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Biomedical subjects

H Cox

Publications and source records attributed to H Cox.

At least 37 records · Page 2Linked to original sources
PubMed1996

A test of Martens, Vealey and Burton's theory of competitive anxiety.

The purpose of this study was to test Martens, Vealey, and Burton's (1990) theoretical model of competitive anxiety. In order to assess the variables corresponding to the model, a sample of 199 (N = 126, male and N = 73, female) individual sport athletes completed the following inventories: the Sport Anxiety Scale (SAS; Smith, Smoll, & Schutz, 1990), items related to the uncertainty of outcome, items related to the importance of outcome, and the Competitive State Anxiety Inventory-2 (CSAI-2; Martens, Burton, Vealey, Bump, & Smith, 1990). In addition, the short-form of the Marlowe-Crowne Social Desirability Scale (M-C SDS; Reynolds, 1982) was completed by all subjects. The variables corresponding to the model underwent psychometric evaluation as well as a check for social desirability effects before they were used in a LISREL causal path model procedure. Results showed no concrete support for the basic propositions advanced through the model. Trait-anxiety did not significantly affect perception of threat and perception of threat had minimal effect on state-anxiety. Recommendations for future research are discussed.

Adolescent↗
PubMed1995

Postprandial sympatho-adrenal activity: its relation to metabolic and cardiovascular events and to changes in meal frequency.

1. Sympatho-adrenal activity was measured after the consumption of a 3.15 MJ mixed meal. Whole-body noradrenaline spillover rates, forearm plasma noradrenaline spillover and adrenaline secretion rates were derived using isotope dilution methodology. Heart rate and blood pressure spectral analysis measurements were also made. The relation of sympathoadrenal activity to thermogenic and cardiovascular events was studied. Sympathetic nervous and thermogenic responses were measured for 120 min after the single 3.15 MJ meal and compared with those after three 1.05 MJ meals, given 30 min apart. 2. Whole-body and forearm plasma noradrenaline spillover, and the 0.1 Hz component of systolic pressure power all increased significantly postprandially, while the 0.1 Hz component of heart rate variability, an indirect index of cardiac sympathetic nervous activity, remained unaltered. Adrenaline secretion was unaltered postprandially. Whole-body plasma noradrenaline spillover and thermogenesis during the 120 min postprandial period were 37% and 36% higher after the single meal as compared with the multiple meals, although this was not statistically significant. 3. The sympathetic neural responses were delayed in relation to peak plasma insulin levels and sustained in the face of declining insulin levels. Energy expenditure increased significantly postprandially, but there was no direct quantitative relationship to plasma noradrenaline spillover. Forearm oxygen consumption did not increase postprandially despite significant increases in regional noradrenaline spillover. Thus, no close relation was demonstrated between postprandial sympathetic nervous activation and either insulin secretion or thermogenesis.

Adult↗
PubMed1995

Thick bone section preparation using a silicon-rubber-based sealant.

A method has been developed, using a silicon-rubber-based sealant, which allows 2-3-mm-thick specimens to be maintained in a protected fluid environment for a number of months, without risk of dehydration. Following this, the specimen can be retrieved, stained, embedded and sectioned further. For example, 2-mm-thick sections of fixed unstained bone are easily examined by means of epi-illuminated polarized light and fluorescence microscopies using either conventional or confocal optics. The method could easily be extended to other tissues, for example brain tissue.

Bone and Bones↗
PubMed1995

Visceral leishmaniasis: rapid response to AmBisome treatment.

There appears to be an increase in imported cases of visceral leishmaniasis in Northern Europe; many are children infected on holiday in the Mediterranean. Making the diagnosis in young children can be difficult especially when an adequate travel history is not obtained at presentation. Two infants with visceral leishmaniasis are presented who were initially felt to have alternative diagnoses and who subsequently responded dramatically to a short course of liposomal amphotericin B (AmBisome).

Amphotericin B↗
PubMed1995

Regional epinephrine kinetics in human heart failure: evidence for extra-adrenal, nonneural release.

