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Abstract Background Obesity is a state of chronic low-grade inflammation. Chronic low-grade inflammation is associated with the pathophysiology of both type-2 diabetes and atherosclerosis. Prevention or reduction of chronic low-grade inflammation may be advantageous in relation to obesity related co-morbidity. In this study we investigated the acute effect of dietary protein sources on postprandial low-grade inflammatory markers after a high-fat meal in obese non-diabetic subjects. Methods We conducted a randomized, acute clinical intervention study in a crossover design. We supplemented a fat rich mixed meal with one of four dietary proteins - cod protein, whey isolate, gluten or casein. 11 obese non-diabetic subjects (age: 40-68, BMI: 30.3-42.0 kg/m2) participated and blood samples were drawn in the 4 h postprandial period. Adiponectin was estimated by ELISA methods and cytokines were analyzed by multiplex assay. Results MCP-1 and CCL5/RANTES displayed significant postprandial dynamics. CCL5/RANTES initially increased after all meals, but overall CCL5/RANTES incremental area under the curve (iAUC) was significantly lower after the whey meal compared with the cod and casein meals (P = 0.0053). MCP-1 was initially suppressed after all protein meals. However, the iAUC was significantly higher after whey meal compared to the cod and gluten meals (P = 0.04). Conclusion We have demonstrated acute differential effects on postprandial low grade inflammation of four dietary proteins in obese non-diabetic subjects. CCL5/RANTES initially increased after all meals but the smallest overall postprandial increase was observed after the whey meal. MCP-1 was initially suppressed after all 4 protein meals and the whey meal caused the smallest overall postprandial suppression. Trial Registration ClinicalTrials.gov ID: NCT00863564

Abstract Background The educational climate is crucial in postgraduate medical education. Although leaders are in the position to influence the educational climate, the relationship between leadership skills and educational climate is unknown. This study investigates the relationship between the educational climate in clinical departments and the leadership skills of clinical consultants responsible for education. Methods The study was a trans-sectional correlation study. The educational climate was investigated by a survey among all doctors (specialists and trainees) in the departments. Leadership skills of the consultants responsible for education were measured by multi-source feedback scores from heads of departments, peer consultants, and trainees. Results Doctors from 42 clinical departments representing 21 specialties participated. The response rate of the educational climate investigation was moderate 52% (420/811), Response rate was high in the multisource-feedback process 84.3% (420/498). The educational climate was scored quite high mean 3.9 (SD 0.3) on a five-point Likert scale. Likewise the leadership skills of the clinical consultants responsible for education were considered good, mean 5.4 (SD 0.6) on a seven-point Likert scale. There was no significant correlation between the scores concerning the educational climate and the scores on leadership skills, r = 0.17 (p = 0.29). Conclusions This study found no relation between the educational climate and the leadership skills of the clinical consultants responsible for postgraduate medical education in clinical departments with the instruments used. Our results indicate that consultants responsible for education are in a weak position to influence the educational climate in the clinical department. Further studies are needed to explore, how heads of departments and other factors related to the clinical organisation could influence the educational climate.

Background: Exaggerated postprandial triglyceride concentration is believed to be atherogenic, and to influence the risk of thrombosis. Both elevated plasminogen inhibitor 1 (PAI-1) and increased factor VII coagulant activity (FVIIc) are potential important contributors to the increased risk of cardiovascular disease in type 2 diabetes., Aim: We aimed to investigate the effect of adding four different protein types (i.e. casein, whey, cod, and gluten) to a fat-rich meal on postprandial responses of PAI-1 and FVIIc in type 2 diabetic patients., Methods: Twelve type 2 diabetic patients ingested four isocaloric test meals in random order. The test meals contained 100 g of butter and 45 g of carbohydrate in combination with 45 g of casein (Cas-meal), whey (Whe-meal), cod (Cod-meal), or gluten (Glu-meal), respectively. Plasma concentrations of PAI-1 and FVIIc were measured before meal, and at regular intervals for 8-h postprandially., Results: The postprandial PAI-1 concentration decreased significantly by 49% to 56% in response to the four test meals. There were no significant differences between the outcomes from the four test-meals. The FVIIc levels decreased by 8% to 11% after the meals. Again, we observed no significant differences in outcomes between the four protein-enriched meals., Conclusions: The four proteins casein, whey, cod, and gluten, added to a fat-rich meal, all decreased the PAI-1 and FVIIc concentrations postprandially in type 2 diabetic subjects. However, postprandial levels of PAI-1 and FVIIc were not acutely influenced by the protein source.