Biomedical subjects

T R Hall

Publications and source records attributed to T R Hall.

At least 73 records · Page 4Linked to original sources

PubMed1986

Mesenchymal hamartomas of the liver in childhood: sonographic and CT findings.

Mesenchymal hamartomas of the liver usually present within the first 2 years of life. Abdominal enlargement and respiratory distress are the most common presenting features. Pathologically, the lesion is composed of large cysts separated by septations. Review of sonograms and CT scans in nine patients shows that a large, predominantly cystic mass with internal septae is characteristic of the tumor. Angiography shows peripheral hypervascularity with a septated avascular center. A confident preoperative diagnosis of mesenchymal hamartoma based on these features is possible.

Angiography↗

PubMed1985

Calcium control of growth hormone release from chicken pituitary glands in vitro.

The influence of calcium on the basal and stimulated release of growth hormone (GH) from chicken pituitary glands has been determined in vitro. Basal GH release occurred in Ca2+ deficient media, although it was increased in proportion to the medium Ca2+ concentration. Growth hormone release was stimulated by 10(-7)-10(-9) M thyrotrophin-releasing hormone (TRH), maximal stimulation being observed in the presence of 10(-8) M TRH and 1.5 mM Ca2+. Decreases in the Ca2+ concentration (to 0.75, 0.375, or 0 mM) suppressed the GH response to 10(-8) M TRH, as did increases (to 3.0 and 6.0 mM) in the Ca2+ concentration. These results suggest that GH release in chickens is regulated by Ca2+-dependent mechanisms.

Animals↗

PubMed1985

Effects of putative neurotransmitters on release of prolactin from pituitary glands of the domestic fowl co-incubated with hypothalamic tissue.

Pituitary glands and hypothalami from broiler fowl heads were incubated alone or together with histamine, gamma-aminobutyric acid (GABA) or acetylcholine (ACh) as well as with catecholamines or neurotransmitter antagonists. Histamine and ACh stimulated, whereas GABA inhibited, the hypothalamus-induced release of prolactin, responses blocked by their specific antagonists. The dopamine antagonist pimozide, but not adrenergic (both alpha and beta), serotoninergic or cholinergic antagonists, prevented the actions of histamine and GABA. None of the antagonists except the cholinergic blocker, atropine, affected ACh-induced release of prolactin. Neither histamine nor ACh prevented inhibition of prolactin release by dopamine or stimulation of prolactin release by noradrenaline. GABA did not affect the response to noradrenaline. Furthermore, histamine, GABA and ACh had no effects on thyrotrophin releasing hormone-stimulated release of prolactin directly at the pituitary level. These results suggest that histamine and GABA affect prolactin release from chicken pituitaries in vivo by modifying the activity of the dopaminergic system. Acetylcholine may stimulate the secretion of prolactin releasing factor from the hypothalamus.

Acetylcholine↗

PubMed1985

Evidence for negative feedback control of the release of [3H]serotonin from superfused mouse cerebellum slices induced by electrical field stimulation.

Slices of mouse cerebellum preloaded with [3H]serotonin were superfused with a solution of Krebs-Ringer phosphate. The effects of exogenous serotonin, serotonin antagonists, fluoxetine, Ca2+ absence, Ca2+ chelation and frequency of stimulation on basal and electrically induced tritium overflow were investigated. Exogenous unlabeled serotonin decreased the stimulus-evoked tritium overflow in a concentration-related manner. This effect was blocked by simultaneous administration of methiothepin, but not by methysergide. When given alone, methiothepin did not alter the electrically induced tritium overflow at 50 Hz, but did potentiate the increased tritium overflow produced at 100 Hz. The basal tritium efflux was increased by exogenous serotonin, but this effect was reversed by the simultaneous administration of fluoxetine. Under this condition exogenous serotonin reduced the basal tritium efflux in a concentration-related manner. Superfusion of the slices with a Ca2+-free solution alone or in the presence of EGTA, reduced the basal tritium efflux and the stimulated tritium overflow. These results support the existence of serotoninergic presynaptic inhibitory autoreceptors in the cerebellum of the mouse.

