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Biomedical subjects

D J Klass

Publications and source records attributed to D J Klass.

32 records · Page 2Linked to original sources
PubMed1991

The accuracy of standardized patient presentation.

The accuracy of standardized patient clinical problem presentation was evaluated by videotape rating of a random sample of 839 student-patient encounters, representing 88 patients, 27 cases and two university test sites. Patient-student encounters were sampled from a collaborative inter-university final-year clinical examination of fourth-year medical students which was conducted at the University of Manitoba and Southern Illinois University in 1987 and 1988. The accuracy, replicability and portability of standardized patient cases were evaluated. The average accuracy of patient presentation was 90.2% in 1987 and 93.4% in 1988. Perfect accuracy scores were obtained by 15 patients; however, 11 patients had average scores below 80% with the accuracy of presentation in some encounters being as low as 30%. There were significant differences in the accuracy score achieved by patients trained together for the same case in 6 of 35 possible comparisons. There was also a systematic trend for patients trained at Southern Illinois to be more accurate in their presentation than patients trained at the University of Manitoba. These differences were significant in 5 of the 15 cases used in the examination.

Clinical Clerkship↗
PubMed1988

Performance and perception in a simulated clinical encounter.

The feasibility of using data arising from a simulated patient encounter to determine the nature of the relationship between patient satisfaction and examinee performance during a clinical examination is explored. Satisfaction (on dimensions of sensitivity, participation and thoroughness) is shown to be related to aspects of the physical examination and the history taking.

Clinical Competence↗
PubMed1986

The pulmonary disposition of theophylline and its influence on human alveolar macrophage bactericidal function.

We studied the pulmonary disposition of theophylline by performing bronchoalveolar lavage on 19 normal, nonsmoking volunteers who had taken theophylline orally for 14 days. In addition, we determined the influence of theophylline on human alveolar macrophage bacterial phagocytosis, intracellular killing, and hydrogen peroxide release. We found a 1:1 relationship between serum and bronchoalveolar lavage theophylline concentrations when lavage fluid concentrations were corrected for saline dilution. We found marked impairment of the bactericidal activity of alveolar macrophages from theophylline-treated subjects (intracellular killing efficiency of 24.7 +/- 1.5% compared with 60.2 +/- 0.9% by macrophages from control subjects; p less than 0.001). This defect in alveolar macrophage bactericidal activity was inversely correlated with the bronchoalveolar lavage theophylline concentrations, and was corrected after the alveolar macrophages were cultured under serum-free conditions for 48 h. Theophylline significantly impaired alveolar macrophage release of hydrogen peroxide. Hence, theophylline may compromise lung host defenses by suppressing alveolar macrophage bactericidal activity and oxidative metabolite release.

Adult↗
PubMed1984

Functional heterogeneity of isopycnic fractions of rat alveolar macrophages.

Rat alveolar macrophages separated into four isopycnic fractions on Percoll gradients were functionally heterogeneous in bacterial phagocytosis, intracellular killing, superoxide anion release, and lysosomal enzyme activity but not in hydrogen peroxide release. With increasing alveolar macrophage density, phagocytosis, intracellular killing, superoxide anion release, and lysozyme activity increase, and acid hydrolase activity decreases.

Animals↗
PubMed1984

Rat lung lavage surfactant enhances bacterial phagocytosis and intracellular killing by alveolar macrophages.

We have tested the effect of a preparation of rat lung lavage surfactant (SAM) on phagocytosis and intracellular killing of Staphylococcus aureus by rat alveolar macrophages (AMs). The SAM was isolated and purified by density gradient centrifugation. It was highly enriched in disaturated phosphatidylcholine, and invariably lowered the surface tension of a clean saline solution to less than 10 dynes/cm at 37 degrees C. We used a radiometric assay to measure phagocytosis as uptake by AMs of 14C phenylalanine labelled staphylococci, and intracellular killing as incorporation of 3H thymidine by viable staphylococci from the lysed AMs. When staphylococci were incubated with 100 to 300 micrograms of SAM, both phagocytosis and intracellular killing efficiency were enhanced. The mean numbers of intracellular staphylococci/AM were 24.3 +/- 3.8 and 18.3 +/- 3.0 in the SAM and control groups, respectively (p less than 0.001). The mean intracellular killing efficiency was 59.6 +/- 6.76% and 39.7 +/- 7.17% in the SAM and control groups, respectively (p less than 0.001). Previous studies have shown that unpurified rat lung lavage fluid enhances intracellular killing of staphylococci by AMs. Our results suggest that SAM may be the active principle in lung lavage fluid that enhances intracellular killing. In addition, in our test system, SAM enhanced staphylococcal phagocytosis by AMs.

Animals↗
PubMed1984

Human lung lavage surfactant enhances staphylococcal phagocytosis by alveolar macrophages.

We tested the effect of a preparation of human lung lavage surfactant (SAM) on phagocytosis and intracellular killing of Staphylococcus aureus by human alveolar macrophages (AM). When staphylococci were incubated with 100 to 300 micrograms of SAM, AM phagocytosis but not intracellular killing efficiency was enhanced. The mean numbers of intracellular staphylococci/AM were 36.0 +/- 2.7 and 23.3 +/- 2.8 in the SAM and control groups, respectively (p less than 0.001). The AM intracellular killing efficiency was 40.9 +/- 3.3% and 39.5 +/- 3.9% in the SAM and control groups, respectively (p greater than 0.05). Our results suggest that SAM is an important nonimmune opsonin for bacterial phagocytosis by human AM.

