Em defesa da sociedade: a invenção dos cuidados paliativos e a produção de subjetividades

O artigo é uma reflexão teórica que faz parte de um estudo denominado Em Defesa da Sociedade: a invenção dos Cuidados Paliativos. Para articular tal discussão, utilizamos o manual de Cuidados Paliativos, publicado no ano de 2007 pela Organização Mundial da Saúde (OMS), entendendo-o como parte de um artefato capaz de produzir subjetividades e governar condutas. Nesse sentido, pretendemos descobrir como os discursos sobre os Cuidados Paliativos se articulam e efetuam a invenção de uma nova disciplina que funcionaria como uma estratégia biopolítica para defender a sociedade. A partir da análise textual do discurso instituído pelo manual, com o auxílio do referencial dos Estudos Culturais e sob a inspiração dos escritos de Michel Foucault, articulamos uma das possíveis leituras deste guia. Desta maneira observamos a (re)organização e a (re)invenção de uma disciplina que investe na subjetividade dos indivíduos constituindo aparatos de verdade que regulam e governam a população

Prostaglandin E2 Signals Through PTGER2 to Regulate Sclerostin Expression

The Wnt signaling pathway is a robust regulator of skeletal homeostasis. Gain-of-function mutations promote high bone mass, whereas loss of Lrp5 or Lrp6 co-receptors decrease bone mass. Similarly, mutations in antagonists of Wnt signaling influence skeletal integrity, in an inverse relation to Lrp receptor mutations. Loss of the Wnt antagonist Sclerostin (Sost) produces the generalized skeletal hyperostotic condition of sclerosteosis, which is characterized by increased bone mass and density due to hyperactive osteoblast function. Here we demonstrate that prostaglandin E2 (PGE2), a paracrine factor with pleiotropic effects on osteoblasts and osteoclasts, decreases Sclerostin expression in osteoblastic UMR106.01 cells. Decreased Sost expression correlates with increased expression of Wnt/TCF target genes Axin2 and Tcf3. We also show that the suppressive effect of PGE2 is mediated through a cyclic AMP/PKA pathway. Furthermore, selective agonists for the PGE2 receptor EP2 mimic the effect of PGE2 upon Sost, and siRNA reduction in Ptger2 prevents PGE2-induced Sost repression. These results indicate a functional relationship between prostaglandins and the Wnt/β-catenin signaling pathway in bone

Prática da ginástica laboral por trabalhadores das indústrias do Rio Grande do Sul, Brasil

O presente estudo identificou a prevalência e os fatores associados à prática de ginástica laboral por trabalhadores da indústria no Estado do Rio Grande do Sul, Brasil. Realizou-se análise secundária dos dados de um estudo de delineamento transversal, com amostra probabilística de 2.265 trabalhadores, de ambos os sexos. O instrumento de pesquisa foi o questionário autoadministrado "Estilo de vida e hábitos de lazer dos trabalhadores das indústrias brasileiras", previamente validado. A variável dependente foi a prática de ginástica laboral, definida pela resposta positiva à questão: "Você participa do programa de ginástica na empresa (ginástica laboral)?". Foram coletadas informações demográficas, socioeconômicas, comportamentais e relacionadas à saúde, como potenciais fatores associados. Na análise de dados, empregou-se o teste Qui-quadrado de Pearson e o modelo de regressão de Poisson com variância robusta, nas análises bruta e ajustada, respectivamente. A prática de ginástica laboral foi referida por 40,3% dos respondentes (IC95%: 38,2; 42,3), sendo mais prevalente nos trabalhadores do sexo feminino, com maiores níveis de escolaridade, naqueles mais ativos no lazer e que relatavam menores intensidades de esforço no trabalho. Não se observou associação da variável dependente com idade, estado civil, renda familiar bruta, tabagismo, autopercepção de saúde e autopercepção do nível de estresse. Programas de ginástica laboral devem desenvolver estratégias de promoção da saúde que priorizem subgrupos de trabalhadores menos envolvidos, em especial, indivíduos do sexo masculino e com menor escolaridade. Desse modo, será possível reduzir as disparidades, beneficiando trabalhadores, independentemente de suas características sociodemográficas, a melhores condições saúde e bem-estar no ambiente das indústrias

Tauroursodeoxycholic Acid Improves Motor Symptoms in a Mouse Model of Parkinson's Disease

