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Biomedical subjects

J B Martin

Publications and source records attributed to J B Martin.

At least 271 records · Page 15Linked to original sources
PubMed1981

Ultrastructural localization and biochemical features of immunoreactive LEU-enkephalin in monkey dorsal horn.

Leu-enkephalin is an opioid peptide that has been found to modulate nociception in the spinal cord. Both pre- and postsynaptic interactions by enkephalins have been proposed. By the peroxidase . anti-peroxidase immunocytochemical method, we studied the distribution and ultrastructure of neuronal elements in the monkey dorsal horn to elucidate possible morphological substrates for postulated opioid actions. Biochemical analysis of immunoreactive Leu-enkephalin-like peptides in the cord was performed to characterize the forms present in labeled neurons and terminals. At the light microscopic level, fiber immunostaining was found in most areas of gray matter, especially in laminae I to V, and in the dorsolateral funiculus. Cell bodies were located in laminae I, II, III, and V. At the ultrastructural level, in the superficial dorsal horn, we found that neurons with Leu-enkephalin receive numerous types of axon inputs, some of which have been identified previously as originating from the dorsal root. Leu-enkephalin terminals formed primarily axosomatic and axodendritic synapses and less frequently synapsed with other axons. With the same Leu-enkephalin antiserum as used in the immunocytochemistry, a peptide physicochemically similar to intact Leu-enkephalin and two larger Leu-enkephalin-like peptides were identified in monkey spinal cord extracts. It is likely that a family of Leu-enkephalin-like peptides is present in monkey spinal cord and that the labeled elements may contain any or all of these substances. It is concluded that both pre- and postsynaptic physiologic effects of Leu-enkephalin are possible, although the preponderance of axodendritic synapses favors a principal postsynaptic site of action. The anatomical results suggest that neurons containing immunoreactive Leu-enkephalin in the dorsal horn, some of which may receive input from primary afferents, modulate nociception by directly synapsing with cells of origin of the spinothalamic tract and also by interacting with primary afferent terminals.

Animals↗
PubMed1980

Preparation and use of teaser bulls.

Bilateral partial epididymectomy was performed on 23 bulls. These bulls were used to detect oestrus under two different management systems. The results obtained were compared with simultaneous plasma progesterone assays, and indicated that teaser bulls can provide accurate detection of oestrus.

Animals↗
PubMed1980

Neuroendocrinology and brain peptides.

To date about thirty peptides--low-molecular-weight, single-chain amino acid compounds--are known to be distributed widely in the central nervous system within selective neuron pathways. These findings, combined with a large body of neuropharmacological, behavioral, and electrophysiological data, open new horizons in neurobiology, force a reexamination of old and accepted hypotheses, and hold important implications for the clinician. There is evidence that substance P and the opioid peptides play a major role in the pain pathway, particularly at the level of the spinal cord. Available evidence also implicates vasoactive intestinal polypeptide in the control of cerebral circulation, cholecystokinin in the regulation of appetite, and vasopressin and adrenocorticotropic hormone in memory. Many questions, however, remain. For most peptides there is little information on mechanisms of biosynthesis, release, interaction with receptors, and termination of biological effect. Another important question is the interaction of peptides with other neurotransmitters. The evidence that both "classic" neurotransmitters and peptides can be found in the same neuronal necessitates reformulation of Dale's "one neuron, one neurotransmitter" hypothesis. It may be that a single cell, while containing different classes of neurotransmitter, will contain only one member of any particular class. It is not too early to speculate on the role of the numerous and diverse peptides in neuronal tissue and on the implications of peptide abnormalities in a variety of neurological diseases. The answers to these and other questions pose a fascinating challenge to neurobiologist and clinician alike.

Adrenocorticotropic Hormone↗
PubMed1980

Effect of chronic treatment with thyrotropin-releasing hormone (TRH) or an analog of TRH (linear beta-alanine TRH) on the hypothalamic-pituitary-thyroid axis.

