Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0011570 (depression)
 172,036 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

To determine whether the development of cardiomyopathies is associated with alterations in creatine kinase function, the functional properties of cardiac contractile apparatus and mitochondria were studied in two different models of cardiomyopathies, the Syrian hamster (hereditary dilated cardiomyopathy, strain UM-X7.1, 200 days old) and the diabetic rat (4-6 weeks after injection of streptozotocin) using ventricular skinned fibers. After Triton X-100 treatment, the hereditary cardiomyopathic fibers demonstrated decreased maximal calcium-activated tension and unchanged calcium sensitivity, whereas fibers from diabetic hearts exhibited unchanged maximal tension and increased calcium sensitivity, when compared with their respective controls. In both cases myofibrillar creatine kinase appeared unchanged. The functional properties of total tissue mitochondria were evaluated using saponin-skinned fibers. Coupling between oxidation and phosphorylation was not altered in cardiomyopathies. Respiration rate (per unit of tissue dry weight) was normal in hereditary cardiomyopathy but was considerably lower in diabetic fibers compared with control fibers. In both models of cardiomyopathies, creatine-stimulated respiration was significantly lower than in controls, thus indicating the depression of functional activity of mitochondrial creatine kinase.
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PMID:Creatine kinase and mechanical and mitochondrial functions in hereditary and diabetic cardiomyopathies. 191 31

Nineteen cases are described, including 12 cases from three different families and 7 nonfamilial cases, in which multisystem neurological disease was associated with acanthocytosis in peripheral blood and normal plasma lipoproteins. Mild acanthocytosis can easily be overlooked, and scanning electron microscopy may be helpful. Some neurologically asymptomatic relatives with significant acanthocytosis were identified during family screening, including some who were clinically affected. The mean age of onset was 32 (range 8-62) yrs and the clinical course was usually progressive but there was marked phenotypic variation. Cognitive impairment, psychiatric features and organic personality change occurred in over half the cases, and more than one-third had seizures. Orofaciolingual involuntary movements and pseudobulbar disturbance commonly caused dysphagia and dysarthria that was sometimes severe, but biting of the lips or tongue was rarely seen. Chorea was seen in almost all symptomatic cases but dystonia, tics, involuntary vocalizations and akinetic-rigid features also occurred. Two cases had no movement disorder at all. Computerized tomography often demonstrated cerebral atrophy. Caudate atrophy was seen less commonly, and nonspecific focal and symmetric signal abnormalities from the caudate or lentiform nuclei were seen by magnetic resonance imaging in 3 out of 4 cases. Depression or absence of tendon reflexes was noted in 13 cases and neurophysiological abnormalities often indicated an axonal neuropathy. Sural nerve biopsies from 3 cases showed evidence of a chronic axonal neuropathy with prominent regenerative activity, predominantly affecting the large diameter myelinated fibres. Serum creatine kinase activity was increased in 11 cases but without clinical evidence of a myopathy. Postmortem neuropathological examination in 1 case revealed extensive neuronal loss and gliosis affecting the corpus striatum, pallidum, and the substantia nigra, especially the pars reticulata. The cerebral cortex appeared spared and the spinal cord showed no evidence of anterior horn cell loss. Two examples of the McLeod phenotype, an X-linked abnormality of expression of Kell blood group antigens, were identified in a single family and included 1 female. The genetics of neuroacanthocytosis are unclear and probably heterogeneous, but the available pedigree data and the association with the McLeod phenotype suggest that there may be a locus for this disorder on the short arm of the X chromosome.
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PMID:Neuroacanthocytosis. A clinical, haematological and pathological study of 19 cases. 199 79

The impact of restricted zinc availability on myoblast differentiation was investigated. Lack of zinc prevented myoblast fusion and the increase in muscle-specific creatine kinase activity. The depression of activity of creatine kinase in the zinc-deficient cultures was accompanied by a similar decrease in the concentration of creatine kinase mRNA and was apparent even when fusion of the myoblasts was inhibited by cytochalasin B. Thus zinc appears to be necessary for the expression of creatine kinase during myoblast differentiation.
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PMID:Inhibition of myoblast differentiation by lack of zinc. 203 64

