O ensino da filosofia no Brasil: um breve olhar sobre algumas das principais tendências no debate entre os anos de 1934 a 2008

Fundação de Amparo à Pesquisa do Estado de São Paulo (FAPESP)

Instituto do Concurso Público na Constituição Federal de 1934

Pós-graduação em Ciências Sociais - FCLAR

A tradução do conto Lange Schatten de Marie Luise Kaschnitz

The principal objective of this project is to present a literary translation from German to Portuguese of the short story 'Lange Schatten', in the collection of the same name, Lange Schatten Erzählungen, published in 1960, written by Marie Luise Kaschnitz. Kaschnitz was born in 1901 in Karlsruhe, south-west Germany. The translation was completed with the aid of virtual and printed dictionaries, in addition to books on the history of German literature and some translation theories. Also, this paper provides brief commentaries on topics related to translation, particularly those concerned with the difficulties posed by translation of this project

Análise da qualidade de vida de pacientes com a doença de Charcot-Marie-Tooth tipo 1A

A doença de Charcot-Marie-Tooth (CMT) é a mais freqüente das neuropatias hereditárias, mas a sua história natural é pouco conhecida. Apesar da maioria dos pacientes apresentarem uma evolução com características mais “benignas”, é associado à doença com um comprometimento funcional, o que pode ser acompanhado de limitações e incapacitações. O presente estudo teve como objetivo avaliar a qualidade de vida de pacientes afetados pela CMT1A. Considerando que a qualidade de vida pode sofrer influência de variáveis sócio-culturais, um estudo neste contexto mostra-se oportuno. Nenhum estudo de nosso conhecimento realizou tal avaliação no contexto brasileiro. Fizeram parte deste estudo pacientes com CMT decorrente da duplicação 17p11.2-p12 (CMT1A) que foram avaliados quanto ao comprometimento funcional por meio da aplicação do SF-36. Esse questionário é utilizado internacionalmente para aferir a qualidade de vida dos indivíduos. Os resultados obtidos foram submetidos à análise estatística. Como resultados não se observaram associações entre o gênero e os domínios avaliados para a qualidade de vida. Os dados obtidos revelaram que a qualidade de vida dos pacientes com CMT1A se mostrou comprometida principalmente quanto aos seus Aspectos Sociais (p = 0,02) e Aspectos emocionais (p = 0,04). Adicionalmente, houve uma tendência ao comprometimento da Capacidade Funcional (p = 0,08), sendo que os outros índices de avaliação de comprometimento físico se mostraram preservados. A presença ou ausência de ocupação parece influenciar os Aspectos Sociais apresentando uma tendência de diferença significativa (p = 0,07), possuindo o grupo com ocupação valores superiores. Apesar da CMT1A apresentar piora clínica ao longo dos anos, a idade mais avançada não implicou em uma pior percepção da qualidade de vida no grupo de pacientes estudados no presente trabalho... (Resumo completo, clicar acesso eletrônico abaixo)

A eugenia no humor da Revista Ilustrada Careta: raça e cor no Governo Provisório (1930-1934)

Pós-graduação em História - FCLAS

Botucatu: modernização e infraestrutura urbana no interior paulista (1928-1934)

Pós-graduação em História - FCLAS

Diversidade e evolução do gênero Adenomera Steindachner, 1867 (Anura, Leptodactylidae)

Fundação de Amparo à Pesquisa do Estado de São Paulo (FAPESP)

A imprensa brasileira e a política cardenista (1934-1940)

Pós-graduação em História - FCLAS

Resposta comportamental da broca-do-café Hypothenemus hampei (Ferrari, 1867) (Coleoptera: Curculionidae: Scolytinae) a voláteis de frutos de café

Pós-graduação em Agronomia (Entomologia Agrícola) - FCAV

Sistemática de Piabina Reinhardt, 1867 (Ostariophysi: Characidae)

Coordenação de Aperfeiçoamento de Pessoal de Nível Superior (CAPES)

Cocaine effects on mouse incentive-learning and human addiction are linked to alpha 2 subunit-containing GABA(A) receptors

