Paleomagnetic properties of igneous rocks from several DSDP and ODP sites, western Pacific

Oceanic basalts and other related igneous rocks are considered excellent recorders of the Earth's paleomagnetic field. Consequently, basalt core paleomagnetic data are valuable for the constraints they provide on plate tectonic motions, especially for oceanic plates such as the Pacific. Unfortunately, few Deep Sea Drilling Project (DSDP) and Ocean Drilling Program (ODP) boreholes have been cored very deeply into the ocean crust. The result is that there are only a few sites at which a large enough number of basalt flows have been cored to properly average secular variation (e.g., Kono, 1980, doi:10.2973/dsdp.proc.55.135.1980; Cox and Gordon, 1984, doi:10.1029/RG022i001p00047). Furthermore, there are a number of sites where basaltic core samples were retrieved but the cores were not measured. Often this occurs because leg scientists had more important sections to work on, or the section was ignored because it was too short to record enough time to average secular variation and obtain a reliable paleolatitude. Even though it may not be possible to determine a precise paleolatitude from such short sections, measurements from a small number of flows are important because they can be combined with other coeval paleomagnetic data from the same plate to calculate a paleomagnetic pole (Gordon and Cox, 1980, doi:10.1111/j.1365-246X.1980.tb02642.x; Cox and Gordon, 1984, doi:10.1029/RG022i001p00047). For this reason, I obtained samples for paleomagnetic measurements from eight Pacific sites (169, 170, 171, 581, 597, 800, 803, and 865), most of which have not been previously measured for paleomagnetism.

Myeloid differentiation factor 88 is required for resistance to Neospora caninum infection

Neospora caninum is an intracellular parasite that causes major economic impact on cattle raising farms, and infects a wide range of warm-blooded hosts worldwide. Innate immune mechanisms that lead to protection against this parasite are still unknown. In order to investigate whether myeloid differentiation factor 88 (MyD88) is required for resistance against N. caninum, genetically deficient mice (MyD88(-/-)) and wild type littermates were infected with live tachyzoites and the resistance to infection was evaluated. We found that sub-lethal tachyzoite doses induced acute mortality of MyD88(-/-) mice, which succumbed to infection due to uncontrolled parasite replication. Higher parasitism in MyD88(-/-) mice was associated with the lack of IL-12 production by dendritic cells, delayed IFN-gamma responses by NKT, CD4(+) and CD8(+) T lymphocytes, and production of high levels of IL-10. MyD88(-/-) mice replenished with IL-12 and IFN-gamma abolished susceptibility as the animals survived throughout the experimental period. We conclude that protective IFN-gamma-mediated immunity to N. caninum is dependent on initial MyD88 signaling, in a mechanism triggered by production of IL-12 by dendritic cells. Further knowledge on Toll-like receptor recognition of N. caninum antigens is encouraged, since it could generate new prophylactic and therapeutic tools to control parasite burden.

Blockade of vascular smooth muscle cell proliferation and intimal thickening after balloon injury by the sulfated oligosaccharide PI-88: Phosphomannopentaose sulfate directly binds FGF-2, blocks cellular signaling, and inhibits proliferation

Percutaneous transluminal coronary angioplasty is a frequently used interventional technique to reopen arteries that have narrowed because of atherosclerosis. Restenosis, or renarrowing of the artery shortly after angioplasty, is a major limitation to the success of the procedure and is due mainly to smooth muscle cell accumulation in the artery wall at the site of balloon injury. In the present study, we demonstrate that the antiangiogenic sulfated oligosaccharide, PI-88, inhibits primary vascular smooth muscle cell proliferation and reduces intimal thickening 14 days after balloon angioplasty of rat and rabbit arteries. PI-88 reduced heparan sulfate content in the injured artery wall and prevented change in smooth muscle phenotype. However, the mechanism of PI-88 inhibition was not merely confined to the antiheparanase activity of this compound. PI-88 blocked extracellular signal-regulated kinase-1/2 (ERK1/2) activity within minutes of smooth muscle cell injury. It facilitated FGF-2 release from uninjured smooth muscle cells in vitro, and super-released FGF-2 after injury while inhibiting ERK1/2 activation. PI-88 inhibited the decrease in levels of FGF-2 protein in the rat artery wall within 8 minutes of injury. PI-88 also blocked injury-inducible ERK phosphorylation, without altering the clotting time in these animals. Optical biosensor studies revealed that PI-88 potently inhibited (K-i 10.3 nmol/L) the interaction of FGF-2 with heparan sulfate. These findings show for the first time the capacity of this sulfated oligosaccharide to directly bind FGF-2, block cellular signaling and proliferation in vitro, and inhibit injury-induced smooth muscle cell hyperplasia in two animal models. As such, this study demonstrates a new role for PI-88 as an inhibitor of intimal thickening after balloon angioplasty. The full text of this article is available online at http://www.circresaha.org.