Animals↗

PubMed1985

Changes in mouse brain serotonin turnover following chronic imipramine administration.

Mice were injected daily for 2 weeks with saline, tryptophan or p-chlorophenylalanine, alone or in combination with the tricyclic antidepressant imipramine. Serotonin turnover in several brain regions was determined by the accumulation of serotonin after pargyline and 5-hydroxyindoleacetic acid after probenecid. Both methods agreed closely. Imipramine tended to depress serotonin turnover. This effect was more marked in hypothalamus, which has high serotonin activity, and was much less in cerebellum, which has low serotonin activity. Chronic imipramine treatment completely abolished the increase in serotonin turnover induced by tryptophan, but had no effect on serotonin turnover in mice treated with p-chlorophenylalanine, which itself reduced serotonin activity.

Animals↗

PubMed1985

Biochemistry and physiology of monoamine oxidase (MAO) activity in the ring dove (Streptopelia risoria). I. Characteristics of MAO activity in vitro.

Monoamine oxidase (MAO) activity was measured in ring dove (Streptopelia risoria) tissues using a fluorometric assay with kynuramine as substrate. Harmaline inhibited MAO activity in a time-dependent manner, and preincubation of enzyme with the drug did not affect its activity. Pargyline produced a slow-onsetting inhibition of activity which was enhanced by preincubation of enzyme and inhibitor. Harmaline displayed reversible non-competitive inhibition of MAO activity. Oxygen is also a substrate for dove MAO, and the reaction apparently involves "ping-pong", double-displacement kinetics. Dove MAO activity is temperature-dependent, with an activation energy of 13.1 kcal/mole.

Animals↗

PubMed1985

Biochemistry and physiology of monoamine oxidase (MAO) activity in the ring dove (Streptopelia risoria). II. Distribution of MAO in different tissues.

Monoamine oxidase (MAO) activity was measured fluorometrically in liver, kidney, intestine and brain of adult male and female ring doves. Liver MAO was inhibited in a concentration-related fashion by clorgyline and harmaline (MAO type A inhibitors) where a plateau in the inhibition curve occurred with about 15% activity remaining, and also by the type B inhibitor deprenyl, which produced a plateau when about 85% activity remained. Kidney, intestine and brain MAO were inhibited in a biphasic manner by harmaline. Results with inhibitors suggest that 85% of liver MAO, 86% of kidney MAO, 88% of intestine and 75% of brain MAO is type A. Using 10(-6) M harmaline to differentiate between MAO-A and MAO-B type activities, the apparent maximal velocities (Vmax) and Michaelis constants (Km) were determined in different tissues. Most activity occurred in the intestine, with proportionally lesser amounts of kidney, liver and brain. The majority of MAO present was in the A form. Except for kidney, Km of MAO-B was higher than that of MAO-A. Both MAO-A and -B activities were higher in the intestines of male birds, although sex differences in content and type of MAO activity were not observed in other tissues of the ring dove.

Animals↗

PubMed1985

Effects of prostaglandin F2 alpha on prolactin secretion in the fowl.

The plasma concentration of prolactin in immature cockerels was increased between 10 and 40 min after the intravenous administration of prostaglandin (PG) F2 alpha (200 micrograms/kg body weight). Lower doses had no effect on plasma prolactin concentration. The addition of PGF2 alpha (10(-9) to 10(-6) M) to incubation media had no effect on the basal release of pituitary prolactin but reduced the release of prolactin from pituitary-hypothalamus co-incubations. The addition of noradrenaline (10(-7) M), serotonin (10(-7) M), acetylcholine (10(-6) M) or histamine (10(-6) M) to the co-incubation increased the hypothalamus-induced prolactin release, although these effects were not observed in the presence of 10(-7) M PGF2 alpha. The in vitro release of pituitary prolactin was increased by adding chicken hypothalamic extract in the presence or absence of PGF2 alpha. These results suggest a dual effect on PGF2 alpha of prolactin secretion in the fowl; its stimulation in vivo may result from a peripheral action.

