940 resultados para 1042


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© 2015 Authors; published by Portland Press Limited. This work was supported by the Marie Curie Initial Training Network AccliPhot financed by the European Union [grant number PITN-GA-2012-316427 (to A.M. and O.E.)]; and the Deutsche Forschungsgemeinschaft [Cluster of Excellence on Plant Sciences, CEPLAS (EXC 1028) (to O.E.)].

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Funding This work was supported by the British Heart Foundation [grant number FS/11/2/28579]. © 2016 Authors; published by Portland Press Limited.

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Postprint

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We evaluate phosphorus (P) and biogenic barium (bio-Ba) as nutrient burial and export productivity indicators for the Late Cretaceous and early Paleogene, combining these with calcium carbonate (CaCO3), organic carbon (C), and bulk CaCO3 C isotopes (d13C). Sample ages span 36-71 Ma (~1 sample/0.5 m.y.) for a depth transect of sites in the western North Atlantic (Blake Nose, Ocean Drilling Program Leg 171B, Sites 1052, 1051, and 1050). We use a multitracer approach including redox conditions to investigate export productivity surrounding the global Paleocene d13C maximum (~57 Ma). Reducing conditions render most of the bio-Ba record not useful for export productivity interpretations. P and organic C records indicate that regional nutrient and organic C burial were high at ~61 and ~69 Ma, and low during the Paleocene d13C maximum, a time of proposed global high relative organic C burial. Observed organic C burial changes at Blake Nose cannot explain this C isotope excursion.

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In early atherosclerosis the frequency of activated monocytes in the peripheral circulation is amplified, and migration of monocytes into the walls of the aorta and large arteries is increased, due partly to de novo expression or activation of monocyte adhesion molecules. Although there is increasing evidence that CMRs (chylomicron remnants) are strongly atherogenic, the outcomes of interactions between blood monocytes and circulating CMRs are not known. Here, we have studied the effects of CRLPs (CMR-like particles) on THP-1 human monocyte oxidative burst. The particles induced a significant increase in reactive oxygen species within 1 h, which persisted for 24 h. We suggest that monocyte–CMR interactions may be important in early atherosclerosis when many activated monocytes are found in susceptible areas of the artery wall.

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The accumulation of foam cells in the artery wall causes fatty streaks, the first lesions in atherosclerosis. LDL (low-density lipoprotein) plays a major role in foam cell formation, although prior oxidation of the particles is required. Recent studies, however, have provided considerable evidence to indicate that CMRs (chylomicron remnants), which carry dietary lipids in the blood, induce foam cell formation without oxidation. We have shown that CMRs are taken up by macrophages and induce accumulation of both triacylglycerol and cholesterol, and that the rate of uptake and amount of lipid accumulated is influenced by the type of dietary fat in the particles. Furthermore, oxidation of CMRs, in striking contrast with LDL, inhibits, rather than enhances, their uptake and induction of lipid accumulation. In addition, the lipid accumulated after exposure of macrophages to CMRs is resistant to efflux, and this may be due to its sequestration in lysosomes. These findings demonstrate that CMRs induce pro-atherogenic changes in macrophages, and that their effects may be modulated by dietary factors including oxidized fats, lipophilic antioxidants and the type of fat present.

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A sufficiently complex set of molecules, if subject to perturbation, will self-organise and show emergent behaviour. If such a system can take on information it will become subject to natural selection. This could explain how self-replicating molecules evolved into life and how intelligence arose. A pivotal step in this evolutionary process was of course the emergence of the eukaryote and the advent of the mitochondrion, which both enhanced energy production per cell and increased the ability to process, store and utilise information. Recent research suggest that from its inception life embraced quantum effects such as “tunnelling” and “coherence” while competition and stressful conditions provided a constant driver for natural selection. We believe that the biphasic adaptive response to stress described by hormesis – a process that captures information to enable adaptability, is central to this whole process. Critically, hormesis could improve mitochondrial quantum efficiency, improving the ATP/ROS ratio, while inflammation, which is tightly associated with the aging process, might do the opposite. This all suggests that to achieve optimal health and healthy ageing, one has to sufficiently stress the system to ensure peak mitochondrial function, which itself could reflect selection of optimum efficiency at the quantum level.