Because GABA(A) receptors containing alpha 2 subunits are highly represented in areas of the brain, such as nucleus accumbens (NAcc), frontal cortex, and amygdala, regions intimately involved in signaling motivation and reward, we hypothesized that manipulations of this receptor subtype would influence processing of rewards. Voltage-clamp recordings from NAcc medium spiny neurons of mice with alpha 2 gene deletion showed reduced synaptic GABA(A) receptor-mediated responses. Behaviorally, the deletion abolished cocaine`s ability to potentiate behaviors conditioned to rewards (conditioned reinforcement), and to support behavioral sensitization. In mice with a point mutation in the benzodiazepine binding pocket of alpha 2-GABA(A) receptors (alpha 2H101R), GABAergic neurotransmission in medium spiny neurons was identical to that of WT (i.e., the mutation was silent), but importantly, receptor function was now facilitated by the atypical benzodiazepine Ro 15-4513 (ethyl 8-amido-5,6-dihydro-5-methyl-6-oxo-4H-imidazo [1,5-a] [1,4] benzodiazepine-3-carboxylate). In alpha 2H101R, but not WT mice, Ro 15-4513 administered directly into the NAcc-stimulated locomotor activity, and when given systemically and repeatedly, induced behavioral sensitization. These data indicate that activation of alpha 2-GABA(A) receptors (most likely in NAcc) is both necessary and sufficient for behavioral sensitization. Consistent with a role of these receptors in addiction, we found specific markers and haplotypes of the GABRA2 gene to be associated with human cocaine addiction.

Lufaxin, a Novel Factor Xa Inhibitor From the Salivary Gland of the Sand Fly Lutzomyia longipalpis Blocks Protease-Activated Receptor 2 Activation and Inhibits Inflammation and Thrombosis In Vivo

Objective-Blood-sucking arthropods' salivary glands contain a remarkable diversity of antihemostatics. The aim of the present study was to identify the unique salivary anticoagulant of the sand fly Lutzomyia longipalpis, which remained elusive for decades. Methods and Results-Several L. longipalpis salivary proteins were expressed in human embryonic kidney 293 cells and screened for inhibition of blood coagulation. A novel 32.4-kDa molecule, named Lufaxin, was identified as a slow, tight, noncompetitive, and reversible inhibitor of factor Xa (FXa). Notably, Lufaxin's primary sequence does not share similarity to any physiological or salivary inhibitors of coagulation reported to date. Lufaxin is specific for FXa and does not interact with FX, Dansyl-Glu-Gly-Arg-FXa, or 15 other enzymes. In addition, Lufaxin blocks prothrombinase and increases both prothrombin time and activated partial thromboplastin time. Surface plasmon resonance experiments revealed that FXa binds Lufaxin with an equilibrium constant approximate to 3 nM, and isothermal titration calorimetry determined a stoichiometry of 1:1. Lufaxin also prevents protease-activated receptor 2 activation by FXa in the MDA-MB-231 cell line and abrogates edema formation triggered by injection of FXa in the paw of mice. Moreover, Lufaxin prevents FeCl3-induced carotid artery thrombus formation and prolongs activated partial thromboplastin time ex vivo, implying that it works as an anticoagulant in vivo. Finally, salivary gland of sand flies was found to inhibit FXa and to interact with the enzyme. Conclusion-Lufaxin belongs to a novel family of slow-tight FXa inhibitors, which display antithrombotic and anti-inflammatory activities. It is a useful tool to understand FXa structural features and its role in prohemostatic and proinflammatory events. (Arterioscler Thromb Vasc Biol. 2012;32:2185-2196.)

