PubMed Health⌕ Search

Biomedical subjects

P R Saunders

Publications and source records attributed to P R Saunders.

At least 19 recordsLinked to original sources
PubMed2001

Chronic fatigue syndrome: neurological findings may be related to blood--brain barrier permeability.

Despite volumes of international research, the etiology of chronic fatigue syndrome (CFS) remains elusive. There is, however, considerable evidence that CFS is a disorder involving the central nervous system (CNS). It is our hypothesis that altered permeability of the blood-brain barrier (BBB) may contribute to ongoing signs and symptoms found in CFS. To support this hypothesis we have examined agents that can increase the blood-brain barrier permeability (BBBP) and those that may be involved in CFS. The factors which can compromise the normal BBBP in CFS include viruses, cytokines, 5-hydroxytryptamine, peroxynitrite, nitric oxide, stress, glutathione depletion, essential fatty acid deficiency, and N-methyl-D-aspartate overactivity. It is possible that breakdown of normal BBBP leads to CNS cellular dysfunction and disruptions of neuronal transmission in CFS. Abnormal changes in BBBP have been linked to a number of disorders involving the CNS; based on review of the literature we conclude that the BBB integrity in CFS warrants investigation.

Blood-Brain Barrier↗
PubMed2000

Nature over nurture: temperament, personality, and life span development.

Temperaments are often regarded as biologically based psychological tendencies with intrinsic paths of development. It is argued that this definition applies to the personality traits of the five-factor model. Evidence for the endogenous nature of traits is summarized from studies of behavior genetics, parent-child relations, personality structure, animal personality, and the longitudinal stability of individual differences. New evidence for intrinsic maturation is offered from analyses of NEO Five-Factor Inventory scores for men and women age 14 and over in German, British, Spanish, Czech, and Turkish samples (N = 5,085). These data support strong conceptual links to child temperament despite modest empirical associations. The intrinsic maturation of personality is complemented by the culturally conditioned development of characteristic adaptations that express personality; interventions in human development are best addressed to these.

Adolescent↗
PubMed1999

Corticotropin-releasing hormone mimics stress-induced colonic epithelial pathophysiology in the rat.

We examined the effect of stress on colonic epithelial physiology, the role of corticotropin-releasing hormone (CRH), and the pathways involved. Rats were restrained or injected intraperitoneally with CRH or saline. Colonic segments were mounted in Ussing chambers, in which ion secretion and permeability (conductance and probe fluxes) were measured. To test the pathways involved in CRH-induced changes, rats were pretreated with hexamethonium, atropine, bretylium, doxantrazole, alpha-helical CRH-(9-41) (all intraperitoneally), or aminoglutethimide (subcutaneously). Restraint stress increased colonic ion secretion and permeability to ions, the bacterial peptide FMLP, and horseradish peroxidase (HRP). These changes were prevented by alpha-helical CRH-(9-41) and mimicked by CRH (50 microgram/kg). CRH-induced changes in ion secretion were abolished by alpha-helical CRH-(9-41), hexamethonium, atropine, or doxantrazole. CRH-stimulated conductance was significantly inhibited by alpha-helical CRH-(9-41), hexamethonium, bretylium, or doxantrazole. CRH-induced enhancement of HRP flux was significantly reduced by all drugs but aminoglutethimide. Peripheral CRH reproduced stress-induced colonic epithelial pathophysiology via cholinergic and adrenergic nerves and mast cells. Modulation of stress responses may be relevant to the management of colonic disorders.

Animals↗
PubMed1999

Complementary health practitioners' attitudes, practices and knowledge related to women's cancers.

OBJECTIVE: To document the attitudes, practices and knowledge of 3 groups of complementary practitioners (naturopathic doctors, chiropractors and massage therapists) regarding women's cancers in general and ovarian cancer specifically. DESIGN: A mailed survey questionnaire was followed by a reminder card and a second mailing of the questionnaire. SETTINGS: National samples were obtained for naturopathic doctors and chiropractors. The massage therapist sample was drawn from Ontario only because of the absence of a national listing of massage therapists. MAIN OUTCOME MEASURES: Practitioners reported response to patients' suspicious symptoms. Practitioners' perceptions of patients' motivations for seeking treatment. Practitioners' satisfaction with interactions with conventional practitioners. Practitioners' perceptions of their role in the care of women at risk of, or diagnosed with, cancer. Practitioners' perceptions of their knowledge regarding women's cancers. Practitioners' knowledge specific to ovarian cancer. RESULTS: A total of 894 completed questionnaires were returned, providing a response rate of 56%. The vast majority of practitioners who saw women with symptoms possibly related to cancer referred them to a family physician or a cancer specialist. Motivations that practitioners most frequently heard expressed by women seeking complementary treatments were "maximizing quality of life," "seeking natural approaches to healing" and "looking to stay well when disease is in remission." Most respondents were dissatisfied with patient-related communication with both family physicians and cancer specialists. The majority of complementary practitioners indicated that they have an important role to play in the postdiagnostic care of women with cancer. Considerable interest was expressed in further education concerning ovarian cancer. CONCLUSIONS: Whereas the professions reached through this survey differ in important ways from each other, they share an interest in being involved in the care of women with cancer, as well as an enthusiasm for the development of continuing professional education programs to help them better serve their clients.