Animals↗

PubMed1985

Age-related changes in prolactin and growth hormone release from pituitary glands in vitro.

The basal release of prolactin from cockerel anterior pituitary glands in vitro declined between 1 and 7 weeks of age, to a level less than that released by pituitary glands from 18 week old (adult) cockerels and hens. Basal growth hormone (GH) release increased between 1 and 7 weeks of age but had declined in adults to a level similar to that released from 4 weeks old cockerels. The responsiveness of the pituitary gland to hypothalamic stimulation, using hypothalami from 8 week old broiler fowl, was also age-related. Prolactin release was considerably higher from pituitaries of 1 week old cockerels compared to the other age groups. Stimulation of GH release by the hypothalamus was higher from pituitaries of both 1 and 7 week old cockerels compared to the other groups of birds. The increase in release of prolactin following incubation with thyrotrophin releasing hormone (TRH) declined between 1 and 7 weeks, but increased slightly in adult birds, whereas the increase in release of GH following TRH was higher from pituitaries of both 1 and 7 week old cockerels. Hypothalamic prolactin (Prl) releasing activity, measured as the ability of the hypothalamus to stimulate hormone release from 8 week old broiler fowl anterior pituitary glands, declined with the age of the donor cockerels. The hypothalami from adult hens secreted significantly more Prl releasing activity than did adult cockerel hypothalami. The secretion of GH releasing activity decreased markedly with the age of the donor bird. These results suggest that maturational patterns of hormone secretion in fowl are partly due to changes in autonomous hormone release, to changing patterns of hypothalamic activity and to differences in pituitary responsiveness to provocative stimuli.

Age Factors↗

PubMed1985

Mechanisms of release of prolactin from fowl anterior pituitary glands incubated in vitro: effects of calcium and cyclic adenosine monophosphate.

Fowl anterior pituitary glands were bisected and each half was pretreated in either Medium 199 or medium containing EGTA to deplete endogenous calcium (Ca2+) stores, after which they were incubated in Medium 199, or Ca2+-free medium, containing prolactin release-stimulating agents and verapamil, a Ca2+ channel blocker. High K+ concentrations, hypothalamic extract, synthetic thyrotrophin-releasing hormone (TRH) and dibutyryl cyclic AMP (dbcAMP) all stimulated release of prolactin from control (non EGTA-treated) hemianterior pituitary glands. The effects of TRH and dbcAMP were not additive, but the response to submaximal concentrations of TRH was augmented by theophylline, a phosphodiesterase inhibitor. Reduction of Ca2+ availability with EGTA or verapamil reduced basal release of prolactin, prevented the prolactin-stimulating effects of high K+ concentrations and TRH, and markedly attenuated responses to hypothalamic extract and dbcAMP, EGTA being more effective than verapamil. Increasing the Ca2+ concentration of the medium did not augment basal or stimulated release of prolactin. These results suggest that both Ca2+ and cyclic AMP may act as intracellular mediators in the release of prolactin. Both basal and stimulated release of prolactin depend upon the presence of Ca2+. Although influx from the medium may be the major source of Ca2+, endogenous stores of Ca2+, perhaps mobilized by dbcAMP, may be able to maintain some release of prolactin. The prolactin-stimulating effects of TRH may be mediated by cyclic AMP.

Animals↗

PubMed1985

Familial gastroesophageal reflux and development of Barrett's esophagus.