Anti-inflammatory Effects of Aerobic Exercise in Mice Exposed to Air Pollution

VIEIRA, R. D. P., A. C. TOLEDO, L. B. SILVA, F. M. ALMEIDA, N. R. DAMACENO-RODRIGUES, E. G. CALDINI, A. B. G. SANTOS, D. H. RIVERO, D. C. HIZUME, F. D. T. Q. S. LOPES, C. R. OLIVO, H. C. CASTRO-FARIA-NETO, M. A. MARTINS, P. H. N. SALDIVA, and M. DOLHNIKOFF. Anti-inflammatory Effects of Aerobic Exercise in Mice Exposed to Air Pollution. Med. Sci. Sports Exerc., Vol. 44, No. 7, pp. 1227-1234, 2012. Purpose: Exposure to diesel exhaust particles (DEP) results in lung inflammation. Regular aerobic exercise improves the inflammatory status in different pulmonary diseases. However, the effects of long-term aerobic exercise on the pulmonary response to DEP have not been investigated. The present study evaluated the effect of aerobic conditioning on the pulmonary inflammatory and oxidative responses of mice exposed to DEP. Methods: BALB/c mice were subjected to aerobic exercise five times per week for 5 wk, concomitantly with exposure to DEP (3 mg.mL (1); 10 mu L per mouse). The levels of exhaled nitric oxide, reactive oxygen species, cellularity, interleukin 6 (IL-6), and tumor necrosis factor alpha (TNF-alpha) were analyzed in bronchoalveolar lavage fluid, and the density of neutrophils and the volume proportion of collagen fibers were measured in the lung parenchyma. The cellular density of leukocytes expressing IL-1 beta, keratinocyte chemoattractant (KC), and TNF-alpha in lung parenchyma was evaluated with immunohistochemistry. The levels of IL-1 beta, KC, and TNF-alpha were also evaluated in the serum. Results: Aerobic exercise inhibited the DEP-induced increase in the levels of reactive oxygen species (P < 0.05); exhaled nitric oxide (P < 0.01); total (P < 0.01) and differential cells (P < 0.01); IL-6 and TNF-alpha levels in bronchoalveolar lavage fluid (P < 0.05); the level of neutrophils (P < 0.001); collagen density in the lung parenchyma (P < 0.05); the levels of IL-6, KC, and TNF-alpha in plasma (P < 0.05); and the expression of IL-1 beta, KC, and TNF-alpha by leukocytes in the lung parenchyma (P < 0.01). Conclusions: We conclude that long-term aerobic exercise presents protective effects in a mouse model of DEP-induced lung inflammation. Our results indicate a need for human studies that evaluate the pulmonary responses to aerobic exercise chronically performed in polluted areas.

Unraveling the drivers of community dissimilarity and species extinction in fragmented landscapes

Communities in fragmented landscapes are often assumed to be structured by species extinction due to habitat loss, which has led to extensive use of the species-area relationship (SAR) in fragmentation studies. However, the use of the SAR presupposes that habitat loss leads species to extinction but does not allow for extinction to be offset by colonization of disturbed-habitat specialists. Moreover, the use of SAR assumes that species richness is a good proxy of community changes in fragmented landscapes. Here, we assessed how communities dwelling in fragmented landscapes are influenced by habitat loss at multiple scales; then we estimated the ability of models ruled by SAR and by species turnover in successfully predicting changes in community composition, and asked whether species richness is indeed an informative community metric. To address these issues, we used a data set consisting of 140 bird species sampled in 65 patches, from six landscapes with different proportions of forest cover in the Atlantic Forest of Brazil. We compared empirical patterns against simulations of over 8 million communities structured by different magnitudes of the power-law SAR and with species-specific rules to assign species to sites. Empirical results showed that, while bird community composition was strongly influenced by habitat loss at the patch and landscape scale, species richness remained largely unaffected. Modeling results revealed that the compositional changes observed in the Atlantic Forest bird metacommunity were only matched by models with either unrealistic magnitudes of the SAR or by models ruled by species turnover, akin to what would be observed along natural gradients. We show that, in the presence of such compositional turnover, species richness is poorly correlated with species extinction, and z values of the SAR strongly underestimate the effects of habitat loss. We suggest that the observed compositional changes are driven by each species reaching its individual extinction threshold: either a threshold of forest cover for species that disappear with habitat loss, or of matrix cover for species that benefit from habitat loss.

Tamoxifen Subcellular Localization; Observation of Cell-Specific Cytotoxicity Enhancement by Inhibition of Mitochondrial ETC Complexes I and III

Recently, a nongenomic cytotoxic component of the chemotherapeutic agent tamoxifen (TAM) has been identified that predominantly triggers mitochondrial events. The present study delineates the intracellular fate of TAM and studies its interaction with a spectrum of cell homeostasis modulators primarily relevant to mitochondria. The subcellular localization of TAM was assessed by confocal fluorescence microscopy. The effect of the modulators on TAM cytotoxicity was assessed by standard MTT assays. Our findings show that in estrogen receptor positive MCF7 breast adenocarcinoma cells and DU145 human prostate cancer cells, TAM largely accumulates in the mitochondria and endoplasmic reticulum, but not lysosomes. Our results further demonstrate that in MCF7, but not in DU145 cells, mitochondrial electron transport chain complex I and III inhibitors exacerbate TAM toxicity with an order of potency of myxothiazol = stigmatellin > rotenone > antimycin A, suggesting a cell-specific cytotoxic interplay between mitochondrial complex I and III function and TAM action.