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Biomedical subjects

T L Munsat

Publications and source records attributed to T L Munsat.

At least 91 records · Page 5Linked to original sources
PubMed1983

Plasmapheresis with immunosuppression in amyotrophic lateral sclerosis.

Four patients with amyotrophic lateral sclerosis and one with progressive muscular atrophy were treated with large-volume plasmapheresis combined with immunosuppression. Assessment of muscle strength and functional ability was performed during a period of time ranging from 6.2 to 13 months. Patients were compared with a clinically matched control group. Both treated and untreated patients continued to show similar deterioration. The results of this study failed to show any therapeutic benefit of plasmapheresis with immunosuppression in patients with amyotrophic lateral sclerosis.

Amyotrophic Lateral Sclerosis↗
PubMed1982

Familial granulovacuolar lobular myopathy with electrical myotonia.

We report 3 patients with a myopathy characterized by profound selective muscle wasting and weakness, electrical myotonia without clinical myotonia and an unusual muscle biopsy. Cryostat sections showed muscle fibers with vacuoles containing hematoxylinophilic granules, and 30% of type I fibers showed demarcation of their sarcoplasm into "lobules" due apparently to reorganization of myofibrillar elements. The electrical myotonia suggests an underlying muscle membrane defect. Two of the patients are siblings suggesting that the disorder may be inherited.

Adult↗
PubMed1982

Familial myoadenylate deaminase deficiency and exertional myalgia.

In 14 members of four families with a hereditary syndrome of exertional myalgia, five of eight muscle biopsies from symptomatic individuals showed histochemical and biochemical absence of myoadenylate deaminase (MADA). In the others, MADA biochemical activity was normal in two and reduced but not absent (intermediate level) in one. Asymptomatic relatives had normal histochemical MADA activity, but three had intermediate biochemical levels. In a survey of 302 routine muscle biopsies, 3 of 36 patient with myalgia had absence of MADA. Three of 266 biopsied for other conditions were MADA-deficient. Despite some inconsistencies, MADA deficiency seems to be relevant to this clinical syndrome.

AMP Deaminase↗
PubMed1981

Retrograde axonal transport of lead in rat sciatic nerve.

A wavelike pattern of retrograde axonal transport of lead was demonstrated in rat sciatic nerve after injection of 203Pb into the triceps surae muscle. The transport rate was about 10 mm per day, and the lead reached the spinal cord by 9 days after injection. The distribution of lead within the spinal cord indicated the possibility of retrograde axonal transport in the upper and lower motor neurons, which might explain how lead enters the central nervous system and could be related to the postulated role of lead in causing amyotrophic lateral sclerosis. Lead may be useful in investigating retrograde transport experimentally.

Animals↗
PubMed1980

Prolonged ethanol consumption produces persistent alterations of cholinergic function in rat brain.

Prolonged ethanol consumption produces neuropathology and neurologic symptoms in humans and experimental animals. As a means of understanding the central nervous system (CNS) consequences of ethanol abuse, we sought whether cholinergic neurochemical functions were altered by long-term ethanol consumption by rats. Eighteen weeks of ethanol consumption in a liquid diet reduced rat striatal and mammillary body choline acetylase (ChAT) by 53% and 58%, respectively. In these same regions, the density of muscarinic cholinergic receptors was elevated 117% and 12%. No such alterations were observed in cortex or in hippocampus. No alterations followed short-term ethanol consumption (2 wk), but they persisted after ethanol withdrawal (4 wk). After 13 mo of ethanol consumption, the number of neuroleptic binding sites in striatum was diminished by 29%. These results demonstrate a persistent, possibly permanent, alteration in brain cholinergic function as a consequence of long-term ethanol ingestion. Since brain acetylcholine is involved in numerous neurologic functions, including memory processes, these findings may be relevant to the lasting memory disorder and other permanent effects associated with chronic alcoholism.

Alcoholism↗
PubMed1980

The effects of acute and chronic ethanol administration on twitch and tetanic force production by rat gastrocnemius muscle in situ.

The effects of acute ethanol injection on force production were measured in normal and chronic alcoholic rats. Acutely injected normal rats, acutely injected chronic alcoholic rats, and noninjected chronic alcoholic rats were compared with control groups: normal nonalcoholic rats and a dietetically deprived control group. Acute ethanol injection increased twitch force in normal rats but not in chronic alcoholic rats. Chronic alcohol ingestion caused a decrease in maximal twitch and tetanic tension. The dietetically deprived control group developed less maximal tetanic force, with no significant decrease in maximal twitch force. Chronic alcohol ingestion seemed to decrease maximal twitch tension, whereas the decrease in maximal tetanic could be attributed to the effects of malnutrition.

