Search

Adolescent eyewitnesses have not been adequately studied. This is problematic given that adolescents are at a heightened risk to be an eyewitness or victim to crime. As a first step in studying adolescent eyewitnesses, the current experiment examined adolescents' (15- to 18-year-old's; N = 470) performance on four lineup procedures—simultaneous, sequential, elimination, wildcard—to determine which resulted in the greatest discriminability. Given that police agencies use different methods for selecting fillers in the real world (Police Executive Research Forum 2013), filler similarity was manipulated in order to test the lineups in a more legally realistic manner. Thus, lineups either contained lower or higher similarity fillers. Using d' as a measure of discriminability, results identified that the wildcard and simultaneous lineups led to the greatest discriminability, while the sequential lineup led to the lowest discriminability. Although the results do not suggest a clear superiority of one lineup procedure over another, what the results do suggest is that the sequential lineup may be the least advantageous to use with adolescents and the wildcard and simultaneous lineups may be the most advantageous. [ABSTRACT FROM AUTHOR]

Background: Despite higher thromboembolism risk, women with atrial fibrillation have lower oral anticoagulation (OAC) use compared to men. The influence of the CHA 2 DS 2‐VASc score or the introduction of non–vitamin K OACs on this relationship is not known. Methods and Results: Using the PINNACLE National Cardiovascular Data Registry from 2008 to 2014, we compared the association of sex with OAC use (warfarin or non–vitamin K OACs) overall and by CHA 2 DS 2‐VASc score and examined temporal trends in OAC use by sex. Multivariable regression models assessed the association between sex and OAC use in those with CHA 2 DS 2‐VASc scores ≥2. Temporal analyses assessed changes in OAC use by sex over time. Of the 691 906 atrial fibrillation patients, 48.5% were women. Women were significantly less likely than men to use any OAC overall (56.7% versus 61.3%; P<0.001) and at all levels of CHA 2 DS 2‐VASc score (adjusted risk ratio 9% to 33% lower, all P<0.001). Compared to other thromboembolic risk factors, female sex was associated with lower use of OAC (risk ratio 0.90, 95%CI 0.90‐0.91). Over time, non–vitamin K OAC use increased at a slightly higher rate in women (56.2% increase per year, 95%CI 54.6% to 57.9%) compared to men (53.6% increase per year, 95%CI 52.0% to 55.2%), yet women remained less likely to receive any OAC at all time points (P<0.001). Conclusions: Among patients with atrial fibrillation, women were significantly less likely to receive OAC at all levels of the CHA 2 DS 2‐VASc score. Despite increasing non–vitamin K OAC use, women had persistently lower rates of OAC use compared to men over time.

Background: Although rates of survival to hospital discharge after in-hospital cardiac arrest (IHCA) have improved over the last decade, it is unknown if these survival gains are sustained after hospital discharge.Objective: To examine 1-year survival trends overall and by rhythm after IHCA.Methods: Using Medicare beneficiaries (age≥65years) with IHCA occurring between 2000 and 2011 at Get With The Guidelines®-Resuscitation Registry participating hospitals we used multivariable regression, to examine temporal trends in risk-adjusted rates of 1-year survival.Results: Among 45,567 patients with IHCA, the unadjusted 1-year survival was 9.4%. Unadjusted 1-year survival was 21.8% among the 9,223 (20.2%) of patients with Ventricular Fibrillation or Pulseless Ventricular Tachycardia (VF/VT) and 6.2% among the 36,344 (79.8%) of patients with Pulseless Electrical Activity or asystole (PEA/asystole). After adjustment for patient and arrest characteristics, 1-year survival increased over time for all IHCA from 8.9% in 2000-2001 to 15.2% in 2011 (adjusted rate ratio [RR] per year, 1.05; 95% CI, 1.03-1.06; P<0.001 for trend). Improvements in 1-year risk adjusted survival were also observed for VF/VT (19.4% in 2000-2001 to 25.6% in 2011 [RR per year, 1.02; 95% CI, 1.01-1.04; P 0.004 for trend]) and PEA/asystole arrests (4.7% in 2000-2001 to 10.2% in 2011 [RR per year, 1.07; 95% CI, 1.05-1.08; P<0.001 for trend]).Conclusion: Among Medicare beneficiaries in the GWTG-Resuscitation registry, 1-year survival after IHCA has increased for over the past decade. Temporal improvements in survival were noted for both shockable and non-shockable presenting arrest rhythms. [ABSTRACT FROM AUTHOR]

Cisplatin is a common platinum-based chemotherapeutic that induces acute kidney injury (AKI) in about 30% of patients. Pharmacokinetic/toxicodynamic (PKTD) models of cisplatin-induced AKI have been used to understand risk factors and evaluate potential mitigation strategies. While both traditional clinical biomarkers of kidney function [e.g. serum creatinine (SCr), blood urea nitrogen (BUN), estimated glomerular filtration rate (eGFR), and creatinine clearance (CrCl)] and newer subclinical biomarkers of kidney injury [e.g. urinary kidney injury molecule 1 (KIM-1), beta-2 microglobulin (B2M), neutrophil gelatinase-associated lipocalin (NGAL), calbindin, etc.] can be used to detect cisplatin-induced AKI, published PKTD models are limited to using only traditional clinical biomarkers. Previously identified risk factors for cisplatin nephrotoxicity have included dose, age, sex, race, body surface area, genetics, concomitant medications, and comorbid conditions. However, the relationships between concentrations and PK of platinum and biomarkers of kidney injury have not been well elucidated. This review discusses the evaluation of cisplatin-induced nephrotoxicity in clinical studies, mouse models, and in vitro models, and examines the available human PK and TD data. Improved understanding of the relationships between platinum PK and TD, in the presence of identified risk factors, will enable the prediction and prevention of cisplatin kidney injury. Significance Statement As cisplatin treatment continues to cause AKI in a third of patients, it is critical to improve the understanding of the relationships between platinum PK and nephrotoxicity as assessed by traditional clinical and contemporary subclinical TD markers of kidney injury. Prediction and prevention of cisplatin-induced nephrotoxicity will be advanced by the evolving development of PKTD models that incorporate kidney injury biomarkers with enhanced sensitivity and include covariates that can impact risk of developing cisplatin-induced AKI., (Copyright © 2024 American Society for Pharmacology and Experimental Therapeutics.)