Blood Vessels, Thrombosis & Hemostasis最新文献

{"title":"Incorporating point-of-care technologies to assess treatment response in sickle cell disease","authors":"Bindu Parachalil Gopalan ∗ , Timothy Quang ∗ , Maria A. Lizarralde-Iragorri , Dianna Lovins , Ann Cullinane , Alina Dulau-Florea , Bruce Tromberg , Arun S. Shet","doi":"10.1016/j.bvth.2024.100009","DOIUrl":"10.1016/j.bvth.2024.100009","url":null,"abstract":"","PeriodicalId":100190,"journal":{"name":"Blood Vessels, Thrombosis & Hemostasis","volume":"1 2","pages":"Article 100009"},"PeriodicalIF":0.0,"publicationDate":"2024-06-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.sciencedirect.com/science/article/pii/S2950327224000093/pdfft?md5=2720a428b76bb505612843d72b3e3c38&pid=1-s2.0-S2950327224000093-main.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141138195","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"HMGA2 promotes platelet-neutrophil complex formation and pulmonary tissue damage in myelodysplastic syndromes","authors":"Natsumi Matsunuma ,&nbsp;Yoshihiro Hayashi ,&nbsp;Marina Fukuda ,&nbsp;Kanako Yuki ,&nbsp;Yasushige Kamimura-Aoyagi ,&nbsp;Hiroki Kobayashi ,&nbsp;Naoki Shingai ,&nbsp;Yuka Harada ,&nbsp;Hironori Harada","doi":"10.1016/j.bvth.2024.100014","DOIUrl":"10.1016/j.bvth.2024.100014","url":null,"abstract":"<div><h3>Abstract</h3><p>High mobility group AT-hook 2 (HMGA2) is an architectural transcription factor that functions as an oncogene in various cancers. Although overexpression of HMGA2 has been reported in several myeloid malignancies, its role varies considerably in different disease contexts. Here, we identified a distinct role of HMGA2 as a mediator of noninfectious pneumonia in myelodysplastic syndrome (MDS). The expression level of <em>HMGA2</em> in CD34⁺ hematopoietic stem cells and progenitors (HSC/Ps) was significantly associated with the incidence of noninfectious pneumonia, a common systemic complication in patients with MDS. Consistent with this clinical investigation, HMGA2 overexpression in a mouse model of an MDS-associated mutation led to the development of lethal noninfectious pneumonia. Mechanistically, HMGA2 overexpression conferred a megakaryocytic lineage bias to HSC/Ps and contributed to platelet activation in MDS mice. P-selectin–positive activated platelets interacted with MDS clone–derived neutrophils that exhibit increased susceptibility to cell death and formed platelet-neutrophil complexes (PNCs). Both the frequency of PNCs and neutrophil cell death within the lung microenvironment increased in MDS mice overexpressing HMGA2. Genetic inhibition of P-selectin attenuated pulmonary tissue damage in MDS mice. These findings indicate that PNCs could be a new therapeutic target for noninfectious pneumonia in patients with MDS and provide new insights into the mechanistic basis of the systemic complications of MDS.</p></div>","PeriodicalId":100190,"journal":{"name":"Blood Vessels, Thrombosis & Hemostasis","volume":"1 2","pages":"Article 100014"},"PeriodicalIF":0.0,"publicationDate":"2024-06-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.sciencedirect.com/science/article/pii/S2950327224000147/pdfft?md5=bb4a2c0bb20376bb8b90b0688c5371f3&pid=1-s2.0-S2950327224000147-main.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141144779","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Venous anomalies: an underrecognized but important cause of venous thromboembolism","authors":"Joanne So ,&nbsp;Caroline Dix ,&nbsp;Warren Clements ,&nbsp;Harry Gibbs ,&nbsp;Huyen Tran ,&nbsp;James D. McFadyen","doi":"10.1016/j.bvth.2024.100013","DOIUrl":"10.1016/j.bvth.2024.100013","url":null,"abstract":"<div><h3>Abstract</h3><p>Anatomical variants, such as May-Thurner syndrome (MTS) and inferior vena cava (IVC) variants, are underrecognized causes of deep venous thrombosis (DVT), despite affecting management. We aimed to identify the proportion of anatomical variants in proximal lower limb DVT. A retrospective cohort study was performed with cases of acute proximal DVT from 2014 to 2021 identified from ICD-10 codes. We identified 4731 DVTs and included 1268 proximal DVTs. Thirty-six (2.84%) had an anatomical variant (25 MTS and 11 IVC variants), with a rate of 14.39% in females &lt;50 years old. Compared with nonvariant DVTs, they were more likely to be unprovoked (81% vs 23%), younger (median age, 37 vs 63 years), female (67% vs 37%), and have postthrombotic syndrome (22% vs 9%). Variants frequently received thrombolysis (58% vs 1%) or angioplasty (47% vs 0%) and indefinite anticoagulation (83% vs 40%). Further investigation for variants should be considered for high-risk patients, as variants affect management.