Journal of Thrombosis and Haemostasis最新文献

{"title":"Commentary on “Antiproliferative agent attenuates post-thrombotic vein wall remodeling in murine and human subjects”","authors":"Peter K. Henke","doi":"10.1016/j.jtha.2024.10.004","DOIUrl":"10.1016/j.jtha.2024.10.004","url":null,"abstract":"","PeriodicalId":17326,"journal":{"name":"Journal of Thrombosis and Haemostasis","volume":"23 1","pages":"Pages 34-35"},"PeriodicalIF":5.5,"publicationDate":"2025-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142971540","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"A novel role for thioredoxin-related transmembrane protein TMX4 in platelet activation and thrombus formation","authors":"Zhenzhen Zhao ,&nbsp;Yucan Wang ,&nbsp;Aizhen Yang ,&nbsp;Yi Lu ,&nbsp;Xiaofeng Yan ,&nbsp;Meinan Peng ,&nbsp;Yue Han ,&nbsp;Chao Fang ,&nbsp;Depei Wu ,&nbsp;Yi Wu","doi":"10.1016/j.jtha.2024.09.007","DOIUrl":"10.1016/j.jtha.2024.09.007","url":null,"abstract":"<div><h3>Background</h3><div>The functions of critical platelet proteins are controlled by thiol-disulfide exchanges, which are mediated by the protein disulfide isomerase (PDI) family. It has been shown that some PDI family members are important in platelet activation and thrombosis with distinct functions. TMX4, a membrane-type PDI family member, is expressed in platelets, but whether it has a role in platelet activation remains unknown.</div></div><div><h3>Objectives</h3><div>To determine the role of TMX4 in platelet activation and thrombosis.</div></div><div><h3>Methods</h3><div>The phenotypes of TMX4-deficient mice were evaluated in tail bleeding time assay and laser-induced and FeCl₃-induced arterial injury models. The functions of TMX4 in platelets were assessed <em>in vitro</em> using TMX4-null platelets, recombinant TMX4 protein, and anti-TMX4 antibody.</div></div><div><h3>Results</h3><div>Compared with the control mice, Tie2-Cre/<em>TMX4</em>^{<em>fl/fl</em>} mice deficient of hematopoietic and endothelial TMX4 exhibited prolonged tail bleeding times and reduced platelet thrombus formation. Pf4-Cre/<em>TMX4</em>^{<em>fl/fl</em>} mice deficient of platelet TMX4 also had prolonged tail bleeding times and decreased thrombus formation, which was rescued by injection of recombinant TMX4 protein. Consistently, TMX4 deficiency inhibited platelet aggregation, integrin αIIbβ3 activation, P-selectin expression, phosphatidylserine exposure, and thrombin generation, without affecting tyrosine phosphorylation of intracellular signaling molecules Syk, LAT, PLCγ2 and calcium mobilization. Recombinant TMX4 protein enhanced platelet aggregation and reduced integrin αIIbβ3 disulfide bonds, and TMX4 deficiency decreased free thiols of integrin αIIbβ3, consistent with a potent reductase activity of TMX4. In contrast, an inactive TMX4 protein and a specific anti-TMX4 antibody inhibited platelet aggregation.</div></div><div><h3>Conclusion</h3><div>TMX4 is a novel PDI family member that enhances platelet activation and thrombosis.</div></div>","PeriodicalId":17326,"journal":{"name":"Journal of Thrombosis and Haemostasis","volume":"23 1","pages":"Pages 277-292"},"PeriodicalIF":5.5,"publicationDate":"2025-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142289957","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Management and outcomes in patients with tumor thrombus: a retrospective cohort study","authors":"Sean Hui ,&nbsp;Khalid Zeid ,&nbsp;Roger Kou ,&nbsp;Ranjeeta Mallick ,&nbsp;Marc Carrier ,&nbsp;Tzu-Fei Wang","doi":"10.1016/j.jtha.2024.10.002","DOIUrl":"10.1016/j.jtha.2024.10.002","url":null,"abstract":"<div><h3>Background</h3><div>Tumor thrombus can be associated with an increased risk of venous thromboembolism (VTE) and poor prognosis. The risks and benefits of anticoagulation remain unclear.</div></div><div><h3>Objectives</h3><div>To evaluate the role of anticoagulation and associated outcomes in patients with tumor thrombus.