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Biomedical subjects

N Ling

Publications and source records attributed to N Ling.

At least 217 records · Page 12Linked to original sources
PubMed1986

Ontogeny of gamma-melanocyte-stimulating hormone in the brain and hypophysis of the rat: an immunohistochemical analysis.

The ontogeny of gamma-melanocyte stimulating hormone (gamma-MSH)-like immunoreactive (gamma-MSHI) structures in the brain and hypophysis was investigated in the rat by means of indirect immunofluorescence. gamma-MSHI neurons in the arcuate nucleus appeared at Day 13 of gestation, in the anterior hypophysis at Day 16, in the intermediate lobe at Day 18, and in the nucleus commissuralis after birth. gamma-MSHI fibers first appeared at Day 15 of gestation in the hypothalamic area and extended dorsally to reach the surface of the diencephalon. At Day 16 of gestation, another gamma-MSHI fiber bundle was found that ran laterally along the ventral surface of the diencephalon. At Day 19, immunoreactive fibers first appeared in the forebrain, diencephalon, midbrain and upper pons, and thereafter they increased in number, reaching a maximum at postnatal Day 15. gamma-MSHI fibers in the lower pons and medulla oblongata first appeared after birth. They also increased in number with age and reached a maximum at postnatal Day 15. The present ontogenetical study has demonstrated the different times of first appearance of each of the 3 major gamma-MSHI structures-containing cell groups in the brain, i.e., the arcuate nucleus, hypophysis and nucleus commissuralis. These findings may reflect the different functions of 3 groups of cells.

Animals↗
PubMed1986

In vitro release of growth hormone-releasing factor from rat hypothalamus: effect of insulin-like growth factor-1.

The release of growth hormone-releasing factor (GHRF) from rat hypothalamus was investigated in vitro. After 60 min preincubation the released GHRF from sliced rat hypothalamic fragments during 60 min incubation was detected by a highly specific and sensitive radioimmunoassay for rat GHRF. The release of GHRF was Ca2+-dependent and enhanced by high concentration of K+. Insulin-like growth factor-1 (IGF-1) significantly decreased GHRF release to 65% and 84% of the control at concentrations of 10(-8) M and 10(-7) M, respectively. These results suggest that this in vitro system is useful for the investigation of the mechanism of GHRF release from the hypothalamus and that IGF-1 is probably involved in the feedback inhibition of growth hormone secretion by attenuating GHRF release from the hypothalamus besides countering the effect of GHRF on the pituitary.

Animals↗
PubMed1986

Purification and characterization of luteinizing hormone-releasing hormone from codfish brain.

We have purified luteinizing hormone-releasing hormone (LH-RH) from codfish brain and have demonstrated its identity with salmon LH-RH (sLH-RH). An antiserum raised against sLH-RH was used in a specific radioimmunoassay (RIA) to monitor purification and to manufacture an immunoaffinity chromatography column for the initial purification step. The cross-reactivity of the sLH-RH RIA with mammalian LH-RH was 0.1%. Acid extracts of codfish brains were sequentially purified by immunoaffinity chromatography, gel-filtration chromatography, and three steps of reverse-phase HPLC. The purified material and synthetic sLH-RH coeluted on reverse-phase HPLC and exhibited similar biological activity in a dispersed pituitary cell bioassay. Furthermore, the amino acid composition of the purified material was identical to salmon LH-RH. These results suggest that there is structural conservation of LH-RH between these species of teleost fish.

Amino Acid Sequence↗
PubMed1986

Subclass distribution of IgG autoantibodies in bullous pemphigoid.

The distribution of IgG subclasses in the antibasement membrane zone autoantibody of pemphigoid in skin and serum was analyzed by use of monoclonal antibodies to human IgG subclasses. The predominant subclass was IgG4 which was present in 23 of 24 skin biopsies, IgG1 was next and IgG3 was found only occasionally. In 3 of 24 biopsies IgG4 was the only IgG subclass detected, C3 was absent in 2 of these, the third contained IgM and C3. Serum autoantibodies were similarly analyzed by indirect immunofluorescence (IIF) when again IgG4 autoantibody was the dominant subclass. No IgE autoantibody was detected by IIF.

Aged↗
PubMed1986

Hypothalamic hypopituitarism following cranial irradiation for nasopharyngeal carcinoma.