The clinical features of acute non-Q wave myocardial infarction (NQMI) with R wave regression and no ST segment depression are distinct from those of acute Q wave myocardial infarction (QMI). NQMI patients showed ST segment elevation at admission, and significantly earlier regression of the ST segment elevation and appearance of coronary T waves were observed compared to QMI patients. In addition to the significantly lower level of mean peak serum creatine kinase activity and the significantly lower incidence of pump failure during the acute phase, the incidences of in-hospital mortality and multivessel disease were significantly lower in the NQMI patients. With respect to acute-phase coronary angiographic features within 48 h after the onset, the rate of spontaneous opening of infarct-related vessels was significantly higher in the NQMI patients. Thirteen of the 19 NQMI patients responded to urokinase infusion. These facts suggest that transient, intermittent or incomplete obstruction may favor this type of NQMI over QMI, and that thrombus might be an important factor in the pathogenesis of this type of NQMI.
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PMID:Coronary angiographic features within 48 hours from onset of non-Q wave myocardial infarction with R wave regression and no ST segment depression. 211 28

Reperfusion of rabbit hearts after 15 min of global ischemia at 37 degrees C depressed developed pressure by 36% (myocardial stunning). Changes in myofilament function were investigated as causes of this depression. Kinetic analysis of the effects of stunning on myofibrillar catalyzed ATP hydrolysis showed that stunning lowered Michaelis constant (Km) slightly and left maximal enzyme reaction velocity unaltered in the stunned myofilaments. The myofilament end of the creatine kinase (CK) shuttle was also found to be unaffected in the stunned myofibrils. The Km ADP for myofibrillar CK from control and stunned hearts was 60.45 +/- 3.45 and 68.04 +/- 2.42 microM, respectively, and the CK activity at 100 microM ADP was 0.63 +/- 0.08 and 0.67 +/- 0.04 IU/mg myofibrillar protein from control and stunned hearts, a rate three times greater than the myofibrillar adenosinetriphosphatase (ATPase) rate and a rate sufficient to deliver ATP to the myofilaments. Myofilament Ca2+ sensitivity was assessed by measuring Ca2(+)-dependent myofibrillar Mg2(+)-ATPase activity at free [Ca2+] ranging from 10 nM to 32 microM and [Mg.ATP] of 0.8, 1.6, and 3.2 mM. The sensitivity of myofilaments to activation by Ca2+ was unaltered in the myofibrils isolated from stunned hearts. It is concluded from these analyses that the depression of pressure development observed in stunned hearts is not due to a defect in myofilament function.
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PMID:Effect of global myocardial stunning on Ca2(+)-sensitive myofibrillar ATPase activity and creatine kinase kinetics. 214 2

2,4-D, an extensively used herbicide, was intentionally ingested by a 61-year-old woman. An initial serum 2,4-D concentration of 392 mg/L was measured. The prominent clinical feature was marked central nervous system depression; primary laboratory abnormalities were extreme elevation of creatine kinase activity, and transitory elevation of AST and lactate dehydrogenase enzyme activities. Alkaline diuresis was initiated early and decreased the half-life of the drug from an initial 39.5 to 2.7h. It is concluded that alkaline diuresis to produce urine pH in the range of 7.5 to 8.5 should be considered in the management of an overdose patient with central nervous system depression and a history of 2,4-D ingestion.
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PMID:Clinical presentation and management of acute 2,4-D oral ingestion. 232 26

This study tested the hypothesis that membrane transport is the major biochemical system of the myocardium altered in furazolidone-induced cardiomyopathy (round heart disease), before the development of myocardial failure, and that metabolic enzymes and contractile proteins are less affected. Compared with controls, maximal percentage depression of activities of myocardium from furazolidone-treated birds were 40 for creatine kinase, 30 for glycolysis, 30 for glycogen, 20 for myofibrils, 20 for Krebs's cycle enzymes, 15 for fatty acid oxidation and 10 for total soluble protein. Sodium and potassium transport, antioxidant system activity, myosin, myosin isoenzyme patterns and amino acid aminotransferases were unaffected. In marked contrast, the calcium-transport ATPase activity of the sarcoplasmic reticulum had undergone a 60 per cent compensatory increase in activity. The pattern of biochemical changes observed is consistent with a role of ischaemia in the pathogenesis of round heart disease and indicates that calcium transport by the sarcoplasmic reticulum is the major biochemical system affected.
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PMID:Myocardial biochemical changes in furazolidone-induced cardiomyopathy of turkeys. 232 37

