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1.
BMC Med Educ ; 11: 93, 2011 Nov 14.
Artículo en Inglés | MEDLINE | ID: mdl-22082174

RESUMEN

BACKGROUND: There is a growing acknowledgement that doctors need to develop leadership and management competences to become more actively involved in the planning, delivery and transformation of patient services. We undertook a systematic review of what is known concerning the knowledge, skills and attitudes of medical students regarding leadership and management. Here we report the results pertaining to the attitudes of students to provide evidence to inform curriculum development in this developing field of medical education. METHODS: We searched major electronic databases and citation indexes within the disciplines of medicine, education, social science and management. We undertook hand searching of major journals, and reference and citation tracking. We accessed websites of UK medical institutions and contacted individuals working within the field. RESULTS: 26 studies were included. Most were conducted in the USA, using mainly quantitative methods. We used inductive analysis of the topics addressed by each study to identity five main content areas: Quality Improvement; Managed Care, Use of Resources and Costs; General Leadership and Management; Role of the Doctor, and Patient Safety. Students have positive attitudes to clinical practice guidelines, quality improvement techniques and multidisciplinary teamwork, but mixed attitudes to managed care, cost containment and medical error. Education interventions had variable effects on students' attitudes. Medical students perceive a need for leadership and management education but identified lack of curriculum time and disinterest in some activities as potential barriers to implementation. CONCLUSIONS: The findings from our review may reflect the relatively little emphasis given to leadership and management in medical curricula. However, students recognise a need to develop leadership and management competences. Although further work needs to be undertaken, using rigorous methods, to identify the most effective and cost-effective curriculum innovations, this review offers the only currently available summary of work examining the attitudes of students to this important area of development for future doctors.


Asunto(s)
Actitud del Personal de Salud , Curriculum , Liderazgo , Estudiantes de Medicina/psicología , Selección de Profesión , Conocimientos, Actitudes y Práctica en Salud , Humanos , Rol del Médico
2.
J Physiol ; 544(Pt 1): 195-209, 2002 Oct 01.
Artículo en Inglés | MEDLINE | ID: mdl-12356892

RESUMEN

Adenosine, prostaglandins (PG) and nitric oxide (NO) have all been implicated in hypoxia-evoked vasodilatation. We investigated whether their actions are interdependent. In anaesthetised rats, the PG synthesis inhibitors diclofenac or indomethacin reduced muscle vasodilatation evoked by systemic hypoxia or adenosine, but not that evoked by iloprost, a stable analogue of prostacyclin (PGI(2)), or by an NO donor. After diclofenac, the A(1) receptor agonist CCPA evoked no vasodilatation: we previously showed that A(1), but not A(2A), receptors mediate the hypoxia-induced muscle vasodilatation. Further, in freshly excised rat aorta, adenosine evoked a release of NO, detected with an NO-sensitive electrode, that was abolished by NO synthesis inhibition, or endothelium removal, and reduced by ~50 % by the A(1) antagonist DPCPX, the remainder being attenuated by the A(2A) antagonist ZM241385. Diclofenac reduced adenosine-evoked NO release by ~50 % under control conditions, abolished that evoked in the presence of ZM241385, but did not affect that evoked in the presence of DPCPX. Adenosine-evoked NO release was also abolished by the adenyl cyclase inhibitor 2',5'-dideoxyadenosine, while dose-dependent NO release was evoked by iloprost. Finally, stimulation of A(1), but not A(2A), receptors caused a release of PGI(2) from rat aorta, assessed by radioimmunoassay of its stable metabolite, 6-keto PGF(1alpha), that was abolished by diclofenac. These results suggest that during systemic hypoxia, adenosine acts on endothelial A(1) receptors to increase PG synthesis, thereby generating cAMP, which increases the synthesis and release of NO and causes muscle vasodilatation. This pathway may be important in other situations involving these autocoids.


Asunto(s)
Adenosina/metabolismo , Hipoxia/fisiopatología , Óxido Nítrico/metabolismo , Prostaglandinas/metabolismo , Teofilina/análogos & derivados , Vasodilatación , Adenosina/antagonistas & inhibidores , Animales , Aorta/efectos de los fármacos , Aorta/metabolismo , Inhibidores de la Ciclooxigenasa/farmacología , Diclofenaco/farmacología , Técnicas In Vitro , Indometacina/farmacología , Masculino , Músculo Esquelético/irrigación sanguínea , Ratas , Ratas Wistar , Teofilina/farmacología , Vasodilatación/efectos de los fármacos
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