Eight patients, one male and seven females, with no pre-existing hypothalamic-pituitary disease, who developed symptoms of hypopituitarism following cranial irradiation for nasopharyngeal carcinoma were studied 5 years or more after radiotherapy. All were GH deficient. Four of the patients with no GH response during insulin tolerance tests (ITT) showed increased GH in response to synthetic human growth hormone releasing factor (GRF-44). Four patients had impaired cortisol responses to ITT, and gradual but diminished cortisol responses to ovine corticotrophin releasing factor (CRF-41). There was no significant difference between mean peak increments in response to ITT and those in response to CRF-41. TSH responses to TRH were delayed in five and absent in two patients; four of these had low free T4 index. Prolactin was raised in all seven women and increased further in response to TRH. Two patients had impaired gonadotrophin responses to LHRH. None of the patients had clinical or biochemical evidence of diabetes insipidus. These data suggest that post-irradiation hypopituitarism in these patients results from radiation damage to the hypothalamus leading to varying degrees of deficiency of the hypothalamic releasing or inhibitory factors.

Adult↗
PubMed1986

A divergence of plasma growth hormone response between growth hormone-releasing factor and insulin-induced hypoglycaemia among middle-aged healthy male subjects.

The capability of the anterior pituitary gland to secrete GH in response to an intravenous injection of growth hormone-releasing factor (GRF) and insulin-induced hypoglycaemia was evaluated in 9 healthy male subjects ranging in age between 37 and 52 years old. Plasma GH response to 100 micrograms human GRF showed considerable intersubject variation and the increment of the peak value from the basal did not exceed 5 ng/ml in four out of 9 subjects. In contrast, insulin-induced hypoglycaemia resulted in a consistent stimulation of GH that exceeded 21 ng/ml in all subjects. The mean peak GH response after insulin-induced hypoglycaemia was significantly higher than that after GRF (27.4 +/- 1.6 vs 10.6 +/- 1.9 ng/ml). These results demonstrate that a significant divergence exists in plasma GH responses between the two provocative tests in the middle-aged subjects and suggest that the stimulation of GH following insulin-induced hypoglycaemia is not mediated solely by endogenous GRF.

Adult↗
PubMed1986

Relative potencies of human, rat, bovine/caprine, porcine and ovine hypothalamic growth hormone-releasing factors to release growth hormone by the rat anterior pituitary in vitro.

Synthetic rat, human, bovine/caprine, porcine and ovine growth hormone-releasing factor (GRF) were tested for their capacity to release growth hormone (GH) by the rat anterior pituitary in vitro. All peptides elicited parallel and dose-dependent increases in GH release and produced similar maximal GH secretion. Rat GRF was 3-6 times more potent in stimulating the release of GH than all other GRFs, while human, bovine/caprine, porcine and ovine GRF had potencies that were not statistically different. The increased potency of both rat GRF(1-27)NH2 and rat GRF(1-23)NH2 when compared to human GRF(1-27)NH2 and human GRF(1-23)NH2, respectively, suggests that the increased potency of this molecule resides in structural differences in the amino terminal of native GRF. The results demonstrate increased sensitivity of rat pituitary cells for their homologous releasing factor.

Animals↗
PubMed1986

Growth hormone-releasing factor: a new chapter in neuroendocrinology.

The isolation and characterization of growth hormone-releasing factor (GRF) has initiated a new and exciting era in our understanding of the neuroendocrine regulation of pituitary growth hormone (GH) secretion. This report briefly describes the isolation and characterization of GRF, factors which modulate the GH response to GRF and the effects of chronic administration and deprivation of GRF on somatic growth. The intent of this report is to serve as a general introduction on biochemical and physiological aspects of GRF. The following reports from this symposium will then cover many of these topics in much greater detail.

Animals↗
PubMed1986

Immunohistochemical evidence that growth hormone-releasing factor (GRF) neurons contain an amidated peptide derived from cleavage of the carboxyl-terminal end of the GRF precursor.

