Valoração de bens e serviços ecossistêmicos associados a projetos de recuperação e conservação ambiental no reservatório de Três Irmãos: carbono, uso público e recursos pesqueiros / Valuation of ecosystem goods and services associated with environmental recovery and conservation projects in the Três Irmãos reservoir: carbon, public use and fishing resources

O objetivo da pesquisa “Metodologia de Valoração de Bens e Serviços Ecossistêmicos Associados a Projetos de Recuperação e Conservação Ambiental em Reservatórios Hidrelétricos” foi estabelecer metodologias adaptadas ao setor hidrelétrico brasileiro, demonstrando que é possível – e necessário – estimar a importância social e econômica das ações de proteção ambiental, com estudo de caso para a UHE Três Irmãos. Para tal, metodologias de valoração ambiental foram aplicadas às ações de conservação conduzidas pelas concessionárias. O presente artigo examina esses benefícios obtidos em termos de balanço de carbono, uso público e recursos pesqueiros. As ações de reflorestamento e de conservação contribuíram para reduzir o volume de carbono na atmosfera. No cenário corrente de reflorestamento, estima-se que o valor do benefício em termos de carbono capturado supere R$8,5 milhões por ano (reflorestamento já realizado), podendo chegar a R$ 60,5 milhões caso o reflorestamento se aproxime do cenário de uma faixa de 250 metros de extensão das margens do reservatório. O VPL desses benefícios foi estimado em R$66,5 milhões e em R$ 473,2 milhões até 2027, respectivamente. Estendendo o horizonte de tempo até 2037, o VPL dos benefícios superaria R$103,7 milhões e R$ 736,1 milhões nos cenários supracitados. Outro benefício das ações de conservação ambiental foi a garantia de um grande fluxo de turismo (mais de 500 mil visitantes em 2017), cujos gastos induziram um aumento de mais de R$90 milhões na economia local, com impacto fiscal de mais de R$ 4 milhões nas receitas das prefeituras

Prolonged maternal separation induces undernutrition and systemic inflammation with disrupted hippocampal development in mice

Objective: Prolonged maternal separation (PMS) in the first 2 wk of life has been associated with poor growth with lasting effects in brain structure and function. This study aimed to investigate whether PMS-induced undernutrition could cause systemic inflammation and changes in nutrition-related hormonal levels, affecting hippocampal structure and neurotransmission in C57BL/6J suckling mice. Methods: This study assessed mouse growth parameters coupled with insulin-like growth factor-1 (IGF-1) serum levels. In addition, leptin, adiponectin, and corticosterone serum levels were measured following PMS. Hippocampal stereology and the amino acid levels were also assessed. Furthermore, we measured myelin basic protein and synapthophysin (SYN) expression in the overall brain tissue and hippocampal SYN immunolabeling. For behavioral tests, we analyzed the ontogeny of selected neonatal reflexes. PMS was induced by separating half the pups in each litter from their lactating dams for defined periods each day (4 h on day 1, 8 h on day 2, and 12 h thereafter). A total of 67 suckling pups were used in this study. Results: PMS induced significant slowdown in weight gain and growth impairment. Significant reductions in serum leptin and IGF-1 levels were found following PMS. Total CA3 area and volume were reduced, specifically affecting the pyramidal layer in PMS mice. CA1 pyramidal layer area was also reduced. Overall hippocampal SYN immunolabeling was lower, especially in CA3 field and dentate gyrus. Furthermore, PMS reduced hippocampal aspartate, glutamate, and gammaaminobutyric acid levels, as compared with unseparated controls. Conclusion: These findings suggest that PMS causes significant growth deficits and alterations in hippocampal morphology and neurotransmission.This work was supported in part by National Institutes of Health (NIH) research grant 5R01HD053131, funded by the Eunice Kennedy Shriver National Institute of Child Health and Human Development and the NIH Office of Dietary Supplements, and Brazilian grants from CNPq and CAPES (Grant # RO1 HD053131). The authors would like to thank Dr. Patricia Foley for veterinarian technical support and Dr. Jose Paulo Andrade for the excellent comments and suggestions to improve this manuscript. N.S. contributed with the stereological studies. I.L.F. and R.B.O. contributed with the behavioral studies. I.L.F., R.B.O., and R.L.G. contributed with the study design, study analysis, and manuscript preparation. G.A.M. and P.B.F. contributed with neurochemical brain analyses. J.I.A.L. and G.M.A. contributed with hormonal and CRP serum analyses. D.G.C., K.M.C., and R.S.R. contributed with animal experimentation and data collection

NANOG Reporter Cell Lines Generated by Gene Targeting in Human Embryonic Stem Cells

Background: Pluripotency and self-renewal of human embryonic stem cells (hESCs) is mediated by a complex interplay between extra- and intracellular signaling pathways, which regulate the expression of pluripotency-specific transcription factors. The homeodomain transcription factor NANOG plays a central role in maintaining hESC pluripotency, but the precise role and regulation of NANOG are not well defined. Methodology/Principal Findings: To facilitate the study of NANOG expression and regulation in viable hESC cultures, we generated fluorescent NANOG reporter cell lines by gene targeting in hESCs. In these reporter lines, the fluorescent reporter gene was co-expressed with endogenous NANOG and responded to experimental induction or repression of the NANOG promoter with appropriate changes in expression levels. Furthermore, NANOG reporter lines facilitated the separation of hESC populations based on NANOG expression levels and their subsequent characterization. Gene expression arrays on isolated hESC subpopulations revealed genes with differential expression in NANOG high and NANOG low hESCs, providing candidates for NANOG downstream targets hESCs. Conclusion/Significance: The newly derived NANOG reporter hESC lines present novel tools to visualize NANOG expression in viable hESCs. In future applications, these reporter lines can be used to elucidate the function and regulation of NANO

