Burnout, compassion satisfaction, and intention to quit among long-term care nursing assistants in the time of COVID-19

Context: The COVID-19 pandemic has greatly exacerbated the stress and burden of those employed in long-term care (LTC) facilities due to staff shortages, increased risks on the job, and ever-changing COVID-19 protocol requirements. Objective: This study examines potential differences in pre-COVID-19 and current COVID-19 on burnout, compassion satisfaction, job satisfaction, and intent to quit of nursing assistants employed in LTC facilities. Methods: The sample included 81 nursing assistants employed in LTC facilities across the United States, with data collected prior to (n = 42) and during COVID-19 related shutdowns (n = 39). Participants completed the Professional Quality of Life Scale 5 (ProQOL 5), a single-item self-report measure of job satisfaction, and a two-item selfreport measure of intent to quit their current employment. Findings: Nursing assistants during COVID-19 reported a higher level of burnout and lower level of compassion satisfaction than nursing assistants pre-COVID-19. However, there were no differences in job satisfaction or intent to quit. Limitations: The study did not measure levels of burnout and compassion satisfaction throughout the entire pandemic. No causal statements can be made regarding the impact of the pandemic on nursing assistant burnout, compassion satisfaction, job satisfaction, or intention to quit. Implications: The results suggest there may be additional factors that influence an individual’s decision to remain employed above and beyond the impacts of burnout and compassion satisfaction that may be unique to the caring professions. Future research might investigate factors that influence an individual’s decision to remain employed as a nursing assistant during periods of increased stress and burnout

A Comparison of Aquatic- vs. Land-Based Plyometrics on Various Performance Variables

International Journal of Exercise Science 8(2) : 134-144, 2015. The purpose of this study was to compare the effects of an aquatic- (W) and land-based (L) plyometric program on balance, vertical jump height, and isokinetic quadriceps and hamstring strength. Thirty-four participants were randomized into three groups, W (n = 12), L (n = 11), and control (n = 11). The W and L groups completed an eight-week plyometric program. A two-way repeated measures ANOVA revealed a significant main effect of condition (F = 346.95, p \u3c 0.001) and interaction between condition by time (F = 1.88, p = 0.01). Paired samples t-tests revealed statistically significant improvements from pre- to post-testing in the L group for isokinetic quadriceps strength at 60 degrees per second (p = 0.02) and hamstring strength at 120 degrees per second (p = 0.02). Statistically significant improvements were observed from pre- to post-testing in the W group for balance (p = 0.003), vertical jump height (p = 0.008), isokinetic quadriceps strength at 60 and 120 degrees per second (p \u3c 0.001), and hamstring strength at 120 degrees per second (p = 0.03). Results demonstrate that aquatic-based plyometric training can be a valid form of training by producing improvements in balance, force output, and isokinetic strength while concurrently decreasing ground impact forces

Osteoarthritis accelerates and exacerbates Alzheimer's disease pathology in mice

<p>Abstract</p> <p>Background</p> <p>The purpose of this study was to investigate whether localized peripheral inflammation, such as osteoarthritis, contributes to neuroinflammation and neurodegenerative disease <it>in vivo</it>.</p> <p>Methods</p> <p>We employed the inducible Col1-IL1β^XATmouse model of osteoarthritis, in which induction of osteoarthritis in the knees and temporomandibular joints resulted in astrocyte and microglial activation in the brain, accompanied by upregulation of inflammation-related gene expression. The biological significance of the link between peripheral and brain inflammation was explored in the APP/PS1 mouse model of Alzheimer's disease (AD) whereby osteoarthritis resulted in neuroinflammation as well as exacerbation and acceleration of AD pathology.</p> <p>Results</p> <p>Induction of osteoarthritis exacerbated and accelerated the development of neuroinflammation, as assessed by glial cell activation and quantification of inflammation-related mRNAs, as well as Aβ pathology, assessed by the number and size of amyloid plaques, in the APP/PS1; Col1-IL1β^XATcompound transgenic mouse.</p> <p>Conclusion</p> <p>This work supports a model by which peripheral inflammation triggers the development of neuroinflammation and subsequently the induction of AD pathology. Better understanding of the link between peripheral localized inflammation, whether in the form of osteoarthritis, atherosclerosis or other conditions, and brain inflammation, may prove critical to our understanding of the pathophysiology of disorders such as Alzheimer's, Parkinson's and other neurodegenerative diseases.</p

Equipping Health Professions Educators to Better Address Medical Misinformation

As part of a cooperative agreement with the US Centers for Disease Control and Prevention (Federal Award Identification Number [FAIN]: NU50CK000586), the Association of American Medical Colleges (AAMC) began a strategic initiative in 2022 both to increase confidence in COVID-19 vaccines and to address medical misinformation and mistrust through education in health professions contexts. Specifically, the AAMC solicited proposals for integrating competency-based, interprofessional strategies to mitigate health misinformation into new or existing curricula. Five Health Professions Education Curricular Innovations subgrantees received support from the AAMC in 2022 and reflected on the implementation of their ideas in a series of meetings over several months. Subgrantees included the Donald and Barbara Zucker School of Medicine at Hofstra/Northwell, Florida International University Herbert Wertheim College of Medicine, the Jacobs School of Medicine and Biomedical Sciences at the University at Buffalo, the Maine Medical Center/Tufts University School of Medicine, and the University of Chicago Pritzker School of Medicine. This paper comprises insights from each of the teams and overarching observations regarding the challenges and opportunities involved with leveraging health professions education to address medical misinformation and improve patient health

