E-cadherin in gastric cancer

Cadherin is an adhesion molecule and a superfamily of calcium-mediated membrane glycoproteins. E-cadherin is the prototype of the class E-cadherin that links to catenins to form the cytoskeleton. Recent evidence has shown that E-cadherin not only acts as an adhesive, but also plays important roles in growth development and carcinogenesis. It has been recently viewed as an invasion as well as a growth suppressor gene. This review summarizes the recent discoveries on E-cadherin and its role in gastric cancer. In particular, our work on E-cadherin in gastric cancer, including its relation with Helicobacter pylori and clinical applications, are described in detail.published_or_final_versio

Exploring Twitter as a Source of an Arabic Dialect Corpus

Given the lack of Arabic dialect text corpora in comparison with what is available for dialects of English and other languages, there is a need to create dialect text corpora for use in Arabic natural language processing. What is more, there is an increasing use of Arabic dialects in social media, so this text is now considered quite appropriate as a source of a corpus. We collected 210,915K tweets from five groups of Arabic dialects Gulf, Iraqi, Egyptian, Levantine, and North African. This paper explores Twitter as a source and describes the methods that we used to extract tweets and classify them according to the geographic location of the sender. We classified Arabic dialects by using Waikato Environment for Knowledge Analysis (WEKA) data analytic tool which contains many alternative filters and classifiers for machine learning. Our approach in classification tweets achieved an accuracy equal to 79%

Serum soluble E-cadherin is a good prognostic marker in gastric cancer

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Methylation of E-caderin gene in gastric cancer and in normal gastric mucosa from patients with and without Helicobacter pylori infection

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Cholestatic jaundice caused by sequential carbimazole and propylthiouracil treatment for thyrotoxicosis

A 36-year-old Chinese man presented to the Queen Mary Hospital in August 1999 with a 2-week history of jaundice due to propylthiouracil treatment for thyrotoxicosis. He had previously received carbimazole but had developed an urticarial skin rash after 2 weeks of treatment. The patient developed liver failure and fulminant pneumonitis shortly after hospital admission. Despite receiving treatment with broad-spectrum antibiotics and intravenous immunoglobulin, he died 11 days after the onset of the respiratory symptoms. Postmortem examination using electron microscopy showed typical glycogen bodies within the cytoplasm of the hepatocytes, which corresponded to eosinophilic cytoplasmic inclusion bodies visible under light microscopy. Immunohistochemical studies of the inclusion bodies were positive for carcinoembryonic antigen and albumin, and negative for fibrinogen, complement protein C3, immunoglobulins G, M, and A, α-fetoprotein, and α-1-antitrypsin. This is the first report of a patient who received two sequential antithyroid drugs and developed predominate cholestasis with unique histological features. Extreme caution should be taken when a patient develops allergy to one type of antithyroid drug, because cross-reactivity may develop to the other type.published_or_final_versio

Interferon and ribavirin therapy for chronic hepatitis C virus genotype 6: A comparison with genotype 1

Because there is a lack of data on the treatment outcome of patients who carry hepatitis C virus (HCV) genotype 6, we conducted a prospective study, to compare the effect of interferon and ribavirin therapy in HCV genotypes 1 and 6, of patients with seropositive anti-HCV, persistently elevated alanine transaminase levels, and detectable HCV RNA. Patients were treated with subcutaneous recombinant interferon α-2b and ribavirin for 12 months. Of 40 patients, 16 had genotype 6, and 24 had genotype 1. An end-of-treatment response was detected in 12 (75%) patients with genotype 6 and in 10 (41.6%) patients with genotype 1 (P = .05). A sustained virological response (SVR) was present in 10 (62.5%) patients with genotype 6 and in 7 (29.2%) patients with genotype 1 (P = .04). Genotype 6 has a better response than genotype 1 and is associated with a higher SVR.published_or_final_versio

Increasing prevalence of advanced colonic polyps in young patients undergoing colonoscopy in a referral academic hospital in Hong Kong

Aim: To investigate the distribution and frequency of advanced polyps over eight years. Methods: 6424 colonoscopies were reviewed during the study period 1998 to 2005. The study period was subdivided into period I: 1998 to 2001 and period II: 2002-2005. Results: 1856 polyps (33% advanced polyps) and 328 CRCs were detected. The mean ages of the patients with advanced polyps and cancer were 69.2 ± 12.0 and 71.6 ± 13.8 years, respectively. Advanced polyps were mainly left sided (59.5%). Advanced polyps were found in patients ≤ 60 years from 17.7% in period I to 26.3% in period II (P 0.05). Conclusion: Advanced polyps increased significantly in the younger male group in the most recent period and there seems to be a shift towards a proximal location. © 2007 WJG. All rights reserved.published_or_final_versio

