Eosinophilic gastroenteritis.
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Biomedical subjects
Publications and source records attributed to G A Higgins.
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In the rat, somatostatin immunoreactivity was identified in neurons of the central nucleus of the amygdala that were retrogradely labeled by injection of fluorescent dyes into the nucleus tractus solitarius and dorsal motor nucleus of the vagus nerve. The double-labeled neurons are located in the medial subdivision of the central nucleus and appear to comprise less than one fifth of the descending pathway. These results suggest that somatostatin may act as a neurotransmitter in a pathway which mediates cardiovascular and other autonomic responses to fear-producing and other emotional stimuli.
Anatomical and electrophysiological studies with neurotensin and somatostatin were performed to assess the integrity of primary explants of the preoptic anterior hypothalamus (POAH) maintained in organ culture as a model to study peptidergic neurons in vitro. POAH neurons maintained in vitro were found to be morphologically similar to those visualized histologically in situ. Somatostatin- and neurotensin-immunoreactive neurons were also present in both preparations. Additionally, electrophysiological responses of neurons in vitro to neurotensin and somatostatin were qualitatively similar to neuronal responses in situ. The striking morphological and pharmacological similarity between POAH neurons in vitro and in situ suggests that primary explants of the POAH are organotypic.
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A comparative study was made of the serum calcitonin levels of patients with hyperparathyroidism. The mean serum calcitonin of those with hyperparathyroidism did not differ significantly from normal persons (mean +/- SEM: 130 +/- 16 pg/ml vs 124 +/- 7 pg/ml, respectively.) Only 0.5% of patients with hyperparathyroidism had values exceeding the upper limits of normal. In contrast, the mean serum calcitonin of patients with hypercalcemia of nonparathyroid etiology was considerably higher than normal (354 +/- 75 pg/ml, p < 0.001)), and 41% exceeded the upper limits of normal. Calcium infusion induced less of an increase in serum calcitonin for patients with hyperparathyroidism than for normal persons. In addition, the diminished responsibility was also present postoperatively. These findings suggest that the prolonged hypercalcemia associated with hyperparathyroidism results in a decreased calcitonin reserve which may persist for unknown reasons. In the clinical evaluation of hypercalcemic patient, the finding of hypercalcitonemia is suggestive evidence against the diagnosis of hyperparathyroidism.