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enterocolitis/hypoxia

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Strana 1 od 313 výsledky

Protective effects of recombinant human interleukin-10 on intestines of hypoxia-induced necrotizing enterocolitis in immature rats.

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OBJECTIVE The role of cytokines in the pathogenesis of hemodynamic instability or tissue destruction in patients with necrotizing enterocolitis (NEC) remains undefined. The aim of this study was to determine the effects of recombinant human interleukin-102 (rhIL-10) on intestines of hypoxia-induced

Supplementation with Saccharomyces boulardii ameliorates hypoxia/reoxygenation-induced necrotizing enterocolitis in young mice.

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Intestinal bacterial proliferation is an important aspect of gastrointestinal injury in neonatal necrotizing enterocolitis (NEC). In the present investigation, we examined the protective action of oral supplementation with Saccharomyces boulardii (S. boulardii), non-pathogen probiotic yeast, against

Intraluminal intestinal microdialysis detects markers of hypoxia and cell damage in experimental necrotizing enterocolitis.

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OBJECTIVE Necrotizing enterocolitis (NEC) represents one of the gravest complications in premature infants and carries significant morbidity and mortality. There is a great need for improved diagnostic methods to reduce the severity and incidence of NEC. The aim of the study was to investigate if

Hypoxia, PAF, and necrotizing enterocolitis.

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Necrotizing enterocolitis (NEC) is an important neonatal disease with a high mortality rate. The pathophysiology is unclear but epidemiologic studies suggest that hypoxia and infection are important risk factors. In this review we discuss the effect of hypoxia and platelet-activating factor (PAF) on

The therapeutic effect of recombinant human trefoil factor 3 on hypoxia-induced necrotizing enterocolitis in immature rat.

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Trefoil peptides are a new class of regulatory peptides involved in mucosal protection and repair in the gastrointestinal tract. Among them, trefoil factor 3 (TFF3) (intestinal trefoil factor) is known to be cytoprotective in the gut. The aim of this study was to determine the effect of recombinant

Hypoxia-induced necrotizing enterocolitis in the immature rat: the role of lipid peroxidation and management by vitamin E.

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The authors developed an experimental model of necrotizing enterocolitis (NEC) by hypoxia-reoxygenation, and determined the content of malondialdehyde levels as an index of lipid peroxidation, related with a free-radical reaction in the gastrointestinal tract of newborn rats. They also investigated

Platelet-activating factor, tumor necrosis factor, hypoxia and necrotizing enterocolitis.

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The pathogenesis of necrotizing enterocolitis (NEC) is poorly understood. We have established several animal models of NEC by using a combination of various stimuli and stress, including endotoxin, PAF, TNF, and hypoxia. We discuss the mechanism of their actions and the possible roles of these
Oxygen-derived free radicals are important components of gastrointestinal injury in necrotizing enterocolitis (NEC). In the present investigation, we examined the protective actions of L-arginine, a nitric oxide synthase substrate, and L-carnitine against hypoxia-reoxygenation (H/R) induced NEC in
OBJECTIVE Necrotizing enterocolitis (NEC) is a multifactorial syndrome in the neonate. Enteral feeding practices are an important component of gastrointestinal injury in neonatal NEC. In the present study, we examined the protective effect of oral supplementation with L-glutamine, an important
The traditional and most frequently employed surgical approach to perforated necrotizing enterocolitis (NEC), laparotomy and bowel resection with enterostomy creation, has been associated with an unacceptably high mortality and major morbidity (sepsis, short-gut syndrome, strictures, long-term total

Pentoxifylline does not prevent hypoxia/reoxygenation-induced necrotizing enterocolitis. An experimental study.

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Hypoxia/reoxygenation (H/R)-induced intestinal injury plays a significant role in the development of necrotizing enterocolitis (NEC). We experimentally explored the effect of pentoxifylline (PTX) on an NEC model. Twenty-one newborn rabbits were divided into three groups: group 1 (control), group 2

Formula feeding and systemic hypoxia synergistically induce intestinal hypoxia in experimental necrotizing enterocolitis.

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OBJECTIVE Feeding and systemic hypoxia are major stresses inducing necrotizing enterocolitis (NEC). This study aims to investigate the role of systemic hypoxia in NEC and its effect before and after feeding. METHODS Neonatal mice were studied in three groups. Control (N = 9): breast feeding; NEC A
BACKGROUND Hypoxia is an important risk factor for development of necrotizing enterocolitis (NEC) in premature infants. Hypoxia-inducible factor (HIF)-1 is a transcription factor that plays a critical role in cellular responses to hypoxia and can be induced by phosphatidylinositol 3-kinase (PI3-K)

Formula Feeding and Immature Gut Microcirculation Promote Intestinal Hypoxia leading to Necrotizing Enterocolitis.

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Major risk factors for necrotizing enterocolitis (NEC) are formula feeding and prematurity, however, their pathogenic mechanisms are unknown. We found that insufficient arginine/nitric oxide synthesis limits blood flow in the intestinal microvasculature, leading to hypoxia, mucosa damage and NEC in

Importance of multiple episodes of hypoxia or cold stress on the development of enterocolitis in an animal model.

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Necrotizing enterocolitis, a highly lethal disease in the newborn infant characterized by ischemic necrosis of the gastrointestinal tract frequently leading to perforation, is seen primarily in low birth weight infants who have undergone stress, such as hypoxia. In an animal model it was
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