The recognition and further investigation of human factors in OSCEs is needed to improve examiner experience and behaviour in order to influence delivery, candidate experience and quality assurance of these examinations.

In response to the Accreditation Council of Graduate Medical Education mandated resident work hour restrictions, our residency program used a night float system in 2003. We undertook a survey of attending staff and residents to assess its effects on patient care and resident education. An anonymous survey was administered to attending staff and residents 1 year and 3 years after work hour restrictions took effect. The areas of disagreement include: beneficial effect on education (residents vs faculty: in 2004, 87% vs 22%, respectively, P = 0.02; in 2006, 71% vs 22%, P = 0.03); beneficial effect on patient care (in 2004, 53% vs 10%, P = 0.03); and compromised continuity of care (in 2004, 27% vs 70%, P = 0.04; in 2006, 7% vs 89%, P = 0.0002). One area of agreement was that residents’ quality of life had improved. Both disagreed that more errors were being made and that work hour restrictions should be mandated on practicing surgeons. Attending staff and residents have deeply held opinions regarding the effects of work hour restrictions. This reflects a continuing dissatisfaction with providing patient care and educating residents under a set of requirements that solely addresses resident sleepiness and fatigue.

The monoclonal theory of atherosclerosis postulates that a subpopulation of vascular smooth muscle cells (VSMCs) is selectively expanded in response to pathologic stimuli and accumulates in vascular intima. The purpose of this research was to clone VSMC, determine growth rates of the clones and their ability to release the mitogenic cytokine tumor necrosis factor-α (TNF-α). With approval of the institutional animal care and use committee, VSMCs were isolated and cultured from the thoracic aortas of three rats. To confirm that the cells in primary culture were of smooth muscle origin, they were immunostained with anti-α-smooth muscle-actin antibodies. Single cell-derived individual colonies with uniform appearance were surrounded by cloning rings, released with trypsin, and expanded. Growth rates of the clones were assessed by the mitochondrial dependent reduction of methyltetrazolium (MTT) to formazan after 24-hour stimulation with 10 per cent serum. Additionally, cloned cells were stimulated with 0.1, 1,10, and 20 μg/mL lipopolysaccharide (LPS) for 24 hours, and TNF-α was determined in the culture medium. Data were analyzed by ANOVA. Two clones were isolated that could be divided into categories based on distinctly different morphology: 1) spindle-shaped (SP) or 2) epithelioid-shaped (EP) VSMCs. The SP clone had a growth rate that was 25 per cent higher than the EP clone ( P < 0.05). Also, the SP clone had significantly higher release of TNF-α in response to LPS. For instance, TNF-α released in response to 0.1 μg/mL of LPS in the SP clone was 157 ± 45 pg/mL versus 21 ± 8.5 pg/mL in the EP clone ( P < 0.05). Primary cultures of rat VSMCs are heterogeneous and consist of at least two morphologically distinct cell types. These clones are different in growth rate and cytokine production. It is possible that selective expansion of one of these clones contributes to formation of stenotic vascular lesions.

In the current study, we test the hypothesis that norepinephrine has greater anti-inflammatory effects versus dopamine over a range of doses in a model of lipopolysaccharide (LPS)-stimulated cytokine release in human saphenous vein. Segments of saphenous vein were cut and separated into 1 mm x 1 mm squares and placed into two 24-well plates. These small segments of vessels were incubated in the presence of 20 μg/mL bacterial LPS, alone as a control or with 10x-6, 10x-5, 10x-4, 10x-3 concentration of dopamine or norepinephrine and LPS. The general linear models (GLM) statistical analysis for least squares means and adjustment for multiple comparisons was chosen to analyze the data. Both norepinephrine and dopamine were able to suppress the production of tumor necrosis factor (TNF) in a dose-dependent fashion. Over the range of doses, norepinephrine is a more potent inhibitor of TNF production than dopamine. This is a statistically significant linear trend ( P < .0001). Both norepinephrine and dopamine are powerful antiinflammatory agents. Norepinephrine is a more potent inhibitor of TNF than dopamine.