A framework for developing excellence as a clinical educator.

The current emphasis on providing quality undergraduate and postgraduate medical education has focused attention on the educational responsibilities of all doctors. There is a greater awareness of the need to train doctors as educators and courses have been set up to satisfy this need. Some courses, such as those on how to conduct appraisal, are specific to one task facing a medical educator. Other courses take a broader view and relate educational theory to practice. In this paper we describe an outcome-based approach in which competence in teaching is defined in terms of 12 learning outcomes. The framework provides a holistic approach to the roles of the teacher and supports the professionalism of teaching. Such a framework provides the basis for the development of a curriculum for teaching excellence. It helps to define important competences for different categories of teachers, communicate the areas to be addressed in a course, identify gaps in course provision, evaluate courses, assist in staff planning and allow individuals to assess their personal learning needs. The framework is presented to encourage wider debate.

Effects of dietary vitamin E and selenium on in vitro cellular immune responses in cattle.

Four groups of calves depleted of alpha-tocopherol and selenium (Se) were supplemented with alpha-tocopherol or Se or alpha-tocopherol and Se or received no supplement. In vitro lymphocyte proliferative responses were measured in fetal calf serum (FCS), in autologous serum and in pooled sera from each group. In FCS, the responses to pokeweed mitogen were significantly enhanced for calves supplemented with alpha-tocopherol. In autologous serum, the mean responses to keyhole limpet haemocyanin (KLH) were greatest for calves supplemented with Se alone. In pooled sera from each group, lymphocytes from calves supplemented with Se alone showed enhanced responses to KLH in the presence of serum from calves supplemented with alpha-tocopherol. The calves depleted of alpha-tocopherol had increased circulating percentages of BoCD2 lymphocytes, apparently due to changes in the BoCD4 subpopulation. The percentages of B cells were greatest in calves supplemented with alpha-tocopherol and Se. The results indicate that alpha-tocopherol and Se have interactive effects on lymphocyte responses to antigen and suggest that micronutrient status is important when interpreting the results of in vitro assays of lymphocyte function.

Antioxidant enzyme activity in the muscles of calves depleted of vitamin E or selenium or both.

Feeding diets depleted of vitamin E and Se to cattle can induce a disease known as nutritional degenerative myopathy. It is believed that an increased peroxidative challenge in muscle is involved in the pathogenesis of this disease. A number of species can up-regulate the activity of some antioxidant enzymes, including glutathione reductase (EC 1.6.4.2), glutathione transferase (EC 2.5.1.18), glucose-6-phosphate dehydrogenase (EC 1.1.1.49), catalase (EC 1.11.1.6), and superoxide dismutase (EC 1.15.1.1), in an attempt to mitigate the effects of a peroxidative challenge. A 2 x 2 factorial study was set up to examine possible changes in the activities of these antioxidant enzymes in muscles of ruminant calves fed on diets low in either vitamin E or Se. Four groups of four calves each were fed on a basal diet of NaOH-treated barley which was supplemented with alpha-tocopherol or Se or both for a total of 50 weeks. Calves fed on diets depleted of vitamin E, but not those fed on diets low in Se, developed subclinical myopathy, as judged by increases in the activity of plasma creatinine kinase (EC 2.7.3.2), and had increased muscle concentrations of two indices of lipid peroxidation, namely thiobarbituric acid-reactive substances, with and without ascorbate activation. Feeding diets depleted of vitamin E and diets low in Se both increased muscle activities of glucose-6-phosphate dehydrogenase in heart, biceps and supraspinatus. This change may have occurred in an attempt to maintain intracellular pools of reduced glutathione. No other changes in antioxidant enzyme activity were observed.

Improved performance in commercial broiler flocks with subclinical infectious bursal disease when fed diets containing increased concentrations of vitamin E.

