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Biomedical subjects

H Somer

Publications and source records attributed to H Somer.

At least 109 records · Page 6Linked to original sources
PubMed1981

Creatine kinase isoenzymes in acute brain injury.

Brain-type creatine kinase (CK) isoenzyme (CK-BB) was detected in the serum in 13 out of 26 patients with acute brain injury (50%). The peak of CK-BB activity ranged from 5 to 188 U/liter, constituting, on average, 10.5% of the total CK activity. The highest activities were seen in patients with gunshot wounds. High CK-BB activity was associated with poor prognosis, but minimal CK-BB elevations did not have prognostic significance. Heart-type creatine kinase isoenzyme (CK-MB) was detected in the serum in 17 out of 26 patients (65%). The peak activity ranged from 5 to 115 U/liter, constituting, on average, 6.6% of total CK activity. Electrocardiogram taken from 20 patients revealed transient T-wave inversions in the precordial leads in four patients; three of them also showed serum CK-MB activity. Subendocardial hemorrhage was detected at autopsy in three of the five CK-MB-positive patients, but in none of the four CK-MB-negative cases. Present findings suggest that acute brain injury may be secondarily cause myocardial damage.

Adolescent↗
PubMed1980

Enzyme release from isolated erythrocytes and lymphocytes in Duchenne muscular dystrophy.

The release of lactate dehydrogenase (LDH) was studied in erythrocytes and lymphocytes from patients with Duchenne muscular dystrophy. Erythrocytes were incubated in Krebs-Ringer with or without 30 mM adenosine and in autologous plasma. There was little release of enzyme in Krebs-Ringer solutions up to 24 h or in autologous plasma up to 48 h, with no statistical difference between Duchenne patients and controls. Addition of 30 mM adenosine reduced the release of LDH in Duchenne erythrocytes at 48 h from 32.4 +/- 5.66% (SE) to 6.2 +/- 1.76% (P < 0.05) and in controls from 38.1 +/- 5.93% to 23.5 +/- 4.63% (n.s.). Lymphocytes incubated in Krebs-Ringer containing 33 mM glucose released LDH faster than Duchenne patients and controls. The adenosine effect could be due to abnormal adenosine uptake (because of a generalized membrane defect) or indicate intrinsic differences in the adenine nucleotide metabolism.

Adolescent↗
PubMed1980

Duchenne carriers: lactate dehydrogenase isoenzyme 5 in serum and muscle.

Only two (5.5%) of 36 possible of known carriers of the gene in Duchenne dystrophy showed increased lactate dehydrogenase isoenzyme 5 (LDH-5) (L/M) in serum, while creatine kinase (CK) was increased in ten (27.8%). LDH-5 and CK did not increase simultaneously; in all five known carriers CK activity was abnormal but LDH-5 was normal. In muscle biopsy, LDH-5 was reduced in patients with Duchenne dystrophy (25.6 +/- 11.5% of total, mean +/- SD; control 59.9 +/- 10.3%; p less than 0.01) and in two of nine possible carriers, but as a group the carriers did not differ from controls: (49.9 +/- 12.1%; p less than 0.05).

Adolescent↗
PubMed1979

Capillary circulation and morphology in Duchenne muscular dystrophy.

Muscle blood flow (MBF) and capillary diffusion capacity (CDC) were determined in 8 patients with Duchenne muscular dystrophy and 5 age-matched control males by measuring the simultaneous clearance of 133Xe and 131I-. MBF was significantly decreased in older patients with severe dystrophy: 35.1 +/- 5.8 ml/100 g/min in 4 advanced Duchenne patients and 45.8 +/- 6.5 ml/100 g/min in controls (p less than 0.005). MBF in 4 early cases did not differ from controls (44.0 +/- 7.9 ml/100 g/min). There was no significant difference in CDC in Duchenne patients and controls. No structural abnormalities in muscle microvasculature were found by light microscopy. In the electron microscope, the Duchenne basement membranes had duplicated or multiple layers of electron-dense material in 63.9% of muscle capillaries while only 6.6% of the control capillaries showed this. These results do not support an ischemic etiology of Duchenne muscular dystrophy.

Adolescent↗
PubMed1979

Erythrocytes in Duchenne dystrophy: osmotic fragility and membrane deformability.

Duchenne erythrocytes showed increased osmotic fragility as compared to controls (p less than 0.01), but individual values overlapped with controls, and only half of the Duchenne erythrocyte values were abnormal. When the effect of the smaller mean corpuscular volume of Duchenne erythrocytes was taken into account, there was no significant difference from controls in membrane deformability, as determined by microsieving or flow channel measurements. The increased osmotic fragility suggests minor changes in erythrocyte membrane properties in Duchenne muscular dystrophy.

Adolescent↗
PubMed1979

Myasthenia gravis and monoclonal IgG gammopathy.

Monoclonal IgG gammopathy of the lambda light-chain type was detected in a 51-year-old woman who had unexplained fever, muscle fatigue, and myalgia. One year later, myasthenia gravis was diagnosed. There was no evidence of myelomatosis or other malignancy. On the assumption that her M-component (gammopathic paraprotein) was related to myasthenia, she was treated with melphalan and cyclophosphamide, but her clinical condition was not improved. Despite therapeutic trials of other agents and a time course of 6 years, the quantity of the M-component remained unchanged. Serum AChR antibody activity was not located in the paraprotein peak. The findings do not support a relationship between the M-component and myasthenia gravis.

Acetylcholine↗
PubMed1979

Inactivation of creatine kinase in physiological saline solutions.

