tracking echocardiography allows for the identification of 3 phenotypically distinct, reproducible, and clinically meaningful RV strain-derived post-systolic patterns. This study hypothesized that left ventricular (LV) enlargement in Barlow disease can be explained by accounting for the total volume load that consists of transvalvular mitral regurgitation (MR) and the prolapse volume. Barlow disease is characterized by long prolapsing mitral leaflets that can harbor a significant amount of blood-the prolapse volume-at end-systole. The LV in Barlow disease can be disproportionately enlarged relative to MR severity, leading to speculation of Barlow cardiomyopathy. Cardiac magnetic resonance (CMR) was used to compare MR, prolapse volume, and heart chambers remodeling in patients with Barlow disease (bileaflet prolapse [BLP]) and in single leaflet prolapse (SLP). A total of 157 patients (81 with BLP, 76 with SLP) were included. Patients with SLP were older and more had hypertension. Patients with BLP had more heart failure. Indexed LV end-diastolic volume was larger in BLP despite similar transvalvular MR. However, the prolapse volume was larger in BLP, which led to larger total volume load compared with SLP. Increasing tertiles of prolapse volume and MR both led to an incremental increase in LV end-diastolic volume in BLP. Using the total volume load improved the correlation with indexed LV end-diastolic volume in the BLP group, which closely matched that of SLP. A multivariable model that incorporated the prolapse volume explained left heart chamber enlargement better than a MR-based model, independent of prolapse category. The prolapse volume is part of the total volume load exerted on the LV during the cardiac cycle and could help explain the disproportionate LV enlargement relative to MR severity noted in Barlow disease.The prolapse volume is part of the total volume load exerted on the LV during the cardiac cycle and could help explain the disproportionate LV enlargement relative to MR severity noted in Barlow disease. This study describes the cardiac phenotypes and markers of adverse outcome in athletes with ventricular arrhythmias with no other discernable etiology than high exercise doses. Little is known about phenotypes and risk markers of life-threatening arrhythmic events in athletes with ventricular arrhythmia. We compared high-performance athletes who have ventricular arrhythmia with healthy controls using clinical data and cardiac imaging. None of the patients had family history of arrhythmogenic cardiomyopathy or any other discernable etiology of ventricular arrhythmia. Right (RV) and left ventricular (LV) function was assessed by echocardiographic longitudinal strain (right ventricular free wall strain longitudinal [RVFWSL] and left ventricular global longitudinal strain [LVGLS]). Mechanical dispersion was defined as the standard deviation of time to peak strain in 16 LV segments. RV ejection fraction and presence of late gadolinium enhancement was assessed by cardiac magnetic resonance. We included 43 aosis comparedto healthy athletes. Athletes with life-threatening arrhythmic events had additional LV contraction abnormalities. These phenotypes mimic arrhythmogenic cardiomyopathy and may potentially be induced by high dosesofexercise in susceptible individuals.Athletes with ventricular arrhythmias had impaired RV function and more myocardial fibrosis compared to healthy athletes. Athletes with life-threatening arrhythmic events had additional LV contraction abnormalities. These phenotypes mimic arrhythmogenic cardiomyopathy and may potentially be induced by high doses of exercise in susceptible individuals.Behavioural change techniques are currently used by many global organisations and public institutions. The amassing evidence base is used to answer practical and scientific questions regarding what cognitive, affective, and environment factors lead to successful behavioural change in the laboratory and in the field. In this piece we show that there is also value to examining interventions that inadvertently fail in achieving their desired behavioural change (e.g., backfiring effects). We identify the underlying causal pathways that characterise different types of failure, and show how a taxonomy of causal interactions that result in failure exposes new insights that can advance theory and practice.We highlight two alternative, yet complementary, solutions for harnessing available neural resources for improving integration of artificial limbs (ALs) through embodiment. 'Hard' embodiment exploits neural and cognitive body mechanisms by closely mimicking their original biological functions. 'Soft' embodiment exploits these same mechanisms by recycling them to support a different function altogether.Increasingly, online platforms are being used to deliver psychotherapy. Ziprasidone mw This, along with the growth in computational psychiatry, provides scientists with new opportunities to quantify how patient-therapist relationships relate to treatment outcomes. We argue that it is necessary to investigate markers and mechanisms that enable successful psychotherapy, and the establishment of therapeutic alliance in particular, using computational tools.Machines do not 'think fast and slow' in the sense that humans do in dual-process models of cognition. However, the people who create the machines may attempt to emulate or simulate these fast and slow modes of thinking, which will in turn affect the way end users relate to these machines. In this opinion article we consider the complex interplay in the way various stakeholders (engineers, user experience designers, regulators, ethicists, and end users) can be inspired, challenged, or misled by the analogy between the fast and slow thinking of humans and the Fast and Slow Thinking of machines.This review discusses impact of advancements in biologic understanding of prostate cancer (PCa) on definition and diagnosis of castration-resistant PCa (CRPC), predictive factors for progression to CRPC and treatment strategies. More sensitive assays confirm that bilateral orchiectomy reduces serum testosterone (T) closer to less then 20 ng/dL than less then 50 ng/dL, and evidence suggests that achieving T less then 20 ng/dL improves outcomes and delays CRPC emergence. Regular T assessments will evaluate whether T is adequately suppressed in the setting of potential progression to CRPC, given that late dosing may result in T escape. More advanced imaging modalities and biomarker assays allow earlier detection of disease progression. Predictive factors for progression to CRPC include Gleason grade, extent of metastatic spread, germline hereditary factors such as gene mutations affecting androgen receptor amplification or DNA repair deficiency mutations, prostate-specific antigen kinetics, and biomarker analyses.