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Biomedical subjects

C Dawson

Publications and source records attributed to C Dawson.

At least 91 records · Page 5Linked to original sources
PubMed1985

Hypertension, perceived clinician empathy, and patient self-disclosure.

The purpose of this study was to compare groups of outpatient hypertensive and diabetic patients to a control group (no known chronic illnesses) on their perceptions of clinician empathy and the importance and difficulty of disclosing information about themselves to health care providers. It was hypothesized that hypertensives would differ from the other groups in perceiving less clinician empathy and in attributing less importance, but greater difficulty, to self-disclosing. The sample was 54 hypertensives, 47 diabetics, and 115 nonchronically ill patients. Each subject completed the Empathy scale of the Barrett-Lennard Relationship Inventory and a patient self-disclosure questionnaire. The empathy hypothesis was supported but the self-disclosure hypotheses were not. Hypertensive patients differed from other patients in perceiving the least clinician empathy and in attributing the greatest importance to discussing their responses to health care.

Adolescent↗
PubMed1985

Muscarinic cholinergic receptors in rabbit retina.

Binding sites with high affinity and specificity for [3H]-quinuclidinyl benzilate are present in rabbit retinal homogenates. Only one set of binding sites was detected with an apparent dissociation constant of 2.13 X 10(-10) M and a density of 59.2 fmol mg-1 of protein. The pharmacological characteristics of specific binding were similar to those in the goldfish, chicken and cow.

Animals↗
PubMed1985

Hypoxic induction of Ca2+-dependent action potentials in small pulmonary arteries of the cat.

Small pulmonary arteries (less than 300 micron) from cats were mounted in myographs to record mechanical and electrical responses to hypoxia. When these preparations were exposed to a PO2 of 30-50 Torr after equilibration at 300 Torr they consistently developed active force, which increased or decreased in amplitude as [Ca2+] was raised or lowered, respectively, and was blocked on addition of verapamil. Intracellular electrical recording with glass microelectrodes demonstrated membrane depolarization and action potential generation when PO2 was lowered. Steady-state voltage vs. applied current curves obtained before and during hypoxia showed a significant reduction in input resistance. The relationship between membrane potential and extracellular K+ was not different during hypoxia compared with control, suggesting that there were not marked changes in K+ permeability under this condition. In the presence of verapamil to block Ca2+ inward current the hypoxia-induced action potentials were abolished concomitant with partial membrane repolarization. The results of these studies suggest that in certain isolated pulmonary arteries hypoxia induces contraction by a mechanism involving an increased Ca2+ conductance. These data suggest that the sensor involved in hypoxic pulmonary vasoconstriction may lie within the vessel wall and somehow mediates changes in smooth muscle ionic conductances.

Action Potentials↗
PubMed1985

A membrane electrical mechanism for hypoxic vasoconstriction of small pulmonary arteries from cat.

Using specially fabricated muscle myographs, we examined electrical and mechanical responses to reduction of PO2 in small (less than 300 micron) pulmonary arteries excised from cat lungs. Upon lowering PO2 from 400 to 50 mm Hg, these preparations consistently developed contractile responses concomitant with membrane depolarization and action potential generation. The largest changes in electromechanical responses to reduction of PO2 occurred between 150 and 50 mm Hg. These data strongly suggest that hypoxic activation of small pulmonary arteries is mediated by direct effects of reduced PO2 on muscle cell membrane ionic conductance systems.

Animals↗
PubMed1984

Herpes simplex virus infection causes the accumulation of a heat-shock protein.

