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M Jacobson

Publications and source records attributed to M Jacobson.

At least 199 records · Page 11Linked to original sources

Hiatus hernia.

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Antacids↗

Absence of adaptive modification in developing retinotectal connections in frogs after visual deprivation or disparate stimulation of the eyes.

Action potentials evoked in the tectum by visual stimulation of the ipsilateral eye were absent in frog larvae and developed during metamorphosis. Formation of the connections underlying these responses is not based on the animal's visual experience. The development of the ipsilateral retinotectal projection occurred normally in frogs reared through metamorphosis in the dark from midlarval stages to adults. Inversion of one eye of frog larvae did not affect the development of ipsilateral retinotectal projections, which developed according to the inherent correspondences between the retinae regardless of the disparities produced by changing the relative positions of the eyes. No compensatory changes occurred in the retinotectal projections in response to the surgical derangement. Skin grafts completely occluding one eye, which were made at early larval stages and left in place for up to 88 days, did not affect the development of normal ipsilateral retinotectal connections. However, abnormal ipsilateral tectal responses evoked by stimulation through either the normal eye or the occluded eye were found in adult frogs after occlusion of one eye from larval stages for more than 121 days. It was concluded that visual stimulation is not required for the normal development of ipsilateral retinotectal connections but is required for their long-term maintenance.

Action Potentials↗

Plasma insulin disturbances in primary hyperparathyroidism.

Plasma insulin dynamics were evaluated in 10 patients with primary hyperparathyroidism before and after parathyroidectomy and correction of hypercalcemia. Before surgery fasting plasma insulin concentrations and insulin responses to administered glucose, tolbutamide, and glucagon were significantly greater than postoperative values. Hyperinsulinemia was not associated with altered glucose curves during glucose or glucagon tolerance tests, but a relatively greater insulin response to tolbutamide resulted in an increased hypoglycemic effect following its administration. The glucose-lowering action of intravenous insulin was slightly impaired before treatment. Intramuscular injections of parathormone to six normal men for 8 days induced mild hypercalcemia and hypophosphatemia and reproduced augmented plasma insulin responses to oral glucose and intravenous tolbutamide. 4-hr intravenous infusions of calcium to another group of six normal men raised serum calcium concentrations above 11 mg/100 ml. This did not alter glucose or insulin curves during oral glucose tolerance but markedly accentuated insulin responses to tolbutamide and potentiated its hypoglycemic effect. When highly purified parathormone was incubated with isolated pancreatic islets of male rats, glucose-stimulated insulin secretion was unaffected. These findings suggest that chronic hypercalcemia of hyperparathyroidism sustains a form of endogenous insulin resistance that necessitates augmented insulin secretion to maintain plasma glucose homeostasis. This state is insufficient to oppose tolbutamide-induced hypoglycemia because of an additional direct, selective enhancement of hypercalcemia on pancreatic beta cell responsiveness to the sulfonylurea. The possible direct role of parathormone in these events has not been established.

Adenoma↗

Brain enhancement in tadpoles: increased DNA concentration after somatotrophin or prolactin.

Frog tadpoles, injected with prolactin or somatotrophin during early stages when the brain cell population is rapidly increasing, exhibited marked increases over sham-injected controls in body weight, brain weight, and brain DNA, throughout subsequent development. Animals treated with somatotrophin attained the increase in brain DNA during the infection period. Prolactin had little effect during this period, but brain DNA accumulation continued at an accelerated rate over the next 15 days, when the rate of DNA increment normally declined. Patterns of incorporation of tritiated thymidine confirmed that both hormones increased DNA accumulation, suggesting increased cell proliferation rather than decreased cell death.

Animals↗