Biomedical subjects
A Bower
Publications and source records attributed to A Bower.
Absolutely fabulous? The TV ads promise easy rock-hard abdominals, but studies show there's no such thing as a free six-pack.
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Clinical teaching: maintaining an educational role for doctors in the new health care environment.
CONTEXT AND OBJECTIVES: Good clinical teaching is central to medical education but there is concern about maintaining this in contemporary, pressured health care environments. This paper aims to demonstrate that good clinical practice is at the heart of good clinical teaching. METHODS: Seven roles are used as a framework for analysing good clinical teaching. The roles are medical expert, communicator, collaborator, manager, advocate, scholar and professional. RESULTS: The analysis of clinical teaching and clinical practice demonstrates that they are closely linked. As experts, clinical teachers are involved in research, information retrieval and sharing of knowledge or teaching. Good communication with trainees, patients and colleagues defines teaching excellence. Clinicians can 'teach' collaboration by acting as role models and by encouraging learners to understand the responsibilities of other health professionals. As managers, clinicians can apply their skills to the effective management of learning resources. Similarly skills as advocates at the individual, community and population level can be passed on in educational encounters. The clinicians' responsibilities as scholars are most readily applied to teaching activities. Clinicians have clear roles in taking scholarly approaches to their practice and demonstrating them to others. CONCLUSION: Good clinical teaching is concerned with providing role models for good practice, making good practice visible and explaining it to trainees. This is the very basis of clinicians as professionals, the seventh role, and should be the foundation for the further development of clinicians as excellent clinical teachers.
Relations of scores on the Stanford Binet Fourth Edition and form L-M: concurrent validation study with children who have mental retardation.
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Sympathetic denervation of the iris dilator in noninsulin-dependent diabetes.
Twenty-three subjects with noninsulin-dependent diabetes mellitus (NIDDM) and 23 age- and sex-matched controls were tested for sympathetic denervation of the iris dilator by comparing the mydriatic effect of the combination of 1% phenylephrine and 1% tropicamide with that of 1% tropicamide alone. Most of the diabetic subjects had no clinical signs of severe diabetic complications. Nine diabetics and two controls showed sympathetic denervation, defined as a 1 mm or greater dilation due the addition of 1% phenylephrine. One of those two controls had a recent history of vascular headache. The diabetics with pupillary neuropathy had higher glycosylated hemoglobin percentages and a history of higher fasting blood sugars (FBS's) than the diabetics with normal pupils. Our results show that pupillary neuropathy can develop in persons with diabetes, often before the other complications of diabetes become manifest.
Cellular mechanisms controlling melanophore stimulating hormone (MSH) release.
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Biogenic amines and control of melanophore stimulating hormone release.
Release of melanophore stimulating hormone (MSH) from the vertebrate pars intermedia is under inhibitory control by the hypothalamus. Removal of the rat pituitary or the neurointermediate lobe of the frog (Rana pipiens) to in vitro incubation medium results in rapid uninhibited release of MSH. This secretion is inhibited by norepinephrine, epinephrine, phenylephrine, and dopamine, and the inhibition is antagonized by alpha-adrenergic receptor blocking agents. Isoproterenol stimulation of MSH secretion from isolated glands is blocked by pro-pranolol, a beta-adrenergic receptor antagonist. These results implicate dopaminergic or classical alpha-adrenergic receptors (or both) in inhibition of MSH release by catecholamines, and implicate beta-adrenergic receptors in stimulation of MSH release by the bioamines.
Regulation of melanophore stimulating hormone (MSH) release.
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Melanophore stimulating hormone: release inhibition by ring structures of neurohypophysial hormones.
Tocinamide and tocinoic acid, ring structures of oxytocin, are potent inhibitors of the release of melanophore stimulating hormone from the rat and hamster pituitary in vitro. Tocinamide is effective at concentrations as low as 10-(14)M on the mammalian pituitary. These peptides do not affect release of the hormone on the frog (Rana pipiens) pars intermedia, but they do inhibit release in the bullfrog (Rana catesbeiana) and the toad (Bufo marinus). The specificity of the peptides on inhibition of the hormone is demonstrated by the fact that oxytocin, lysine vasopressin, and pressinoic acid and pressinamide (ring structures of the vasopressins) do not show such inhibitory activity. Hypothalamic extracts of either the frog (Rana pipiens) or the rat inhibit release of the hormone from pituitaries of either species. The inhibitory effects of tocinamide and tocinoic acid, like that of hypothalamic extracts, are reversible.
Ionic requirements for melanophore-stimulating hormone (MSH) release.
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Comparative MSH release-inhibiting activities of tocinoic acid (the ring of oxytocin), and L-pro-L-leu-gly-NH 2 (the side chain of oxytocin).
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