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1.  Delivery and use of individualised feedback in large class medical teaching 
BMC Medical Education  2013;13:63.
Background
Formative feedback that encourages self-directed learning in large class medical teaching is difficult to deliver. This study describes a new method, blueprinted feedback, and explores learner’s responses to assess its appropriate use within medical science teaching.
Methods
Mapping summative assessment items to their relevant learning objectives creates a blueprint which can be used on completion of the assessment to automatically create a list of objectives ranked by the attainment of the individual student. Two surveys targeted medical students in years 1, 2 and 3. The behaviour-based survey was released online several times, with 215 and 22 responses from year 2, and 187, 180 and 21 responses from year 3. The attitude-based survey was interviewer-administered and released once, with 22 responses from year 2 and 3, and 20 responses from year 1.
Results
88-96% of learners viewed the blueprinted feedback report, whilst 39% used the learning objectives to guide further learning. Females were significantly more likely to revisit learning objectives than males (p = 0.012). The most common reason for not continuing learning was a ‘hurdle mentality’ of focusing learning elsewhere once a module had been assessed.
Conclusions
Blueprinted feedback contains the key characteristics required for effective feedback so that with further education and support concerning its use, it could become a highly useful tool for the individual and teacher.
doi:10.1186/1472-6920-13-63
PMCID: PMC3704919  PMID: 23642040
Feedback; Objective; Assessment; Blueprint
2.  TBK1 Kinase Addiction in Lung Cancer Cells Is Mediated via Autophagy of Tax1bp1/Ndp52 and Non-Canonical NF-κB Signalling 
PLoS ONE  2012;7(11):e50672.
K-Ras dependent non-small cell lung cancer (NSCLC) cells are ‘addicted’ to basal autophagy that reprograms cellular metabolism in a lysosomal-sensitive manner. Here we demonstrate that the xenophagy-associated kinase TBK1 drives basal autophagy, consistent with its known requirement in K-Ras-dependent NSCLC proliferation. Furthermore, basal autophagy in this context is characterised by sequestration of the xenophagy cargo receptor Ndp52 and its paralogue Tax1bp1, which we demonstrate here to be a bona fide cargo receptor. Autophagy of these cargo receptors promotes non-canonical NF-κB signalling. We propose that this TBK1-dependent mechanism for NF-κB signalling contributes to autophagy addiction in K-Ras driven NSCLC.
doi:10.1371/journal.pone.0050672
PMCID: PMC3510188  PMID: 23209807
3.  The cyclin-dependent kinase PITSLRE/CDK11 is required for successful autophagy 
Autophagy  2011;7(11):1295-1301.
(Macro)autophagy is a membrane-trafficking process that serves to sequester cellular constituents in organelles termed autophagosomes, which target their degradation in the lysosome. Autophagy operates at basal levels in all cells where it serves as a homeostatic mechanism to maintain cellular integrity. The levels and cargoes of autophagy can, however, change in response to a variety of stimuli, and perturbations in autophagy are known to be involved in the etiology of various human diseases. Autophagy must therefore be tightly controlled. We report here that the Drosophila cyclindependent kinase PITSLRE is a modulator of autophagy. Loss of the human PITSLRE ortholog, CDK11, initially appears to induce autophagy, but at later time points CDK11 is critically required for autophagic flux and cargo digestion. Since PITSLRE/CDK11 regulates autophagy in both Drosophila and human cells, this kinase represents a novel phylogenetically conserved component of the autophagy machinery.
doi:10.4161/auto.7.11.16646
PMCID: PMC3242795  PMID: 21808150
PITSLRE; CDK11; cyclin-dependent kinase; autophagy; human; Drosophila
4.  Ian Louttit Wilkinson 
BMJ : British Medical Journal  2008;336(7656):1315.
doi:10.1136/bmj.a149
PMCID: PMC2413387
5.  PUMA and Bax-induced Autophagy Contributes to Apoptosis 
Cell death and differentiation  2009;16(8):1135-1145.
The p53-inducible BH3-only protein PUMA is a key mediator of p53-dependent apoptosis, and PUMA has been shown to function by activating Bax and mitochondrial outer membrane permeabilization. In this study we describe an ability of PUMA to induce autophagy that leads to the selective removal of mitochondria. This function of PUMA depends on Bax/Bak and can be reproduced by overexpression of Bax. The induction of autophagy coincides with cytochrome c release, and taken together the results suggest that PUMA functions through Bax to induce mitochondrial autophagy in response to mitochondrial perturbations. Surprisingly, inhibition of PUMA or Bax-induced autophagy dampens the apoptotic response, suggesting that under some circumstances the selective targeting of mitochondria for autophagy can enhance apoptosis.
doi:10.1038/cdd.2009.28
PMCID: PMC2711052  PMID: 19300452
PUMA; Bax; autophagy
6.  Tumor Antigen LRRC15 Impedes Adenoviral Infection: Implications for Virus-Based Cancer Therapy▿ †  
Journal of Virology  2008;82(12):5933-5939.
Adenoviruses for gene or oncolytic therapy are under development. Notable among these strategies is adenoviral delivery of the tumor suppressor p53. Since all therapeutics have limitations in certain settings, we have undertaken retroviral suppressor screens to identify genes conferring resistance to adenovirus-delivered p53. These studies identified the tumor antigen LRRC15, which is frequently overexpressed in multiple tumor types, as a repressor of cell death due to adenoviral p53. LRRC15, however, does not impede p53 function per se but impedes adenoviral infection. Specifically, LRRC15 causes redistribution of the coxsackievirus-adenovirus receptor away from the cell surface. This effect is manifested in less adenoviral binding to the surfaces of LRRC15-expressing cells. This discovery, therefore, not only is important for understanding adenoviral biology but also has potentially important implications for adenovirus-based anticancer therapeutics.
doi:10.1128/JVI.02273-07
PMCID: PMC2395123  PMID: 18385238
7.  Biomedical models and healthcare systems 
BMJ : British Medical Journal  2005;330(7488):419.
PMCID: PMC549148  PMID: 15718550
15.  The concept of disease 
British Medical Journal  1979;2(6202):1440.
PMCID: PMC1597132
16.  Analysis of finite dose dermal absorption data: Implications for dermal exposure assessment 
A common dermal exposure assessment strategy estimates the systemic uptake of chemical in contact with skin using the fixed fractional absorption approach: the dermal absorbed dose is estimated as the product of exposure and the fraction of applied chemical that is absorbed, assumed constant for a given chemical. Despite the prominence of this approach there is little guidance regarding the evaluation of experiments from which fractional absorption data are measured. An analysis of these experiments is presented herein, and limitations to the fixed fractional absorption approach are discussed. The analysis provides a set of simple algebraic expressions that may be used in the evaluation of finite dose dermal absorption experiments, affording a more data-driven approach to dermal exposure assessment. Case studies are presented that demonstrate the application of these tools to the assessment of dermal absorption data.
doi:10.1038/jes.2013.23
PMCID: PMC3868874  PMID: 23715085
risk assessment; skin absorption; percent absorption; fractional absorption; dermal load; maximum flux; evaporation

Results 1-16 (16)