960 resultados para Juba II., King of Mauritania.


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"Poems ('Vers libre') by Carmen Sylva": vol. II, p. 175-222.

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Five manganese complexes in an N 4O 2 donor environment have been prepared. Four of the compounds involve aroyl hydrazone as ligands and manganese is in a +2 oxidation state. The fifth compound was prepared using N,Nprime-o-phenylenebis(salicylideneimine) and imidazole as ligands where manganese is present in +3 oxidation state. X-ray crystal structure of one Mn +2 compound and the Mn +3 compound was determined. The relative stabilities of the Mn +2 and Mn +3 oxidation states were analyzed using the structural data and MO calculations. Manganese(II) complexes of four aroyl hydrazone ligands were prepared and characterized by different physicochemical techniques. The complexes are of the type Mn(L) 2, where L stands for the deprotonated hydrazone ligand. One of the compounds, Mn(pybzhz) 2, was also characterized by single crystal structure determination. In all these complexes, the Mn(II) is in an N 4O 2 donor environment and the Mn(II) center cannot be oxidized either chemically or electrochemically. However, when another ligand Ophsal is used to give the compound [Mn(Ophsal)(imzH) 2]ClO 4, which was also characterized by X-ray crystal structure determination, manganese can easily avail the +3 oxidation state. The relative stabilities of the +2 and +3 oxidation states of manganese were analyzed and it was concluded that the extent of distortion from the perfect octahedral geometry is the main controlling factor in these cases. © 2004 Elsevier B.V. All rights reserved.

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The exponential growth of studies on the biological response to ocean acidification over the last few decades has generated a large amount of data. To facilitate data comparison, a data compilation hosted at the data publisher PANGAEA was initiated in 2008 and is updated on a regular basis (doi:10.1594/PANGAEA.149999). By January 2015, a total of 581 data sets (over 4 000 000 data points) from 539 papers had been archived. Here we present the developments of this data compilation five years since its first description by Nisumaa et al. (2010). Most of study sites from which data archived are still in the Northern Hemisphere and the number of archived data from studies from the Southern Hemisphere and polar oceans are still relatively low. Data from 60 studies that investigated the response of a mix of organisms or natural communities were all added after 2010, indicating a welcomed shift from the study of individual organisms to communities and ecosystems. The initial imbalance of considerably more data archived on calcification and primary production than on other processes has improved. There is also a clear tendency towards more data archived from multifactorial studies after 2010. For easier and more effective access to ocean acidification data, the ocean acidification community is strongly encouraged to contribute to the data archiving effort, and help develop standard vocabularies describing the variables and define best practices for archiving ocean acidification data.

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vol. II. Idylls of the king. To the queen.- vol. III. The princess. Maud. Enoch Arden. In memoriam.- vol. IV. Queen Mary. Harold. The lover's tale. Ballads and other poems. Sonnets. Translations, etc.- Vol. V. Tiresias and other poems. The promise of May. Demeter and other poems.- vol. VI. Becket. The cup. The falcon. The foresters. Balin and Balan. The death of Oenone, and other poems. Complete indexes.

