281. Endoscopy in patients on antiplatelet or anticoagulant therapy, including direct oral anticoagulants: British Society of Gastroenterology (BSG) and European Society of Gastrointestinal Endoscopy (ESGE) guidelines.
作者: Andrew M Veitch.;Geoffroy Vanbiervliet.;Anthony H Gershlick.;Christian Boustiere.;Trevor P Baglin.;Lesley-Ann Smith.;Franco Radaelli.;Evelyn Knight.;Ian M Gralnek.;Cesare Hassan.;Jean-Marc Dumonceau.
来源: Gut. 2016年65卷3期374-89页
The risk of endoscopy in patients on antithrombotics depends on the risks of procedural haemorrhage versus thrombosis due to discontinuation of therapy. P2Y12 RECEPTOR ANTAGONISTS CLOPIDOGREL, PRASUGREL, TICAGRELOR: For low-risk endoscopic procedures we recommend continuing P2Y12 receptor antagonists as single or dual antiplatelet therapy (low quality evidence, strong recommendation); For high-risk endoscopic procedures in patients at low thrombotic risk, we recommend discontinuing P2Y12 receptor antagonists five days before the procedure (moderate quality evidence, strong recommendation). In patients on dual antiplatelet therapy, we suggest continuing aspirin (low quality evidence, weak recommendation). For high-risk endoscopic procedures in patients at high thrombotic risk, we recommend continuing aspirin and liaising with a cardiologist about the risk/benefit of discontinuation of P2Y12 receptor antagonists (high quality evidence, strong recommendation).
283. Deletion of Men1 and somatostatin induces hypergastrinemia and gastric carcinoids.
作者: Sinju Sundaresan.;Anthony J Kang.;Michael M Hayes.;Eun-Young K Choi.;Juanita L Merchant.
来源: Gut. 2017年66卷6期1012-1021页
Gastric carcinoids are slow growing neuroendocrine tumours arising from enterochromaffin-like (ECL) cells in the corpus of stomach. Although most of these tumours arise in the setting of gastric atrophy and hypergastrinemia, it is not understood what genetic background predisposes development of these ECL derived tumours. Moreover, diffuse microcarcinoids in the mucosa can lead to a field effect and limit successful endoscopic removal.
284. Interferon-microRNA signalling drives liver precancerous lesion formation and hepatocarcinogenesis.
作者: Yingcheng Yang.;Ximeng Lin.;Xinyuan Lu.;Guijuan Luo.;Tao Zeng.;Jing Tang.;Feng Jiang.;Liang Li.;Xiuliang Cui.;Wentao Huang.;Guojun Hou.;Xin Chen.;Qing Ouyang.;Shanhua Tang.;Huanlin Sun.;Luonan Chen.;Frank J Gonzalez.;Mengchao Wu.;Wenming Cong.;Lei Chen.;Hongyang Wang.
来源: Gut. 2016年65卷7期1186-201页
Precancerous lesion, a well-established histopathologically premalignant tissue with the highest risk for tumourigenesis, develops preferentially from activation of DNA damage checkpoint and persistent inflammation. However, little is known about the mechanisms by which precancerous lesions are initiated and their physiological significance.
285. Defective monocyte oxidative burst predicts infection in alcoholic hepatitis and is associated with reduced expression of NADPH oxidase.
作者: Nikhil Vergis.;Wafa Khamri.;Kylie Beale.;Fouzia Sadiq.;Mina O Aletrari.;Celia Moore.;Stephen R Atkinson.;Christine Bernsmeier.;Lucia A Possamai.;Gemma Petts.;Jennifer M Ryan.;Robin D Abeles.;Sarah James.;Matthew Foxton.;Brian Hogan.;Graham R Foster.;Alastair J O'Brien.;Yun Ma.;Debbie L Shawcross.;Julia A Wendon.;Charalambos G Antoniades.;Mark R Thursz.
来源: Gut. 2017年66卷3期519-529页
In order to explain the increased susceptibility to serious infection in alcoholic hepatitis, we evaluated monocyte phagocytosis, aberrations of associated signalling pathways and their reversibility, and whether phagocytic defects could predict subsequent infection.
286. Reversal of murine alcoholic steatohepatitis by pepducin-based functional blockade of interleukin-8 receptors.
作者: Verena Wieser.;Timon E Adolph.;Barbara Enrich.;Athan Kuliopulos.;Arthur Kaser.;Herbert Tilg.;Nicole C Kaneider.
来源: Gut. 2017年66卷5期930-938页
Alcoholic steatohepatitis is a life-threatening condition with short-term mortality up to 40%. It features hepatic neutrophil infiltration and blood neutrophilia, and may evolve from ethanol-induced breakdown of the enteric barrier and consequent bacteraemia. Signalling through CXCR1/2 G-protein-coupled-receptors (GPCRs), the interleukin (IL)-8 receptors, is critical for the recruitment and activation of neutrophils. We have developed short lipopeptides (pepducins), which inhibit post-ligand GPCR activation precisely targeting individual GPCRs.
