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Biomedical subjects

J V Martin

Publications and source records attributed to J V Martin.

17 recordsLinked to original sources
PubMed1992

Characterization of the hypnotic effects of triazolam microinjections into the medial preoptic area.

We have previously reported that microinjections of the benzodiazepine hypnotic triazolam into the medial preoptic area (MPA) of the hypothalamus enhance sleep in rats. The present study further characterizes this effect, by examining its anatomical specificity, determining whether it is mediated by interaction with central benzodiazepine receptors, and assessing whether sleep induction is associated with changes in core temperature. It was found that microinjections of 0.25 and 0.5 micrograms triazolam into two nearby structures, the lateral preoptic area and diagonal band of Broca, failed to alter sleep. Total sleep time was enhanced by microinjection of triazolam into the MPA, and this effect was blocked by co-administration of the benzodiazepine receptor blocker RO 15-1788. Sleep enhancement by triazolam was not associated with significant alterations in core body temperature. These observations continue to suggest that the MPA may be a site which mediates the hypnotic effect of triazolam, and add to the growing body of data emphasizing the importance of hypothalamic function in the regulation of sleep and waking.

Body Temperature↗
PubMed1992

Purification and characterization of iotrochotin, a novel toxin from the Caribbean sponge Iotrochota birotulata, which selectively permeabilizes synaptosomes.

A protein termed iotrochotin (IOT) was isolated from the exudate of the Caribbean sponge Iotrochota birotulata using as an assay its stimulation of the release of radioactivity from synaptosomes preloaded with [3H]choline. Sephadex G-50 chromatography of the exudate produced one peak, with a mol. wt of approximately 18,000, which was further resolved into two active fractions by anion exchange chromatography. The more tightly bound of the two fractions was characterized and referred to as IOT. The action of IOT was essentially complete by 0.5-1.0 min and was independent of the Ca2+ or Na+ content of the incubation mixture. Released radioactivity included about 50% each of [3H]acetylcholine and [3H]choline. Release of radioactivity increased as a function of IOT concentration and then reached a maximum. Extrapolated asymptotic release was nearly equal to that obtained by lysing the synaptosomes. IOT also released radioactivity from synaptosomes which had been preincubated with other tritiated neurotransmitters or with 2-[3H]deoxy-D-glucose. Lactate dehydrogenase and choline acetyltransferase activities were not released from synaptosomes by treatment with IOT, but were released by digitonin. IOT therefore releases some of the smaller molecular weight components of synaptosomes, but does not permeabilize the synaptosomal membrane in the same way as digitonin treatment.

Animals↗
PubMed1991

Diazepam enhances intrasynaptosomal free calcium concentrations.

Synaptosomes prepared from brains of rats were incubated in different concentrations of diazepam under conditions designed to reduce the action of a reversed Na+/Ca2+ exchanger. In synaptosomes depolarized in the presence of added Ca2+, doses of diazepam ranging from 0.1 to 100 microM were found to significantly enhance Ca2+ levels measured with the fluorescent dye fura-2, compared to control incubations without drug. Furthermore, doses of diazepam as low as 1 microM significantly increased the concentration of Ca2+ in non-depolarized synaptosomes without added Ca2+ in the medium. The effects of depolarization and diazepam treatment were synergistic in increasing the levels of intrasynaptosomal Ca2+.

Analysis of Variance↗
PubMed1990

Accidental death from a black-powder rifle breech plug.

Authentic black-powder muzzle-loader weapons and replicas are used today primarily for hunting game such as deer and hogs. The following is a case presentation of accidental death from cerebral trauma caused by a .45-caliber black-powder-rifle breech plug implanting in the victim's brain.

Accidents↗
PubMed1990

Monoamine receptors in an animal model of affective disorder.

After a relatively mild course of uncontrollable shocks, two distinct groups of rats can be defined in terms of their performance in learning to escape from a controllable stressor. Response-deficient (RD) rats do not learn to terminate the controllable stressor, whereas nondeficient (ND) rats learn this response as readily as do untreated control rats. The current studies were designed to determine the neurochemical correlates of the behavioral differences between these groups of rats. The major findings concerned postsynaptic beta-adrenergic effects in the hippocampus of RD rats. These included an up-regulation of beta-adrenergic receptors and, in parallel experiments, an increase in the sensitivity of adenylyl cyclase to stimulation by norepinephrine. There was no difference in brain levels of catecholamines between the three groups of rats. A statistically significant increase in levels of 5-hydroxytryptamine was noted in the hippocampus and hypothalamus of RD rats as compared to levels in ND rats, but no significant differences were measured between groups of rats in terms of S1 or S2 serotonergic receptor binding. These results implicate both beta-adrenergic and serotonergic mechanisms in the behavioral deficit caused by uncontrollable shock.

Adenylyl Cyclases↗
PubMed1979

2,4,5--T.

Explore the source record for details and available documents.

2,4,5-Trichlorophenoxyacetic Acid↗
PubMed1977

Elevation of serum alkaline phosphatase activity and related enzymes in diabetes mellitus.

