Katherine Schulz-Heik, Jaimohan Ramachandran, W. Ageno, R. Strey, T. Siegemund, Christine Schubert, G. Schuster, Karin Wulff, F. Herrmann, M. Šabovič, Vida Bojec, D. Imberti, J. Jesty, A. Siegemund, L. Mattar, I. C. Ferrari, Guareide Carelli, I. Zupan, D. Bluestein, L. Carvalho, I. A. Thomazini-Santos, B. Salobir, F. Maffei, A. Ihara, Kengo Matsumoto, T. Kawamoto, S. Shouno, J. Kawamoto, Akira Katayama, M. Yoshitatsu, H. Izutani, Petra Bratina, J. Ponikvar, M. Fouassier, D. Moreau, F. Thiolliére, C. Frère, A. Marquès-Verdier, B. Souweine
{"title":"Contents Vol. 34, 2005","authors":"Katherine Schulz-Heik, Jaimohan Ramachandran, W. Ageno, R. Strey, T. Siegemund, Christine Schubert, G. Schuster, Karin Wulff, F. Herrmann, M. Šabovič, Vida Bojec, D. Imberti, J. Jesty, A. Siegemund, L. Mattar, I. C. Ferrari, Guareide Carelli, I. Zupan, D. Bluestein, L. Carvalho, I. A. Thomazini-Santos, B. Salobir, F. Maffei, A. Ihara, Kengo Matsumoto, T. Kawamoto, S. Shouno, J. Kawamoto, Akira Katayama, M. Yoshitatsu, H. Izutani, Petra Bratina, J. Ponikvar, M. Fouassier, D. Moreau, F. Thiolliére, C. Frère, A. Marquès-Verdier, B. Souweine","doi":"10.1159/000093990","DOIUrl":"https://doi.org/10.1159/000093990","url":null,"abstract":"","PeriodicalId":19817,"journal":{"name":"Pathophysiology of Haemostasis and Thrombosis","volume":"34 1","pages":"291 - 292"},"PeriodicalIF":0.0,"publicationDate":"2006-06-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1159/000093990","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"64340929","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Katherine Schulz-Heik, Jaimohan Ramachandran, W. Ageno, R. Strey, T. Siegemund, Christine Schubert, G. Schuster, Karin Wulff, F. Herrmann, M. Šabovič, Vida Bojec, D. Imberti, J. Jesty, A. Siegemund, L. Mattar, I. C. Ferrari, Guareide Carelli, I. Zupan, D. Bluestein, L. Carvalho, I. A. Thomazini-Santos, B. Salobir, F. Maffei, A. Ihara, Kengo Matsumoto, T. Kawamoto, S. Shouno, J. Kawamoto, Akira Katayama, M. Yoshitatsu, H. Izutani, Petra Bratina, J. Ponikvar, M. Fouassier, D. Moreau, F. Thiolliére, C. Frère, A. Marquès-Verdier, B. Souweine
{"title":"Subject Index Vol. 34, 2005","authors":"Katherine Schulz-Heik, Jaimohan Ramachandran, W. Ageno, R. Strey, T. Siegemund, Christine Schubert, G. Schuster, Karin Wulff, F. Herrmann, M. Šabovič, Vida Bojec, D. Imberti, J. Jesty, A. Siegemund, L. Mattar, I. C. Ferrari, Guareide Carelli, I. Zupan, D. Bluestein, L. Carvalho, I. A. Thomazini-Santos, B. Salobir, F. Maffei, A. Ihara, Kengo Matsumoto, T. Kawamoto, S. Shouno, J. Kawamoto, Akira Katayama, M. Yoshitatsu, H. Izutani, Petra Bratina, J. Ponikvar, M. Fouassier, D. Moreau, F. Thiolliére, C. Frère, A. Marquès-Verdier, B. Souweine","doi":"10.1159/000093989","DOIUrl":"https://doi.org/10.1159/000093989","url":null,"abstract":"","PeriodicalId":19817,"journal":{"name":"Pathophysiology of Haemostasis and Thrombosis","volume":"34 1","pages":"289 - 290"},"PeriodicalIF":0.0,"publicationDate":"2006-06-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1159/000093989","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"64341349","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
{"title":"Title Page / Table of Contents","authors":"","doi":"10.1159/000093465","DOIUrl":"https://doi.org/10.1159/000093465","url":null,"abstract":"","PeriodicalId":19817,"journal":{"name":"Pathophysiology of Haemostasis and Thrombosis","volume":"19 1","pages":"145 - 148"},"PeriodicalIF":0.0,"publicationDate":"2006-05-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1159/000093465","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"64336872","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
{"title":"Subject Index Vol. 34, No. 4–5, 2005","authors":"","doi":"10.1159/000093467","DOIUrl":"https://doi.org/10.1159/000093467","url":null,"abstract":"","PeriodicalId":19817,"journal":{"name":"Pathophysiology of Haemostasis and Thrombosis","volume":"34 1","pages":"247 - 247"},"PeriodicalIF":0.0,"publicationDate":"2006-05-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1159/000093467","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"64336754","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
