What is the impact of shift work on the psychological functioning and resilience of nurses? An integrative review

Aim: To synthesize existing research to determine if nurses who work shifts have poorer psychological functioning and resilience than nurses who do not work shifts. Background: Research exploring the impact of shift work on the psychological functioning and resilience of nurses is limited compared with research investigating the impact of shifts on physical outcomes. Design: Integrative literature review. Data Sources: Relevant databases were searched from January 1995-August 2016 using the combination of keywords: nurse, shift work; rotating roster; night shift; resilient; hardiness; coping; well-being; burnout; mental health; occupational stress; compassion fatigue; compassion satisfaction; stress; anxiety; depression. Review Methods: Two authors independently performed the integrative review processes proposed by Whittemore and Knafl and a quality assessment using the mixed-methods appraisal tool by Pluye et al. Results: A total of 37 articles were included in the review (32 quantitative, 4 qualitative and 1 mixed-methods). Approximately half of the studies directly compared nurse shift workers with non-shift workers. Findings were grouped according to the following main outcomes: (1) general psychological well-being/quality of life; (2) Job satisfaction/burnout; (3) Depression, anxiety and stress; and (4) Resilience/coping. We did not find definitive evidence that shift work is associated with poorer psychological functioning in nurses. Overall, the findings suggest that the impact of shift work on nurse psychological functioning is dependent on several contextual and individual factors. Conclusion: More studies are required which directly compare the psychological outcomes and resilience of nurse shift workers with non-shift workers

SARS-CoV-2 susceptibility and COVID-19 disease severity are associated with genetic variants affecting gene expression in a variety of tissues

Variability in SARS-CoV-2 susceptibility and COVID-19 disease severity between individuals is partly due to genetic factors. Here, we identify 4 genomic loci with suggestive associations for SARS-CoV-2 susceptibility and 19 for COVID-19 disease severity. Four of these 23 loci likely have an ethnicity-specific component. Genome-wide association study (GWAS) signals in 11 loci colocalize with expression quantitative trait loci (eQTLs) associated with the expression of 20 genes in 62 tissues/cell types (range: 1:43 tissues/gene), including lung, brain, heart, muscle, and skin as well as the digestive system and immune system. We perform genetic fine mapping to compute 99% credible SNP sets, which identify 10 GWAS loci that have eight or fewer SNPs in the credible set, including three loci with one single likely causal SNP. Our study suggests that the diverse symptoms and disease severity of COVID-19 observed between individuals is associated with variants across the genome, affecting gene expression levels in a wide variety of tissue types

A first update on mapping the human genetic architecture of COVID-19

peer reviewe

Sleep alterations following exposure to stress predict fear-associated memory impairments in a rodent model of PTSD

Sleep abnormalities such as insomnia, nightmares, hyper-arousal, and difficulty initiating or maintaining sleep, are diagnostic criteria of post-traumatic stress disorder (PTSD). The vivid dream state, rapid eye movement (REM) sleep, has been implicated in processing emotional memories. We have hypothesized that REM sleep is maladaptive in those suffering from PTSD. However, the precise neurobiological mechanisms regulating these sleep disturbances following trauma exposure are poorly understood. Using single prolonged stress (SPS), a well-validated rodent model of PTSD, we measured sleep alterations in response to stress exposure and over a subsequent 7-day isolation period during which the PTSD-like phenotype develops in rats. SPS resulted in acutely increased REM sleep, transition to REM sleep, and decreased waking in addition to alterations in sleep architecture. The severity of the PTSD-like phenotype was later assessed by measuring freezing levels on a fear-associated memory test. Interestingly, the change in REM sleep following SPS was significantly correlated with freezing behavior during extinction recall assessed more than a week later. We also report reductions in theta (4–10 Hz) and sigma (10–15 Hz) band power during transition to REM sleep which also correlated with impaired fear-associated memory processing. These data reveal that changes in REM sleep, transition to REM sleep, waking, and theta and sigma power may serve as sleep biomarkers to identify individuals with increased susceptibility to PTSD following trauma exposure