A monoclonal antibody, produced from mice immunized with a herpes simplex virus (HSV)-infected cell extract, reacts with a molecule which is present in uninfected cells and which accumulates in large amounts during HSV 2 infection. In uninfected cells this molecule is growth regulated, in that exponentially growing cells have intense nuclear immunofluorescence, whereas confluent quiescent cells have little. It has a mol. wt. of 57 000 (p57) in exponential cells, and one of 61 000 (p61) in quiescent cells. In HSV 2-infected cells, p57 accumulates and nuclear and cytoplasmic immunofluorescence increases. In uninfected cells, p57 also accumulates during heat-shock treatment, and this is associated with a new immunofluorescence throughout the cytoplasm. We suggest that HSV 2 infection induces a cellular stress response which is involved in the shut-off of host cell polypeptide synthesis.

Animals↗
PubMed1984

A patient self-disclosure instrument.

Four studies in which a patient self-disclosure questionnaire was developed and tested are reported. The instrument was designed to include only content judged by both patients and clinicians as important. Three areas of patient difficulty in disclosing to a health care provider were measured: personal problems and feelings, responses to health care, and life style. Patient difficulty in disclosure was assessed by 21 7-point rating scales, 7 for each disclosure area; ratings were summed to obtain scores. A correlation matrix of the ratings of 216 patients was subjected to a three-factor principal components analysis with varimax rotation; the solution accounted for 59% of the total variance. High internal consistency and test re-test reliability for the total scale and subscales were obtained; Cronbach's alpha .82-.83, n = 214; r = .81-.87, n = 66. In separate tests of construct validity patient self-disclosure was shown to be influenced by locus of control and perception of clinician empathy, and to covary with heart rate changes.

Adolescent↗
PubMed1984

Taurine uptake processes in the isolated rabbit retina and the effects of light.

As part of a study on the mechanisms involved in regulating photoreceptor taurine levels, we have examined the characteristics of [3H]-taurine uptake by the isolated rabbit retina. The effects of light on taurine accumulation have also been studied. Rabbit retinas quickly accumulated [3H]-taurine and tissue: medium ratios of 50:1 were attained after 60 min incubation at 37 degrees C. Under these conditions no metabolites of [3H]-taurine were detected in the tissue. The efflux of [3H]-taurine from the retina was extremely slow, less than 5% of the accumulated radioactivity being released in a 30 min incubation in fresh medium. Thus, in subsequent experiments the accumulation of radioactivity was taken as a measure of [3H]-taurine uptake. Non-linear regression analysis of kinetic data revealed that taurine was accumulated by separate high- and low-affinity transport processes, the kinetic parameters being Kmh = 93 +/- 12 microM; Vmh = 72 +/- 7; KmL = 8.8 +/- 5 mM; VML = 274 +/- 79 nmol min-1 g-1 wet weight respectively. The properties of the high- and low-affinity taurine uptake processes were very similar. Both were temperature sensitive, particularly between 25 and 37 degrees C and sodium- and chloride-dependent, and were inhibited by metabolic inhibitors. The substrate specificities of the high- and low-affinity uptake processes were also similar, both processes being inhibited by beta-alanine, guanidinoethylsulphonate (GES) and GABA, but not by alpha-alanine or glycine. Hypotaurine selectively inhibited the high-affinity uptake process for [3H]-taurine. Exposure of retinas to continuous light did not affect either the high- or the low-affinity uptake of [3H]-taurine compared with dark-adapted controls. However, flickering light (0.5-30 Hz, 25% duty cycle) reduced the high-affinity accumulation of [3H]-taurine by as much as 50%. The reduction in [3H]-taurine may be due to a localized decrease in uptake (or possibly an increased release) by the photoreceptors because the same reduction was found when synaptic transmission in the retina was blocked by exposure to medium containing high Mg/low Ca. High Mg/low Ca did not itself affect taurine accumulation.

Amino Acids↗
PubMed1983

Evidence for a cholinergic inhibitory feed-back mechanism in the rabbit retina.

