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Compression, tension and high-velocity plate impact experiments were performed on a typical tough Zr41.2Ti13.8Cu10Ni12.5Be22.5 (Vit 1) bulk metallic glass (BMG) over a wide range of strain rates from similar to 10(-4) to 10(6) s(-1). Surprisingly, fine dimples and periodic corrugations on a nanoscale were also observed on dynamic mode I fracture surfaces of this tough Vit 1. Taking a broad overview of the fracture patterning of specimens, we proposed a criterion to assess whether the fracture of BMGs is essentially brittle or plastic. If the curvature radius of the crack tip is greater than the critical wavelength of meniscus instability [F. Spaepen, Acta Metall. 23 615 (1975); A.S. Argon and M. Salama, Mater. Sci. Eng. 23 219 (1976)], microscale vein patterns and nanoscale dimples appear on crack surfaces. However, in the opposite case, the local quasi-cleavage/separation through local atomic clusters with local softening in the background ahead of the crack tip dominates, producing nanoscale periodic corrugations. At the atomic cluster level, energy dissipation in fracture of BMGs is, therefore, determined by two competing elementary processes, viz. conventional shear transformation zones (STZs) and envisioned tension transformation zones (TTZs) ahead of the crack tip. Finally, the mechanism for the formation of nanoscale periodic corrugation is quantitatively discussed by applying the present energy dissipation mechanism.

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Resumen: Este texto muestra la importancia de la conversión como parte esencial de la tarea pensante de la teología a la hora de la Nueva Evangelización. El autor relaciona la eficacia de la palabra teológica en diálogo con la actual cultura posmoderna, con la exigencia –para la teología– de superar críticamente sus propias posibles idolatrías, entrando decidida y gozosamente en la via eminentiae, en el camino incesante hacia el “Dios siempre mayor”, que es, a la vez, el camino hacia lo auténticamente humano. El itinerario del apóstol Pedro ilustra ejemplarmente el planteo que propone el autor.

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The paper investigates whether the growing GDP share of the services sector can contribute to explain the great moderation in the US. We identify and analyze three oil price shocks and use a SVAR analysis to measure their economic impact on the US economy at both the aggregate and the sectoral level. We find mixed support for the explanation of the great moderation in terms of shrinking oil shock volatilities and observe that increases (decreases) in oil shock volatilities are contrasted by a weakening (strengthening) in their transmission mechanism. Across sectors, services are the least affected by any oil shock. As the contribution of services to the GDP volatility increases over time, we conclude that a composition effect contributed to moderate the conditional volatility to oil shocks of the US GDP.

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Jean Le Clerc nasceu em Genebra em 1657 e morreu em Amsterdã em 1736. Erudito suíço distinguiu-se como historiador, crítico, teólogo e filósofo. Suas doutrinas filosóficas carecem de unidade e foram, basicamente, fundamentadas em obras de escritores ingleses. Como pastor protestante exerceu o sacerdócio em Londres, tendo aplicado em seus estudos de teologia e exegese bíblica um critério de extrema liberdade, o que o levou a ser acusado de sociniano. Alguns de seus trabalhos foram publicados sob o pseudônimo de Joannes Phereponus. ‘Ars critica’ teve sua primeira edição em 1697. Editado em dois volumes. Contém regras para o estudo dos autores gregos e latinos clássicos, constituindo um tratado de crítica geral e dicionário para o entendimento desses autores. A quarta edição de ‘Ars critica’ foi acrescida de um terceiro volume. Considera-se a edição de 1730 a melhor dentre as publicadas. E uma obra que exigiu uma imensa erudição e grande conhecimento filosófico para sua realização

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Background: Human melanoma frequently colonizes bone marrow (BM) since its earliest stage of systemic dissemination, prior to clinical metastasis occurrence. However, how melanoma cell adhesion and proliferation mechanisms are regulated within bone marrow stromal cell (BMSC) microenvironment remain unclear. Consistent with the prometastatic role of inflammatory and angiogenic factors, several studies have reported elevated levels of cyclooxygenase-2 (COX-2) in melanoma although its pathogenic role in bone marrow melanoma metastasis is unknown. Methods: Herein we analyzed the effect of cyclooxygenase-2 (COX-2) inhibitor celecoxib in a model of generalized BM dissemination of left cardiac ventricle-injected B16 melanoma (B16M) cells into healthy and bacterial endotoxin lipopolysaccharide (LPS)-pretreated mice to induce inflammation. In addition, B16M and human A375 melanoma (A375M) cells were exposed to conditioned media from basal and LPS-treated primary cultured murine and human BMSCs, and the contribution of COX-2 to the adhesion and proliferation of melanoma cells was also studied. Results: Mice given one single intravenous injection of LPS 6 hour prior to cancer cells significantly increased B16M metastasis in BM compared to untreated mice; however, administration of oral celecoxib reduced BM metastasis incidence and volume in healthy mice, and almost completely abrogated LPS-dependent melanoma metastases. In vitro, untreated and LPS-treated murine and human BMSC-conditioned medium (CM) increased VCAM-1-dependent BMSC adherence and proliferation of B16M and A375M cells, respectively, as compared to basal medium-treated melanoma cells. Addition of celecoxib to both B16M and A375M cells abolished adhesion and proliferation increments induced by BMSC-CM. TNF alpha and VEGF secretion increased in the supernatant of LPS-treated BMSCs; however, anti-VEGF neutralizing antibodies added to B16M and A375M cells prior to LPS-treated BMSC-CM resulted in a complete abrogation of both adhesion-and proliferation-stimulating effect of BMSC on melanoma cells. Conversely, recombinant VEGF increased adherence to BMSC and proliferation of both B16M and A375M cells, compared to basal medium-treated cells, while addition of celecoxib neutralized VEGF effects on melanoma. Recombinant TNFa induced B16M production of VEGF via COX-2-dependent mechanism. Moreover, exogenous PGE2 also increased B16M cell adhesion to immobilized recombinant VCAM-1. Conclusions: We demonstrate the contribution of VEGF-induced tumor COX-2 to the regulation of adhesion-and proliferation-stimulating effects of TNFa, from endotoxin-activated bone marrow stromal cells, on VLA-4-expressing