Search PubMed⌕ Search

Biomedical subjects

S R Max

Publications and source records attributed to S R Max.

At least 73 records · Page 4Linked to original sources
PubMed1980

Aromatization of androgens to estrogens mediates increased activity of glucose 6-phosphate dehydrogenase in rat levator ani muscle.

Administration of testosterone propionate to immature male rats caused a 50% increase in the specific activity of glucose 6-phosphate dehydrogenase, the rate-limiting enzyme of the pentose phosphate pathway, in the levator ani muscle. This effect appears to be mediated by conversion of testosterone to estradiol because of the following results: 1) the effect was not mimicked by the nonaromatizable androgens fluoxymesterone or 5 alpha-dihydrotestosterone; 2) it was mimicked by 17 beta-estradiol and diethylstilbestrol; 3) it was blocked by an estrogen antagonist but not by an androgen antagonist; 4) the inactive steroid 17 alpha-estradiol was without effect on glucose 6-phosphate dehydrogenase; and 5) the effect of testosterone was blocked by an inhibitor of androgen aromatase. These results demonstrate a direct effect of estrogen on striated muscle.

Androgens↗
PubMed1978

Nerve growth factor-mediated induction of tyrosine hydroxylase in rat superior cervical ganglia in vitro.

Exposure of rat sympathetic ganglia to 3 microgram/ml of 2.5 S nerve growth factor (NGF) resulted in a 100% increase in tyrosine hydroxylase activity within 48 h. Pulselabeling of proteins with [3H]leucine, followed by immunoprecipitation with antibodies to tyrosine hydorxylase and isolation of the precipitated enzyme by gel electrophoresis, demonstrated that the increase in tyrosine hydroxylase activity was due to enhanced de novo synthesis. The incorporation of [3H]leucine into tyrosine hydroxylase was increased by 150% compared to a 17% increase in total protein synthesis, which was not statistically significant. The fact that the half-life of pulse-labeled tyrosine hydroxylase was the same for NGF-treated and control organ cultures of superior cervical ganglia excludes the possibility that enhanced tyrosine hydroxylase labeling by NGF is due to decreased degradation. We conclude that, without modulatory factors which play a role in vivo, NGF can enhance the synthesis of tyrosine hydroxylase in sympathetic ganglia in vitro, provided organ culture conditions which permit optimal survival of adrenergic neurons are selected.

Animals↗
PubMed1978

The pentose phosphate pathway in regenerating skeletal muscle.

1. The activities of the oxidative enzymes (glucose 6-phosphate dehydrogenase and 6-phosphogluconate dehydrogenase) and of the non-oxidative enzymes (transaldolase, tranketolase, ribose 5 phosphate isomerase and ribulose 5-phosphate 3-epimerase) of the pentose phosphate pathway were measured at various times during the first 24h of skeletal-muscle regeneration after administration of Marcaine, a mytoxic local anesthetic. 2. The activities of the oxidative enzymes increased after Marcaine injection and rose to 9 times control activities by 24h. 3. The activities of all non-oxidative enzymes were increased after Marcaine administration, but to a much smaller extent than the oxidative enzymes (1.1-1.7-fold). 4. Histochemical analysis localized glucose 6-phosphate dehydrogenase activity within muscle fibres of control and Marcaine-treated muscles. 5. Cycloheximide or actinomycin D prevented the increase in oxidative enzyme activities, suggesting a requirement for synthesis of protein and RNA.

Animals↗
PubMed1977

Neural regulation of muscle acetylcholinsterase: effects of batrachotoxin and 6-aminonicotinamide.

Batrachotoxin (BTX), which causes increased Na+ permeability and blocks axoplasmic transport, or 6-aminonicotinamide (6-AN), which causes neuronal damage, was injected into the subarachnoid space of rat lumbar spinal cord. The activity of acetylcholinesterase (AChE) was measured in homogenates of the fast-twitch extensor digitorum longus (EDL) muscle and the slow-twitch soleus (SOL) muscle 10 days after injection. Both drug treatments significantly decreased AChE in EDL and SOL. Correlative electrophysiological measurements were made in intact EDL and SOL after injection of BTX or 6-AN. The results support the hypothesis that AChE in muscle is neurotrophically controlled.