287. Implantation of healthy matrix-embedded endothelial cells rescues dysfunctional endothelium and ischaemic tissue in liver engraftment.
Liver transplantation is limited by ischaemic injury which promotes endothelial cell and hepatocyte dysfunction and eventually organ failure. We sought to understand how endothelial state determines liver recovery after hepatectomy and engraftment.
288. Titanium dioxide nanoparticles exacerbate DSS-induced colitis: role of the NLRP3 inflammasome.
作者: Pedro A Ruiz.;Belen Morón.;Helen M Becker.;Silvia Lang.;Kirstin Atrott.;Marianne R Spalinger.;Michael Scharl.;Kacper A Wojtal.;Anne Fischbeck-Terhalle.;Isabelle Frey-Wagner.;Martin Hausmann.;Thomas Kraemer.;Gerhard Rogler.
来源: Gut. 2017年66卷7期1216-1224页
Western lifestyle and diet are major environmental factors playing a role in the development of IBD. Titanium dioxide (TiO2) nanoparticles are widely used as food additives or in pharmaceutical formulations and are consumed by millions of people on a daily basis. We investigated the effects of TiO2 in the development of colitis and the role of the nucleotide-binding oligomerisation domain receptor, pyrin domain containing (NLRP)3 inflammasome.
289. Oral versus intravenous iron replacement therapy distinctly alters the gut microbiota and metabolome in patients with IBD.
作者: Thomas Lee.;Thomas Clavel.;Kirill Smirnov.;Annemarie Schmidt.;Ilias Lagkouvardos.;Alesia Walker.;Marianna Lucio.;Bernhard Michalke.;Philippe Schmitt-Kopplin.;Richard Fedorak.;Dirk Haller.
来源: Gut. 2017年66卷5期863-871页
Iron deficiency is a common complication in patients with IBD and oral iron therapy is suggested to exacerbate IBD symptoms. We performed an open-labelled clinical trial to compare the effects of per oral (PO) versus intravenous (IV) iron replacement therapy (IRT).
290. Role of bismuth in improving Helicobacter pylori eradication with triple therapy.
In most regions of the world, antimicrobial resistance has increased to the point where empirical standard triple therapy for Helicobacter pylorieradication is no longer recommended. The treatment outcome in a population is calculated as the sum of the treatment success in the subpopulation with susceptible infections plus treatment success in the subpopulation with resistant infections. The addition of bismuth (i.e., 14-day triple therapy plus bismuth) can improve cure rates despite a high prevalence of antimicrobial resistance. The major bismuth effect is to add an additional 30%-40% to the success with resistant infections. The overall result is therefore dependent on the prevalence of resistance and the treatment success in the subpopulation with resistant infections (eg, with proton-pump inhibitor-amoxicillin dual therapy). Here, we explore the contribution of each component and the mechanisms of how bismuth might enhance the effectiveness of triple therapy. We also discuss the limitations of this approach and provide suggestions how triple therapy plus bismuth might be further improved.
291. Fungal microbiota dysbiosis in IBD.
作者: Harry Sokol.;Valentin Leducq.;Hugues Aschard.;Hang-Phuong Pham.;Sarah Jegou.;Cecilia Landman.;David Cohen.;Giuseppina Liguori.;Anne Bourrier.;Isabelle Nion-Larmurier.;Jacques Cosnes.;Philippe Seksik.;Philippe Langella.;David Skurnik.;Mathias L Richard.;Laurent Beaugerie.
来源: Gut. 2017年66卷6期1039-1048页
The bacterial intestinal microbiota plays major roles in human physiology and IBDs. Although some data suggest a role of the fungal microbiota in IBD pathogenesis, the available data are scarce. The aim of our study was to characterise the faecal fungal microbiota in patients with IBD.
292. Periodontitis induced by Porphyromonas gingivalis drives periodontal microbiota dysbiosis and insulin resistance via an impaired adaptive immune response.
作者: Vincent Blasco-Baque.;Lucile Garidou.;Céline Pomié.;Quentin Escoula.;Pascale Loubieres.;Sandrine Le Gall-David.;Mathieu Lemaitre.;Simon Nicolas.;Pascale Klopp.;Aurélie Waget.;Vincent Azalbert.;André Colom.;Martine Bonnaure-Mallet.;Philippe Kemoun.;Matteo Serino.;Rémy Burcelin.
来源: Gut. 2017年66卷5期872-885页
To identify a causal mechanism responsible for the enhancement of insulin resistance and hyperglycaemia following periodontitis in mice fed a fat-enriched diet.
