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Biomedical subjects

J C Lissitzky

Publications and source records attributed to J C Lissitzky.

At least 55 records · Page 3Linked to original sources
PubMed1984

Regulation of expression of opioid peptide genes.

In the past three years it has been shown by recombinant DNA approaches that there are at least three different genes that code for opioid peptides. The basic structures of the three polyprotein precursor molecules from which bioactive opioid peptides are derived are remarkably similar. There are also similarities in the structure of the genes that code for these precursor molecules. Using immunological techniques, it has been shown that the levels of the opioid peptides can be regulated by altering the rates of protein processing or secretion. Recently, complementary DNA clones of the opioid peptide precursor molecules have been used as hybridization probes to determine that regulation also occurs at the level of gene expression (transcription of the opioid peptide genes).

Adrenalectomy↗
PubMed1984

The primate thyroid gland contains receptors for androgens.

The gonadal steroids have long been known to modulate thyroid function. Most studies suggest that the gonadal steroids act indirectly through the hypothalamic-pituitary axis to modulate thyroid function. The following studies were conducted to determine whether there are receptors for androgens in the thyroid itself. Cytosols from male and female euthyroid patients were analyzed for the presence of androgen with the synthetic analog methyltrienolone [( 3H]R1881). No evidence of androgen receptors was found in any of the cytosols prepared from female patients. In all males studied, androgen receptors were found in concentrations ranging from 100-150 fmol/10 mg DNA for the cytosols and from 690-2800 fmol/10 mg DNA for the nuclear extracts. The receptors had a dissociation constant (Kd) of approximately 5-10 X 10(-10) M for the cytosol and approximately 10-15 X 10(-10) M for the nuclear extracts. In addition to the human studies, studies in baboons were conducted to determine the possible cell type which might contain receptors for androgens. Male and female baboons were injected with [3H] dihydrotestosterone and killed between 1 and 1 1/2 h later. The thyroids were removed and processed for autoradiography. In autoradiograms from animals injected with [3H]dihydrotestosterone, nuclear localization of radioactivity was found in virtually all of the follicular cells. Also, label was found overlying the colloid, with heaviest labeling near the cells. These data suggest that there may be direct actions of androgens on follicular cells.

Animals↗
PubMed1983

Glucocorticoids regulate proopiomelanocortin gene expression in vivo at the levels of transcription and secretion.

After adrenalectomy, the plasma levels of adrenocorticotropic hormone (corticotropin, ACTH)/endorphin peptides in rats rise dramatically in the first 4 hr while pituitary peptide levels fall sharply. Eight hours after adrenalectomy, plasma levels are near control values again but they then increase continuously over the next 8 days. Proopiomelanocortin (POMC) mRNA levels in the anterior pituitary (quantitated by hybridization with cloned POMC cDNA) increase 2-fold in the first 24 hours, reaching 15- to 20-fold the control level 18 days after adrenalectomy. When dexamethasone is administered to rats 8 days after adrenalectomy, the above events are reversed. Plasma ACTH falls to control levels within 2 hr whereas anterior pituitary POMC mRNA requires 5 days of treatment for return to control levels. The levels of POMC mRNA in the neurointermediate lobe and the hypothalamus are not altered by either treatment. Adrenalectomy increases transcription of the POMC gene in the anterior pituitary approximately 20-fold and halves transcription of the growth hormone gene within 1 hr of operation. Administration of dexamethasone immediately after adrenalectomy suppresses the increase in transcription of the POMC gene and increases the transcription of the growth hormone gene. Transcription of the POMC gene(s) in the neurointermediate lobe is not altered by either of these treatments.

Adrenalectomy↗
PubMed1982

Influence of endogenous somatostatin on growth hormone and thyrotropin secretion in neonatal rats.