To determine the optimal conditions for measuring the activity of creatine kinase released from isolated skeletal muscle preparations, we investigated the stability of the enzyme during storage in saline solutions of varying composition. Parameters studied were temperature, presence of albumin or dithiothreitol, calcium concentration and anionic composition. It is concluded that maximal activity is retained when samples are kept at 4 degrees C and analyzed within 24 hours in the presence of a thiol-protective compound. If longer storage periods are anticipated, inactivation is significantly retarded by addition of albumin or by decreasing the free calcium concentration of the storage salines.

Animals↗
PubMed1978

A new cause of increased serum aspartate aminotransferase activity.

Two healthy young women had an unexplained persistent elevation of aspartate aminotransferase (ASAT) activity. In both cases electrophoresis of serum ASAT isoenzymes displayed an abnormally moving fraction that comprised the whole serum activity, while liver and muscle revealed the normal cytoplasmic and mitochondrial isoenzymes. In the first case serum ASAT was found to be bound by serum IgG, in the second case the binding protein remained unidentified.

Adult↗
PubMed1978

Heart type creatine kinase isoenzyme (CK MB) in acute cerebral disorders.

Heart type creatine kinase isoenzyme (CK MB) was detected in the serum in 23 out of 53 patients (43%) with acute cerebrovascular, traumatic, or infectious brain damage. Electrocardiogram disclosed abnormalities suggestive of acute myocardial injury in 15 of these 23 patients. Eleven of them also showed increased LD1 activity. Subendocardial haemorrhage was detected in 3 out of 8 necropsied patients with serum CK MB activity. Among those 30 patients in whom no CK MB activity was found electrocardiographic abnormalities suggestive of acute myocardial injury were observed in 2 and increased LD1 was seen in 4 cases. The mortality was higher if either CK MB isoenzyme or electrocardiographic abnormalities suggestive of acute myocardial injury were present, compared with the patients lacking these signs (P less than 0.01). Present findings suggest that acute brain damage may secondarily cause myocardial damage more often than has been believed before. Results also indicate that a combination of acute brain damage and acute myocardial injury often indicated a poor prognosis.

Acute Disease↗
PubMed1977

Brain-type creatine kinase isoenzyme. Occurrence in serum in acute cerebral disorders.

Acute brain damage-cerebrovascular or cardiovascular, traumatic or infectious-released brain-type isoenzyme of creatine kinase (BB-CK) into the circulation within a few hours in 16 of 62 patients (26%). Occurrence of BB-CK was transient in the serum. BB-CK activity was found in the peripheral blood in 13 of 23 patients with diffuse brain damage compared to three of 39 patients with a local cerebrovascular accident (P less than .0005). The mortality of patients having BB-CK in their serum was 63% compared to 39% of those without BB-CK activity in their serum (P less than .05).

Adult↗
PubMed1976

Creatine kinase isoenzymes in neuromuscular diseases.

Determination of the creatine kinase isoenzyme pattern in 62 biopsy samples obtained from patients with neuromuscular disease revealed changes mainly in Duchenne muscular dystrophy. The BB isoenzyme was detected in 10 out of 17 cases with Duchenne muscular dystrophy and the relative amount of MB+BB isoenzyme was significantly increased in this group (P less than 0.005). In serum the MB isoenzyme was detected in all 28 cases with progressive muscular dystrophy and frequently also in other neuromuscular diseases. Among 152 control samples the MB isoenzyme was detected only in 2 cases. It is suggested that the finding of MB isoenzyme in the serum with normal or only slightly elevated total CK activity may be a further proof of neuromuscular disorder, but the finding is not specific for any particular disease.

Adult↗
PubMed1975

Nothing dehydrogenase reaction as an artefact in serum isoenzyme analyses.

A nonspecific staining occurs in serum in isoenzyme methods based on tetrazolium staining reactions. The artefact is pronounced when a large application volume, a prolonged incubation time, distinctly alkaline conditions, or excess of phenazine methosulphate is used. Only phenazine methosulphate and a tetrazolium stain are required for the appearance. Inhibition studies and histochemical staining reactions give evidence that protein-bound sulphydryl groups are responsible for the artefact in serum.

Chloromercuribenzoates↗
PubMed1975

Congenital muscular dystrophy: a clinico-pathological and follow-up study of 15 patients.

Fifteen patients with a presumptive diagnosis of congenital muscular dystrophy were followed for up to 15 years. The diagnosis was based on clinical, enzyme, histological and neurophysiological examinations. The group formed nine per cent of the 160 children suffering from neuromuscular disorders seen at the same hospital during a period of ten years. The muscle weakness was generalized and also involved respiratory muscles and the face. 60 per cent of the children had congenital contractures; these were well amenable to treatment. However, there was a strong tendency for new contractures to form from the second to third year onwards. There were also other signs indicating that the disease process was changing with time. The deep tendon reflexes were present in the beginning but later were usually lost. The serum creatine kinase was raised even to high levels in the first one to two years and gradually sank to normal or near normal values. The histopathological findings changed with time from relatively slight changes compatible with a muscle destroying process to inactive type lesions characterized by fibrotic and particularly adipose tissue replacing muscle fibres. On the basis of these findings it can be assumed that the active disease process is at its height during intrauterine and early postnatal life and then wanes leaving an outburnt or cicatrical state in which new contractures easily develop causing possible deterioration with time. Active treatment is thus of great importance both to overcome neonatal contractures and to prevent new ones to develop.

Adolescent↗
PubMed1975

Brain creatine kinase in blood after acute brain injury.

Severe cold injury of the brain increased significantly both total creatine kinase and the corresponding brain isoenzyme (CKBB) activity in confluens sinuum samples. CKBB could be detected also in peripheral blood a few hours after severe brain injury in eight of 12 patients. Finding of CKBB in human plasma may prove a useful indicator of severe brain injury.

Animals↗