Should Antipsychotics' Risks Be Accepted by Clinicians on Behalf of Patients to Achieve Benefits of Mitigating Older Adults' Behavioral Symptoms in Short-Staffed Units?

This commentary on a case considers risks and benefits of pharmacological and nonpharmacological management of agitation in patients with dementia. Specifically, it considers beneficence and nonmaleficence in treatment decisions that affect both patients and staff as well as autonomy and surrogate decision making.

Aftermath of the Parkland Shooting: A Case Report of Post-traumatic Stress Disorder in an Adolescent Survivor.

The Journal of Child and Family Studies states that there have been more mass shootings within the last 18 years than in the entire 20th century combined, with 77% carried out by adolescents. This case study aims to evaluate the clinical presentation of post-traumatic stress disorder (PTSD) in an adolescent by highlighting the clinical course of a school shooting survivor. Here, we present the case of a 15-year-old female who presented to the emergency department (ED) of the University Hospital Medical Center (UHMC) under the Baker Act by the police for self-injury and self-harm. She had been admitted three times to the psychiatric hospital, all following the trauma of surviving the shooting. She met the criteria for PTSD and was triggered by graphics in the news outlets and social media.  As clinicians working with PTSD adolescents, we must be cognizant of these factors as we think about prognosis and create a comprehensive treatment plan. This case study brings to our attention how complex and multifaceted PTSD patients can be in this day and age where social media, news outlets, and television are so pervasive. Three clinical pearls to take home from this patient encounter are: understanding the importance of news and media in modern-day PTSD diagnosis, how certain avoidance behaviors can delay remission, and how uncontrolled re-exposure can lead to poorer outcomes in children and adolescents specifically. It is no longer a rare occurrence to have a patient who has survived a mass school shooting. As a result of this unfortunate reality, clinicians need to be able to recognize and treat symptoms of PTSD in adolescent patients. We must be equipped to expect the interplay of modern triggers such as social media and news media and how it may affect adolescent patients.

Acute heart failure with cardiomyocyte atrophy induced in adult mice by ablation of cardiac myosin light chain kinase.

AIMS: Under pressure overload, initial adaptive hypertrophy of the heart is followed by cardiomyocyte elongation, reduced contractile force, and failure. The mechanisms governing the transition to failure are not fully understood. Pressure overload reduced cardiac myosin light chain kinase (cMLCK) by ∼80% within 1 week and persists. Knockdown of cMLCK in cardiomyocytes resulted in reduced cardiac contractility and sarcomere disorganization. Thus, we hypothesized that acute reduction of cMLCK may be causative for reduced contractility and cardiomyocyte remodelling during the transition from compensated to decompensated cardiac hypertrophy. METHODS AND RESULTS: To mimic acute cMLCK reduction in adult hearts, the floxed-Mylk3 gene that encodes cMLCK was inducibly ablated in Mylk3(flox/flox)/merCremer mice (Mylk3-KO), and compared with two control mice (Mylk3(flox/flox) and Mylk3(+/+)/merCremer) following tamoxifen injection (50 mg/kg/day, 2 consecutive days). In Mylk3-KO mice, reduction of cMLCK protein was evident by 4 days, with a decline to below the level of detection by 6 days. By 7 days, these mice exhibited heart failure, with reduction of fractional shortening compared with those in two control groups (19.8 vs. 28.0% and 27.7%). Severely convoluted cardiomyocytes with sarcomeric disorganization, wavy fibres, and cell death were demonstrated in Mylk3-KO mice. The cardiomyocytes were also unable to thicken adaptively to pressure overload. CONCLUSION: Our results, using a new mouse model mimicking an acute reduction of cMLCK, suggest that cMLCK plays a pivotal role in the transition from compensated to decompensated hypertrophy via sarcomeric disorganization.