urea/necrotisch

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In vitro induction of apoptosis vs. necrosis by widely used preservatives: 2-phenoxyethanol, a mixture of isothiazolinones, imidazolidinyl urea and 1,2-pentanediol.

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Preservatives are added to many final products, such as detergents, cosmetics, pharmaceuticals and vaccines. We conducted an in vitro investigation of the apoptosis- and necrosis-inducing potential of brief applications (10 min) of four common preservatives: ethylene glycol monophenyl ether,

Development of N-2,4-pyrimidine-N-phenyl-N'-phenyl ureas as inhibitors of tumor necrosis factor alpha (TNF-alpha) synthesis. Part 1.

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A new class of tumor necrosis factor alpha (TNF-alpha) synthesis inhibitors based on an N-2,4-pyrimidine-N-phenyl-N'-phenyl urea scaffold is described. Many of these compounds showed low-nanomolar activity against lipopolysaccharide stimulated TNF-alpha production. X-ray co-crystallization studies

Development of N-2,4-pyrimidine-N-phenyl-N'-alkyl ureas as orally active inhibitors of tumor necrosis factor alpha (TNF-alpha) synthesis. Part 2.

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A new class of tumor necrosis factor alpha (TNF-alpha) synthesis inhibitors based on a N-2,4-pyrimidine-N-phenyl-N'-alkyl urea scaffold is described. Many of these compounds showed low-nanomolar activity against lipopolysaccharide stimulated TNF-alpha production. Two analogs were tested in an in

[Dependence of the rate of development of Zenker's necrosis in the fibers of the frog sartorius muscle on the concentration of chloral hydrate, urea and urethane].

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The spreading necrosis in dissected m. sartorius of Rana temporaria changes its speed in the phasic mode in relation to the concentrations of chloral hydrate, urea and uretan, added to the Ringer solution. The number and size of the phases are also dependent on the temperature and the initial

Tumor necrosis factor-alpha acutely up-regulates urea synthesis in vivo in rats--a hepatic component of inflammatory catabolism?

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BACKGROUND Catabolism is a serious problem in patients with active inflammation. The tissue nitrogen (N) depletion is related to increased hepatic capacity for elimination of N via conversion of amino-N into urea-N. This is caused by the inflammatory process, but the mediators responsible are

The fractional excretion of urea in the differential diagnosis of prerenal failure and acute tubular necrosis in neonates.

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BACKGROUND Acute renal failure (ARF) in a newborn is a common problem. Fractional excretion of sodium (FENa) has been used to distinguish between the two main causes of ARF, prerenal failure and acute tubular necrosis (ATN). However, the clinical usefulness of FENa could be limited by furosemide

Prediction model based on blood urea nitrogen and the leukocyte count for intestinal necrosis in patients with portal vein system thrombosis: a retrospective study.

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Portal vein system thrombosis (PVST) is a serious and potentially fatal disease. No definite parameter can predict intestinal necrosis in patients with PVST to justify early surgical intervention. The current study aimed to explore a simple and accurate model to predict the occurrence

Hepatocyte heterogeneity in ammonia metabolism: impairment of glutamine synthesis in CCl4 induced liver cell necrosis with no effect on urea synthesis.

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After induction of a perivenous liver cell necrosis by CCl4 pretreatment of the rat, ammonia uptake by perfused liver is decreased. This was due to an inhibition of glutamine synthesis from added ammonia, whereas urea synthesis was not affected by CCl4 pretreatment. The data confirm recent findings

Admission Hematocrit and Rise in Blood Urea Nitrogen at 24 h Outperform other Laboratory Markers in Predicting Persistent Organ Failure and Pancreatic Necrosis in Acute Pancreatitis: A Post Hoc Analysis of Three Large Prospective Databases.

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Predicting severe acute pancreatitis (AP) remains a challenge. The present study compares admission blood urea nitrogen (BUN), hematocrit, and creatinine, as well as changes in their levels over 24 h, aiming to determine the most accurate laboratory test for predicting persistent organ failure and

Erratum: Admission Hematocrit and Rise in Blood Urea Nitrogen at 24 h Outperform other Laboratory Markers in Predicting Persistent Organ Failure and Pancreatic Necrosis in Acute Pancreatitis: A Post Hoc Analysis of Three Large Prospective Databases.

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Evaluation of plasma leptin, tumor necrosis factor-α, and prealbumin as prognostic biomarkers during clinical recovery from acute exacerbations of chronic obstructive pulmonary disease.

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BACKGROUND Inflammatory and nutritional biomarkers have an important bearing on outcomes of acute exacerbations of chronic obstructive pulmonary disease (AECOPD), but the temporal profile of these compounds during an acute episode is unclear. METHODS Plasma leptin, prealbumin, and tumor necrosis

Renal papillary necrosis and urinary protein alterations induced in Fischer-344 rats by D-ormaplatin.

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D-ormaplatin (previously called tetraplatin) produced dose-related renal papillary necrosis when given intravenously to Fischer-344 rats at doses of 2, 4, and 9 mg/kg. The lesions were most severe at 4 days postdosing and had repaired by day 9 in the 2- and 4-mg/kg dose groups. Blood urea nitrogen

Elevated serum levels of the type I and type II receptors for tumor necrosis factor-alpha as predictive factors for ARF in patients with septic shock.

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BACKGROUND Acute renal failure (ARF), a common and serious complication in patients with septic shock, has high mortality. Recent data suggest that proinflammatory cytokines may contribute to sepsis-associated ARF. METHODS To examine the role of proinflammatory cytokines, we evaluated 537 patients

P16INK4a played a critical role in exacerbating acute tubular necrosis in acute kidney injury.

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Acute kidney injury (AKI) is a common clinical syndrome with high morbidity and mortality, which is mostly caused by acute tubular necrosis (ATN). AKI is associated with many factors, including cell senescence, inflammatory infiltration, apoptosis and excessive accumulation of reactive oxygen

Caspase-1-deficient mice are protected against cisplatin-induced apoptosis and acute tubular necrosis.

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BACKGROUND Cisplatin is a commonly used chemotherapeutic agent which causes apoptosis or necrosis of renal tubular epithelial cells in vitro. Caspases are a family of cysteine proteases that mediate apoptosis (caspase-3) and inflammation (caspase-1). Although well studied in vitro, caspases have not

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