112 resultados para Insurance Contracts Act 54


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This is the first in a two-part analysis of Northern Ireland’s engagement with the climate governance regime created by the UK Climate Change Act 2008. It contends that UK devolution has shaped this national regime and may itself be shaped by the national low carbon transition, particularly in the case of the UK’s most devolved region. In essence, while Northern Ireland’s consent to the application of the Act appeared to represent a long-term commitment to share power in the interests of present and future generations and thus to devolution itself, this first article argues that it was also potentially illusory. The second article argues that making an effective commitment to climate governance will require its devolved administration to allow constitutional arrangements designed for conflict resolution to mature. Failure to do so will have important implications for the UK’s putative ‘national’ low carbon transition and the longer term viability of devolution in the region.

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The 1867 Reform Act in Britain extended the electoral franchise to the skilled but propertyless urban working classes. Using stock market data and exploiting the fact that foreign and domestic equities traded simultaneously on the London market, this paper finds that investors in British firms reacted negatively to the passage of this Act. We suggest that this finding is consistent with investors foreseeing future alterations of property rights arising from the pressure that the large newly enfranchised group would bring to bear on government policy. We also suggest that our findings appear to be more consistent with the Tory political competition explanation for the Act rather than the Whig threat-of-revolution explanation.

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There is an implicit assumption in the UK Treasury’s publications on public-private partnerships (PPP) – also more commonly known in the United Kingdom as private finance initiative (PFI) - that accountability and value for money (VFM) are related concepts. While recent academic studies on PPP/PFI (from now on as PFI) have focused on VFM, there is a notable absence of studies exploring the ‘presumed’ relationships between accountability and VFM. Drawing on Dubnick’s (Dubnick and Romzek, 1991, 1993; Dubnick, 1996, 1998, 2003, 2005; Dubnick and Justice, 2002) framework for accountability and PFI literature, we develop a research framework for exploring potential relationships between accountability and VFM in PFI projects by proposing alternative accountability cultures, processes and mechanisms for PFI. The PFI accountability model is then exposed to four criteria - warrantability, tractability, measurability and feasibility. Our preliminary interviews provide us guidance in identifying some of the cultures, processes and mechanisms indicated in our model which should enable future researchers to test not only the UK Government’s claimed relationships between accountability and VFM using more specific PFI empirical data, but also a potential relationship between accountability and performance in general.

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Artemisinin and related compounds are potent and widely used antimalarial drugs but their biochemical mode of action is not clear. There is strong evidence that ATP-dependent calcium transporters are a key target in the malarial parasite. However, work using Saccharomyces cerevisiae suggests that disruption of mitochondrial function is critical in the cell killing activity of these compounds. Here it is shown that, in the absence of reducing agents, artemisinin and artesunate targeted the S. cerevisiae calcium channels Pmr1p and Pmc1p. Both compounds affected the growth of yeast on fermentable and nonfermentable media. This growth inhibition was not seen in a yeast strain in which the genes encoding both calcium channels were deleted. In the presence of reducing agents, which break the endoperoxide bridge in the drugs, growth inhibition was only observed in nonfermentable media. This inhibition could be partially relieved by the addition of a free radical scavenger. These results suggest that the drugs have two biochemical modes of action - one acting by specific binding to calcium channels and one involving free radical production in the mitochondria.

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Hypertension, a key risk factor for stroke, cardiovascular disease and dementia, is associated with chronic vascular inflammation, and although poorly understood, putative mechanisms include proinflammatory responses induced by mechanical stretching, with cytokine release and associated upregulated expression of adhesion molecules. Because blood pressure increases with age, we measured baseline and tumour necrosis alpha (TNF-a)-stimulated CD11b/CD18 adhesion molecule expression on leucocytes to assess any association between the two. In 38 subjects (mean age 85 years), consecutively enrolled from Belfast Elderly Longitudinal Free-Living Aging Study (BELFAST), baseline and TNF-a-stimulated CD11b/CD18 expression on separated monocytes and neutrophils increased with systolic blood pressure >120 mmHg (p=0.05) and for lymphocytes, with diastolic blood pressure >80 mmHg (p<0.05).These findings show increased potential stickiness of intravascular cells with increasing blood pressure which is accentuated by TNF-a, and suggest mechanistic reasons why better hypertension control is important. 

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The results of a kinetic study of the oxidative dissolution of ruthenium dioxide hydrate to ruthenium tetroxide by periodate ions, IO4-, in acidic solution are described. The kinetics of dissolution give a good fit to a 'soft-centre' model in which the particles of RuO2.xH2O are assumed to be monodispersed, spherical but inhomogeneous in composition, comprising a difficult-to-corrode outer shell and a more easy-to-corrode inner core. In this work metaperiodate appears to act as a two-electron oxidant. The observed kinetics fit a reaction scheme in which the rate-determining step is the reaction between a surface site and an adsorbed IO4 ion and there is competitive adsorption by any IO3- present. In the absence and presence of an excess of IO3- ions, the overall activation energy for the corrosion reaction was determined to be 38 +/- 2 and 54 +/- 4 kJ mol-1, respectively.

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