Journal of Thrombosis and Haemostasis (J THROMB HAEMOST)
The mission of the new Journal of Thrombosis and Haemostasis will be to advance science related to the important medical problems of thrombosis, bleeding disorders and vascular biology through the diffusion and exchange of information and ideas within the international research community. The Journal publishes high quality, original research reports, state-of-the art reviews, invited commentary and debate on timely topics, letters and announcements. Editors invite both laboratory and clinical reports. The Journal of Thrombosis and Haemostasis is now available in print and online.
- Impact factor5.73Show impact factor historyHide impact factor history
- WebsiteJournal of Thrombosis and Haemostasis website
Other titlesJournal of thrombosis and haemostasis, JTH
Material typeDocument, Periodical, Internet resource
Document typeInternet Resource, Computer File, Journal / Magazine / Newspaper
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Publications in this journal
Journal of Thrombosis and Haemostasis 06/2013; In press.
Article: Increased anticoagulant response to low-molecular-weight heparin in plasma from patients with advanced cirrhosis.[show abstract] [hide abstract]
ABSTRACT: INTRODUCTION: Cirrhotic patients may present thrombotic complications that warrant anticoagulant therapy. However, the efficacy of low-molecular-weight heparin (LMWH) in this clinical setting is still unclear. AIMS/METHODS: To evaluate the in vitro effect of LMWH on thrombin generation (TG) in cirrhotic patients at different stages of liver disease. Thirty cirrhotics (10 Child Pugh A, 10 Child Pugh B and 10 Child Pugh C), 10 subjects with inherited type 1 antithrombin (AT) defect and 10 healthy controls were studied. TG was determined at baseline and with anti-Xa levels after the addition of enoxaparin at 0.35 and 0.7 U anti-Xa mL. The endogenous thrombin potential (ETP) ratio at 0.35 and 0.7 U anti-Xa mL was obtained by dividing ETP with LMWH by ETP at baseline. RESULTS: Mean AT levels in all cirrhotic subgroups and in patients with AT deficiency were significantly lower than in controls. The 0.35 ETP ratio was significantly lower in cirrhotic patients than in controls (0.26 ± 0.1 vs. 0.48 ± 0.1, P < 0.001) and the reduction paralleled the severity of liver disease, in spite of the concomitant decrease in AT and anti-Xa activity. AT-deficient subjects showed a significantly increased 0.35 ETP ratio compared with both cirrhotic patients and controls (0.69 ± 1 vs. 0.26 ± 0.1, P < 0.001, and vs. 0.48 ± 0.1, P = 0.04 respectively). LMWH at 0.7 U anti-Xa mL completely inhibited TG in 9/30 cirrhosis patients with more advanced liver disease (Child Pugh B and C), whereas complete TG abolition was seen in only 1/10 controls. CONCLUSIONS: Cirrhotic patients show an increased response to LMWH, which correlates with the severity of liver disease, in spite of reduced AT and anti-Xa activity levels. Thrombin generation may be a useful tool to monitor the response to LMWH in cirrhotic patients. © 2012 International Society on Thrombosis and Haemostasis.Journal of Thrombosis and Haemostasis 09/2012; 10(9):1823-9.
Journal of Thrombosis and Haemostasis 04/2012;
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ABSTRACT: BACKGROUND: Most physiologic processes exhibit diurnal fluctuations controlled by the circadian regulation of sleep-wake behavior and feeding cycles. In addition, many cell types express endogenous circadian rhythms that affect cell-specific processes. Independent reports support the hypothesis that thrombopoietin (TPO) is under circadian control. OBJECTIVES: The current study tested the hypothesis that CLOCK, a circadian transcription factor, may regulate Thpo, the gene encoding TPO. METHODS: Circadian gene expression patterns were analyzed in mice and in human cell lines, Small interfering RNA was used to knock down CLOCK expression in cell lines, and gene expression was also examined in Clock(Delta19/Delta19) mutant mice. RESULTS: It was found that there was a diurnal rhythm in the expression of Thpoin vivo in mice, and that this was associated with concomitant rhythms of protein abundance. Thpo was rhythmically expressed in human cell lines, consistent with the gene being directly or indirectly regulated by the circadian clock. Silencing of CLOCK in the Huh7 human hepatoma cell line led to a significant reduction in the rhythmicity of Thpo expression. The expression of Mpl in murine marrow also displayed diurnal rhythmicity in vivo. In Clock(Delta19/Delta19) mutant mice, Thpo and Mpl expression was disrupted and there was an increase in the number of mature megakaryocytes, but no change in the ploidy distribution within the megakaryocyte population. CONCLUSIONS: These findings establish that Clock regulates Thpo and Mpl expression in vivo, and demonstrate an important link between the body's circadian timing mechanisms and megakaryopoiesis.Journal of Thrombosis and Haemostasis 04/2012; 10(4):662-9.
