6,963 publications from this institution
Conference Abstract| December 01 1984 Nifedipine Prolongs Isoprenaline-Induced Bronchodilatation in Normal Subjects Francis M. Cuss; Francis M. Cuss 1Department of Medicine, Royal Postgraduate Medical School, Hammersmith Hospital, London W12 OHS Search for other works by this author on: This Site PubMed Google Scholar Sharyn E. Mannix; Sharyn E. Mannix 1Department of Medicine, Royal Postgraduate Medical School, Hammersmith Hospital, London W12 OHS Search for other works by this author on: This Site PubMed Google Scholar Peter J. Barnes Peter J. Barnes 1Department of Medicine, Royal Postgraduate Medical School, Hammersmith Hospital, London W12 OHS Search for other works by this author on: This Site PubMed Google Scholar Clin Sci (Lond) (1984) 67 (s9): 62P. https://doi.org/10.1042/cs067062Pa Views Icon Views Article contents Figures & tables Video Audio Supplementary Data Peer Review Share Icon Share Twitter LinkedIn Cite Icon Cite Get Permissions Citation Francis M. Cuss, Sharyn E. Mannix, Peter J. Barnes; Nifedipine Prolongs Isoprenaline-Induced Bronchodilatation in Normal Subjects. Clin Sci (Lond) 1 December 1984; 67 (s9): 62P. doi: https://doi.org/10.1042/cs067062Pa 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. © 1984 The Biochemical Society and the Medical Research Society1984 Article PDF first page preview Close Modal You do not currently have access to this content.
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Conference Article| August 01 1993 How to assess regression of the atherosclerotic plaque J. de Feyter Pirn; J. de Feyter Pirn * 1Catheterization Laboratory, Thoraxcenter Bd 432, University Hospital Dijkzigt, Erasmus University Rotterdam, P.O. Box 1738, 3000 DR Rotterdam, The Netherlands *To Whom correspondence should be addressed Search for other works by this author on: This Site PubMed Google Scholar C. Di Mario; C. Di Mario 1Catheterization Laboratory, Thoraxcenter Bd 432, University Hospital Dijkzigt, Erasmus University Rotterdam, P.O. Box 1738, 3000 DR Rotterdam, The Netherlands Search for other works by this author on: This Site PubMed Google Scholar P. W. Serruys; P. W. Serruys 1Catheterization Laboratory, Thoraxcenter Bd 432, University Hospital Dijkzigt, Erasmus University Rotterdam, P.O. Box 1738, 3000 DR Rotterdam, The Netherlands Search for other works by this author on: This Site PubMed Google Scholar J. R. T. C. Roelandt J. R. T. C. Roelandt 1Catheterization Laboratory, Thoraxcenter Bd 432, University Hospital Dijkzigt, Erasmus University Rotterdam, P.O. Box 1738, 3000 DR Rotterdam, The Netherlands Search for other works by this author on: This Site PubMed Google Scholar Biochem Soc Trans (1993) 21 (3): 642–647. https://doi.org/10.1042/bst0210642 Article history Received: March 30 1993 Views Icon Views Article contents Figures & tables Video Audio Supplementary Data Peer Review Share Icon Share Twitter LinkedIn Cite Icon Cite Get Permissions Citation J. de Feyter Pirn, C. Di Mario, P. W. Serruys, J. R. T. C. Roelandt; How to assess regression of the atherosclerotic plaque. Biochem Soc Trans 1 August 1993; 21 (3): 642–647. doi: https://doi.org/10.1042/bst0210642 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 JournalsBiochemical Society Transactions Search Advanced Search This content is only available as a PDF. © 1993 Biochemical Society1993 Article PDF first page preview Close Modal You do not currently have access to this content.
Review(s) of: The church as the image of the trinity: A critical evaluation of Miroslav Volf 's ecclesial model, by Kevin Bidwell (Oregon: Wipf and Stock, 2011), 280pp., ISBN 9781610973731, $US30.00.
PURPOSE: There is still scarce data about the incidence of (late) stent thrombosis (ST) following implantation of drug-eluting stents in patients treated for multivessel coronary artery disease (MVD). Recent concerns were raised about a possible erosion of the long-term treatment benefit of sirolimus-eluting stents (SES) due to ST. Our aim was to assess the impact of ST on Major Adverse Cardiac Events (MACE) up to 3 years in patients treated with SES for MVD in the Arterial Revascularization Therapies Study part II (ARTS-II) trial. METHODS: ARTS-II is a non-randomized, open label, stratified trial with 607 patients exclusively treated with SES for multivessel coronary artery disease including mandatory involvement of the LAD. The 3-year clinical data from ARTS-II were re-adjudicated by an independent clinical events committee for the incidence of ST according to the definitions recently proposed by an Academic Research Consortium (ARC) using the categories of definite (angiography or autopsy), probable (myocardial infarction in target area, unexplained death within 30 days), and possible ST (unexplained death). RESULTS: The majority of patients (53.5%) had 3-vessel disease. Total stented length was 72.5 ± 32.1mm, and 3.7 ± 1.5 stents were implanted per patient on average. At 3 years, 18/607patients died (3.0%), and MI was observed in 49/607 patients (8.1%). Stent thrombosis occurred in 39/607 patients (6.4%), 21 patients had ``definite” ST, and 32 patients had ``definite or probable” ST according to the ARC classification. From the 39 patients experiencing ST only 8 died, 7 of which were contributed by the ARC ``possible” ST category. CONCLUSIONS: In ARTS-II, the majority of deaths in patients with ST was contributed by the ARC possible category. The final impact of ST on the individual MACE categories will be presented at the conference.
Alveolar macrophages from COPD patients exhibit reduced bacterial phagocytosis compared to those from healthy controls and this defect is associated with increased exacerbation frequency. The defective phagocytosis extends to different bacterial species, fungal spores and apoptotic cells, suggesting a common defective mechanism, and is replicated in monocyte-derived macrophages (MDM) providing a useful cell model. Phagocytosis requires cytoskeletal rearrangements involving protein transporters such as dynein. We hypothesised that regulation of dynein motors is aberrant in COPD and related to reduced phagocytosis and increased pro-inflammatory cytokine release. To test this, the effect of a dynein motor inhibitor, ciliobrevin D, on macrophage phagocytosis was examined. Monocytes from non-smokers (n=8), smokers (n=3) and COPD patients (n=4) were incubated in GM-CSF for 12 days to generate MDM. MDM were treated with ciliobrevin D (1-100µM) for 30 min prior to 4h incubation with fluorescently-labelled H. influenzae (HI) or S. pneumoniae (SP), and phagocytosis measured by fluorimetry. Cytokine release was measured by ELISA (IL-10, TNFα and CXCL8). Ciliobrevin D caused a concentration-dependent increase in phagocytosis of HI in COPD macrophages that was maximal (↑86±36%) in COPD MDM at 100µM (p<0.05). A similar trend was seen with non-smokers and smokers. There was also a trend for a concentration-dependent increase in phagocytosis of SP by MDM from all subjects. However, there was no effect on bacterial-stimulated cytokine release.
