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  • 1
    Electronic Resource
    Electronic Resource
    Springer
    Digestive diseases and sciences 43 (1998), S. 2309-2316 
    ISSN: 1573-2568
    Keywords: GROWTH FACTORS ; WOUND REPAIR ; ESOPHAGUS
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract Factors and mechanisms involved in esophagealmucosal injury and repair are not well known. The aim ofthis study was to assess the effects of growth factorsand prostaglandins on esophageal mucosal cell repair activities. Rabbit esophageal cells wereisolated, cultured, and exposed to different growthfactors and prostaglandin E2. Subconfluentcell cultures were used to study proliferative responsesdetermined by [3H]thymidine incorporation intoDNA. Restitution was studied in confluent monolayerswounded by mechanical denudation. Restitution was themain mechanism involved in wound repair within the first24 hr. HGF, IGF-I, and EGF dose-dependentlystimulated cell proliferation but did not affectrestitution. TGF-β1 inhibited bothproliferation and restitution while PDGF-BB andprostaglandin E2 had no effect. Esophageal epithelial cell restitution andproliferation are affected by growth factors. HGF,IGF-I, EGF (stimulation), and TGF-β1(inhibition) are major growth factors affecting in vitroesophageal wound repair activities, which, unlike those ofother areas of the digestive tract, are not affected byprostaglandins.
    Type of Medium: Electronic Resource
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  • 2
    Electronic Resource
    Electronic Resource
    Springer
    Digestive diseases and sciences 43 (1998), S. 1230-1240 
    ISSN: 1573-2568
    Keywords: FIBROBLASTS ; ULCER HEALING ; PLATELET-DERIVED GROWTH FACTOR ; TRANSFORMING GROWTH FACTOR-β ; PROSTAGLANDINS
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract Fibroblasts modulate epithelial biologicalactivities and play a key role in the ulcer healingprocess. There is no information regarding thebiological response of human gastric fibroblasts toregulatory compounds. The aim of this study was to assessthe effects of growth factors and prostaglandins on anin vitro model of human gastric fibroblast wound repair.Subconfluent fibroblast cultures were used to study proliferative responses, determined by[3H]thymidine incorporation into DNA. Invitro wound repair was determined in confluentfibroblast monolayers after mechanical denudation. Thepresence of putative growth factors secreted by fibroblastswas studied in conditioned medium by heparin-affinitychromatography and immunodetection with specificantibodies. Serum and platelet-derived growth factor (PDGF)-BB induced a dramatic increase in bothgastric fibroblast proliferation and closure of woundedcell monolayers, whereas these activities were inhibitedby both transforming growth factor(TGF)-β1 and prostaglandin E1. Basalactivities in unstimulated gastric fibroblasts werelower than those obtained in skin fibroblasts.Conditioned medium stimulated fibroblast proliferationand wound repair activity, which was inhibited by the addition of suramin,and was partially dependent on the presence of PDGF-likefactor. PDGF is a major, autocrine promotor of humangastric fibroblast-dependent wound repair activities, which are inhibited by prostaglandins andTGF-β. These findings might be important for futuretherapeutic ulcer healing approaches.
    Type of Medium: Electronic Resource
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  • 3
    Electronic Resource
    Electronic Resource
    Springer
    Digestive diseases and sciences 42 (1997), S. 1003-1012 
    ISSN: 1573-2568
    Keywords: ESOPHAGITIS ; PEPSIN ; ADAPTATION ; EPIDERMAL GROWTH FACTOR ; NITRIC OXIDE
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract To study whether the esophageal mucosa was ableto elicit mucosal adaptation, we induced esophagealdamage by perfusing acidified pepsin in rabbits. Mucosaladaptation was induced by preexposing the esophageal mucosa to a mild irritant (acidified saline)for 60 min prior to acidified pepsin (strong irritant).Macroscopic and microscopic esophageal injury, cellproliferation, and mucosal barrier function(H+, K+, hemoglobin flux rates)were studied. Preexposure of the esophageal mucosa toacidified saline significantly decreased both themucosal damage and the mucosal barrier dysfunctioninduced by acidified pepsin. The development of this phenomenon wasnondependent on cell proliferation. Concomitanttreatment with either the nitric oxide synthaseinhibitor, NG-nitro-L-arginine, or theperfusion of immunospecific EGF-receptor antibodies or tyrphostin-25, aninhibitor of the tyrosine kinase activities ligated tothe intracytoplasmatic domain of the EGF receptor,during the preexposure period completely reversed the protection induced by acid. We conclude thatthe rabbit esophageal mucosa shows mucosal adaptation toacid and pepsin. The development of this phenomenon isfast, not dependent on cell proliferation, and dependent, at least in part, on nitric oxideand EGF-receptor-mediated mechanisms.