Adult↗
PubMed1998

Stress stimulates transepithelial macromolecular uptake in rat jejunum.

Evidence suggests that stress may be a contributing factor in intestinal inflammatory disease; however, the involved mechanisms have not been elucidated. We previously reported that acute stress alters epithelial physiology of rat intestine. In this study, we documented stress-induced macromolecular transport across intestinal epithelium. After exposure of Wistar-Kyoto rats to acute restraint stress, transport of a model protein, horseradish peroxidase (HRP), was assessed in isolated segments of jejunum. The flux of intact HRP was significantly enhanced across intestine from stressed rats compared with controls. Electron microscopy revealed HRP-containing endosomes within enterocytes, goblet cells, and Paneth cells of stressed rats. The number and area of HRP endosomes within enterocytes were found to be significantly increased by stress. HRP was also visualized in paracellular spaces between adjacent epithelial cells only in intestine from stressed rats. Atropine treatment of rats prevented the stress-induced abnormalities of protein transport. Our results suggest that stress, via a mechanism that involves release of acetylcholine, causes epithelial dysfunction that includes enhanced uptake of macromolecular protein antigens. We speculate that immune reactions to such foreign proteins may initiate or exacerbate inflammation.

Animals↗
PubMed1998

Epithelial ion transport and barrier abnormalities evoked by superantigen-activated immune cells are inhibited by interleukin-10 but not interleukin-4.

Many studies have indicated an association between bacteria and the severity of enteric secretory or inflammatory disorders. We previously showed that monolayers of human T84 epithelial cells display altered ion transport and permeability after coculture with Staphylococcus aureus enterotoxin B (SEB, a model superantigen)-activated immune cells, where interferon-gamma and tumor necrosis factor-alpha were key mediators in the pathophysiology. Here we examined whether the regulatory Th2-type cytokines, interleukin (IL)-10 and IL-4, could prevent these epithelial irregularities. T84 monolayers were cocultured with human peripheral blood mononuclear cells (PBMC) or T cell-enriched, monocyte-depleted PBMC (T + B cells) +/- SEB for 20 hr in the presence or absence of IL-10 or IL-4. Subsequently, T84 monolayers were mounted in Ussing chambers and ion transport (short-circuit current (Isc) and DeltaIsc evoked by forskolin) and permeability (ion resistance and probe fluxes) were assessed. IL-10 dose-dependently inhibited the increased T84 permeability and the reduced responsiveness to forskolin that were evoked by coculture with SEB-activated PBMC or T + B cells. Similar changes in T84 function occurred in response to conditioned medium from SEB-activated immune cells; however, addition of IL-10 to the conditioned medium did not prevent the changes in epithelial function. In contrast, when PBMC were stimulated with SEB in the presence of IL-10, the subsequent conditioned medium was less effective in evoking altered epithelial function. These data suggest that the affect of IL-10 was due to effects on the immune cells and not directly on the epithelium. In contrast to IL-10, IL-4 did not ameliorate any of the immune-mediated changes in T84 function. We conclude that IL-10 can reduce the epithelial functional changes caused by SEB-activated immune cells and this data adds further support for IL-10 immunotherapy in the treatment of intestinal secretory or inflammatory disorders.

Cell Line↗
PubMed1997

Cholinergic nerves mediate stress-induced intestinal transport abnormalities in Wistar-Kyoto rats.

We have previously reported that acute stress alters intestinal transport physiology in Wistar-Kyoto rats, a stress-susceptible strain. In this study, we tested the hypothesis that the abnormalities in these rats are due to cholinergic mechanisms. Atropine- or saline-treated rats were exposed to acute restraint stress, and, subsequently, electrophysiological parameters of excised jejunal segments were assessed in Ussing chambers. Compared with the parent Wistar rat strain, Wistar-Kyoto rats demonstrated significantly greater stress-induced changes in ion secretion and permeability. The activity of cholinesterase in intestinal mucosal homogenates was significantly less in Wistar-Kyoto than in Wistar rats. Atropine pretreatment of rats before stress corrected the epithelial pathophysiology. Our results suggest that stress stimulated the release of acetylcholine, resulting in altered epithelial function in these genetically predisposed rats.

Animals↗
PubMed1994

Propofol infusion and the suppression of consciousness: the EEG and dose requirements.