The effects of treatment for 5 or 9 days with varying doses of thyrotropin-releasing hormone (TRH) or the linear beta-alanine TRH congener (pGlu-His-Pro-beta-Ala-NH2) on serum levels of TSH, T3, and T4 were studied in mice and rats. At low doses in rats treatment with TRH for 9 days significantly increased serum levels of T3 but not serum T4 whereas a higher dose of TRH (10 mg/kg) reduced serum T3 levels. beta-Ala TRH (0.1--10 mg/kg IP) treatment for 9 days in rats significantly reduced serum T4 levels whereas serum T3 levels were only depressed at higher doses (1--10 mg/kg IP) of the peptide. In mice treatment for 5 days with TRH (1 and 10 mg/kg IP) significantly reduced serum levels of T3 and T4. In addition, TRH (0.1--10 mg/kg IP) or beta-Ala TRH treatment (1.0--10 mg/kg IP) for 9 days significantly reduced serum TSH levels in rats. TRH (10 mg/kg IP for 9 days) also significantly reduced serum GH levels in rats. No alteration in hypothalamic content of TRH and LHRH was observed after chronic TRH treatment. Some, but not all, of our findings support the hypothesis that treatment with high doses of TRH reduce pituitary-thyroid axis functions by a direct effect on hypophysial TRH receptors.

Animals↗
PubMed1980

The release of biologically and immunologically reactive somatostatin from perifused hypothalamic fragments.

The purpose of this investigation was to 1) develop a hypothalamic perifusion system which would allow measurement of spontaneous basal somatostatin (SRIF) release, 2) compare the immunological and biological activities of released SRIF, and 3) study the effect of membrane depolarization, extracellular calcium, and several neurotransmitters on SRIF release. Release was greater at the beginning of the perifusion and decayed with time for 90 min, after which it stabilized and remained constant for 3 h, the period used to determine the mean rates of release. Basal release was 20.2 pg/fragment x 10 min. Membrane depolarization with 55 mK K+ increased SRIF release 30 to 4-fold in a calcium-dependent manner. The immunoreactivity and biological activity of SRIF concentrated by affinity chromatography of hypothalamic perifusates were compared to those of synthetic SRIF and rat hypothalamic extract. Biological activity was assessed by the inhibition of radioimmunoassayable rat GH released from cultured dispersed rat anterior pituitary cells. Hypothalamic fragments were exposed to several neurotransmitters as well as other substances known to influence rat GH secretion. Our results may be summarized as follows. 1) The perifused medial basal hypothalamus releases immunoactive and bioactive SRIF at a constant basal rate. 2) Membrane depolarization with high potassium stimulates a small releasable pool of SRIF in a calcium-dependent manner. 3) Affinity chromatography is an alternative technique to collect and concentrate SRIF released from tissues. 4) Common neurotransmitter agents did not modify SRIF release from the medial basal hypothalami under the present conditions.

Animals↗
PubMed1980

Mesocestoides (Cestoda) in a child in Mississippi treated with paromomycin sulfate (humatin).

The fifth case of human infection with Mesocestoides in the United States is reported in a 17-month-old child living in Mississippi. The child was asymptomatic and the source of the infection in unknown. Stools examined after treatment with paromomycin sulfate (Humatin) revealed no further evidence of infection. This is the 18th case of Mesocestoides infection in man reported in the literature.

Cestode Infections↗
PubMed1980

Functions of central nervous system neurotransmitters in regulation of growth hormone secretion.

Pituitary growth hormone (GH) secretion is regulated by two hypothalamic factors: somatostatin, a characterized tetradecapeptide, which inhibits secretion, and GH-releasing factor, unidentified, which stimulates secretion. Biogenic amines, including norepinephrine, dopamine, serotonin, acetylcholine, and gamma-aminobutyric acid have excitatory or inhibitory effects at brain sites to modulate hypothalamic control. alpha-Adrenergic mechanisms have been shown to be of particular importance in the regulation of physiologic GH secretion, which is characterized by episodic surges of release.

Acetylcholine↗
PubMed1979

Immunoreactive and biologically active somatostatin-like material in rat retina.