</p></div>","PeriodicalId":100190,"journal":{"name":"Blood Vessels, Thrombosis & Hemostasis","volume":"1 3","pages":"Article 100013"},"PeriodicalIF":0.0,"publicationDate":"2024-05-22","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.sciencedirect.com/science/article/pii/S2950327224000135/pdfft?md5=101383f35f94ec4ed05c4461416ff731&pid=1-s2.0-S2950327224000135-main.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141133282","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Clusterin can mediate apoptosis-induced molecular mechanisms in immune thrombocytopenia","authors":"Tea Stein ,&nbsp;Christina Bitsina ,&nbsp;Michelle Seiler ,&nbsp;Markus Schmugge ,&nbsp;Francesca D. Franzoso","doi":"10.1016/j.bvth.2024.100012","DOIUrl":"10.1016/j.bvth.2024.100012","url":null,"abstract":"<div><h3>Abstract</h3><p>Abnormalities in the apoptosis pathway have been implicated into the pathogenesis of various autoimmune diseases, including immune thrombocytopenia (ITP). Our data suggest that mechanisms associated with impaired clusterin-mediated apoptosis might play a role in the pathophysiology of ITP platelets and their production by MKs. Platelet-rich plasma from 10 patients with ITP compared with healthy controls was used for the apoptosis proteomic profiling and clusterin (<em>CLU</em>) expression validation by reverse transcription polymerase chain reaction. We used the megakaryoblastic (MEG-01) cell line, treated for 2 hours with plasma from patients with newly diagnosed ND), chronic ITP or healthy controls and pan-caspase inhibitor (Z-VAD-FMK), apoptosis inducer ABT-737, rotenone (Rot), or rapamycin (Rap). Our apoptosis proteomic profiling revealed significantly increased expression levels of certain apoptotic genes such as CLU, phospho-p53 (S46), procaspase-3, and cleaved caspase 3 (<em>CASP-3</em>) in patients with ITP compared with healthy controls. Treatment with pan-caspase inhibitor or Rap had a significant downregulatory effect at messenger RNA (mRNA) level for CLU; CASP-3, -8, and -9; p53; and B-cell lymphoma-2–associated X protein (<em>BAX</em>) in ITP plasma–treated cells in comparison with control plasma–treated MEG-01 cells, whereas Rot or ABT-737 had opposite effects. We observed a significant downregulation of mRNA expression levels of these apoptotic markers in ITP plasma–treated and <em>CLU</em> or glucose-regulated protein 78 small interfering RNA–transfected MEG-01 cells. Our results indicate an upregulation of CLU and <em>BAX</em> in platelets and MKs which may contribute to deciphering the cause of platelet destruction in ITP disease.</p></div>","PeriodicalId":100190,"journal":{"name":"Blood Vessels, Thrombosis & Hemostasis","volume":"1 3","pages":"Article 100012"},"PeriodicalIF":0.0,"publicationDate":"2024-05-21","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.sciencedirect.com/science/article/pii/S2950327224000123/pdfft?md5=6b8a4dce22601fd3b7c37e71e3a35d40&pid=1-s2.0-S2950327224000123-main.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141953339","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Tailoring caplacizumab administration using ADAMTS13 activity for immune-mediated thrombotic thrombocytopenic purpura","authors":"Sean G. Yates ,&nbsp;Sandra L. Hofmann ,&nbsp;Ibrahim F. Ibrahim ,&nbsp;Yu-Min P. Shen ,&nbsp;Allen P. Green ,&nbsp;Ravi Sarode","doi":"10.1016/j.bvth.2024.100010","DOIUrl":"10.1016/j.bvth.2024.100010","url":null,"abstract":"<div><h3>Abstract</h3><p>Caplacizumab, a nanobody targeting the A1 domain of von Willebrand factor (VWF), rapidly inhibits VWF interaction with platelets. This inhibition effectively prevents microthrombus formation and has led to its increasing