The economic effects of increased vitamin E supplementation in 79 commercial broiler flocks incorporating over 1.5 million birds was assessed. Approximately half of the flocks were fed on either a high (178 IU/kg) or normal (48 IU/kg) vitamin E-containing diet. In addition, in approximately half of the flocks subclinical infectious bursal disease (IBD) was present. Analysis of the performance data demonstrated that flocks with subclinical IBD were consistently worse (P< 0.001) for net income, feed conversion ratio and average weight per bird than flocks without the subclinical disease. The trial also indicated that the average net income of flocks with subclinical IBD and fed a high vitamin E-containing diet was 10% better (P < 0.05) than flocks with subclinical IBD and fed a normal vitamin E-containing diet. However, the trial also demonstrated that the difference between the average net income achieved by flocks without subclinical IBD and being fed on either a high or a normal vitamin E-containing diet was only 2% and not significantly different. It is suggested that the increased improved performance from high vitamin E-containing diets recorded in flocks with subclinical IBS is due to enhanced immunocompetence and increased resistance to disease. It is also suggested that under field conditions, high dietary inputs of vitamin E are most beneficial where there is a challenge to the host's defence system and significantly improved performance will occur more predictably under such conditions.

Vitamin E and selenium deficiencies increase indices of lipid peroxidation in muscle tissue of ruminant calves.

Indices of lipid peroxidation were investigated in muscle tissues of 1) calves depleted of vitamin E and/or Se and 2) calves depleted of vitamin E and Se and fed daily supplements of polyunsaturated fatty acids (PUFA). Calves deficient in both vitamin E and Se or deficient in vitamin E alone showed elevated muscle concentrations of thiobarbituric acid-reactive substances (TBARS), ascorbate-induced TBARS (ATBARS), ascorbate-induced hexanal and iron-induced 4-hydroxynonenal (HNE). Muscle tissue of calves depleted of Se alone showed no increases in these indices of lipid peroxidation. Two further groups of calves were fed diets either sufficient or deficient in both vitamin E and Se. Both of these groups were then fed linseed oil, protected against ruminal hydrogenation, as a source of PUFA. The deficient animals had higher muscle concentrations of all three indices of lipid peroxidation than the supplemented calves. Furthermore, feeding PUFA to vitamin E and Se deficient animals increased muscle concentrations of induced HNE to levels above those in deficient animals not fed PUFA supplements.

Sequential changes in plasma methylmalonic acid and vitamin B12 in sheep eating cobalt-deficient grass.

Methylmalonic acid (MMA) concentrations are elevated in plasma as a result of vitamin B12 deficiency. This study reports the sequential changes in plasma MMA in lambs maintained on a cobalt-deficient pasture compared with supplemented controls. The results indicate that MMA is elevated in the early stages of deficiency, preceding the onset of loss of production and clinical signs of disease. It remains elevated as long as the lambs are unsupplemented with cobalt (Co). The most striking clinical sign was a loss of body condition as opposed to weight. The defect in the methylmalonyl CoA mutase is obviously an early defect in cobalt deficiency.

Effects of d- versus l-amphetamine, food deprivation, and current intensity on self-stimulation of the lateral hypothalamus, substantia nigra, and medial frontal cortex of the rat.

Intracranial sefl-stimulation (ICSS) was studied in rats with chronically implanted lateral hypothalamic, substantia nigra, or medial frontal cortex bipolar electrodes. A comparison of the effects of d- and l-amphetamine on ICSS response rate indicated that the d isomer had a greater facilitatory effect than the l isomer at lateral hypothalamic and substantia nigra electrode sites but that neither isomer significantly affected medial frontal cortex ICSS. d-Amphetamine resulted in a dose-related increase in motor activity, but the same doses of the l isomer resulted in decreased motor activity. Only lateral hypothalamic ICSS response rates increased significantly in response to food deprivation. Increases in current intensity above the level used for amphetamine and food-deprivation testing facilitated lateral hypothalamic and substantia nigra ICSS response rates but did not significantly affect medial frontal cortex response rates. The responsiveness of ICSS at each electrode site appeared to be correlated with the fiber- and cell-body densities of catecholaminergic systems in the brain.

Motivational and neuroanatomical specificity of hypodipsia for aversive solutions produced by medial preoptic injury to the rat.

Bilateral medial preoptic lesions in rats dramatically lowered the rejection threshold for quinine-adulterated water but not for food in 24-hr forced-choice tests. The detection threshold for quinine in a two-bottle choice test, however, was unaffected by the medial preoptic lesion. Bilateral septal and lateral preoptic lesions had no effect on any quinine-adulteration tests. The enhanced rejection of quinine-adulterated water in a forced-choice test by medial-preoptic-damaged rats was also observed after 24-hr of water deprivation. Furthermore, the plasma osmolality of medial preoptic rats was significantly elevated above controls after 24-hr of water deprivation. These findings were interpreted as suggesting that a medial preoptic lesion produces a deficit in thirst-motivated behavior.