When gestating rats were injected iv with an antiserum to somatostatin (SRIF-AS) during the last week of gestation, serum GH levels in fetuses and 6-h-old newborn rats were not significantly different from controls. Similarly, 2 h after the ip administration of SRIF-AS, no change in serum GH concentration was observed in 2-h-old rats. However, under the same conditions, a significant increase in serum GH was observed in 24-h-old rats and in 2- to 60-day-old rats. The injection of SRIF-AS neither changed basal serum TSH levels during the neonatal development nor in the adult stage. A significant increase in TRH-induced TSH release was observed after the third postnatal day. It is concluded that endogenous SRIF plays a physiological role in GH release by 24 h of age in the rat and that the fall in GH secretion that normally occurs during the first week of life is due to the development of inhibitory mechanisms mediated by hypothalamus SRIF. Additionally the results suggest that the influence of SRIF upon TSH secretion is present before that of TRH.

Aging↗
PubMed1982

Corticolipotropin immunoreactivity in silent chromophobe adenomas: a light and electron microscopic study.

Twenty silent human pituitary adenomas were morphologically studied. Immunoperoxidase methods showed numerous adrenocorticotropic hormone-immunoreactive tumor cells in 14 cases by light microscopy and in one additional case by electron microscopy. Three of these cases were positive for beta-endorphin and one for beta-lipotropin by electron microscopy. These immunoreactions were found in undifferentiated tumors as well as in oncocytic adenomas, and could not be related to the presence of basophils by light microscopy. The peptides so detected in silent adenomas may have no biological activity and may correspond to common precursor molecule subunits.

Adenoma, Chromophobe↗
PubMed1981

Parallel stimulation of ACTH, beta-LPH + beta-endorphin and alpha-MSH release by alpha-adrenergic agents in rat anterior pituitary cells in culture.

Characteristics of the alpha-adrenergic stimulation of ACTH, beta-endorphin + beta-LPH and alpha-MSH release were studied in rat anterior pituitary cells in primary culture. Parallel changes of ACTH, beta-endorphin + beta-LPH and alpha-MSh release were found under all stimulatory and inhibitory conditions by natural and synthetic catecholamine agonists and antagonists. (-)Epinephrine and (-)norepinephrine lead to a 8--10-fold stimulation of peptide release at ED50 values of 20 and 90 nM, respectively. The stereoselectivity of the alpha-adrenergic stimulatory action on peptide release is indicated by a 100-fold higher activity of (-)- than (+)norepinephrine while (-)epinephrine is 10 times more potent than the corresponding (+) stereoisomer. The involvement of a typical alpha-adrenergic mechanism in the control of release of ACTH, beta-endorphin and related peptides in rat anterior pituitary gland is indicated by the following order of potency of a series of catecholaminergic agents (ED50 values): (-)epinephrine (20 nM) greater than (-)norepinephrine (90 nm) greater than phenylephrine (400 nM) greater than isoproterenol (6000 nM). The stimulatory effect of (-)epinephrine or phenylephrine is completely reversed by low concentrations of the alpha-adrenergic antagonist phentolamine while the beta-adrenergic antagonist propranolol has no effect up to 10 muM. Beside providing an easily accessible pure population of post-synaptic alpha-adrenergic receptors having potential applications as a model for other less accessible alpha-adrenergic brain systems, the present data suggest the possibility of the direct involvement of a catecholamine in the physiological control of ACTH secretion in the rat anterior pituitary gland.

Adrenergic alpha-Agonists↗
PubMed1981

Influence of thyrotropin-releasing hormone on the secretion of thyrotropin in neonatal rats.

Two hours after the ip administration of TRH antiserum, no change in serum TSH concentration was observed in the rat from birth through day 5 of life. Under the same conditions, a significant reduction in serum TSH was observed in 7- to 14-day-old rats. Similarly, in neonatal hypothyroidism, TSH levels did not change in 1-day-old rats, whereas a significant decrease was observed on day 7. The administration of synthetic TRH during the neonatal period induced a significant increase of serum TSH in the newborn; however, TSH release by the pituitary gland increased progressively from days 3-10. Immunoreactive TRH was undetectable in the serum of newborn rats. Adult levels were reached when the rats were 10 days old. It is concluded that neonatal pituitary-thyroid function in the rat is not physiologically dependent upon TRH secretion, although synthetic TRH is able to stimulate the secretion of TSH at birth.