use as a frontline disease-modifying agent. Clinical trial and postmarketing data suggest that caplacizumab administration guided by ADAMTS13 (a disintegrin and metalloprotease with thrombospondin type 1 motif, member 13) recovery may be as effective and possibly safer than the dosing recommended by the manufacturer. Accordingly, this before-after cohort study sought to compare historical cases of immune thrombotic thrombocytopenic purpura (iTTP) (20 episodes) managed without caplacizumab with cases of iTTP (20 episodes) using a tailored approach to caplacizumab administration based on ADAMTS13 activity measured twice weekly during the hospital stay. Caplacizumab was discontinued when the ADAMTS13 activity was ≥20% on 2 consecutive occasions. Caplacizumab-treated patients received 6 doses (range, 2-30), an 81% reduction relative to the number of doses based on the manufacturer’s recommendations (35+), leading to cost savings of $6 466 800. Platelet count normalization occurred at 4 days in caplacizumab-treated patients vs 6 days in the non-caplacizumab cohort (<em>P</em> = .2). Rates of exacerbation and relapse were similar between both groups. Ultimately, these findings suggest that tailoring caplacizumab administration based on ADAMTS13 activity recovery leads to a marked reduction in the caplacizumab doses required. Despite this reduction, clinical and laboratory data were similar to those described in clinical trials and postmarketing studies while generating significant cost savings. Given these findings, prospective studies using ADAMTS13 activity to guide individualized caplacizumab therapy are warranted.</p></div>","PeriodicalId":100190,"journal":{"name":"Blood Vessels, Thrombosis & Hemostasis","volume":"1 3","pages":"Article 100010"},"PeriodicalIF":0.0,"publicationDate":"2024-05-20","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.sciencedirect.com/science/article/pii/S295032722400010X/pdfft?md5=56d7c205f9e439a85649a8226120009f&pid=1-s2.0-S295032722400010X-main.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141140252","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Real-world insights on the management of immune-mediated thrombotic thrombocytopenic purpura with caplacizumab","authors":"Daan Dierickx ,&nbsp;Thierry Connerotte ,&nbsp;Julie Dallemagne ,&nbsp;Ann De Becker ,&nbsp;Ine Moors ,&nbsp;Sylvia Snauwaert ,&nbsp;Anne Sonet ,&nbsp;Koen Theunissen ,&nbsp;Dimitri Breems ,&nbsp;Adrien De Voeght ,&nbsp;Aurélie Jaspers ,&nbsp;Catherine Lambert ,&nbsp;Bert Heyrman ,&nbsp;Joris Hautekiet ,&nbsp;Sofie Lyna ,&nbsp;Chantal Maertens ,&nbsp;Vanessa Delrieu","doi":"10.1016/j.bvth.2024.100008","DOIUrl":"10.1016/j.bvth.2024.100008","url":null,"abstract":"","PeriodicalId":100190,"journal":{"name":"Blood Vessels, Thrombosis & Hemostasis","volume":"1 2","pages":"Article 100008"},"PeriodicalIF":0.0,"publicationDate":"2024-05-03","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.sciencedirect.com/science/article/pii/S2950327224000081/pdfft?md5=ae0ed1e3c0a98ab76962842e53d150e4&pid=1-s2.0-S2950327224000081-main.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141037208","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"A multicellular vessel-on-a-chip model reveals context-dependent roles for platelets in inflammation and inflammatory hemostasis","authors":"Rebecca B. Riddle ,&nbsp;Karin Jennbacken ,&nbsp;Kenny M. Hansson ,&nbsp;Matthew T. Harper","doi":"10.1016/j.bvth.2024.100007","DOIUrl":"https://doi.org/10.1016/j.bvth.2024.100007","url":null,"abstract":"<div><h3>Abstract</h3><p>The immune system identifies and destroys invading pathogens. However, chronic inflammation and excessive tissue damage can occur if inflammation is not resolved or if the immune system misidentifies a threat. Therefore, the immune system must be tightly controlled. However, the complex cell-cell and cell-microenvironment interactions that regulate immune-cell recruitment are challenging to recapitulate in 2-dimensional in vitro models, and poorly representative of human physiology in in vivo animal models. Organ-on-a-chip technology has the potential to overcome these limitations and provide powerful preclinical