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)

Total creatine kinase measurement in serum has remained the best overall marker for detection and monitoring of skeletal muscle diseases, despite that different human tissues exhibit varying distributions of cytoplasmic and mitochondrial isoenzymes of creatine kinase. Acute myocardial infarction aside, increases in total serum creatine kinase, as reflected by the MM isoenzyme, are most commonly caused by injury or diseases to striated muscle. Enzyme markers of skeletal muscle injury that have been previously used (eg, aldolase, enolase, aspartate aminotransferase, and lactate dehydrogenase isoenzyme 5) are not as specific as creatine kinase and have limited clinical utility. However, new enzyme and protein markers are currently being investigated, eg, troponin and carbonic anhydrase III, which are more specific than creatine kinase toward particular tissues. Moreover, measurement of creatine kinase isoforms may provide information about whether muscle turnover is acute or chronic.
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PMID:Clinical applications of muscle enzymes and proteins. 145 75

Total serum protein, serum albumin, total urine protein excretion, and the serum activity of several enzymes--aldolase (ALS), cholinesterase (CHS), leucine aminopeptidase (LAP), isocitrate dehydrogenase (ICD), aspartate aminotransferase (AST), alanine aminotransferase (ALT), lactate dehydrogenase (LDH), alpha-hydroxybutyrate dehydrogenase (HBD), creatine kinase (CK), alkaline phosphatase (ALP), and gamma-glutamyl transferase (GGT)--were estimated in rats with nephrotic syndrome (NS) at 2, 4, 6, 8, 10, 12, 16, 20, and 30 days after a single injection of puromycin aminonucleoside (PAN). It was found that: (a) total serum protein and serum albumin diminished on day 4 and returned to control values on days 20 and 30, respectively; (b) total urine protein excretion rose on day 4, reached a peak value on day 8, and then fell substantially but still remained higher than control values on day 30; (c) ALS and CHS activities increased; (d) LAP, ICD, and AST activities showed a biphasic pattern, first increasing and then decreasing; (e) ALT, LDH, HBD, CK, and ALP activities decreased; and (f) GGT activity remained unchanged. The differences in the profiles of the enzyme activities suggest their independent regulation in experimental NS induced by PAN.
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PMID:Activity of serum enzymes in puromycin aminonucleoside-induced nephrotic syndrome. 146 3

In recent years, captopril has attracted considerable clinical attention as an agent for use in treating heart failure. We administered 15 mg/kg of captopril or 1.5 mg/kg of enalapril to 5-week-old J-2-N cardiomyopathic hamsters for 10 or 15 weeks, and investigated the roles of the renin-angiotensin-aldosterone and kallikrein-kinin systems in the onset and progress of cardiomyopathy. In the untreated group, serum creatine kinase levels increased in accordance with the progression of cardiomyopathy, but this increase was markedly inhibited by the administration of captopril. The rise in serum aldolase levels was similarly inhibited. Serum malondialdehyde levels were significantly reduced by the administration of captopril. ECG findings and the ventricular myosin isoenzyme pattern were also markedly improved by captopril. The improvement in all these parameters was less with enalapril. These differences between captopril and enalapril suggest that increases in tissue bradykinin and vasodilatory prostaglandins may play an important role in the beneficial effects of captopril.
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PMID:The effects of angiotensin converting enzyme inhibitors and the role of the renin-angiotensin-aldosterone system in J-2-N cardiomyopathic hamsters. 153 90

The association of glycolytic enzymes with the particulate fraction of the cell was assessed in the brain of the freshwater turtle, Pseudemys scripta elegans, using three different methodologies. Each method showed that a large percentage of each of eight enzymes was bound in brain. The effect of environmental anoxia (5 or 20 h submergence in N2-bubbled water at 7 degrees C) on the distribution of enzymes between free and bound states was analyzed. All three techniques showed a significant increase in the percentages of brain aldolase and glyceraldehyde-3-phosphate dehydrogenase bound during anoxia and no change in lactate dehydrogenase or creatine kinase binding. Two methodologies also showed an increase in the percent bound during anoxia for hexokinase, phosphofructokinase, and phosphoglycerate kinase. An increased association of glycolytic enzymes with structural elements of the cell during anoxia may physically position the glycolytic pathway to facilitate coupling between this ATP-generating pathway and ATP-utilizing processes, such as membrane ion pumps.
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PMID:Subcellular enzyme binding and the regulation of glycolysis in anoxic turtle brain. 153 98

