A stress correction procedure for the analysis of inelastic frames under transient dynamic loads

This paper attempts to present an algorithm (as a set of conditions and equations) for the correction of stresses of both strain-hardening and perfectly-plastic materials, for the analysis of frames under transient dynamic loadings. The validity of the proposed conditions and equations is verified through numerical experiments

Dietary Omega-3 Fatty Acids Do Not Change Resistance of Rat Brain or Liver Mitochondria to Ca2+ and/or Prooxidants

Omega-3 polyunsaturated fatty acids (n-3 PUFAs) block apoptotic neuronal cell death and are strongly neuroprotective in acute and chronic neurodegeneration. Theoretical considerations, indirect data, and consideration of parsimony lead to the hypothesis that modulation of mitochondrial pathway(s) underlies at least some of the neuroprotective effects of n-3 PUFAs. We therefore systematically tested this hypothesis on healthy male FBFN1 rats fed for four weeks with isocaloric, 10% fat-containing diets supplemented with 1, 3, or 10% fish oil (FO). High resolution mass spectrometric analysis confirmed expected diet-driven increases in docosahexaenoic acid (DHA, 22:6, n-3) and eicosapentaenoic acid (EPA, 20:5, n-3) in sera, liver and nonsynaptosomal brain mitochondria. We further evaluated the resistance of brain and liver mitochondria to Ca2+ overload and prooxidants. Under these conditions, neither mitochondrial resistance to Ca2+ overload and prooxidants nor mitochondrial physiology is altered by diet, despite the expected incorporation of DHA and EPA in mitochondrial membranes and plasma. Collectively, the data eliminate one of the previously proposed mechanism(s) that n-3 PUFA induced augmentation of mitochondrial resistance to the oxidant/calcium-driven dysfunction. These data furthermore allow us to define a specific series of follow-up experiments to test related hypotheses about the effect of n-3 PUFAs on brain mitochondria

Análise proteômica do estresse hídrico em cafeeiro.

Déficit hídrico é um dos fatores ambientais mais importantes para a diminuição da produtividade do cafeeiro, tanto no Brasil quanto em outros países produtores. O estabelecimento de estratégias para obtenção de cultivares tolerantes ao estresse hídrico depende da compreensão das respostas biológicas ao nível genético, molecular e bioquímico. Para estudar a resposta ao estresse hídrico no gênero Coffea, foi estabelecida uma rede de pesquisa em proteômica (PROTEOPAR ? Programa Proteoma do Paraná) constituída de oito laboratórios. Quatro genótipos de Coffea, com diferentes respostas fisiológicas à seca, foram analisados: C. canephora (Clone 14, tolerante e Clone 109A, sensível) e C. arabica (BA10, tolerante e Geisha, sensível). Proteínas foram extraídas de folhas e raízes de plantas (18 meses de idade) mantidas em casa-de-vegetação, utilizando-se o método de SDS-Fenol modificado. Os regimes hídricos constituíram-se dos seguintes tratamentos: controle irrigado, estresse hídrico severo (-4,0 MPa de potencial de água) e recuperação pós-estresse (36 horas após irrigação). Os extratos protéicos foram distribuídos aos laboratórios do PROTEOPAR para obtenção e análise do padrão de expressão protéica diferencial via eletroforese bidimensional. O método de identificação de proteínas PMF (?Peptide mass fingerprinting?) foi aplicado utilizando-se um espectrômetro de massa (MS) do tipo MALDI-TOF e comparando os espectros de digestão tríptica contra bancos de dados baseados em ESTs de Coffea

Dysregulation of MicroRNA-34a Expression in Head and Neck Squamous Cell Carcinoma Promotes Tumor Growth and Tumor Angiogenesis

MicroRNAs (miRs) are small non-coding RNAs that play an important role in cancer development where they can act as oncogenes or as tumor-suppressors. miR-34a is a tumor-suppressor that is frequently downregulated in a number of tumor types. However, little is known about the role of miR-34a in head and neck squamous cell carcinoma (HNSCC).miR-34a expression in tumor samples, HNSCC cell lines and endothelial cells was examined by real time PCR. Lipofectamine-2000 was used to transfect miR-34a in HNSCC cell lines and human endothelial cells. Cell-proliferation, migration and clonogenic survival was examined by MTT, Xcelligence system, scratch assay and colony formation assay. miR-34a effect on tumor growth and tumor angiogenesis was examined by in vivo SCID mouse xenograft model. Our results demonstrate that miR-34a is significantly downregulated in HNSCC tumors and cell lines. Ectopic expression of miR-34a in HNSCC cell lines significantly inhibited tumor cell proliferation, colony formation and migration. miR-34a overexpression also markedly downregulated E2F3 and survivin levels. Rescue experiments using microRNA resistant E2F3 isoforms suggest that miR-34a-mediated inhibition of cell proliferation and colony formation is predominantly mediated by E2F3a isoform. In addition, tumor samples from HNSCC patients showed an inverse relationship between miR-34a and survivin as well as miR-34a and E2F3 levels. Overexpression of E2F3a completely rescued survivin expression in miR-34a expressing cells, thereby suggesting that miR-34a may be regulating survivin expression via E2F3a. Ectopic expression of miR-34a also significantly inhibited tumor growth and tumor angiogenesis in a SCID mouse xenograft model. Interestingly, miR-34a inhibited tumor angiogenesis by blocking VEGF production by tumor cells as well as directly inhibiting endothelial cell functions.Taken together, these findings suggest that dysregulation of miR-34a expression is common in HNSCC and modulation of miR34a activity might represent a novel therapeutic strategy for the treatment of HNSCC