{"title":"Author Index Vol. 34, No. 4–5, 2005","authors":"","doi":"10.1159/000093466","DOIUrl":"https://doi.org/10.1159/000093466","url":null,"abstract":"","PeriodicalId":19817,"journal":{"name":"Pathophysiology of Haemostasis and Thrombosis","volume":"34 1","pages":"246 - 246"},"PeriodicalIF":0.0,"publicationDate":"2006-05-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1159/000093466","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"64336664","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
{"title":"Oral and Poster Presentations","authors":"Redakcja Nt","doi":"10.1159/000093567","DOIUrl":"https://doi.org/10.1159/000093567","url":null,"abstract":"","PeriodicalId":19817,"journal":{"name":"Pathophysiology of Haemostasis and Thrombosis","volume":"7 1","pages":"199 - 248"},"PeriodicalIF":0.0,"publicationDate":"2006-05-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1159/000093567","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"64337766","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
{"title":"Aspirin resistance.","authors":"Alan D Michelson","doi":"10.1159/000093570","DOIUrl":"https://doi.org/10.1159/000093570","url":null,"abstract":"Platelets are small cells of great importance in thrombosis and inflammation (1). Platelets have a welldefined, critical role in coronary artery thrombosis and other common cardiovascular diseases including stroke, peripheral arterial disease, and diabetes mellitus (1;2). Platelet function tests have been studied in cardiovascular diseases as a means to predict clinical outcomes and to monitor antiplatelet drugs (3). Aspirin irreversibly acetylates serine 529 of cyclooxygenase (COX)-1, resulting in inhibition of thromboxane A2 release from platelets and prostacyclin from endothelial cells (4). Thromboxane A2 induces platelet activation, whereas prostacyclin inhibits platelet activation. Because platelets lack the synthetic machinery to generate significant amounts of new COX, aspirininduced COX-1 inhibition lasts for the lifetime of the platelet. In contrast, endothelial cells retain their capacity to generate new COX and recover normal function shortly after exposure to aspirin. Aspirin is, therefore, an antithrombotic agent.","PeriodicalId":19817,"journal":{"name":"Pathophysiology of Haemostasis and Thrombosis","volume":"35 1-2","pages":"5-9"},"PeriodicalIF":0.0,"publicationDate":"2006-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1159/000093570","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"26153383","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Olivier Morel, Florence Toti, Babé Bakouboula, Lélia Grunebaum, Jean-Marie Freyssinet
{"title":"Procoagulant microparticles: 'criminal partners' in atherothrombosis and deleterious cellular exchanges.","authors":"Olivier Morel, Florence Toti, Babé Bakouboula, Lélia Grunebaum, Jean-Marie Freyssinet","doi":"10.1159/000093538","DOIUrl":"https://doi.org/10.1159/000093538","url":null,"abstract":"<p><p>Procoagulant microparticles (MP) constitute valuable hallmarks of vascular cell damage at the crossroad of atherothrombosis processes. Detectable at low concentrations in the blood flow of healthy individuals, elevated levels of procoagulant microparticles are characteristic features of most cardiovascular risk factors. Circulating MP support cellular cross-talk leading to vascular inflammation, endothelial dysfunction, leukocyte adhesion and recruitment possibly contributing to plaque growth with consecutive development of local thrombosis and altered vasomotion. Within the plaque, MP shed by apoptotic monocytes and smooth muscle cells are major determinant of plaque thrombogenicity mainly through the presence of tissue factor (TF) activity. Besides this procoagulant potential, trapped MP could contribute to plaque vulnerability through multiple pathways including angiogenesis, extracellular matrix proteolysis, recruitment of inflammatory cells, smooth muscle cell and endothelial apoptosis. Having long been considered sufficient to initiate coagulation following plaque disruption, the role assigned to plaque-bound TF does not appear physically realistic at a macroscopic scale, the swift growth of the thrombus probably involving blood-borne TF conveyed by circulating MP. As participants in crucial steps of atherosclerotic disease, MP can now be viewed as \"partners in crime\" in acute ischemic syndromes.</p>","PeriodicalId":19817,"journal":{"name":"Pathophysiology of Haemostasis and Thrombosis","volume":"35 1-2","pages":"15-22"},"PeriodicalIF":0.0,"publicationDate":"2006-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1159/000093538","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"26153387","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
