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Biomedical subjects

M Brown

Publications and source records attributed to M Brown.

At least 793 records · Page 44Linked to original sources
PubMed1979

The night comes alive with laughter.

A sense of isolation is often felt by the elderly who may be unable to go out and meet people. In Castleford an evening group has been set up to try to alleviate this and give families an evening off from caring for their elderly relatives. In this Joint Care Award entry Malcolm Hornby, hospital social services officer, Wakefield, and Mike Brown, district general administrator, Wakefield AHA, describe how the scheme was set up; its success is self-evident.

Aged↗
PubMed1979

Antiallergy agents. 1. 1,6-Dihydro-6-oxo-2-phenylpyrimidine-5-carboxylic acids and esters.

The synthesis of some 1,6-dihydro-6-oxo-2-phenylpyrimidine-5-carboxylic acids and esters with potent oral and intravenous antiallergic activity against passive cutaneous anaphylaxis in the rat is described. Requirements for high activity include a free NH group in the pyrimidinone nucleus and a small to medium size ortho alkoxy or alkenyloxy group on the phenyl ring. It is suggested that in the case of the highly active compounds hydrogen bonding occurs between a nitrogen of the pyrimidine ring and the ethereal oxygen. The nature of this bonding and its possible contribution to an optimum configuration for the molecules is discussed.

Animals↗
PubMed1979

Effect of baroreceptor deafferentation on central catecholamines in the rat.

1. Sinoaortic deafferentation in the rat leads to increased blood pressure and heart rate. 2. Early increases in tyrosine hydroxylase activity both in brain stem and hypothalamus suggest that increased noradrenaline synthesis may contribute to the development of neurogenic hypertension. 3. After 4 weeks, phenylethanolamine-N-methyltransferase activity was reduced in the hypothalamus. 4. Noradrenaline- and adrenaline, but not dopamine-containing neurones may participate in regulation of sympathetic efferent activity.

Afferent Pathways↗
PubMed1979

Morphine acute effects on spontaneous multiunit activity recorded simultaneously from medial thalamus and caudate nucleus in freely behaving rats.

Treatment with varying doses of morphine and its antagonist naloxone produced different response patterns in "spontaneous" multiunit discharges recorded from the medial thalamus and caudate nucleus of freely behaving rats previously implanted, stereotaxically, with permanent semimicro-electrodes. The changes in electrical discharges induced by incremental doses of morphine exhibited dose-related patterns, and could be reversed by naloxone. This procedure, testing several incremental doses of a drug, provides a tool with which to identify and classify the specific response patterns induced by morphine. The two structures examined in the present study exhibited four response patterns to the treatments but only one pattern of response was similar in the two nuclei. The medial thalamic units are more sensitive to morphine than those recorded from the caudate nucleus. The present finding, i.e., acute effects of morphine, provides basic information with which to examine the physiological properties underlying the chronic effects of morphine.

Animals↗
PubMed1979

Systems development: trends, issues and implications.

Integrated systems are developing and growing in the U.S. health care industry. This phenomenon has many implications for health care institutions, communities and health care consumers across the country.

Centralized Hospital Services↗
PubMed1979

Genetic Analysis of a Baculovirus, Autographa californica Nuclear Polyhedrosis Virus I. Isolation of Temperature-Sensitive Mutants and Assortment into Complementation Groups.

Temperature-sensitive (ts) mutants were isolated from the baculovirus Autographa californica (alfalfa looper) MNPV, grown in Spodoptera frugiperda (fall armyworm) cells in the presence of N-methyl-N'-nitro-N-nitrosoguanidine. Of 567 plaque isolates screened, 27 were temperature sensitive (ts), representing a mutation frequency of 4.8%. Ten ts mutants were studied in detail: six failed to yield nonoccluded virus at 33 degrees C (NOV mutants), whereas the other four produced nonoccluded virus but were restricted in formation of polyhedra at 33 degrees C (Poly mutants). One of the six NOV mutants failed to synthesize viral DNA. Reversion and leak frequencies were determined, and the mutants were assorted into complementation groups based on the yield of polyhedrin synthesis in cells coinfected with pairs of mutants at 33 degrees C, as measured by radioimmunoassay. For NOV mutants, complementation indexes were also based on virus yield and were consistent with those based on polyhedrin synthesis. Nine mutants were assorted into five complementation groups. One mutant remained unclassified.

Journal Article↗
PubMed1979

A test for bladder neck competence: the fluid bridge test.

The momentary entry of urine into the proximal urethra during coughing can be demonstrated by a new test which can be conducted using apparatus now commonly available for urodynamic investigations. If the bladder neck opens, a fluid bridge is established between points of pressure measurement in the bladder and in the proximal urethra. Thus, the pressures at these two points momentarily become equal. The clinical value and relevance to physiology may not become clear for some time, but the relatively simple apparatus and procedure, and the ease with which the results can be translated into physical facts, provide important advantages over other dynamic tests of the urethra which are currently possible.

