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Sökning: hsv:(MEDICIN OCH HÄLSOVETENSKAP) hsv:(Klinisk medicin) hsv:(Gastroenterologi) > (2010-2019) > (2012)

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1.
  • Carlsson, Lena M S, 1957, et al. (författare)
  • Bariatric surgery and prevention of type 2 diabetes in Swedish obese subjects.
  • 2012
  • Ingår i: The New England journal of medicine. - : Massachusetts Medical Society. - 1533-4406 .- 0028-4793. ; 367:8, s. 695-704
  • Tidskriftsartikel (övrigt vetenskapligt/konstnärligt)abstract
    • Weight loss protects against type 2 diabetes but is hard to maintain with behavioral modification alone. In an analysis of data from a nonrandomized, prospective, controlled study, we examined the effects of bariatric surgery on the prevention of type 2 diabetes.
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  • Keszthelyi, D., et al. (författare)
  • Revisiting concepts of visceral nociception in irritable bowel syndrome
  • 2012
  • Ingår i: European Journal of Pain. - : Wiley. - 1090-3801. ; 16:10, s. 1444-1454
  • Forskningsöversikt (refereegranskat)abstract
    • Background and Objective Irritable bowel syndrome (IBS) is a common disorder characterized by abdominal pain related to defecation with a change in bowel habit. Patients with IBS often exhibit increased visceral sensitivity, which can be tested clinically by rectal balloon distension procedures. This paper aims to give an overview of mechanisms involved in visceral hypersensitivity in IBS by reviewing recent literature. Databases and Data Treatment A literature search in the electronic databases Pubmed and MEDLINE was executed using the search terms visceral pain or visceral nociception or visceral hypersensitivity and irritable bowel syndrome. Both original articles and review articles were considered for data extraction. Results Recent advances in molecular neurophysiology provide knowledge to better understand the underlying mechanism in pain generation in the human gut, in particular, in IBS patients. Sensitization of peripheral nociceptive afferents, more specifically high-threshold afferents, has been proposed as one of the principle mechanism in the development of visceral hypersensitivity. On the other hand, central mechanisms also play an important role. In terms of clinical testing of visceral perception, considerable discrepancies remain, however, across different centres. Conclusion Alterations in the modulatory balance of pro- and antinociceptive central processing of noxious peripheral input may serve as in integrative hypothesis for explaining visceral hypersensitivity in IBS. Nevertheless, it remains troublesome to estimate the contribution of central and peripheral factors in visceral hypersensitivity, posing a challenge in determining effective therapeutic entities.
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  • Reinhardt, Christopher, et al. (författare)
  • Tissue factor and PAR1 promote microbiota-induced intestinal vascular remodelling
  • 2012
  • Ingår i: Nature. - : Springer Science and Business Media LLC. - 0028-0836 .- 1476-4687. ; 483, s. 627-631
  • Tidskriftsartikel (refereegranskat)abstract
    • The gut microbiota is a complex ecosystem that has coevolved with host physiology. Colonization of germ-free (GF) mice with a microbiota promotes increased vessel density in the small intestine, but little is known about the mechanisms involved. Tissue factor (TF) is the membrane receptor that initiates the extrinsic coagulation pathway, and it promotes developmental and tumour angiogenesis. Here we show that the gut microbiota promotes TF glycosylation associated with localization of TF on the cell surface, the activation of coagulation proteases, and phosphorylation of the TF cytoplasmic domain in the small intestine. Anti-TF treatment of colonized GF mice decreased microbiota-induced vascular remodelling and expression of the proangiogenic factor angiopoietin-1 (Ang-1) in the small intestine. Mice with a genetic deletion of the TF cytoplasmic domain or with hypomorphic TF (F3) alleles had a decreased intestinal vessel density. Coagulation proteases downstream of TF activate protease-activated receptor (PAR) signalling implicated in angiogenesis. Vessel density and phosphorylation of the cytoplasmic domain of TF were decreased in small intestine from PAR1-deficient (F2r-/-) but not PAR2-deficient (F2rl1-/-) mice, and inhibition of thrombin showed that thrombin-PAR1 signalling was upstream of TF phosphorylation. Thus, the microbiota-induced extravascular TF-PAR1 signalling loop is a novel pathway that may be modulated to influence vascular remodelling in the small intestine. © 2012 Macmillan Publishers Limited. All rights reserved.
