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Biomedical subjects

G M Tyce

Publications and source records attributed to G M Tyce.

At least 145 records · Page 8Linked to original sources
PubMed1977

Demethylation of O-methyl metabolites of catecholamines in erythrocytes: a methanol-forming reaction.

When lysates of erythrocytes of 11 species, including man, were incubated at pH 7.8 with L-3-methoxy-4-hydroxy [U-14C]phenylalanine or with [7-3H]normetanephrine, these were demethylated and formed 3,4-dihydroxy[14C]phenylalanine or [3H]norepinephrine. These catechols were identified by column and paper chromatographic methods. When [14C-methoxy]normetanephrine was incubated with lysates of rat erythrocytes, the one-carbon product was identified as [14C]methanol by the isolation in the incubation mixture of [14C]methanol-3,5-dinitrobenzoate and its recrystallization to constant specific radioactivity. Metanephrine, 3-methoxytyramine, vanilmandelic acid, and 3-methoxy-4-hydroxyphenylglycol were also O-demethylated by rat erythrocytes; epinephrine was not N-demethylated. The reaction was not influenced by the addition of S-adenosylmethionine. The reaction appears to be different from that catalyzed by the "methanol-forming enzyme" previously described in erythrocytes and in other tissues.

Animals↗
PubMed1977

Patterns of dystonia ("I-D-I" and "D-I-D-") in response to l-dopa therapy for Parkinson's disease.

The clinical, biochemical, and pharmacologic responses to L-dopa were studied in 87 patients with Parkinson's disease. Eleven of the 87 patients had a long-duration response, 39 had a short-duration response, and 37 had a combination of both. Thirty-four of the 39 patients with short-duration response to L-dopa experienced a consistent and reproducible sequence of clinical and biochemical events after each dose, characterized by improvement of parkinsonism and a single phase of dystonia occurring during or shortly after the peak of dopa concentration in plasma and during maximal clinical improvement. We have called this the I-D-I- response, for Parkinsonism-Improvement-Dystonia-Improvement-Parkinsonism. The remaining five patients all had the onset of the disease at an unusually young age and showed a distinctly different response pattern consisting of a first phase of dystonia, before there was any improvement, followed by a phase of improvement without dystonia and then by a second phase of dystonia before the abrupt return of parkinsonism. We have called this the D-I-D response, for Parkinsonism-Dystonia-Improvement-Dystonia-Parkinsonsim. Dystonia occurs in the D-I-D- response when the concentration of dopa in plasma passes through a critical but relatively low level, whereas it remains absent as long as the concentration of dopa remains above that level. In the I-D-I- response, dystonia is avoided by keeping the plasma concentration of dopa low, in the D-I-D- response by keeping it high. It is postulated that in the D-I-D response postsynaptic depolarization blockade due to supramaximal stimulation of the neuronal system mediating dystonia occurs, whereas in the I-D-I response the postsynaptic members of the same neuronal population respond with excitation but not with depolarization blockade.

Dose-Response Relationship, Drug↗
PubMed1975

Parathyroid function in patients with pheochromocytoma.

Serum calcium, serum immunoreactive parathyroid hormone (PTH), and plasma immunoreactive calcitonin were measured in 12 patients with catecholamine-secreting tumors. Only two patients had high serum calcium and immunoreactive PTH concentrations (one also had high basal immunoreactive calcitonin); in both, the hypercalcemia persisted after removal of their pheochromocytomas but was corrected by removal of hyperplastic parathyroid glands and medullary thyroid carcinomas. Of the 10 patients with normal serum calcium and immunoreactive PTH concentrations, 2 had high immunoreactive calcitonin concentrations and medullary thyroid carcinomas alone were found. Our results suggest that [1] hypercalcemia occurs infrequently in patients with pheochromocytoma, [2] chronic circulating catecholamine excess does not cause increased immunoreactive PTH or immunoreactive calcitonin secretion in patients with pheochromocytoma, and [3] the parathyroid disease in patients with pheochromocytoma is a genetically determined component of multiple endocrine neoplasia.

Adolescent↗
PubMed1975

Bilateral adrenal medullary hyperplasia in multiple endocrine neoplasia, type 2: the precursor of bilateral pheochromocytoma.

An asymptomatic 12-year-old girl with multiple endocrine neoplasia, type 2, had high urinary levels of vanillylmandelic acid that suggested pheochromocytoma; she also had bilateral medullary thyroid carcinoma and hyperparathyroidism. Her mother and maternal aunt and uncle had bilateral pheochromocytoma (metastatic in the former two). Bilateral adrenalectomy was performed. Diffuse, non-nodular adrenal medullary hyperplasia was present. This hyperplasia was characterized by increased medullary mitotic activity, decreased corticomedullary ratio, increased total adrenal weight, and increased total catecholamine content (left adrenal). The results in this case suggest that diffuse hyperplasia of the adrenal medulla may be the precursor of pheochromocytoma in patients with this syndrome.

Adrenal Cortex↗
PubMed1975

Effect of L-DOPA on endogenous histamine metabolism.

To estimate the effect of long-term administration of L-3,4-dihydroxyphenylalanine (L-Dopa) on methylation of compounds not formed from it, the urinary excretion of histamine and its methylated metabolites was studied in rats and guinea pigs fed L-Dopa in their diets and in patients with Parkinson's disease being treated with L-Dopa. In the guinea pigs, but not in the rats, L-Dopa administration decreases excretion of histamine and of its methylated metabolites, methylhistamine and 1-methylimidazole-4-acetic acid. Because excretion of 1-methylimidazole-5-acetic acid, which comes from the diet and is not a metabolite of histamine, was unaffected by the L-Dopa treatment, the decreases were due to a specific effect of L-Dopa on histamine metabolism. When compared to normal control subjects, patients with Parkinson's disease excreted less histamine and methylhistamine, both before and during treatment with L-Dopa. Administration of the peripheral aromatic L-amino acid decarboxylase inhibitor, L-alpha-methyldopa hydrazine (MK 486), decreased urinary excretion of histamine markedly. Neither L-Dopa nor MK 486 appeared to influence excretion of the imidazoleacetic acids in the patients. The results suggest that L-Dopa may decrease histamine formation or release in some species but that it does not influence histamine methylation.

Acetates↗