</div></div><div><h3>Methods</h3><div>We conducted a single-center retrospective cohort study in patients with tumor thrombus from 2019 to 2022. All patients were followed for 12 months from the diagnosis of tumor thrombus or until death if death occurred earlier. The primary outcome was the percentage of patients prescribed any dose of anticoagulation for tumor thrombus (or concurrent bland thrombus/VTE). The secondary outcomes included new thrombosis, major bleeding, clinically relevant nonmajor bleeding, and mortality. We calculated the 6- and 12-month cumulative incidence of outcomes with 95% CI and compared those given anticoagulation vs not, considering death as a competing risk.</div></div><div><h3>Results</h3><div>We included 211 patients, among whom 106 (50.2%; 95% CI, 47.9%-52.6%) were given anticoagulation for tumor thrombus or concurrent VTE (present in 21.8%). The most common type of cancer was hepatocellular carcinoma (28%). Splanchnic veins were the most commonly involved (49.3%). Anticoagulation was more likely used if tumor thrombus involved the inferior vena cava and/or the heart, with concurrent VTE, or if thrombosis service was consulted. The overall 12-month incidence of new VTE was 11.4% (95% CI, 7.3%-16.5%), that of major bleeding + clinically relevant nonmajor bleeding was 36.6% (95% CI, 29.6%-43.5%), and mortality of 52.5% (95% CI, 44.8%-59.6%), with no significant differences among groups given anticoagulation or not.</div></div><div><h3>Conclusion</h3><div>Patients with tumor thrombus carry high risks of VTE, bleeding, and mortality. The impact of anticoagulation remains unclear.</div></div>","PeriodicalId":17326,"journal":{"name":"Journal of Thrombosis and Haemostasis","volume":"23 1","pages":"Pages 201-209"},"PeriodicalIF":5.5,"publicationDate":"2025-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142468672","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Aptamer BT200 is protective against myocardial ischemia-reperfusion injury in mice","authors":"Xinyuan Chen,&nbsp;Xianying Liao,&nbsp;Guiping Lu,&nbsp;Yue Ma,&nbsp;Ruowen Wang,&nbsp;Ancai Yuan,&nbsp;Yuquan Xie,&nbsp;Jun Pu","doi":"10.1016/j.jtha.2024.09.032","DOIUrl":"10.1016/j.jtha.2024.09.032","url":null,"abstract":"<div><h3>Background</h3><div>Myocardial ischemia-reperfusion (MI/R) injury tends to affect cardiac function and leads to poor patient prognosis, and there is still no effectively targeted drug to develop anti–von Willebrand factor (VWF) aptamer in acute coronary heart disease. However, the newly anti-VWF aptamer BT200 is applied not only for stroke and hemophilia but also for antithrombolism function in clinical development. The role of BT200 in acute myocardial injury during MI/R is still unknown.</div></div><div><h3>Objectives</h3><div>To investigate the cardioprotective effect of aptamer BT200 in a mouse model of MI/R.</div></div><div><h3>Methods</h3><div>C57BL/6 mice were subjected to 30-minute ischemia and 24-hour reperfusion to establish MI/R model. Mice were treated with intravenous injection of cy3-labeled BT200 and were observed by an <em>in vivo</em> imaging system at different time points. Then, mice were sampled and evaluated by echocardiography, Evans triphenyltetrazolium chloride staining, histopathologic, western blotting, and real-time quantitative polymerase chain reaction assays to detect cardiac injury and inflammation response after 24-hour reperfusion.</div></div><div><h3>Results</h3><div>BT200 aptamer can enter and infiltrate into the ischemic myocardium after 24-hour reperfusion. BT200 was shown to inhibit VWF A1 activity and prolong bleeding time in MI/R mice. Moreover, BT200-treated mice had a significant reduction in infarct size and an improvement in cardiac function post-MI/R. BT200 treatment can also alleviate MI/R-induced microvascular obstruction, inflammation response, and cardiomyocyte apoptosis.</div></div><div><h3>Conclusion</h3><div>Pharmacologic targeting of VWF with BT200 alleviates acute MI/R injury in a murine model and may be a novel therapy strategy for acute myocardial infarction.