Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: EC:2.6.1.1 (aspartate aminotransferase)
 21,665 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Recent studies indicate that in animals with marked cardiac hypertrophy, there is depressed function of Ca2+ sequestration by myocardial sarcoplasmic reticulum (SR) because of down regulation of the Ca(2+)-ATPase gene. However, in several animal models we have observed enhancement of myocardial Ca2+ sequestration in response to chronic cardiac stimulation. We tested the hypothesis that in animals with mild cardiac hypertrophy, there is enhanced Ca(2+)-cycling activity by the SR Ca2+ pump and Ca(2+)-release channel. Because creatine kinase activity is consistently decreased in cardiomyopathy, we also determined whether enhanced Ca2+ cycling was accompanied by down regulation or inhibition of the creatine kinase system. Mild cardiac hypertrophy was induced by volume overload; 2% salt was added to the diet of 2-week-old turkey poults for 4 weeks. Compared with age-matched controls, volume overload resulted in 14.3% increase in heart weight and 21.5% increase in heart-to-body weight ratios. The hypertrophied heart had approximately 20% increased activities of the SR Ca2+ pump and the SR Ca2+ channel. Net Ca2+ transport was increased by 16.5%. Compared with controls and in contrast to several other myocardial enzymes, creatine kinase activity was diminished in the hypertrophied hearts by 23% and creatine content was decreased by 8%. Differences between groups were not detected for lactate dehydrogenase, aspartate transaminase, and alanine transaminase. We concluded that an early adaptation of the myocardium undergoing hypertrophy in compensatory response to functional overload is an enhancement of Ca2+ cycling activity by the Ca2+ pump and Ca2+ channel of the SR.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Effects of mild cardiac hypertrophy, induced by volume overload in turkeys, on myocardial sarcoplasmic reticulum calcium-pump and calcium-channel activities and on the creatine kinase system. 165 61

To determine if liver dysfunction in children affects energy and macronutrient homeostasis, we performed 13 metabolic studies in 11 patients (age, 17.8 +/- 5.9 months [mean +/- SEM]) with extrahepatic biliary atresia (EHBA). Nutritional balance, indirect calorimetry, anthropometry, and biochemical liver function tests were utilised. Sixty-four percent of the energy losses were in the form of stool fat. Energy expenditure (68 kcal/kg/d) was 29% higher than normal (P less than 0.0025). Only one third of the metabolisable energy intake (37 kcal/kg/d) was stored in the body for new tissue synthesis. In spite of the bountiful protein intake for age, the increased protein oxidation (2g/kg/d) resulted in a virtually zero mean nitrogen balance. In addition, four patients oxidised endogenous protein as well. The respiratory quotient was 0.96, and did not change significantly between pre- and post-meal measurements, suggesting a predominant utilisation of carbohydrate for energy metabolism. Net lipid oxidation was severely diminished. We found that the higher the serum aspartate aminotransferase level (previously named SGOT), the lower the net fat oxidation, and the higher the conversion of glucose to fat. These data suggest that markedly increased energy expenditure contributes to the malnutrition of patients with EHBA. We characterised for the first time how severe liver disease in infants and children affects carbohydrate, fat, and protein metabolism, thus inducing protein-energy malnutrition.
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PMID:Resting energy expenditure is increased in infants and children with extrahepatic biliary atresia. 273 18

In two feeding experiments fattening bulls received on average a daily supplement of 170 or 200 mg Monensin. In a further 8-week experiment the daily Monensin supplement was 0; 500 or 1 000 mg per day. Ergotropic Monensin supplements (experiments 1 and 2) did not change the blood count and the Ca, P and Mg content of blood serum and the activity of AP, AST and LAP in the serum remained unchanged. Net acid base excretion and the content of Na, K and Mg in urine were not significantly influenced either. The influence of 500 mg Monensin per animal and day on the feed intake of animals previously given lower supplements was insignificant. 1 000 mg Monensin per animal and day resulted in a 40% decrease of feed intake and permanent diarrhoea. It was connected with a diminishing of the glucose content in the blood and an increase of net acid base, Na and P excretion in urine. The blood count did not change after the Monensin overdose. In conclusion one can say that the ergotropic Monensin supplement did not change the metabolism parameters.
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PMID:[The influence of the rumen fermoregulator monensin, on selected parameters of the metabolism of fattening bulls]. 370 55

Pseudoisocytidine (psi ICyd) is a C-nucleoside with enhanced stability and resistance to enzymatic deamination when compared to 5-azacytidine and 1-beta-D-arabinofuranosylcytosine. Elimination kinetics in plasma using [14C]psi ICyd showed a beta-phase for t1/2 for 14C of 2 hr and a beta-phase t1/2 of unchanged psi ICyd of 1.5 hr. Net recovery of radioactivity in urine over 24 hr varied between 40 and 80% of the administered dose; 50 to 90% was unchanged drug and the rest was pseudouridine. Human leukemic cells in vitro deaminated psi ICyd very slowly, formed appreciable quantities of pseudoisocytidine triphosphate, and incorporated small amounts into RNA and DNA. Clinical trials were done using a daily i.v. injection for 5 consecutive days. Hematological or intestine toxicities were not seen, nor was depression of white blood cell count observed in leukemic patients. Hepatic toxicity proved to be dose limiting; this was characterized by an early phase with elevation of prothrombin time and aspartate aminotransferase. A later phase with cirrhosis was observed in two patients. Autopsy showed massive hepatic necrosis in patients dying of acute toxicity and micronodular cirrhosis in one patient dying with the chronic form.
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PMID:Biochemical, pharmacological, and phase I clinical evaluation of pseudoisocytidine. 747 Oct 64

In the JSCC, recommended methods for eight items of enzymes and 9 items of non-enzyme (one item for Na, K, and Cl) have been presented since the recommended methods of activity measurements of AST, ALT, CK, and LD were prepared in 1989. These recommended methods were prepared by placing priority on the actual situation of the measurement methods of those days in Japan, and there are some differences with IFCC recommended methods or primary reference procedures. Recently, from the viewpoint of global standardization, measured values that can be shared with data overseas are required even on clinical exami- nation, and overseas inspection facilities are sometimes used to avoid differences in measurement methods in international clinical trials. With this situation, when the recommended methods of JSCC and IFCC are compared, there are the following differences: - PALP for AST and ALT: not added in JSCC method/ added in IFCC method. - Buffer solution (pH) for LD: EAE (pH 8.8) in JSCC method/ NMG (pH 9.4) in IFCC method. Buffer solution for ALP: EAE in JSCC method/ AMP in IFCC method. Free glycerol for TG: not included on JSCC method/ included in ID-GC/MS method of NIST and CDC. It is necessary to consider from various aspects whether or not these differences affect the implementation of global standardization. In consideration, it is necessary to add the point of how the method should be linked directly to the international traceability of CRMLN (Cholesterol Reference Method Laboratory Net- work) and JCTLM (Joint Committee for Traceability in Laboratory Medicine) to the domestic surveillance and to judge it. [Review].
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PMID:[The Future Topics of Discussion on JSCC Recommended Methods]. 3069 65