Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: EC:4.1.2.13 (aldolase)
3,461 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

A 39-year-old female with several past psychiatric hospitalization for schizophrenia was admitted to our hospital because of severe pain and swelling of her legs. A few days before onset, she had often sat down upon her heels in water closet, agitated and talking to herself for many hours. Two days before the admission, she had suffered from severe pain and swelling of her bilateral calf-muscles, and her urine became brownish. On admission, neurological findings revealed delirious state, moderate rigidity of limbs, hyporeflexia of legs, marked swelling and severe spontaneous pain in bilateral legs. She was afebrile with body temperature of 36.4 degrees C. Laboratory data showed marked increase of levels of serum CK to 163,000 U/1, myoglobin to 9,860 ng/ml and aldolase to 42.8 IU/1, and the diagnosis of rhabdomyolysis was made. Although she fell into acute renal failure, the renal function recovered after repeated hemodialysis. Several days after admission, swelling and pain of calf-muscles began to improve, and serum CK, myoglobin and aldolase decreased rapidly. One month later, she was able to walk on her own legs. In the literature, rhabdomyolysis associated with immobile posture caused by schizophrenia is extremely rare, and this is the first case reported in Japan. The relationship between rhabdomyolysis and schizophrenia was discussed.
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PMID:[A case of rhabdomyolysis following long time immobile posture caused by schizophrenia]. 259 45

To evaluate the participation of proteins derived from mitochondrial genes in the adaptive response of skeletal muscle to increased contractile activity, we administered chloramphenicol (CAP; 200-1,000 mg.kg-1.day-1), an inhibitor of translation from mitochondrial ribosomes, to adult rabbits undergoing electrical stimulation of the tibialis anterior muscle of one hind limb. In unmedicated animals, 10 days of electrical stimulation increased maximum velocity (Vmax) of cytochrome oxidase and citrate synthase by 214 +/- 17 and 201 +/- 16% (P less than 0.01). In a dose-dependent manner, CAP abolished activity-induced increases in cytochrome oxidase Vmax, suggesting that augmented mitochondrial protein synthesis is necessary for the adaptive response of enzymes that require protein subunits encoded by mitochondrial genes. However, CAP failed to inhibit activity-induced changes in Vmax of enzymes derived exclusively from nuclear genes (citrate synthase and aldolase). CAP also failed to inhibit activity-induced increases in mRNA transcribed from the nuclear genes encoding beta-F1 ATPase or myoglobin, or from the mitochondrial genes encoding 12S rRNA, 16S rRNA, or cytochrome b. These latter findings suggest that mitochondrial translation products do not participate in pretranslational regulation of these nuclear or mitochondrial genes in response to changes in contractile activity of skeletal muscle.
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PMID:Effects of inhibition of mitochondrial protein synthesis in skeletal muscle. 289 13

We report the clinical and laboratory characteristics of measles infection in an unselected group of 461 young adults. Otitis media was diagnosed in 9.8%, sinusitis in 4.1%, pneumonia in 3.7%, and keratitis in 3.3% of the patients. Minor T-wave changes on electrocardiogram were observed in only 0.7% and jaundice in 0.4%. Elevated liver enzymes were found in 51% of the patients. Creatine kinase (CK) MM fraction was high in 44%. Traces of myoglobin were found in the urine of 14% of those with a high CK, and of the 13 patients with the higher CKs, 12 had an abnormal serum aldolase. We emphasize several points of interest in this large and unselected group of young adults. There was 1) possible evidence of rhabdomyolisis in some of our patients; 2) a lower rate of electrocardiogram abnormalities than previously reported; 3) no evident correlation between initial laboratory values and subsequent complications; and 4) lack of a clinical or laboratory difference between patients who had been vaccinated with an attenuated virus during childhood and those who had not.
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PMID:An outbreak of measles among young adults. Clinical and laboratory features in 461 patients. 337 86