Role of hepatitis B virus genotypes in chronic hepatitis B exacerbation

Hepatitis B virus (HBV) genotypes and precore and core promoter mutations were determined in 318 patients with HBV. Patients infected with HBV genotype B had a higher median alanine aminotransferase level and bilirubin level and a lower median albumin level during exacerbations of disease, compared with patients infected with HBV genotype C (all P < .001). By logistic regression analysis, HBV genotype B infection (P = .014) and low albumin levels (P = .006) were independently associated with a higher risk of hepatic decompensation during severe exacerbations of disease. Patients infected with genotype B had a significantly higher mortality due to hepatic decompensation than did patients with genotype C (70% vs. 27.8%; P = .05).published_or_final_versio

Macrophage migration inhibitory factor stimulated by Helicobacter pylori increases proliferation of gastric epithelial cells

Aim: Helicobacter pylori (H pylori) is associated with increased gastric inflammatory and epithelial expression of macrophage migration inhibitory factor (MIF) and gastric epithelial cell proliferation. This study aimed at determining whether H pylori directly stimulates release of MIF in monocytes, whether the cag pathogenicity island (PAI) is involved for this function, and whether MIF stimulated by H pylori increases gastric epithelial cell proliferation in vitro. Methods: A cytotoxic wild-type H pylori strain (TN2), its three isogenic mutants (TN2Δcag, TN2ΔcagA and TN2ΔcagE) were co-cultured with cells of a human monocyte cell line, THP-1, for 24 h at different organism/cell ratios. MIF in the supernatants was measured by an ELISA. Cells of a human gastric cancer cell line, MKN45, were then co-cultured with the supernatants, with and without monoclonal anti-MIF antibody for 24 h. The cells were further incubated for 12 h after addition of 3H-thymidine, and the levels of incorporation of 3H-thymidine were measured with a liquid scintillation counter. Results: The wild-type strain and the isogenic mutants, TN2ΔcagA and TN2ΔcagE, increased MIF release at organism/cell ratios of 200 /1 and 400/1, but not at the ratios of 50/1 and 100/1. However, the mutant TN2Δcag did not increase the release of MIF at any of the four ratios. 3H-thymidine readings for MKN-45 cells were significantly increased with supernatants derived from the wild-type strain and the mutants TN2ΔcagA and TN2ΔcagE, but not from the mutant TN2Δcag. Moreover, in the presence of monoclonal anti-MIF antibody, the stimulatory effects of the wild-type strain on cell proliferation disappeared. Conclusion: H pylori stimulates MIF release in monocytes, likely through its cag PAI, but not related to cagA or cagE. H pylori-stimulated monocyte culture supernatant increases gastric cell proliferation, which is blocked by anti-MIF antibody, suggesting that MIF plays an important role in H pylori-induced gastric epithelial cell proliferation. © 2005 The WJG Press and Elsevier Inc. All rights reserved.published_or_final_versio

Differing coping mechanisms, stress level and anorectal physiology in patients with functional constipation

Aim: To investigate coping mechanisms, constipation symptoms and anorectal physiology in 80 constipated subjects and 18 controls. Methods: Constipation was diagnosed by Rome II criteria. Coping ability and anxiety/depression were assessed by validated questionnaires. Transit time and balloon distension test were performed. Results: 34.5% patients were classified as slow transit type of constipation. The total colonic transit time (56 h vs 10 h, P<0.0001) and rectal sensation including urge sensation (79 mL vs 63 mL, P = 0.019) and maximum tolerable volume (110 mL vs 95 mL, P = 0.03) differed in patients and controls. Constipated subjects had significantly higher anxiety and depression scores and lower SF-36 scores in all categories. They also demonstrated higher scores of 'monitoring' coping strategy (14±6 vs 9±3, P = 0.001), which correlated with the rectal distension sensation (P = 0.005), urge sensation (P=0.002), and maximum tolerable volume (P = 0.035). The less use of blunting strategy predicted slow transit constipation in both univariate (P = 0.01) and multivariate analysis (P = 0.03). Conclusion: Defective or ineffective use of coping strategies may be an important etiology in functional constipation and subsequently reflected in abnormal anorectal physiology. © 2005 The WJG Press and Elsevier Inc. All rights reserved.published_or_final_versio