Search PubMed⌕ Search

Biomedical subjects

J Engel

Publications and source records attributed to J Engel.

At least 559 records · Page 31Linked to original sources

Human cytoplasmic actin proteins are encoded by a multigene family.

We characterized nine human actin genes that we isolated (Engel et al., Proc. Natl. Acad. Sci. U.S.A. 78:4674-4678, 1981) from a library of cloned human DNA. Measurements of the thermal stability of hybrids formed between each cloned actin gene and alpha-, beta-, and gamma-actin mRNA demonstrated that only one of the clones is most homologous to sarcomeric actin mRNA, whereas the remaining eight clones are most homologous to cytoplasmic actin mRNA. By the following criteria we show that these nine clones represent nine different actin gene loci rather than different alleles or different parts of a single gene: (i) the restriction enzyme maps of the coding regions are dissimilar; (ii) each clone contains sufficient coding region to encode all or most of an entire actin gene; and (iii) each clone contains sequences homologous to both the 5' and 3' ends of the coding region of a cloned chicken beta-actin cDNA. We conclude, therefore, that the human cytoplasmic actin proteins are encoded by a multigene family.

Actins↗

Osteoarthritis of the trapezio-metacarpal joint. Results of treatment with a silicone cap implant.

The results of surgical treatment for arthritis of the first carpometacarpal joint using Kessler's silicone implant were examined in a group of 23 patients. The mean follow-up period was 24 months. Pain relief was obtained in 18 patients (78 per cent), functional improvement in daily activities in 16 patients, and power of pinch and power of grasp were improved in 10 out of 13 patients. Limitation of abduction complicated surgery in 6 patients. A high incidence of subluxation was found without correlation to the subjective results. Most of our patients were satisfied with the functional end results.

Adult↗

Recent developments in the diagnosis and therapy of epilepsy.

Recent advances in the diagnosis of epilepsy include the development of a clinically useful classification of epileptic seizures and the recognition of specific epileptic disorders. These advances have been aided by the advent of x-ray computed tomography, long-term electroencephalographic telemetry, and video monitoring. Techniques for functional imaging of the human brain promise even greater diagnostic capabilities. New antiepileptic drugs have improved medical management, and technical and theoretical advances in pharmacokinetics have permitted physicians to design balanced dosing for individual patients. Although currently underused, surgical treatment of partial complex epilepsy can be safe and effective when used appropriately. Operant conditioning of electroencephalography may become another practical alternative therapy. Contributions of basic research to understanding the complications of status epilepticus have influenced treatment protocols and greatly improved the prognosis of this potentially lethal condition.

Anticonvulsants↗

The effect of chronic ethanol administration on lipids and fatty acids in subcellular fractions of rat brain.

In this study we have investigated the proportion of lipids and of fatty acids in brain membranes and blood serum from rats which received ethanol over a long period. Nine Sprague-Dawley rats were given ethanol in their drinking water for five months. Nine age-matched rats given pure water served as controls. Subcellular fractions (myelin, synaptosomes and mitochondria) were prepared in a discontinuous gradient of sucrose from each of the 18 rats. Blood serum was collected at decapitation. The fractions were assayed for their concentrations of protein, cholesterol, phospholipids and for the proportions of fatty acids in individual phosphoglycerides. No significant differences in the concentration of the major lipids were obtained between the ethanol-exposed rats and the control rats. In the synaptosomal fraction from ethanol-exposed rats, the proportion of oleic acid in phosphatidylcholine was increased and that of arachidonic acid in phosphatidylethanolamine decreased. These two fatty acids were also changed in the blood serum and there was a significant correlation between the changes in the brain and blood serum. The results suggest that during ethanol exposure there is an increased disposition toward modification of synaptosomal membranes by changes in the blood plasma fatty acid pattern.

Animals↗

The regulation of striatal DOPA synthesis by alpha 2-adrenoreceptors.

The administration of alpha 2-adrenoreceptor antagonists SKF 64139 or SKF 72223 (TIQ derivatives) elicits an increase in striatal DOPA synthesis. The findings that the enhanced DOPA synthesis is reversed by pretreatment of the animals with clonidine or with the D beta H inhibitor FLA-63 suggest that action of the TIQ derivatives is related to their ability to block alpha-adrenoreceptors. It is being postulated that the enhanced striatal DOPA synthesis elicited by the TIQ derivatives is a result of inhibition of dopaminergic neurotransmission.

Adrenergic beta-Antagonists↗

[The tourniquet].

Explore the source record for details and available documents.

Tourniquets↗

Symphalangism with multiple anomalies of the hands and feet: a new genetic trait.