Somatostatin-like activity, as determined by radioimmunoassay and bioassay, is present in HCl extracts of rat retina. The concentrations of immunoreactive somatostatin are 612 +/- 43 (mean +/- SEM)pg per whole retina of 0.621 +/- 0.044 pg/microgram of protein in retinas from rats killed by decapitation, values which are not significantly different from those in retinas from rats killed by ether inhalation. The immunoreactive somatostatin was partially purified and concentrated by immunoaffinity chromatography. Both the crude retinal extracts and the immunoaffinity-purified immunoreactive somatostatin inhibited, in a dose-related manner, the release of rat growth hormone from dispersed rat anterior pituitary cells in culture. When the immunoaffinity-purified immunoreactive somotostatin was subjected to gel filtration chromatography, 96% of the recovered somatostatin eluted as a peak corresponding in position to that of synthetic somatostatin. Retinas from a group of rats with hereditary degeneration of the photoreceptor cells and another group of rats studied 1 year after transection of the optic nerves demonstrated an increased concentration of immunoreactive somatostatin compared to controls.

Animals↗
PubMed1979

The use of length of stay distributions to predict hospital discharges.

Many hospital admissions scheduling or admissions control systems reported in the literature rely on estimates of future discharges to help control the variance in daily patient census. One of the two most frequently reported methods of estimating discharges attempts to explain the variance in historical length of stay (LPS) data. This paper explores the relationship between LOS variance explanation and the ability to predict discharges and concludes that even a large improvement in the ability to explain LOS variance will only marginally reduce the errors in the associated discharge predictions. In drawing this conclusion, a general discharge prediction model is developed and a more relevant statistic than per cent variance explained is introduced.

Admitting Department, Hospital↗
PubMed1979

Effect of anterior hypothalamic lesions on neurohypophysial and peripheral tissue concentrations of somatostatin in the rat.

Somatostatin (SRIF) is present in nerve endings in the median eminence (ME) and posterior pituitary. Hypothalamic SRIF containing neuronal perikarya are predominantly located in the anterior hypothalamic area (AHA), a region implicated in the inhibitory control of GH secretion. The effect of AHA lesions on SRIF in the ME, posterior pituitary, pancreas, stomach, and small intestine was studied in the rat in order to elucidate the source of ME and posterior pituitary SRIF and to determine if depletion of hypothalamic SRIF affects peripheral organ concentrations of the peptide. Lesioned animals showed a highly significant (P less than 0.01) 83% and 82% reduction in ME and posterior pituitary SRIF and to determine if depletion of hypothalamic SRIF affects peripheral organ concentrations of the peptide. Lesioned animals showed a highly significant (P less than SRIF concentrations in the pancreas, stomach, and small intestine of the lesioned animals. Plasma and pancreatic insulin and pancreatic glucagon were likewise unchanged. These data suggest that the hypothalamic SRIF pathway begins in the AHA, from where axons of somatostatinergic neurosecretory neurons project to both ME and posterior pituitary. AHA lesions have no effect on gut and pancreatic SRIF or pancreatic insulin and glucagon.

Animals↗
PubMed1979

Chromatographic and biological properties of immunoreactive somatostatin in hypothalamic and extrahypothalamic brain regions of the rat.

A sheep antiserum to somatostatin was used to develop RIA and immunoaffinity chromatography methods for the study of immunoreactive somatostatin (IRS) in brain tissue. IRS extracted from rat median eminence, anterior hypothalamic-preoptic area, amygdala, and parietal cortex bound reversibly to immunoaffinity columns, providing a technique for concentration and partial purification. Immunoaffinity purified IRS from each of the four brain regions eluted as four peaks on gel filtration chromatography. Each peak possessed biological activity, as determined by inhibitory effects on the release of GH from cultured rat anterior pituitary cells. No differences were detected by the methods employed between IRS from the anterior hypothalamic-preoptic area, which is rich in IRS-containing neuronal cell bodies, and that from the median eminence, where IRS is localized predominantly in nerve terminals.

Animals↗
PubMed1979

Episodic and TRH induced growth hormone release in primary hypothyroidism of man and rat.

In 27 hypothyroid subjects studied over 20 to 120 minutes, the concentration of serum growth hormone (GH) was variable with the amplitude and frequency of the secretory patterns similar to those reported by others for normal individuals. Serum GH, after the administration of thyrotropin releasing hormone (TRH) did not differ from values observed as spontaneous surges, in contrast to a consistent increase in thyrotropin and prolactin. Episodic secretion of GH persisted in thyroidectomized rats and did not differ significantly from that present in intact controls. It is concluded that episodic GH secretion is not abolished in primary hypothyroidism and that TRH is not a constant GH secretagogue in human subjects with hypothyroidism.

Adolescent↗