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Cardiovascular diseases (CVDs) including, hypertension, coronary heart disease and heart failure are the leading cause of death worldwide. Hypertension, a chronic increase in blood pressure above 140/90 mmHg, is the single main contributor to deaths due to heart disease and stroke. In the heart, hypertension results in adaptive cardiac remodelling, including LV hypertrophy to normalize wall stress and maintain cardiac contractile function. However, chronic increases in BP results in the development of hypertensive heart disease (HHD). HHD describes the maladaptive changes during cardiac remodelling which result in reduced systolic and diastolic function and eventually heart failure. This includes ventricular dilation due to eccentric hypertrophy, cardiac fibrosis which stiffens the ventricular wall and microvascular rarefaction resulting in a decrease in coronary blood flow albeit an increase in energy demand. Chronic activation of the renin-angiotensin-system (RAS) with its effector peptide angiotensin (Ang)II plays a key role in the development of hypertension and the maladaptive changes in HHD. Ang II acts via the angiotensin type 1 receptor (AT1R) to mediate most of its pathological actions during HHD, including stimulation of cardiomyocyte hypertrophy, activation of cardiac fibroblasts and increased collagen deposition. The counter-regulatory axis of the RAS which is centred on the ACE2/Ang-(1-7)/Mas axis has been demonstrated to counteract the pathological actions of Ang II in the heart and vasculature. Ang-(1-7) via the Mas receptor prevents Ang II-induced cardiac hypertrophy and fibrosis and improves cardiac contractile function in animal models of HHD. In contrast, less is known about Ang-(1-9) although evidence has demonstrated that Ang-(1-9) also antagonises Ang II and is anti-hypertrophic and anti-fibrotic in animal models of acute cardiac remodelling. However, so far it is not well documented whether Ang-(1-9) can reverse established cardiac dysfunction and remodelling and whether it is beneficial when administered chronically. Therefore, the main aim of this thesis was to assess the effects of chronic Ang-(1-9) administration on cardiac structure and function in a model of Ang II-induced cardiac remodelling. Furthermore, this thesis aimed to investigate novel pathways contributing to the pathological remodelling in response to Ang II. First, a mouse model of chronic Ang II infusion was established and characterised by comparing the structural and functional effects of the infusion of a low and high dose of Ang II after 6 weeks. Echocardiographic measurements demonstrated that low dose Ang II infusion resulted in a gradual decline in cardiac function while a high dose of Ang II induced acute cardiac contractile dysfunction. Both doses equally induced the development of cardiac hypertrophy and cardiac fibrosis characterised by an increase in the deposition of collagen I and collagen III. Moreover, increases in gene expression of fibrotic and hypertrophic markers could be detected following high dose Ang II infusion over 6 weeks. Following this characterisation, the high dose infusion model was used to assess the effects of Ang-(1-9) on cardiac structural and functional remodelling in established disease. Initially, it was evaluated whether Ang-(1-9) can reverse Ang II-induced cardiac disease by administering Ang-(1-9) for 2-4 weeks following an initial 2 week infusion of a high dose of Ang II to induce cardiac contractile dysfunction. The infusion of Ang-(1-9) for 2 weeks was associated with a significant improvement of LV fractional shortening compared to Ang II infusion. However, after 4 weeks fractional shortening declined to Ang II levels. Despite the transient improvement in cardiac contractile function, Ang-(1-9) did not modulate blood pressure, LV hypertrophy or cardiac fibrosis. To further investigate the direct cardiac effects of Ang-(1-9), cardiac contractile performance in response to Ang-(1-9) was evaluated in the isolated Langendorff-perfused rat heart. Perfusion of Ang-(1-9) in the paced and spontaneously beating rat heart mediated a positive inotropic effect characterised by an increase in LV developed pressure, cardiac contractility and relaxation. This was in contrast to Ang II and Ang-(1-7). Furthermore, the positive inotropic effect to Ang-(1-9) was blocked by the AT1R antagonist losartan and the protein kinase A inhibitor H89. Next, endothelial-to-mesenchymal transition (EndMT) as a novel pathway that may contribute to Ang II-induced cardiac remodelling was assessed in Ang II-infused mice in vivo and in human coronary artery endothelial cells (HCAEC) in vitro. Infusion of Ang II to mice for 2-6 weeks resulted in a significant decrease in myocardial capillary density and this was associated with the occurrence of dual labelling of endothelial cells for endothelial and mesenchymal markers. In vitro stimulation of HCAEC with TGFβ and Ang II revealed that Ang II exacerbated TGF-induced gene expression of mesenchymal markers. This was not correlated with any changes in SMAD2 or ERK1/2 phosphorylation with co-stimulation of TGFβ and Ang II. However, superoxide production was significantly increased in HCAEC stimulated with Ang II but not TGFβ. Finally, the role of Ang II in microvesicle (MV)-mediated cardiomyocyte hypertrophy was investigated. MVs purified from neonatal rat cardiac fibroblasts were found to contain detectable Ang II and this was increased by stimulation of fibroblasts with Ang II. Treatment of cardiomyocytes with MVs derived from Ang II-stimulated fibroblasts induced cardiomyocyte hypertrophy which could be blocked by the AT1R antagonist losartan and an inhibitor of MV synthesis and release brefeldin A. Furthermore, Ang II was found to be present in MVs isolated from serum and plasma of Ang II-infused mice and SHRSP and WKY rats. Overall, the findings of this thesis demonstrate for the first time that the actions of Ang-(1-9) in cardiac pathology are dependent on its time of administration and that Ang-(1-9) can reverse Ang II-induced cardiac contractile dysfunction by acting as a positive inotrope. Furthermore, this thesis demonstrates evidence for an involvement of EndMT and MV signalling as novel pathways contributing to Ang II-induced cardiac fibrosis and hypertrophy, respectively. These findings provide incentive to further investigate the therapeutic potential of Ang-(1-9) in the treatment of cardiac contractile dysfunction in heart disease, establish the importance of novel pathways in Ang II-mediated cardiac remodelling and evaluate the significance of the presence of Ang II in plasma-derived MVs.

