Pathophysiology of Haemostasis and Thrombosis最新文献

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Contents Vol. 35, 2006 目录2006年第35卷
Pathophysiology of Haemostasis and Thrombosis Pub Date : 2007-06-01 DOI: 10.1159/000103876
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引用次数: 0
Subject Index Vol. 35, 2006 主题索引第35卷,2006年
Pathophysiology of Haemostasis and Thrombosis Pub Date : 2007-06-01 DOI: 10.1159/000103875
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引用次数: 0
Author Index Vol. 35, 2006 作者索引,2006年第35卷
Pathophysiology of Haemostasis and Thrombosis Pub Date : 2007-06-01 DOI: 10.1159/000103874
{"title":"Author Index Vol. 35, 2006","authors":"","doi":"10.1159/000103874","DOIUrl":"https://doi.org/10.1159/000103874","url":null,"abstract":"","PeriodicalId":19817,"journal":{"name":"Pathophysiology of Haemostasis and Thrombosis","volume":"26 1","pages":"457 - 457"},"PeriodicalIF":0.0,"publicationDate":"2007-06-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1159/000103874","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"64425041","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}
引用次数: 0
Statin therapy alone and in combination with an acyl-CoA:cholesterol O-acyltransferase inhibitor on experimental atherosclerosis. 他汀类药物单独治疗和与酰基辅酶a:胆固醇o -酰基转移酶抑制剂联合治疗实验性动脉粥样硬化。
Pathophysiology of Haemostasis and Thrombosis Pub Date : 2007-01-01 Epub Date: 2008-03-06 DOI: 10.1159/000112634
Stephen G Worthley, Gérard Helft, Roberto Corti, Matthew I Worthley, Derek P Chew, Zahi A Fayad, Azfar G Zaman, John T Fallon, Valentin Fuster, Juan J Badimon
{"title":"Statin therapy alone and in combination with an acyl-CoA:cholesterol O-acyltransferase inhibitor on experimental atherosclerosis.","authors":"Stephen G Worthley,&nbsp;Gérard Helft,&nbsp;Roberto Corti,&nbsp;Matthew I Worthley,&nbsp;Derek P Chew,&nbsp;Zahi A Fayad,&nbsp;Azfar G Zaman,&nbsp;John T Fallon,&nbsp;Valentin Fuster,&nbsp;Juan J Badimon","doi":"10.1159/000112634","DOIUrl":"https://doi.org/10.1159/000112634","url":null,"abstract":"<p><p>The ability to modify the enzymatic processes involved in promoting atherosclerotic plaque disruption and to serially monitor atherosclerotic evolution could provide novel information in the management of patients with atherosclerosis. We studied the effects of a statin (atorvastatin) and its combination with an acyl-CoA:cholesterol O-acyltransferase (ACAT) inhibitor (avasimibe) on atherosclerotic regression and plaque stability as measured by matrix metalloproteinase 1 and 3 (MMP-1 and MMP-3) levels. Watanabe Heritable Hyperlipidemic (WHHL) rabbits treated with atorvastatin alone experienced an attenuated increase in atherosclerotic burden versus controls as determined by MR imaging. The mean vessel wall area (VWA) prior to drug therapy was 5.57 +/- 0.01 mm2. The VWA increased to 6.71 +/- 0.03 and 7.16 +/- 0.03 mm2, respectively, in atorvastatin-treated and control groups (p < 0.0001 for both). The combination of atorvastatin and avasimibe induced a significant regression of the previously established atherosclerotic lesions, with the VWA decreasing to 4.54 +/- 0.04 mm2 (p = 0.009). Atorvastatin alone induced a nonsignificant reduction in the percent staining of MMP-1 in atherosclerotic lesions, but the combination treatment with avasimibe led to a significant reduction versus controls (p = 0.005). However, a reduction in MMP-3 staining was significant for rabbits treated with both atorvastatin alone (p = 0.007) and in combination with avasimibe (p = 0.04) versus controls. In this animal model, the addition of avasimibe to atorvastatin has beneficial effects on both atherosclerotic plaque regression and stabilization.</p>","PeriodicalId":19817,"journal":{"name":"Pathophysiology of Haemostasis and Thrombosis","volume":"36 1","pages":"9-17"},"PeriodicalIF":0.0,"publicationDate":"2007-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1159/000112634","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"27315118","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}
引用次数: 10
Platelet activation and red blood cell phosphatidylserine exposure evaluated by flow cytometry in patients with Behçet's disease: are they related to thrombotic events? 用流式细胞术评估behet病患者的血小板活化和红细胞磷脂酰丝氨酸暴露:它们与血栓事件有关吗?
