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Biomedical subjects

B Simon

Publications and source records attributed to B Simon.

At least 433 records · Page 24Linked to original sources
PubMed1977

Human fat cell adenylate cyclase. Modulation of parathyroid hormone action by guanine nucleotides.

The effects of guanine nucleotides on basal and parathyroid hormone-stimulated adenylate cyclase of human fat cell ghosts were studied. GTP (10(-7)-10(-3) M) caused a dose-dependent inhibition of basal enzyme activity, but it had no significant effect on PTH-stimulated rates of cAMP-formation. The guanine nucleotide analogue 5'-guanylyl-imidodiphosphate GMP (PNP) when applied in the same concentration range, stimulated basal as well as PTH-activated adenylate cyclase activity up to 300%. GMP (PNP) activation was non-linear with time. PTH-activated the human fat cell adenylate cyclase via an individual receptor distinct from beta-adrenergic receptor sites.

Adenylyl Cyclases↗
PubMed1977

[Recurrent retroperitoneal giant lipoma (author's transl)].

A giant lipoma weighing 9.1 kg situated retroperitoneally which was removed by operation from a 74-year-old woman is reported. The diagnosis of tumors is discussed. The characteristics of this primary benign tumor such as the rapid growth, tendency to malignant degeneration and recurrence make radical surgical removal necessary.

Aged↗
PubMed1977

[Poisoning after ingestion of mussels (mytilus edulis) (author's transl)].

Symptoms of poisoning occurred in 19 persons in the Rhein-Main region in October 1976, after they had eaten mussels (Mytilus edulis) imported from Vigo, Spain. Mild oral paraesthesias, tingling in the fingertips and feet were followed by generalised numbness and dizziness. All symptoms disappeared within 48 hours. They had been caused by saxitoxin which is produced by a dinoflagellate and accumulated in the mussels, as confirmed by testing confiscated samples of mussels. Toxin concentration ranged from 6000 to 20 000 MU (mice units) per 100 g mussel meat.

Adolescent↗
PubMed1977

Catecholamine-sensitive adenylate cyclase of human fat cell ghosts. Inhibition of isoproterenol-stimulation by dihydroergotamine.

Isoproterenol-activation of the adenylate cyclase system of human fat cell ghosts was markedly inhibited by dihydroergotamine which had no effect on basal and NaF-stimulated enzyme activity. Our results indicate that the antilipolytic action of this substance in human adipose tissue is probably due to inhibition of catecholamine-sensitive adenylate cyclase activity.

Adenylyl Cyclases↗
PubMed1977

beta-adrenergic receptor coupled-adenylate cyclase of human fat cell ghosts.

The effects of beta-adrenergic agonists such as isoproterenol, norepinephrine and epinephrine upon the adenylate cyclase activity of human fat cell ghosts were tested, each alone and in combination with the beta-blocking agent propranolol. Saturating concentrations of these agents showed a 2-6.5-fold increase of enzyme activity without addition of any artificial cofactors. Isoproterenol was more potent in stimulating the enzyme system than epinephrine and nor-epinephrine. Propranolol caused a dose-dependent rightward shift of the log-dose response curve of these beta-adrenergic agonists. The assay of human fat cell adenylate cyclase in vitro may provide a simple anc convenient assay system for the screening of beta-adrenergic drugs of potential therapeutic importance.

Adenylyl Cyclases↗
PubMed1977

Catecholamine-sensitive adenylate cyclase of human fat cell ghosts: a comparative study using different beta-adrenergic agents.

Some of the effects of beta-adrenergic agonists and antagonists on the adenylate cyclase system of human fat cell ghosts were studied. Isoproterenol, by causing about a fourfold increase of enzyme activity, was more potent than epinephrine and norepinephrine (about 2.5--3.0-fold stimulation). The beta2-adrenergic agonists salbutamol, terbutalin, and fenoterol were considerably less effective than the naturally occurring catecholamines. The stimulatory actions of isoproterenol and beta2-adrenergic agonists were competitively inhibited by the beta-blocking agent propranolol. Isoproterenol stimulation was also inhibited by the selective beta1-adrenergic antagonist practolol. This compound, however, was less potent than propranolol. The results are suggestive for an adenylate cyclase system in human fat cell ghosts coupled to beta1-adrenergic receptor sites. These receptors differ from the cardiac beta receptors with respect to practolol affinity.

Adenylyl Cyclases↗
PubMed1977

Effects of clofibrate on the human fat cell adenylate cyclase system.

The effects of chlofibrate on the adenylate cyclase system of human adipocytes were studied. Clofibrate reduced basal as well as hormone-NaF)stimulated adenylate cyclase activities to about the same extent (45% inhibition at 1 mg/ml clofibrate). The relative extent of hormonal stimulation was not altered by this compound. The inhibitory action of clofibrate was non-competitive with respect to the substrate ATP and cofactors (Mg2+-ions). Inhibition of enzyme activity was detectable after 2.5 min. Our results suggest that the antilipolytic activity of clofibrate is mediated via inhibition of the catalytic subunit of the fat cell adenylate cyclase.

Adenosine Triphosphate↗
PubMed1977

Human fat cell adenylate cyclase: regional differences in adrenaline responsiveness.

The effect of adrenaline on adenylate cyclase activity in membranes prepared from human abdominal and gluteal adipose tissue was examined. Basal enzyme activity averaged 1.0 mmol cAMP/mg protein/15 min in abdominal tissue and 0.68 nmol cAMP/mg protein/15 min in ghosts from the buttock. Maximally effective concentrations of sodium fluoride (20 mmol/1) induced an eight-fold increase in both membrane preparations. The maximal response to adrenaline (1.0 mmol/1) averaged 170% in ghosts of abdominal tissue compared with 60% in gluteal membranes. The concentrations of adrenaline required to produce half-maximal stimulation were similar in membrane preparations of both regions (about 5 X 10(-5) mol/1).

Abdomen↗