844. Vedolizumab affects antibody responses to immunisation selectively in the gastrointestinal tract: randomised controlled trial results.
作者: Tim Wyant.;Tim Leach.;Serap Sankoh.;Yuemei Wang.;Jonathan Paolino.;Marcela F Pasetti.;Brian G Feagan.;Asit Parikh.
来源: Gut. 2015年64卷1期77-83页
The α4β7 integrin monoclonal antibody vedolizumab is hypothesised to be gut selective. Effects of vedolizumab on immune responses to parenterally or enterally administered antigens were investigated.
845. Higher proportion of viral basal core promoter mutant increases the risk of liver cirrhosis in hepatitis B carriers.
作者: Tai-Chung Tseng.;Chun-Jen Liu.;Hung-Chih Yang.;Chi-Ling Chen.;Wan-Ting Yang.;Cheng-Shiue Tsai.;Stephanie Fang-Tzu Kuo.;Femke Carolien Verbree.;Tung-Hung Su.;Chia-Chi Wang.;Chen-Hua Liu.;Pei-Jer Chen.;Ding-Shinn Chen.;Jia-Horng Kao.
来源: Gut. 2015年64卷2期292-302页
Precore (PC) variant (G1896A) and basal core promoter (BCP) variant (A1762T/G1764A) of HBV are associated with risk of hepatocellular carcinoma in HBV carriers. However, little is known about their impact on the adverse outcomes of hepatitis B e antigen (HBeAg)-negative hepatitis and liver cirrhosis.
847. Peginterferon alfa-2a with or without low-dose ribavirin for treatment-naive patients with hepatitis C virus genotype 2 receiving haemodialysis: a randomised trial.
作者: Chen-Hua Liu.;Chun-Jen Liu.;Chung-Feng Huang.;Jou-Wei Lin.;Chia-Yen Dai.;Cheng-Chao Liang.;Jee-Fu Huang.;Peir-Haur Hung.;Hung-Bin Tsai.;Meng-Kun Tsai.;Chih-Yuan Lee.;Shih-I Chen.;Sheng-Shun Yang.;Tung-Hung Su.;Hung-Chih Yang.;Pei-Jer Chen.;Ding-Shinn Chen.;Wan-Long Chuang.;Ming-Lung Yu.;Jia-Horng Kao.
来源: Gut. 2015年64卷2期303-11页
Data comparing the efficacy and safety of combination therapy with peginterferon plus low-dose ribavirin and peginterferon monotherapy in treatment-naive haemodialysis patients with hepatitis C virus genotype 2 (HCV-2) infection are limited.
848. Simvastatin is associated with reduced risk of acute pancreatitis: findings from a regional integrated healthcare system.
To characterise the relationship between simvastatin and risk of acute pancreatitis (AP).
849. Increased colonic bile acid exposure: a relevant factor for symptoms and treatment in IBS.
作者: Antal Bajor.;Hans Törnblom.;Mats Rudling.;Kjell-Arne Ung.;Magnus Simrén.
来源: Gut. 2015年64卷1期84-92页
Bile acids may play a role in the pathogenesis of IBS. We investigated the potential effects of bile acids entering the colon and its role in the symptom pattern in IBS.
850. The combination of autofluorescence endoscopy and molecular biomarkers is a novel diagnostic tool for dysplasia in Barrett's oesophagus.
作者: Massimiliano di Pietro.;David F Boerwinkel.;Mohammed Kareem Shariff.;Xinxue Liu.;Emmanouil Telakis.;Pierre Lao-Sirieix.;Elaine Walker.;George Couch.;Leanne Mills.;Tara Nuckcheddy-Grant.;Susan Slininger.;Maria O'Donovan.;Mike Visser.;Sybren L Meijer.;Philip V Kaye.;Lorenz Wernisch.;Krish Ragunath.;Jacques J G H M Bergman.;Rebecca C Fitzgerald.
来源: Gut. 2015年64卷1期49-56页
Endoscopic surveillance for Barrett's oesophagus (BO) is limited by sampling error and the subjectivity of diagnosing dysplasia. We aimed to compare a biomarker panel on minimal biopsies directed by autofluorescence imaging (AFI) with the standard surveillance protocol to derive an objective tool for dysplasia assessment.
851. Effects of HDV infection and pegylated interferon α treatment on the natural killer cell compartment in chronically infected individuals.
作者: Sebastian Lunemann.;David F G Malone.;Jan Grabowski.;Kerstin Port.;Vivien Béziat.;Birgit Bremer.;Karl-Johan Malmberg.;Michael P Manns.;Johan K Sandberg.;Markus Cornberg.;Hans-Gustaf Ljunggren.;Heiner Wedemeyer.;Niklas K Björkström.
