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Biomedical subjects

N Ling

Publications and source records attributed to N Ling.

At least 325 records · Page 18Linked to original sources
PubMed1983

[Increase by somatocrinin of a cyclic AMP-dependent protein kinase activity in adenohypophyseal, secretory granules in the hog].

This study shows that the growth hormone hypothalamic releasing factor (somatocrinin) stimulates the activity of cyclic AMP-dependent protein kinase associated with a purified fraction of hog anterior pituitary secretory granules. Threshold, half-maximal and maximal concentrations (0.3, 35 pM and 10 nM, respectively, in the presence of 50 nM cyclic AMP) are similar to those observed for in vitro stimulation of growth hormone release by somatocrinin.

Animals↗
PubMed1982

Immunohistochemical distribution of pro-somatostatin-related peptides in hippocampus.

By using immune sera which recognize one or more of the 3 peptides, somatostatin-14 (SS14), somatostatin-28 (SS28) and somatostatin-28(1-12) (SS28(1-12)) we have characterized their immunohistochemical distribution in the hippocampal formation. There exist at least two independent neuronal systems containing pro-somatostatin-related peptides: an intrinsic system of cells in the polymorphic layers which branch locally, and a dense terminal field in the molecular layer of the dentate gyrus that may constitute a portion of the entorhinal-dentate projection. In addition, SS28 is the dominant form present in cell bodies, whereas SS28(1-12) is preferentially localized in neuronal processes and terminals. We could not detect SS14 immunohistochemically.

Animals↗
PubMed1982

Somatostatin-28 inhibits thyroid-stimulating hormone release in man.

The effects of an equimolar (1,8 nmol/kg body weight) infusion of somatostatin-28 (SS-28) and somatostatin-14 (SS-14) on the thyroid-stimulating hormone (TSH) response to a combined pituitary function test consisting of 200 micrograms thyrotrophin-releasing hormone (TRH) as well as 100 micrograms luteinizing hormone-releasing hormone (LH-RH) and insulin 0.1 U/kg were compared in 5 normal men. SS-28 significantly inhibited the TSH response to TRH compared with the control infusion. SS-14 was ineffective in 1 subject but overall did not differ significantly from SS-28. In 1 of the subjects the inhibitory effects of SS-28 on the TSH response was determined at three different doses of SS-28. In this subject SS-28 was found to be approximately 16 times more potent than SS-14 in the inhibition of TSH release. Suppression of TSH by SS-28 adds further support for a hormonal role for the peptide.

Adult↗
PubMed1982

[Somatomedin inhibition of the growth hormone secretion stimulated by the hypothalamic factor somatocrinin or the synthetic peptide hpGRF].

In the in vitro monolayer pituitary cell culture system somatomedin-C and IGF-I are practically equipotent to inhibit the secretion of growth hormone stimulated by hypothalamic growth hormone releasing factor (GRF) or the synthetic peptide hpGRF-44 (3-200 x 10(-12)M). Highly purified somatomedin-C or IGF-I are active to inhibit the effect of GRF at concentrations of 0.5 to 10 ng/ml(1.0 x 10(-10) M - 1.3 x 10(-9) M) in either short-term (3-4 hrs.) or long-term (24 hrs.) incubation, with no statistical difference between the results obtained in either duration of incubation. IGF-II is less potent than IGF-I as an inhibitor of GRF. The effect of the somatomedins is specific for the secretion of growth hormone and is not duplicated by other growth factors such as epidermal growth factor (EGF) or fibroblast growth factor (FGF).

Animals↗
PubMed1982

Growth hormone-releasing factor from a human pancreatic tumor that caused acromegaly.

A 44 amino acid peptide with growth hormone-releasing activity has been isolated from a human tumor of the pancreas that had caused acromegaly. The primary structure of the tumor-derived peptide is H-Tyr-Ala-Asp-Ala-Ile-Phe-Thr-Asn-Ser-Tyr-Arg-Lys-Val-Leu-Gly-Gln-Leu-Ser-Ala- Arg-Lys-Leu-Leu-Gln-Asp-Ile-Met-Ser-Arg-Gln-Gln-Gly-Glu-Ser-Asn-Gln-Glu-Arg-Gly -Ala-Arg-Ala-Arg-Leu-NH2. The synthetic replicate has full biological activity in vitro and in vivo specifically to stimulate the secretion of immunoreactive growth hormone. The tumor-derived peptide is identical in biological activity and similar in physiochemical properties to the still uncharacterized growth hormone-releasing factor present in extracts of hypothalamic tissues.