A number of neurohumoral processes are activated in heart failure, including an increase in the plasma concentration of epinephrine. Radiotracer methods were applied in 42 patients with severe heart failure and 31 healthy volunteers to ascertain the rate at which epinephrine is released to plasma and to evaluate the contribution of extra-adrenal sources. The increase in arterial plasma epinephrine observed in the heart failure patients was explained principally by a 34% (P < 0.001) reduction in the whole body clearance rate of epinephrine from plasma. Regional venous sampling from the heart, lungs, and hepatomesenteric beds was performed in a subgroup of the study population, revealing a significant increase in the release rate of epinephrine to plasma from these organs in heart failure which accounted for 26% of the whole body plasma epinephrine appearance rate. To establish whether the cardiac epinephrine release was of neuronal origin, a physical (cycling) or mental (difficult mental arithmetic) stressor was applied as a sympathoexcitatory stimulus, given that a proportional release of norepinephrine and epinephrine could be expected if sympathetic nerves were the source. These interventions caused significant increases in the regional spillover of norepinephrine to plasma but not that of epinephrine. These findings suggest that nonadrenal tissues contribute significantly to the whole body epinephrine release rate in heart failure and that this may arise from a site other than sympathetic neurons.

Adrenal Glands↗
PubMed1995

Effects of aging on epinephrine secretion and regional release of epinephrine from the human heart.

In contrast to the sympathetic nervous system, which is activated by aging in at least some sympathetic nervous outflows, epinephrine release from the adrenal medulla appears to be either normal or low in the elderly. Using isotope dilution methodology, we studied the effect of aging on the secretion of epinephrine in 19 men, aged 20-30 yr, and 15 men, aged 60-75 yr. Measurements were made both at rest and during the application of laboratory stressors, as diminished adrenal medullary responsiveness possibly contributes to the impairment of some cardiovascular and metabolic responses to stress described previously in the elderly. Epinephrine secretion at rest was lower in the older men (mean +/- SEM, 0.86 +/- 0.10 nmol/min) than in the younger men (1.45 +/- 0.17 nmol/min; P < 0.05). Due to 20% lower plasma epinephrine clearance in the older men (P < 0.01), the reduction in the plasma concentration of epinephrine (0.37 +/- 0.03 vs. 0.52 +/- 0.06 nmol/L; P = 0.06) was proportionally less than that in epinephrine secretion. In the younger men, epinephrine secretion doubled or tripled during mental stress, isometric exercise, and dynamic exercise. Epinephrine responses to the stressors were reduced in older men, being equivalent to only 44% (P < 0.05), 44% (P = 0.1), and 33% (P = 0.01) of the corresponding responses in the younger men. After uptake from plasma, in some circumstances epinephrine is released from sympathetic nerves as a cotransmitter, where it can augment the release of the major sympathetic transmitter, norepinephrine. We also measured regional extraadrenal release of epinephrine from the heart to test whether the previously described increased release of norepinephrine from the cardiac sympathetic nerves with aging might result from facilitator effects of epinephrine released as a cotransmitter. At rest, epinephrine was released from the heart (9.4 +/- 2.6 pmol/min) in older men only (P < 0.01) despite the fact that adrenal medullary secretion of epinephrine was reduced. Failure of epinephrine and norepinephrine spillover from the heart to increase in parallel in the elderly during the sympathetic excitation accompanying exercise suggested that epinephrine lay outside the sympathetic nerves, perhaps arising from extraneuronal synthesis in the heart. We have not yet tested whether extraneuronal, in contrast to neuronal, epinephrine release in the heart could contribute to the observed higher rates of norepinephrine release in the elderly.

Adult↗
PubMed1994

Cellular localization of putative odorant receptor mRNAs in olfactory and chemosensory neurons: a non radioactive in situ hybridization study.

