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1.  Do students learn to be more conscientious at medical school? 
BMC Medical Education  2012;12:54.
Professionalism in medical students is not only difficult to define but difficult to teach and measure. As negative behaviour in medical students is associated with post-graduate disciplinary action it would be useful to have a model whereby unprofessional behaviour at the undergraduate level can easily be identified to permit appropriate intervention. We have previously developed a scalar measure of conscientiousness, the Conscientiousness Index (CI), which positively correlates to estimates of professional behaviour in undergraduate medical students. By comparing CI points awarded in year 1 and year 2 of study we were able to use the CI model to determine whether teaching and clinical exposure had any effect on students’ conscientiousness.
CI points were collected by administrative staff from 3 successive cohorts of students in years 1 and 2 of study. Points were awarded to students for activities such as submission of immunisation status and criminal record checks, submission of summative assignments by a specified date and attendance at compulsory teaching sessions. CI points were then converted to a percentage of maximal possible scores (CI %) to permit direct comparison between years 1 and 2 of study.
CI % scores were generally high with each year of study for each cohort showing negatively skewed normal distributions with peaks > 89%. There was a high degree of correlation of CI % scores between year 1 and year 2 of study for each cohort alone and when cohort data was combined. When the change in CI % from year 1 to year 2 for all students was compared there was no significant difference in conscientiousness observed.
We have provided evidence that use of a CI model in undergraduate medical students provides a reliable measure of conscientiousness that is easy to implement. Importantly this study shows that measurement of conscientiousness by the CI model in medical students does not change between years 1 and 2 study suggesting that it is a stable characteristic and not modified by teaching and clinical exposure.
PMCID: PMC3434045  PMID: 22784434
2.  Connexin-mimetic peptides dissociate electrotonic EDHF-type signalling via myoendothelial and smooth muscle gap junctions in the rabbit iliac artery 
British Journal of Pharmacology  2004;144(1):108-114.
Synthetic peptides corresponding to the Gap 26 and Gap 27 domains of the first and second extracellular loops of the major vascular connexins (Cx37, Cx40 and Cx43), designated as 43Gap 26, 40Gap 27, 37,40Gap 26 and 37,43Gap 27 according to Cx homology, were used to investigate the role of gap junctions in the spread of endothelial hyperpolarizations evoked by cyclopiazonic acid (CPA) through the wall of the rabbit iliac artery.Immunostaining and confocal microscopy demonstrated that gap junction plaques constructed from Cx37 and Cx40 were abundant in the endothelium, whereas Cx43 was the dominant Cx visualized in the media.None of the Cx-mimetic peptides affected endothelial hyperpolarizations evoked by CPA directly.When administered individually, 40Gap 27, 37,40Gap 26 and 37,43Gap 27, but not 43Gap 26, attenuated endothelium-dependent subintimal smooth muscle hyperpolarization. By contrast, only 43Gap 26 and 37,43Gap 27 reduced the spread of subintimal hyperpolarization through the media of the rabbit iliac artery. The site of action of the peptides therefore correlated closely with the expression of their target Cxs in detectable gap junction plaques.The findings provide further evidence that the EDHF phenomenon is electrotonic in nature, and highlight the contribution of myoendothelial and homocellular smooth muscle communication via gap junctions to arterial function.
PMCID: PMC1575982  PMID: 15644874
Gap junctions; connexin; EDHF; hyperpolarization
3.  Enhanced inhibition of the EDHF phenomenon by a phenyl methoxyalaninyl phosphoramidate derivative of dideoxyadenosine 
British Journal of Pharmacology  2004;142(1):27-30.
In rabbit arteries endogenous production of cAMP facilitates electrotonic signalling via gap junctions, thus explaining the ability of P-site inhibitors of adenylyl cyclase to attenuate EDHF-type responses. In the present study, we show that a lipophilic phosphoramidate pronucleotide derivative of dideoxyadenosine, 2′,3′-ddA-PMAPh, exhibits enhanced activity as an inhibitor of EDHF-type smooth muscle hyperpolarizations induced by acetylcholine (ACh) compared to the parent nucleoside 2′,3′-ddA, and that the effects of both compounds can be reversed by the cAMP phosphodiesterase inhibitor IBMX. Neither 2′,3′-ddA nor 2′,3′-ddA-PMAPh depress ACh-evoked endothelial hyperpolarization directly. Modifications in the lipophilicity of dideoxyadenosine and its direct intracellular delivery as a mononucleotide may thus enhance the ability to inhibit adenylyl cyclase and depress electrotonic signalling via myoendothelial gap junctions.
PMCID: PMC1574937  PMID: 15131001
cAMP; adenylyl cyclase; gap junctions; connexin
4.  Inhibition of the gap junctional component of endothelium-dependent relaxations in rabbit iliac artery by 18-α glycyrrhetinic acid 
The gap junction inhibitor 18-α-glycyrrhetinic acid (α-GA, 100 μM) attenuated endothelium-dependent relaxations to acetylcholine and cyclopiazonic acid by ∼20% in rings of pre-constricted rabbit iliac artery. The nitric oxide synthase inhibitor NG-nitro-L-arginine methyl ester (L-NAME, 300 μM) inhibited relaxations to both agents by ∼65% and these were further attenuated by α-GA to <10% of control. In endothelium-denuded preparations, relaxations to sodium nitroprusside were not affected by α-GA. Heterocellular gap junctional communication may therefore account for nitric oxide-independent relaxations evoked both by receptor-dependent and -independent mechanisms in rabbit iliac artery.
PMCID: PMC1565609  PMID: 9776336
Gap junctions; glycyrrhetinic acid; nitric oxide; endothelium-derived hyperpolarizing factor (EDHF)

Results 1-4 (4)