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Percutaneous coronary intervention (PCI) of multivessel and/or left main stem disease have been shown to be potentially legitimate revascularization alternatives in appropriately selected patients. Risk stratification is an important component in guiding patients to identify the most appropriate revascularization modality (PCI or coronary artery bypass grafting [CABG]) in conjunction with the Heart Team. The aim of this paper is to give the clinician a concise overview of the important established and evolving contemporary risk models in aiding this decision-making process. Risk models, based on clinical and anatomical variables alone, the novel concept of functional anatomical risk scores, and risk models combining aspects from both clinical and anatomical scores, are all discussed. The emerging concepts of the patient-empowered risk/benefit tradeoff between PCI and CABG to help personalize the choice of revascularization modality are also explored.
Conference Abstract| February 01 1983 Steroids Selectively Increase β-Adrenoceptors in Foetal Alveoli: Autoradiographic Evidence Peter J. Barnes; Peter J. Barnes 1Cardiovascular Research Institute, University of California, San Francisco, U.S.A. Search for other works by this author on: This Site PubMed Google Scholar M. M. Jacobs; M. M. Jacobs 2Cardiovascular Research Institute, University of California, San Francisco, U.S.A. Search for other works by this author on: This Site PubMed Google Scholar J. M. Roberts J. M. Roberts 3Cardiovascular Research Institute, University of California, San Francisco, U.S.A. Search for other works by this author on: This Site PubMed Google Scholar Author and article information Publisher: Portland Press Ltd Online ISSN: 1470-8736 Print ISSN: 0143-5221 © 1983 The Biochemical Society and the Medical Research Society1983 Clin Sci (Lond) (1983) 64 (2): 10P. https://doi.org/10.1042/cs064010P Views Icon Views Article contents Figures & tables Video Audio Supplementary Data Peer Review Share Icon Share Facebook Twitter LinkedIn Email Cite Icon Cite Get Permissions Citation Peter J. Barnes, M. M. Jacobs, J. M. Roberts; Steroids Selectively Increase β-Adrenoceptors in Foetal Alveoli: Autoradiographic Evidence. Clin Sci (Lond) 1 February 1983; 64 (2): 10P. doi: https://doi.org/10.1042/cs064010P Download citation file: Ris (Zotero) Reference Manager EasyBib Bookends Mendeley Papers EndNote RefWorks BibTex toolbar search Search Dropdown Menu toolbar search search input Search input auto suggest filter your search All ContentAll JournalsClinical Science Search Advanced Search This content is only available as a PDF. © 1983 The Biochemical Society and the Medical Research Society1983 Article PDF first page preview Close Modal You do not currently have access to this content.
Aluminum alloys are employed in a range of structural engineering applications, supported by many international design standards, but plastic design methods are generally not permitted. In the second part of this study, an extensive numerical parametric study is conducted to assess the effect of key parameters, such as cross section slenderness, cross section aspect ratio, and moment gradient on the strength, strain hardening, and moment redistribution behavior of aluminum alloy continuous beams. The key input parameters and findings are reported herein. Based on both the experimental and parametric numerical results, the design provisions of the American, Australian/New Zealand, and European specifications as well as the traditional plastic design method, the plastic hinge method, and the continuous strength method (CSM) for indeterminate structures, the scope of which is extended in the present study, have been evaluated. The design strengths predicted by the three specifications were found to be rather conservative, while the predications of the latter three methods are more precise and consistent. The results reveal that strain hardening at the cross-sectional level and moment redistribution at the global system level have significant influence on the performance of stocky (plastic and compact sections) aluminum alloy members, which should be accounted for in design. Following reliability analysis, proposals are made for revised design provisions.
Intravascular imaging has enabled in vivo assessment of coronary artery pathology and detection of plaque characteristics that are associated with increased vulnerability. Prospective invasive imaging studies of coronary atherosclerosis have demonstrated that invasive imaging modalities can detect lesions that are likely to progress and cause cardiovascular events and provided unique insights about atherosclerotic evolution. However, despite the undoubted value of the existing imaging techniques in clinical and research arenas, all the available modalities have significant limitations in assessing plaque characteristics when compared with histology. Hybrid/multimodality intravascular imaging appears able to overcome some of the limitations of standalone imaging; however, there are only few histology studies that examined their performance in evaluating plaque pathobiology. In this article, we review the evidence about the efficacy of standalone and multi-modality/hybrid intravascular imaging in assessing plaque morphology against histology, highlight the advantages and limitations of the existing imaging techniques and discuss the future potential of emerging imaging modalities in the study of atherosclerosis.
