A crucial step in clarifying and consolidating the learning gained from simulations in healthcare is to debrief those simulation experiences-that is, to methodically review what happened and why. Leading a debriefing is a learned skill, and can be improved with practice and feedback. The Debriefing Assessment for Simulation in Healthcare （DASHTM） Handbook and Rating Forms are designed to assist in evaluating and developing debriefing skills. Additional information, rating forms, and contact information can be found at the DASH website: http:／／www.harvardmedsim.org／dash.html.

The left atrium and left atrial appendage have unique genetic anatomical and physiological features. Recently, advances in diagnostic imaging technology have provided much new knowledge. Clinically, the risk of developing atrial fibrillation increases with age. In order to reduce the public health burden such as cerebral infarction caused by atrial fibrillation, we need to find some predictive risk factors and preventive strategies for cerebral infarction and more effective treatments. The new concept of atrial myopathy has emerged, and animal models and human studies have revealed close interactions between atrial myopathy, atrial fibrillation, and stroke through various mechanisms. Structural and electrical remodeling such as fibrosis and deterioration of the balance of autonomic nerves and complicated interactions between these mechanisms lead to deterioration of atrial fibrillation and a continuous vicious cycle, and finally thrombosis in the left atrial appendage. Although anticoagulant therapy for patients with atrial fibrillation is strongly recommended, it is difficult for many patients to continue optimal treatment. In the nearly future, it will be important to understand the anatomy and physiology of the left atrial appendage and to understand the shape changes, size and the changes of autonomic function, and thrombus formation conditions associated with LAA remodeling during atrial fibrillation, and then we should provide early therapeutic intervention.

Background/Aims: Several studies have assessed the effect of cool temperature on colonic peristalsis. Transient receptor potential melastatin 8 (TRPM8) is a temperature-sensitive ion channel activated by mild cooling expressed in the colon. We examined the antispasmodic effect of cool temperature on colonic peristalsis in a prospective, randomized, single-blind trial and based on the video imaging and intraluminal pressure of the proximal colon in rats and TRPM8-deficient mice. Methods: In the clinical trial, we randomly assigned a total of 94 patients scheduled to undergo colonoscopy to 2 groups: the mildly cool water (n = 47) and control (n = 47) groups. We used 20 mL of 15°C water for the mildly cool water. The primary outcome was the proportion of subjects with improved peristalsis after treatment. In the rodent proximal colon, we evaluated the intraluminal pressure and performed video imaging of the rodent proximal colon with cool water administration into the colonic lumen. Clinical trial registry website (Trial No. UMIN-CTR; UMIN000030725). Results: In the randomized controlled trial, after treatment, the proportion of subjects with no peristalsis with cool water was significantly higher than that in the placebo group (44.7% vs 23.4%; P < 0.05). In the rodent colon model, cool temperature water was associated with a significant decrease in colonic peristalsis through its suppression of the ratio of peak frequency (P < 0.05). Cool temperaturetreated TRPM8-deficient mice did not show a reduction in colonic peristalsis compared with wild-type mice. Conclusion For the first time, this study demonstrates that cool temperature-dependent suppression of colonic peristalsis may be associated with TRPM8 activation.