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  • Björkman, Eleonora, 1981, et al. (författare)
  • In vitro assessment of epithelial electrical resistance in human esophageal and jejunal mucosae and in Caco-2 cell layers.
  • 2012
  • Ingår i: Scandinavian journal of gastroenterology. - : Informa UK Limited. - 1502-7708 .- 0036-5521. ; 47:11, s. 1321-1333
  • Tidskriftsartikel (refereegranskat)abstract
    • Abstract Objective. There is a need for a technique allowing studies of human mucosal specimens collected during different clinical conditions. This study elucidates if square wave pulse analysis discriminates between epithelial and transmural electrical resistance and if there is an association with transepithelial permeability of molecular probes. Methods. Mucosae from esophagus (surgical resections: n = 14; endoscopic biopsies: n = 15) and jejunum (n = 12) and Caco-2 cell monolayers were investigated in Ussing chambers. Transmural and epithelial electrical resistance were recorded by the use of standardized current pulses. Permeability was assessed using two fluorescein-labeled probes (weight 376 and 4000 Da). Results. Baseline epithelial electrical resistance was higher in esophageal mucosa (∼280 Ω*cm(2)), than in jejunal (∼10 Ω*cm(2)) and Caco-2 cells (∼140 Ω*cm(2)). The subepithelial contribution to the transmural resistance was higher in jejunal preparations (+88%) and Caco-2 cells (+75%), than in esophageal (+30%). During hypoxia the subepithelial resistance was unchanged, whereas the epithelial resistance decreased significantly in jejunal mucosa and Caco-2 cells. These findings coincided with increased transepithelial probe permeability and signs of disturbed morphology. Esophageal epithelia were resistant to hypoxia. However, exposure to deoxycholic acid and trypsin abolished the esophageal epithelial resistance and increased probe permeability. Endoscopic esophageal biopsies from patients with erosive reflux disease exhibited significantly lower epithelial resistance and higher current than healthy subjects. Conclusion. Square wave pulse analysis in Ussing chambers is suitable for assessment of epithelial electrical resistance that can reflect transepithelial permeability of molecular probes with known size. Moreover, the technique discriminated between healthy and reflux-diseased esophageal mucosal biopsies.
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  • Ellegård, Lars, 1958 (författare)
  • D-vitamin efter tarmoperation
  • 2012
  • Ingår i: ILCO-bladet. - 0345-4908. ; :2
  • Tidskriftsartikel (övrigt vetenskapligt/konstnärligt)
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  • Ellegård, Lars, 1958 (författare)
  • Nutrition vid tarmsvikt efter tarmischemi.
  • 2012
  • Ingår i: Läkartidningen. - 0023-7205. ; 109:49-50, s. 2294-2295
  • Tidskriftsartikel (refereegranskat)abstract
    • Patienter med tarmischemi drabbas akut av tarmsvikt, som oftast blir kronisk. Vid ileocekal resektion krävs livslång substitution med vitamin B12. Vid stomiflöden överstigande 1–2 l/dygn ökar risken för dehydrering och natriumbrist, vilket bäst diagnostiseras via lågt urin-Na, och magnesiumbrist som ger kramper. Om >1 meter tunntarm plus kolon återstår kan patienten vanligen klara sig med peroralt intag, som kompenserar de ökade förlusterna. För optimal rehabilitering bör samlad kompetens inom kirurgi, nutrition och stomivård erbjudas. Det ger goda möjligheter till kateterinläggning, kuratorskontakt och bestämning av bentäthet och kroppssammansättning.
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