Diálogo entre Design, Arte e Moda e o Nascimento dos Ideais de Projeto e Estilismo no Brasil por Meio das Iniciativas do MASP e Rhodia

Este texto visa demonstrar que as noções de projeto e estilismo engendradas pelas iniciativas do IAC do MASP, entre a Rhodia e o MASP e o CIT da Rhodia, entre as décadas de 1950 e 1990, podem ter influenciado a constituição de uma noção de projeto nascida e cultivada no meio acadêmico, há quase três décadas, desde o início do funcionamento do curso da Faculdade Santa Marcelina por meio da atuação de professores e profissionais que estiveram de alguma forma vinculados ao MASP ou à Rhodia e que, transferiram seu conhecimento aos discentes da FASM. A pesquisa que originou o presente artigo se pautou pela coleta e análise de fontes primárias, em especial, entrevistas com os pioneiros do campo acadêmico da moda. Elas permitiram avançar no sentido de compreender que o ensino e a prática de estilismo e projeto se fundem ainda hoje e que isso se deve, possivelmente, ao surgimento dessas noções ter acontecido de forma híbrida

Éware Tchoni: Caracterização dos desembarques pesqueiros no município de São Paulo de Olivença, Amazonas, Brasil/ Éware Tchoni: Characterization of fishing landings in the municipality of São Paulo de Olivença, Amazonas, Brazil

Este trabalho objetivou caracterizar o desembarque pesqueiro efetuado no município de São Paulo de Olivença, Alto Solimões, estado do Amazonas. O desembarque pesqueiro foi amostrado diariamente, nos anos de 2008, 2009, 2011 e 2012, através de entrevistas com uso de questionários estruturados aplicados aos pescadores no momento do desembarque.  Os resultados indicam as canoas conduzidas por dois pescadores como as principais embarcações utilizadas na pesca, realizada principalmente no rio Solimões, com uso de malhadeiras. Foram registradas 56 espécies, distribuídas em 6 Ordens e 17 famílias. Identificou-se dois picos de produção de pescado na região, composto principalmente por Characiformes migradores. Espécies não valorizadas, ou até mesmo rejeitadas em outras regiões são comuns nos desembarques nessa região, com destaque para os Doradídeos. As informações geradas neste trabalho são importantes, pois fornecem subsídios para ações de ordenamento pesqueiro nesta região

Indoor NO2 air pollution and lung function of professional cooks

Studies ofcooking- generated NO2 effects are rare in occupational epidemiology. in the present study, we evaluated the lung function of professional cooks exposed to NO2 in hospital kitchens. We performed spirometry in 37 cooks working in four hospital kitchens and estimated the predicted FVC, FEV1 and FEF25-75, based on age, sex, race, weight, and height, according to Knudson standards. NO2 measurements were obtained for 4 consecutive days during 4 different periods at 20-day intervals in each kitchen. Measurements were performed inside and outside the kitchens, simultaneously using Palm diffusion tubes. A time/exposure indicator was defined as representative of the cumulative exposure of each cook. No statistically significant effect of NO2 exposure on FVC was found. Each year of work as a cook corresponded to a decrease in predicted FEV1 of 2.5% (P=0.046) for the group as a whole. When smoking status and asthma were included in the analysis the effect of time/exposure decreased about 10% and lost statistical significance. On predicted FEF25-75, a decrease of 3.5% (P=0.035) was observed for the same group and the inclusion of controllers for smoking status and asthma did not affect the effects of time/exposure on pulmonary function parameter. After a 10-year period of work as cooks the participants of the study may present decreases in both predicted FEV1 and FEF25-75 that can reach 20 and 30%, respectively. the present study showed small but statistically significant adverse effects of gas stove exposure on the lung function of professional cooks.Univ São Paulo, Fac Med, Lab Poluicao Atmosfer Expt, BR-01246903 São Paulo, SP, BrazilUniversidade Federal de São Paulo, Escola Paulista Med, Dept Med, Disciplina Clin Med,Grp Fisiopatol Pulmonar & Pol, São Paulo, SP, BrazilABC, Fac Med, Dept Saude Coletividade, Santo Andre, SP, BrazilUniv Catolica Santos, Programa Posgrad Saude Coletiva, Santos, SP, BrazilCtr Univ Araraquara, Lab Fisioterapia Cardioresp, Araraquara, SP, BrazilUniv Estadual Paulista, Inst Quim, Araraquara, SP, BrazilHarvard Univ, Sch Publ Hlth, Dept Environm Hlth, Exposure Epidemiol & Risk Program, Boston, MA 02115 USAUniv Santo Amaro, Fac Med, Programa Pediat Ambiental, São Paulo, SP, BrazilUniversidade Federal de São Paulo, Escola Paulista Med, Dept Med, Disciplina Clin Med,Grp Fisiopatol Pulmonar & Pol, São Paulo, SP, BrazilWeb of Scienc