Plasma indicators of muscle cell leakage and of hemolysis were studied in 23 runners before and after a marathon race. Blood samples were drawn from an antecubital vein the morning before the race (baseline), at 3 p.m., i.e., 2 h before the start, on arrival, 12 and 36 h, and 7 days later. Compared with the baseline values, the plasma creatinine phosphokinase MM and MB subfractions, aldolase and glutamicoxaloacetic transaminase activity were increased immediately after the race, rose further 12 h after the marathon, and remained elevated the race, rose further 12 h after the marathon, and remained elevated 36 h and 7 days later. The plasma lactate dehydrogenase activity and myoglobin concentration were increased on arrival and returned to the pre-race activity 7 days after the marathon. Compared with the pre-race values, the plasma haptoglobin concentration was decreased immediately and 12 h after the marathon. Our data show that indicators of muscle cell leakage and of hemolysis in plasma, withdrawn after a marathon race, remained elevated for up to 7 days after the race.
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PMID:Indicators of cell breakdown in plasma of men during and after a marathon race. 338 15

Three cases of Crohn's disease (CD) which showed an elevation of creatine phosphokinase (CPK) during the course were reported. In two cases, elevations of serum myoglobin and aldolase were also observed which indicated rhabdomyolysis. Rhabdomyolysis occurred unrelated to the activity of CD and it was asymptomatic. It was unable to identify an apparent known cause for rhabdomyolysis. All three cases were under elemental diet (ED) but the causality of ED for rhabdomyolysis was uncertain. So far as we know, there is no report on rhabdomyolysis during ED treatment and there are only two reports in which rhabdomyolysis was documented in CD. The latter was rhabdomyolysis due to electrolyte depletion secondary to malabsorption in CD which was not encountered in our cases. Our department dealt only three cases of CD and all of them had an elevation of CPK which had been measured as one of routine blood chemistry in our hospital. These observations led to a following conclusion that subclinical rhabdomyolysis may be one of extra-intestinal complications of CD.
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PMID:Rhabdomyolysis associated with Crohn's disease. 362 67

We studied the behaviour of serum myoglobin and of serum enzymes in 25 young men, before and after physical stress. The stress appeared to markedly increase myoglobin, aldolase and CK activity and to a lesser extent GOT. Myoglobin, aldolase return to normal levels within 24 hours but CK appeared to decrease more slowly. The simultaneous determination of some organic-specific enzymes (CK-MB, gamma-GT, GPT) permitted us to state that the myocardium and liver are not involved in the increase of tests following muscular stress.
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PMID:[Variations in serum myoglobin due to physical exertion]. 613 26

Some experimental and clinical studies were done from the metabolic viewpoint to elucidate the characteristics of myonephropathic-metabolic syndrome. In experimental dogs with their femoral arteries ligated and two third of femoral muscles divided, aldolase and myoglobin showed remarkable increase without significant changes in electrolytes. Slight increase of GPT and GOT was observed. Amino acids showed elevation in urea, taurin, leucin, isoleucin, valine, threonine, 3-methylhistidine, phenylalanine, histidine, lysine, methionine, tyrosine and anserin and decrease in glutamine, alanine, glycine, proline, carnosine, citrullin and arginine. In patients with acute arterial occlusion, potassium, GOT, LDH, CPK, lactate and pyruvate increased moderately and myoglobin showed remarkable increase and aldolase slight increase. Amino acids showed remarkable increase in 3-methylhistidine and beta-amino-isobutyric acid and moderate increase in phenylalanine and arginine. These results revealed that measurement of free amino acid concentration, especially that of methylhistidine as well as myoglobin, pyruvate, lactate and some other enzymes might be of great help to predict the prognosis of patients with acute arterial occlusion of the extremities.
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PMID:[Metabolic study on acute arterial occlusion of the extremities]. 667 89

