uremia/protease

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Enzyme cytochemistry of rat organs after uremia with special reference to proteases.

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Wistar rat organs and tissues were investigated after acute and chronic uremia using enzyme cytochemical means whereby special attention was paid to plasma membrane and lysosomal proteases. Heart muscle, pancreas, spleen, stomach, duodenum, jejunum, colon and skeletal muscle did not show any

Increased plasma glycosidase and protease activity in uraemia: possible role in the aetiology of the anaemia of chronic renal failure.

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We have measured plasma N-acetyl-beta-D-glucosaminidase (EC 3.2.1.30) and neuraminidase (EC 3.2.1.18) activities as markers of glycosidase activity and immunoreactive trypsin (EC 3.4.21.4) levels as a marker of proteolytic potential in the plasma of normal and uraemic subjects. The levels of all of

Signals regulating accelerated muscle protein catabolism in uremia.

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In chronic renal failure (CRF), the ATP-dependent, ubiquitin-proteasome proteolytic pathway is activated with concurrent increases in the transcription of genes encoding proteins of this pathway in muscle. We have shown that the stimuli for these responses include acidosis and glucocorticoids, but

Calpain is activated in experimental uremia: is calpain a mediator of uremia-induced myocardial injury?

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BACKGROUND The cysteine proteases calpain and caspase-3 are known mediators of cell death. The aim of this study was to assess their contribution to the tissue damage found in experimental uremia. METHODS Calpain and caspase-3 activities were measured in the hearts of rats that were sham-operated

Plasma and platelet von Willebrand factor defects in uremia.

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OBJECTIVE Several mechanisms have been proposed to explain the prolonged bleeding times and clinical bleeding in chronic renal failure. Recent evidence has implicated an abnormality in the structure or function of the von Willebrand factor or in its interaction with uremic platelets. We investigated

Mechanisms for protein catabolism in uremia: metabolic acidosis and activation of proteolytic pathways.

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Accelerated protein catabolism in uremia occurs in animals and patients with acute (ARF) and chronic renal failure (CRF). Possible causes include resistance to both insulin-induced inhibition of protein-degradation and insulin-induced stimulation of protein synthesis. The mechanisms for these

Increased platelet phosphatidylserine exposure and caspase activation in chronic uremia.

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Platelet activation is associated with exposure of the aminophospholipid phosphatidylserine (PS) to the outer hemi-leaflet of the plasma membrane bilayer, which seems to be involved in the coagulation process. Because platelet activation may occur in patients suffering from chronic uremia, which is

Chronic ethanol ingestion enhances catabolism and muscle protease activity in acutely uremic rats.

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Skeletal muscle wasting in men as well as enhanced urea production in animals due to ethanol consumption has been demonstrated by numerous authors. Furthermore, the outcome of acute renal failure is closely related to the extent of catabolism. The present study was performed to investigate whether

Mechanisms that cause protein and amino acid catabolism in uremia.

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Anorexia and/or a protein- and calorie-restricted diet can cause protein wasting by limiting the intake of essential amino acids (EAA) and, hence, protein synthesis. By this mechanism plus the effects of inadequate calories, restricted diets could contribute to the loss of lean body mass of uremic

Inhibitor of marrow thymidine incorporation from sera of patients with uremia.

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A low-molecular-weight fraction of serum samples from 14 patients with uremia inhibited tritiated thymidine incorporation (18 +/- 2%) by cultured rabbit marrow whereas an identical fraction from nonazotemic subjects did not. A similar effect on ferrous 59 incorporation into heme was observed. A

Role of proteases in hypercatabolic patients with renal failure.

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Proteolytic enzymes exist in plasma ultrafiltrates, concentrated dialysates, and urine fractions of patients with posttraumatic acute renal failure (ARF), as well as in urine fractions of patients with nephrotic syndrome and in concentrated dialysates of patients or routine dialysis therapy (RDT).

Effect of acute uremia on protein degradation and amino acid release in the rat hemicorpus.

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Protein synthesis and degradation and net uptake and release of amino acids and minerals were investigated in the perfused hemicorpus of acutely uremic and sham-operated control Sprague-Dawley rats. Rats underwent bilateral nephrectomy or sham surgery and were studied 30 hours after surgery. The

Salmon spawning migration and muscle protein metabolism: the August Krogh principle at work.

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The August Krogh principle, stating that for any particular question in biology, nature holds an ideal study system, was applied by choosing the anorexic, long-distance migration of salmon as a model to analyze protein degradation and amino acid metabolism. Reexamining an original study done over 20

ADAMTS-13 deficiency following Hemiscorpius lepturus scorpion sting.

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Hemiscorpius lepturus is a lethal scorpion with potentially cytotoxic venom. Various degrees of local and systemic toxicity have been observed after its envenomation ranging from local erythema to disseminated intravascular coagulation, renal failure and severe pulmonary hemorrhage. In this case

A possible mechanism of immunoregulation produced by alpha 2-macroglobulin.

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Most of the plasma suppressive activity was associated with alpha 2M in both normal subjects and cancer patients. alpha 2M binding to physiological levels of proteases was associated with an increase in the ability to suppress lymphocyte reactivity in the TEEM test. alpha 2M binding to proteases

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