4 rows where subject = "["Gastroenterology"]"
✎ View and edit SQL
Suggested facets: references-count, award_numbers, funder_names, funder_dois, subject (array), ISSN (array), orcids (array), names (array), award_numbers (array), funder_names (array)
|1||1||["Human gut microbiome: hopes, threats and promises"]||10.1136/gutjnl-2018-316723||http://dx.doi.org/10.1136/gutjnl-2018-316723||2018-06-22T16:20:25Z||["Gastroenterology"]||132||230||["0017-5749", "1468-3288"]||Gut||<jats:p>The microbiome has received increasing attention over the last 15 years. Although gut microbes have been explored for several decades, investigations of the role of microorganisms that reside in the human gut has attracted much attention beyond classical infectious diseases. For example, numerous studies have reported changes in the gut microbiota during not only obesity, diabetes, and liver diseases but also cancer and even neurodegenerative diseases. The human gut microbiota is viewed as a potential source of novel therapeutics. Between 2013 and 2017, the number of publications focusing on the gut microbiota was, remarkably, 12 900, which represents four-fifths of the total number of publications over the last 40 years that investigated this topic. This review discusses recent evidence of the impact of the gut microbiota on metabolic disorders and focus on selected key mechanisms. This review also aims to provide a critical analysis of the current knowledge in this field, identify putative key issues or problems and discuss misinterpretations. The abundance of metagenomic data generated on comparing diseased and healthy subjects can lead to the erroneous claim that a bacterium is causally linked with the protection or the onset of a disease. In fact, environmental factors such as dietary habits, drug treatments, intestinal motility and stool frequency and consistency are all factors that influence the composition of the microbiota and should be considered. The cases of the bacteria <jats:italic>Prevotella copri</jats:italic> and <jats:italic>Akkermansia muciniphila</jats:italic> will be discussed as key examples.</jats:p>||1||["http://orcid.org/0000-0003-2040-2448"]||["Patrice D Cani"]||||["FP7 Ideas: European Research Council", "Fonds Baillet Latour", "Fonds De La Recherche Scientifique - FNRS", "WELBIO"]||["10.13039/100011199", "10.13039/501100010563", "10.13039/501100002661", [""]]|
|7||7||["Update on lactose malabsorption and intolerance: pathogenesis, diagnosis and clinical management"]||10.1136/gutjnl-2019-318404||http://dx.doi.org/10.1136/gutjnl-2019-318404||2019-08-19T15:35:18Z||["Gastroenterology"]||95||13||["0017-5749", "1468-3288"]||Gut||<jats:p>Lactose is the main source of calories in milk, an essential nutriedigestion, patients with visceral hypersensitivity nt in infancy and a key part of the diet in populations that maintain the ability to digest this disaccharide in adulthood. Lactase deficiency (LD) is the failure to express the enzyme that hydrolyses lactose into galactose and glucose in the small intestine. The genetic mechanism of lactase persistence in adult Caucasians is mediated by a single C→T nucleotide polymorphism at the LCTbo −13’910 locus on chromosome-2. Lactose malabsorption (LM) refers to any cause of failure to digest and/or absorb lactose in the small intestine. This includes primary genetic and also secondary LD due to infection or other conditions that affect the mucosal integrity of the small bowel. Lactose intolerance (LI) is defined as the onset of abdominal symptoms such as abdominal pain, bloating and diarrhoea after lactose ingestion by an individual with LM. The likelihood of LI depends on the lactose dose, lactase expression and the intestinal microbiome. Independent of lactose digestion, patients with visceral hypersensitivity associated with anxiety or the Irritable Bowel Syndrome (IBS) are at increased risk of the condition. Diagnostic investigations available to diagnose LM and LI include genetic, endoscopic and physiological tests. The association between self-reported LI, objective findings and clinical outcome of dietary intervention is variable. Treatment of LI can include low-lactose diet, lactase supplementation and, potentially, colonic adaptation by prebiotics. The clinical outcome of these treatments is modest, because lactose is just one of a number of poorly absorbed carbohydrates which can cause symptoms by similar mechanisms.</jats:p>||4||["http://orcid.org/0000-0002-8719-5175", "http://orcid.org/0000-0003-4394-5584"]||["Benjamin Misselwitz", "Matthias Butter", "Kristin Verbeke", "Mark R Fox"]||[""]||[""]||[""]|
|35||35||["Efficacy of psychological therapies for irritable bowel syndrome: systematic review and network meta-analysis"]||10.1136/gutjnl-2020-321191||http://dx.doi.org/10.1136/gutjnl-2020-321191||2020-04-10T21:25:23Z||["Gastroenterology"]||0||2||["0017-5749", "1468-3288"]||Gut||<jats:sec><jats:title>Objectives</jats:title><jats:p>National guidelines for the management of irritable bowel syndrome (IBS) recommend that psychological therapies should be considered, but their relative efficacy is unknown, because there have been few head-to-head trials. We performed a systematic review and network meta-analysis to try to resolve this uncertainty.