Postmortem biochemical indices may provide a useful adjunct to morphological studies in the identification of antemortem brain insult. We studied 34 routine medico-legal cases categorising them into one of four diagnostic groups. There were 11 cases of head trauma, 7 of 'hypoxia' (3 hangings and 4 carbon monoxide or drug poisonings), 7 sudden cardiac deaths and 9 miscellaneous cases. Survival time and postmortem interval was known for each case. The degree of cranio-cerebral trauma was graded. Cerebro-spinal fluid (CSF) and vitreous humour were analysed for calcium, glucose, total proteins, aldolase, aspartate transaminase (AST), alanine transaminase (ALT), gamma glutamyltransferase (GGT), lactate dehydrogenase (LDH), creatine kinase (CK) and creatine kinase BB isoenzyme (CK-BB). CK-BB was also measured in superior vena cava serum. In CSF there was a significant correlation between the severity of cranio-cerebral trauma and levels of aldolase, CK-BB, AST, ALT and total proteins. CSF CK-BB, median units/l (range), for the groupings of head trauma, hypoxia, sudden cardiac death and miscellaneous were respectively 823 (2-3431); 96 (2-187); 4 (2-25); 5 (1-69). Corresponding serum CK-BB levels were 240 (28-322); 390 (26-411); 180 (20-482); 79 (18-530).
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PMID:Efficacy of cerebro-spinal fluid biochemistry in the diagnosis of brain insult. 160 50

We reported a 40-year-old male with adult-onset nemaline myopathy (adult-onset rod disease) showing muscular hypertrophy of distal limbs. At the age of 25, he noticed thinness of his thighs. Difficulty in climbing stairs slowly progressed from the age of 35. On admission neurological examination revealed muscular weakness and atrophy of proximal limbs and hypertrophy of distal flexors. Normal laboratory tests included serum creatine kinase, myoglobin, aldolase and pyruvate. Electromyography revealed severe neurogenic changes in the right biceps brachial muscle and the right quadriceps muscle, and moderate changes in the right gastrocnemius. Biopsy specimen of the deltoid muscle demonstrated type 1 fiber predominance and type 1 fiber atrophy, and there was small group atrophy and type grouping. Abundant nemaline rods were found mainly in type 1 fibers (81.5%). In order to evaluate hypertrophy of calf muscles, T1-weighted MRI of lower extremity was performed. While transaxial images through mid thigh showed moderate fatty replacement, increased volume and little fatty replacement were found in the mid calf. Therefore, hypertrophy of the calf muscle seemed to be compensative hypertrophy. But in this case neurogenic factors were indicated electromyographically and histologically. These findings may advocate the notion that neurogenic factors involved not only congenital but adult-onset rod disease.
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PMID:[A case of adult-onset nemaline myopathy (adult-onset rod disease) with distal muscular hypertrophy]. 165 78

Didemnin B (NSC 325,319), a cyclic depsipeptide isolated from a Caribbean tunicate, exhibits potent preclinical antitumor activity. In previous phase I studies, 3.47 mg/m2 was the maximally tolerated dose, with nausea and vomiting being the dose-limiting toxicity. The drug was given in a single bolus infusion over 30 min every 28 days. In the current study, 30 patients presenting with previously treated non-small-cell lung cancer (NSCLC) received 46 courses of the drug at doses ranging from 3.47 to 9.1 mg/m2. Neuromuscular toxicity was dose-limiting. Nausea and vomiting appeared to be correlated with dose levels and were ameliorated by a combination of antiemetics including dexamethasone. Other side effects included a mild rise in hepatic enzymes and an allergic reaction that was preventable by the addition of corticosteroids to the premedication regimen. In all, 2 minor responses were seen among 24 evaluable patients. Because neuromuscular toxicity is dose-limiting, we recommend that routine measurements of creatine kinase and aldolase, a careful neurologic evaluation, and electromyography and muscle biopsy (if indicated) be incorporated into phase II trials. The recommended dose for phase II studies using a single bolus schedule is 6.3 mg/m2, following the premedication of patients with antiemetics.
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PMID:Phase I/II clinical trial of didemnin B in non-small-cell lung cancer: neuromuscular toxicity is dose-limiting. 166 19

