The structural response of Elliptical Hollow Sections (EHS) under combined biaxial bending and compression is investigated in this paper. The research is conducted at the cross-sectional level and is based primarily upon laboratory testing and Finite element modelling. A series of experiments with various load eccentricities about both the major and minor axes have been conducted so as to investigate the interaction between compression and biaxial bending. The measured geometric and material properties of the test specimens, together with the full load-deformation histories have been reported. The test data have been supplemented by further results generated through parallel numerical studies. The combined structural performance data have been used to verify proposed interaction expressions; these have been developed in accordance with Eurocode 3 for ease of future incorporation.
"9. Why Does Asthma Become Persistent?." American Journal of Respiratory and Critical Care Medicine, 153(6_pt_2), pp. S23–S25
Tubular construction is synonymous with modern architecture. The familiar range of tubular sections – square, rectangular and circular hollow sections – has been recently extended to include elliptical hollow sections (EHSs). Due to differing flexural rigidities about the two principal axes, these new sections combine the elegance of circular hollow sections with the improved structural efficiency in bending of rectangular hollow sections. Following the introduction of structural steel EHSs, a number of investigations into their structural response have been carried out. This paper presents a state-of-the-art review of recent research on EHSs together with a sample of practical applications. The paper addresses fundamental research on elastic local buckling and post-buckling, cross-section classification, response in shear, member instabilities, connections and the behaviour of concrete-filled EHSs. Details of full-scale testing and numerical modelling studies are described, and the generation of statistically validated structural design rules, suitable for incorporation into international design codes, is outlined.
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At present, asthma represents a substantial burden on health care resources in all countries so far studied. The costs of asthma are largely due to uncontrolled disease, and are likely to rise as its prevalence and severity increase. Costs could be significantly reduced if disease control is improved. A large proportion of the total cost of illness is derived from treating the consequences of poor asthma control-direct costs, such as emergency room use and hospitalizations. Indirect costs, which include time off work or school and early retirement, are incurred when the disease is not fully controlled and becomes severe enough to have an effect on daily life. In addition, quality of life assessments show that asthma has a significant socioeconomic impact, not only on the patients themselves, but on the whole family. Underuse of prescribed therapy, which includes poor compliance, significantly contributes towards the poor control of asthma. The consequences of poor compliance in asthma include increased morbidity and sometimes mortality, and increased health care expenditure. To improve asthma management, international guidelines have been introduced which recommend an increase in the use of prophylactic therapy. The resulting improvements in the control of asthma will reduce the number of hospitalizations associated with asthma, and may ultimately produce a shift within direct costs, with subsequent reductions in indirect costs. In addition, costs may be reduced by improving therapeutic interventions and through effective patient education programmes. This paper reviews current literature on the costs of asthma to assess how effectively money is spent and, by estimating the proportion of the cost attributable to uncontrolled disease, will identify where financial savings might be made.
The rise in life expectancy worldwide has been accompanied by an increased incidence of age-related diseases, representing an enormous burden on healthcare services and society. All vital organs lose function with age, and this is well described in the lung, with a progressive decline in pulmonary function after the age of about 25 years. The lung ages, like any other organ, with progressive functional impairment and reduced capacity to respond to environmental stresses and injury. Normal physiological ageing results in enlarged alveolar spaces and loss of lung elasticity in the elderly known as 'senile emphysema', whereas in COPD there is destruction of the alveolar walls and fibrosis of peripheral airways. However, COPD shows striking age-associated features, such as an increase in cellular senescence, stem cell exhaustion, increased oxidative stress, alteration in the extracellular matrix and a reduction in endogenous antiageing molecules and protective pathways such as autophagy. In this review we discuss the evidence showing how oxidative stress induces accelerated ageing by upregulating the phosphatidylinositol-4,5-bisphosphate 3-kinase/AKT/mechanistic target of rapamycin signalling pathway resulting in depletion of stem cells, defective autophagy, reduced antioxidant responses and defective mitochondrial function thus generating further oxidative stress. Understanding the mechanisms of accelerated ageing in COPD may identify novel therapeutic approaches.