Air pollution and the respiratory system

A poluição atmosférica encontra-se presente nos mais diferentes cenários ao longo dos últimos 250 anos, desde que a Revolução Industrial acelerou o processo de emissão de poluentes que, até então, estava limitado ao uso doméstico de combustíveis vegetais e minerais e às emissões vulcânicas intermitentes. Hoje, aproximadamente 50% da população do planeta vivem em cidades e aglomerados urbanos e estão expostas a níveis progressivamente maiores de poluentes do ar. Este estudo é uma revisão não sistemática sobre os diferentes tipos e fontes de poluentes do ar e os efeitos respiratórios atribuídos à exposição a esses contaminantes. Podem ser creditados aos poluentes particulados e gasosos, emitidos por diferentes fontes, aumentos nos sintomas de doenças, na procura por atendimentos em serviços de emergência e no número de internações e de óbitos. Mais do que descompensar doenças pré-existentes, exposições crônicas têm ajudado a aumentar o número de casos novos de asma, de DPOC e de câncer de pulmão, tanto em áreas urbanas quanto em áreas rurais, fazendo com que os poluentes atmosféricos rivalizem com a fumaça do tabaco pelo papel de principal fator de risco para estas doenças. Na rotina de clínicos e pneumologistas, esperamos contribuir para consolidar a importância da investigação sobre a exposição aos poluentes do ar e o reconhecimento de que esse fator de risco merece ser levado em conta na adoção da melhor terapêutica para o controle das descompensações agudas das doenças respiratórias e para a sua manutenção entre as crises

Brain zinc chelation by diethyldithiocarbamate increased the behavioral and mitochondrial damages in zebrafish subjected to hypoxia

The increase in brain levels of chelatable zinc (Zn) in dysfunctions involving oxygen deprivation has stimulated the treatment with Zn chelators, such as diethyldithiocarbamate (DEDTC). However, DEDTC is a redox-active compound and it should be better evaluated during hypoxia. We use the hypoxia model in zebrafish to evaluate DEDTC effects. The exploratory behavior, chelatable Zn content, activities of mitochondrial dehydrogenases, reactive species levels (nitric oxide, superoxide anion, hydroxyl radical scavenger capacity) and cellular antioxidants (sulfhydryl, superoxide dismutase) of zebrafish brain were assessed after recovery, with or without 0.2mM DEDTC. The increased brain levels of chelatable Zn induced by hypoxia were mitigated by DEDTC. However, the novel tank task indicated that DEDTC did further enhance the exploratory deficit caused by hypoxia. Furthermore, these behavioral impairments caused by DEDTC were more associated with a negative action on mitochondrial activity and brain oxidative balance. Thus, due to apparent pro-oxidant action of DEDTC, our data do not support its use for neuroprotection in neuropathologies involving oxygen deprivation

TLR2, TLR4 and the MYD88 Signaling Pathway Are Crucial for Neutrophil Migration in Acute Kidney Injury Induced by Sepsis

The aim of this study was to investigate the role of TLR2, TLR4 and MyD88 in sepsis-induced AKI. C57BL/6 TLR2(-/-), TLR4(-/-) and MyD88(-/-) male mice were subjected to sepsis by cecal ligation and puncture (CLP). Twenty four hours later, kidney tissue and blood samples were collected for analysis. the TLR2(-/-), TLR4(-/-) and MyD88(-/-) mice that were subjected to CLP had preserved renal morphology, and fewer areas of hypoxia and apoptosis compared with the wild-type C57BL/6 mice (WT). MyD88(-/-) mice were completely protected compared with the WT mice. We also observed reduced expression of proinflammatory cytokines in the kidneys of the knockout mice compared with those of the WT mice and subsequent inhibition of increased vascular permeability in the kidneys of the knockout mice. the WT mice had increased GR1(+low) cells migration compared with the knockout mice and decreased in GR1(+high) cells migration into the peritoneal cavity. the TLR2(-/-), TLR4(-/-), and MyD88(-/-) mice had lower neutrophil infiltration in the kidneys. Depletion of neutrophils in the WT mice led to protection of renal function and less inflammation in the kidneys of these mice. Innate immunity participates in polymicrobial sepsis-induced AKI, mainly through the MyD88 pathway, by leading to an increased migration of neutrophils to the kidney, increased production of proinflammatory cytokines, vascular permeability, hypoxia and apoptosis of tubular cells.Fundação de Amparo à Pesquisa do Estado de São Paulo (FAPESP)Conselho Nacional de Desenvolvimento Científico e Tecnológico (CNPq)National Institute of Science and Technology (INCT)Universidade Federal de São Paulo, Dept Med, Disciplina Nefrol, São Paulo, BrazilUniv São Paulo, Dept Imunol, Lab Imunobiol Transplantes, São Paulo, BrazilHosp Israelita Albert Einstein, IIEP, São Paulo, BrazilUniv Fed Triangulo Mineiro, Uberaba, BrazilUniversidade Federal de São Paulo, Dept Med, Disciplina Nefrol, São Paulo, BrazilFAPESP: 07/07139-3Web of Scienc

