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arginase/necrosis

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Pagina 1 a partire dal 335 risultati
Serum concentrations of arginase, glutamic pyruvic transaminase (SGPT) and glutamic oxaloacetic transaminase (SGOT) in dogs, cats, horses, cattle, sheep and pigs were determined before and after oral administration of CCl(4) at doses known to cause hepatic necrosis. Following CCl(4) administration,

Expression of arginase by mouse myeloid leukemic cell differentiation in vitro induced with tumor necrosis factor.

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Induction of arginase activity in mouse myeloid leukemic M1 cells by treatment with recombinant human tumor necrosis factor (rH-TNF) or TNF-elicited mouse serum (TNS) were examined in vitro. M1 cells differentiated into macrophage-like cells by addition of rH-TNF or TNS. The differentiated cells
Changes in the serum concentrations of aspartic aminotransferase (AST), alanine aminotransferase (ALT), rhodanese and arginase were measured in dogs, sheep and cattle with hepatic necrosis induced by the oral administration of carbon tetrachloride. A new method for arginase assay was based on the
Aging is associated with glucose intolerance. Arginase-II (Arg-II), the type-II L-arginine-ureahydrolase, is highly expressed in pancreas. However, its role in regulation of pancreatic β-cell function is not known. Here we show that female (not male) mice deficient in Arg-II (Arg-II-/-) are

Comparative studies on plasma arginase and transaminases in hepatic necrosis.

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Recombinant human arginase toxicity in mice is reduced by citrulline supplementation.

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Human recombinant arginase I cobalt coupled to polyethylene glycol 5000 (HuArg I [Co]-PEG5000) achieved potent in vitro depletion of arginine from tissue culture medium and cytotoxicity to many cancer cell lines. The recombinant enzyme also produced tumor growth inhibition of hepatocellular

Arginase inhibition ameliorates adipose tissue inflammation in mice with diet-induced obesity.

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This study examined whether oral administration of an arginase inhibitor regulates adipose tissue macrophage infiltration and inflammation in mice with high fat diet (HFD)-induced obesity. Male C57BL/6 mice (n = 30) were randomly assigned to control (CTL, n = 10), HFD only (n = 10), and HFD with
Catalase is an antioxidant enzyme that has been shown to inhibit apoptotic or necrotic neuronal death induced by hydrogen peroxide. We report the purification of a contaminating antiapoptotic activity from a commercial bovine liver catalase preparation by following its ability to inhibit apoptosis

EXPERIMENTAL LIVER NECROSIS; I. THE HEXON BASES.

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1. The liver of the dog in which necrosis has been produced by injection of haematoxic immune sera is characterized in the less marked forms by a storing up of nitrogen in the persisting living cells, while in the diffuse forms the total nitrogen content is but slightly above the normal. This last

Increased levels of circulating arginase I in overweight compared to normal weight adolescents.

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OBJECTIVE Overweight and the metabolic syndrome have become major problems, especially in children and adolescents. Obesity at a young age increases the risk for cardiovascular diseases and diabetes mellitus later in life. An early event in the development of cardiovascular disease is endothelial

Aging alters the production of iNOS, arginase and cytokines in murine macrophages.

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The limited amount of information on the primary age-related deficiencies in the innate immune system led us to study the production of inducible nitric oxide synthase (iNOS), arginase, and cytokines in macrophages of young (8 weeks old) and old (72 weeks old) female BALB/c mice. We first evaluated

EXPERIMENTAL LIVER NECROSIS; II. ENZYMES.

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1. The presence of blood serum has a decided inhibitory effect on autolysis. Thus in the normal unwashed organs the non-coagulable nitrogen increase was 100 to 300 per cent., while in the washed it amounted to 450 per cent. The washed necrotic livers showed an increase of from 600 to 850 per cent.,
OBJECTIVE Inflammation plays an important role in atherosclerosis. Arginase I (Arg I) promotes the proliferation of vascular smooth muscle cells; however, the effect of Arg I on inflammation remains unknown. The present study investigated the role of Arg I in inflammation in vitro and in

The influence of L-arginine on the regulation of epidermal arginase.

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Topical preparations containing urea are firmly established in dermatological therapy and nursing care therapy. In addition, urea is frequently used as an inactive ingredient with disinfecting, keratoplastic and penetration-promoting action in topical preparations. Despite good tolerance and ensured

Liver I/R injury is improved by the arginase inhibitor, N(omega)-hydroxy-nor-L-arginine (nor-NOHA).

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Liver ischemia-reperfusion (I/R) injury is associated with profound arginine depletion due to arginase release from injured hepatocytes. The purpose of this study was to determine whether arginase inhibition with N(omega)-hydroxy-nor-l-arginine (nor-NOHA) would increase circulating arginine levels
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