We investigated the use of PCR primers designed to conserved exons within nuclear DNA to amplify potentially variable regions such as introns or hypervariable exons from a wide range of species. We then explored various approaches to assay population-level variation in these PCR products. Primers designed to amplify regions within the histone H2AF, myoglobin, MHC DQA, and aldolase (ALD) genes gave clean amplifications in diverse mammals (DQA), and in birds, reptiles and mammals (aldolase, H2AF, myoglobin). The sequenced PCR products generally, but not always, confirmed that the correct locus had been amplified. Several primer sets produced smaller size fragments consistent with preferential amplification of intronless pseudogenes; this was confirmed by sequencing seal and reptile H2AF PCR products. Digestion with randomly selected four-base recognizing enzymes detected variation in some cases but not in others. In species/gene combinations with either low (e.g. seal H2AF, ALD-A) or high (e.g. skink ALD-1) nucleotide diversity it was more efficient to sequence a small number of distantly related individuals (e.g. one per geographic population) and from these data to identify informative or potentially informative restriction enzymes for 'targeted' digestion. We conclude that for studies of population-level variation, the optimal approach is to use a battery of primers for initial PCR of both mtDNA and scnDNA loci, select those that give clean amplifications, and sequence one sample from each population to (i) confirm gene identity, (ii) estimate the amount of variation and, (iii) search for diagnostic restriction sites. This will allow determination of the most efficient approach for a large-scale study.
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PMID:Rapid assessment of single-copy nuclear DNA variation in diverse species. 790 60

A 22-year-old man developed transient unconsciousness during running. He developed fever, nausea, vomiting, diarrhea and general fatigue. Next day, he was admitted to National Hospital Nayoro because of high serum CK level of 13,610U/l. Biochemical analyses revealed elevated serum myoglobin, increased CK-MM isozyme, aldolase and lactate dehydrogenase, increased serum osmolality, increased uric acid, and decreased serum potassium levels. Therefore, he was diagnosed as having rhabdomyolysis. In addition, serum CK-MB isozyme, cardiac myosin light chain I and troponin T were increased, suggesting the damage of cardiac muscle. Electrocardiogram showed elevated ST segment and inverted T on V2-4, which were not observed previously. He had no preceding infectious disease, drug ingestion or an underlying metabolic disorder. The rhabdomyolysis may be precipitated by the superimposition of dehydration and loss of potassium due to diarrhea and vomiting. The myocardial injury, probably produced by transient myocardial ischemia, should be paid attention in case of rhabdomyolysis.
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PMID:[A case of rhabdomyolysis complicated with myocardial injury]. 856 47

Oral L-carnitine has been reported to lower the elevated serum myoglobin of renal failure in chronic peritoneal dialysis patients, and intravenous L-carnitine can improve muscle fatigue and cramps in chronic hemodialysis patients. In this study oral L-carnitine, 1.98 g/day, was administered to 6 chronic hemodialysis patients for 8 weeks. Serum levels of myoglobin, creatine kinase, and aldolase, as well as skeletal muscle symptoms (cramps during dialysis, fatigue, and weakness) were monitored biweekly for 12 weeks. Mean baseline serum myoglobin level was 337 +/- 34 ng/mL. By 6 and 8 weeks mean serum myoglobin was 234 +/- 39 and 233 +/- 40 ng/mL, significantly lower by the Friedman test (p < 0.05). Four weeks after carnitine was discontinued, mean serum myoglobin had risen to 320 +/- 118 ng/mL. Serum creatine kinase and aldolase levels were normal throughout the study. All 6 patients noted improvement in muscular symptoms, with maximal effect at 8 weeks, although 2 patients did not improve until 2 to 4 weeks after carnitine was stopped. We conclude that oral L-carnitine may lower serum myoglobin and improve muscle cramps and weakness in hemodialysis patients. The maximal effect of carnitine on myoglobin occurs 2 weeks before the maximal improvement in muscular symptoms.
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PMID:Effect of oral L-carnitine on serum myoglobin in hemodialysis patients. 882 May 5


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