The family of an elderly man with Barrett's esophagus was examined for gastroesophageal reflux and development of Barrett's esophagus. All five living children have gastroesophageal reflux or esophagitis, or both, and three have unequivocal Barrett's esophagus. Two third-generation descendents have gastroesophageal reflux. This pattern suggests autosomal dominant transmission of the gastroesophageal reflux trait. The family also has a high prevalence of cancer, which may represent the cancer family syndrome.

Adolescent↗

PubMed1984

Aspects of the neuroendocrine control of ovulation and broodiness in the domestic hen.

The neuroendocrine control of ovulation and broodiness in the domestic hen involves complex interactions between hypothalamic neuropeptides, neurotransmitters, and ovarian steroids which regulate the secretion of luteinizing hormone (LH) and prolactin. Nuclear progesterone receptor is localized in many neurons throughout the hypothalamus but is absent from LHRH neurons. Hence, the positive feedback action of progesterone on LH release is not mediated by a genomic mechanism within the LHRH neuron. Precursors of 5-hydroxytryptamine (5HT) and dopamine (DA) inhibit the preovulatory release of LH, while the turnover rates of these neurotransmitters in the anterior hypothalamus decrease when preovulatory levels of LH are at their highest. Further, a population of receptors for 5HT which occurs in the anterior hypothalamus in laying birds is absent in nonlaying, incubating hens. Taken together, these observations suggest that the preovulatory surge of LH is mediated by a transitory decrease in the inhibitory action of 5HT and possibly DA, on the secretion of LHRH. Neurons containing 5HT may play a role in the regulation of prolactin release and, more specifically, in the control of broodiness. Drugs which enhance the function of 5HT neurons stimulate prolactin release while increased prolactin secretion in incubating hens is associated with an increase in the turnover of 5HT in the anterior hypothalamus. No receptors for 5HT were demonstrable in the anterior pituitary gland, showing that the prolactin-releasing activity of 5HT must be mediated by a prolactin-releasing factor (PRF). A candidate for a physiological PRF is vasoactive intestinal polypeptide (VIP).(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗

PubMed1984

Stress and adrenal function.

The natural environment is composed of various potentially hostile stressors. It is a basic requirement of life that the cells of an organism must be maintained within closely defined physiological limits. The maintenance of a constant interior mileu results from physiological and behavioural homeostatic adaptations. The physiological regulation of homeostatis is achieved by complex endocrine interactions, principally by the hormones secreted from the adrenal glands. In this brief review the responses of the avian adrenal glands to stressful stimuli, the mechanism of adrenal activation, and the function of the adrenal responses will be considered.

Adaptation, Physiological↗

PubMed1984

Adrenocortical and adrenomedullary responses of fowl to treadmill exercise.

Adrenomedullary and adrenocortical responses of 40-day-old cockerels to treadmill exercise (0.4 km/hr, 0 degrees incline) were determined. Plasma concentrations of adrenaline were increased above both resting and control levels (P less than 0.001) after 30 min exercise and continued to increase (P less than 0.01) until the cessation of exercise. Plasma noradrenaline and dopamine levels were increased after 60 min of exercise (P less than 0.01 and 0.05, respectively). The adrenaline component of the plasma catecholamine response increased significantly above that of noradrenaline (P less than 0.001). Plasma corticosterone levels were also increased (P less than 0.001) during exercise and were closely correlated with plasma adrenaline concentrations. Exercise depleted (P less than 0.01) adrenal stores of adrenaline, which were inversely proportional to plasma adrenaline concentrations (P less than 0.001). Neither adrenal noradrenaline nor dopamine were significantly correlated with their plasma levels. These results suggest that adrenocortical (corticosterone) and adrenomedullary (adrenaline) responses during exercise may occur in response to similar stimuli or may be interrelated.

Adrenal Cortex↗

PubMed1984

Oestradiol 17 beta modifies fowl pituitary prolactin and growth hormone secretion in vitro.