Portaria n?? 88, de 13 de junho de 2014: recomp??e a Comiss??o Gestora do Plano de Gest??o de Log??stica Sustent??vel da ENAP

Recomp??e a Comiss??o Gestora do Plano de Gest??o de Log??stica Sustent??vel da ENAP, criada pela Portaria n?? 259, de 20 de dezembro de 2012, com o intuito de elaborar, monitorar, avaliar e revisar o Plano de Gest??o de Log??stica Sustent??vel ??? PLS da ENAP, conforme determina o ?? 2?? do art. 6?? da Instru????o Normativa SLTI/MPOG n?? 10, de 12 de novembro de 2012. Esta Comiss??o homologa e acompanha o atendimento das metas pactuadas pela ENAP junto ?? Secretaria Executiva do Minist??rio do Planejamento, Or??amento e Gest??o, com vistas ?? utiliza????o racional de recursos combatendo o desperd??cio, promovendo a redu????o do consumo e a melhoria do gasto.

Auxílios de Estado sob a forma fiscal: O caso Açores - Proc. C-88/03

Mestrado em Fiscalidade

Imagens da catástrofe ecológica na ficção científica brasileira, de " Parada 88: o limite de alerta" a " Acquaria"

Dissertação apresentada para cumprimento dos requisitos necessários à obtenção do grau de Mestre em Ciências da Comunicação, área de especialização em Cinema e Televisão

Estudo comparativo entre estibogluconato de sódio BP 88® e antimoniato de meglumina no tratamento da leishmaniose cutânea II. Toxicidade bioquímica e cardíaca

Foi avaliada a toxicidade de dois antimoniais pentavalentes em 111 pacientes com leishmaniose cutânea. Quarenta e sete pacientes receberam antimoniato de meglumina (Grupo I) e 64 pacientes, estibogluconato de sódio BP 88® (Grupo II), 20mg SbV/kg/dia por 20 dias. Realizou-se a avaliação de aminotransferases, fosfatase alcalina, amilase, creatinina, uréia, exame de urina e eletrocardiograma, antes do tratamento e no décimo e vigésimo dias. Observou-se maior freqüência de valores anormais de aminotransferases no décimo e vigésimo dias de tratamento no grupo II (p < 0,001) e maior proporção de valores anormais de amilase no décimo dia no mesmo grupo (p < 0,001). Houve maior variação dos níveis de aminotransferases, fosfatase alcalina e amilase nos primeiros dez dias no grupo II (p < 0,01). No vigésimo dia observou-se maior variação nos níveis de aminotransferases no grupo II (p = 0,02 e p = 0,03, respectivamente). Quarenta e três porcento dos pacientes do grupo I e 54% dos pacientes do grupo II apresentaram alterações eletrocardiográficas (p = 0,30).

Óbito durante tratamento da leishmaniose tegumentar americana com stibogluconato de sódio bp 88® (shandong xinhua)

Os autores relatam a ocorrência de óbito em paciente portador da forma cutânea da LTA no município de Caxias-MA. Trata-se de paciente do sexo masculino, 22 anos, gari, portador de lesão ulcerada no membro inferior (perna esquerda), diagnosticado, após encontro do parasita (Leishmania) na lesão, tratado com stibogluconato de sódio BP88® (Shandong Xinhua) na dose de 10mg/Sb+5/kg/dia/20 dias. Após a 3ª dose apresentou dores articulares, naúseas, mal estar geral. Com a continuação da medicação houve agravamento do quadro com dor epigástrica e no hipocôndrio direito irradiando-se para o hemitórax homolateral. Após a 7ª dose apresentou dispnéia associado à dor torácica de leve intensidade. Na 9ª dose houve piora do quadro, mesmo assim continuou a usar o medicamento até a 11ª dose quando seu estado agravou-se. Foi internado, necessitando de tratamento intensivo. Nos exames realizados apresentou: 4,4 milhões de eritócitos, 10,6% de hemoglobina, 35% de hematócrito, 26.400 de leucócitos, basófilos e mielócitos (0), 59% de segmentados, 30% de linfócitos, 2% de monócitos, plaquetas (normais), glicose 42mg%, uréia 73mg%, creatinina (2,4mg%), eletrocardiograma (bloqueio de ramo direito). Veio a falecer tendo como causa do óbito, insuficiência cárdio respiratória. O relato atual mostra a necessidade de esclarecimento das equipes de saúde quanto ao uso dos Sb+5 e também lembrar o Ministério da Saúde quando da aquisição de novos produtos, preocupar-se com a qualidade e procedência do mesmo.