{"title":"HDL--associated paraoxonase 1 (PON1) and dietary antioxidants attenuate lipoprotein oxidation, macrophage foam cells formation and atherosclerosis development.","authors":"Michael Aviram","doi":"10.1159/000093558","DOIUrl":"https://doi.org/10.1159/000093558","url":null,"abstract":"Dietary antioxidants act as a first line of defense against lipids peroxidation in lipoproteins and in arterial cells, including macrophage foam cells. A second line of defense by antioxidants could be related to stimulation of paraoxonases (PONs). PON1 is associated in serum with high density lipoprotein (HDL). The activity of serum PON1 was shown to be inversely associated with the risk for atherosclerosis development and this phenomenon could be related to the ability of PON 1 to protect lipids in LDL, HDL and arterial cells against oxidation, secondary to its hydrolytic action on specific oxidized lipids. PON1 was shown to play a major role in protecting against oxidative stress and its consequent cardiovascular diseases development. Dietary intervention with appropriate nutraceuticals, with most potent and diverse antioxidative properties most efficiently attenuate cardiovascular diseases progression. Major risk factors for atherosclerosis development include the quantity and quality of low density lipoprotein (LDL, “The bad cholesterol”) and that of high density lipoprotein (HDL, “the good cholesterol”). High","PeriodicalId":19817,"journal":{"name":"Pathophysiology of Haemostasis and Thrombosis","volume":"35 1-2","pages":"146-51"},"PeriodicalIF":0.0,"publicationDate":"2006-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1159/000093558","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"26154350","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Elisabeth Koller, Ivo Volf, Aner Gurvitz, Franz Koller
{"title":"Modified low-density lipoproteins and high-density lipoproteins. From investigation tools to real in vivo players.","authors":"Elisabeth Koller, Ivo Volf, Aner Gurvitz, Franz Koller","doi":"10.1159/000093225","DOIUrl":"https://doi.org/10.1159/000093225","url":null,"abstract":"<p><p>It has long been known that the oxidative state of the various plasma lipoproteins modulates platelet aggregability, thereby contributing to atherogenesis. Low-density lipoprotein (LDL), occurring in vivo both in the native and oxidised forms, interacts directly with platelets, by binding to specific receptors. While the identity of the receptors for native LDL and some subfractions of high-density lipoproteins (HDL) remains disputed, apoE-containing HDL(2) binds to LRP8. The nature of these interactions as well as the distinction between candidate receptor proteins was elucidated using covalently modified apolipoproteins, which pointed to the participation of apolipoproteins in high affinity binding. However, the platelet effects initiated by binding of native lipoproteins remain controversial. Some of this ambiguity can be traced to the fact that native LDL inevitably undergoes substantial oxidisation upon modification, including by radiolabelling. The platelet-activating effects provoked by oxidised LDL are irrefutable, but many details remain unknown. The role of CD36 in platelet binding by oxidised LDL is well established, although additional receptors may exist. Much less is known about the interaction of oxidised HDL with platelets, since platelet activation was observed in some, but not all studies. Various frequently applied in vitro oxidation methods produce modified lipoprotein species that may not be relevant in vivo. Based on the reported modifications obtained by in vitro oxidation of LDL, early investigations focused mainly on the formation and the eventual effects of oxidised lipids. More recently, alterations to lipoproteins performed using hypochloric acid and myeloperoxidase redirected the attention to the role of modified apoproteins in triggering platelet responses.</p>","PeriodicalId":19817,"journal":{"name":"Pathophysiology of Haemostasis and Thrombosis","volume":"35 3-4","pages":"322-45"},"PeriodicalIF":0.0,"publicationDate":"2006-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1159/000093225","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"26172118","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}