</div></div>","PeriodicalId":17326,"journal":{"name":"Journal of Thrombosis and Haemostasis","volume":"23 1","pages":"Pages 222-234"},"PeriodicalIF":5.5,"publicationDate":"2025-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142502849","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Déjà vu all over again: a recurrent flaw in anticoagulant study design","authors":"Bethany Samuelson Bannow ,&nbsp;Alison Edelman ,&nbsp;Marc Carrier","doi":"10.1016/j.jtha.2024.10.019","DOIUrl":"10.1016/j.jtha.2024.10.019","url":null,"abstract":"<div><div>The availability of direct oral anticoagulants rapidly changed the landscape of anticoagulation between 2010 and the present. Randomized controlled trials demonstrating efficacy with similar or superior safety compared with warfarin led to the widespread use of direct oral anticoagulants in male and female patients of all ages. Years later, postmarketing data demonstrated a markedly increased rate of heavy menstrual bleeding (HMB) with rivaroxaban that had gone undetected in registry trials.</div><div>Factor (F)XI inhibitors are currently being investigated as another alternative to available anticoagulation agents. While generally mild, the phenotype of inherited FXI deficiency includes bleeding in tissues with enhanced fibrinolysis, including HMB. Thus, we aimed to perform a systematic review of published studies on FXI inhibitors in order to estimate rates of HMB. However, we found that few studies included menstruating individuals, and even fewer specifically reported on uterine bleeding, highlighting once again a flaw in our approach to conducting trials of new anticoagulants.</div></div>","PeriodicalId":17326,"journal":{"name":"Journal of Thrombosis and Haemostasis","volume":"23 1","pages":"Pages 23-26"},"PeriodicalIF":5.5,"publicationDate":"2025-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142546156","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Genetic engineering of megakaryocytes from blood progenitor cells using messenger RNA lipid nanoparticles","authors":"Jerry Leung ,&nbsp;Asel Primbetova ,&nbsp;Colton Strong ,&nbsp;Brenna N. Hay ,&nbsp;Han Hsuan Hsu ,&nbsp;Andrew Hagner ,&nbsp;Leonard J. Foster ,&nbsp;Dana Devine ,&nbsp;Pieter R. Cullis ,&nbsp;Peter W. Zandstra ,&nbsp;Christian J. Kastrup","doi":"10.1016/j.jtha.2024.09.008","DOIUrl":"10.1016/j.jtha.2024.09.008","url":null,"abstract":"<div><h3>Background</h3><div>Platelets are an essential component of hemorrhage control and management, and engineering platelets to express therapeutic proteins could expand their use as a cell therapy. Genetically engineered platelets can be achieved by modifying the platelet precursor cells, megakaryocytes (MKs). Current strategies include transfecting MK progenitors <em>ex vivo</em> with viral vectors harboring lineage-driven transgenes and inducing the production of <em>in vitro</em> modified platelets. The use of viruses, however, poses challenges in clinical implementation, and no methods currently exist to genetically modify MKs with nonviral techniques. Lipid nanoparticles (LNPs) are a nonviral delivery system that could enable a facile strategy to modify MKs with a variety of nucleic acid payloads.</div></div><div><h3>Objectives</h3><div>To investigate whether LNPs can transfect cultured hematopoietic stem/progenitor cell–derived MKs to express exogenous proteins and induce functional changes.</div></div><div><h3>Methods</h3><div>MK and MK progenitors differentiated from cord blood–derived hematopoietic stem/progenitor cells were treated with LNP formulations containing messenger RNA and resembling the clinically approved LNP formulations. Transfection efficiency was assessed through flow cytometry by expression of enhanced green fluorescent protein. Functional changes to the MKs were assessed through rotational thromboelastometry by expression of exogenous coagulation factor (F)VII, a representative physiologically relevant protein.</div></div><div><h3>Results</h3><div>LNPs enabled transfection efficiencies of 99% in MKs and did not impair MK maturation, viability, and morphology. MKs engineered to express exogenous FVII decreased clotting time in FVII-deficient plasma following clot initiation.</div></div><div><h3>Conclusion</h3><div>This approach provides an easy-to-use modular platform to genetically modify MK and MK progenitors, which can be potentially extended to producing genetically modified cultured platelets.