来源: Gut. 2015年64卷3期469-82页
Although hepatitis delta is considered an immune-mediated disease, adaptive immune responses to hepatitis delta virus (HDV) are hardly detectable. Thus, the role of other immune responses, including those mediated by natural killer (NK) cells, must be considered in HDV pathogenesis and in treatments with immune-stimulating agents such as interferon (IFN)α. However, the phenotype and function of NK cells in chronic HDV infection, or in HDV-infected individuals undergoing IFNα treatment, have not been extensively studied.
852. Targeting mTOR dependency in pancreatic cancer.
作者: Douglas C Morran.;Jianmin Wu.;Nigel B Jamieson.;Agata Mrowinska.;Gabriela Kalna.;Saadia A Karim.;Amy Y M Au.;Christopher J Scarlett.;David K Chang.;Malgorzata Z Pajak.; .;Karin A Oien.;Colin J McKay.;C Ross Carter.;Gerry Gillen.;Sue Champion.;Sally L Pimlott.;Kurt I Anderson.;T R Jeffry Evans.;Sean M Grimmond.;Andrew V Biankin.;Owen J Sansom.;Jennifer P Morton.
来源: Gut. 2014年63卷9期1481-9页
Pancreatic cancer is a leading cause of cancer-related death in the Western world. Current chemotherapy regimens have modest survival benefit. Thus, novel, effective therapies are required for treatment of this disease.
854. OCT1 is a determinant of synbindin-related ERK signalling with independent prognostic significance in gastric cancer.
作者: Jin Qian.;Xuan Kong.;Niantao Deng.;Patrick Tan.;Haoyan Chen.;Jilin Wang.;Zhaoli Li.;Ye Hu.;Weiping Zou.;Jie Xu.;Jing-Yuan Fang.
来源: Gut. 2015年64卷1期37-48页
Octamer transcription factor 1 (OCT1) was found to be expressed in intestinal metaplasia and gastric cancer (GC), but the exact roles of OCT1 in GC remain unclear. The objective of this study was to determine the functional and prognostic implications of OCT1 in GC.
858. Oesophageal adenocarcinoma and prior diagnosis of Barrett's oesophagus: a population-based study.
作者: Shivaram K Bhat.;Damian T McManus.;Helen G Coleman.;Brian T Johnston.;Christopher R Cardwell.;Una McMenamin.;Finian Bannon.;Blanaid Hicks.;Grace Kennedy.;Anna T Gavin.;Liam J Murray.
来源: Gut. 2015年64卷1期20-5页
Endoscopic surveillance of Barrett's oesophagus (BO) provides an opportunity to detect early stage oesophageal adenocarcinoma (OAC). We sought to determine the proportion of OAC patients with a prior diagnosis of BO on a population basis and to evaluate the influence of a prior diagnosis of BO on survival, taking into account lead and length time biases.
859. Update on basic and clinical aspects of eosinophilic oesophagitis.
The identification of a distinct syndrome, designated eosinophilic oesophagitis (EoE), with its own clinical and histopathological characteristics, was first described in the early 1990s. Meanwhile intense research has uncovered many molecular, immunological and clinical aspects of this chronic-inflammatory disorder. This article focuses exclusively on basic and clinical insights of EoE gathered during the last few years. Regarding aetiopathogenesis it has become clear that EoE is a food-triggered disease with milk and wheat as the dominant culprit food categories. However, it is still debated whether a disturbed mucosal integrity allowing allergens to cross the mucosal barrier, or changes in wheat and milk manufacturing might induce these inflammatory responses. Furthermore, basic science and clinical studies have accordingly confirmed that a chronic eosinophilic inflammation leads to a remodelling of the oesophagus with micro- and macro-morphological alterations, ending in a strictured oesophagus with impaired function. Fortunately, long-term therapeutic trials, using either topical corticosteroids or dietary allergen avoidance, have demonstrated that this sequela can be prevented or even reversed. This finding is of clinical relevance as it supports the initiation of a consistent anti-inflammatory therapy. Nevertheless, EoE is still an enigmatic disease and the long list of unanswered questions will certainly stimulate further research.
860. Identification of inflammatory mediators in patients with Crohn's disease unresponsive to anti-TNFα therapy.
作者: Raquel Franco Leal.;Núria Planell.;Radhika Kajekar.;Juan J Lozano.;Ingrid Ordás.;Isabella Dotti.;Miriam Esteller.;M Carme Masamunt.;Harsukh Parmar.;Elena Ricart.;Julián Panés.;Azucena Salas.
来源: Gut. 2015年64卷2期233-42页
Anti-tumour necrosis factor α (TNFα) therapy effectively induces and maintains remission in Crohn's disease (CD). Up to 40% of patients, however, fail to respond to anti-TNFα.
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