The effects of muscarine, atropine and nicotinic antagonists on the light-evoked release of radioactivity from rabbit retinas previously exposed to [3H]choline (Ch) was studied. On the basis of previous experiments, this light-evoked release of total radioactivity was taken as a measure of the light-evoked release of [3H]acetylcholine (ACh) from the cholinergic amacrine cells. Atropine (1 microM) in the presence, but not the absence, of eserine more than doubled the light-evoked release of [3H]ACh. Eserine (30 microM) itself had no significant effect on either the spontaneous resting release or the light-evoked release of [3H]ACh. Muscarine (10 microM) in the presence or absence of eserine reduced the light-evoked release of [3H]ACh from the retina by 50%. This effect of muscarine was blocked by atropine used in the absence of eserine. The nicotinic antagonists pempidine, hexamethonium and gallamine had no significant effect on retinal [3H]ACh release. Strychnine (20 microM), which alone had no effect on retinal [3H]ACh release, abolished the effects of both muscarine and atropine on the light-evoked release of [3H]ACh. Bicuculline (5 microM) did not affect the actions of muscarine or atropine on the light-evoked release of [3H]ACh. Previous experiments had shown that glycine and gamma-aminobutyric acid (GABA) reduce the light-evoked release of [3H]ACh from the retina and that these inhibitory effects are selectively blocked by strychnine (20 microM) and bicuculline (5 microM) respectively. These results suggest the presence in the retina of a cholinergic inhibitory feed-back mechanism which involves a neuronal loop, rather than presynaptic or post-synaptic inhibitory muscarinic receptors on the cholinergic amacrine cells themselves. Our experiments do not provide evidence on the nature of the proposed inhibitory loop, except that it apparently includes a glycinergic or taurinergic (amacrine) cell.

Acetylcholine↗
PubMed1981

Thygeson's superficial punctate keratitis.

Thygeson's superficial keratitis is a chronic disease of the cornea characterized by focal epithelial lesions. We studied 45 cases of Thygeson's superficial punctate keratitis. Twenty-eight were male and 17 were female patients. The disease had been active in our patients from one month to 24 years. The clinical findings, course, outcome, and response to therapy were studied. Viral cultures and microscopic studies were performed on the corneal epithelial scrapings from ten cases. The average course of the disease was prolonged in patients who received topical steroid therapy. Subepithelial opacities were seen more frequently in patients who had received treatment with idoxuridine (IDU).

Adolescent↗
PubMed1979

Stimulation of peroxidase by chlamydial infection: cytochemistry of guinea pig conjunctival epithelium.

Guinea pig inclusion conjunctivitis, a naturally occurring chlamydial disease of guinea pigs, resolves spontaneously after 3 to 4 weeks. The factors responsible for curbing the infection have not yet been specifically defined. Since Iwata (Invest. Ophthalmol. 15:297-301, 1976) reported cytochemical activity for peroxidase in the conjunctival epithelium of the normal rat, we undertook these studies to determine whether a similar activity exists in the guinea pig, and if so, whether it functions in the elimination of this Chlamydia psittaci infection. Tarsal conjunctivas of 14 normal guinea pigs, 34 infected ones, and 7 control guinea pigs (inoculated with yolk sac only) were excised and tested for peroxidase by the Graham and Karnovsky method (J. Histochem. Cytochem. 14:291-302, 1966). We found that peroxidase activity, virtually absent in normal animals, was intensely stimulated by the infection. This enzymatic activity appeared 2 days after inoculation of the conjunctiva with chlamydia and persisted for 6 to 7 weeks. The enzyme was localized in the rough endoplasmic reticulum and perinuclear cisternae of all layers of the conjunctival epithelium from the external surface to the basal lamina, including cells with no apparent inclusions as well as those heavily parasitized. Reaction in the Golgi complex was variable. No reaction, however, was ever evident in the chlamydial vacuoles or lysosomes, and the organisms continued to grow and multiply during peak enzymatic activity. We therefore concluded that the stimulated enzyme is apparently not directly responsible for the waning of the infection, but instead reflects an alteration of host metabolism that occurs as a consequence of the infection.

Animals↗