Alcoholism↗
PubMed1979

Identification of direct competition for, and indirect influences on, striatal muscarinic cholinergic receptors: in vivo [3H]quinuclidinyl benzilate binding in rats.

[3H]Quinuclidinyl benzilate (QNB) binds to specific muscarinic receptors of rat striatum, in vivo. The binding is saturable and displaceable by muscarinic drugs. Clozapine and thioridazine are unique antipsychotic agents with low liability for extrapyramidal side-effects, and both displaced ONB, while several other neuroleptics did not. In addition to this apparent direct competition for cholinergic receptors, morphine and amphetamine increased ONB binding by indirect influences on muscarinic receptors. In vivo QNB binding not only confirms in vitro findings, but it also detects indirect, probably transsynaptic, alterations of muscarinic cholinergic receptor dynamics.

Animals↗
PubMed1977

Programmed feeding as a model of chronic alcoholism in the rat.

Programmed-feeding polydipsia results in a reliable model of chronic alcoholism in the rat. High oral ethanol comsumption and a predictable withdrawal reaction associated with audiogenic seizures are produced. The maintenance of high blood ethanol levels for three weeks in 18 male Charles River rats was associated with audiogenic seizures after 6 or 8 hours of withdrawal. These chronic alcoholic rats had enhanced blood clearance of ethanol. The cerebral cortical crude mitochondrial fraction showed a decrease in total and magnesium-dependent adenosine triphosphatase activity in alcoholic and control (water-fed) rats compared with normal rats.

Adenosine Triphosphatases↗
PubMed1977

Serum creatine phosphokinase levels and prednisone treated muscle weakness.

Evidence is cited from the literature and from personal experience with the "inflammatory" form of facioscapulohumeral syndrome that the creatine phosphokinase reduction occurring during pharmacologic treatment of various neuromuscular diseases does not necessarily imply therapeutic benefit.

Adolescent↗
PubMed1977

Experimental serotonin myopathy.

One hundred and eight Wistar rats were injected with serotonin (20 mg per kilogram of body weight intraperitoneally) or imipramine hydrochloride (20 mg per kilogram intraperitoneally), or both, in a single cycle or in multiple (up to 18 weeks) weekly cycles. In contrast to previous reports, a characteristic myopathy was produced with serotonin alone, identical to that produced by serotonin and imipramine in combination. Imipramine alone produced no significant change. The myopathy produced was characterized by (1) preferential damage to myofibers with high oxidative capacity (types I and IIA), (2) prominent regenerative activity occurring as early as 48 hours, and (3) degeneratio of capillary endothelium (thickening, vacuolar degeneration, proliferation of marginal folds, dissolution of mitochondria). Small groups of degenerating fibers and increased connective tissue were not observed. There was no loss of myofibers or fat replacement. The changes suggested repeated acute insults followed the complete recovery. These observations suggest that although the pathogenesis of serotonin and serotonin-imipramine myopathy is primarily ischemic, it is not a satisfactory model of human Duchenne muscular dystrophy.

Animals↗
PubMed1976

Effects of nerve stimulation on human muscle.

A phasic program of femoral nerve stimulation was used to reduce refractory knee flexion contractures in five patients. In one, rectus femoris was tenotomized before starting stimulation to reduce hip flexion contracture. Muscle biopsies were performed before and after 5 to 12 weeks of intermittent stimulation at separated sites on the same muscle. In the four patients where muscle contraction was isometric, type I fibers increased 3.7%, 6.4%, 48.4%, anand 30.4%, respectively. Both fiber types in each patient showed an increase in size ( p less than .001). In the tenotomized muscle, where contraction was isotonic at a shortened length, the proportion of type I fibers decreased from 40.2% to 25.4%, and their mean diameter also decreased (p less than .001). These observations suggest that the physical conditions of contraction may be more important than the pattern of neuronal discharge in determining the metabolic profile of human muscle fibers.

Axons↗
PubMed1976

Dominant inheritance of McArdle syndrome.

Myophosphorylase deficiency (McArdle syndrome) is an uncommon condition characterized by exercise intolerance, muscle cramping, and myoglobinuria. Although the original report by McArdle dealt with a sporadic case, subsequent cases reported in the literature show high familial incidence and consanguinity, implying that the defect is transmitted as a rare recessive gene or a possible sex-limited mode of inheritance. The present report describes the clinical, histoenzymatic, and biochemical findings in a 40-year-old woman with myophosphorylase deficiency. The family history reveals that four other members are also affected: an older sister, a younger brother, a 10-year-old son, and her 75-year-old mother, and possibly her maternal grandmother. Because of this particular pattern of direct transmission in this family, a dominant inheritance is postulated.

Adolescent↗