The effect of isosorbide dinitrate (ISDN) spray on release of the isoenzyme creatine kinase-MB (CK-MB) after myocardial ischemia induced by atrial pacing was evaluated in 8 patients with coronary artery disease. Atrial pacing to ischemia (ST-segment depression of greater than or equal to 1.5 mm for greater than or equal to 80 ms) resulted in elevation of CK-MB levels in plasma drawn from the coronary sinus, from 1.8 +/- 1.5 to 6.8 +/- 7.0 ng/ml (p less than 0.001) at 30 minutes after onset of ischemia. When atrial pacing was repeated at the same rate after 1 squirt of ISDN spray, 1.25 mg, the CK-MB levels were not altered despite significant ischemic ST-segment depression. It is concluded that ISDN prevents the process responsible for myocardial release of CK-MB, being either micronecroses or a reversible consequence of ischemia.
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PMID:Prevention of creatine kinase-MB release in coronary artery disease and pacing-induced myocardial ischemia by isosorbide dinitrate spray. 234 14

The present study was undertaken to elucidate the possible effects of tanshinone VI, one of the extracts from the root of Salvia, on post-hypoxic recovery of cardiac contractile force. For this purpose, rat hearts were perfused for 45 min under reoxygenated conditions following 20-min hypoxic perfusion, and changes in tissue high-energy phosphates and calcium contents, and release of ATP metabolites and creatine kinase were examined. Post-hypoxic recovery of cardiac contractile force was augmented when hearts were treated with 42 nM tanshinone VI during hypoxia. This beneficial recovery was accompanied by enhanced restoration of myocardial high-energy phosphates, depression of hypoxia- and reoxygenation-induced increase in tissue calcium content, and suppression of release of ATP metabolites such as adenosine, inosine and hypoxanthine from the perfused heart. The results suggest that tanshinone VI is beneficial for the recovery of cardiac contractility after a certain period of oxygen-deficiency, possibly through mechanisms involving improvement of myocardial energy production upon oxygen-replenishment and/or inhibition of calcium accumulation in the cardiac cell.
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PMID:Beneficial effect of tan-shen, an extract from the root of Salvia, on post-hypoxic recovery of cardiac contractile force. 239 Jan 9

Inclusion body myositis (IBM) was suspected on light microscopic grounds in 48 of 170 consecutive patients with inflammatory myopathies. One or more vacuoles containing membranous material, groups of atrophic fibres, and an autoaggressive endomysial inflammatory exudate occurred in 100, 96 and 92% of the muscle specimens. All three of these features were present in 88% of the specimens. Electron microscopy confirmed the presence of filamentous inclusions in 40 of 43 patients. The inclusions are typically near vacuoles and a minimum of three vacuolated fibres must be scrutinized to detect them with confidence. There is no electromyographic pattern that can reliably distinguish IBM from other inflammatory myopathies. The typical clinical features in the patients diagnosed by histological criteria as IBM were: insidious onset after age 50 yrs with painless, proximal lower extremity weakness; slow but relentless progression with selectively severe involvement of quadriceps, iliopsoas, tibialis anterior, biceps and triceps muscles; relatively early depression of the knee reflexes; and a normal or mildly elevated serum creatine kinase level. The male: female ratio was 3:1. Distal weakness occurred in about 50%, but only in 35% was it as great or greater than proximal weakness. Significant associated illnesses include other autoimmune disorders (15%), diabetes mellitus (20%), and diffuse peripheral neuropathy (18%). Prednisone treatment at dose levels frequently effective in polymyositis failed to prevent disease progression in those patients observed for 2 or more years. Our findings support the notion that IBM is a distinct entity in which a set of pathological features is associated with a constellation of clinical findings.
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PMID:Inclusion body myositis. Observations in 40 patients. 254 78


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