This Guide has been written to provide guidance for individuals involved in curriculum design who wish to develop research skills and foster the attributes in medical undergraduates that help develop research. The Guide will provoke debate on an important subject, and although written specifically with undergraduate medical education in mind, we hope that it will be of interest to all those involved with other health professionals' education. Initially, the Guide describes why research skills and its related attributes are important to those pursuing a medical career. It also explores the reasons why research skills and an ethos of research should be instilled into professionals of the future. The Guide also tries to define what these skills and attributes should be for medical students and lays out the case for providing opportunities to develop research expertise in the undergraduate curriculum. Potential methods to encourage the development of research-related attributes are explored as are some suggestions as to how research skills could be taught and assessed within already busy curricula. This publication also discusses the real and potential barriers to developing research skills in undergraduate students, and suggests strategies to overcome or circumvent these. Whilst we anticipate that this Guide will appeal to all levels of expertise in terms of student research, we hope that, through the use of case studies, we will provide practical advice to those currently developing this area within their curriculum.

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Alzheimer patients have increased levels of both the 42 amyloid-beta-peptide (Abeta) and the amyloid binding alcohol dehydrogenase (ABAD), which is an intracellular binding site for Abeta. The overexpression of Abeta and ABAD in transgenic mice has shown that the binding of Abeta to ABAD results in amplified neuronal stress and impairment of learning and memory. From a proteomic analysis of the brains from these animals, we have identified for the first time that the protein endophilin I increases in Alzheimer diseased brain. The increase in endophilin I levels in neurons is linked to an increase in the activation of the stress kinase c-Jun N-terminal kinase with the subsequent death of the neurons. We also demonstrate in living animals that the expression level of endophilin I is an indicator for the interaction of ABAD and Abeta as its expression levels return to normal if this interaction is perturbed. Therefore this identifies endophilin I as a new indicator of the progression of Alzheimer disease.

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Bidirectional transepithelial K+ flux measurements across 'high-resistance' epithelial monolayers of MDCK cells grown upon millipore filters show no significant net K+ flux. Measurements of influx and efflux across the basal-lateral and apical cell membranes demonstrate that the apical membranes are effectively impermeable to K+. K+ influx across the basal-lateral cell membranes consists of an ouabain-sensitive component, an ouabain-insensitive component, an ouabain-insensitive but furosemide-sensitive component, and an ouabain- and furosemide-insensitive component. The action of furosemide upon K+ influx is independent of (Na+ - K+)-pump inhibition. The furosemide-sensitive component is markedly dependent upon the medium K+, Na+ and Cl- content. Acetate and nitrate are ineffective substitutes for Cl-, whereas Br- is partially effective. Partial Cl- replacement by NO3 gives a roughly linear increase in the furosemide-sensitive component. Na+ replacement by choline abolishes the furosemide-sensitive component, whereas Li+ is a partially effective replacement. Partial Na+ replacement by choline abolishes the furosemide-sensitive component, whereas Li+ is a partially effective replacement. Partial Na+ replacement with choline gives an apparent affinity of approximately 7 mM Na, whereas variation of the external K+ content gives an affinity of the furosemide-sensitive component of 1.0 mM. Furosemide inhibition is of high affinity (K1/2 = 3 micrometer). Piretanide, ethacrynic acid, and phloretin inhibit the same component of passive K+ influx as furosemide; amiloride, 4,-aminopyridine, and 2,4,6-triaminopyrimidine partially so. SITS was ineffective. Externally applied furosemide and Cl- replacement by NO3- inhibit K+ efflux across the basal-lateral membranes indicating that the furosemide-sensitive component consists primarily of K:K exchange.