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acidosis/phosphatase
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Pagina 1 a partire dal 278 risultati
[Changes in the serum alkaline phosphatase of sheep and cattle with acute acidosis of the forestomach].
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Experimental acidosis of the forestomach was induced in 6 lambs and 29 ewes and rams, using starch (5-10 g/kg body mass), lactic acid (0.4-0.5 per cent of the live weight) or concentrates (50-60 g/kg body mass). Acidosis occurred spontaneously in 10 calves and 14 cows following the intake of great
Pyruvate dehydrogenase phosphatase deficiency: a cause of congenital chronic lactic acidosis in infancy.
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A male child presented on the first day of life with metabolic acidosis with elevated blood lactate (15 mM), pyruvate (0.4 mM), and free fatty acid (1.3 mM) levels and a blood pH of 7.16. The severity of the acidosis was diminished by intravenous administration of glucose in large doses and by
Automated determination of blood metabolic acidosis, total acid phosphatase, angiotensin converting enzyme, fructosamine and urinary oxalate and citrate on the ABX Pentra 400.
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We have adapted automated assays for quantification of pyruvate (PYR), acetoacetate (AA), and betahydroxybutyrate (BOHB) in plasma, total acid phosphatase (TAP), angiotensin converting enzyme (ACE) and fructosamine (FRUCT) in serum, and oxalate (OXAL) and citrate (CIT) in urine that can be performed
Lactic acidosis due to a defect in the pyruvate dehydrogenase complex: a possible brain pyruvate dehydrogenase phosphatase deficiency.
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Low neutrophil alkaline phosphatase in renal tubular acidosis with hypophosphatemia after toluene sniffing.
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[Changes of leukocytic alkaline phosphatase in acidosis states].
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Renal tubular acidosis, hypokalemia, and acid phosphatase.
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Lanthanum carbonate versus sevelamer hydrochloride: improvement of metabolic acidosis and hyperkalemia in hemodialysis patients.
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Sevelamer hydrochloride (SH) has been reported to aggravate metabolic acidosis and hyperkalemia. This study was performed to evaluate acid-base status and serum potassium changes after replacing SH with lanthanum carbonate (LC) in hemodialysis patients. SH was prescribed for 24 weeks in 14 stable
Acidosis environment promotes osteoclast formation by acting on the last phase of preosteoclast differentiation: a study to elucidate the action points of acidosis and search for putative target molecules.
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Acidosis promoted tartaric acid-resistant acid phosphatase-positive multinuclear cell (TRAP+MNC) or osteoclast formation. Large osteoclast or TRAP+LMNC formation was observed far more in an acidosis environment than in a physiologically neutral environment. One of the major action points of acidosis
Convergent signaling by acidosis and receptor activator of NF-kappaB ligand (RANKL) on the calcium/calcineurin/NFAT pathway in osteoclasts.
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Systemic acidosis has detrimental effects on the skeleton, and local acidosis coincides with bone destruction in inflammatory and metastatic diseases. Acidification dramatically enhances osteoclastic resorption, although the underlying mechanism has remained elusive. We investigated the effect of
Effects of correction of metabolic acidosis on blood urea and bone metabolism in patients with mild to moderate chronic kidney disease: a prospective randomized single blind controlled trial.
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BACKGROUND
There are no controlled trials on the efficacy of oral bicarbonate therapy in patients with mild to moderate chronic kidney disease (CKD). This prospective randomized controlled study was done to evaluate the effects of correction of metabolic acidosis on renal functions and bone
Influence of metabolic acidosis on serum 1,25(OH)2D3 levels in chronic renal failure.
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Metabolic acidosis has been shown to alter vitamin D metabolism. There is also evidence that calcium may modulate 1,25(OH)2D3 by a parathyroid hormone (PTH)-independent mechanism. To investigate the effect of rapid correction of chronic metabolic acidosis on serum 1,25(OH)2D3 levels by free calcium
Acute Lymphoblastic Leukemia Presenting with Liver Infiltration and Severe Lactic Acidosis.
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BACKGROUND Type-B lactic acidosis is a rare complication of solid tumors and hematological malignancies. It occurs secondary to Warburg effect, when glucose metabolism in cancer cells switches from the oxidative pathway to the glycolytic pathway. Malignant lactic acidosis is a life-threatening
Metabolic acidosis in patients receiving anticonvulsants.
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Blood pH, bicarbonate, PCO2, serum calcium, alkaline phosphatase and red cell carbonic anhydrase were measured in 37 selected patients receiving anticonvulsants. Patients with metabolic acidosis showed a high incidence of hypocalcemia with increased alkaline phosphatase and a significant reduction
[Studies on the mechanism of metabolic acidosis observed in the children treated with anticonvulsants].
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Clinical and experimental studies were performed on the mechanisms of metabolic acidosis observed in the children with epilepsy who had long been treated with anticonvulsants such as phenobarbital (PB) or diphenylhydantoin (DPH). The effect of the anticonvulsants was studied on the erythrocyte
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