Travail et maladie: congés psychiatriques chez les professionnels de la santé en milieu hospitalier / Trabajo y enfermedad: licencia psiquiátrica para profesionales sanitarios en hospitales / Trabalhar e adoecer: análise da licença psiquiátrica entre profissionais de saúde do trabalho hospitalar / Work and illness: psychiatric leave for health professionals in hospitals

L'article présente les résultats d'une recherche qui porte sur l'analyse des congés médico-psychiatriques, suite à un diagnostic d'anxiété et/ou de dépression, chez les professionnels de la santé (infirmiers et travailleurs sociaux), fonctionnaires des hôpitaux publics. L'approche théorique est la psychosociologie, discipline qui articule expériences subjectives et rapports sociaux. La méthode des «histoires de vie professionnelle¼ permet une analyse des récits et de l'avènement du congé psychiatrique; six dimensions socio-cliniques ont été identifiées: (1) la fragilité psychosociale; (2) la hiérarchie dans le travail hospitalier; (3) la perte de l'acte pouvoir sur le travail; (4) la souffrance éthico-politique; (5) la régulation de la souffrance; (6) le retour à une nouvelle condition de travailleur. Selon les personnes interrogées, avant l'arrêt, le travail était un organisateur de vie et un espace d'insertion sociale important; après ce congé, suite au congé maladie, - le côté organisateur de l'existence n'est plus présent. D'autres dimensions commencent à opérer. Le congé maladie crée une rupture: les professionnels élaborent de nouveaux sens à leur vie et leur condition de travailleurs, et ce, suite à la façon dont ils ont été traités par les institutions de santé.(AU)

The article presents the results of a research which focuses on the analysis of medico-psychiatric leave, following a diagnosis of anxiety and / or depression, among health professionals (nurses and social workers), civil servants of public hospitals. The theoretical approach is psychosociology, a discipline which articulates subjective experiences and social relationships. The method of "professional life stories" allows an analysis of the stories and the advent of psychiatric leave; six socio-clinical dimensions have been identified: (1) psychosocial fragility; (2) hierarchy in hospital work; (3) the part of power over work; (4) ethical-political suffering; (5) the regulation of suffering; (6) the return to a new condition of worker. According to the people questioned, before the stoppage, work was an important organizer of life and a space for social integration; after this leave, following sick leave, - the organizing side of life is no longer present. Other dimensions are starting to operate. Sick leave creates a rupture: professionals develop new meanings in their life and their condition as workers, following the way in which they have been treated by health institutions.(AU)

El artículo presenta los resultados de una investigación que se centra en el análisis de la baja médico-psiquiátrica, tras un diagnóstico de ansiedad y / o depresión, entre profesionales de la salud (enfermeras y trabajadores sociales), funcionarios de hospitales públicos. El enfoque teórico es la psicosociología, disciplina que articula experiencias subjetivas y relaciones sociales. El método de las "historias de vida profesional" permite analizar las historias y el advenimiento de la licencia psiquiátrica; Se han identificado seis dimensiones socio-clínicas: (1) fragilidad psicosocial; (2) jerarquía en el trabajo hospitalario; (3) la pérdida del acto de poder sobre el trabajo; (4) sufrimiento ético-político; (5) la regulación del sufrimiento; (6) el regreso a una nueva condición de trabajador. Según las personas entrevistadas, antes del paro, el trabajo era un importante organizador de la vida y un espacio de integración social; después de esta licencia, después de la licencia por enfermedad, el lado organizativo de la vida ya no está presente. Comienzan a operar otras dimensiones. La baja por enfermedad crea una ruptura: los profesionales desarrollan nuevos significados en su vida y en su condición de trabajadores, siguiendo la forma en que han sido tratados por las instituciones de salud.(AU)

O artigo apresenta os resultados de uma investigação que tem como foco a análise dos afastamentos médico-psiquiátricos, após um diagnóstico de ansiedade e/ou depressão, entre profissionais de saúde (enfermeiros e assistentes sociais), funcionários de hospitais públicos. O enfoque teórico é a psicossociologia, disciplina que articula experiências subjetivas e relações sociais. O método das "histórias de vida profissional" permite analisar as histórias e o advento da licença psiquiátrica. A análise das narrativas dos profissionais sobre o evento das licenças psiquiátricas permitiu compreender o sofrimento psíquico e o adoecimento mental no trabalho hospitalar, considerando a articulação de seis dimensões socioclínicas: (1) a fragilidade psicossocial; (2) a hierarquia no trabalho hospitalar; (3) a perda do ato-poder sobre o trabalho; (4) o sofrimento ético-político; (5) a tentativa de regulação do sofrimento; e (6) a religação a uma nova condição de trabalhador. O trabalho era um organizador de vida e espaço significativo de inserção social; advindo o acontecimento da licença, surgem outros organizadores da existência, e novas construções de sentido para o trabalho são produzidas. A licença produz uma ruptura em que nada mais se apresenta como antes, pois os profissionais ressignificam sua vida e sua condição de trabalhador.(AU)

Nuclear sensing of breaks in mitochondrial DNA enhances immune surveillance.