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Gracias al crecimiento, expansión y popularización de la World Wide Web, su desarrollo tecnológico tiene una creciente importancia en la sociedad. La simbiosis que protagonizan estos dos entornos ha propiciado una mayor influencia social en las innovaciones de la plataforma y un enfoque mucho más práctico. Nuestro objetivo en este artículo es describir, caracterizar y analizar el surgimiento y difusión del nuevo estándar de hipertexto que rige la Web; HTML5. Al mismo tiempo exploramos este proceso a la luz de varias teorías que aúnan tecnología y sociedad. Dedicamos especial atención a los usuarios de la World Wide Web y al uso genérico que realizan de los Medios Sociales o "Social Media". Sugerimos que el desarrollo de los estándares web está influenciado por el uso cotidiano de este nuevo tipo de tecnologías y aplicaciones. 

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vol. 19, n. 2, p. 211-223, jul./dez. 2015.

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v. 19, n. 2, p. 191-210, jul./dez. 2015.

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ASA (acetylsalicylic acid) is an NSAID (non-steroidal anti-inflammatory drug). ASA has gained attention as a potential chemopreventive and chemotherapeutic agent for several neoplasms. The aim of this study was to analyse the possible antitumoural effects of ASA in two erythroleukaemic cell lines, with or without the MDR (multidrug resistance) phenotype. The mechanism of action of different concentrations of ASA were compared in K562 (non-MDR) and Lucena (MDR) cells by analysing cell viability, apoptosis and necrosis, intracellular ROS (reactive oxygen species) formation and bcl-2, p53 and cox-2 gene expression. ASA inhibited the cellular proliferation or induced toxicity in K562 and Lucena cell lines, irrespective of the MDR phenotype. The ASA treatment provoked death by apoptosis and necrosis in K562 cells and only by necrosis in Lucena cells. ASA also showed antioxidant activity in both cell lines. The bcl-2, p53 and cox-2 genes in both cell lines treated with ASA seem to exhibit different patterns of expression. However, normal lymphocytes treated with the same ASA concentrations were more resistant than tumoral cells. The results of this work show that both cell lines responded to treatment with ASA, demonstrating a possible antitumoral and anti-MDR role for this drug.

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Vale la pena aclarar que este trabajo fue realizado a finales del año 2000, por consiguiente las cifras que aquí se encuentran han podido sufrir variaciones durante el presente año. ¿Existe alguna relación entre esta guerra que nos azota desde hace más de cuatro décadas y los niveles de pobreza que presenta el país? Por conflicto armado me refiero básicamente al problema con la guerrilla. A los secuestros, a las extorsiones, a los bloqueos a las carreteras, a las voladuras de torres de energía y oleoductos, y a las demás acciones terroristas. Mientras que por pobreza hago alusión a una mayor escasez de nuestros limitados recursos. A que la «torta de la riqueza» que nos tenemos que repartir todos los colombianos se hace cada vez más pequeña. Y lo que es peor aún, que la porción que les corresponde a los ciudadanos menos favorecidos es la más afectada. ¿El conflicto armado que actualmente está padeciendo nuestro país es entonces una causa o una consecuencia de la pobreza? Por una parte, la incapacidad del Estado para satisfacer las necesidades básicas de muchos ciudadanos (educación, salud, seguridad, empleo, etc.) es causa directa de nuestro conflicto armado. Por otra, el conflicto armado le quita competitividad a nuestros productos, provoca una fuga masiva de capital tanto económico como humano, produce desempleo, etc. El problema adquiere más bien la dimensión y las características de un círculo vicioso. Yo considero que se genera violencia cuando hay un Estado incapaz de satisfacer las necesidades más elementales de algunos miembros de la sociedad. Sin embargo, de la misma manera creo que toda forma de violencia destruye la riqueza. Sin embargo, el Estado colombiano es ineficiente y no alcanza a proporcionarle a una enorme cantidad de compatriotas.