</div></div>","PeriodicalId":17326,"journal":{"name":"Journal of Thrombosis and Haemostasis","volume":"23 1","pages":"Pages 306-313"},"PeriodicalIF":5.5,"publicationDate":"2025-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142349115","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Loss of function in protein Z (PROZ) is associated with increased risk of ischemic stroke in the UK Biobank","authors":"Amelia K. Haj ,&nbsp;Justine Ryu ,&nbsp;Sean J. Jurgens ,&nbsp;Sharjeel Chaudhry ,&nbsp;Satoshi Koyama ,&nbsp;Xin Wang ,&nbsp;Seung Hoan Choi ,&nbsp;Cody Hou ,&nbsp;Simone Sanna-Cherchi ,&nbsp;Christopher D. Anderson ,&nbsp;Patrick T. Ellinor ,&nbsp;Pavan K. Bendapudi","doi":"10.1016/j.jtha.2024.09.016","DOIUrl":"10.1016/j.jtha.2024.09.016","url":null,"abstract":"<div><h3>Background</h3><div>The vitamin K–dependent coagulation factor protein Z (PZ), encoded by the <em>PROZ</em> gene, is canonically considered to have anticoagulant effects through negative regulation of factor Xa. Paradoxically, higher circulating PZ concentrations have repeatedly been associated with an elevated risk of acute ischemic stroke.</div></div><div><h3>Objectives</h3><div>We performed a large-scale genetic association study to examine the relationship between germline genetic variants in <em>PROZ</em> and the risk of ischemic stroke.</div></div><div><h3>Methods</h3><div>Using whole-exome sequencing and clinical data for 416 711 participants in the UK Biobank (UKB), we identified individuals with rare (minor allele frequency ≤0.1%) putatively function-altering variants in <em>PROZ</em>. Using Firth’s logistic regression and controlling for known stroke risk factors, we evaluated the association between variant carrier status and noncardioembolic ischemic stroke (NCEIS). Additionally, we evaluated differences in the plasma levels of 1472 proteins between <em>PROZ</em> variant carriers and noncarriers in a subset of 48 893 UKB participants.</div></div><div><h3>Results</h3><div>After accounting for missing data, qualifying variants in <em>PROZ</em> were identified in 414 UKB participants (99.0% heterozygous). Variant carriers had a significantly increased risk of NCEIS (odds ratio, 2.34; 95% CI, 1.15-4.13; <em>P</em> = .02) but not of venous thromboembolism, myocardial infarction, or peripheral artery disease. Plasma proteomics analysis revealed that <em>PROZ</em> variant carriers had significantly elevated levels of 2 proteins related to the response to cerebral ischemia, peroxiredoxins 1 and 6 (PRDX1: fold change, 1.83; <em>P</em> = 1.3 × 10⁻⁵; PRDX6: fold change, 1.78; <em>P</em> = 9.6 × 10⁻¹⁰).</div></div><div><h3>Conclusion</h3><div>Lifelong exposure to decreased PZ levels confers a significantly increased risk of NCEIS, consistent with the role of PZ as an anticoagulant factor.</div></div>","PeriodicalId":17326,"journal":{"name":"Journal of Thrombosis and Haemostasis","volume":"23 1","pages":"Pages 171-180"},"PeriodicalIF":5.5,"publicationDate":"2025-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142391506","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Phosphatidylserine-blocking nanoparticles inhibit thrombosis without increased bleeding in mice","authors":"Jeremy G.T. Wurtzel ,&nbsp;Brian D. Gray ,&nbsp;Koon Y. Pak ,&nbsp;Xuefei Zhao ,&nbsp;Peisong Ma ,&nbsp;Steven E. McKenzie ,&nbsp;Michelle Tanujaya ,&nbsp;Victor Rizzo ,&nbsp;Fabiola Del Carpio-Cano ,&nbsp;A. Koneti Rao ,&nbsp;Parkson Lee-Gau Chong ,&nbsp;Lawrence E. Goldfinger","doi":"10.1016/j.jtha.2024.10.007","DOIUrl":"10.1016/j.jtha.2024.10.007","url":null,"abstract":"<div><h3>Background</h3><div>Phosphatidylserine (PS) is a procoagulant phospholipid enriched on surfaces of activated vascular cells including platelets, endothelium, monocytes, and microvesicles. As a molecular driver of thrombosis accessible to drug blockade, PS is an attractive pharmacologic target for modulating thrombogenesis, with potentially reduced bleeding risk compared to anticoagulant and antiplatelet therapies.</div></div><div><h3>Objectives</h3><div>Test antithrombotic capabilities of a liposomal formulation, Zn-dipicolylamine cyanine-3[22,22]/1-palmitoyl-2-oleoyl-<em>sn</em>-glycero-3-phosphocholine (molar ratio, 3:97), designated as DPAL, which we previously described binds selectively to PS-enriched cell surfaces, compared with effects on bleeding, in mouse models.