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Background: The outbreak of COVID-19 in China was a sudden bio-disaster, which may bring a negative impact on the job burnout of health care professionals (HCPs).Objective: We aim to find out the association factors, especially those closely related to this outbreak, of job burnout in Chinese HCPs.Method: The cross-sectional survey about HCPs' job burnout based on a network platform was conducted in high and low infection regions during the COVID-19 outbreak in China. The demographic characteristics, medical-work-related factors, risk of getting infected due to occupational exposure, and family factors were collected by the self-reported questionnaire. The Chinese version of the Maslach Burnout Inventory (CMBI) and the Trait Coping Style Questionnaire (TCSQ) were employed in this study to evaluate the job burnout and coping style, respectively. Furthermore, statistical analysis was done to find out the associated factors of job burnout.Results: We collected 880 complete questionnaires from doctors and nurses from February 9, 2020 to February 11, 2020. In this study, the positive rates of three dimensions of burnout (emotional exhaustion, depersonalization, and reduced personal accomplishment) and overall burnout were 9.09, 50.57, 56.59, and 73.98%, respectively. After the statistical analysis, we found that several factors can independently affect the dimensions. Working in the high infection region and negative coping styles can affect all three dimensions at once. More night shift quantity and having symptoms could increase emotional exhaustion and depersonalization, while higher work intensity and senior title could increase emotional exhaustion and reduce personal accomplishment, respectively.Conclusion: The rate of moderate and severe burnout had increased due to the outbreak. More attention should be paid to burnout in HCPs, especially those with negative coping. There were some potential ways to reduce burnout, such as reducing their workload and providing better protection from the virus.

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Minocycline protects animals against cerebral ischemia by inhibiting inflammation. To determine whether minocycline protects PC12 cells from in vitro ischemic-like injury and affects pro-inflammatory 5-lipoxygenase activation, the cell viability and 5-lipoxygenase translocation to nuclear membrane were observed after oxygen-glucose deprivation (OGD). We found that OGD reduced cell viability, which was attenuated by minocycline and 5-lipoxygenase inhibitor caffeic acid. 5-Lipoxygenase protein was detected in PC12 cells by immunohistochemical and Western blot analyses. OGD induced 5-lipoxygenase translocation to nuclear membranes, which was abolished by minocycline and caffeic acid. Thus, minocycline can protect PC12 cells from in vitro ischemic-like injury, and this effect may be partly related to the inhibition of 5-lipoxygenase activation.

White matter is primarily composed of myelin and myelinated axons. Structural and functional completeness of myelin is critical for the reliable and efficient transmission of information. White matter injury has been associated with the development of many demyelinating diseases. Despite a variety of scientific advances aimed at promoting re-myelination, their benefit has proven at best to be marginal. Research suggests that the failure of the re-myelination process may be the result of an unfavorable microenvironment. Astrocytes, are the most ample and diverse type of glial cells in central nervous system (CNS) which display multiple functions for the cells of the oligodendrocytes lineage. As such, much attention has recently been drawn to astrocyte function in terms of white matter myelin repair. They are different in white matter from those in gray matter in specific regards to development, morphology, location, protein expression and other supportive functions. During the process of demyelination and re-myelination, the functions of astrocytes are dynamic in that they are able to change functions in accordance to different time points, triggers or reactive pathways resulting in vastly different biologic effects. They have pivotal effects on oligodendrocytes and other cell types in the oligodendrocyte lineage by serving as an energy supplier, a participant of immunological and inflammatory functions, a source of trophic factors and iron and a sustainer of homeostasis. Astrocytic impairment has been shown to be directly linked to the development of neuromyelities optica (NMO). In addition, astroctyes have also been implicated in other white matter conditions such as psychiatric disorders and neurodegenerative diseases such as Alzheimer’s disease (AD), multiple sclerosis (MS) and amyotrophic lateral sclerosis (ALS). Inhibiting specifically detrimental signaling pathways in astrocytes while preserving their beneficial functions may be a promising approach for remyelination strategies. As such, the ability to manipulate astrocyte function represents a novel therapeutic approach that can repair the damaged myelin that is known to occur in a variety of white matter-related disorders.

Background Astrocytes are crucial regulators in the central nervous system. Abnormal activation of astrocytes contributes to some behavior deficits. However, mechanisms underlying the effects remain unclear. Here, we studied the activation of A1 astrocytes and their contribution to murine behavior deficits. Methods A1 astrocytes were induced by treatment with lipopolysaccharide (LPS) in vitro. The functional phenotype of astrocytes was determined by quantitative RT-PCR, ELISA, and immunohistochemistry. To assess the role of A1 astrocytes in vivo, mice were injected intraperitoneally with LPS. Then, murine behaviors were tested, and the hippocampus and cortex were analyzed by quantitative RT-PCR, ELISA, and immunohistochemistry. The function of IL-10 and fluorocitrate on A1 astrocyte activation was also examined. Results Our results show that astrocytes isolated from B6.129S6-Il10tm1Flv/J homozygotes (IL-10tm1/tm1) were prone to characteristics of A1 reactive astrocytes. Compared with their wild-type counterparts, IL-10tm1/tm1 astrocytes exhibited higher expression of glial fibrillary acidic protein (GFAP). Whether or not they were stimulated with LPS, IL-10tm1/tm1 astrocytes exhibited enhanced expression of A1-specific transcripts and proinflammatory factors IL-1β, IL-6, and TNFα. In addition, IL-10tm1/tm1 astrocytes demonstrated hyperphosphorylation of STAT3. Moreover, astrocytes from IL-10tm1/tm1 mice showed attenuated phagocytic ability and were neurotoxic. IL-10tm1/tm1 mice demonstrated increased immobility time in the forced swim test and defective learning and memory behavior in the Morris water maze test. Moreover, enhanced neuroinflammation was found in the hippocampus and cortex of IL-10tm1/tm1 mice, accompanying with more GFAP-positive astrocytes and severe neuron loss in the hippocampus. Pretreatment IL-10tm1/tm1 mice with IL-10 or fluorocitrate decreased the expression of proinflammatory factors and A1-specific transcripts in the hippocampus and cortex, and then alleviated LPS-induced depressive-like behavior. Conclusion These results demonstrate that astrocytes isolated from B6.129S6-Il10tm1Flv/J homozygotes are prone to A1 phenotype and contribute to the depression-like behavior and memory deficits. Inhibiting A1 astrocyte activation may be an attractive therapeutic strategy in some neurodegenerative diseases.