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Two distinct maintenance-data-models are studied: a government Enterprise Resource Planning (ERP) maintenance-data-model, and the Software Engineering Industries (SEI) maintenance-data-model. The objective is to: (i) determine whether the SEI maintenance-data-model is sufficient in the context of ERP (by comparing with an ERP case), (ii) identify whether the ERP maintenance-data-model in this study has adequately captured the essential and common maintenance attributes (by comparing with the SEI), and (iii) proposed a new ERP maintenance-data-model as necessary. Our findings suggest that: (i) there are variations to the SEI model in an ERP-context, and (ii) there are rooms for improvements in our ERP case’s maintenance-data-model. Thus, a new ERP maintenance-data-model capturing the fundamental ERP maintenance attributes is proposed. This model is imperative for: (i) enhancing the reporting and visibility of maintenance activities, (ii) monitoring of the maintenance problems, resolutions and performance, and (iii) helping maintenance manager to better manage maintenance activities and make well-informed maintenance decisions.

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The structures of two 1:1 proton-transfer red-black dye compounds formed by reaction of aniline yellow [4-(phenyldiazenyl)aniline] with 5-sulfosalicylic acid and benzenesulfonic acid, and a 1:2 nontransfer adduct compound with 3,5-dinitrobenzoic acid have been determined at either 130 or 200 K. The compounds are 2-(4-aminophenyl)-1-phenylhydrazin-1-ium 3-carboxy-4-hydroxybenzenesulfonate methanol solvate, C12H12N3+.C7H5O6S-.CH3OH (I), 2-(4-aminophenyl)-1-hydrazin-1-ium 4-(phenydiazinyl)anilinium bis(benzenesulfonate), 2C12H12N3+.2C6H5O3S-, (II) and 4-(phenyldiazenyl)aniline-3,5-dinitrobenzoic acid (1/2) C12H11N3.2C~7~H~4~N~2~O~6~, (III). In compound (I) the diaxenyl rather than the aniline group of aniline yellow is protonated and this group subsequently akes part in a primary hydrogen-bonding interaction with a sulfonate O-atom acceptor, producing overall a three-dimensional framework structure. A feature of the hydrogen bonding in (I) is a peripheral edge-on cation-anion association involving aromatic C--H...O hydrogen bonds, giving a conjoint R1/2(6)R1/2(7)R2/1(4)motif. In the dichroic crystals of (II), one of the two aniline yellow species in the asymmetric unit is diazenyl-group protonated while in the other the aniline group is protonated. Both of these groups form hydrogen bonds with sulfonate O-atom acceptors and thee, together with other associations give a one-dimensional chain structure. In compound (III), rather than proton-transfer, there is a preferential formation of a classic R2/2(8) cyclic head-to-head hydrogen-bonded carboxylic acid homodimer between the two 3,5-dinitrobenzoic acid molecules, which in association with the aniline yellow molecule that is disordered across a crystallographic inversion centre, result in an overall two-dimensional ribbon structure. This work has shown the correlation between structure and observed colour in crystalline aniline yellow compounds, illustrated graphically in the dichroic benzenesulfonate compound.

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Healthcare-associated methicillin-resistant Staphylococcus aureus(MRSA) infection may cause increased hospital stay or, sometimes, death. Quantifying this effect is complicated because it is a time-dependent exposure: infection may prolong hospital stay, while longer stays increase the risk of infection. We overcome these problems by using a multinomial longitudinal model for estimating the daily probability of death and discharge. We then extend the basic model to estimate how the effect of MRSA infection varies over time, and to quantify the number of excess ICU days due to infection. We find that infection decreases the relative risk of discharge (relative risk ratio = 0.68, 95% credible interval: 0.54, 0.82), but is only indirectly associated with increased mortality. An infection on the first day of admission resulted in a mean extra stay of 0.3 days (95% CI: 0.1, 0.5) for a patient with an APACHE II score of 10, and 1.2 days (95% CI: 0.5, 2.0) for a patient with an APACHE II score of 30. The decrease in the relative risk of discharge remained fairly constant with day of MRSA infection, but was slightly stronger closer to the start of infection. These results confirm the importance of MRSA infection in increasing ICU stay, but suggest that previous work may have systematically overestimated the effect size.

