171,203 research outputs found
New evidences for C-reactive protein (CRP) deposits in the arterial intima as a cardiovascular risk factor
No full textFabrizio Montecucco, François MachDivision of Cardiology, Foundation for Medical Research, University Hospital, Geneva, SwitzerlandAbstract: Inflammatory processes are orchestrated by several soluble molecules, which interact with cell populations involved. Cytokines, chemokines, acute-phase reactants, and hormones are crucial in the evolution of several inflammatory disorders, such as atherosclerosis. Several evidences suggest that C-reactive protein (CRP) started to be considered as a cardiovascular risk factor, since CRP directly induces atheroslerosis development. The recent demonstration of CRP production not only by the liver, but also within atherosclerotic plaques by activated vascular cells, also suggests a possible dual role, as both a systemic and tissue agent. Although more studies are needed, some therapeutic approaches to reduce CRP levels have been performed with encouraging results. However, given the strong limitations represented by its low specificity and still accordingly with the American Heart Association, there is no need for high sensitivity CRP screening of the entire adult population as a public-health measure. The measure of serum CRP might be useful only for patients who are considered at intermediate risk.Keywords: atherosclerosis, inflammation, plaque, cardiovascular risk, C-reactive protei
The use of acetylated ferricytochrome C for the detection of superoxide radicals produced in biological membranes
No full textAcetylation of 60% of lysine residues of horse heart ferricytochrome c results in more than 95% decrease of its ability to be reduced by mitochondrial and microsomal reductases and to become oxidized (after chemical reduction) by mitochondrial oxidase. The ability of acetylated ferricytochrome c to be reduced by 02- radicals is maintained, making this derivative useful for the detection of 02- radicals in biological systems containing cytochrome c reductases or oxidases. Mitochondrial membranes can reduce acetylated ferricytochrome c at a rate of 0.5 nmoles.min-1.mg-1. Such a reaction is 82% inhibited by 2.8 × 10-8M superoxide dismutase. © 1975 Academic Press, Inc
Different polypeptides of bovine heart cytochrome c oxidase are in contact with cytochrome c
No full textAbstractTwo water-soluble carbodiimides, differing in molecular dimensions, have been used to characterize the cytochrome c binding site of bovine heart cytochrome c oxidase. Several polypeptide components of the enzyme contain acidic residues which are modified by these reagents. Carboxyl groups present in subunit II, VII and polypeptide c, are protected from modification when cytochrome c, equimolar to oxidase, is added and they can cross-link to the substrate once activated by the carbodiimide. Comparison of the modification patterns suggest that the most reactive residues are located on subunit II and VII, the former being also more exposed. The data obtained indicate that eventhough subunit II plays the major role in binding cytochrome c, at least two other lower Mr polypeptides contribute to the cytochrome c binding domain
Diagnostic and therapeutic challenges for patients with ANCA-associated vasculitides at the time of COVID-19. Response to: 'Rituximab for granulomatosis with polyangiitis in the pandemic of COVID-19: Lessons from a case with severe pneumonia' by Guilpain et al
No full textClinical course and outcome of COVID-19 in patients with rheumatic diseases: Are all biological disease-modifying antirheumatic drugs alike? Response to: Â € Increased risk for severe COVID-19 in patients with inflammatory rheumatic diseases treated with rituximab' by Schulze-Koops et al
No full textResponse to: 'Increased rather than decreased incidence of giant-cell arteritis during the COVID-19 pandemic' by Lecler et al
No full textCan hydroxychloroquine protect patients with rheumatic diseases from COVID-19? Response to: Ͽ Does hydroxychloroquine prevent the transmission of COVID-19?' by Heldwein and Calado and SLE, hydroxychloroquine and no SLE patients with COVID-19: A comment' by Joob and Wiwanitkit
No full textThrombotic thrombocytopenic purpura and autoimmunity: a tale of shadows and suspects
No full textBackground and Objective, The key pathogenic feature of TTP is the formation of platelet aggregates within the microcirculation; however, the etiology of such aggregates has been elusive for years. A large amount of evidence points to an abnormal interaction between damaged vascular endothelium and platelets, although the cause of the primary microvascular endothelial cell injury is seldom clear. The autoimmune hypothesis often recurs, and this is based on a number of observations: the claimed superiority of plasma-exchange over plasma infusion, the anecdotal report of the presence of immunocomplexes and autoantibodies in TTP patients, the efficacy of the administration of corticosteroids and other immunosuppressant agents, and the concomitant occurrence of TTP in association with autoimmune diseases, especially systemic lupus erythematosus (SLE). This review will focus on the complex relationships between TTP and humoral autoimmunity; in particular, similarities and differences between TTP, SLE and antiphospholipid (aPL) antibodies syndrome, as well as the putative role of several other antibodies directed towards endothelial cells and/or platelets, including the recently discovered anti-CD36 antibodies and antivWF-cleaving metalloprotease, will be discussed. Design and Methods. The authors have been Involved in the study and treatment of TTP and autoimmune diseases for years; furthermore, the PubMed data base of the National Library of Congress has been extensively searched using the Internet. Conclusions. Although over the years evidence has increased in favor of the autoimmune hypothesis for TTP etiopathogenesis, TTP should not yet be considered an autoimmune disease. Autoantibodies should be regarded as only one of the many different insults which can trigger microvascular thrombosis even though the autoimmune theory of the pathogenesis of TTP is gaining more and more strength. As far as concerns the relationship between TTP, SLE and aPL antibodies-related disorders, these diseases should be distinguished on the basis of both different clinical presentations and accurate antibody screening, although this approach should definitely not delay the prompt start of treatment
Non-steroidal anti-inflammatory treatment during covid-19: Friend or foe? Response to: 'Coronavirus disease 19 (Covid-19) and non-steroidal anti-inflammatory drugs (NSAID)' by Giollo et al
No full text
- …