models. In this study, we developed a vessel-on-a-chip model to investigate the role of platelets in inflammation and inflammatory hemostasis. Endothelial vessels cultured in the OrganoPlate exhibited physiological barrier function to macromolecules and red blood cells (RBCs), which was enhanced by platelets. Cytokine stimulation increased vessel permeability and induced neutrophil transmigration. Leakage of RBCs occurred at sites of inflammation and/or neutrophil transmigration, depending on the extracellular matrix composition. Addition of platelets prevented RBC leakage at these sites, while simultaneously increasing permeability and neutrophil transmigration, demonstrating the multifaceted role of platelets in inflammatory hemostasis. In angiogenic neovessels, platelets played a protective role, preventing leakage of both small molecules and RBCs. Together, our model successfully recapitulated the modulation of endothelial barrier function and inflammation by platelets and demonstrated the feasibility of investigating complex cellular interactions in in vitro models.</p></div>","PeriodicalId":100190,"journal":{"name":"Blood Vessels, Thrombosis & Hemostasis","volume":"1 2","pages":"Article 100007"},"PeriodicalIF":0.0,"publicationDate":"2024-04-30","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.sciencedirect.com/science/article/pii/S295032722400007X/pdfft?md5=edb3e86ad1aba2714f231a2a11968874&pid=1-s2.0-S295032722400007X-main.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"140948054","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Idiopathic multicentric Castleman disease - TAFRO results in high levels of mTOR activator SVEP1, tissue factor, and endotheliopathy","authors":"Chen Lossos ,&nbsp;Jenna Brown ,&nbsp;Sara Sheikhbahaei ,&nbsp;Anne Hubben ,&nbsp;Sharon C. Liu ,&nbsp;Keith R. McCrae ,&nbsp;Shruti Chaturvedi ,&nbsp;Rakhi P. Naik ,&nbsp;Ivo M.B. Francischetti","doi":"10.1016/j.bvth.2024.100006","DOIUrl":"10.1016/j.bvth.2024.100006","url":null,"abstract":"<div><h3>Abstract</h3><p>Idiopathic multicentric Castleman disease (iMCD) is an inflammatory disease associated with a cytokine storm, activation of the PI3K/AKT/mTOR pathway, coagulopathy, and increased risk of thrombosis. The mechanisms underlying these pathologic processes remain elusive. We studied novel markers of mTOR activation and thrombosis in 1 patient with typical features of iMCD with TAFRO (thrombocytopenia, anasarca, fevers, reticulin myelofibrosis, and organomegaly) syndrome (iMCD-TAFRO). Plasma levels of SVEP1 (Sushi, von Willebrand factor type A, epidermal growth factor, and pentraxin domain–containing 1 protein), a newly identified mTOR activator associated with cardiovascular diseases and dementia, in addition to cytokines, chemokines and components of the coagulation cascade and complement system were evaluated by enzyme-linked immunosorbent assay (ELISA) and arrays. Compared with healthy controls, a 15-fold increase in SVEP1 was observed. High levels of factor VIIa/antithrombin and microparticles expressing functional tissue factor (TF) were detected. The anticoagulants thrombomodulin and soluble endothelial protein C receptor were elevated, indicating shedding from endothelial cells. Plasminogen activator inhibitor 1 was increased, consistent with hypofibrinolysis, whereas high levels of C3b and C5a are in keeping with complement activation. Furthermore, markers of endothelial cell activation (e.g. von Willebrand factor, angiopoietin-2), cell adhesion molecules, and angiogenesis mediators were upregulated. SVEP1 emerges as a potential mechanism of mTOR activation in iMCD-TAFRO, while multiple pathways influence coagulopathy. Immunothrombosis emerges as a potential therapeutic target for iMCD.</p></div>","PeriodicalId":100190,"journal":{"name":"Blood Vessels, Thrombosis & Hemostasis","volume":"1 2","pages":"Article 100006"},"PeriodicalIF":0.0,"publicationDate":"2024-04-03","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.sciencedirect.com/science/article/pii/S2950327224000068/pdfft?md5=01d36b9f10240b963e82456d37859b0d&pid=1-s2.0-S2950327224000068-main.