Medical education has traditionally focused on the learners, the educators, and the curriculum, while tending to overlook the role of the designed environment. Experience indicates, however, that processes and outcomes of medical education are sensitive to the qualities and disposition of the spaces in which it occurs. This includes the clinical education within the patient care environment, termed the clinical learning environment (CLE). Recognition of this has informed the design of some new clinical learning spaces for the past decade. Competency-based clinical education can drive design requirements that differ materially from those associated with general purpose educational or clinical spaces. In this article, we outline two conceptual frameworks: (i) materialist spatiality and (ii) actor-network theory and consider how they can guide the design of spaces to support competency-based medical education and to guide the evaluation and discussion of the educational impacts of the spaces once built. We illustrate the use of these frameworks through discussion of the educational ambitions that underpinned the design of some recent clinical educational spaces. We close with practical points for consideration by educators and designers.

Background: Although the role of vitamin D deficiency in causing osteomalacia is well recognised, there is limited evidence to suggest that vitamin D deficiency is associated with osteoporosis. One community based study has suggested a reduction in bone density in females with low vitamin D levels, while another has shown no effect of isolated vitamin D deficiency on population fracture rates. We aimed to assess bone density in a cohort of women with low vitamin D levels but no other identified risk factors for osteoporosis. We wished to see if there was any relationship between the two, in order to clarify whether measurement of vitamin D was justified in aiding selection of patients for DXA, and whether DXA was justified in patients found to have isolated vitamin D deficiency. Methods: We identified 70 women referred to an open access DXA scanning service by their GP with low vitamin D levels (under 48 nmol/l) as their only risk factor. We performed DXA of hip and spine and recorded the absolute bone density and Z scores for each patient, together with their vitamin D levels. We calculated the mean (SD) values for Z score at hip and spine, and compared these to a control group of women referred for baseline DXA prior to commencing aromatase inhibitors for breast cancer. We also compared the results with those obtained from the rest of the GP database for women referred up with a 10 year risk of osteoporotic fractures calculated at over 10% using FRAX. These statistical comparisons were made using unpaired Students t test. Mean values for Z scores at hip and spine were calculated and compared within the index group for those with vitamin D levels above and below 20 nmol/l using Students t test. Correlation coefficients between vitamin D levels and Z scores at hip and spine were also calculated for the index group. Results: Mean (SD) values for Z scores in the hip and spine for patients with isolated vitamin D deficiency were +0.30 (0.87) and +0.46 (0.92) respectively. These were not significantly different from controls whose corresponding values were +0.17 (0.34) and +0.49 (0.45). By contrast, patients with a 10 year risk of fracture of over 10% had lower values at hip −0.01 (0.07) and spine −0.13 (0.09) [p = 0.01]. Mean Z scores for those with very low vitamin D levels (under 20 nmol/l) were not significantly different at either site when compared to those with less severe deficiency (20-48 nmol/l) [p = 0.26]. There was no correlation between vitamin D levels and Z scores at hip or spine [r = 0.01] Conclusions: There was no overall decrease in bone density associated with low vitamin D levels in women in our study. There is no evidence to support the routine measurement of vitamin D to select patients for DXA scanning. There is no reason to perform DXA scans in those patients who have an isolated vitamin D deficiency in the absence of defined risk factors for osteoporosis. Disclosure statement: The authors have declared no conflicts of interest.

BACKGROUND:To avoid ischemic necrosis, compartment syndrome is a surgical emergency treated with decompression once identified. A potentially lethal, oxidant-driven reperfusion injury occurs after decompression. N-acetylcysteine is an antioxidant with the potential to attenuate the reperfusion injury.QUESTIONS/PURPOSES:We asked whether N-acetylcysteine could preserve striated muscle contractility and modify neutrophil infiltration and activation after simulated compartment syndrome release.MATERIALS AND METHODS:Fifty-seven rats were randomized to control, simulated compartment syndrome, and simulated compartment syndrome plus N-acetylcysteine groups. We isolated the rodent cremaster muscle on its neurovascular pedicle and placed it in a pressure chamber. Chamber pressure was elevated above critical closing pressure for 3 hours to simulate compartment syndrome. Experiments were concluded at three times: 1 hour, 24 hours, and 7 days after decompression of compartment syndrome. We assessed twitch and tetanic contractile function and tissue myeloperoxidase activity. Ten additional rats were randomized to control and N-acetylcysteine administration after which neutrophil respiratory burst activity was assessed.RESULTS:The simulated compartment syndrome decreased muscle contractility and increased muscle tissue myeloperoxidase activity compared with controls. Treatment with N-acetylcysteine preserved twitch and tetanic contractility. N-acetylcysteine did not alter neutrophil infiltration (myeloperoxidase activity) acutely but did reduce infiltration at 24 hours, even when given after decompression. N-acetylcysteine reduced neutrophil respiratory burst activity.CONCLUSION:N-acetylcysteine administration before or after simulated compartment syndrome preserved striated muscle contractility, apparently by attenuating neutrophil activation and the resultant oxidant injury.CLINICAL RELEVANCE:Our data suggest a potential role for N-acetylcysteine in the attenuation of muscle injury after release of compartment syndrome and possibly in the prophylaxis of compartment syndrome.

