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Microglia activation and neuroinflammation have been extensively studied in murine models of neurodegenerative diseases; however, to overcome the genetic differences between species, a human cell model of microglia able to recapitulate the activation profiles described in patients is needed. Here we developed human models of Parkinson's like neuroinflammation by using the human microglia clone 3 (HMC3) cells, whose activation profile in response to classic inflammatory stimuli has been controversial and reported only at mRNA levels so far. In fact, we showed the increased expression of the pro-inflammatory markers iNOS, Caspase 1, IL-1β, in response to IFN-γ plus high glucose, a non-specific disease stimulus that emphasized the dynamic polarization and heterogenicity of the microglial population. More specifically, we demonstrated the polarization of HMC3 cells through the upregulation of iNOS expression and nitrite production in response to the Parkinson's like stimuli, 6-hydroxidopamine (6-OHDA) and 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP), the latter depending on the NF-κB pathway. Furthermore, we identified inflammatory mediators that promote the pro-inflammatory activation of human microglia as function of different pathways that can simulate the phenotypic transition according to the stage of the pathology. In conclusion, we established and characterized different systems of HMC3 cells activation as in vitro models of Parkinson's like neuroinflammation., Competing Interests: The authors declare that the research was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest., (Copyright © 2022 De Chirico, Poeta, Babini, Piccolino, Monti and Massenzio.)

Mitochondrial aspartate-glutamate carrier isoform 1 (AGC1) deficiency is an ultra-rare genetic disease characterized by global hypomyelination and brain atrophy, caused by mutations in the SLC25A12 gene leading to a reduction in AGC1 activity. In both neuronal precursor cells and oligodendrocytes precursor cells (NPCs and OPCs), the AGC1 determines reduced proliferation with an accelerated differentiation of OPCs, both associated with gene expression dysregulation. Epigenetic regulation of gene expression through histone acetylation plays a crucial role in the proliferation/differentiation of both NPCs and OPCs and is modulated by mitochondrial metabolism. In AGC1 deficiency models, both OPCs and NPCs show an altered expression of transcription factors involved in the proliferation/differentiation of brain precursor cells (BPCs) as well as a reduction in histone acetylation with a parallel alteration in the expression and activity of histone acetyltransferases (HATs) and histone deacetylases (HDACs). In this study, histone acetylation dysfunctions have been dissected in in vitro models of AGC1 deficiency OPCs (Oli-Neu cells) and NPCs (neurospheres), in physiological conditions and following pharmacological treatments. The inhibition of HATs by curcumin arrests the proliferation of OPCs leading to their differentiation, while the inhibition of HDACs by suberanilohydroxamic acid (SAHA) has only a limited effect on proliferation, but it significantly stimulates the differentiation of OPCs. In NPCs, both treatments determine an alteration in the commitment toward glial cells. These data contribute to clarifying the molecular and epigenetic mechanisms regulating the proliferation/differentiation of OPCs and NPCs. This will help to identify potential targets for new therapeutic approaches that are able to increase the OPCs pool and to sustain their differentiation toward oligodendrocytes and to myelination/remyelination processes in AGC1 deficiency, as well as in other white matter neuropathologies., Competing Interests: The authors declare that the research was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest., (Copyright © 2022 Poeta, Petralla, Babini, Renzi, Celauro, Magnifico, Barile, Masotti, De Chirico, Massenzio, Viggiano, Palmieri, Virgili, Lasorsa and Monti.)

Introduction: Teaching is a stressful profession that exposes workers to the risk of burnout. Techniques involving higher mental functions, such as transcendental meditation and prayer, have been used in stress and burnout prevention programs. In this study, we report the results of an experience conducted in a group of teachers of a religious institute, in which prayer was used as a technique to prevent burnout., Methods: Fifty teachers and support staff employed at a Catholic school of a Congregation of nuns volunteered for this study. They were randomized into two groups: prayer treatment ( n = 25) or control group ( n = 25). The treatment protocol was based on the combination of individual Christian prayer and a focus group of prayer-reflection. The participants received two 30 min training sessions a week over 2 months. Job satisfaction, well-being, and burnout symptoms (emotional exhaustion and depersonalization sub-scales) were measured at baseline and at follow-up (4 months) with the Italian versions of the Maslach Burnout Inventory validated for teaching and education sector, the General Health Questionnaire, and the Warr, Cook, and Wall's Job Satisfaction Scale., Results: At follow-up, a significant improvement of all outcome measures was observed. Emotional exhaustion (16.80-4.92, p < 0.001), depersonalization (3.72-0.60, p < 0.001) levels, and psychological impairment (10.08-2.04, p < 0.001) were significantly decreased, and job satisfaction (45.96-77.00, p < 0.001) was increased. The effect sizes (Glass' Δ) of the therapeutic interventions ranged from 0.53 (satisfaction level) to 2.87 (psychological health), suggesting moderate to large effects., Discussion: Prayer could be effective, no less than meditation and other spiritual or mind-body techniques, in contrasting the negative effects of occupational stress and preventing burnout among teachers and possibly other human service professionals., (Copyright © 2020 Chirico, Sharma, Zaffina and Magnavita.)

Background: This systematic review with meta-analysis was carried out to study the relationship between workplace violence and sleep problems. Methods: The PRISMA statement was used to conduct a systematic search of the literature on PubMed/MEDLINE, Scopus, Sociological abstract, DOAJ, Web of Science, and Google Scholar databases. Of the original number of 749 studies, 34 were included in the systematic review, and 7 in the meta-analysis. Results: A total of 119,361 participants from 15 different countries took part in these studies which were published between 1999 and 2019. Significant heterogeneity was observed among the studies ( I 2 = 96%). In a random-effects meta-analysis model, pooled odds ratio (OR) analysis revealed that there was a direct relationship between occupational exposure to violence and sleep problems (OR = 2.55; 95% CI = 1.77-3.66). According to the GRADE guidelines, the quality of evidence of the association was low. Conclusions: The findings of this study demonstrate that occupational exposure to physical, verbal, or sexual violence is associated with sleep problems. Further research on the relationship between violence and sleep is needed so that appropriate measures can be taken to prevent violence and improve sleep hygiene in the workplace. Trial Registration Number: PROSPERO International prospective register of systematic reviews (CRD42019124903) February 9, 2019., (Copyright © 2019 Magnavita, Di Stasio, Capitanelli, Lops, Chirico and Garbarino.)