</jats:p></jats:sec><jats:sec><jats:title>Design</jats:title><jats:p>We searched the medical literature through January 2020 for randomised controlled trials (RCTs) assessing efficacy of psychological therapies for adults with IBS, compared with each other, or a control intervention. Trials reported a dichotomous assessment of symptom status after completion of therapy. We pooled data using a random effects model. Efficacy was reported as a pooled relative risk (RR) of remaining symptomatic, with a 95% CI to summarise efficacy of each comparison tested, and ranked by therapy according to P score.</jats:p></jats:sec><jats:sec><jats:title>Results</jats:title><jats:p>We identified 41 eligible RCTs, containing 4072 participants. After completion of therapy, the psychological interventions with the largest numbers of trials, and patients recruited, demonstrating efficacy included self-administered or minimal contact cognitive behavioural therapy (CBT) (RR 0.61; 95% CI 0.45 to 0.83, P score 0.66), face-to-face CBT (RR 0.62; 95% CI 0.48 to 0.80, P score 0.65) and gut-directed hypnotherapy (RR 0.67; 95% CI 0.49 to 0.91, P score 0.57). After completion of therapy, among trials recruiting only patients with refractory symptoms, group CBT and gut-directed hypnotherapy were more efficacious than either education and/or support or routine care, and CBT via the telephone, contingency management, CBT via the internet and dynamic psychotherapy were all superior to routine care. Risk of bias of trials was high, with evidence of funnel plot asymmetry; the efficacy of psychological therapies is therefore likely to have been overestimated.</jats:p></jats:sec><jats:sec><…||6||["http://orcid.org/0000-0003-4151-7180", "http://orcid.org/0000-0001-6371-4359"]||["Christopher J Black", "Elyse R Thakur", "Lesley A Houghton", "Eamonn M M Quigley", "Paul Moayyedi", "Alexander C Ford"]||[""]||[""]||[""]|
|70||70||["TGF-\u03b22 silencing to target biliary-derived liver diseases"]||10.1136/gutjnl-2019-319091||http://dx.doi.org/10.1136/gutjnl-2019-319091||2020-01-28T21:17:00Z||["Gastroenterology"]||0||0||["0017-5749", "1468-3288"]||Gut||<jats:sec><jats:title>Objective</jats:title><jats:p>TGF-β2 (TGF-β, transforming growth factor beta), the less-investigated sibling of TGF-β1, is deregulated in rodent and human liver diseases. Former data from bile duct ligated and MDR2 knockout (KO) mouse models for human cholestatic liver disease suggested an involvement of TGF-β2 in biliary-derived liver diseases.</jats:p></jats:sec><jats:sec><jats:title>Design</jats:title><jats:p>As we also found upregulated <jats:italic>TGFB2</jats:italic> in liver tissue of patients with primary sclerosing cholangitis (PSC) and primary biliary cholangitis (PBC), we now fathomed the positive prospects of targeting TGF-β2 in early stage biliary liver disease using the MDR2-KO mice. Specifically, the influence of <jats:italic>TgfB2</jats:italic> silencing on the fibrotic and inflammatory niche was analysed on molecular, cellular and tissue levels.</jats:p></jats:sec><jats:sec><jats:title>Results</jats:title><jats:p><jats:italic>TgfB2</jats:italic>-induced expression of fibrotic genes in cholangiocytes and hepatic stellate cellswas detected. <jats:italic>TgfB2</jats:italic> expression in MDR2-KO mice was blunted using <jats:italic>TgfB2</jats:italic>-directed antisense oligonucleotides (AON). Upon AON treatment, reduced collagen deposition, hydroxyproline content and αSMA expression as well as induced <jats:italic>PparG</jats:italic> expression reflected a significant reduction of fibrogenesis without adverse effects on healthy livers. Expression analyses of fibrotic and inflammatory genes revealed AON-specific regulatory effects on <jats:italic>Ccl3</jats:italic>, <jats:italic>Ccl4</jats:italic>, <jats:italic>Ccl5</jats:italic>, <jats:italic>Mki67</jats:italic> and <jats:italic>Notch3</jats:italic> expression. Further, AON treatment of MDR2-KO mice increased tissue infiltration by F4/80-positive cells including eosinophils, whereas the number of CD45-positive inflammatory cells decreased. In line, <jats:italic>TGFB2</jats:italic> and CD45 expression correlated positively in PS…||29||["http://orcid.org/0000-0002-4840-6240", "http://orcid.org/0000-0001-7953-8927", "http://orcid.org/0000-0003-3135-1359", "http://orcid.org/0000-0002-6022-073X", "http://orcid.org/0000-0003-0336-0581", "http://orcid.org/0000-0003-0211-352X"]||["Anne Dropmann", "Steven Dooley", "Bedair Dewidar", "Seddik Hammad", "Tatjana Dediulia", "Julia Werle", "Vanessa Hartwig", "Shahrouz Ghafoory", "Stefan Woelfl", "Hanna Korhonen", "Michel Janicot", "Katja Wosikowski", "Timo Itzel", "Andreas Teufel", "Detlef Schuppan", "Ana Stojanovic", "Adelheid Cerwenka", "Stefanie Nittka", "Albrecht Piiper", "Timo Gaiser", "Naiara Beraza", "Malgorzata Milkiewicz", "Piotr Milkiewicz", "John G Brain", "David E J Jones", "Thomas S Weiss", "Ulrich M Zanger", "Matthias Ebert", "Nadja M Meindl-Beinker"]||["non"]||["Robert Bosch Stiftung", "Bundesministerium f\u00fcr Bildung und Forschung", "Deutsche Forschungsgemeinschaft", "ESF Baden W\u00fcrttemberg (www.esf-bw.de) and the Ministerium f\u00fcr Wissenschaft, Forschung und Kunst, Baden W\u00fcrttemberg", "EU", "Isarna Therapeutics GmbH", "SPP 1937"]||["10.13039/501100001646", "10.13039/501100002347", "10.13039/501100001659", [""], [""], [""], [""]]|
CREATE TABLE [article] ( [title] TEXT, [DOI] TEXT, [URL] TEXT, [created] TEXT, [subject] TEXT, [references-count] TEXT, [is-referenced-by-count] TEXT, [ISSN] TEXT, [container-title] TEXT, [abstract] TEXT, [author_number] TEXT, [orcids] TEXT, [names] TEXT, [award_numbers] TEXT, [funder_names] TEXT, [funder_dois] TEXT );