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Biomedical subjects

J Schechter

Publications and source records attributed to J Schechter.

At least 55 records · Page 3Linked to original sources
PubMed1988

Activation of anterior pituitary folliculo-stellate cells in the formation of estrogen-induced prolactin-secreting tumors.

The response of folliculo-stellate (FS) cells of the anterior pituitary to estrogen has been studied in two strains of rat which differ in estrogen responsiveness. Fischer 344 (F344) rats are highly estrogen-responsive in comparison to Sprague-Dawley (S-D) rats. Ovariectomized adults were implanted with silastic capsules containing 17 beta-estradiol benzoate. Control and experimental animals were sacrificed 10 and 20 days after implantation of the silastic capsules. Most FS cells of F344 rats revealed dramatic changes, i.e. activation as phagocytes, after 10 and 20 days of estrogen treatment. These activated FS cells separated themselves from adjacent parenchymal cells and frequently contained phagosomes which included portions of granulated cells, mostly somatotrophs and lactotrophs. They also contained a variety of lysosomal dense bodies and dilated cisterns of endoplasmic reticulum. Endfeet processes abutting the parenchymal basal lamina contained large aggregates of dumbbell-shaped granules and tubulo-vesicles. Subjacent to the endfeet processes the basal lamina was often discontinuous, and profiles suggesting uptake of fragments of the basal lamina by FS cells were evident. Most FS cells of estrogen-treated S-D rats either were identical to those of controls or were only minimaly modified. However, a few activated FS cells were present and these contained a variety of lysosomal dense bodies and phagosomes, as well as lipid inclusions and dilated endoplasmic reticulum. Endfeet projections at the parenchymal basal lamina contained very few dumbbell-shaped granules or tubulo-vesicles, and the basal lamina was intact.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1988

Morphological evidence for the presence of arteries in human prolactinomas.

This study was undertaken to clarify the vascular anatomy of human prolactinomas and specifically to determine whether arteries were present. Sixteen prolactinomas were studied by electron microscopy. The presurgical diagnosis of the tumors as prolactinomas was based on the findings of hyperprolactinemia and radiographic abnormalities, and was confirmed by the electron microscopic features of the specimens as well as by immunocytochemical staining for PRL. In addition to the presence of fenestrated endothelial cells, which are characteristic of the normal capillaries of the anterior pituitary, 13 of the 16 prolactinomas contained arteries. These arteries ranged from well formed vessels with multiple layers of smooth muscle cells to abnormal terminal arterioles, i.e. vessels with fenestrated endothelium surrounded by a variable number of smooth muscle cells. Arteries were not found in anterior pituitaries from 8 patients with no pituitary disease. In the prolactinomas, smooth muscle cells also were found, either isolated in the pericapillary connective tissue space or in small cords some distance from the vessel lumen. The results suggest that vascular changes, including arteriogenesis, occur in prolactinomas (and possibly other types of pituitary tumor). The arteries entering the anterior pituitary directly could be congenital or develop during formation of the tumor. An arterial blood supply to a region of the anterior pituitary could result in the escape of that area from hypothalamic regulation, since systemic blood contains negligible levels of hypothalamic hormones. In the case of PRL-secreting cells, which are tonically inhibited by the hypothalamic hormone dopamine, this would result in hypertrophy, hyperplasia, and possibly tumorigenesis.

Adult↗
PubMed1987

Hepatoerythropoietic porphyria: clinical, biochemical, and enzymatic studies in a three-generation family lineage.

Hepatoerythropoietic porphyria is caused by a marked deficiency in the activity of uroporphyrinogen decarboxylase, an enzyme that is essential for heme biosynthesis. It has been hypothesized that uroporphyrinogen decarboxylase deficiency is inherited as a homozygous defect in the disease. This suggestion has been supported by reports of a deficiency of the enzyme in parents of patients with the disorder. Further confirmation would be provided by demonstrating a similar uroporphyrinogen decarboxylase deficiency in the offspring of such patients. This study follows the enzymatic defect throughout three generations of a family in which a second-generation male was shown to have hepatoerythropoietic porphyria. Detailed biochemical and enzymatic analyses revealed a moderate deficiency of uroporphyrinogen decarboxylase in both the proband's parents and in his three children, all of whom were asymptomatic. The mildness of the clinical symptoms in the proband correlated with a higher level of residual enzyme activity than that in previously described patients. We conclude that clinically manifested hepatoerythropoietic porphyria results from the homozygous inheritance of a defect in the uroporphyrinogen decarboxylase gene, that the severity of clinical symptoms is probably related to the level of residual enzyme activity, and that the genetic defect of uroporphyrinogen decarboxylase in hepatoerythropoietic porphyria can be heterogeneous.