Article: Use of a mouse model to elucidate the phenotypic effects of the von willebrand factor cleavage mutants, Y1605A/M1606A and R1597W.Journal of Thrombosis and Haemostasis 01/2012;
Article: High sensitivity cardiac troponin T and interleukin-6 predict adverse cardiovascular events and mortality in anticoagulated patients with atrial fibrillation: a rebuttal.Journal of Thrombosis and Haemostasis 01/2012;
Article: Human neutrophil alpha-defensins induce formation of fibrinogen and thrombospondin-1 amyloid-like structures and activate platelets via glycoprotein IIb/IIIaJournal of Thrombosis and Haemostasis 01/2012; 10:647-661.
Article: Risk Factors for Post-Discharge Bleeding in US Medically ill Patients at Risk of Venous ThromboembolismJournal of Thrombosis and Haemostasis 07/2011;
Article: Risk Factors for pulmonary embolismJournal of Thrombosis and Haemostasis 01/2009; 7(S2):P417.
Article: Comparison of the revised Geneva score with the Wells rule for assessing clinical probability of pulmonary embolism.[show abstract] [hide abstract]
ABSTRACT: The revised Geneva score, a standardized clinical decision rule in the diagnosis of pulmonary embolism (PE), was recently developed. The Wells clinical decision is widely used but lacks full standardization, as it includes subjective clinician's judgement. We have compared the performance of the revised Geneva score with the Wells rule, and their usefulness for ruling out PE in combination with D-dimer measurement. In 300 consecutive patients, the clinical probability of PE was assessed prospectively by the Wells rule and retrospectively using the revised Geneva score. Patients comprised a random sample from a single center, participating in a large prospective multicenter diagnostic study. The predictive accuracy of both scores was compared by area under the curve (AUC) of receiver operating characteristic (ROC) curves. The overall prevalence of PE was 16%. The prevalence of PE in the low-probability, intermediate-probability and high-probability categories as classified by the revised Geneva score was similar to that of the original derivation set. The performance of the revised Geneva score as measured by the AUC in a ROC analysis did not differ statistically from the Wells rule. After 3 months of follow-up, no patient classified into the low or intermediate clinical probability category by the revised Geneva score and a normal D-dimer result was subsequently diagnosed with acute venous thromboembolism. This study suggests that the performance of the revised Geneva score is equivalent to that of the Wells rule. In addition, it seems safe to exclude PE in patients by the combination of a low or intermediate clinical probability by the revised Geneva score and a normal D-dimer level. Prospective clinical outcome studies are needed to confirm this latter finding.Journal of Thrombosis and Haemostasis 02/2008; 6(1):40-4.
Article: Combined tissue factor pathway inhibitor and thrombomodulin deficiency produces an augmented hypercoagulable state with tissue-specific fibrin deposition.[show abstract] [hide abstract]
ABSTRACT: Tissue factor pathway inhibitor (TFPI) and thrombomodulin (TM) are endothelial-associated anticoagulant proteins thought to control hemostasis in specific vascular beds. Here, we have examined the consequences of TFPI deficiency in the presence of a compounding procoagulant state caused by reduced TM function. TFPI(+/-)/TM(pro/pro) mice are born at less than expected frequency in either TFPI(+/-)/TM(pro/+) or TM(pro/pro) mothers but are born at near the expected frequency in TM(pro/+) mothers. Adult TFPI(+/-)/TM(pro/pro) mice have elevated thrombin-antithrombin complex and increased thrombus volume in an electrical injury model of venous thrombosis. In striking contrast to mice with single deficiency of TFPI or TM, TFPI(+/-)/TM(pro/pro) mice exhibit augmented fibrin deposition not only in the liver, but also in the cerebral microvasculature. TFPI(+/-)/TM(pro/pro) mice exhibit partial intrauterine lethality when carried by mothers with an underlying prothrombotic state, providing the first experimental evidence in an animal model that TFPI-dependent control of hemostasis in the vascular bed of the placenta fulfills a critical role for successful pregnancy outcome. In addition to the placenta, partial TFPI deficiency interacts with decreased TM function in an organ selective manner to produce fibrin deposition in other specific vascular beds, the liver and brain.Journal of Thrombosis and Haemostasis 02/2008; 6(1):111-7.
