Wake up and get some sleep : Reviewing workplace napping and charting future directions

Although research demonstrates the importance of napping for health and well-being within work settings, the topic has resulted in limited empirical investigations, fragmented literary results, and an elusive understanding of whether napping should be normalized in the workplace. Also, what needs to be clarified are the benefits of workplace napping (WN) and the role of human resource managers in promoting the practice of WN. A systematic, narrative synthesis approach is used to review the existing WN literature, conceptualize WN, and discuss its benefits for employee relations, productivity, and the role of human resource managers on WN. Finally, based on this conceptual backdrop, future research questions are proposed that help pave the way for the normalization of WN

Wake up and get some sleep:Reviewing workplace napping and charting future directions

Although research demonstrates the importance of napping for health and well-being within work settings, the topic has resulted in limited empirical investigations, fragmented literary results, and an elusive understanding of whether napping should be normalized in the workplace. Also, what needs to be clarified are the benefits of workplace napping (WN) and the role of human resource managers in promoting the practice of WN. A systematic, narrative synthesis approach is used to review the existing WN literature, conceptualize WN, and discuss its benefits for employee relations, productivity, and the role of human resource managers on WN. Finally, based on this conceptual backdrop, future research questions are proposed that help pave the way for the normalization of WN.</p

Wake up and get some sleep:Reviewing workplace napping and charting future directions

Although research demonstrates the importance of napping for health and well-being within work settings, the topic has resulted in limited empirical investigations, fragmented literary results, and an elusive understanding of whether napping should be normalized in the workplace. Also, what needs to be clarified are the benefits of workplace napping (WN) and the role of human resource managers in promoting the practice of WN. A systematic, narrative synthesis approach is used to review the existing WN literature, conceptualize WN, and discuss its benefits for employee relations, productivity, and the role of human resource managers on WN. Finally, based on this conceptual backdrop, future research questions are proposed that help pave the way for the normalization of WN.</p

Resolution of herpes simplex virus reactivation in vivo results in neuronal destruction.

A fundamental question in herpes simplex virus (HSV) pathogenesis is the consequence of viral reactivation to the neuron. Evidence supporting both post-reactivation survival and demise is published. The exceedingly rare nature of this event at the neuronal level in the sensory ganglion has limited direct examination of this important question. In this study, an in-depth in vivo analysis of the resolution of reactivation was undertaken. Latently infected C57BL/6 mice were induced to reactivate in vivo by hyperthermic stress. Infectious virus was detected in a high percentage (60-80%) of the trigeminal ganglia from these mice at 20 hours post-reactivation stimulus, but declined by 48 hours post-stimulus (0-13%). With increasing time post-reactivation stimulus, the percentage of reactivating neurons surrounded by a cellular cuff increased, which correlated with a decrease in detectable infectious virus and number of viral protein positive neurons. Importantly, in addition to intact viral protein positive neurons, fragmented viral protein positive neurons morphologically consistent with apoptotic bodies and containing cleaved caspase-3 were detected. The frequency of this phenotype increased through time post-reactivation. These fragmented neurons were surrounded by Iba1+ cells, consistent with phagocytic removal of dead neurons. Evidence of neuronal destruction post-reactivation prompted re-examination of the previously reported non-cytolytic role of T cells in controlling reactivation. Latently infected mice were treated with anti-CD4/CD8 antibodies prior to induced reactivation. Neither infectious virus titers nor neuronal fragmentation were altered. In contrast, when viral DNA replication was blocked during reactivation, fragmentation was not observed even though viral proteins were expressed. Our data demonstrate that at least a portion of reactivating neurons are destroyed. Although no evidence for direct T cell mediated antigen recognition in this process was apparent, inhibition of viral DNA replication blocked neuronal fragmentation. These unexpected findings raise new questions about the resolution of HSV reactivation in the host nervous system

BAFF and APRIL counterregulate susceptibility to inflammation-induced preterm birth

Summary: Clinical evidence points to a function for B cell-activating factor (BAFF) in pregnancy. However, direct roles for BAFF-axis members in pregnancy have not been examined. Here, via utility of genetically modified mice, we report that BAFF promotes inflammatory responsiveness and increases susceptibility to inflammation-induced preterm birth (PTB). In contrast, we show that the closely related A proliferation-inducing ligand (APRIL) decreases inflammatory responsiveness and susceptibility to PTB. Known BAFF-axis receptors serve a redundant function in signaling BAFF/APRIL presence in pregnancy. Treatment with anti-BAFF/APRIL monoclonal antibodies or BAFF/APRIL recombinant proteins is sufficient to manipulate susceptibility to PTB. Notably, macrophages at the maternal-fetal interface produce BAFF, while BAFF and APRIL presence divergently shape macrophage gene expression and inflammatory function. Overall, our findings demonstrate that BAFF and APRIL play divergent inflammatory roles in pregnancy and provide therapeutic targets for mitigating risk of inflammation-induced PTB

Thermoneutral Housing Enables Studies of Vertical Transmission of Obesogenic Diet-Driven Metabolic Diseases

Vertical transmission of obesity is a critical contributor to the unabated obesity pandemic and the associated surge in metabolic diseases. Existing experimental models insufficiently recapitulate “human-like” obesity phenotypes, limiting the discovery of how severe obesity in pregnancy instructs vertical transmission of obesity. Here, via utility of thermoneutral housing and obesogenic diet feeding coupled to syngeneic mating of WT obese female and lean male mice on a C57BL/6 background, we present a tractable, more “human-like” approach to specifically investigate how maternal obesity contributes to offspring health. Using this model, we found that maternal obesity decreased neonatal survival, increased offspring adiposity, and accelerated offspring predisposition to obesity and metabolic disease. We also show that severe maternal obesity was sufficient to skew offspring microbiome and create a proinflammatory gestational environment that correlated with inflammatory changes in the offspring in utero and adulthood. Analysis of a human birth cohort study of mothers with and without obesity and their infants was consistent with mouse study findings of maternal inflammation and offspring weight gain propensity. Together, our results show that dietary induction of obesity in female mice coupled to thermoneutral housing can be used for future mechanistic interrogations of obesity and metabolic disease in pregnancy and vertical transmission of pathogenic traits