293. Liver PPARα is crucial for whole-body fatty acid homeostasis and is protective against NAFLD.
作者: Alexandra Montagner.;Arnaud Polizzi.;Edwin Fouché.;Simon Ducheix.;Yannick Lippi.;Frédéric Lasserre.;Valentin Barquissau.;Marion Régnier.;Céline Lukowicz.;Fadila Benhamed.;Alison Iroz.;Justine Bertrand-Michel.;Talal Al Saati.;Patricia Cano.;Laila Mselli-Lakhal.;Gilles Mithieux.;Fabienne Rajas.;Sandrine Lagarrigue.;Thierry Pineau.;Nicolas Loiseau.;Catherine Postic.;Dominique Langin.;Walter Wahli.;Hervé Guillou.
来源: Gut. 2016年65卷7期1202-14页
Peroxisome proliferator-activated receptor α (PPARα) is a nuclear receptor expressed in tissues with high oxidative activity that plays a central role in metabolism. In this work, we investigated the effect of hepatocyte PPARα on non-alcoholic fatty liver disease (NAFLD).
294. Global patterns and trends in colorectal cancer incidence and mortality.
作者: Melina Arnold.;Mónica S Sierra.;Mathieu Laversanne.;Isabelle Soerjomataram.;Ahmedin Jemal.;Freddie Bray.
来源: Gut. 2017年66卷4期683-691页
The global burden of colorectal cancer (CRC) is expected to increase by 60% to more than 2.2 million new cases and 1.1 million deaths by 2030. In this study, we aim to describe the recent CRC incidence and mortality patterns and trends linking the findings to the prospects of reducing the burden through cancer prevention and care.
296. Signalling via the osteopontin and high mobility group box-1 axis drives the fibrogenic response to liver injury.
作者: Elena Arriazu.;Xiaodong Ge.;Tung-Ming Leung.;Fernando Magdaleno.;Aritz Lopategi.;Yongke Lu.;Naoto Kitamura.;Raquel Urtasun.;Neil Theise.;Daniel J Antoine.;Natalia Nieto.
来源: Gut. 2017年66卷6期1123-1137页
Liver fibrosis is associated with significant collagen-I deposition largely produced by activated hepatic stellate cells (HSCs); yet, the link between hepatocyte damage and the HSC profibrogenic response remains unclear. Here we show significant induction of osteopontin (OPN) and high-mobility group box-1 (HMGB1) in liver fibrosis. Since OPN was identified as upstream of HMGB1, we hypothesised that OPN could participate in the pathogenesis of liver fibrosis by increasing HMGB1 to upregulate collagen-I expression.
297. The global prevalence of IBS in adults remains elusive due to the heterogeneity of studies: a Rome Foundation working team literature review.
作者: Ami D Sperber.;Dan Dumitrascu.;Shin Fukudo.;Charles Gerson.;Uday C Ghoshal.;Kok Ann Gwee.;A Pali S Hungin.;Jin-Yong Kang.;Chen Minhu.;Max Schmulson.;Arkady Bolotin.;Michael Friger.;Tamar Freud.;William Whitehead.
来源: Gut. 2017年66卷6期1075-1082页
The global prevalence of IBS is difficult to ascertain, particularly in light of the heterogeneity of published epidemiological studies. The aim was to conduct a literature review, by experts from around the world, of community-based studies on IBS prevalence.
299. Raf kinase inhibitor protein mediates intestinal epithelial cell apoptosis and promotes IBDs in humans and mice.
作者: Wenlong Lin.;Chunmei Ma.;Fasheng Su.;Yu Jiang.;Rongrong Lai.;Ting Zhang.;Kai Sun.;Liping Fan.;Zijian Cai.;Zhongqi Li.;He Huang.;Jun Li.;Xiaojian Wang.
来源: Gut. 2017年66卷4期597-610页
Raf kinase inhibitor protein (RKIP) appears to control cancer cell metastasis and its expression in colonic tissue is related to colonic cancer development. We sought to identify the roles of RKIP in maintaining homeostasis of GI tract.
300. Patterns of PD-L1 expression and CD8 T cell infiltration in gastric adenocarcinomas and associated immune stroma.
作者: Elizabeth D Thompson.;Marianna Zahurak.;Adrian Murphy.;Toby Cornish.;Nathan Cuka.;Eihab Abdelfatah.;Stephen Yang.;Mark Duncan.;Nita Ahuja.;Janis M Taube.;Robert A Anders.;Ronan J Kelly.
来源: Gut. 2017年66卷5期794-801页
Recent data supports a significant role for immune checkpoint inhibitors in the treatment of solid tumours. Here, we evaluate gastric and gastro-oesophageal junction (G/GEJ) adenocarcinomas for their expression of programmed death-ligand 1 (PD-L1), infiltration by CD8+ T cells and the relationship of both factors to patient survival.
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