We report a new autosomal dominant condition involving hands and feet of an Arabic father and 5 of his 11 children. This trait is characterized by symphalangism, syndactyly, brachydactyly type D, clinodactyly, and hypoplasia of the thenar and hypothenar eminences. Affected persons had symphalangism and syndactyly plus some or all or part of the other anomalies. Symphalangism, the main defect in this syndrome, showed variable expressivity. A distinct dermatoglyphic pattern was observed in all affected relatives. Linkage studies were done; however, no linkage was demonstrated.

Adult↗

Correlation of criteria used for localizing epileptic foci in patients considered for surgical therapy of epilepsy.

Criteria for anterior temporal lobectomy, performed on seven patients with partial complex seizures, were derived from a battery of fourteen presurgical tests. Seven tests were routine studies aimed at identifying a focus of epileptic excitability, while seven were designed to reveal areas of focal functional deficit. Conflicting information was frequently obtained from the tests of epileptic excitability, suggesting that it is probably inaccurate to view patients with partial complex seizures as having a single epileptogenic focus. Presurgical evaluation must therefore be aimed at identifying the focus most responsible for the patient's habitual seizures. Tests of focal functional deficit provided useful nonconflicting confirmatory information in each of the seven patients studied. The most reliable information was obtained from depth electrode implantation, and this procedure should be considered essential except when all evidence of surface-recorded epileptic excitability, including ictal onset, and evidence of focal functional deficit agree.

Adult↗

Effects of propranolol on the locomotor stimulation induced by activation of postsynaptic catecholamine receptors.

The present study was undertaken in order to clarify the possible involvement of a central beta-adrenoceptor mediated action on the stimulation of locomotor activity by the dopamine agonist apomorphine and the noradrenergic agonist clonidine. The effect of pretreatment with various doses of d-and dl-propranolol on apomorphine- and apomorphine plus clonidine-induced locomotor stimulation in reserpinized mice was measured in photocell activity chambers. Pretreatment with dl-propranolol prolonged the duration of apomorphine-induced locomotor stimulation without affecting the maximal level of activity. A similar tendency was seen after pretreatment with the d-form of propranolol, which has a much lower beta-receptor blocking activity. The potentiation by clonidine of the apomorphine-induced locomotor stimulation in reserpinized mice was dose-dependently reduced by pretreatment with dl-propranolol whereas d-propranolol was found to be ineffective. The results indicate that central beta-receptor mechanisms might be involved in the apomorphine plus clonidine-induced locomotor stimulation of reserpinized mice.

Animals↗

The effect of lithium on the locomotor stimulation induced by dependence-producing drugs.

The present study was performed to investigate how lithium affects locomotor stimulation induced by dependence-producing drugs such as amphetamine, ethanol and morphine. Acute lithium alone was found to suppress exploratory hyperactivity in mice without affecting basal locomotor activity, further supporting the contention that lithium has a neurolept-like behavioural profile. Acute lithium pretreatment suppressed locomotor stimulation in mice induced by all the dependence-producing drugs in a dose-dependent manner. Locomotor stimulation seen after amphetamine and ethanol appeared to be more suppressed by lithium than that seen after morphine. Taken together with the finding that lithium had no effect on apomorphine-clonidine-induced locomotor stimulation after elimination of presynaptic activity the present data suggest that the suppressive effect of lithium is mediated via presynaptic catecholaminergic mechanisms.

Amphetamine↗

The effect of catecholamine receptor antagonists on ethanol-induced locomotor stimulation.

The effect of various catecholamine receptor antagonists, which differ in their potency to block central dopamine and noradrenaline receptors, respectively, on ethanol-induced locomotor stimulation was investigated. It was shown that small doses of both specific dopamine (pimozide, haloperidol) and noradrenaline (phenoxybenzamine, yohimbine) receptor blocking agents statistically significantly suppressed the ethanol-induced locomotor stimulation. Of special interest in this study was the observation that remarkably small doses of clozapine completely antagonized the ethanol-induced locomotor stimulation. The possibility that this effect of clozapine is mediated via its interference with the activity of central noradrenaline and/or GABA neurons is discussed.

Adrenergic alpha-Antagonists↗

Neuronal firing patterns during the spread of an occipital lobe seizure to the temporal lobes in man.

Neuronal recordings from occipital cortex and hippocampus during a seizure originating in the occipital lobe of a patient with an occipito-temporal tumor demonstrated that the visual aura resulted from neuronal activation of medial peristriate and possibly other occipital lobe neurons while the psychomotor automatisms followed 10-20 sec later and were caused by recruitment of hippocampal neurons bilaterally. This confirmed that the complex seizure symptoms were caused by propagation from an occipital lobe focus. The psychomotor symptoms have not recurred for the 6 months since interruption of occipito-temporal connections; however, the spared medial occipital neurons still produce visual auras.

Astrocytoma↗