Mitochondrial DNA double-strand breaks (mtDSBs) are toxic lesions that compromise the integrity of mitochondrial DNA (mtDNA) and alter mitochondrial function1. Communication between mitochondria and the nucleus is essential to maintain cellular homeostasis; however, the nuclear response to mtDSBs remains unknown2. Here, using mitochondrial-targeted transcription activator-like effector nucleases (TALENs)1,3,4, we show that mtDSBs activate a type-I interferon response that involves the phosphorylation of STAT1 and activation of interferon-stimulated genes. After the formation of breaks in the mtDNA, herniation5 mediated by BAX and BAK releases mitochondrial RNA into the cytoplasm and triggers a RIG-I-MAVS-dependent immune response. We further investigated the effect of mtDSBs on interferon signalling after treatment with ionizing radiation and found a reduction in the activation of interferon-stimulated genes when cells that lack mtDNA are exposed to gamma irradiation. We also show that mtDNA breaks synergize with nuclear DNA damage to mount a robust cellular immune response. Taken together, we conclude that cytoplasmic accumulation of mitochondrial RNA is an intrinsic immune surveillance mechanism for cells to cope with mtDSBs, including breaks produced by genotoxic agents.

Low-level blast exposure disrupts gliovascular and neurovascular connections and induces a chronic vascular pathology in rat brain.

Much concern exists over the role of blast-induced traumatic brain injury (TBI) in the chronic cognitive and mental health problems that develop in veterans and active duty military personnel. The brain vasculature is particularly sensitive to blast injury. The aim of this study was to characterize the evolving molecular and histologic alterations in the neurovascular unit induced by three repetitive low-energy blast exposures (3 × 74.5 kPa) in a rat model mimicking human mild TBI or subclinical blast exposure. High-resolution two-dimensional differential gel electrophoresis (2D-DIGE) and matrix-assisted laser desorption/ionization (MALDI) mass spectrometry of purified brain vascular fractions from blast-exposed animals 6 weeks post-exposure showed decreased levels of vascular-associated glial fibrillary acidic protein (GFAP) and several neuronal intermediate filament proteins (α-internexin and the low, middle, and high molecular weight neurofilament subunits). Loss of these proteins suggested that blast exposure disrupts gliovascular and neurovascular interactions. Electron microscopy confirmed blast-induced effects on perivascular astrocytes including swelling and degeneration of astrocytic endfeet in the brain cortical vasculature. Because the astrocyte is a major sensor of neuronal activity and regulator of cerebral blood flow, structural disruption of gliovascular integrity within the neurovascular unit should impair cerebral autoregulation. Disrupted neurovascular connections to pial and parenchymal blood vessels might also affect brain circulation. Blast exposures also induced structural and functional alterations in the arterial smooth muscle layer. Interestingly, by 8 months after blast exposure, GFAP and neuronal intermediate filament expression had recovered to control levels in isolated brain vascular fractions. However, despite this recovery, a widespread vascular pathology was still apparent at 10 months after blast exposure histologically and on micro-computed tomography scanning. Thus, low-level blast exposure disrupts gliovascular and neurovascular connections while inducing a chronic vascular pathology.

Lack of chronic neuroinflammation in the absence of focal hemorrhage in a rat model of low-energy blast-induced TBI.

Blast-related traumatic brain injury (TBI) has been a common cause of injury in the recent conflicts in Iraq and Afghanistan. Blast waves can damage blood vessels, neurons, and glial cells within the brain. Acutely, depending on the blast energy, blast wave duration, and number of exposures, blast waves disrupt the blood-brain barrier, triggering microglial activation and neuroinflammation. Recently, there has been much interest in the role that ongoing neuroinflammation may play in the chronic effects of TBI. Here, we investigated whether chronic neuroinflammation is present in a rat model of repetitive low-energy blast exposure. Six weeks after three 74.5-kPa blast exposures, and in the absence of hemorrhage, no significant alteration in the level of microglia activation was found. At 6 weeks after blast exposure, plasma levels of fractalkine, interleukin-1ß, lipopolysaccharide-inducible CXC chemokine, macrophage inflammatory protein 1α, and vascular endothelial growth factor were decreased. However, no differences in cytokine levels were detected between blast-exposed and control rats at 40 weeks. In brain, isolated changes were seen in levels of selected cytokines at 6 weeks following blast exposure, but none of these changes was found in both hemispheres or at 40 weeks after blast exposure. Notably, one animal with a focal hemorrhagic tear showed chronic microglial activation around the lesion 16 weeks post-blast exposure. These findings suggest that focal hemorrhage can trigger chronic focal neuroinflammation following blast-induced TBI, but that in the absence of hemorrhage, chronic neuroinflammation is not a general feature of low-level blast injury.