Adult↗
PubMed1987

Rathke's pouch grafts in adult brain sites.

Donor tissue containing Rathke's pouch (RP) with its associated mesenchyme and neural lobe was isolated from 15-day fetal rats and stereotaxically transplanted either to hypothalamic hypophysiotropic sites or to cerebral cortex of adult females for 30 days. Hosts either were intact or had been hypophysectomized 2-4 weeks prior to transplantation of Rathke's pouch. Grafts in the hypothalamus of either intact or hypophysectomized hosts were pleomorphic and large, often as wide as 1-2 mm, and occasionally larger. Grafts in the cortex of either intact or hypophysectomized hosts were nodular and occasionally projected upward in association with the meninges (cortex/meninges grafts). Certain features were characteristic of the grafts in all experimental groups, i.e., development of histotypic pars distalis with cell cords and fenestrated capillaries. In all experimental groups gonadotrophs and somatotrophs, when present, were localized at the graft margin adjacent to the connective-tissue interface; mammotrophs, when present, were distributed throughout the graft. Features specific to each experimental group also were apparent. Grafts in the hypothalamus of both intact and hypophysectomized hosts typically were encapsulated by a labyrinthine meshwork of cell processes, whereas cortex/meninges grafts directly abutted dense connective tissue or neural tissue. In hypothalamic grafts in intact hosts, moderately differentiated mammotrophs, gonadotrophs, and somatotrophs could be identified by their cytological features and immunopositivity for prolactin, luteinizing hormone, and growth hormone, respectively. In hypothalamic grafts in hypophysectomized hosts, mammotrophs were absent, and gonadotrophs and somatotrophs were poorly granulated and not abundant. Grafts in the cortex of intact hosts contained numerous, well-differentiated mammotrophs, gonadotrophs, and somatotrophs. Many of the mammotrophs in these grafts were hypertrophied, and profiles of exocytosis were common. In grafts in the cortex of hypophysectomized hosts, mammotrophs were either absent or very few, whereas gonadotrophs and somatotrophs were numerous. Gonadotrophs in these grafts were dramatically hypertrophied, although exocytosis was rare. The results indicate that development of histotypic pars distalis may occur in hypophysiotropic and non-hypophysiotropic brain sites and that the hormonal state of the host as well as implantation site modulate cytodifferentiation of specific pars distalis cell types.

Animals↗
PubMed1987

Estrogen-induced tumors: changes in the vasculature in two strains of rat.

The influence of estrogen on the vasculature of the pars distalis has been studied in two strains of rat that differ in estrogen responsiveness. (Fischer 344 rats are highly estrogen-responsive in comparison to Sprague-Dawley rats.) Ovariectomized adults were implanted with silastic capsules containing 17 beta-estradiol benzoate. Control and experimental animals were sacrificed 10 and 20 days after implantation of the silastic capsules. Pituitary weights and plasma prolactin were elevated dramatically in estrogen-treated Fischer rats in comparison to more moderate increases in Sprague-Dawley rats. Although both strains exhibited the hypertrophy of mammotrophs expected after estrogen stimulation, the vasculature in Fischer rats were dramatically altered from normal. The pars distalis of the 20-day, estrogen-treated Fischer rats contained well-formed arteries. In addition, capillaries frequently were disrupted, contributing to the formation of hemorrhagic lakes unlined by an endothelium. Even in intact capillaries, basal laminae delimiting the pericapillary spaces often were disrupted or absent. Perivascular connective tissue cells were prominent within the perivascular spaces and often contained numerous, large lysosomal dense bodies as well as clusters of small dumbbell-shaped bodies. These granule clusters also were apparent adjacent to the perivascular space within parenchymal cells, most frequently within follicular cells. The vasculature of Sprague-Dawley rats maintained a more normal appearance after estrogen treatment, although perivascular connective tissue cells did appear activated and basal laminae delimiting the pericapillary spaces were disrupted occasionally. However, no capillaries were disrupted, nor were any hemorrhagic lakes evident, and no arteries were present.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