4,038 research outputs found

    A Modified Crank-Nicolson Method

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    In order to obtain a numerical solution to the heat equation using finite differences, either implicit or explicit equations are used to formulate a solution. The advantage in an explicit formulation is its simplicity and minimal computer storage requirements while its disadvantage is its instability. The opposite is true for an implicit formulation such as the Crank-Nicolson method; although it is stable it is more difficult to implement and requires a much larger memory capacity. In this paper we examine the accuracy and stability of a hybrid approach, a modified Crank-Nicolson formulation, that combines the advantageous features of both the implicit and explicit formulations. This hybrid approach results in a 20% reduction in the amount of work required compared to the standard Crank-Nicolson solution if both methods use a special tridiagonal system solver. If Gaussian elimination is used, the modified Crank-Nicolson approach reduces the amount of work by 87%. Regardless of the linear system solver used, the modified Crank-Nicolson approach reduces by 50% the memory requirement of the standard Crank-Nicolson method

    Toronto City Hall and Square

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    Thesis (M.Arch.)--Massachusetts Institute of Technology, Dept. of Architecture, 1958.ACCOMPANYING drawings held by MIT Museum.by David Ernest Horne.M.Arch

    Preservation and the ADA : adapting the historic building for accessibility

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    From Dome to Disease: The Respiratory Toxicity of Volcanic Cristobalite

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    Exposure to fine-grained volcanic ash can potentially cause acute and chronic respiratory disease. The toxicity of ash is likely to vary depending on the type and style of eruption; eruptions at dome-forming volcanoes, in particular, can produce ash containing substantial quantities of respirable crystalline silica, a recognised human carcinogen and causative agent of silicosis. Volcanic domes crystallise crystalline silica as cristobalite, which is metastable at dome-forming temperatures (ca. 850 °C), through deposition from silica-saturated vapours and through devitrification of volcanic glass. Five dome-forming volcanoes are studied to constrain the hazard posed by volcanic cristobalite, including: Colima, Mexico; Merapi, Indonesia; Mount St. Helens, USA; Santiaguito, Guatemala; and Unzen, Japan. The evolution of the cristobalite hazard is investigated from crystallisation in volcanic settings to its potential effect on biological systems, through a series of petrological, physicochemical and toxicological studies. We rationalise the presence of metastable cristobalite below its stability field in all domes studied by way of a textural investigation, and conclude that the incorporation of aluminium and sodium into the silica structure facilitates crystallisation. Since particle toxicology is dependent on composition and structure, the observation of cation substitutions is expanded in a geochemical and thermodynamic investigation of volcanic cristobalite to constrain its mineralogy. We find that incorporation of 1-4 wt. % aluminium leads to a poorly-ordered cristobalite structure. This investigation facilitates a mineralogical comparison of the cristobalite hazard among volcanic locations and provides the framework for assessing volcanic cristobalite toxicity. We investigate the ability of volcanic ash to elicit an in vitro pro-inflammatory response, focusing on silica-mediated experiments, and relate the influence of structure and composition to the potential physiological burden. We find that volcanic cristobalite can be mineralogically considered as a single entity among locations, and that cristobalite-bearing ash is less toxic than expected. Nonetheless, we recommend that eruptions be considered on a case-by-case basis to most effectively aid the risk mitigation work of disaster managers globally

    Vascular regulation of endogenous fibrinolysis in man

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    The initiation, modulation and resolution of thrombus associated with eroded or unstable coronary plaques are critical determinants of acute coronary events. This itself is dependent on the cellular function of the surrounding endothelium and vascular wall. In particular, the regulation of vascular tone and the acute release of tissue plasminogen activator by the endothelium make important contributions to the defence against intravascular thrombosis. These aspects of endothelial function will provide major new insights into the pathophysiology of cardiovascular disease, and to shape future therapeutic interventions.The experimental medicine models presented here originate from an early interest in exploring these novel aspects of endothelial function, and in particular, the acute release of the endothelium-derived fibrinolytic factor, tissue plasminogen activator. This model was initiated, developed and applied to a diverse range of physiological and pathophysiological circumstances that have informed health and disease. Publications are grouped into 5 main sections.Section 1 describes the early validation and exploration of the model to stimulate acute tissue plasminogen activator release using a variety of physiological and pathophysiological mediators. This describes the early identification of potent stimulators of acute tissue plasminogen activator release including substance P, bradykinin, desmopressin and thrombin receptor agonists. This work was extended to demonstrate the important role of nitric oxide and vascular inflammation in this process. Subsequent sections cover the application of these techniques in patient populations with a predisposition to cardiovascular disease (Section 2) as well as with established (Section 3) and end-stage disease (Section 4). These sections also explore the potentially important modulation of the renin-angiotensin system with particular reference to angiotensin-converting enzyme inhibition and the role of bradykinin. Section 5 contains some miscellaneous work and reviews of the subject area bring together the key aspects of the field as well as an important study to address the vascular endothelial function in patients with a rare haematological deficiency, type 3 von Willebrand disease

