enterocolitis/phosphatase

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Intestinal alkaline phosphatase to treat necrotizing enterocolitis.

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BACKGROUND Intestinal alkaline phosphatase (IAP) activity is decreased in necrotizing enterocolitis (NEC), and IAP supplementation prevents NEC development. It is not known if IAP given after NEC onset can reverse the course of the disease. We hypothesized that enteral IAP given after NEC induction

Enteral intestinal alkaline phosphatase administration in newborns decreases iNOS expression in a neonatal necrotizing enterocolitis rat model.

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OBJECTIVE To determine if intestinal alkaline phosphatase (IAP) decreases intestinal injury resulting from experimentally induced necrotizing enterocolitis (NEC). We hypothesized that IAP administration prevents the initial development of NEC related intestinal inflammation. METHODS Pre- and

Factors Known to Influence the Development of Necrotizing Enterocolitis to Modify Expression and Activity of Intestinal Alkaline Phosphatase in a Newborn Neonatal Rat Model.

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BACKGROUND Prematurity, formula feeding, and early weaning strongly influence enterocyte differentiation. Intestinal alkaline phosphatase (IAP), an endogenous protein expressed in the intestines, is one enzyme that is affected by these factors. IAP supplementation decreases the severity of

Differences in Serum Alkaline Phosphatase Levels in Infants with Spontaneous Intestinal Perforation versus Necrotizing Enterocolitis with Perforation

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Introduction: Data on laboratory markers of spontaneous intestinal perforation (SIP) and necrotizing enterocolitis (NEC) remain sparse. Objective: To compare serum alkaline

Intestinal alkaline phosphatase administration in newborns decreases systemic inflammatory cytokine expression in a neonatal necrotizing enterocolitis rat model.

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BACKGROUND Supplementation of intestinal alkaline phosphatase (IAP), an endogenous protein expressed in the intestines, decreases the severity of necrotizing enterocolitis (NEC)-associated intestinal injury and permeability. We hypothesized that IAP administration is protective in a dose-dependent

The protective role of intestinal alkaline phosphatase in necrotizing enterocolitis.

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BACKGROUND Enterocytes produce intestinal alkaline phosphatase (iAP), which detoxifies lipopolysaccharide (LPS), a mediator in necrotizing enterocolitis (NEC) pathogenesis. We hypothesize that aberrant expression or function of iAP contributes to the pathogenesis of NEC. METHODS Newborn Sprague

The relationship between reticulated platelets, intestinal alkaline phosphatase, and necrotizing enterocolitis.

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BACKGROUND Necrotizing enterocolitis (NEC) affects up to 10% of extremely-low-birthweight infants, with a 30% mortality rate. Currently, no biomarker reliably facilitates early diagnosis. Since thrombocytopenia and bowel ischemia are consistent findings in advanced NEC, we prospectively investigated

Single nucleotide polymorphisms in the dual specificity phosphatase genes and risk of necrotizing enterocolitis in premature infant.

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Differences in the susceptibility of preterm infants to develop necrotizing enterocolitis (NEC) implicate potential genetic differences in response to the inflammatory stimuli leading to NEC. Dual specificity phosphatases (DUSPs) are a key suppressor pathway of the mitogen-activated

Intestinal alkaline phosphatase administration in newborns is protective of gut barrier function in a neonatal necrotizing enterocolitis rat model.

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BACKGROUND Previously, we have shown that supplementation of intestinal alkaline phosphatase (IAP) decreased severity of necrotizing enterocolitis (NEC)-associated intestinal injury. We hypothesized that IAP administration is protective of intestinal epithelial barrier function in a dose-dependent

Intestinal alkaline phosphatase prevents the systemic inflammatory response associated with necrotizing enterocolitis.

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BACKGROUND Necrotizing enterocolitis (NEC) is the most common surgical emergency in neonates, with an incidence of 0.5-2.4 cases per 1000 live births and a mortality rate between 10% and 50%. Neonates affected by NEC develop a septic injury that is associated with increased risk of neurological

Association of Intestinal Alkaline Phosphatase With Necrotizing Enterocolitis Among Premature Infants.

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Necrotizing enterocolitis (NEC) in preterm infants is an often-fatal gastrointestinal tract emergency. A robust NEC biomarker that is not confounded by sepsis could improve bedside management, lead to lower morbidity and mortality, and permit patient selection in randomized clinical

[Excretion of enzymes entokinase and alkaline phosphatase with feces of patients with chronic enteritis and enterocolitis].

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Intestinal alkaline phosphatase prevents the systemic inflammatory response associated with necrotizing enterocolitis.

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Inhibition of miR-124 improves neonatal necrotizing enterocolitis via an MYPT1 and TLR9 signal regulation mechanism.

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BACKGROUND Necrotizing enterocolitis (NEC) was one of the main causes of morbidity and mortality in neonates. Our objective was to detect the mechanism of miR-124 in small bowel tissues of NEC. METHODS Hematoxylin and eosin (H&E) staining was used to detect the repair of the damaged tissues in rat

Intestinal alkaline phosphatase is protective to the preterm rat pup intestine.

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BACKGROUND Necrotizing enterocolitis (NEC) is the most common surgical emergency in neonates, with a mortality rate between 10 and 50%. The onset of necrotizing enterocolitis is highly variable and associated with numerous risk factors. Prior research has shown that enteral supplementation with

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