isoleucine/edema

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Evaluation of (1-sarcosine, 8-isoleucine) angiotensin II as a therapeutic agent for oleic acid-induced pulmonary edema.

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(1-Sarcosine, 8-isoleucine) angiotensin II was assessed as a therapeutic agent for acute respiratory distress syndrome with oleic acid pulmonary edema in sheep used as an experimental model. Under general anesthesia with controlled mechanical ventilation with 100% oxygen, 32 sheep received oleic

Metabolomic analysis of the plasma of patients with high-altitude pulmonary edema (HAPE) using 1H NMR.

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Upon rapid ascent to a high altitude, non-acclimatized individuals, although healthy, are highly prone to contracting high-altitude pulmonary edema (HAPE). Early diagnosis is difficult and there is no reliable biomarker available. We used proton ((1)H) NMR metabolomics to profile the altered

Revealing anti-inflammation mechanism of water-extract and oil of forsythiae fructus on carrageenan-Induced edema rats by serum metabolomics.

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Forsythiae Fructus is an important Chinese medicine which shows a significant effect against inflammation. This study aimed to investigate the preventive anti-inflammation mechanism of Forsythiae Fructus by serum metabolomics strategy and compare the difference of the metabolism pathways between

Role of ammonia in the pathogenesis of brain edema.

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The role of hyperammonemia in the pathogenesis of cerebral edema was investigated using mongrel dogs to develop a treatment for cerebral edema in acute hepatic failure. Intravenous infusion of ammonium acetate alone into dogs did not induce brain edema, although blood ammonia reached

Metabolic findings on 3T 1H-MR spectroscopy in peritumoral brain edema.

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OBJECTIVE Little is known about the metabolic properties of brain edema associated with tumors. This work was conducted on the basis of the assumption that, in the presence of intra-axial and extra-axial brain tumors, the white matter involved by the edema is a site of metabolic change that involves

Using a Caesalpinia echinata Lam. protease inhibitor as a tool for studying the roles of neutrophil elastase, cathepsin G and proteinase 3 in pulmonary edema.

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Acute lung injury (ALI) is characterized by neutrophil infiltration and the release of proteases, mainly elastase (NE), cathepsin G (Cat G) and proteinase 3 (PR3), which can be controlled by specific endogenous inhibitors. However, inhibitors of these proteases have been isolated from different

L-ornithine-L-aspartate lowers plasma and cerebrospinal fluid ammonia and prevents brain edema in rats with acute liver failure.

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Brain edema sufficient to cause intracranial hypertension and brain herniation remains a major cause of mortality in acute liver failure (ALF). Studies in experimental animal models of ALF suggest a role for ammonia in the pathogenesis of both encephalopathy and brain edema in this condition. As

Identification of the antivasopermeability effect of pigment epithelium-derived factor and its active site.

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Vascular permeability plays a key role in a wide array of life-threatening and sight-threatening diseases. Vascular endothelial growth factor can increase vascular permeability. Using a model system for nonproliferative diabetic retinopathy, we found that pigment epithelium-derived factor (PEDF)

A profile of amino acid and catecholamine levels during endotoxin-induced acute lung injury in sheep: searching for potential markers of the acute respiratory distress syndrome.

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The identification of plasma markers of the course of the acute respiratory distress syndrome (ARDS) is needed to improve its treatment and to further advance the development of new therapeutic agents. The status of markers of lung injury in ARDS is reviewed and some new potential markers are

Protease-activated receptor 2 and bradykinin-mediated vasodilation in the cerebral arteries of stroke-prone rats.

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Protease-activated receptor 2 (PAR(2)) expression is up-regulated during vascular injury associated with edema. PAR(2) and bradykinin subtype 2 receptor (B(2)) expression and function were assessed in relation to hypertensive encephalopathy (HE) and cerebral hemorrhage (CH) in middle cerebral

Heterogeneity of hemoglobin gamma chains in normal newborns and in cases of alpha and beta thalassemia.

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The ratio of Ggamma to Agamma was studied in 13 normal healthy newborns and in eight neonates with hydrops fetalis due to homozygous alpha-thalassemia. The findings in the normal healthy newborns agreed with those of earlier reports. In homozygous alpha-thalassemia the Ggamma and Agamma ratio

Apoptotic signaling pathways induced by acute administration of branched-chain amino acids in an animal model of maple syrup urine disease.

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Maple Syrup Urine Disease (MSUD) is an inborn error of metabolism caused by a deficiency of the branched-chain α-keto acid dehydrogenase complex activity. This blockage leads to accumulation of the branched-chain amino acids leucine, isoleucine and valine, as well as their corresponding α-keto acids

Quantification of branched-chain amino acids in blood spots and plasma by liquid chromatography tandem mass spectrometry for the diagnosis of maple syrup urine disease.

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Individuals with maple syrup urine disease (MSUD) have an inherited metabolic disorder resulting in a deficiency in the branched-chain keto-acid dehydrogenase complex. As a result, these individuals have elevated concentrations of the branched-chain amino acids valine, isoluecine, allo-isoleucine,

Posttraumatic dental implant placement in a patient with maple syrup urine disease.

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Maple syrup urine disease (MSUD) is an inborn error of metabolism resulting from a defect in the oxidation of the branched-chain amino acids leucine, isoleucine, and valine. Patients present in early infancy with brain edema; delay in diagnosis and treatment is common and associated with residual

Cerebral computed tomography in maple syrup urine disease.

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Maple syrup urine disease (MSUD) is an inherited metabolic disorder due to decreased decarboxylation of branched chain keto acids triggering an accumulation of leucine, isoleucine, and valine. We describe two infants with biochemically confirmed MSUD in whom computed tomography (CT) revealed

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