Humans↗
PubMed1982

Antiarrhythmic effects of cyclic guanosine 3' :5'-monophosphate and sodium nitroprusside on barium chloride arrhythmias in rabbits.

The hypothesis that c GMP and sodium nitroprusside (NP), an activator of guanylate cyclase which elevates levels of c GMP, have antiarrhythmic activity was tested in the barium chloride (BaCl2) model of arrhythmias. Electrocardiograms were recorded continuously on tape in unanesthetized New Zealand white rabbits weighing approximately 2.0 kg. BaCl2, 4 mg/kg i.v. bolus, induced frequent ventricular ectopic beats. These ventricular arrhythmias were abolished by 8-bromo-c GMP, 5 mg/kg, injected into the left ventricle (5/6 rabbits), NP 25.0 microgram/kg/min i.v. (6/6), NP 10 micrograms/kg/min i.v. (3/6), and markedly reduced in frequency by NP 10 micrograms/kg/min (3/6). In temporal association with NP, 4 fold increases in c GMP levels in blood and significant increases in myocardial GMP were found compared to control animals (n = 6). In this model, c GMP and NP have significant antiarrhythmic properties. NP effect may be mediated by alterations in c GMP metabolism.

Animals↗
PubMed1979

Dibutyryl cyclic GMP and hyperventilation promote rat lung phospholipid release.

Ventilation of rats at high inspiratory pressures raises lung tissue content of guanosine 3',5'-cyclic monophosphate (cGMP). Hyperventilation in rabbits augments release of phospholipid into lavage fluid. Can cGMP, in the absence of hyperventilation, increase lung phospholipid release? Sprague-Dawley rats are injected with [14C]palmitate, and after 1.5 h are anesthetized and ventilated for 20 min. Three groups are ventilated at peak inspiratory pressures (PIP) of 10 cmH2O, while saline, dibutyryl adenosine 3',5'-cyclic monophosphate (DBcAMP), or dibutyryl cGMP (DBcGMP) is infused into the pulmonary artery. In a fourth group, saline is infused into the pulmonary artery, but ventilation is performed with PIP of 25 cmH2O. Lung tissue and lavage fluid are then analyzed for phospholipid (PL) content and for incorporation of [14C]palmitate into lavage and tissue PL fractions. Ventilation at increased pressure and infusion of DBcGMP are associated with increases in release of labeled PL into lavage fraction. The findings suggest that the increase in lavage PL release associated with hyperventilation is, at least in part, mediated by cGMP.

Animals↗
PubMed1978

Lung tissue guanosine 3',5'-monophosphate: effects of ventilation and anesthesia.

In vivo levels of guanosine 3',5'-cyclic monophosphate (cGMP) in rat lung were measured by radioimmunoassay. The basal levels of this agent were found to change depending on the method of killing or anesthesia used. Lowest values were found after microwave irradiation to the head (10.2 fmol/mg wet wt). Values after pentobarbitol anesthesia, with or without atropine, were significantly higher (19-24 fmol/mg). In animals anesthetized with pentobarbital and ventilated at pressures of 7 cmH2O with no end-expiratory pressure, lung cGMP was 42-49 fmol/mg. Ventilation at higher pressures resulted in much higher levels of cGMP (20 cmH2O, 105 fmol/mg; 30 cmH2O, 233 fmol/mg). The response of cGMP to ventilation was not blocked by pretreatment of the animals with atropine. High-pressure ventilation was without effect on lung adenosine 3',5'-cyclic monophosphate.

Animals↗
PubMed1976

Effects of prednisolone on the differentiation of mouse lung adenomas in culture.

Explants of pulmonary adenomas, induced in mice by urethan, were cultured with or without prednisolone for 72 hr. After this time, the cuboidal epithelial cells of the tumor contained many more lamellar bodies than the nonsteroid control cultures. Incorporation of labeled palmitic acid into saturated phosphatidylcholine was not significantly increased in these short-term steroid-treated cultures. The results indicate that steroid enhances the maturation of cultured pulmonary adenoma cells into cells morphologically indistinguishable from type II alveolar epithelial cells of normal lung.

Adenoma↗
PubMedDate not supplied

Cigarette smoke exposure in vivo increases cyclic GMP in rat lung.

The enzyme guanylate cyclase is stimulated to produce cycle guanosine 3',5'-monophosphate (GMP) when lung tissue is exposed to cigarette smoke in vitro. These experiments tested whether in vivo exposure in rats to cigarette smoke produces a similar response. Adult rats were anaesthetized with pentobarbital and ventilation with mixtures of air and cigarette smoke at 10 cm H2O inspiratory pressure was achieved after a tracheotomy was performed. Lung tissue samples were taken at intervals during 20 min exposure period and analyzed for levels of cyclic adenosine 3', 5'-monophosphate (AMP) and cycle GMP. Blood carboxyhemoglobin (COHb) levels at 5 min and 15 min of exposure showed high, but sublethal levels of COHb. lung tissue cAMP was unchanged with this exposure, but cGMP levels rose dramatically. Rat lungs showed no changes related to ventilation under similar conditions in the absence of smoke. This observed response of cGMP to cigarette smoke may represent an important pulmonary defense mechanism.

Animals↗