disaccharide/edema

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Generalized morphea with vascular involvement. A case report and disaccharide analysis of the skin glycosaminoglycans.

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We report a 69-year-old man with severe generalized morphea, who showed over 80% of skin involvement, while the internal organs were not affected. We performed histological examinations and analysis of skin disaccharides constituting chondroitinase-digestible glycosaminoglycans in the center and

Structural analysis, molecular docking and molecular dynamics of an edematogenic lectin from Centrolobium microchaete seeds.

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Lectins represent a class of proteins or glycoproteins capable of reversibly binding to carbohydrates. Seed lectins from the Dalbergieae tribe (Leguminosae) have structural variability, carbohydrate specificity, and biological effects, such as inflammation, vasorelaxation and cancer antigen binding.

Effects of trehalose in preservation of canine lung for transplants.

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The effect of trehalose, a non-reducing disaccharide which stabilizes and protects membranes, in the preservation of canine lungs was examined when Euro-Collins solution was basically used as a preservant. In group I, five lungs were perfused and preserved in an Euro-Collins solution modified by

Regulation of MI transport in retinal pigment epithelium by sugars, amiloride, and pH gradients: potential impairment of pump-leak balance in diabetic maculopathy.

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Impairment of transport and metabolism of retinal pigment epithelium (RPE) has been recognized to play a role in the development of diabetic macular edema. To understand the mechanism(s) of action of high glucose levels in alteration of RPE metabolism, primary cultures of RPE cells were used as an

A structure-activity relationship for induction of meningeal inflammation by muramyl peptides.

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Components of bacterial peptidoglycans have potent biological activities, including adjuvant effects, cytotoxicity, and induction of sleep. Mixtures of peptidoglycan components also induce inflammation in the lung, subarachnoid space, and joint, but the structural requirements for activity are

Hepatic encephalopathy. Metabolic consequence of cirrhosis often is reversible.

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Hepatic encephalopathy is a well-recognized clinical complication of chronic liver disease. About 30% of patients with cirrhosis die in hepatic coma. Hepatic encephalopathy can occur in patients with fulminant liver disease without evidence of portal-systemic shunting. These patients have increased

Hepatic encephalopathy: nomenclature, pathogenesis and treatment.

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Hepatic encephalopathy (HE) is a neuropsychiatric syndrome in patients with liver failure and/or a portal-systemic bypass. Since 2002 a new nomenclature of HE exists, that classifies HE in encephalopathy type A (associated with acute liver failure), type B (associated with portal-systemic bypass),

A computational study of the oligosaccharide binding sites in the lectin-like domain of Tumor Necrosis Factor and the TNF-derived TIP peptide.

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The lectin-like domain of Tumor Necrosis Factor (TNF), mimicked by the TIP peptide, activates amiloride-sensitive sodium uptake in type II alveolar epithelial cells and as such increases alveolar liquid clearance in dysfunctional lungs. This protective effect is blunted upon mutation of residues

Increased sulfatation of orbital glycosaminoglycans in Graves' ophthalmopathy.

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Accumulation of interstitial glycosaminoglycans (GAG) in orbital tissue of patients with Graves' ophthalmopathy (GO) leads to edema, increased orbital pressure, and proptosis. In this study, a new, highly sensitive, high performance liquid chromatography method was developed to determine the altered

New management options for end-stage chronic liver disease and acute liver failure: potential for pediatric patients.

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The management of children with end-stage chronic liver disease and acute liver failure mandates a multidisciplinary approach and intense monitoring. In recent years, considerable progress has been made in developing specific and supportive medical measures, but studies and publications have mainly

Pathophysiology and management of hepatic encephalopathy 2014 update: Ammonia toxicity and hyponatremia.

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Hyperammonemia is a major factor involved in the pathogenesis of hepatic encephalopathy (HE). Ammonia elicits astrocyte swelling and causes brain edema. In addition, hyponatremia, a condition frequently observed in hepatic cirrhosis, also exacerbates brain edema, potentially becoming a factor that

Pathophysiology of hepatic encephalopathy: a new look at ammonia.

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Results of neuropathologic, spectroscopic, and neurochemical studies continue to confirm a major role for ammonia in the pathogenesis of the central nervous system complications of both acute and chronic liver failure. Damage to astrocytes characterized by cell swelling (acute liver failure) or

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