Chicken pituitary glands were incubated in medium containing oestradiol 17 beta (E2), alone or together with single whole hypothalami. E2 stimulated prolactin release from the pituitary and increased the prolactin releasing activity of the hypothalamus, but did not affect growth hormone release. Preincubation of pituitaries with E2 dramatically stimulated subsequent prolactin release. Pituitaries primed with E2 were more responsive to the prolactin-stimulating effects of hypothalamic extract (HE) and thyrotrophin-releasing hormone (TRH) and more sensitive to the prolactin-inhibiting effect of dopamine. E2-primed pituitaries were much less sensitive to the growth hormone releasing activity of TRH and HE. These results show that E2 may regulate pituitary function by direct effects on hormone release by modifying pituitary sensitivity to stimulatory or inhibitory influences and by altering hypothalamic releasing activity.

Animals↗

PubMed1984

Stimulatory and inhibitory effects of prostaglandin E2 on prolactin release in the domestic fowl.

In vivo prolactin secretion was increased in immature cockerels 20-30 min after the intravenous administration of prostaglandin (PG) E2 at a dose of 200 micrograms/kg. The addition of PGE2 to incubation medium had no direct effect on the release of pituitary prolactin during short-term (3-hr) culture, but augmented the stimulatory effect of hypothalamic tissue on prolactin secretion. The stimulatory effect of serotonin, noradrenaline, acetylcholine, and histamine on hypothalamus-induced prolactin release was also increased when pituitaries were coincubated with 10(-7)M PGE2, as was the stimulatory effect of thyrotrophin-releasing hormone (TRH) and hypothalamic extract (HE). The long-term (24-hr) preincubation of pituitaries with 10(-7)M PGE2 reduced the responsiveness of the prolactin-secreting cells to TRH or HE stimulation. PGE2 treatment also reduced the stimulatory effect of hypothalamic tissue on prolactin release and diminished the stimulatory effect of serotonin on hypothalamus-induced prolactin secretion. A 24-hr preincubation of hypothalamic tissue with 10(-7)M PGE2 also reduced its stimulatory effect on prolactin release when subsequently incubated with control pituitary glands. These results demonstrate that PGE2 initially stimulates in vivo and in vitro prolactin secretion in the fowl, possibly by increasing the release of hypothalamic prolactin-releasing activity and/or by increasing pituitary sensitivity to provocative stimuli. Chronic PGE2 stimulation appears to result in a reduction in pituitary responsiveness to stimulatory influences and in the release of hypothalamic-releasing activity.

Acetylcholine↗

PubMed1984

Evidence for "short loop" feedback regulation of prolactin and growth hormone secretion in the pigeon.

When pigeons were injected with an extract of chicken hypothalamus, the increase in weight of the crop sac showed that prolactin secretion was stimulated. Crop sac weight was no higher after 16 days of injection than it was after 8 days. Pituitary gland content of prolactin and growth hormone was elevated at 8 days, but showed a relative decrease after a further 8 days of injections. Prolactin and growth hormone releasor activity in the hypothalamus was investigated in vitro. A decline during treatment with hypothalamic extract was seen, and by 8 days no releasor activity could be detected. Injection with ovine prolactin also reduced prolactin releasor activity in the hypothalamus. The results suggest that the secretion of prolactin and possibly also of growth hormone is controlled by a "short loop" negative feedback mechanism which acts on hypothalamic hypophysiotrophic hormones.

Animals↗

PubMed1984

Growth hormone and prolactin secretion in water-deprived chickens.

The deprivation of water for 12 or 24 hr increased the prolactin concentration in the plasma of immature chickens but had no effect on the circulating growth hormone (GH) level. The increase in plasma prolactin level reflected an increase in the basal rate of prolactin release from incubated hemipituitary glands and an increase in the responsiveness of the pituitary gland to hypothalamic releasing factors. The deprivation of water had no effect on basal level of pituitary GH release in vitro but abolished the stimulatory effect of the hypothalamus on in vitro GH secretion.

Animals↗