Pathophysiology of Haemostasis and Thrombosis Pub Date : 2007-01-01 Epub Date: 2008-03-06 DOI: 10.1159/000112635
M Martínez, J M Ricart, S Ruiz-Aja, A Rus, J Todolí, J Calvo, A Vayá
{"title":"Platelet activation and red blood cell phosphatidylserine exposure evaluated by flow cytometry in patients with Behçet's disease: are they related to thrombotic events?","authors":"M Martínez,&nbsp;J M Ricart,&nbsp;S Ruiz-Aja,&nbsp;A Rus,&nbsp;J Todolí,&nbsp;J Calvo,&nbsp;A Vayá","doi":"10.1159/000112635","DOIUrl":"https://doi.org/10.1159/000112635","url":null,"abstract":"<p><p>Behçet's disease (BD) is associated with an increased risk of venous and arterial thromboses that are associated with morbidity and mortality increase, although the mechanisms are not well established. In the present study, we used whole blood cytometry to determine the exposure of CD62 on the surface of platelets and the expression of phosphatidylserine (PS) on the surface of circulating red blood cells. Microparticle and microaggregate formation from platelets were also determined in a well-classified group of 72 patients (39 males, 33 females, aged 46.5 +/- 12.5 years) with BD, in comparison with a well-matched control group of 72 healthy volunteers. Results showed no differences in the above-mentioned parameters when BD patients and controls were compared. However, when we compared BD patients with/without thrombosis using these parameters, there were significant differences between both groups. BD patients with previous thrombosis had a higher percentage of circulating CD62-positive platelets and a higher number of circulating microaggregates than those without thrombosis, suggesting that platelet activation may be involved in the development of thrombotic events in these patients.</p>","PeriodicalId":19817,"journal":{"name":"Pathophysiology of Haemostasis and Thrombosis","volume":"36 1","pages":"18-22"},"PeriodicalIF":0.0,"publicationDate":"2007-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1159/000112635","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"27315119","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}
引用次数: 25
A biochemical study on the effect of proteolysis of beta-thromboglobulin proteins released from activated platelets on fibroblast proliferation. 活化血小板释放β -血小板球蛋白蛋白水解对成纤维细胞增殖影响的生化研究。
Pathophysiology of Haemostasis and Thrombosis Pub Date : 2007-01-01 Epub Date: 2010-03-13 DOI: 10.1159/000296282
Resmi Ravindran, Lissy K Krishnan
{"title":"A biochemical study on the effect of proteolysis of beta-thromboglobulin proteins released from activated platelets on fibroblast proliferation.","authors":"Resmi Ravindran,&nbsp;Lissy K Krishnan","doi":"10.1159/000296282","DOIUrl":"https://doi.org/10.1159/000296282","url":null,"abstract":"<p><p>beta-Thromboglobulin (beta-TG) proteins are a heterogeneous group released from platelet alpha-granules on activation and have an effect on fibroblast migration and proliferation. We have previously reported the action of a metal-dependent protease on platelet-released proteins, which generates low-molecular-weight proteins that could be inhibited by ethylenediaminetetraacetic acid (EDTA). To understand the physiological significance of the breakdown of proteins after release, their effect on fibroblast proliferation in vitro was studied. Platelet releasates were obtained without and with EDTA inhibition designated as R1 and R2, respectively, and proteins were affinity purified for testing. Cell proliferation was measured using [(3)H]-thymidine assay. Both R1 and R2 showed maximum activity at 100 microg/ml and R2 elicited significant proliferation compared to R1. When affinity-purified proteins were tested at 100 ng/ml, high-molecular-weight proteins showed significantly higher proliferation than low-molecular-weight proteins. We have shown that beta-TG is cleaved after being released from activated platelets, thereby becoming less mitogenic for fibroblasts.</p>","PeriodicalId":19817,"journal":{"name":"Pathophysiology of Haemostasis and Thrombosis","volume":"36 6","pages":"285-9"},"PeriodicalIF":0.0,"publicationDate":"2007-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1159/000296282","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"28772026","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}
引用次数: 6
Reflectance changes in clotting native blood: evidence of a red-cell process. 凝血中的反射变化:红细胞过程的证据。
Pathophysiology of Haemostasis and Thrombosis Pub Date : 2007-01-01 Epub Date: 2008-03-06 DOI: 10.1159/000112636
Frank A Greco
