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Abstract Cold‐formed steel (CFS) products are extremely versatile and can be used in multiple applications. Recent experiments tests by the authors have shown that mobilising composite action within systems comprising cold‐formed steel beams and lightweight concrete is feasible and can lead to substantial improvements in structural performance. However, their behaviour subjected to elevated temperatures has yet to be investigated; this is, therefore, the focus of the present study. The results of two tests on CFS‐LWC beams at ambient and elevated temperatures are reported. A numerical modelling study using fire dynamics simulator (FDS) software is then described in which the temperature development was successfully replicated.

No abstract is provided for this article.

Sudden cardiac death or unheralded acute coronary syndromes are common initial manifestations of coronary atherosclerosis and most such events occur at sites of non-flow limiting coronary atherosclerosis. Autopsy data suggests that plaque composition is a key determinant of the propensity of atherosclerotic lesions to provoke clinical events. Most of these events are related to plaque rupture and subsequent thrombotic occlusion at the site of non-flow limiting atherosclerotic lesions in epicardial coronary arteries. Detection of these non-obstructive, lipid rich, high-risk plaques may have an important impact on the prevention of acute myocardial infarction and sudden death. Currently, there are several intravascular tools capable of locally evaluating determinants of plaque vulnerability such as the size of the lipid core, thickness of the fibrous cap, inflammation within the cap and positive remodeling. These new modalities have the potential to provide insights into the pathophysiology of the natural history of coronary plaque by means of prospective studies.

Although intracoronary ultrasonography allows detailed tomographic imaging of the arterial wall, it fails to provide data on the structural architecture and longitudinal extent of arterial disease. This information is essential for decision making during therapeutic interventions. Three-dimensional reconstruction techniques offer visualization of the complex longitudinal architecture of atherosclerotic plaques in composite display. Progress in computer hardware and software technology have shortened the reconstruction process and reduced operator interaction considerably, generating three-dimensional images with delineation of mural anatomy and pathology. The indications for intravascular ultrasonography will grow as the technique offers the unique capability of providing ultrasonic histology of the arterial wall, and the need for a three-dimensional display format for comprehensive analysis is increasingly recognized. Consequently, three-dimensional imaging is being rapidly implemented in the catheterization laboratories for guidance of intracoronary interventions and detailed assessment of their results. However exciting the prospects may be, three-dimensional reconstructions at present remain partially artificial because the true spatial position of the imaging catheter tip is not recorded, and shifts in its location and curves of the arterial lumen result in pseudoreconstructions rather than true reconstructions. In this report, we address the principles of three-dimensional reconstruction with a critical review of its limitations. Potential solutions for refinement of this exciting imaging modality are presented.

To assess the safety and performance of the Nobori drug-eluting stent with biodegradable polymer versus the TAXUS drug-eluting stent with permanent polymer, in the treatment of patients with de novo coronary artery lesions.NOBORI 1 was a multicentre, randomised (2:1), prospective, controlled, clinical trial which enrolled 363 patients (238 Nobori and 125 TAXUS) with up to two de novo lesions in two epicardial vessels. The primary endpoint was in-stent late loss at nine months, while secondary endpoints included safety and efficacy up to five years. At five years, clinical data were available for 350 patients (96%). There were no differences in the composite of death and myocardial infarction (10.9% vs. 11.2%) and target lesion failure (9.2% and 10.4%), while ischaemia- and non-ischaemia-driven target lesion revascularisations were less frequent in the Nobori (6.3%) than in the TAXUS arm (16.0%). The rates of stent thrombosis (definite and probable according to the ARC definitions) were 0.0% and 3.2%, in the Nobori and TAXUS stents, respectively (p=0.014).Five years after implantation, the Nobori DES resulted in durable treatment effects with very low TLR and no stent thrombosis. The study was not powered to assess the differences in clinical endpoints. These data are hypothesis-generating.

Chronic obstructive pulmonary disease (COPD), which is caused primarily by cigarette smoking, is a major health problem worldwide. The progressive decline in lung function that occurs in COPD is a result of persistent inflammation of the airways and destruction of the lung parenchyma. Despite the key role of inflammation in the pathogenesis of COPD, treatment with corticosteroids — normally highly effective antiinflammatory drugs — has little therapeutic benefit. This corticosteroid resistance is largely caused by inactivation of histone deacetylase 2 (HDAC2), which is critical for the transrepressive activity of the glucocorticoid receptor (GR) that mediates the antiinflammatory effect of corticosteroids. Here, we show that in alveolar macrophages from patients with COPD, S-nitrosylation of HDAC2 is increased and that this abolishes its GR-transrepression activity and promotes corticosteroid insensitivity. Cys-262 and Cys-274 of HDAC2 were found to be the targets of S-nitrosylation, and exogenous glutathione treatment of macrophages from individuals with COPD restored HDAC2 activity. Treatment with sulforaphane, a small-molecule activator of the transcription factor nuclear factor erythroid 2–related factor 2 (NRF2), was also able to denitrosylate HDAC2, restoring dexamethasone sensitivity in alveolar macrophages from patients with COPD. These effects of sulforaphane were glutathione dependent. We conclude that NRF2 is a novel drug target for reversing corticosteroid resistance in COPD and other corticosteroid-resistant inflammatory diseases.