We have used Median Power Frequency (MPF) to study changes in the electroencephalogram during propofol infusions in 52 women about to undergo gynaecological surgery. Patients were allocated to receive propofol by one of nine different manually-controlled infusion schemes designed to achieve and maintain a stable blood propofol concentration between 1.0 and 6.0 micrograms ml-1, covering a range of states between conscious sedation and full anaesthesia. We recorded the changes in MPF and the response to clinical signs of loss of consciousness at these different doses and concentrations of propofol. Using probit analysis, we derived MPF values corresponding to 50% and 95% suppression of response to verbal (9.3 Hz and 6.8 Hz), eyelash (8.9 Hz and 6.7 Hz) and venepuncture (5.7 Hz and 3.0 Hz) stimuli. Likewise, we obtained dose and concentration requirements for propofol to suppress these stimuli. The mean (95% confidence intervals) ED50 (5.8 (3.5-6.8) mg kg-1 h-1) and ED95 (8.3 (7.1-16.9) mg kg-1 h-1) propofol doses for suppression of consciousness were similar to the values for suppression of the eyelash reflex (6.2 (5.3-6.8) mg kg-1 h-1 and 8.6 (7.8-10.8) mg kg-1 h-1, respectively). The EC50 for loss of consciousness was a propofol concentration of 2.3 (1.8-2.7) micrograms ml-1 and for 50% suppression of MPF was 3.1 (2.7-3.5) micrograms ml-1. The dose required for 50% suppression of MPF was 7.1 (6.2-8.0) mg kg-1 h-1. After 30 min, at blood propofol concentrations > 4.0 micrograms ml-1, consistent with stable anaesthesia, the mean MPF was 5.6 (4.5-6.3) Hz.

Adolescent↗
PubMed1994

Acute stressors stimulate ion secretion and increase epithelial permeability in rat intestine.

Wistar-Kyoto rats were subjected to 4 h restraint stress (RS) or cold restraint stress (CRS), and jejunal tissues were examined in Ussing chambers for alterations in transport functions compared with tissues from unstressed control rats. The baseline short-circuit current (Isc) was significantly elevated in tissues from RS (approximately 50%) and CRS (100%). Substitution of Cl- eliminated the abnormality, suggesting that stress stimulates Cl- secretion. Electrical transmural stimulation of enteric nerves caused a transient increase in Isc in all tissues. The magnitude of this response was significantly less in tissues from CRS than from control rats; however, the ability of the epithelium to secrete in response to exogenous stimulation with bethanechol or vasoactive intestinal polypeptide was unimpaired, implicating a neural change. Tissue conductance was higher in jejunum from RS and CRS rats than from controls. Increased intestinal epithelial permeability in stressed rats was confirmed by significantly greater fluxes of the inert radiolabeled probes, [3H]mannitol and 51Cr-labeled EDTA. No structural changes were observed. We conclude that acute stressors have profound effects on intestinal epithelial physiology, stimulating ion secretion and reducing barrier function.

Acute Disease↗
PubMed1992

Dexamethasone induces a down regulation of rat mast cell protease II content in rat basophilic leukaemia cells.

Corticosteroids are widely used to treat severe allergic and inflammatory disease in which mast cells have been implicated as playing an important role. It has been previously shown that in vivo treatment with large bolus doses of corticosteroid can induce a down regulation of the number of IMMC in the rat. Previous in vitro studies of the RBL cell line have shown that culture in the presence of high doses of dexamethasone can induce an increase in cellular histamine content similar to that induced by other agents known to reduce the rate of cell division such as 5-hydroxyurea or sodium butyrate. In our studies the rat mucosal mast cell like cell line RBL-2H3 was cultured in the continuous presence of dexamethasone for periods of up to 4 weeks. Cell-associated histamine levels were found not to increase significantly at the doses of the corticosteroid we used. Of greater interest was the observation that levels of the mucosal mast cell specific protease RMCPII were dramatically reduced in these dexamethasone-treated cultures even at doses that might be considered to be physiologically relevant. This effect could be observed at 3 days after dexamethasone treatment and a continued reduction of RMCPII content was noted up to 4 weeks, at which time RMCPII levels were less than 5% of the control values in 10(-7) M dexamethasone treated cells. 5-Hydroxyurea did not reduce cellular RMCPII content even at a concentration which substantially reduced the rate of cell division and significantly increased cell associated histamine content.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1991

Acute suppurative parotitis: a forgotten cause of upper airway obstruction.

A patient had threatened upper airway obstruction as a result of bilateral acute suppurative parotitis. Because of the rarity of this condition in recent times, accurate diagnosis was delayed and fiber-optic intubation in the intensive care unit was required to safeguard the airway. Management is described with reference to the surgical anatomy and previously reported cases.

Acute Disease↗
PubMed1991

A level vaporizer.

Explore the source record for details and available documents.

Anesthesiology↗
PubMed1990

Opisthotonus and other unusual neurological sequelae after outpatient anaesthesia.

Four patients who developed unusual neurological sequelae after outpatient anaesthesia are described. Propofol is strongly implicated as the cause. All four patients were female with no previous history of psychiatric disorder or neurological disease, unpremedicated, and had procedures of duration less than 20 minutes. Hyperreflexia and hypertonicity were present postoperatively and the reactions appeared to be triggered by an external stimulus. Three patients were examined by a neurologist and had a normal electroencephalograph. Two patients were on the same operating list; quality control was carried out on the anaesthetic agents used, and blood samples sent for toxicology showed no abnormalities. Mechanisms underlying these reactions are discussed.

Adult↗