    Type of Medium: Electronic Resource
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  • 4
    Electronic Resource
    Electronic Resource
    Springer
    Digestive diseases and sciences 45 (2000), S. 1802-1809 
    ISSN: 1573-2568
    Keywords: superoxide anion ; nitric oxide ; esophagitis ; superoxide dismutase ; sodium nitroprusside ; nitric oxide synthase inhibitor
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract It has been suggested that free radicals are involved in esophagitis. To study the role and potential interaction of superoxide anion and nitric oxide (NO) in low-grade esophagitis, we perfused acidified pepsin (30 min every 12 hr) for seven days in rabbits treated with different agents to modulate the generation of these radicals. Measurements included macroscopic and microscopic damage, superoxide anion generation, mucosal nitric oxide synthase activity, and peroxynitrite formation. Low-grade esophagitis was associated with increased nitric oxide synthase mucosal activity and mucosal damage was dose-dependently increased by treatment with the NO synthase inhibitor N G-nitro-l-arginine. Superoxide anion was scarcely generated in the mucosa, but this was not accompanied by any change in the activity of mucosal superoxide dismutase. Treatment with superoxide dismutase did not improve mucosal damage. Generation of peroxynitrites was not detected. In conclusion, nitric oxide is involved in the mucosal defense of the esophagus against acid- and pepsin-induced damage. Superoxide anion generation seems irrelevant in the induction of low-grade esophagitis and not sufficient to interact with nitric oxide to generate measurable mucosal peroxynitrite radicals.
    Type of Medium: Electronic Resource
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  • 5
    Electronic Resource
    Electronic Resource
    Springer
    Inflammation 21 (1997), S. 419-429 
    ISSN: 1573-2576
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract Unlike gastric mucosa, it has been considered that lipoxygenase metabolites protect the esophageal mucosa and that prostaglandins are only secreted in the presence of esophageal inflammation. The aim of this study was to determine the profile of arachidonic acid metabolites and their response to regulatory compounds in rabbit esophageal mucosal cells in culture. Eicosanoids secreted into the medium were extracted and identified by HPLC and RIA. Esophageal mucosal cells in culture metabolized arachidonic acid mainly through the cycloxygenase pathway and PGE2 was the major arachidonic acid metabolite secreted. The addition of IL-1β and A23187 (calcium ionophore) stimulated PGE2 synthesis. In basal conditions neither leukotrienes nor HETEs were detected. However, the addition of the NDGA induced the secretion of lipoxygenase metabolites identified as 12–15 HETEs. In conclusion, rabbit esophageal epithelial cells in culture metabolize arachidonic acid via both cycloxygenase and lipoxygenase pathways. In our system, PGE2 was the main arachidonic acid metabolite.
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  • 6
    Electronic Resource
    Electronic Resource
    Weinheim : Wiley-Blackwell
    ISSN: 0935-6304
    Keywords: Chemistry ; Analytical Chemistry and Spectroscopy
    Source: Wiley InterScience Backfile Collection 1832-2000
    Topics: Chemistry and Pharmacology
    Type of Medium: Electronic Resource
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  • 7
    Electronic Resource
    Electronic Resource
    Amsterdam : Elsevier
    Comparative Biochemistry And Physiology 18 (1966), S. 241-248 
    ISSN: 0010-406X
    Source: Elsevier Journal Backfiles on ScienceDirect 1907 - 2002
    Topics: Biology , Chemistry and Pharmacology
    Type of Medium: Electronic Resource
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  • 8
    Electronic Resource
    Electronic Resource
    Amsterdam : Elsevier
    Comparative Biochemistry And Physiology 28 (1969), S. 227-232 
    ISSN: 0010-406X
    Source: Elsevier Journal Backfiles on ScienceDirect 1907 - 2002
    Topics: Biology , Chemistry and Pharmacology
    Type of Medium: Electronic Resource
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  • 9
    Electronic Resource
    Electronic Resource
    [s.l.] : Nature Publishing Group
    Nature 206 (1965), S. 27-28 
    ISSN: 1476-4687
    Source: Nature Archives 1869 - 2009
    Topics: Biology , Chemistry and Pharmacology , Medicine , Natural Sciences in General , Physics
    Notes: [Auszug] IN a previous communication from, our laboratory1 we compared the metabolism of glucose in two strains of Trypanosoma cruzi. In addition to metabolic differences, there was also some difference in the pathogenicity of both the Tulahuen2 and the Peruvian3 strains examined. These facts led us to ...
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  • 10
    Electronic Resource
    Electronic Resource
    Oxford, UK : Blackwell Science Ltd
    ISSN: 1365-2036
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: Background : Aspirin is valuable for preventing vascular events, but information about ulcer frequency is necessary to inform risk-benefit decisions in individual patients.Aim : To determine ulcer prevalence and incidence in a population representative of those given aspirin therapy and evaluate risk predictors.Methods : Patients taking aspirin 75–325 mg daily were recruited from four countries. Exclusions included use of gastroprotectant drugs or other non-steroidal anti-inflammatory drugs. We measured point prevalence of endoscopic ulcers, after quantitating dyspeptic symptoms. Incidence was assessed 3 months later in those eligible to continue (no baseline ulcer or reason for gastroprotectants).Results : In 187 patients, ulcer prevalence was 11% [95% confidence interval (CI) 6.3–15.1%]. Only 20% had dyspeptic symptoms, not significantly different from patients without ulcer. Ulcer incidence in 113 patients followed for 3 months was 7% (95% CI 2.4–11.8%). Helicobacter pylori infection increased the risk of a duodenal ulcer [odds ratio (OR) 18.5, 95% CI 2.3–149.4], as did age 〉70 for ulcers in stomach and duodenum combined (OR 3.3, 95% CI 1.3–8.7).Conclusions : Gastroduodenal ulcers are found in one in 10 patients taking low-dose aspirin, and most are asymptomatic; this needs considering when discussing risks/benefits with patients. Risk factors include older age and H. pylori (for duodenal ulcer).
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