{"title":"Reflectance changes in clotting native blood: evidence of a red-cell process.","authors":"Frank A Greco","doi":"10.1159/000112636","DOIUrl":"https://doi.org/10.1159/000112636","url":null,"abstract":"<p><p>When broadband light illuminates clotting native blood, the reflectance at each wavelength traces a time course with four discernible regions. Clot formation occurs just before the second phase. Two wavelengths, 471 and 771 nm, were selected for more detailed study of the first two phases. Analysis of each time course in native blood demonstrates that both signals track a single process during the first phase, but distinct processes during the second. Experiments on citrated blood identified which blood components contribute to reflectance changes. Comparison of liquid and clotting blood reveals a single process during the first phase, entailing that rouleaux formation determines the time course at both wavelengths. Control experiments eliminate clot propagation and shape change of red cells or platelets as possible factors in the second phase. Exogenous ADP added to EDTA blood evokes the second-phase response at 471 but not 771 nm, a novel phenomenon that requires the presence of red cells. The descriptive name 'ADP-end-response' is suggested for this red cell process until it is further characterized. We propose that the ADP-end-response determines the 471-nm signal during the second phase of clotting native blood and depends upon platelets in the absence of exogenous ADP. The 771-nm signal reports fibrin cross-linking during the second phase. An earlier pilot study demonstrated that rofecoxib effects the 471-nm signal ex vivo, which indicates that reflectance spectroscopy may be useful in the assessment of drug effects on platelet-erythrocyte interactions.</p>","PeriodicalId":19817,"journal":{"name":"Pathophysiology of Haemostasis and Thrombosis","volume":"36 1","pages":"23-31"},"PeriodicalIF":0.0,"publicationDate":"2007-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1159/000112636","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"27315120","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}
引用次数: 2
Increased platelet cholesterol and decreased percentage volume of platelets as a secondary risk factor for coronary artery disease. 血小板胆固醇升高和血小板体积百分比降低是冠状动脉疾病的次要危险因素。
Pathophysiology of Haemostasis and Thrombosis Pub Date : 2007-01-01 Epub Date: 2008-03-06 DOI: 10.1159/000112639
Resmi Ravindran, Lissy K Krishnan
{"title":"Increased platelet cholesterol and decreased percentage volume of platelets as a secondary risk factor for coronary artery disease.","authors":"Resmi Ravindran,&nbsp;Lissy K Krishnan","doi":"10.1159/000112639","DOIUrl":"https://doi.org/10.1159/000112639","url":null,"abstract":"<p><p>Platelet hyperactivity is likely to contribute to the progression of atherogenesis and organized thrombus formation on vascular surfaces. The purpose of this study was to examine the effect of hypercholesterolemia on the cholesterol content of platelets, on platelet responsiveness and other platelet indices using platelets from 5 groups of age-matched subjects (n = 30 each), which includes healthy controls. All groups except controls had a high plasma lipid profile. While subjects in group I had only hyperlipidemia, those in groups II and III had hyperlipidemia in conjunction with diabetes mellitus and hypertension, respectively. The fourth group consisted of patients with confirmed coronary artery disease (CAD). The parameters studied include packed cell volume of platelets (platelet crit), platelet distribution width (PDW), platelet cholesterol and platelet aggregation in response to adenosine diphosphate and collagen. All the patient groups showed increased platelet aggregation (p < 0.05) and low platelet crit compared with controls (p < 0.05). In addition, platelet cholesterol was increased in patients with coronary disease, hyperlipidemia and diabetes mellitus (p < 0.05) but not in patients with hypertension (p > 0.05); PDW was high only in CAD (p < 0.05). A higher PDW indicated a prothrombotic tendency in CAD patients. Our data suggest that hyperlipidemia increases the lipid content in platelets and enhances their reactivity. Hyperactive platelets with increased platelet cholesterol may contribute to accelerated atherogenesis associated with CAD.</p>","PeriodicalId":19817,"journal":{"name":"Pathophysiology of Haemostasis and Thrombosis","volume":"36 1","pages":"45-51"},"PeriodicalIF":0.0,"publicationDate":"2007-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1159/000112639","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"27315077","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}
引用次数: 36
Genistein and its analogue enhanced tissue plasminogen activator activity in HeLa S3. 染料木素及其类似物可增强 HeLa S3 中组织纤溶酶原激活剂的活性。
Pathophysiology of Haemostasis and Thrombosis Pub Date : 2007-01-01 Epub Date: 2010-03-13 DOI: 10.1159/000296280