Of 101 consecutive hospitalised diabetic patients, 29 had elevated serum enzyme activities attributable to recognized clinical entities; 17% of the remainder had raised alkaline phosphatase (AP) activity, 15% had raised aspartate aminotransferase (GOT) activity, and 12% raised lactate dehydrogenase (LDH) activity in serum. Ketoacidosis and death within 3 months were commoner among patients with elevated serum enzyme activities than among those with normal enzymes. Study of 200 consecutive new untreated diabetics when first seen at an out-patient clinic revealed 15 with clinically explainable abnormal serum enzyme activities. Of the remainder, 11% had raised AP activity, 12% raised GOT activity, and 21% raised LDH activity in serum; these patients tended to have higher blood sugar concentrations than the subjects with normal serum enzymes. These abnormalities seem to be an intrinsic feature of diabetes mellitus which do not relate to duration, complications, or treatment of the disease. They do not seem to be directly related to hepatic involvement.

Adolescent↗
PubMed1976

Enzyme inducation as a possible cause of increased serum-trigylcerides after oral contraceptives.

Serial studies on twenty patients before and during oral-contraceptive therapy demonstrated a significant positive association between serum gamma-glutamyl-transpeptidase (G.G.T.) activity and triglyceride concentrations, both of which rose after treatment. The association between serum G.G.T. and triglyceride, and their increase after treatment with oral contraceptives, may reflect hepatic microsomal enzyme induction of both the rate-limiting enzymes of triglyceride synthesis, and G.G.T.

Adolescent↗
PubMed1976

The association between serum triglycerides and gamma glutamyl transpeptidase activity in diabetes mellitus.

A study conducted on 228 diabetic patients has shown a significant positive association between serum gamma-glutamyl transpeptidase (GGT) and triglyceride levels. Both fall with treatment, the most marked reduction occurring in patients on insulin. We suggest that the association between serum GGT and triglyceride levels and also the higher incidence of raised GGT and triglyceride levels in new diabetics may reflect hepatic microsomal enzyme induction of the rate-limiting enzymes of triglyceride synthesis. Serum GGT does not seem to correlate with hepatomegaly in diabetes mellitus.

Adolescent↗
PubMed1976

The excitation and inhibition of sexual receptivity in female hamsters by progesterone: time and dose relationships, neural localization and mechanisms of action.

Ovariectomized hamsters were administered estradiol benzoate (EB) and 44 h later, progesterone (P.) Lordosis behavior was induced. When an additional dose of P was given up to 24 h prior to or 24 h after the EB, EB-P facilitation of lordosis was inhibited. Additional hamsters were given varying doses of P (25-200 mu) following EB using both excitatory and inhibitory paradigms. Inhibition of EB-induced lordosis was effected with a lower dose of P than was the facilitation of EB induced lordosis by P. Hamsters were also given intracerebral implants of P using excitatory and inhibitory paradigms. No excitatory loci were found. Inhibition of EB-induced lordosis was effected by implants in the posterior hypothalamus and anterior mesencephalon, but not by diencephalic implants. Other hamsters were administered tritiated estradiol (E2) plus P prior to, concurrent with, or shortly after the E2. P had no effect upon the accumulation of E2 by any brain sites, although E2 was found to concentrate to a greater degree in the diencephalon than in the mesencephalon or cortex. The estrogen-induced depletion and replenishment of hypothalamic cytosol estrogen receptors was also studied. Concurrent P treatment had no effect upon the receptor depletion-replenishment process. It was concluded that P can both facilitate and inhibit estrogen-induced lordosis and that the inhibitory effects of P are not upon estrogen-sensitive cells in the brain.

Animals↗
PubMed1975

Gamma-glutamyl transpeptidase, triglycerides, and enzyme induction.

A study conducted on 109 consecutive patients submitted for routine lipid and lipoprotein screening has shown a significant positive association between serum gamma-glutamyl transpeptidase (gamma-GT) activity and the serum triglyceride concentration and between serum gamma-GT activity and the serum pre-beta-lipoprotein concentration. We suggest that these associations may reflect hepatic microsomal enzyme induction in hyperlipidaemic subjects which increases the hepatic content of the rate-limiting enzyme(s) for triglyceride synthesis.

Aged↗
PubMed1975

Role of gamma-glutamyl transpeptidase activity in the diagnosis of hepatobiliary disease.

The enzyme gamma-glutamyl transpeptidase is widely distributed throughout the body, notably kidney, seminal vesicles, pancreas, liver, spleen and brain. Being one of the enzymes of the gamma-glutamyl cycle, it is involved in aminoacid transport, catalysing a transpeptidation reaction between gamma-glutamyl peptides and most common amino acids. Methods of assay of the enzyme are based on its ability also to act on synthetic amides of glutamic acid; kinetic methods monitoring the release of p-nitroaniline from the substrate L-gamma-glutamyl p-nitroanilide are the most satisfactory. In diseases of the liver, the highest levels occur in association with cirrhosis, alcoholism, hepatic secondaries and cholestasis. As the enzyme is present in the endoplasmic reticulum of the hepatocyte, its activity is increased in situations leading to microsomal enzyme induction. Raised levels can also occur in pancreatitis, diabetes, myocardial infarction, congestive cardiac failure, chronic renal failure, cerebrovascular accidents, cerebral tumours and chronic obstructive pulmonary disease. Although the lack of specificity must be recognised, the estimation can be useful in the elucidation of some clearly defined problems arising during investigation of patients with suspected hepatic disease, especially where performed as part of a biochemical profile.

Alcoholism↗