Salud de los trabajadores

Actividad física y su relación con los factores de riesgo cardiovascular de carteros chilenosAnálisis de resultados: riesgos psicosociales en el trabajo Suceso-Istas 21 en Cesfam QuellónAusentismo laboral por enfermedades oftalmológicas, Chile 2009Brote de diarreas por norovirus, posterremoto-tsunami, Constitución, Región del MauleCalidad de vida en profesionales de la salud pública chilenaCaracterización del reposo laboral en personal del SSMN durante el primer semestre de 2010Concentración de nicotina en pelo en trabajadores no fumadores expuestos a humo de tabaco ambientalCondiciones de trabajo y bienestar/malestar docente en profesores de enseñanza media de SantiagoDisfunción auditiva inducida por exposición a xilenoErgonomía aplicada al estudio del síndrome de dolor lumbar en el trabajoEstimación de la frecuencia de factores de riesgo cardiovascular en trabajadores de una empresa mineraExposición a plaguicidas inhibidores de la acetilcolinesterasa en Colombia, 2006-2009Factores de riesgo y daños de salud en conductores de una empresa peruana de transporte terrestre, 2009Las consecuencias de la cultura en salud y seguridad ocupacional en una empresa mineraPercepción de cambios en la práctica médica y estrategias de afrontamientoPercepción de la calidad de vida en la Universidad del BiobíoPesos máximos aceptables para tareas de levantamiento manual de carga en población laboral femeninaRiesgo coronario en trabajadores mineros según la función de Framingham adaptada para la población chilenaTrastornos emocionales y riesgo cardiovascular en trabajadores de la salu

Influenza A Virus Nucleoprotein Exploits Hsp40 to Inhibit PKR Activation

BACKGROUND: Double-stranded RNA dependent protein kinase (PKR) is a key regulator of the anti-viral innate immune response in mammalian cells. PKR activity is regulated by a 58 kilo Dalton cellular inhibitor (P58(IPK)), which is present in inactive state as a complex with Hsp40 under normal conditions. In case of influenza A virus (IAV) infection, P58(IPK) is known to dissociate from Hsp40 and inhibit PKR activation. However the influenza virus component responsible for PKR inhibition through P58(IPK) activation was hitherto unknown. PRINCIPAL FINDINGS: Human heat shock 40 protein (Hsp40) was identified as an interacting partner of Influenza A virus nucleoprotein (IAV NP) using a yeast two-hybrid screen. This interaction was confirmed by co-immunoprecipitation studies from mammalian cells transfected with IAV NP expressing plasmid. Further, the IAV NP-Hsp40 interaction was validated in mammalian cells infected with various seasonal and pandemic strains of influenza viruses. Cellular localization studies showed that NP and Hsp40 co-localize primarily in the nucleus. During IAV infection in mammalian cells, expression of NP coincided with the dissociation of P58(IPK) from Hsp40 and decrease PKR phosphorylation. We observed that, plasmid based expression of NP in mammalian cells leads to decrease in PKR phosphorylation. Furthermore, inhibition of NP expression during influenza virus replication led to PKR activation and concomitant increase in eIF2α phosphorylation. Inhibition of NP expression also led to reduced IRF3 phosphorylation, enhanced IFN β production and concomitant reduction of virus replication. Taken together our data suggest that NP is the viral factor responsible for P58(IPK) activation and subsequent inhibition of PKR-mediated host response during IAV infection. SIGNIFICANCE: Our findings demonstrate a novel role of IAV NP in inhibiting PKR-mediated anti-viral host response and help us understand P58(IPK) mediated inhibition of PKR activity during IAV infection

Tyrosine kinase signalling in breast cancer: Epidermal growth factor receptor and c-Src interactions in breast cancer

Both the non-receptor tyrosine kinase, c-Src, and members of the epidermal growth factor (EGF) receptor family are overexpressed in high percentages of human breast cancers. Because these molecules are plasma membrane-associated and involved in mitogenesis, it has been speculated that they function in concert with one another to promote breast cancer development and progression. Evidence to date supports a model wherein c-Src potentiates the survival, proliferation and tumorigenesis of EGF receptor family members, in part by associating with them. Phosphorylation of the EGF receptor by c-SRC is also critical for mitogenic signaling initiated by the EGF receptor itself, as well as by several G-protein coupled receptors (GPCRs), a cytokine receptor, and the estrogen receptor. Thus, c-Src appears to have pleiotropic effects on cancer cells by modulating the action of multiple growth-promoting receptors

Profile of Central and Effector Memory T Cells in the Progression of Chronic Human Chagas Disease

Chagas disease is a parasitic infection caused by protozoan Trypanosoma cruzi that affects approximately 11 million people in Latin America. The involvement of the host's immune response on the development of severe forms of Chagas disease has not been fully elucidated. Studies on the immune response against T. cruzi infection show that the immunoregulatory mechanisms are necessary to prevent the deleterious effect of excessive immune response stimulation and consequently the fatal outcome of the disease. A recall response against parasite antigens observed in in vitro peripheral blood cell culture clearly demonstrates that memory response is generated during infection. Memory T cells are heterogeneous and differ in both the ability to migrate and exert their effector function. This heterogeneity is reflected in the definition of central (TCM) and effector memory (TEM) T cells. Our results suggest that a balance between regulatory and effectors T cells may be important for the progression and development of the disease. Furthermore, the high percentage of central memory CD4+ T cells in indeterminate patients after stimulation suggests that these cells may modulate host's inflammatory response by controlling cell migration to tissues and their effector role during chronic phase of the disease