Background: Curriculum reform poses significant challenges for medical schools across the globe. This paper describes the reforms that took place at the medical school of the Royal College of Surgeons in Ireland (RCSI) between 2005 and 2008 and the institutional self review process that accompanied these reforms. Results: Although fully accredited with the Irish Medical Council the RCSI sought additional detailed review of all aspects of its undergraduate medical program. Five medical educationalists were invited to visit the College in 2005 and again in 2008 to act as ‘critical friends’ and guide the self review using the World Federation for Medical Education (WFME) standards which had recently been adopted in Ireland. Conclusion: The process of institutional self review (as opposed to more high stakes accreditation) can bring about significant reform, especially when supported by a panel of ‘critical friends’ working alongside faculty to help guide and support sustained curriculum reform. The WFME standards continue to provide a useful framework to consider all medical education activities within a medical school engaged in continuous renewal. Adequate preparation for such reviews is critical to the success of such an undertaking and should be supported by a comprehensive communication strategy and project plan.

Objective. Myocardial dysfunction is often seen during the inflammatory response to major surgery at 4 to 6h postoperatively. The aim of this study was to investigate the effect of glutamine pretreatment, as a means of preconditioning, on lipopolysaccharide-induced myocardial dysfunction.Methods. C57BL/6 mice were randomized into four groups: Control; lipopolysaccharide; glutamine plus lipopolysaccharide; and Quercetin, an inhibitor of heat shock protein synthesis plus glutamine and lipopolysaccharide. Left ventricular function was assessed at 6h following lipopolysaccharide (LPS) insult by invasive hemodynamics. Heat shock protein (HSP)72 in heart tissue was determined by Western immunoblot at 12h after glutamine administration.Results. Administration of lipopolysaccharide resulted in significant decrease in left ventricular end systolic pressure (LVESP) (69.1 +/- 2.52 mm Hg versus 106.3 +/- 3.36 mm Hg in controls), reduced dP/dtmax (4704.1 +/- 425.31 mm Hg/s versus 9389.8 +/- 999.4 mm Hg/s in controls), and the increase in left ventricular end diastolic pressure (LVEDP) (5.10 +/- 0.28 mm Hg versus 2.16 +/- 0.27 mm Hg in controls) (P < 0.05). Peritoneal injection of 25g/kg of glutamine 12 h prior to lipopolysaccharide exposure induced HSP72 expression in heart tissues and attenuated lipopolysaccharide-induced left ventricular dysfunction: LVESP 85.94 +/- 3.8 mm Hg (P < 0.05), dP/dtmax 8331 425 mm Hg (P < 0.05), LVEDP 2.32 +/- 0.23 mm Hg (P < 0.01). Quercetin partially attenuated glutamine induced HSP72 expression and blocked the protective response of glutamine.Conclusion. These data demonstrate that cardio-protection with glutamine is associated with induction of HSP72 and may be an approach to activating the preconditioning response in the heart in clinical practise. (C) 2010 Elsevier Inc. All rights reserved.

The focus of this investigation was on adduct formation, and its consequences, between organotin(IV) Lewis acids and the tetradentate salicylaldimine ligands H(2)3-MeOsalen [N,N'-bis(3-methoxysalicylidine)1,2-ethane diamine] and H(2)3-MeOsalbiphen [N,N'-bis(3-methoxysalicylidine)2,2'-biphenyl diamine]. (SnBu2Cl2)-Cl-n reacted with H(2)3-MeOsalen to give a 1/1 adduct, A, containing a dangling salicylaldimine ligand but failed to yield a solid state adduct with H(2)3-MeOsalbiphen, even though it exists in dynamic equilibrium with the latter ligand in solution. The stronger Lewis acids SnPh2Cl2 and (SnBuCl3)-Cl-n yielded 2/1 solid state adducts D and E, respectively, with H(2)3-MeOsalbiphen in each of which the ligand bridges to six-coordinated tin centers and donor bonds are via phenolic and methoxy oxygen atoms. SnB2n(NCS)(2) reacted with H(2)3-MeOsalen to give an adduct, B, having a solid state ionic structure of formulation {[SnBu2n(NCS)(H(2)3-MeOsalen)](2)(mu-H(2)3-MeOsalen)}[SnBu2n(NCS)(4)]. The cation of B displays both bridging and dangling ligands and seven-coordinated tin. The ionic structure gives way to a nonionic symmetric cyclic trimeric structure of formulation [SnBu2n(NCS)(2)(mu-H(2)3-MeOsalen)](3) in solution. The latter reacted with NaCl and (SnBu2Cl2)-Cl-n to yield a new adduct, C, which in the solid state has an the ionic formulation [(SnBu2Cl)-Cl-n(mu-H(2)3-MeOsalen)](2)[SnBu2n (2)(NCS)(4)], the cation of which has a centrosymmetric structure and seven-coordinated tin. The solid state ionic structure of C is not retained in solution. Crystallographic data are also reported for the free ligands H(2)3-MeOsalen and H(2)3-MeOsalbiphen (two crystal modifications of the latter were identified). The structural data clearly identify that donor bond formation through the salicylaldimine phenolic oxygen has the concomitant effect of phenolic hydrogen transfer to the imine nitrogen, a process that accounts for the imine hydrolysis which frequently occurs when the salicylaldimine ligands react with Lewis acids. Salicylaldehyde does not assume a zwitterionic form in its 1/1 adduct, F, with SnMe2Cl2 (the structure of this adduct was reinvestigated in the present study), and consequently the role of the phenolic oxygen is reduced to that of a very weak donor, participating merely in secondary bonding.