Nitric oxide (NO) plays a key role as a vasodilator, neurotransmitter, and inflammatory mediator in the airways and is produced in increased amounts in asthma. It may have beneficial effects on airways function as a bronchodilator and is the neurotransmitter of bronchodilator nerves in human airways. On the other hand, NO may have deleterious effects on the airways as a vasodilator by increasing plasma exudation, and may also amplify the asthmatic inflammatory response. Proinflammatory cytokines and oxidants increase the expression of an inducible form of NO synthase (NOS) in airway epithelial cells in asthma, and this may underlie the increased levels of NO found in exhaled air of asthmatic patients. Inducible NOS is inhibited by glucocorticoids, but selective inhibitors of this enzyme may have therapeutic potential in asthma.
Autonomic nerves control many aspects of airway function, including smooth muscle tone, epithelial cell function, mucus secretion, bronchial flow and permeability, and inflammatory mediator release. There is considerable evidence that there may be abnormalities of autonomic function in asthma, perhaps as a result of airway inflammation. Inflammatory mediators might stimulate bronchial afferent receptors (irritant receptors and C-fibre endings) to produce reflex cholinergic bronchoconstriction. Anticholinergic drugs have not proved to be very effective in controlling clinical asthma, however, suggesting that cholinergic reflex mechanisms may not play a major role. Adrenergic abnormalities have been described in asthma. There is no direct sympathetic neural control of airway smooth muscle, suggesting that circulating catecholamines may regulate airway tone, and counteract the effect of inflammatory mediators in asthma. Surprisingly, the concentration of adrenaline in plasma does not rise in asthmatic subjects with induced bronchoconstriction, or even during an acute asthma attack. The function of beta-adrenoceptors in asthma is uncertain, but there is some evidence that beta-receptor function may be impaired, possibly as a result of inflammatory mediator release. alpha-Adrenoceptor function may be enhanced in asthma; inflammatory mediators may 'turn on' bronchoconstrictor alpha-adrenergic responses in airway smooth muscle, and alpha-agonists may have a bronchoconstrictor effect in asthmatic subjects. But specific alpha-blockers have little effect on airway function, and the role of alpha-receptors in asthma is questionable. Non-adrenergic, non-cholinergic nerves are the only neural bronchodilator mechanism in human airways. The neurotransmitter has not yet been identified but vasoactive intestinal peptide (VIP) is a possible candidate.(ABSTRACT TRUNCATED AT 250 WORDS)
Alveolar macrophages (Mφ) from COPD patients show defective bacterial phagocytosis, which may be linked to increased oxidative stress in the lungs. Scavenger receptors mediate phagocytosis, but may become damaged by oxidative stress. In this study, the effect oxidative stress on phagocytosis and cell surface receptor expression was studied in monocyte-derived Mφ (MDM). MDM from non-smokers (NS), smokers (S) or COPD patients were cultured in GM-CSF for 12 d (n=5-7), then treated ± 200µM H<sub>2</sub>O<sub>2</sub> for 24h. MDM were exposed to fluorescently labelled <i>H.influenzae</i> (HI) or <i>S.pneumoniae</i> (SP) for 4 h, labelled with antibodies for HLA-DR, CD36, CD80, CD163, CD206, α<sub>v</sub>β<sub>3</sub> and ICAM-3, and analysed by flow cytometry. At baseline, COPD MDM expressed 68% less HLA-DR compared to NS (p<0.05). In NS and S MDM, phagocytosis of HI, increased expression of CD80 (NS 229%, S 797%, p<0.05), α<sub>v</sub>β<sub>3</sub> (NS 354%, S 313%, p<0.05), and ICAM-3 (NS 248%, S 892%, p<0.01). In COPD MDM, phagocytosis did not change receptor expression. H<sub>2</sub>0<sub>2</sub> decreased phagocytosis of HI (NS 35%, S 16%, COPD 17% p<0.05) and SP (NS 54%, S 30%, COPD 43%, p<0.05). In NS MDM only, H<sub>2</sub>0<sub>2</sub> caused a decrease in ICAM-3 expression after HI phagocytosis (37% p<0.05), but had no effect on other receptors. MDM from COPD patients display differential scavenger receptor profiles compared to healthy MDM in response to phagocytosis of bacteria. This could contribute to Mφ dysfunction in COPD. Exogenous oxidative stress decreased phagocytosis in all patient groups, which may be linked to decreased expression of ICAM-3. Identifying the mechanisms involved in receptor expression may prove advantageous in developing novel therapies.