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"140757920","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Angiopoietin-2 is associated with sickle cell complications, including stroke risk, and decreases with hydroxyurea therapy","authors":"Thomas F. Siegert ,&nbsp;Robert O. Opoka ,&nbsp;Maria Nakafeero ,&nbsp;Aubri Carman ,&nbsp;Kagan A. Mellencamp ,&nbsp;Teresa Latham ,&nbsp;Heather Hume ,&nbsp;Adam Lane ,&nbsp;Russell E. Ware ,&nbsp;John M. Ssenkusu ,&nbsp;Chandy C. John ,&nbsp;Andrea L. Conroy","doi":"10.1016/j.bvth.2024.100001","DOIUrl":"10.1016/j.bvth.2024.100001","url":null,"abstract":"<div><h3>Abstract</h3><p>Hydroxyurea reduces morbidity and mortality in children with sickle cell anemia (SCA). The endothelium is central to SCA-related complications including stroke. However, hydroxyurea’s impact on the endothelium is not well described. To address this gap, we measured plasma levels of endothelial activation markers (angiopoietin-2, P-selectin, soluble endothelial selectin [sE-selectin], soluble intercellular cellular adhesion molecule 1, and soluble vascular endothelial cellular adhesion molecule) by enzyme-linked immunosorbent assay after initiation of hydroxyurea therapy. Samples were collected from Ugandan children with SCA enrolled in a clinical trial evaluating hydroxyurea vs placebo (NOHARM trial). Samples were collected at enrollment; and then after 2, 4, and 12 months of follow-up. Longitudinal changes in biomarker levels were evaluated using linear mixed effects models. Transcranial Doppler (TCD) velocities were measured at 10 to 12 months follow-up to assess cerebral blood flow and primary stroke risk. Mediation analysis was used to explore causal pathways of hydroxyurea-mediated effects on TCD velocities. In total, 798 plasma samples were tested from 205 children (mean enrollment age, 2.2 years). At enrollment, higher levels of angiopoietin-2 were associated with a previous medical history of dactylitis, vaso-occlusive crises, acute chest syndrome, and transfusion (<em>P</em> &lt; .05 for all). Hydroxyurea therapy at a fixed dose of 20 mg/kg per day decreased plasma angiopoietin-2, P-selectin, and sE-selectin levels over the study period (<em>P</em> &lt; .05 for all). Angiopoietin-2 and sE-selectin were associated with higher TCD velocities. Mediation analysis suggests that hydroxyurea decreases TCD velocities through an increase in fetal and total hemoglobin. Increased fetal and total hemoglobin, and decreased white blood cell count may decrease TCD velocity, in part, through an angiopoiten-2–mediated pathway. This trial was registered at <span>www.ClinicalTrials.gov</span><svg><path></path></svg> as #NCT01976416.</p></div>","PeriodicalId":100190,"journal":{"name":"Blood Vessels, Thrombosis & Hemostasis","volume":"1 1","pages":"Article 100001"},"PeriodicalIF":0.0,"publicationDate":"2024-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.sciencedirect.com/science/article/pii/S2950327224000019/pdfft?md5=f1c5ca1f4a1bdaab750c18dd27ec29af&pid=1-s2.0-S2950327224000019-main.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"139897487","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Evaluating research collaboration networks among venous thromboembolism researchers before and during the COVID-19 pandemic","authors":"Divya Karsanji ,&nbsp;James A. King ,&nbsp;Jenny Godley ,&nbsp;Deborah M. Siegal ,&nbsp;Teresa M. Chan ,&nbsp;Grégoire Le Gal ,&nbsp;Marc Carrier ,&nbsp;Susan R. Kahn ,&nbsp;Tobias Tritschler ,&nbsp;Nicole J. Langlois ,&nbsp;Chad Saunders ,&nbsp;Ramy Saleh ,&nbsp;Alexandra Garven ,&nbsp;Caleb MacGillivray ,&nbsp;Marc A. Rodger ,&nbsp;Leslie Skeith","doi":"10.1016/j.bvth.2024.100004","DOIUrl":"https://doi.org/10.1016/j.bvth.2024.100004","url":null,"abstract":"","PeriodicalId":100190,"journal":{"name":"Blood Vessels, Thrombosis & Hemostasis","volume":"1 1","pages":"Article 100004"},"PeriodicalIF":0.0,"publicationDate":"2024-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.sciencedirect.com/science/article/pii/S2950327224000044/pdfft?md5=aa71f0d53b40103720a335466fc1712d&pid=1-s2.0-S2950327224000044-main.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"140113270","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}