The precise cellular localization of mRNAs for putative odorant receptors was investigated in the mouse chemosensory system (olfactory epithelium, septal organ and vomeronasal organ). Four additional members of the odorant receptor family were cloned from mouse olfactory mucosa and in situ hybridization was performed with paraffin-embedded tissue using digoxigenin labelled, non-radioactive antisense RNA probes for these individual receptor genes. The results clearly demonstrated expression of odorant receptors within single individual receptor neurons and there was no receptor expression either in the basal cells (stem cells) or supporting cells (sustentacular cells). In contrast to the uniform expression of olfactory marker protein mRNA within the layer of mature neurons, odorant receptor expression was localized in scattered individual cells but with a bilateral symmetry. The number of positive cells was far less than the number detected with the olfactory marker protein probe. Interestingly, rostro-caudal and dorso-ventral sites of expression were specific to each receptor probe. Under the highly stringent hybridization and washing conditions used here, even mixed RNA probes prepared from 4 different odorant receptor genes were only expressed in a maximum of 20-60 neurons per section (i.e. less than 0.1% of the population of total receptor neurons) suggesting the size of odorant receptor superfamilies to be larger than previously estimated. Some chemoreceptor neurons in the septal organ and vomeronasal organ also expressed odorant receptor mRNAs suggesting that these two additional non-olfactory chemosensory systems share the same chemoreceptive pathway as the olfactory system.

Amino Acid Sequence↗
PubMed1994

Mineralocorticoid induced hypertension and noradrenaline spillover in man.

This study examined haemodynamics and noradrenaline spillover in five normal men before and on day 7 of oral fludrocortisone treatment, 0.3 mg/day. Resting systolic (105 to 115 mm Hg, standard error of the difference +/- 2.0, p < 0.01) and diastolic (65 to 73 mm Hg, +/- 3.0, p < 0.05) blood pressure increased, as did cardiac output, from 5.0 to 5.7 L/min (+/- 0.1, p < 0.01). Calculated total peripheral resistance fell from 21.2 to 20.0 mm Hg/L/min (+/- 0.4, p < 0.05). Fludrocortisone produced a fall in plasma potassium, renin and aldosterone concentrations and haematocrit and a rise in body weight. Cold pressor responses were increased by fludrocortisone, from 7.5 to 20 mm Hg (+/- 3.0, p < 0.01), and forearm vascular resistance rose 12 arbitrary resistance units (R) before and 36 R units after treatment (+/- 5.0, p < 0.01). Total body spillover of noradrenaline was decreased from 9.48 to 7.36 ng/kg/min (+/- 0.86, p < 0.05). There were no changes in forearm noradrenaline spillover at rest or during cold pressor stimulation. It appears unlikely that the sympathetic nervous system plays a major role in the pathogenesis of mineralocorticoid hypertension in man.

Adult↗
PubMed1993

Multiparameter flow cytometric analysis of a novel cytotoxin (factor 2) induced tumor cell membrane permeability.

An improved twin-probe multiparameter flow cytometric technique was applied to examine a novel cytotoxin, Factor (F2), induced tumor cell permeability. Ability to retain preloaded intracellular bis-carboxyethyl carboxyfluorescein (BCECF, green fluorescence) and to exclude extracellular propidium (red fluorescence) was measured simultaneously with forward and right-angle scatter. In addition to the two expected cell populations which were stained green negative, red positive ("membrane-damaged" and "non-viable", Region 2), and green positive, red negative ("membrane intact" and "viable", Region 3), a third population was seen which fluoresced neither green nor red and displayed intermediate light scatter characteristics (Region 1). K562 cells progressed from Region 3 to Region 1, and then from Region 1 to Region 2 after treatment with F2. These results suggest that sequential changes in membrane structure lead to increased permeability, first with respect to intracellular BCECF and then in turn to extracellular propidium. Flow cytometric changes caused by F2 were detectable 10 min after treatment with 2.5 U/ml of F2, and 5 min after 10 or 40 U/ml of F2. Flow cytometric analysis showed that F2-induced tumor cell lysis and growth inhibition were accompanied by rapid alternations in tumor cell membrane permeability. Flow cytometric analysis also distinguished F2 cytotoxicity from phorbol myristate acetate (PMA) associated cytotoxicity to K562 cells and determined that F2 produced spontaneously or induced by PMA and/or ciprofloxacin had a similar ability to induce tumor cell membrane permeability change.