Aging↗
PubMed1980

Influence of haloperidol on ACTH and beta-endorphin secretion in the rat.

The injection of haloperidol, a dopamine receptor blocker, was followed by a large increase of plasma ACTH and beta-endorphin-like immunoreactivity (beta-EI) in the rat. This effect was prevented when the rats were previously treated with corticosteroids. These results suggest that catecholamines inhibit ACTH and beta-endorphin secretion in the rat.

Adrenocorticotropic Hormone↗
PubMed1980

beta-Endorphin is present in high concentration in the hypophysial portal vessels of rats.

beta-Endorphin-like immunoreactivity (beta-ELI) was measured in hypophysial portal and arterial blood of intact, adrenalectomized and hypophysectomized rats. beta-ELI levels were 61 times higher in the long portal vessels than in the general circulation. Circulating, and especially portal, levels of beta-ELI were significantly increased after adrenalectomy. After removal of the pituitary gland, the mean level of beta-ELI in portal blood was significantly lower than in intact rats. beta-ELI in portal blood displayed the same chromatographic properties as synthetic beta-endorphin.

Adrenalectomy↗
PubMed1980

[Hypothalamic control of ACTH secretion].

The hypothalamic regulation of ACTH secretion has been reviewed. Recent biochemical investigations on corticotropin-releasing factor (CRF) suggest that CRF is present in the hypothalamus under two or more different molecular weight forms, their structure being not elucidated yet. Vasopressin has a CRF-like activity. However, contradictory results have been reported on the role of AVP as a physiological CRF. The synthesis of CRF appears to occur in a large hypothalamic area outside the median eminence. CRF-carrying fibers are thought to pass through the lateral retrochiasmatic area and project on the hypophysial portal vessels at the junction between the pituitary stalk and the median eminence. Conflicting data have been published on the influence of monoamines on ACTH secretion. In the dog, ACTH release is inhibited by the alpha-adrenergic receptors, this effect being not as clearly demonstrated in other species. The stimulation of nicotinic and muscarinic receptors followed by increased ACTH secretion. Glucocorticoids appear to lower ACTH secretion through an action at both the hypothalamic and pituitary levels.

Acetylcholine↗
PubMed1980

[Lipocorticotropic peptides in Cushing's disease: in vitro studies].

The immunologic patterns of 3 human pituitary adenomas of Cushing's disease have been studied after gel exclusion chromatography (Sephadex G-50). The immunologic characteristics were examined with three radioimmunoassays specific for human corticotropin (ACTH), lipotropin (LPH) and beta-endorphin (beta-End). In cell tumor extracts, chromatographic peaks corresponding to beta-LPH, gamma-LPH, beta-End and ACTH were identified. The ACTH/beta-LP-beta-End ratio was 1 in the 3 cases. Additionally, in the 3 cases, a chromatographic peak, partially cross-reacting in the beta-End assay, was eluted after beta-End, thus suggesting the presence of a fragment of the molecule. In 1 case, a peak of large molecular weight material with N- and C-terminal beta-LPH and ACTH immunoreactivity was observed, which corresponded to the precursor material. The release and the effects of various stimuli were studied on dispersed tumor cells in primary culture. The tumor cells had a biphasic basal secretion rate with a rapid increase of ACTH/beta-LPH-beta-End in the culture medium during the first 2 h. Then the release, studied during 2 days, was slower. Chromatographic studies showed that the beta-LPH/beta-End ratio was 0.8 in the cells and 0.3 in the medium, due essentially to the release of beta-End and beta-End-like materials. The cells released ACTH and beta-LPH-beta-End in equimolar ratio after stimulation with arginine vasopressin (AVP). The maximum effect was obtained with 10(-6) M AVP (D50 = 1 10(-9) M). Dibutyryl cyclic AMP (2. 10(-3) M) induced maximal release of ACTH/beta-LPH-beta-End. This stimulation was suppressed by a 48-hour preincubation with dexamethasone (10(-8)-10(-6) M). There was no effect of TRH and LH-RH on cell release. Dopamine (10(-6) M) specifically blocked the release of ACTH/beta-LPH-beta-End in 1 case. These data showed (a) heterogeneity of chromatographic profiles from case to case; (b) the presence of material in the tumor, cell extracts and culture medium corresponding to fragment(s) of beta-End; (c) culture studies demonstrated that tumor cells remain responsive to AVP stimulation and dexamethasone suppression, and (d) the dopamine inhibition of ACTH and beta-End release needs further investigation.