Article: Networking with fibrinogen: a prerequisite for fibroblast growth factor-2 (FGF-2)-stimulated tumor growth?Journal of Thrombosis and Haemostasis 02/2008; 6(1):174-5.
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ABSTRACT: Blood coagulation factor (F) Va is the essential protein cofactor to the serine protease FXa. Factor Va stimulates the thrombin-to-prothrombin conversion by the prothrombinase complex, by at least five orders of magnitude. Factor Va binds with very high affinity to phosphatidylserine containing phospholipid membranes, which allows the visualization of its membrane-bound state by transmission electron microscopy (EM). In this paper we present an averaged three-dimensional structure of FVa molecules attached to phosphatidylserine containing lipid tubes, as determined by EM and single particle analysis. The low-resolution FVa three-dimensional structure is compared with the available atomic models for FVa. The experimental data are combined with the most suitable atomic model and a membrane-bound FVaEM model is proposed that best fits the protein density defined by EM. In the FVaEM model, the C1 and C2 membrane-binding domains are juxtaposed onto the membrane surface and the model geometries indicate a deeper insertion of both C domains into the lipid bilayer than has been previously suggested. The present structure is a first step towards a higher-resolution experimental structure of a human FVa molecule in its membrane-bound conformation, allowing the visualization of individual domains within FVa and its association with the membrane.Journal of Thrombosis and Haemostasis 02/2008; 6(1):76-82.
Article: Carboxypeptidase U (TAFIa) activity is induced in vivo in ischemic stroke patients receiving thrombolytic therapy.Journal of Thrombosis and Haemostasis 02/2008; 6(1):200-2.
Article: Pharmacogenetic dose refinement prevents warfarin overdose in a patient who is highly warfarin-sensitive.Journal of Thrombosis and Haemostasis 02/2008; 6(1):207-9.
Article: Association between inherited thrombophilic abnormalities and central venous catheter thrombosis in patients with cancer: a meta-analysis.[show abstract] [hide abstract]
ABSTRACT: The risk of deep vein thrombosis (DVT) is increased in cancer patients with central venous catheters (CVC). Factor (F)V Leiden and the G20210A prothrombin mutation (PTM) may play a role in causing catheter-related DVT in patients with cancer. However, information on the association between these thrombophilic abnormalities and CVC-related thrombosis are scarce. To assess the risk of CVC-related thrombosis associated with these two thrombophilic disorders. MEDLINE and EMBASE databases (up to March 2007); reference lists of retrieved articles. Studies comparing the prevalence of prothrombotic abnormalities in cancer patients with CVC-related thrombosis and in a control group of cancer subjects with CVC without thrombosis. Two reviewers independently selected studies and extracted study characteristics, quality and outcomes. Odds ratios (ORs) and 95% confidence intervals (CIs) were calculated for each trial and pooled. Ten studies involving 1000 patients were included. The pooled OR for CVC-related thrombosis was 4.6 (95% CI: 2.6, 8.1) in patients with FV Leiden. The pooled OR for CVC-related thrombosis was 4.9 (95% CI: 1.7, 14.3) in patients with PTM. The estimated attributable risk of CVC-related thrombosis was 13.1% for FV Leiden and 4.5% for PTM. Our meta-analysis suggests that the presence of FV Leiden and PTM is associated with CVC-related thrombosis.Journal of Thrombosis and Haemostasis 02/2008; 6(1):70-5.
Article: Heparin-independent activation of platelets by heparin-induced thrombocytopenia antibodies: a common occurrence.Journal of Thrombosis and Haemostasis 02/2008; 6(1):197-200.
Data provided are for informational purposes only. Although carefully collected, accuracy cannot be guaranteed. The impact factor represents a rough estimation of the journal's impact factor and does not reflect the actual current impact factor. Publisher conditions are provided by RoMEO. Differing provisions from the publisher's actual policy or licence agreement may be applicable.
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