Parkinson's disease (PD) is characterized by severe motor symptoms, and currently there is no treatment that retards disease progression or reverses damage prior to the time of clinical diagnosis. Tauroursodeoxycholic acid (TUDCA) is neuroprotective in the 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP) mouse model of PD; however, its effect in PD motor symptoms has never been addressed. In the present work, an extensive behavior analysis was performed to better characterize the MPTP model of PD and to evaluate the effects of TUDCA in the prevention/improvement of mice phenotype. MPTP induced significant alterations in general motor performance paradigms, including increased latency in the motor swimming, adhesive removal and pole tests, as well as altered gait, foot dragging, and tremors. TUDCA administration, either before or after MPTP, significantly reduced the swimming latency, improved gait quality, and decreased foot dragging. Importantly, TUDCA was also effective in the prevention of typical parkinsonian symptoms such as spontaneous activity, ability to initiate movement and tremors. Accordingly, TUDCA prevented MPTP-induced decrease of dopaminergic fibers and ATP levels, mitochondrial dysfunction and neuroinflammation. Overall, MPTP-injected mice presented motor symptoms that are aggravated throughout time, resembling human parkinsonism, whereas PD motor symptoms were absent or mild in TUDCA-treated animals, and no aggravation was observed in any parameter. The thorough demonstration of improvement of PD symptoms together with the demonstration of the pathways triggered by TUDCA supports a subsequent clinical trial in humans and future validation of the application of this bile acid in PD.National funds, through the Foundation for Science and Technology (Portugal) (FCT), under the scope of the projects PTDC/NEU-NMC/0248/2012, UID/DTP/04138/2013 and POCI-01-0145-FEDER-007038, and post-doctoral grants SFRH/BPD72891/2010 (to A.I.R.), SFRH/BPD/95855/2013 (to M.J.N.), SFRH/BPD/98023/2013 (to A.N.C.), SFRH/BPD/91562/2012 (to A.S.F.) and UMINHO/BI/248/2016 (to S.D.S.). This work has also been developed under the scope of the project NORTE-01-0145-FEDER-000013, supported by the Northern Portugal Regional Operational Program (NORTE 2020), under the Portugal 2020 Partnership Agreement, through the European Regional Development Fund (FEDER), and by FEDER funds, through the Competitiveness Factors Operational Program (COMPETE)info:eu-repo/semantics/publishedVersio

Causal Pathways from Enteropathogens to Environmental Enteropathy: Findings from the MAL-ED Birth Cohort Study

Background Environmental enteropathy (EE), the adverse impact of frequent and numerous enteric infections on the gut resulting in a state of persistent immune activation and altered permeability, has been proposed as a key determinant of growth failure in children in low- and middle-income populations. A theory-driven systems model to critically evaluate pathways through which enteropathogens, gut permeability, and intestinal and systemic inflammation affect child growth was conducted within the framework of the Etiology, Risk Factors and Interactions of Enteric Infections and Malnutrition and the Consequences for Child Health and Development (MAL-ED) birth cohort study that included children from eight countries. Methods Non-diarrheal stool samples (N = 22,846) from 1253 children from multiple sites were evaluated for a panel of 40 enteropathogens and fecal concentrations of myeloperoxidase, alpha-1-antitrypsin, and neopterin. Among these same children, urinary lactulose:mannitol (L:M) (N = 6363) and plasma alpha-1-acid glycoprotein (AGP) (N = 2797) were also measured. The temporal sampling design was used to create a directed acyclic graph of proposed mechanistic pathways between enteropathogen detection in non-diarrheal stools, biomarkers of intestinal permeability and inflammation, systemic inflammation and change in length- and weight- for age in children 0–2 years of age. Findings Children in these populations had frequent enteric infections and high levels of both intestinal and systemic inflammation. Higher burdens of enteropathogens, especially those categorized as being enteroinvasive or causing mucosal disruption, were associated with elevated biomarker concentrations of gut and systemic inflammation and, via these associations, indirectly associated with both reduced linear and ponderal growth. Evidence for the association with reduced linear growth was stronger for systemic inflammation than for gut inflammation; the opposite was true of reduced ponderal growth. Although Giardia was associated with reduced growth, the association was not mediated by any of the biomarkers evaluated. Interpretation The large quantity of empirical evidence contributing to this analysis supports the conceptual model of EE. The effects of EE on growth faltering in young children were small, but multiple mechanistic pathways underlying the attribution of growth failure to asymptomatic enteric infections had statistical support in the analysis. The strongest evidence for EE was the association between enteropathogens and linear growth mediated through systemic inflammation