Oxidative Stress and Modification of Renal Vascular Permeability Are Associated with Acute Kidney Injury during P. berghei ANKA Infection

Malaria associated-acute kidney injury (AKI) is associated with 45% of mortality in adult patients hospitalized with severe form of the disease. However, the causes that lead to a framework of malaria-associated AKI are still poorly characterized. Some clinical studies speculate that oxidative stress products, a characteristic of Plasmodium infection, as well as proinflammatory response induced by the parasite are involved in its pathophysiology. Therefore, we aimed to investigate the development of malaria-associated AKI during infection by P. berghei ANKA, with special attention to the role played by the inflammatory response and the involvement of oxidative stress. For that, we took advantage of an experimental model of severe malaria that showed significant changes in the renal pathophysiology to investigate the role of malaria infection in the renal microvascular permeability and tissue injury. Therefore, BALB/c mice were infected with P. berghei ANKA. To assess renal function, creatinine, blood urea nitrogen, and ratio of proteinuria and creatininuria were evaluated. The products of oxidative stress, as well as cytokine profile were quantified in plasma and renal tissue. The change of renal microvascular permeability, tissue hypoxia and cellular apoptosis were also evaluated. Parasite infection resulted in renal dysfunction. Furthermore, we observed increased expression of adhesion molecule, proinflammatory cytokines and products of oxidative stress, associated with a decrease mRNA expression of HO-1 in kidney tissue of infected mice. The measurement of lipoprotein oxidizability also showed a significant increase in plasma of infected animals. Together, our findings support the idea that products of oxidative stress, as well as the immune response against the parasite are crucial to changes in kidney architecture and microvascular endothelial permeability of BALB/c mice infected with P. berghei ANKA.State of Sao Paulo Foundation for Research Support (FAPESP)State of Sao Paulo Foundation for Research Support (FAPESP) [07/07139-3, 10/52180-4, 12/02270-2]CAPESCAPESBrazilian Council of Scientific and Technologic Development (International Associated Laboratory of Renal Immunopathology, CNPq/Inserm)Brazilian Council of Scientific and Technologic Development (International Associated Laboratory of Renal Immunopathology, CNPq/Inserm)Complex Fluids INCT (FAPESP/CNPq)Complex Fluids INCT (FAPESP/CNPq

MyD88 Signaling Pathway Is Involved in Renal Fibrosis by Favoring a T(H)2 Immune Response and Activating Alternative M2 Macrophages

Inflammation contributes to the pathogenesis of chronic kidney disease (CKD). Molecules released by the inflamed injured tissue\ud can activate toll-like receptors (TLRs), thereby modulating macrophage and CD4+ T-cell activity. We propose that in renal fibrogenesis,\ud M2 macrophages are recruited and activated in a T helper subset 2 cell (TH2)-prone inflammatory milieu in a MyD88-\ud dependent manner. Mice submitted to unilateral ureteral ligation (UUO) demonstrated an increase in macrophage infiltration with\ud collagen deposition after 7 d. Conversely, TLR2, TLR4 and MyD88 knockout (KO) mice had an improved renal function together with\ud diminished TH2 cytokine production and decreased fibrosis formation. Moreover, TLR2, TLR4 and MyD88 KO animals exhibited less M2\ud macrophage infiltration, namely interleukin (IL)-10+ and CD206+ CD11bhigh cells, at 7 d after surgery. We evaluated the role of a TH2\ud cytokine in this context, and observed that the absence of IL-4 was associated with better renal function, decreased IL-13 and TGF-\ud β levels, reduced arginase activity and a decrease in fibrosis formation when compared with IL-12 KO and wild-type (WT) animals.\ud Indeed, the better renal outcomes and the decreased fibrosis formation were restricted to the deficiency of IL-4 in the hematopoietic\ud compartment. Finally, macrophage depletion, rather than the absence of T cells, led to reduced lesions of the glomerular filtration\ud barrier and decreased collagen deposition. These results provide evidence that future therapeutic strategies against renal\ud fibrosis should be accompanied by the modulation of the M1:M2 and TH1:TH2 balance, as TH2 and M2 cells are predictive of fibrosis\ud toward mechanisms that are sensed by innate immune response and triggered in a MyD88-dependent pathway.Brazilian Foundation - FAPESP (Fundacao de Apoio a Pesquisa do Estado de Sao Paulo) [07/07139-3, 10/52180-4]Brazilian Foundation FAPESP (Fundacao de Apoio a Pesquisa do Estado de Sao Paulo)International Associated Laboratory (CNPq/Inserm)International Associated Laboratory (CNPq/Inserm)National Institute of Science and Technology (INCT)National Institute of Science and Technology (INCT