† Disorders classified as TSRDs in the Diagnostic and Statistical Manual of Mental Disorders (DSM-5) include posttraumatic stress disorder (PTSD), acute stress disorder (ASD), and adjustment disorders (ADs), among others. § Unpaid adult caregiver status was self-reported. The definition of an unpaid caregiver for adults was a person who had provided unpaid care to a relative or friend aged ≥18 years to help them take care of themselves at any time in the last 3 months. Examples provided included helping with personal needs, household chores, health care tasks, managing a person's finances, taking them to a doctor's appointment, arranging for outside services, and visiting regularly to see how they are doing. ¶ Essential worker status was self-reported. The comparison was between employed respondents (n = 3,431) who identified as essential versus nonessential. For this analysis, students who were not separately employed as essential workers were considered nonessential workers.

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Astrocytes regulate synaptic connectivity in the CNS through secreted signals. Here we identified two astrocyte-secreted proteins, hevin and SPARC, as regulators of excitatory synaptogenesis in vitro and in vivo. Hevin induces the formation of synapses between cultured rat retinal ganglion cells. SPARC is not synaptogenic, but specifically antagonizes synaptogenic function of hevin. Hevin and SPARC are expressed by astrocytes in the superior colliculus, the synaptic target of retinal ganglion cells, concurrent with the excitatory synaptogenesis. Hevin-null mice had fewer excitatory synapses; conversely, SPARC-null mice had increased synaptic connections in the superior colliculus. Furthermore, we found that hevin is required for the structural maturation of the retinocollicular synapses. These results identify hevin as a positive and SPARC as a negative regulator of synapse formation and signify that, through regulation of relative levels of hevin and SPARC, astrocytes might control the formation, maturation, and plasticity of synapses in vivo.F ormation of the correct type and number of synaptic connections is crucial for the proper development and function of our nervous systems. In the past decade, astrocytes have emerged as important regulators of synaptic connectivity (1, 2).By using a purified retinal ganglion cell (RGC) culture system (3), we previously showed that astrocyte-secreted factors, including a family of ECM proteins, thrombospondins (TSPs), significantly increase the number of synapses formed between RGCs (4-6). These in vitro findings paved the way for recognition of astrocytes, and the TSPs they secrete, as important regulators of synapse formation and injury-mediated synaptic remodeling in vivo (4,5,7).TSPs belong to a subclass of secreted proteins called matricellular proteins. Matricellular proteins function by modulation of cell-cell and cell-matrix interactions, and thereby regulate the adhesion state of cells (8). Astrocytes express a number of matricellular proteins in addition to TSPs, and their expression is developmentally regulated and overlaps with early postnatal periods of synaptic development in the CNS (9, 10).In the present study we investigated whether other astrocytesecreted matricellular proteins could modulate synapse formation. Gene expression profiling of astrocytes suggested the matricellular proteins hevin [also known as secreted protein acidic and rich in cysteine (SPARC)-like 1] and SPARC as possible candidates. Hevin and SPARC are members of the SPARC family (11). Hevin was first identified as a synaptic glycoprotein and was initially termed synaptic cleft-1, or SC1 (12). It is localized to excitatory CNS synapses (13). Astrocytes in the developing brain express high levels of hevin and SPARC mRNA, with hevin mRNA being one of the highest-level mRNAs expressed by astrocytes (10). Unlike TSP1 and TSP2, the expression of which is decreased during maturation, hevin and SPARC mRNA levels remain high in the adult (9, 14-16).Here we investigated whether hevin and SPARC p...

Objective To determine the association between poor sleep quality, fatigue, and self-reported safety outcomes among Emergency Medical Services (EMS) workers. Methods We used convenience sampling of EMS agencies and a cross-sectional survey design. We administered the 19-item Pittsburgh Sleep Quality Index (PSQI), 11-item Chalder Fatigue Questionnaire (CFQ), and 44-item EMS Safety Inventory (EMS-SI) to measure sleep quality, fatigue, and safety outcomes, respectively. We used a consensus process to develop the EMS-SI, which was designed to capture three composite measurements of EMS worker injury, medical errors and adverse events (AE), and safety compromising behaviors. We used hierarchical logistic regression to test the association between poor sleep quality, fatigue, and three composite measures of EMS worker safety outcomes. Results We received 547 surveys from 30 EMS agencies (a 35.6% mean agency response rate). The mean PSQI score exceeded the benchmark for poor sleep (6.9, 95%CI 6.6, 7.2). Greater than half of respondents were classified as fatigued (55%, 95%CI 50.7, 59.3). Eighteen percent of respondents reported an injury (17.8%, 95%CI 13.5, 22.1), forty-one percent a medical error or AE (41.1%, 95%CI 36.8, 45.4), and 89% (95%CI 87, 92) safety compromising behaviors. After controlling for confounding, we identified 1.9 greater odds of injury (95%CI 1.1, 3.3), 2.2 greater odds of medical error or AE (95%CI 1.4, 3.3), and 3.6 greater odds of safety compromising behavior (95%CI 1.5, 8.3) among fatigued respondents versus non-fatigued respondents. Conclusions In this sample of EMS workers, poor sleep quality and fatigue is common. We provide preliminary evidence of an association between sleep quality, fatigue, and safety outcomes.