Antisera were raised against synthetic replicates of the carboxyl-terminal (C-terminal) fragment of the precursor to human GH-releasing factor (GRF) (pre-proGRF) whose structure was predicted from the complementary DNA cloned from a pancreatic tumor. These antisera were used along with antisera to human GRF itself to search for the presence of related molecules in the human hypothalamus, with an immunohistochemical approach. The antisera to pre-proGRF that recognize specifically the C-terminal amidated form of pre-proGRF stain GRF neurons in their cell bodies, fibers, and nerve endings that are in contact with portal capillaries of the median eminence. Antisera against the nonamidated form of the molecule did not give any staining in the hypothalamus. These results strongly suggest that human hypothalamic GRF derives from a precursor immunologically related (and probably identical) to the tumorous one and that this precursor is cleaved inside GRF cell bodies to give, in addition to the GRF-44-NH2 a second amidated peptide, the C-terminal pre-proGRF that is transported distally to nerve endings and most probably coreleased with GRF into portal capillaries.

Adult↗
PubMed1986

The effect of glucose and free fatty acids on growth hormone (GH)-releasing factor-mediated GH secretion in rats.

We have examined the effect of glucose and FFA on GH-releasing factor (GHRF)-mediated GH secretion in rats under pentobarbital anesthesia. Hyperglycemia did not affect GH secretion induced by administration of 20, 100, and 200 ng GHRF/100 g body weight. In contrast, GH response to 50 ng GHRF/100 g body weight in lipid heparin-treated rats, which showed high plasma FFA levels, was significantly suppressed compared with the control group (plasma peak GH: control, 1526 +/- 263 ng/ml; lipid-heparin group, 377 +/- 69 ng/ml P less than 0.05, mean +/- SEM). This suppressive effect of FFA on GH secretion was abolished by pretreatment with antisomatostatin serum (ASS) (GH level at 4 min after GHRF administration: ASS-saline group, 1606 +/- 210 ng/ml; ASS-lipid-heparin group, 1531 +/- 174 ng/ml; mean +/- SEM). These results suggest that hyperglycemia does not change the GH response to GHRF and that elevation of plasma FFA suppresses GHRF-induced GH secretion by the stimulation of somatostatin secretion in rats.

Animals↗
PubMed1986

The responses of plasma adrenocorticotropin and cortisol to corticotropin-releasing hormone (CRH) and cerebrospinal fluid immunoreactive CRH in anorexia nervosa patients.

Pituitary-adrenocortical responses to the iv injection of 100 micrograms synthetic ovine corticotropin-releasing hormone (CRH) were studied in 13 patients with anorexia nervosa, and the concentrations of immunoreactive CRH in cerebrospinal fluid were measured in 7 of them. Mean basal levels of plasma ACTH and cortisol were 32 +/- 5 pg/ml (+/- SEM) and 21.1 +/- 1.5 micrograms/dl, respectively. The latter value was significantly higher than that in age-matched normal women (P less than 0.005). The mean increments of plasma ACTH and cortisol in response to CRH injection in those 13 patients were 21 +/- 5 pg/ml and 5.3 +/- 1.7 micrograms/dl, respectively, significantly lower than those in normal women (58 +/- 6 pg/ml and 15.3 +/- 7.7 micrograms/dl, respectively; P less than 0.005). When 4 patients were reexamined after weight gains of between 3 and 22 kg, their responses to the CRH injection increased. The mean concentration of immunoreactive CRH in the cerebrospinal fluid of seven patients was 30.8 +/- 3.9 pg/ml (+/- SEM), which was higher than the value of 18.4 +/- 1.1 pg/ml (P less than 0.005) in control subjects with cervical spondylosis. These findings suggest the possibility that hypersecretion of CRH may occur in patients with anorexia nervosa.

Adolescent↗
PubMed1986

Thyroid-stimulating autoantibodies usually contain only lambda-light chains: evidence for the "forbidden clone" theory.