</div></div><div><h3>Methods</h3><div>PS-dependent DPAL binding to human and murine platelets was tested <em>in vitro</em>. Thrombosis and bleeding after DPAL intravenous administration were tested in C57Bl/6J mice following FeCl₃ carotid arterial injury and tail tip amputation, respectively. Incorporation in hemostatic clots was investigated in the cremaster muscle laser injury model. Toxicity was tested by direct exposure to human endothelial cell cultures.</div></div><div><h3>Results</h3><div>DPAL bound agonist-stimulated, PS-positive human and murine platelets, blocked by Annexin V or Ano6 deletion, which ablate PS exposure. DPAL prolonged prothrombin time, but did not prevent thrombin-induced fibrinogen receptor activation or aggregation, nor alter blood cell counts including platelets. Following arteriolar laser injury, DPAL bound wound surfaces and edges without destabilizing plugs. DPAL dose-dependently blocked FeCl₃-induced arterial thrombosis but did not substantially increase bleeding, or induce endothelial cell death.</div></div><div><h3>Conclusion</h3><div>DPAL reduces thrombogenesis with minimal effects on bleeding in mouse models via selective binding to PS. DPAL may support novel approaches to modulate pathogenic thrombin generation with improved safety profiles in multiple contexts.</div></div>","PeriodicalId":17326,"journal":{"name":"Journal of Thrombosis and Haemostasis","volume":"23 1","pages":"Pages 108-122"},"PeriodicalIF":5.5,"publicationDate":"2025-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142468675","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"High-dose intravenous immunoglobulin G and usual heparin anticoagulation for urgent cardiac surgery in a patient with severe autoimmune heparin-induced thrombocytopenia","authors":"Theodore E. Warkentin ,&nbsp;William Geerts ,&nbsp;Jo-Ann I. Sheppard ,&nbsp;Cameron B. Guest ,&nbsp;Gideon Cohen ,&nbsp;Pablo Perez d’Empaire ,&nbsp;Ishac Nazy ,&nbsp;Donald M. Arnold","doi":"10.1016/j.jtha.2024.10.035","DOIUrl":"10.1016/j.jtha.2024.10.035","url":null,"abstract":"<div><div>A 56-year-old woman required urgent cardiac surgery for <em>Streptococcus mitis</em> mitral valve infective endocarditis complicated by severe autoimmune heparin-induced thrombocytopenia (aHIT). We reasoned that the combination of high-dose intravenous immunoglobulin G (IVIG; to mitigate aHIT antibody-mediated platelet activation in the presence of heparin) together with the high concentrations of heparin attained during cardiac surgery (which typically produces less platelet activation <em>in vitro</em> vs usual therapeutic heparin concentrations) might prove effective. Accordingly, our patient underwent cardiac surgery with heparin following high-dose IVIG (1 g/kg × 2) without intra- or postoperative thrombosis. Serial serotonin release assays, using blood obtained pre-/post-IVIG, showed minimal platelet activation (∼30% serotonin release) post-IVIG at heparin concentrations typically obtained during cardiac surgery (2-5 U/mL) and significantly less than pre-IVIG serum in heparin’s absence (∼85% serotonin release). In the setting of urgent cardiac surgery, preoperative high-dose IVIG appears to be a reasonable strategy to reduce platelet-activating effects of heparin-induced thrombocytopenia (including aHIT) antibodies, permitting safe use of standard intraoperative heparin dosing.</div></div>","PeriodicalId":17326,"journal":{"name":"Journal of Thrombosis and Haemostasis","volume":"23 1","pages":"Pages 321-324"},"PeriodicalIF":5.5,"publicationDate":"2025-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142648388","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Platelets welcome a new protein disulfide isomerase family member","authors":"Robert Flaumenhaft","doi":"10.1016/j.jtha.2024.10.006","DOIUrl":"10.1016/j.jtha.2024.10.006","url":null,"abstract":"","PeriodicalId":17326,"journal":{"name":"Journal of Thrombosis and Haemostasis","volume":"23 1","pages":"Pages 36-38"},"PeriodicalIF":5.5,"publicationDate":"2025-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142971477","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}