Acromegaly↗
PubMed1982

Noradrenergic terminal excitability: effects of opioids.

The local infusion of morphine or D-Ala2, Met5-enkephalinamide into the frontal cortical terminal fields of noradrenergic neurons of the nucleus locus coeruleus resulted in a decrease in the excitability of the axon terminal regions to direct electrical stimulation. These effects were concentration dependent and could be blocked or partially reversed by the local infusion of naloxone. Some evidence was obtained for a differential antagonizing effect of naloxone upon the effects of morphine and D-Ala2, Met5-enkephalinamide. These results are discussed with respect to an effect of opioids on the polarization and/or ionic conductance of the terminal fields of locus coeruleus neurons, and to the possible regulation of neurotransmitter release by presynaptic opiate receptors.

Animals↗
PubMed1982

Beta-endorphin concentrations in serum, hypothalamus and central gray of hypophysectomized and mediobasal hypothalamus lesioned rats.

The serum and brain concentrations of beta-endorphin immunoreactivity have been studied in intact, mediobasal hypothalamus (MBH) lesioned and hypophysectomized male rats. After hypophysectomy there is a major reduction (90%) of beta-endorphin concentration in the serum but only a partial reduction (20%) in the mediobasal hypothalamus. However, MBH lesions enhance beta-endorphin serum values in previously hypophysectomized rats. Long-term MBH lesions alone lead to an almost complete disappearance of beta-endorphin in the central gray matter with a slight decrease in the serum. These data clearly show that: (1) the pituitary is the major source of beta-endorphin in the serum; (2) the hypothalamus is the major source of beta-endorphin in the central gray matter; and (3) there is clear influence of the pituitary on hypothalamic beta-endorphin.

Animals↗
PubMed1982

Inhibition of gastric and pancreatic secretions by cerebroventricular injections of gastrin-releasing peptide and bombesin in rats.

It has been suggested that mammalian gastrin-releasing peptide (GRP) and bombesin (BBS) might inhibit gastric secretion by a central nervous system action. The present investigations were intended to define the gastric effect and to look for an effect on the exocrine pancreas. Wistar male rats were provided with a chronic cannula allowing cerebroventricular injections in the 3rd ventricle, and with chronic gastric and/or pancreatic fistulas allowing the collection of gastric and/or pancreatic secretions in conscious animals. Both basal secretions were studied. Gastric secretion was stimulated with a 75 mg/kg s.c. injection of 2-deoxyglucose (2-dGlc). The dose range of bombesin was 0.01-1 microgram (6-600 pmol) and GRP was 0.01-10 microgram/rat (3.5 pmol to 3.5 nmol). A significant dose related decrease of basal gastric secretion was observed with the two peptides. The gastric acid response to 2-dGlc was inhibited by both peptides in a dose-related fashion and the reduction of gastric acid output mainly resulted from a decrease in the volume of gastric juice. The exocrine pancreatic secretion was also decreased by 30-55% after GRP but the BBS inhibitory effect was poorly dose-related. No significant difference was found after removal of gastric secretion, indicating that most of the pancreatic inhibition was independent of gastric secretion.

Animals↗
PubMed1982

Growth hormone releasing factor, somatocrinin, releases pituitary growth hormone in vitro.

Purified (rat) hypothalamic growth hormone releasing factor (GRF), native human GRF isolated from an islet cell tumor of the pancreas that had caused acromegaly, and the synthetic replicates of the human material are potent secretagogues of immunoreactive growth hormone (GH) by primary cultures of rat pituitary cells. Native or synthetic peptides give identical dose-response curves, with identical slopes and identical maximal effects. The median effective dose of the tumor-derived GRF is 15 x 10(-12) M. The effect of hypothalamic GRF or of a synthetic replicate of tumor-derived GRF is immediate, being demonstrable in less than or equal to 30 sec after contact in a pituitary cell perifusion system. The effect of hypothalamic GRF or of tumor-derived GRF is highly specific for stimulating release of immunoreactive growth hormone; there is no demonstrable concomitant effect on the secretion of other pituitary hormones. Somatostatin-28 and somatostatin-14 inhibit the release of growth hormone produced by hypothalamic GRF or tumor-derived GRF in typical noncompetitive antagonism. On the basis of the results reported here, hypothalamic GRF and tumor-derived GRF are qualitatively indistinguishable in their ability to stimulate the secretion of immunoreactive growth hormone in vitro. The name "somatocrinin" is proposed to replace the acronym GRF.