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This study aimed to identify: i) the prevalence of malnutrition according to the scored Patient Generated-Subjective Global Assessment (PG-SGA); ii) utilization of available nutrition resources; iii) patient nutrition information needs; and iv) external sources of nutrition information. An observational, cross-sectional study was undertaken at an Australian public hospital on 191 patients receiving oncology services. According to PG-SGA, 49% of patients were malnourished and 46% required improved symptom management and/or nutrition intervention. Commonly reported nutrition-impact symptoms included: peculiar tastes (31%), no appetite (24%) and nausea (24%). External sources of nutrition information were accessed by 37%, with popular choices being media/internet (n=19) and family/friends (n=13). In a sub-sample (n=65), 32 patients were aware of the available nutrition resources, 23 thought the information sufficient and 19 patients had actually read them. Additional information on supplements and modifying side effects was requested by 26 patients. Malnutrition is common in oncology patients receiving treatment at an Australian public hospital and almost half require improved symptom management and/or nutrition intervention. Patients who read the available nutrition information found it useful, however awareness of these nutrition resources and the provision of information on supplementation and managing symptoms requires attention.

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This thesis is a study of naturally occurring radioactive materials (NORM) activity concentration, gamma dose rate and radon (222Rn) exhalation from the waste streams of large-scale onshore petroleum operations. Types of activities covered included; sludge recovery from separation tanks, sludge farming, NORM storage, scaling in oil tubulars, scaling in gas production and sedimentation in produced water evaporation ponds. Field work was conducted in the arid desert terrain of an operational oil exploration and production region in the Sultanate of Oman. The main radionuclides found were 226Ra and 210Pb (238U - series), 228Ra and 228Th (232Th - series), and 227Ac (235U - series), along with 40K. All activity concentrations were higher than the ambient soil level and varied over several orders of magnitude. The range of gamma dose rates at a 1 m height above ground for the farm treated sludge had a range of 0.06 0.43 µSv h 1, and an average close to the ambient soil mean of 0.086 ± 0.014 µSv h 1, whereas the untreated sludge gamma dose rates had a range of 0.07 1.78 µSv h 1, and a mean of 0.456 ± 0.303 µSv h 1. The geometric mean of ambient soil 222Rn exhalation rate for area surrounding the sludge was mBq m 2 s 1. Radon exhalation rates reported in oil waste products were all higher than the ambient soil value and varied over three orders of magnitude. This study resulted in some unique findings including: (i) detection of radiotoxic 227Ac in the oil scales and sludge, (ii) need of a new empirical relation between petroleum sludge activity concentrations and gamma dose rates, and (iii) assessment of exhalation of 222Rn from oil sludge. Additionally the study investigated a method to determine oil scale and sludge age by the use of inherent behaviour of radionuclides as 228Ra:226Ra and 228Th:228Ra activity ratios.

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Nitric oxide is known to be an important inflammatory mediator, and is implicated in the pathophysiology of a range of inflammatory disorders. The aim of this study was to determine the localization and distribution of endothelial NOS (NOS-II) in human gingival tissue, and to ascertain if human gingival fibroblasts express NOS-II when stimulated with interferon gamma (IFN-gamma) and bacterial lipopolysaccharide (LPS). The distribution of NOS-II in inflamed and non-inflamed specimens of human gingivae was studied using a monoclonal antibody against nitric oxide synthase II. Cultures of fibroblasts derived from healthy human gingivae were used for the cell culture experiments. The results from immunohistochemical staining of the tissues indicated an upregulation of NOS-II expression in inflamed compared to non-inflamed gingival tissue. Fibroblasts and inflammatory cells within the inflamed connective tissue were positively stained for NOS-II. In addition, basal keratinocytes also stained strongly for NOS-II, in both healthy and inflamed tissue sections. When cultured human gingival fibroblasts were stimulated by INF-gamma and Porphyromonas gingivalis LPS, NOS-II was more strongly expressed than when the cells were exposed to LPS or IFN-gamma alone. These data suggest that, as for other inflammatory diseases, NO plays a role in the pathophysiology of periodontitis.