Cell Membrane Permeability↗
PubMed1993

Elevated total body noradrenaline spillover in normotensive members of hypertensive families.

1. In prehypertension, abnormalities in cardiovascular control mechanisms have been described. It has been postulated that this may involve hereditary disturbances in the sympathetic regulation of blood pressure. Since the neurochemical methods used to test sympathetic nervous system activity have been rather imprecise, in the present study we have applied noradrenaline plasma kinetic methodology to evaluate sympathetic activity in normotensive subjects with a familial predisposition to essential hypertension. 2. Total body noradrenaline spillover to plasma, an index of integrated sympathetic nerve firing rates, was calculated during infusion of l-[7-3H]noradrenaline in 11 normotensive offspring of essential hypertensive parents and 11 age-, height- and weight-matched normotensive offspring of normotensive parents. 3. The resting arterial plasma noradrenaline concentration was higher in healthy subjects with a family history of essential hypertension (1.41 +/- 0.15 nmol/l, mean +/- SEM, P < 0.002) than in normotensive subjects with no family history of essential hypertension (0.82 +/- 0.07 nmol/l). The overall rate of spillover of noradrenaline to plasma was also elevated in the normotensive offspring of hypertensive parents (4.34 +/- 0.54 nmol/min) compared with subjects with a negative family history of essential hypertension (2.02 +/- 0.20 nmol/min). Similarly, the arterial plasma concentration of the noradrenaline precursor 3,4-dihydroxyphenylalanine was higher in subjects with a positive family history of essential hypertension (7.55 +/- 0.24 nmol/l) than in normotensive control subjects (5.97 +/- 0.30 nmol/l, P < 0.001).(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1993

Evaluation of a novel fluorescence polarization immunoassay for teicoplanin.

A fluorescence polarization immunoassay (FPI) for teicoplanin that uses the TDx Instrument System (Abbott, Irving, Tex.) as an automated analyzer has been developed by Innotron of Oregon Inc. and was evaluated in patients with staphylococcal infections enrolled in a clinical trial of the antibiotic. The assay proved accurate in estimating concentrations of between 5 and 100 mg/liter. The intraassay coefficient of variation was < 7.3%, while the interassay variance was < 11.6% against three commercially prepared standards at known concentrations of approximately 5, 35, and 75 mg/liter. Against routinely prepared standards at 10 concentrations between 5 and 100 mg/liter analyzed in a single run, the coefficient of variance did not exceed 4.3%. Compared with bioassay, the FPI demonstrated good correlation in terms of reliability (r = 0.909) in samples containing teicoplanin only and specificity (r = 0.916) in samples containing both teicoplanin and gentamicin. With a turnaround time of 20 min and with only 50 microliters of serum needed for estimation of the amount of drug in a sample, the FPI described here should provide a useful method of teicoplanin measurement in routine diagnostic laboratories.

Biological Assay↗
PubMed1992

Characterization of the interaction of the cervane alkaloid, imperialine, at muscarinic receptors in vitro.

The action of the cervane alkaloid, imperialine, has been assessed at M1, M2 and M3 receptors in functional assays and at M1, M2, M3 and putative M4 sites in binding studies. In functional studies, imperialine acted as a selective surmountable antagonist at M2 receptors in guinea-pig isolated atria and uterus (-log KB = 7.7 and 7.4, respectively), in comparison to M1 receptors in canine isolated saphenous vein (-log KB = 6.9) or M3 receptors in a range of guinea-pig isolated smooth muscles including ileum, trachea, fundus, seminal vesicle or oesophagus (-log KB = 6.6-6.8). In rat aorta, the -log KB value at the M3 receptor (5.9) was slightly, but significantly, lower. In competition radioligand binding studies, imperialine was also selective toward to M2 sites in rat myocardium (-log Ki = 7.2) with respect to M1 and M3 sites (rat cerebral cortex, rat submaxillary gland; -log Ki = 6.1 and 5.7, respectively). However, it did not significantly discriminate between rat cardiac M2 sites and putative M4 sites in rabbit lung (-log Ki = 6.9). Imperialine resembles the alkaloid himbacine in terms of its pharmacological profile at muscarinic receptor subtypes in that it acts as an M2 selective antagonist with respect to M1 or M3 sites. It may also provide a second, commercially available, antagonist with which to discriminate between M1 and M4 receptors.