    Recognition of Foreign Governments and Its Effect on Private Rights

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    Studies into endogenous fibrinolysis in the peripheral and coronary vascular beds of man

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    BACKGROUND: Acute myocardial infarction is caused by thrombotic occlusion of a coronary artery compromised by atheromatous plaque. The interplay between acute plaque rupture or erosion and the local haemostatic and fibrinolytic activities are critical determinants in the initiation and resolution of the thrombotic complications of coronary atheroma. This is exemplified by the high rate of spontaneous reperfusion in the infarct related artery after acute myocardial infarction.OBJECTIVES: The aims of the thesis were: first, to establish a selective, specific and reproducible model for assessing endothelial function and acute endogenous fibrinolytic capacity in vivo in the peripheral circulation of man; second, to characterise the underlying mechanisms of the fibrinolytic response in this model; third, to compare the acute endogenous fibrinolytic capacity in health and disease; fourth, to examine the influence of therapeutic intervention on the fibrinolytic response; and finally, fifth, to apply this model to the coronary circulation in order to determine the acute coronary fibrinolytic response and assess its relationship with the extent of coronary atheroma.METHODS: Peripheral circulation. Blood flow and plasma fibrinolytic parameters were determined in both forearms using venous occlusion plethysmography and blood samples withdrawn from the antecubital fossae. The brachial artery of the nondominant forearm was cannulated and intra-artenal drugs administered. Plasma fibrinolytic parameters were determined using enzyme linked immunosorbant and photometric methods. The mechanisms of substance P action were explored using neurokinin type 1 receptor antagonism, nitric oxide synthase inhibition and the nitric oxide donor, sodium nitroprusside. The acute fibrinolytic response was examined in habitual cigarette smokers and patients with hypercholesterolaemia: the latter were also assessed following 6 weeks of lipid lowering therapy. Coronary circulation. Following diagnostic coronary angiography, the proximal coronary artery plaque volume was determined using computerised three dimensional reconstruction of intravascular ultrasound images. Blood flow and fibrinolytic responses to selective left anterior descending coronary artery infusion were assessed using intracoronary ultrasound and Doppler, and coronary sinus and arterial blood sampling.RESULTS: Intrabrachial substance P infusion was well tolerated and produced reproducible increases in forearm blood flow and tissue plasminogen activator release without affecting plasminogen activator inhibitor type 1 and von Willebrand factor concentrations. In contrast, endothelin-1 and L-monomethyl arginine infusion did not cause acute tissue plasminogen activator release. The response to substance P infusion appears to be dependent on the endothelial cell neurokinin type 1 receptor, and is, in part, mediated by the L-arginine:nitric oxide pathway. Whilst endothelium-dependent vasomotion was impaired in both cigarette smokers and patients with hypercholesterolaemia, tissue plasminogen activator release was diminished only in cigarette smokers and was unaffected by hypercholesterolaemia or lipid lowering therapy. Coronary fibrinolytic activity, but not endothelium-dependent coronary vasodilatation, inversely correlated with the volume of coronary artery atheroma.CONCLUSIONS: A model to assess the acute endogenous fibrinolytic capacity has been developed and characterised which was well tolerated and reproducible. Cigarette smoking, but not hypercholesterolaemia, is associated with an impairment of the acute tissue plasminogen activator release which may, in part, explain the increased propensity of smokers to sustain an acute myocardial infarction as well as to respond more favourably to thrombolytic therapy. The apparently normal fibrinolytic response in patients with hypercholesterolaemia indicates that endothelial dysfunction can be manifest in separate distinct pathways depending upon the nature of the insult. Finally, the demonstration of an association between the extent of coronary atheroma and the local endogenous fibrinolytic response provides a potentially important mechanism through which endothelial dysfunction can directly contribute to the thrombotic consequences of coronary artery disease

    La Pensee Morale Et Religieuse De Francois De La Mothe Le Vayer

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