A fasciitis-sclerodermia-eosinophilia syndrome developed in four female patients, aged between 55 and 75 years, after the ingestion of tryptophan, 1.5-6.0 g daily, for 13 months to 7 years. It began characteristically with hard oedema of the limbs, sometimes also of the trunk. Later there occurred diffuse indurations of the body surface with fixation of the skin to fascial planes. This was associated with mainly sensory peripheral neuropathy. Three of the patients had an eosinophilia (12-30%). Histological examination revealed a cell-poor fasciitis, fibrosis of the cutis and subcutis, perimyositis and epidermal atrophy of varying degree. Erythrocyte sedimentation rate was at most slightly increased. Antinuclear antibodies were demonstrated in one patient (1:80). Serum aldolase concentration was raised (3.4-5.4 U/l), while creatine kinase was normal. The disease progressed even after tryptophan was discontinued, in only one patient there was improvement during glucocorticoid treatment. In two cases the skin induration regressed slowly after administration of methotrexate (15 mg weekly) and hydroxychloroquine (400 mg daily).
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PMID:[Tryptophan-induced fasciitis-scleroderma-eosinophilia syndrome]. 186 Apr 21

Generalized komuragaeri disease (Satoyoshi disease) is a rare disorder of unknown etiology, characterized by painful muscle spasms, alopecia, diarrhea and various endocrine disorders. We administered glucocorticoid to a girl with this disease, resulting in a marked improvement of all clinical features. The patient was a 15-year-old girl. Since the age of 13 years, she had had intermittent painful muscle spasms, which affected any skeletal muscles 5 to 15 times a day at exercise and at rest and lasted for a few minutes. At the age of 14 years, she had idiopathic thrombocytopenic purpura which responded to the glucocorticoid treatment. Amenorrhea and orthostatic hypotension developed at the age of 14 years. Then the loss of body and head hair was noticed and progressed slowly. She had not experienced severe diarrhea. On admission, her physical and neurological examinations showed no abnormalities except for the thin hair and frequent muscle spasms. Laboratory examinations showed elevated levels of serum creatine kinase and aldolase, positive antinuclear antibody of speckled pattern and a mild disturbance in carbohydrate absorption. Endocrinological tests suggested the dysfunction of hypothalamus as a cause of amenorrhea. Electromyogram showed large action potentials on spasms. She was treated with glucocorticoid, 2 mg/kg on alternate days. The muscle spasms decreased gradually in frequency and duration in 1 month of treatment, and disappeared in 4 months. The growth of her hair was noticed and orthostatic hypotension disappeared in 4 months. Menstruation became regular in 7 months. The muscle spasms worsened when the dosage of glucocorticoid was reduced, and they improved on the increased dosage. She was free of symptoms at 6 months after the successful diminution of glucocorticoid. The etiology of this disease has not been revealed. The association of autoimmune disorders and the responsiveness of all clinical features to glucocorticoid suggest that an autoimmune process is involved in the pathogenesis of generalized komuragaeri disease.
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PMID:[A case of generalized komuragaeri disease (Satoyoshi disease) treated with glucocorticoid]. 204 11

The purpose of the present study was to investigate the effects of 8 months of a specific and controlled sprint training programme on three groups of young athletes (two groups of males and one of females). Biopsies of vastus lateralis were taken before and after the period of training. The type percentage and diameter of the fibres, as well as the glycogen content and the activities of the enzymes of glycogen metabolism (glycogen synthase and glycogen phosphorylase), glycolysis (phosphofructokinase, pyruvate kinase, aldolase and lactate dehydrogenase), oxidative metabolism (succinate dehydrogenase) and creatine kinase and aminotransferases were studied. The results show an increase in the percentage of type I fibres and an increase in the diameter of both fibre types. A significant increase was also observed in glycogen content, and in the activities of glycogen synthase, glycogen phosphorylase, phosphofructokinase, pyruvate kinase, succinate dehydrogenase, aspartate aminotransferase and alanine aminotransferase. We conclude that a long period of sprint training induces a biochemical muscle adaptation to anaerobic exercise. This metabolic adaptation is followed by a morphological adaptation, although this is probably not as specific as the biochemical one.
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PMID:Biochemical and histochemical adaptation to sprint training in young athletes. 208 3


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