3,4-Methylenedioxymethamphetamine (MDMA, “Ecstasy”) is a potent psychedelic drug inducing euphoria and hyper-sociability in humans, as well as hyperactivity and anxiety in rodents. Adult zebrafish (Danio rerio) have become a widely used species in neurobehavioral research. Here, we explore the effects of a wide range (0.25–120 mg/L) of acute MDMA doses on zebrafish behavior in the novel tank test. While MDMA was inactive at lower doses (0.25–10 mg/L), higher doses reduced bottom swimming and immobility (40–120 mg/L) and impaired intra-session habituation (10–120 mg/L). MDMA also elevated brain c-fos expression, collectively confirming the utility of zebrafish models for screening of hallucinogenic compounds.
In the index hospitalization, CR in STEMI patients is associated with significant risk reduction in cardiac death and revascularization and a non-significant reduced trend of CI-AKI, despite increased use of contrast when compared with IRA.
Purpose: Degenerative mitral stenosis (DMS) is an increasingly recognized cause of mitral stenosis. The goal of this study was to compare echocardiographic differences between DMS and rheumatic mitral stenosis (RMS), identify echocardiographic variables reflective of DMS severity, and propose a dimensionless mitral stenosis index (DMSI) for assessment of DMS severity. Methods: This is a single-center, retrospective cohort study. We included patients with at least mild MS and a mean transmitral pressure gradient (TMPG) [?] 4 mmHg. Mitral valve area by the continuity equation (MVACEQ) was used as an independent reference. The DMSI was calculated as follows: DMSI = VTILVOT / VTIMV. All-cause mortality data were collected retrospectively. Results: A total of 64 patients with DMS and 24 patients with RMS were identified. MVACEQ was larger in patients with DMS (1.43 ? 0.4 cm2) than RMS (0.9 ? 0.3 cm2) by~0.5 cm2 (p = <0.001) and mean TMPG was lower in the DMS group (6.0? 2 vs. 7.9?3 mmHg, p=0.003). A DMSI of ? 0.50 and [?] 0.351 were associated with MVACEQ [?] 1.5 and MVACEQ [?] 1.0 cm2 (p<0.001), respectively. With the progression of DMS from severe to very severe, there was a significant drop in DMSI. There was a non-significant trend towards worse survival in patients with MVACEQ [?] 1.0 cm2 and DMSI [?] 0.35, suggesting severe stenosis severity. Conclusion: Our results show that TMPG correlates poorly with MVA in patients with DMS. Proposed DMSI may serve as a simple echocardiographic indicator of hemodynamically significant DMS.
Purpose: Degenerative mitral stenosis (DMS) is an increasingly recognized cause of mitral stenosis. The goal of this study was to compare echocardiographic differences between DMS and rheumatic mitral stenosis (RMS), identify echocardiographic variables reflective of DMS severity, and propose a dimensionless mitral stenosis index (DMSI) for assessment of DMS severity. Methods: This is a single-center, retrospective cohort study. We included patients with at least mild MS and a mean transmitral pressure gradient (TMPG) ≥4 mm Hg. Mitral valve area by the continuity equation (MVA CEQ) was used as an independent reference. The DMSI was calculated as follows: DMSI = VTI LVOT / VTI MV. All-cause mortality data were collected retrospectively. Results: A total of 64 patients with DMS and 24 patients with RMS were identified. MVA CEQ was larger in patients with DMS (1.43 ± 0.4 cm 2) than RMS (0.9 ± 0.3 cm 2) by ~0.5 cm 2 (P = <.001), and mean TMPG was lower in the DMS group (6.0 ± 2 vs 7.9 ± 3 mm Hg, P = .003). A DMSI of ≤0.50 and ≤0.351 was associated with MVA CEQ ≤1.5 and MVA CEQ ≤1.0 cm 2 (P < .001), respectively. With the progression of DMS from severe to very severe, there was a significant drop in DMSI. There was a nonsignificant trend toward worse survival in patients with MVA CEQ ≤1.0 cm 2 and DMSI ≤0.35, suggesting severe stenosis severity. Conclusion: Our results show that TMPG correlates poorly with MVA in patients with DMS. Proposed DMSI may serve as a simple echocardiographic indicator of hemodynamically significant DMS.
Cardiovascular disease (CVD) comprises a vast spectrum of disease states ranging from hypertension (HTN) to valvular heart disease (VHD). CVD is known to be the leading cause of morbidity, mortality, and health-care expenditure throughout the world. According to the World Health Organization, coronary artery disease (CAD) and stroke, both subsets of CVD, are the world's biggest killers, accounting for a combined 15 million deaths in 2015. These diseases have remained the leading causes of death globally in the last 15 years. In 2010, CAD alone was projected to cost the U.S. $108.9 billion including the cost of health-care services, medications, and lost productivity. The presence of frailty signiicantly worsens outcomes for patients sufering from CAD. With just this one example of how frailty afects CVD, it is clear that understanding the impact of frailty upon patients alicted with the spectrum of cardiovascular disease is integral for the care of this very signiicant patient population.
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