Adenoma↗
PubMed1979

Parallel release of ACTH, beta-endorphin, alpha-MSH and beta-MSH-like immunoreactivities in rat anterior pituitary cells in culture.

Specific radioimmunoassays (RIAs) for ACTH, beta-endorphin, alpha-MSH and beta-MSH were used to identify the immunoreactive components released during incubation of rat anterior pituitary cells in primary culture. Such measurements were performed after separation of the incubation media by chromatography on Sephadex G-50 or G-75. The ACTH-RIA measured approximately equal amounts of 13 and 4.5K ACTH while equal proportions of components migrating at the position of beta-LPH and beta-endorphin were measured in the beta-endorphin RIA system. Immunoreactive components migrating at the position of gamma-LPH and alpha-MSH were measured in the beta-MSH and alpha-MSH RIA systems, resp. 3 purified corticotropin-releasing fractions (CRF) prepared from porcine hypothalami and increasing concentrations of N6,O2'-dibutyryl cyclic AMP and theophylline led to parallel release of ACTH, beta-endorphin, beta-MSH and alpha-MSH immunoreactivities while preincubation with dexamethasone led to a 30-60% inhibition of the release of all peptides. The present data show that the release of ACTH, beta-LPH, beta-endorphin, gamma-LPH and alpha-MSH-like immunoeactivities occurs in parallel in anterior pituitary cells in culture both under basal and acute stimulatory or inhibitory conditions of release.

Adrenocorticotropic Hormone↗
PubMed1979

[Immunocytochemical similarities between basophilic and chromophobe pituitary adenomas. Light and electron microscopic study of 13 cases (author's transl)].

ACTH, beta MSH, beta LPH, beta endorpSin, leucine and methionine enkephalin activities were tested in four Cushing pituitary basophilic adenomas and nine "chromophobe" adenomas with immunoperoxidase methods. The antisera gave various positive reactions in both of these groups. ACTH, alpha MSH and enkephalins were predominant. The reason why these hormones are clinically silent in "chromophobe" or, even, basophilic adenomas is still to be elucidated.

Adenoma, Basophil↗
PubMed1978

Localization of alpha-melanocyte-stimulating hormone in rat brain and pituitary.

The distribution of alpha-melanocyte-stimulating hormone (alpha-MSH) was studied in the rat brain with an immunoperoxidase technique. alpha-MSH-containing cells were found in the arcuate nucleus of the hypothalamus. Cells staining for alpha-MSH were also localized in the intermediate lobe of the pituitary. alpha-MSH-containing nerve fibers extended throughout regions of the hypothalamus, thalamus, and midbrain. Two weeks after hypophysectomy, alpha-MSH-positive cells anf fibers were still present in the brain. These results indicate that alpha-MSH of non-pituitary origin is synthesized and stored by neural structures in the rat brain. The detection of alpha-MSH by radioimmunoassay in the rat brain and pituitary supports these observations.

Animals↗