Amino Acid Sequence↗
PubMed1982

Presence of somatostatin-28-(1-12) in hypothalamus and pancreas.

Acid extracts from rat pancreas and hypothalamus were analyzed for the presence of the antigenic determinant corresponding to the NH2 terminus of somatostatin-28 (SS28), using an antiserum directed against amino acids 1 to less than or equal to 11 of the SS28 molecule. On gel permeation chromatography the majority of the immunoreactive material from each tissue extract eluted in one zone compatible with a peptide of 1250 daltons. Purification of this immunoreactive material by reverse-phase HPLC and cation-exchange chromatography yielded two immunoreactive peptides from each tissue extract. The amino acid compositions of both peptides in pancreas and hypothalamus correspond to the fragment 1-12 of SS28. The more hydrophobic peptide from each tissue coeluted with synthetic SS28-(1-12) on HPLC, while the other one coeluted with synthetic SS28-(1-12)-amide. We conclude that the prosomatostatin fragment Ser-Ala-Asn-Ser-Asn-Pro-Ala-Met-Ala-Pro-Arg-Glu-OH is present in both rat hypothalamus and rat pancreas.

Amino Acid Sequence↗
PubMed1982

Molecular forms of the putative enkephalin precursor BAM-12P in bovine adrenal, pituitary, and hypothalamus.

A highly specific radioimmunoassay for one of the putative adrenomedullary [Met]enkephalin precursors, BAM-12P (Tyr-Gly-Gly-Phe-Met-Arg-Arg-Val-Gly-Arg-Pro-Glu-OH), has been developed. The BAM-12P antibodies recognize the COOH-terminal fragment of the peptide from Arg7 to Glu12 and do not crossreact with [Met5]- or [Leu5]enkephalin or any of their COOH-terminal lysine or arginine extended analogs. Specificity for the COOH-terminal Glu-OH is suggested by the 100% crossreactivity with BAM-12P5-12 and 0.3% crossreactivity with BAM-12P5-12 amide. Using these antibodies, we have measured three forms of BAM-12P-like immunoreactivity in extracts of bovine adrenal medulla, of which the major form (greater than 90%) corresponds to BAM-12P by molecular weight. Extracts of bovine adrenal cortex contain 1% the amount of a BAM-12P-like material (Mr approximately 1400; 20 ng per gland), possibly due to crosscontamination with adrenomedullary tissue. The major form of BAM-12P-like material in extracts of bovine neurointermediate pituitaries is of higher molecular weight than authentic BAM-12P (Mr approximately 4000); the remaining material (10%) corresponds to BAM-12P by molecular weight. There is no detectable BAM-12P-like immunoreactivity in crude or purified extracts of bovine anterior pituitaries. Extracts of bovine hypothalamic tissues contain small amounts of BAM-12P immunoreactivity (approximately 2 ng per fragment) which can be detected as one molecular form corresponding to a 1400-dalton molecule. The results indicate that the enkephalin precursor found in the adrenal medulla also may be present in the pituitary and hypothalamus. Furthermore, the processing of this molecule appears to be tissue-specific.

Adrenal Cortex↗
PubMed1982

Somatostatin-28 inhibits LHRH-stimulated gonadotrophin secretion in man.

The LH and FSH responses to 100 micrograms LHRH in a combined pituitary stimulation test were compared to five normal men during infusions of somatostatin-28 (SS-28) and somatostatin (SS-14) and during control infusions of haemacel. SS-28 and SS-14 were administered in equimolar concentrations of 1.8 nmol/kg body weight over 210 min and LHRH was injected as a bolus at 120 min after commencement of the infusion. SS-28 significantly reduced both LH and FSH responses to LHRH compared with control infusions. SS-14 did not significantly alter the FSH response but caused a significant reduction in the LH concentration 75 and 90 min after LHRH injection. These findings demonstrate that SS-28 has distinct biological activity in addition to its role as a putative precursor of SS-14. Inhibition of gonadotropin hormone secretion by SS-14 and SS-28 suggest that these hypothalamic peptides may play a part in the regulation of LH and FSH secretion.

Adult↗