EMF1 and PRC2 Cooperate to Repress Key Regulators of Arabidopsis Development

EMBRYONIC FLOWER1 (EMF1) is a plant-specific gene crucial to Arabidopsis vegetative development. Loss of function mutants in the EMF1 gene mimic the phenotype caused by mutations in Polycomb Group protein (PcG) genes, which encode epigenetic repressors that regulate many aspects of eukaryotic development. In Arabidopsis, Polycomb Repressor Complex 2 (PRC2), made of PcG proteins, catalyzes trimethylation of lysine 27 on histone H3 (H3K27me3) and PRC1-like proteins catalyze H2AK119 ubiquitination. Despite functional similarity to PcG proteins, EMF1 lacks sequence homology with known PcG proteins; thus, its role in the PcG mechanism is unclear. To study the EMF1 functions and its mechanism of action, we performed genome-wide mapping of EMF1 binding and H3K27me3 modification sites in Arabidopsis seedlings. The EMF1 binding pattern is similar to that of H3K27me3 modification on the chromosomal and genic level. ChIPOTLe peak finding and clustering analyses both show that the highly trimethylated genes also have high enrichment levels of EMF1 binding, termed EMF1_K27 genes. EMF1 interacts with regulatory genes, which are silenced to allow vegetative growth, and with genes specifying cell fates during growth and differentiation. H3K27me3 marks not only these genes but also some genes that are involved in endosperm development and maternal effects. Transcriptome analysis, coupled with the H3K27me3 pattern, of EMF1_K27 genes in emf1 and PRC2 mutants showed that EMF1 represses gene activities via diverse mechanisms and plays a novel role in the PcG mechanism

GA4GH: International policies and standards for data sharing across genomic research and healthcare.

The Global Alliance for Genomics and Health (GA4GH) aims to accelerate biomedical advances by enabling the responsible sharing of clinical and genomic data through both harmonized data aggregation and federated approaches. The decreasing cost of genomic sequencing (along with other genome-wide molecular assays) and increasing evidence of its clinical utility will soon drive the generation of sequence data from tens of millions of humans, with increasing levels of diversity. In this perspective, we present the GA4GH strategies for addressing the major challenges of this data revolution. We describe the GA4GH organization, which is fueled by the development efforts of eight Work Streams and informed by the needs of 24 Driver Projects and other key stakeholders. We present the GA4GH suite of secure, interoperable technical standards and policy frameworks and review the current status of standards, their relevance to key domains of research and clinical care, and future plans of GA4GH. Broad international participation in building, adopting, and deploying GA4GH standards and frameworks will catalyze an unprecedented effort in data sharing that will be critical to advancing genomic medicine and ensuring that all populations can access its benefits

The effect of oxidized guanines on DNA synthesis by DNA polymerase β

DNA replication is the fundamental biological task of duplicating genetic information for passing on to a daughter cell. DNA polymerases are the molecular machines that read the parent DNA strand and instruct the addition of correct corresponding nucleotides (also termed fidelity) to form a new DNA strand. DNA replication is extremely accurate to prevent deleterious alterations to the genetic code. However, DNA is damaged more than 10,000 times per cell per day. 8-oxo-7,8-dihydro-2ʹ-guanosine (8-oxo-G) is a form of DNA oxidative damage that threatens fidelity by base pairing with both a canonical cytosine and a non-canonical adenine. Due to its dual coding potential, DNA polymerases frequently make the mistake of inserting adenine instead of cytosine during DNA replication. We hypothesized that other oxidized guanines, such as 4,6-diamino-5-formamidopyrimidine (Fapy•dG) and 7,8-dihydro-8-oxo-riboguanosine (r8-oxo-G), may also be error-prone during DNA polymerase processing. To evaluate the mutagenicity of Fapy•dG and r8-oxo-G, we employed a well-characterized human DNA polymerase involved in DNA repair, DNA polymerase β (pol β). This work broadly shows that pol β has similar strategies for excluding damaged nucleotide triphosphates, but unique mechanistic barriers in response to different oxidized guanines in different DNA positions. By furthering our understanding of damaged DNA processing by DNA polymerase β, this work expands the current literature of DNA polymerase discrimination mechanisms and informs on the mutagenic properties of formerly uncharacterized damaged DNA substrates

Factors Correlated With Successful Pediatric Post-Discharge Phone Call Attempt and Connection

OBJECTIVES: Postdischarge phone calls can identify discharge errors and gather information following hospital-to-home transitions. This study used the multisite Project IMPACT (Improving Pediatric Patient Centered Care Transitions) dataset to identify factors associated with postdischarge phone call attempt and connectivity. METHODS: This study included 0- to 18-year-old patients discharged from 4 sites between January 2014 and December 2017. We compared demographic and clinical factors between postdischarge call attempt and no-attempt and connectivity and no-connectivity subgroups and used mixed model logistic regression to identify significant independent predictors of call attempt and connectivity. RESULTS: Postdischarge calls were attempted for 5528 of 7725 (71.6%) discharges with successful connection for 3801 of 5528 (68.8%) calls. Connection rates varied significantly among sites (52% to 79%, P \u3c .001). Age less than 30 days (P = .03; P = .01) and age 1 to 6 years (P = .04; P = .04) were independent positive predictors for both call attempt and connectivity, whereas English as preferred language (P \u3c .001) and the chronic noncomplex clinical risk group (P = .02) were independent positive predictors for call attempt and connectivity, respectively. In contrast, readmission within 3 days (P = .004) and federal or state payor (P = .02) were negative independent predictors for call attempt and call connectivity, respectively. CONCLUSIONS: This study suggests that targeted interventions may improve postdischarge call attempt rates, such as investment in a reliable call model or improvement in interpreter use, and connectivity, such as enhanced population-based communication