Chieko Yatagai, Tatsuya Singu, Masugi Maruyama, Hiroyuki Sumi
{"title":"Genistein and its analogue enhanced tissue plasminogen activator activity in HeLa S3.","authors":"Chieko Yatagai, Tatsuya Singu, Masugi Maruyama, Hiroyuki Sumi","doi":"10.1159/000296280","DOIUrl":"10.1159/000296280","url":null,"abstract":"<p><p>Soybean isoflavones of genistein and biochanin A, its analogue, promote the activity for generating tissue-plasminogen activator (tPA) from human cervical cancer cells (HeLa S3) and human umbilical vein endothelial cells (HUVEC). At a concentration of 50 microM, each of 14 types of isoflavones were added to HeLa culture solution and incubated. After 24 h, the culture solution was replaced, and then incubated for another 24 h. When fibrinolytic activity was checked in the resulting culture solution using the fibrin plate method, substantial fibrinolytic activity was confirmed for two types of isoflavones. Genistein showed the highest level of fibrinolytic activity at 12.4 times the control, and for biochanin A, an analogue of genistein, the level was 3.5 times the control. Checking fibrinolytic activity and molecular weight of the protein bands separated by zymography, a rise in the protein band concentration in proportion to the concentration of the reagents added was confirmed for the protein band with activity in the same position as the standard reference tPA, which has a molecular weight of about 68 kDa. ELISA also demonstrated that the concentration of tPA in the culture solution was higher than that of plasminogen activator-1. Fibrinolytic activity of HUVEC incubated with 25 microM of biochanin A was much higher than that of the control, which suggests that these soybean isoflavones could have beneficial effects on blood circulation in vivo.</p>","PeriodicalId":19817,"journal":{"name":"Pathophysiology of Haemostasis and Thrombosis","volume":"36 6","pages":"298-304"},"PeriodicalIF":0.0,"publicationDate":"2007-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1159/000296280","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"28772024","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}
引用次数: 1
Reverse effect of aspirin: is the prothrombotic effect after aspirin discontinuation mediated by cyclooxygenase 2 inhibition? 阿司匹林的逆转作用:阿司匹林停药后的血栓前作用是由环氧化酶2抑制介导的吗?
Pathophysiology of Haemostasis and Thrombosis Pub Date : 2007-01-01 Epub Date: 2008-03-06 DOI: 10.1159/000112638
Christian Doutremepuich, Omar Aguejouf, Francisco X Eizayaga, Vanessa Desplat
{"title":"Reverse effect of aspirin: is the prothrombotic effect after aspirin discontinuation mediated by cyclooxygenase 2 inhibition?","authors":"Christian Doutremepuich,&nbsp;Omar Aguejouf,&nbsp;Francisco X Eizayaga,&nbsp;Vanessa Desplat","doi":"10.1159/000112638","DOIUrl":"https://doi.org/10.1159/000112638","url":null,"abstract":"<p><strong>Background: </strong>While aspirin is the drug most often used to prevent cardiovascular complications, its discontinuation induces an increased risk of acute coronary syndrome and ischemic stroke in some patients.</p><p><strong>Objectives: </strong>We hypothesized that infinitesimal concentrations of aspirin could persist in plasma after its discontinuation, thereby inducing a prothrombotic effect that could be due to a modification in the mechanism of action of aspirin via the cyclooxygenase 1 (COX-1) and COX-2 pathways.</p><p><strong>Methods and results: </strong>We studied the effects of ultra-low-dose aspirin (ULDA) as well as those of sc-560 and ns-398, specific COX-1 and COX-2 inhibitors, on induced hemorrhagic time and in a model of laser-induced thrombosis in rats. In the laser-induced thrombosis model, ULDA treatment increased the number of emboli and the duration of embolization, thereby confirming its prothrombotic effect described in previous publications. This effect was also observed in rats pretreated with sc-560 but not in those pretreated with ns-398.</p><p><strong>Conclusions: </strong>We demonstrated that ULDA induced a prothrombotic effect in the rats studied. This strongly suggests that a very small amount of aspirin could remain in the patient's blood after aspirin therapy, leading to cardiovascular complications. This effect may be mediated by the COX-2 pathway.</p>","PeriodicalId":19817,"journal":{"name":"Pathophysiology of Haemostasis and Thrombosis","volume":"36 1","pages":"40-4"},"PeriodicalIF":0.0,"publicationDate":"2007-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1159/000112638","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"27315076","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}
引用次数: 29
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