Search PubMed⌕ Search

Biomedical subjects

E Dillmann

Publications and source records attributed to E Dillmann.

7 recordsLinked to original sources
PubMed1993

Multicultural issues in medical curriculum: implications for Canadian physicians.

This descriptive study explored multicultural issues in medical education which should be included in the curricula of both the undergraduate and residency programs of the Faculty of Medicine, The University of Calgary. Face-to-face interviews were conducted with 21 male and female ethnic patients to determine their expectations of and experiences with the health care they had received in Canada. Telephone interviews were conducted with ten primary care physicians to determine their experiences of providing care to new immigrants from cultures other than their own. Content analyses and comparison of the two sets of interview data revealed barriers to satisfaction, diagnosis and treatment. Some barriers were perceived both by the physicians and the ethnic patients, e.g. language, and attitudes towards medical technology and treatment. Others were perceived just by the physicians, e.g. patients' belief in traditional practices. Still others were perceived just by the ethnic patient, e.g. perceived racial discrimination. Based on the data from the interviews, two simulated patients were developed and presented to the students of medicine, both undergraduate and resident, to teach them about multicultural health care. This study demonstrates how local data about multicultural health issues can be used to develop simulated patients for inclusion in the medical curriculum.

Adult↗
PubMed1984

Effect of exposure to low temperature on normal and iron-deficient subjects.

Twenty-one Venezuelan peasants were segregated into three groups on the basis of measurements of iron status: seven normal subjects, six iron-deficient subjects with normal hemoglobin and eight iron-deficient subjects with a hemoglobin concentration of less than 9 g/dl. All subjects were placed in a water bath at an initial temperature of 36 degrees C. The water temperature was then rapidly lowered to 28 degrees C, and observations were made over the period of 1 h. Mean oral temperature of the first group fell 0.2, the second group 0.5, and the third group 0.9 degrees C. Mean plasma norepinephrine levels in both groups of iron-deficient subjects were significantly higher at 36 degrees C and during cold exposure compared with control subjects. Oxygen consumption was also significantly increased in both groups of iron-deficient subjects after cold exposure.

Adult↗
PubMed1979

Catecholamine elevation in iron deficiency.

Iron-deficient rats have increased blood and urinary catecholamines regardless of whether anemia is or is not present. The catecholamine response in both iron-deficient and control animals is largely temperature dependent, showing little difference at the isothermic temperature of 30 degrees C but a two- to threefold increase in iron-deficient animals over controls at lower temperatures. The iron-deficient rat is unable to maintain body temperature at 4 degrees C and this is independent of anemia or of food intake. When animals are run on the treadmill for 4 h, body temperatures increase but the difference observed at 4 degrees C between iron-deficient and control animals persists. The underlying abnormality in temperature regulation and in catecholamine response disappeared after 6 days of iron therapy.

Animals↗
PubMed1979

Lactic acidosis as a result of iron deficiency.

Iron-deficient rats have an impaired work performance, even when their anemia is corrected by exchange transfusion. Muscle activity is associated with a higher blood lactate concentration than is observed in iron-replete animals. The accumulation of lactate is a result of excessive production as lactate clearance from the blood was shown to be unaffected. By adjusting the work load to a lower level, it was possible to divide iron-deficient animals into two groups, one capable of continued treadmill running and another in which animals stopped before 20 min. In the former, blood lactate concentration reached a plateau at moderate levels, whereas it continued to increase in the latter until the animal stopped running. Levels of alpha-glycerophosphate oxidase in skeletal muscle mitochondria were found to be much lower in the second group (P < 0.001). Lactate infusion into normal animals was shown to interfere with work performance, and maintenance of a normal pH in iron-deficient and iron-replete animals did not prevent the impairment in work associated with high blood lactate concentrations. Additional evidence was obtained that energy substrate (blood glucose and free fatty acids, muscle glycogen) was adequate in irondeficient animals. Oxygen tension in their vena caval blood was higher than in controls. Furthermore, the in situ behavior of electrically stimulated gastroenemius and soleus muscles appeared similar to that of control animals. Because the stimulation of the single muscle in the iron-deficient animal did not result in appreciable elevation of blood lactate and did not show impaired contractility further supported the hypothesis that the elevation of blood lactate caused the decreased work performance. It is concluded that iron deficiency by a depletion in the iron-containing mitochondrial enzyme, alpha-glycerophosphate oxidase, impairs glycolysis, resulting in excess lactate formation, which at high levels leads to cessation of physical activity.

Acidosis↗