Female↗
PubMed1979

Somatostatin analogs inhibit somatostatin release.

To determine if, like insulin, somatostatin inhibits its own secretion from the pancreas, nonimmunoreactive analogs of somatostatin were perfused in an isolated dog pancreaticoduodenal preparation using a nonrecirculating system. [D-Trp8-D-Cys14]somatostatin, at a concentration of 200 ng/ml, blocked the response of somatostatin-like immunoreactivity (SLI) to cholecystokinin and arginine. When perfusion of the analog was discontinued, SLI release increased. At a concentration of 0.1 ng/ml, des Asn5-[D-Trp8]somatostatin lowered SLI levels significantly without significantly reducing glucagon levels. At a concentration of 1 ng/ml, des Asn5-[D-Trp8]somatostatin significantly inhibited SLI as well as insulin and glucagon release. Perfusion of glucagon at a concentration of 10 ng/ml failed to overcome the blockade of SLI and insulin release caused by 50 ng/ml des Asn5-[D-Trp8]somatostatin. The results are compatible with a direct inhibitory effect of somatostatin analogs upon SLI release and raise the possibility of a self-inhibiting action of the native hormone.

Animals↗
PubMed1979

Somatostatin: central nervous system actions on glucoregulation.

Somatostatin (SRIF) has been tested for its actions on the central nervous system to affect glucoregulation. In doses ineffective when given systemically , SRIF and SRIF analogs given intracisternally (ic) reduce hyperglycemia and hyperglucagonemia after ic bombesin administration. The SRIF analog, des-AA1, 2, 4, 5, 12, 13-[D-Trp8]SRIF, decreases plasma insulin and elevates plasma glucose and glucagon when given systemically. However, when given ic, this peptide prevents the rise in glucose and glucagon after ic bombesin administration and is 10 times more potent than SRIF in reducing bombesin-induced hyperglycemia. Other analogs of SRIF and various unrelated peptides were found to be ineffective in reducing bombesin-induced hyperglycemia. des-AA1, 2, 4, 5, 12, 13-[D-Trp]SRIF prevented the hyperglycemia induced by surgical stress or by ic administration of beta-endorphin or carbacol. des-AA1, 2, 4, 5, 12, 13-[D-Trp]SRIF given ic did not prevent hyperglycemia induced by systemic administration of epinephrine, arginine, or glucagon. These studies suggest that SRIF and its analogs may act within the brain to affect glucoregulation.

Animals↗
PubMed1979

Effects of neuropeptides on adenohypophyseal hormone response to acute stress in male rats.

The effects of bombesin and other unrelated oligopeptides on hormonal changes induced by stress were studied in conscious adult male rats. Restraint in the cold for 1 h increased plasma corticosterone and PRL levels and decreased GH values but had no effect on LH levels. Bombesin (5 microgram), given intracerebroventricularly (ivt) before stress, inhibited the PRL rise without affecting corticosterone, GH, or LH response. A complete blockade of PRL rise was observed with doses of bombesin ranging from 5 microgram to 100 ng ivt, regardless of the duration (15, 30, 45, or 60 min) or the nature (cold exposure or restraint at room temperature) of the stressor agents. Bombesin was 10(3) more potent as a PRL inhibitor when given ivt than when given iv, and its ivt effect was not reversed by naloxone (1 or 10 mg/kg). Among other unrelated peptides tested (beta-endorphin, neurotensin, substance P, and TRH; 5 microgram ivt), only neurotensin decreased plasma PRL levels in rats subjected to restraint in the cold for 1 h. These results show that in conscious male rats, centrally administered bombesin has a very potent and long acting inhibitory effect on PRL release induced by acute stress. Since a bombesin-like peptide has been found in rat brain, its physiological role in PRL regulation remains to be elucidated.

Animals↗
PubMed1979

Central nervous system action of bombesin: mechanism to induce hyperglycemia.

Bombesin acts within the brain to produce a prompt and sustained hyperglycemia, hyperglucagonemia, and relative or absolute hypoinsulinemia. Bombesin does not decrease plasma glucose turnover. Acute adrenalectomy but not hypophysectomy prevents hyperglycemia and hyperglucagonemia after intracisternal administration of bombesin. Administration of bombesin into the lateral ventricle of awake, unrestrained animals results in elevation of plasma glucose, preceded by a significant increase in plasma epinephrine and no increase in plasma norepinephrine or dopamine. Systemic administration of somatostatin prevents bombesin-induced hyperglycemia and hyperglucagonemia. These data support the conclusion that bombesin acts within the brain to increase sympathetic outflow resulting in increased adrenalmedullary epinephrine secretion, followed by depression of plasma insulin and elevation of plasma glucagon and glucose.

Adrenal Glands↗