http://www.biomedcentral.com/bmcgastroenterol/ The editor's pick of recent articles published by BMC Gastroenterology 2012-05-24T00:00:00Z Background: The objective of this study was to conduct a systematic review with meta-analysis of studiesassessing the association between living in an urban environment and the development of theCrohn's disease (CD) or ulcerative colitis (UC). Methods: A systematic literature search of MEDLINE (1950-Oct. 2009) and EMBASE (1980-Oct.2009) was conducted to identify studies investigating the relationship between urbanenvironment and IBD. Cohort and case-control studies were analyzed using incidence rateratio (IRR) or odds ratio (OR) with 95 % confidence intervals (CIs), respectively. Stratifiedand sensitivity analyses were performed to explore heterogeneity between studies and assesseffects of study quality. Results: The search strategy retrieved 6940 unique citations and 40 studies were selected forinclusion. Of these, 25 investigated the relationship between urban environment and UC and30 investigated this relationship with CD. Included in our analysis were 7 case-control UCstudies, 9 case-control CD studies, 18 cohort UC studies and 21 cohort CD studies. Based ona random effects model, the pooled IRRs for urban compared to rural environment for UCand CD studies were 1.17 (1.03, 1.32) and 1.42 (1.26, 1.60), respectively. These associationspersisted across multiple stratified and sensitivity analyses exploring clinical and studyquality factors. Heterogeneity was observed in the cohort studies for both UC and CD,whereas statistically significant heterogeneity was not observed for the case-control studies. Conclusions: A positive association between urban environment and both CD and UC was found.Heterogeneity may be explained by differences in study design and quality factors. http://www.biomedcentral.com/1471-230X/12/51 Ing Shian Soon Natalie A Molodecky Doreen M Rabi William A Ghali Herman W Barkema Gilaad G Kaplan BMC Gastroenterology 2012, 12:51 2012-05-24T00:00:00Z 10.1186/1471-230X-12-51 Urban environment and risk of IBD Analysis of previously publshed research indicates that a positive association exists between living in an urban environment and the risk of developing inflammatory bowel diseases (IBDs) such as Crohn's disease and ulcerative colitis. /content/figures/1471-230X-12-51-toc.gif BMC Gastroenterology 1471-230X 12 51 2012-05-24T00:00:00Z PDF Background: Arginine (ARG) and nitric oxide maintain the mucosal integrity of the intestine in various intestinal disorders. In the present study, we evaluated the effects of oral ARG supplementation on intestinal structural changes, enterocyte proliferation and apoptosis following methotrexate (MTX)-induced intestinal damage in a rat. Methods: Male rats were divided into four experimental groups: Control rats, CONTR-ARG rats, were treated with oral ARG given in drinking water 72 hours before and 72 hours following vehicle injection, MTX rats were treated with a single dose of methotrexate, and MTX-ARG rats were treated with oral ARG following injection of MTX. Intestinal mucosal damage, mucosal structural changes, enterocyte proliferation and enterocyte apoptosis were determined 72 hours following MTX injection. RT-PCR was used to determine bax and bcl-2 mRNA expression. Results: MTX-ARG rats demonstrated greater jejunal and ileal bowel weight, greater ileal mucosal weight, greater ileal mucosal DNA and protein levels, greater villus height in jejunum and ileum and crypt depth in ileum, compared to MTX animals. A significant decrease in enterocyte apoptosis in the ileum of MTX-ARG rats (vs MTX) was accompanied by decreased bax mRNA and protein expression and increased bcl-2 protein levels. Conclusions: Treatment with oral ARG prevents mucosal injury and improves intestinal recovery following MTX- injury in the rat. http://www.biomedcentral.com/1471-230X/12/41 Tal Koppelmann Yulia Pollak Jorge Mogilner Jacob Bejar Arnold G Coran Igor Sukhotnik BMC Gastroenterology 2012, 12:41 2012-04-30T00:00:00Z 10.1186/1471-230X-12-41 Oral arginine reduces intestinal injury In a rat model, dietary L-Arginine supplementation prevents mucosal injury, decreases cell death via apoptosis and improves intestinal recovery following methotrexate (MTX)-induced intestinal injury, suggesting that oral arginine may have clinical value for the treatment of chemotherapy-induced mucositis. /content/figures/1471-230X-12-41-toc.gif BMC Gastroenterology 1471-230X 12 41 2012-04-30T00:00:00Z XML Background: Luteolin is a 3',4',5,7-tetrahydroxyflavone found in various fruits and vegetables. We have shown previously that luteolin reduces HT-29 cell growth by inducing apoptosis and cell cycle arrest. The objective of this study was to examine whether luteolin downregulates the insulin-like growth factor-I receptor (IGF-IR) signaling pathway in HT-29 cells. Methods: In order to assess the effects of luteolin and/or IGF-I on the IGF-IR signaling pathway, cells were cultured with or without 60 μmol/L luteolin and/or 10 nmol/L IGF-I. Cell proliferation, DNA synthesis, and IGF-IR mRNA levels were evaluated by a cell viability assay, [3H]thymidine incorporation assays, and real-time polymerase chain reaction, respectively. Western blot analyses, immunoprecipitation, and in vitro kinase assays were conducted to evaluate the secretion of IGF-II, the protein expression and activation of IGF-IR, and the association of the p85 subunit of phophatidylinositol-3 kinase (PI3K) with IGF-IR, the phosphorylation of Akt and extracellular signal-regulated kinase (ERK)1/2, and cell division cycle 25c (CDC25c), and PI3K activity. Results: Luteolin (0 - 60 μmol/L) dose-dependently reduced the IGF-II secretion of HT-29 cells. IGF-I stimulated HT-29 cell growth but did not abrogate luteolin-induced growth inhibition. Luteolin reduced the levels of the IGF-IR precursor protein and IGF-IR transcripts. Luteolin reduced the IGF-I-induced tyrosine phosphorylation of IGF-IR and the association of p85 with IGF-IR. Additionally, luteolin inhibited the activity of PI3K activity as well as the phosphorylation of Akt, ERK1/2, and CDC25c in the presence and absence of IGF-I stimulation. Conclusions: The present results demonstrate that luteolin downregulates the activation of the PI3K/Akt and ERK1/2 pathways via a reduction in IGF-IR signaling in HT-29 cells; this may be one of the mechanisms responsible for the observed luteolin-induced apoptosis and cell cycle arrest. http://www.biomedcentral.com/1471-230X/12/9 Do Lim Han Cho Jongdai Kim Chu Nho Ki Lee Jung Park BMC Gastroenterology 2012, 12:9 2012-01-23T00:00:00Z 10.1186/1471-230X-12-9 Luteolin reduces IGF-IR signalling Luteolin, a flavonoid found in fruits and vegetables, reduces insulin-like growth factor-I receptor (IGF-IR) signaling in colon cancer cells, suggesting that this mechanism may contribute to luteolin-induced apoptosis and cell cycle arrest. /content/figures/1471-230X-12-9-toc.gif BMC Gastroenterology 1471-230X 12 9 2012-01-23T00:00:00Z XML