated neoplasia development. METHODS: The expression of EPHB2 and EPHB4 in CRC clinical specimens and cell lines were determined by immunohistochemistry, Western blot, and real-time PCR. Cell proliferation and invasion were evaluated by MTT and chamber kits, luciferase assay and co-immunoprecipitation were used to detect the transcriptional regulation and protein-protein interactions, respectively. The immunofluorescence assay was employed to confirm the subcellular location of Notch intracellular domain (NICD), and chromatin immunoprecipitation assay was implied to detect the modification types of H3K4me3 and H3K27me3. Mice xenograft model was used to detect the in vivo effects of EPHB2 and EPHB4 genes on cell growth. RESULTS: In CRC clinical specimens and cell lines, we found that EPHB2 was significantly decreased, while EPHB4 was elevated in the CRC tissues, and these aberrant expression manners correlated with worse overall survival rates in the clinic. When the EPHB2 and EPHB4 expressions were manipulated by overexpression or knockdown in the SW620 cells, the cell proliferation and invasion were obviously suppressed, whereas EPHB2 knockdown or EPHB4 overexpression showed the opposite phenotypes. We also found that Notch signaling pathway was abnormally activated and treatment of Notch signaling ligand human Jagged1 peptide downregulated EPHB2 and upregulated EPHB4 in the SW620 cells, as well as promoted the chromatin modification protein Jumonji domain-containing protein-3 (JMJD3) cytonuclear trans-localization with the NICD, which indicated that NICD brought JMJD3 to the EPHB4 enhancer region to decrease the H3K27me3 level. CONCLUSION: Taken together, we provide a new mechanistic option in understanding the role of Notch signaling and the roles of EPHB2 and EPHB4 in CRC.

[Effects of Lactobacilli on regulating NF-kappaB activation and IL-8 secretion in SGC7901 cell impacted by Helicobacter pylori].

OBJECTIVE: In vitro to investigate the regulation effects of Lactobacillus acidophilus ATCC4356 and L. bulgaricus (LB) on the activation of NF-kB and IL-8 secretion of SGC7901 cell, which Helicobacter pylori induced. METHODS: SGC7901 cell was cultured to reach the exponential growth phase, then adjusted to cell concentration (2.5 x 10(5)/mL), and planted into six shadow mask and incubated for 24 hours. Until reaching exponential growth phase, the cultured ATCC4356 and LB were adjusted to different concentration to incubation with SGC7901 cell together for one hour, and then added H. pylori into them for culturing 3 hours. For the contrast analysis of result, the experiment subgroups were designed as follow: normal control, H. pylori stimulating group (H. pylori group), ATCC4356 intervention group (ATCC4356 group) and LB intervention group (LB group). The nuclear factor-kB of SGC7901 cell was detected by immunohistochemistry. The release of IL-8 in cells was detected by ELISA. RESULTS: The percentage of NF-kB p65 positive nuclei-stained cell and the secreting level of IL-8 from cells in H. pylori group significantly increased compared with those in control group (P < 0.01). When the Lactobacillus concentration was 3 x 10(6) cfu/mL, 3 x 10(7) cfu/mL and 3 x 10(8) cfu/mL respectively, the percentage of NF-kB p65 positive nuclei-stained cell of ATCC4356 group was significantly decreased compared with that of H. pylori group (P < 0.01). When the Lactobacillus concentration was 3 x 10(6) cfu/ mL and 3 x 10(7) cfu/mL respectively, the IL-8 secretory volume of cells of ATCC4356 group could be significantly decreased compared with that of H. pylori group (P < 0.01). When the Lactobacillus concentration was 3 x 10(6) cfu/ mL, 3 x 10(7) cfu/mL and 3 x 10(8) cfu/mL respectively, the percentage of NF-kB p65 positive nuclei-stained cell of LB group was significantly decreased compared with that of H. pylori group (P < 0.05). When the Lactobacillus concentration was 3 x 10(7) cfu/mL or 3 x 10(8) cfu/mL respectively, the cell IL-8 secretory volume of LB group was significantly decreased compared with that of H. pylori group (P < 0.05). However, if the level of Lactobacillus concentration showed too high, the ATCC4356 and LB might have no above mentioned inhibitory action, the percentage of NF-kB p65 positive nuclei-stained cell and the level of IL-8 secretion of cells in those experiment groups significantly increased compared with those in H. pylori group. CONCLUSION: In some concentration range, both ATCC4356 and LB can inhibit the cell inflammatory reaction induced by H. pylori, but if the concentration is too high, they may make the inflammatory reaction become more serious. These can explain in partial why lactobacillus as primary common bacterium maintains the proper proportion concentration is very important for the keeping on microecological balance in stomach.