Alkaloids↗
PubMed1992

Relationship between the sympatholytic action of nebivolol and hypotension.

Nebivolol, a chemically novel beta 1-adrenoceptor antagonist, acutely lowers blood pressure in spontaneously hypertensive rats, anaesthetised normotensive dogs, and hypertensive patients. We have investigated the actions of dl-nebivolol in five conscious normotensive rabbits (sham, mean blood pressure (BP) of 82.2 +/- 4.1 mm Hg, mean +/- SEM) and four hypertensive rabbits (renal wrap hypertension) (wrap, mean BP of 117.6 +/- 1.5 mm Hg). Nebivolol (1 mg/kg i.v.) did not significantly lower the BP or heart rate in either group 30 min after injection. In the same rabbits, on another day, after autonomic blockade (mecamylamine), nebivolol (0.1, 0.3, and 1.0 mg/kg i.v.) right shifted the bolus i.v. isoproterenol tachycardia dose-response curves by dose ratios of 5, 18, and 90 in sham rabbits, respectively, and 5, 11, and 23 in wrap rabbits, respectively, indicating significant cardiac beta 1-adrenoceptor antagonism. In guinea pig isolated right atria pretreated with atropine (1 microM) and desipramine (DMI, 0.1 microM), norepinephrine concentration-response curves were antagonised competitively by nebivolol (3-100 nM), giving a pKb of 7.90. In separate atria without DMI pretreatment, neither nebivolol (100 nM) nor propranolol (100 nM) had any significant effect on the increase in the rate of norepinephrine efflux following electrical field stimulation (0.5-2 Hz, 3 min). These findings suggest that at concentrations of nebivolol that show substantial beta 1-adrenoceptor antagonism, there is no evidence of hypotension or bradycardia nor additional effects on cardiac norepinephrine release. Why nebivolol lowers blood pressure in some species but not in the conscious rabbit is not known.

Adrenergic beta-Antagonists↗
PubMed1991

c-myc protein product is a marker of DNA synthesis but not of malignancy in human gastrointestinal tissues and tumours.

c-myc is a conserved cellular gene. The gene product is a nuclear-bound 62,000 molecular weight phosphoprotein (p62c-myc). Although p62c-myc levels have been measured in colorectal cancers, little is known about the expression of the protein in upper gastrointestinal tumours and tissues. Studies were performed on tumour and mucosal specimens from 87 patients with colorectal cancer, from two with polyposis coli, from six with squamous oesophageal carcinomas and from 18 with gastric carcinomas. The mean p62c-myc content was measured in units of fluorescence in the G1 diploid and G2 diploid peaks of the cell cycle by multiparameter flow cytometry using the 6E10 antibody. The nuclear p62c-myc content increased with DNA synthesis in tumours and mucosa. G2 levels of p62c-myc were higher in glandular mucosa than in adenocarcinomas. No differences in peak nuclear c-myc expression were found in relation to histological grade or to anatomical site of colorectal tumours. There was a broadly inverse relationship between G2 p62c-myc levels in tumours and mucosa and their in vivo 5-bromo-2'-deoxyuridine labelling indices. Nuclear p62c-myc levels are cell cycle related but the protein has not been shown to be a marker of increased tissue proliferation or of gastrointestinal malignancy. The reduction of the nuclear p62c-myc content of many adenocarcinoma cells compared with glandular mucosa cells suggests that reduced synthesis or nuclear retention of the normal protein may be a factor in the development of gastrointestinal adenocarcinomas, although the mechanism by which this may occur is not clear.

Adenocarcinoma↗