Burnet's "forbidden clone" theory would predict that in patients with Graves' disease the pathogenic thyroid-stimulating autoantibody (TSab)-secreting clones arise by somatic mutation. Because each lymphocyte and its progeny are permanently committed to producing antibodies of a single light chain type, a clone arising by somatic mutation occurring in a single cell would be expected to produce autoantibodies of exclusively kappa or exclusively lambda type in an individual patient. Using affinity chromatographic techniques and monoclonal antibodies, we investigated the light chain type of TSab in 11 patients with Graves' disease. In all patients tested, TSab activity was confined to a single light chain type, confirming the recent work of Zakarija who used affinity chromatography with polyclonal antisera, but contrasting with earlier studies which used immuno-precipitation methods. Furthermore, the light chain type was lambda in 10 of the 11 patients. These observations provide support for the forbidden clone theory. In addition, the marked preponderance of patients producing TSab of the lambda-light chain type indicates that TSab are more likely to arise from the lambda repertoire of clones than from the kappa repertoire and suggests that immunoglobulin light chain V genes may be genetic determinants for susceptibility to Graves' disease.

Antibodies, Monoclonal↗
PubMed1986

Studies on the response of growth hormone (GH) secretion to GH-releasing hormone, thyrotropin-releasing hormone, gonadotropin-releasing hormone, and somatostatin in acromegaly.

The plasma GH response to GH-releasing hormone (GHRH), TRH, or GnRH administration was examined in 25 acromegalic patients. Plasma GH levels increased in 21 patients after GHRH, in 19 after TRH, and in 4 after GnRH. The four GHRH nonresponders had had acromegaly longer than had the GHRH responders. No specific combination of GH responsiveness to these 3 releasing hormones was found among the patients. Infusion of 1 mg GHRH for 150 min gradually increased plasma GH levels, with some fluctuations, from the beginning to the end of infusion in normal subjects and in 7 patients who were GHRH responders, but a bolus injection of 100 micrograms GHRH at the end of the infusion did not further elevate plasma GH levels. These results suggest that desensitization to GHRH occurred in the normal subjects and acromegalic patients. However, in 5 acromegalic patients who responded to both GHRH and TRH, a bolus injection of 500 micrograms TRH given at the end of the 150-min infusion of 1 mg GHRH evoked a further plasma GH rise. In 5 normal subjects and 2 patients who were responders to GHRH but not TRH, a bolus injection of 500 micrograms TRH did not cause plasma GH elevation at the end of 150-min infusion of 1 mg GHRH. These results imply that TRH and GnRH stimulate GH secretion from the adenoma cells in vivo through receptors different from those for GHRH. In vitro studies using cultured pituitary adenoma cells from 2 patients revealed that the responses of GH secretion to GHRH were similar to those in vivo. These data, therefore, suggest that the responsiveness of GH secretion to stimuli is determined by the specificity of the receptors on adenoma cells. The action of somatostatin-28 was more potent than that of somatostatin-14 in the suppression of GH secretion from adenoma cells.

Acromegaly↗
PubMed1986

Cross-sectional seroepidemiologic study of the prevalence of cytomegalovirus and herpes simplex virus infection in a Canadian Inuit (Eskimo) community.

The prevalence of antibody to cytomegalovirus (CMV) and herpes simplex virus (HSV) was determined, using enzyme-linked immunosorbent assay techniques, in a cross-sectional serologic survey of an isolated northern Canadian Inuit (Eskimo) community. The population studied included 155 Inuit and 11 Caucasian residents. By 6 years of age, 80% of the Inuit population were seropositive for CMV and 100% for herpes simplex virus. While only 7/63 Inuit greater than 20 years were seronegative for CMV, 5/11 Caucasian residents were seronegative (p = 0.01). For the Inuit population, no association between seropositivity for CMV and seropositivity for hepatitis A or hepatitis B was observed. This prevalence survey shows a serologic profile for infection with CMV and HSV in this northern Inuit community with an early age of acquisition and high prevalence of infection characteristic of socioeconomically deprived populations throughout the world, and is distinct from that observed in many other North American populations.

Adolescent↗
PubMed1985

Primary structure of bovine brain acidic fibroblast growth factor (FGF).

The major anionic mitogenic polypeptide for endothelial cells, acidic fibroblast growth factor (FGF), has been purified to homogeneity from bovine brain and its complete primary structure established by gas-phase sequence analysis. The 140 amino acid (Mr 16,000) protein has been previously shown to be a potent growth factor for many diverse cell types of mesodermal origin, in vitro, and an angiogenic agent, in vivo. The amino acid sequence of bovine brain acidic FGF has a 53% absolute homology with that of bovine pituitary basic FGF suggesting that these endothelial cell mitogens are derived from a single ancestral gene.

Amino Acid Sequence↗