Effect of Nature-Themed Recharge Room on Healthcare Workers' Level of Stress and Anxiety.

OBJECTIVE: To determine if there is a difference in stress and anxiety before and after the use of the nature-themed recharge room. BACKGROUND: Psychological support measures have been noted to be relevant to nurses; however, the effect of the pandemic on the healthcare workers' emotional and psychological well-being led to urgent calls to implement psychological support measures more widely. METHODS: The study utilized a 1-group pretest and posttest design. One hundred sixty hospital employees utilized the recharge room, with 131 completed questionnaires counted in the data analysis. Data were collected using the demographic form, Perceived Stress Scale, and State-Trait Anxiety Inventory. RESULTS: Most participants were between 25 and 35 years old, female, worked the morning shift, had 3 to 5 years of experience, preferred a water feature theme, and used the room for 10 minutes. The mean stress preintervention score was 7.44, and postintervention score was 7.17, with the difference not statistically significant. The mean anxiety preintervention score was 14.17, and postintervention score was 8.48, with the difference statistically significant at a P < 0.05. Females working in the hospital for 1 to 5 years were physicians/residents, nursing support staff, and leaders with the highest mean stress (4-item Perceived Stress Scale) and anxiety (6-item State-Trait Anxiety Inventory) preintervention scores. Comparing the preintervention and postintervention anxiety levels, the highest reduction was noted among females working in the hospital for 1 to 3 years and nursing support staff who have used the room for 5 to 15 minutes with 2 or fewer people. CONCLUSION: Organizational leaders should offer psychological support programs, such as the nature-themed recharge room, to help reduce the healthcare workers' stress and anxiety.

Reactivation of Simian Varicella Virus in Rhesus Macaques after CD4 T Cell Depletion.

Rhesus macaques intrabronchially inoculated with simian varicella virus (SVV), the counterpart of human varicella-zoster virus (VZV), developed primary infection with viremia and rash, which resolved upon clearance of viremia, followed by the establishment of latency. To assess the role of CD4 T cell immunity in reactivation, monkeys were treated with a single 50-mg/kg dose of a humanized monoclonal anti-CD4 antibody; within 1 week, circulating CD4 T cells were reduced from 40 to 60% to 5 to 30% of the total T cell population and remained low for 2 months. Very low viremia was seen only in some of the treated monkeys. Zoster rash developed after 7 days in the monkey with the most extensive CD4 T cell depletion (5%) and in all other monkeys at 10 to 49 days posttreatment, with recurrent zoster in one treated monkey. SVV DNA was detected in the lung from two of five monkeys, in bronchial lymph nodes from one of the five monkeys, and in ganglia from at least two dermatomes in three of five monkeys. Immunofluorescence analysis of skin rash, lungs, lymph nodes, and ganglia revealed SVV ORF63 protein at the following sites: sweat glands in skin; type II cells in lung alveoli, macrophages, and dendritic cells in lymph nodes; and the neuronal cytoplasm of ganglia. Detection of SVV antigen in multiple tissues upon CD4 T cell depletion and virus reactivation suggests a critical role for CD4 T cell immunity in controlling varicella virus latency.IMPORTANCE Reactivation of latent VZV in humans can result in serious neurological complications. VZV-specific cell-mediated immunity is critical for the maintenance of latency. Similar to VZV in humans, SVV causes varicella in monkeys, establishes latency in ganglia, and reactivates to produce shingles. Here, we show that depletion of CD4 T cells in rhesus macaques results in SVV reactivation, with virus antigens found in zoster rash and SVV DNA and antigens found in lungs, lymph nodes, and ganglia. These results suggest the critical role of CD4 T cell immunity in controlling varicella virus latency.

Cell differentiation modifies the p53 transcriptional program through a combination of gene silencing and constitutive transactivation.

The p53 transcription factor is a master regulator of cellular responses to stress that is commonly inactivated in diverse cancer types. Despite decades of research, the mechanisms by which p53 impedes tumorigenesis across vastly different cellular contexts requires further investigation. The bulk of research has been completed using in vitro studies of cancer cell lines or in vivo studies in mouse models, but much less is known about p53 action in diverse non-transformed human tissues. Here, we investigated how different cellular states modify the p53 transcriptional program in human cells through a combination of computational analyses of publicly available large-scale datasets and in vitro studies using an isogenic system consisting of induced pluripotent stem cells (iPSCs) and two derived lineages. Analysis of publicly available mRNA expression and genetic dependency data demonstrated wide variation in terms of expression and function of a core p53 transcriptional program across various tissues and lineages. To monitor the impact of cell differentiation on the p53 transcriptome within an isogenic cell culture system, we activated p53 by pharmacological inhibition of its negative regulator MDM2. Using cell phenotyping assays and genome wide transcriptome analyses, we demonstrated that cell differentiation confines and modifies the p53 transcriptional network in a lineage-specific fashion. Although hundreds of p53 target genes are transactivated in iPSCs, only a small fraction is transactivated in each of the differentiated lineages. Mechanistic studies using small molecule inhibitors and genetic knockdowns revealed the presence of two major regulatory mechanisms contributing to this massive heterogeneity across cellular states: gene silencing by epigenetic regulatory complexes and constitutive transactivation by lineage-specific transcription factors. Altogether, these results illuminate the impact of cell differentiation on the p53 program, thus advancing our understanding of how this tumor suppressor functions in different contexts.