Ischemia/reperfusion (I/R) results in endothelial dysfunction, seen as loss of endothelium-dependent vasodilatation. In prolonged ischemia, this can result in marked vasospasm or no reflow in the microvasculature. Thermotolerance (T) attenuates I/R-induced microvascular injury. The aim of this study was to investigate the effect of thermotolerance on I/R-induced vasomotor changes and "no reflow." Sprague-Dawley rats were randomized into an ischemia/reperfusion group (I/R group) and a group in which thermotolerance (41 + 0.5 degrees C for 15 min 18 h prior to I/R) was induced (T + I/R group). IR injury was established by occlusion of the superior mesenteric and celiac vascular pedicle for 30 min, followed by 60 min of reperfusion. Vasomotor function [arteriolar constriction:dilatation (C:D) ratio] measured by response to acetylcholine (endothelium-dependent) and sodium nitroprusside (endothelium-independent) and "no-reflow" phenomenon were determined in mesenteric arterioles by intravital microscopy. Data are expressed as means +/- SEM and were analyzed using ANOVA and chi(2) test. I/R caused a significant decrease in endothelium-dependent vasodilatation (C:D = 1.37+/-0.31 in IR group vs. 2.06+/-0.20 in baseline, P<0.01) and no reflow in arterioles in 16 of 28 unheated rats. Endothelium-independent dilatation was not altered by I/R. Thermotolerance attenuated this impairment of endothelium-dependent dilatation (P<0.01 vs. IR; C:D = 1.95+/-0.19) and reduced no-reflow phenomenon to 4 of 16 rats (P<0.05 vs. IR). This study demonstrated that thermotolerance preserves endothelial vasomotor function and markedly reduces "no reflow" in arterioles.

Chen, Gang MD; Moneley, Dana; Kelly, Cathal; Chen, Hong MD; Leahy, Austin; Bouchier-Hayes, David Author Information

Thermotolerance describes the process in which hyperthermia induces a transient resistance of the stressed cells to subsequent episodes of oxidative stress. The aims of this study were first, to assess the effect of ischemia-reperfusion (IR) injury on renal function and the expression of the ICAM-1 receptor and MHC antigens, and second, to evaluate the protective effects of thermotolerance on IR induced renal injury and its potential for decreasing allograft rejection, by decreasing alloantigen expression. Sprague-Dawley rats were randomized into three groups: control, IR, and hyperthermia + IR (HIR) (n=8 per group). Thermotolerance was induced 18 hr prior to IR by increasing the core body temperature to 41 degrees C+/-0.5 degrees C for 15 min. After left uninephrectomy, IR was induced by clamping the right renal pedicle for 45 min, followed by 2 hr reperfusion. Myeloperoxidase (MPO) activity was used as an indicator of renal neutrophil influx. Kidney edema was assessed using the weight difference between left and right kidneys. Renal function was evaluated by measuring serum creatinine and urea 2 hr following clamp removal. Immunocytochemistry was used to measure expression of ICAM-1 and MHC antigen. Renal function was significantly impaired by IR with serum creatinine and urea levels of 131.5+/-5.01 microM and 11.2+/-0.71 mM, respectively, compared with controls of 67.9+/-5.11 microM and 8.1+/-0.36 mM, P<0.005 in both cases. Renal function was preserved in the HIR group, serum creatinine (84.8+/-8.58 microM) and urea (9.0+/-0.52 mM) were comparable to that of controls. Renal endothelium was activated in the IR group compared with controls, with increased ICAM-1, and tubular epithelium showed increased class II MHC expression. This up-regulation was prevented by prior induction of thermotolerance. Endothelial permeability was increased in the IR group with MPO activity of 0.8+/-0.08 units/g tissue--twice that of control levels P<0.05--and a marked increase in organ edema. Thermotolerance preserved endothelial barrier function. Thermotolerance may prevent IR injury by preventing endothelium activation and has the potential to modify allograft rejection by decreasing expression of ICAM-1, an important T cell receptor, and class II MHC.

Cancer patients are often at high risk for perioperative complications because of preexisting conditions, the magnitude of surgery, and the use of aggressive multimodality treatment. It is essential to identify risk factors preoperatively, correct any deficits, and monitor organ dysfunction. During the perioperative period prophylaxis and surveillance for cardiopulmonary, hematologic, and septic complications should minimize morbidity and mortality. Finally, nutritional support should be given to malnourished patients undergoing extensive operative procedures.