Background: Reliable and valid methods of evaluating operative performance are essential for surgical training programs and education research. Laparoscopic surgery entails a unique skill set, but it is unclear whether it requires a specific assessment form or whether more general assessment tools can be applied. The primary purpose of this study was to assess the concurrent validity of 2 previously validated assessment scales. One of these scales was designed specifically to assess laparoscopic skills and the other to assess more general surgical skills. Construct validity and reliability of both scales were also assessed.Methods: Postgraduate year (PGY) 1–5 general surgery and urology residents (N = 33) performed a live human laparoscopic cholecystectomy. Three attending surgeon raters scored their performance using previously validated objective structured assessment of technical skills (OSATS) and Global Operative Assessment of Laparoscopic Skills (GOALS) global rating scales.Results: Pearson's correlation coefficient between OSATS and GOALS was 0.975 (P = .01). Evidence of construct validity was demonstrated for both OSATS and GOALS with senior residents (PGY 3–5) demonstrating significantly higher scores than the junior (PGY 1–2) group (P < .001). Both OSATS and GOALS demonstrated reliability with a Cronbach's alpha of 0.959 and 0.957, respectively.Conclusions: Reliability and construct validity were confirmed for both OSATS and GOALS global rating scales. The near total correlation between the 2 scales questions the need for separate laparoscopic assessment tools. This study highlights the real strengths of OSATS, the use of which allows for more consistent nomenclature and standardized skills assessment across surgical platforms.

Dietary flaxseed has significant anti-atherogenic effects. However, the limits of this action and its effects on vascular contractile function are not known. We evaluated the effects of flaxseed supplementation on atherosclerosis and vascular function under prolonged hypercholesterolemic conditions in New Zealand White rabbits assigned to one of four groups for 6, 8, or 16 wk of feeding: regular diet (RG), 10% flaxseed-supplemented diet (FX), 0.5% cholesterol-supplemented diet (CH), and 0.5% cholesterol- and 10% flaxseed-supplemented diet (CF). Cholesterol feeding resulted in elevated plasma cholesterol levels and the development of atherosclerosis. The CF group had significantly less atherosclerotic lesions in the aorta and carotid arteries after 6 and 8 wk than the CH animals. However, the anti-atherogenic effect of flaxseed supplementation was completely attenuated by 16 wk. Maximal tension induced in aortic rings either by KCl or norepinephrine was not impaired by dietary cholesterol until 16 wk. This functional impairment was not prevented by including flaxseed in the high-cholesterol diet. Aortic rings from the cholesterol-fed rabbits exhibited an impaired relaxation response to acetylcholine at all time points examined. Including flaxseed in the high-cholesterol diet completely normalized the relaxation response at 6 and 8 wk and partially restored it at 16 wk. No significant changes in the relaxation response induced by sodium nitroprusside were observed in any of the groups. In summary, dietary flaxseed is a valuable strategy to limit cholesterol-induced atherogenesis as well as abnormalities in endothelial-dependent vasorelaxation. However, these beneficial effects were attenuated during prolonged hypercholesterolemic conditions.

Clinical data and molecular experiments have strongly linked coronary artery diseases to infection by Chlamydia pneumonia (Cpn). However, the role of Cpn infection as a causative atherogenic factor remains to be proven. Our investigation hypothesizes that Cpn infection of the coronary artery induces atherosclerotic pathology in the absence of a host immune system. Methods: Porcine left anterior descending coronary artery (LAD) was explanted, dissected into 3mm-long sections and cultured in 20% fetal bovine serum. On Day 3 post explant, LAD sections were either infected by 1 × 105 plaque forming unit of Cpn (strain AR-39) or an equivalent amount of heat killed Cpn. Sections were collected on day 4, 5, 6, 7, 8, 9 and 10 post infection (pi). Results: Cpn inclusion bodies (IB, Cpn progeny) were strongly detected on day 5, 6, 9 and 10 pi. in the smooth muscle intimal layer. Very few IB were detected between day 1–4 and 7–8 pi. The emergence of IB on day 5/6 and day 9/10 indicated successful completions of Cpn life cycles. Cpn-infected vessels exhibited physically detached muscle cells, porous zones in the intimal layer and neointimal growth which strongly resembled in vivo atherosclerotic lesions. Detection of porous zones in the intimal layer correlated with active bacterial metabolism and occurred when IB were absent (day 1–4, day 7–8 pi.). There was significant PCNA expression along sites where muscle layers were detached. From days 7–10 pi., the intimal to lumen ratio increased only in the CPn-infected LAD. Overall, we conclude that Cpn infection can induce atherosclerosis independent of inflammation, by causing smooth muscle cell injury and structural damage to a vessel. Further investigation on related cellular pathways will help unravel the mechanism of infection-induced atherogenesis, stroke and vascular diseases.