6-Aminonicotinamide↗
PubMed1977

Release of acetylcholinesterase by cultured spinal cord cells.

The release of acetylcholinesterase from neurons was studied using cultured chick-embryo spinal-cord cells. Cells dissociated from 12-day-old chick-embryo spinal cords were grown in culture for 10-12 days. Numerous well differentiated spinal neurons were found after 7-10 days in culture. Acetylcholinesterase activity per dish increased by 60-fold from days 2-12. Acetylcholinesterase was released into the surrounding media by the cells when they were incubated either in the standard culture medium or the serum-free medium. Acetylcholinesterase release was significantly reduced when protein synthesis and microtubules were disrupted by cycloheximide and colchicine, respectively. Histochemical localization of acetylcholinesterase indicated that the synthesis and relase of acetylcholinesterase are attributable to neurons. Cultured chick-embryo brain and neuroblastoma cells also released acetylcholinesterase into the media. These results are discussed with regard to possible physiological roles for acetylcholinesterase secretion from neurons.

Acetylcholinesterase↗
PubMed1977

Developmental patterns of glycolytic enzymes in regenerating skeletal muscle after autogenous free grafting.

Extensor digitorum longus muscles of rats were removed and injected with a solution of Marcaine plus hyaluronidase. After incubation in Marcaine solution for 10 min, the muscles were grafted into their original beds. The grafts and the contralateral control muscles were removed from the rats at 0, 1-5, 7, 11, 36, and 69 days postoperatively. The muscles were then frozen in dry ice and isopentane and subsequently homogenized and centrifuged. The supernatant was analyzed for a number of enzymes, the regenerative patterns of which can be classified into 3 groups: (1) early increase in activity: hexokinase, glucose-6-phosphate dehydrogenase; (2) early decrease in activity with failure to recover to control levels: phosphorylase, phosphofructokinase, alpha-glycerophosphate dehydrogenase; and (3) early decrease followed by return to control levels: lactate dehydrogenase, pyruvate kinase, creatine phosphokinase, adenylate kinase. These patterns are not identical to those reported for embryogenesis of muscle. The data are discussed with regard to correlative histological studies of muscle regeneration.

Adenylate Kinase↗
PubMed1976

GM3 gangliosidosis: a novel human sphingolipodystrophy.

A male infant of nonconsanguinous Jewish parents had clinical features of pseudo-Hurler's syndrome. A maternal uncle with similar features had previously died at 21/2 months of age. Following death at 3 1/2 months of age, analysis of the patient's brain and liver revealed increased amounts of ganglioside GM3, a virtual absence of higher ganglioside homologues (GM3, GM1, GD1a, and GT1) and a deficiency of the biosynthetic enzyme, UDP-Gal NAc:GM3 N-acetylgalactosaminyl-transferase. Since the biochemical findings denote a novel state of ganglioside deficiency, clinical findings emphasizing points of distinction from other causes of pseudo-Hurler's syndrome are presented.

Brain↗
PubMed1975

Deficient Ganglioside Biosynthesis: a novel human sphingolipidosis.

An unusual lipid storage disese is chracterized by the accumulation of hematoside (Gms3) in the patient's liver and brain. In contrast to the other sphingoliidoses, the accumulation of Gm3 is not the result of a defective catabolic reaction, but is the first disorder caused by deficiency in ganglioside biosynthesis to be described in man.

Brain↗
PubMed1975

Cerebral sponginess and GM3 gangliosidosis; ultrastructure and probable pathogenesis.

Extensive multifocal vacuolation of the cerebral hemispheres, brain stem, cerebellum, optic nerves and spinal cord were demonstrated in a 3 1/2 month-old infant. This co-existed with marked increases in cerebral and hepatic ganglioside GM3 (hematoside), absence of its higher homologues (GM1 and GM2) and absence of tissue N-acetylgalactosaminyl transferase. Ultrastructurally, there are major abnormalities in myelin and astroglia. The absence of identifiable "storage" material is believed to correlate with an enzymatic defect involved in ganglioside anabolism. A familial occurrence of this disorder is strongly suggested by the clinical history.

Astrocytes↗