Seminars in thrombosis and hemostasis最新文献

{"title":"Alterations in the Blood-Brain Barrier in Mood Disorders and Neurodegenerative Diseases.","authors":"Ismael Conejero, Mathias Chea, Philippe Courtet, Sylvie Bouvier, Fabricio Pereira","doi":"10.1055/s-0045-1804893","DOIUrl":"https://doi.org/10.1055/s-0045-1804893","url":null,"abstract":"<p><p>Depressive disorders and suicidal behaviors represent major causes of health loss. Modifications of brain microvasculature, and specifically alterations of the blood-brain barrier have been supposed to participate in the vulnerability to those disorders along with cognitive impairment, especially in the older adults. In this article, we addressed evidence linking blood-brain barrier impairments with mood disorders and suicide. Secondly, we investigated their relationship with depression in old age, and with neurodegenerative processes. Particular attention was drawn toward the potential interactions between the coagulation processes and the blood-brain barrier dysfunctions, as innovative treatment strategies may emerge from research in those fields. Overall, the studies reviewed highlight the implication of multiple dysfunctions of the blood-brain barrier in mood disorders and suicide. Impairments of the blood-brain barrier show relationships with altered expression of endothelial cell junction proteins. These modifications also implicate receptors of the extracellular matrix, the vascular endothelial growth factor, changes in perivascular astrocytes, and has links with local and systemic inflammatory processes. Dysfunctions of the blood-brain barrier underly chronic stress and participate in psychiatric diathesis in old age. In addition, we outline that coagulation processes are likely to interact with the blood-brain barrier and further contribute to neurodegenerative disorders. In conclusion, new pathophysiological models offer perspectives toward detecting new biomarkers in mood disorders and suicide. In parallel, these models open avenues for developing innovative therapeutic agents, although further considering their potential risks and eventual benefits is needed.</p>","PeriodicalId":21673,"journal":{"name":"Seminars in thrombosis and hemostasis","volume":" ","pages":""},"PeriodicalIF":3.6,"publicationDate":"2025-03-09","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143586794","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":"Laboratory and Molecular Diagnosis of Factor XI Deficiency.","authors":"Simon Davidson, Keith Gomez","doi":"10.1055/s-0044-1792033","DOIUrl":"10.1055/s-0044-1792033","url":null,"abstract":"<p><p>The prevalence of factor XI (FXI) deficiency is 1 per 10 to 20,000 in the general population, much higher than that reported in most texts. The prevalence is higher in Ashkenazi Jews where it is about 1:20. Clinically, FXI deficiency presents as a mild bleeding disorder mostly associated with posttraumatic or postsurgical hemorrhages or unexplained minor bleeding. It is often discovered due to incidental finding of a prolonged activated partial thromboplastin time (aPTT) on routine laboratory screening. FXI deficiency is an autosomal recessive bleeding disorder with many causative <i>F11</i> gene defects. Diagnosis is based on FXI activity, antigen levels, and molecular diagnostics. As FXI levels do not correlate with bleeding symptoms, identification of pathogenic genetic variants may be a more accurate predictor of bleeding risk and therefore aid in the clinical management of the patient. Two variants in the <i>F11</i> gene account for most cases found in the Jewish and Arab populations. Patients with FXI deficiency can develop inhibitors to FXI although spontaneously acquired inhibitors are extremely rare. We will discuss laboratory and molecular assays used to diagnose FXI deficiency as well as interferences that can complicate diagnosis including new anticoagulants and acquired FXI inhibitors.</p>","PeriodicalId":21673,"journal":{"name":"Seminars in thrombosis and hemostasis","volume":" ","pages":"145-154"},"PeriodicalIF":3.6,"publicationDate":"2025-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11906224/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142576857","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":"Glanzmann Thrombasthenia 10 Years Later: Progress Made and Future Directions.","authors":"Alan T Nurden, Paquita Nurden","doi":"10.1055/s-0044-1782519","DOIUrl":"10.1055/s-0044-1782519","url":null,"abstract":"<p><p>Glanzmann thrombasthenia (GT) is the most common inherited platelet disorder (IPD) with mucocutaneous bleeding and a failure of platelets to aggregate when stimulated. The molecular cause is insufficient or defective αIIbβ3, an integrin encoded by the <i>ITGA2B</i> and <i>ITGB3</i> genes. On activation αIIbβ3 undergoes conformational changes and binds fibrinogen (Fg) and other proteins to join platelets in the aggregate. The application of next-generation sequencing (NGS) to patients with IPDs has accelerated genotyping for GT; progress accompanied by improved mutation curation. The evaluation by NGS of variants in other hemostasis and vascular genes is a major step toward understanding why bleeding varies so much between patients. The recently discovered role for glycoprotein VI in thrombus formation, through its binding to fibrin and surface-bound Fg, may offer a mechanosensitive back-up for αIIbβ3, especially at sites of inflammation. The setting up of national networks for IPDs and GT is improving patient care. Hematopoietic stem cell therapy provides a long-term cure for severe cases; however, prophylaxis by monoclonal antibodies designed to accelerate fibrin formation at injured sites in the vasculature is a promising development. Gene therapy using lentil-virus vectors remains a future option with CRISPR/Cas9 technologies offering a promising alternative route.</p>","PeriodicalId":21673,"journal":{"name":"Seminars in thrombosis and hemostasis","volume":" ","pages":"196-208"},"PeriodicalIF":3.6,"publicationDate":"2025-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"140158966","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":"Factor XIII Deficiency: Laboratory, Molecular, and Clinical Aspects.","authors":"Akbar Dorgalaleh, Sina Jozdani, Masoumeh Kiani Zadeh","doi":"10.1055/s-0044-1796673","DOIUrl":"10.1055/s-0044-1796673","url":null,"abstract":"<p><p>Factor XIII-A (FXIII-A) deficiency is an ultra-rare bleeding disorder characterized by high rates of morbidity and mortality, primarily resulting from intracranial hemorrhage, umbilical cord bleeding, and miscarriage, whereas patients with severe FXIII-B deficiency present with a milder phenotype. Although the estimated incidence of severe FXIII-A deficiency is one per 2 million, a high prevalence ranging from 0.8 to 3.5% has been observed for heterozygous FXIII-A deficiency. Unlike most bleeding disorders, individuals with heterozygous FXIII-A deficiency, particularly women, are more likely to experience hemorrhagic complications during hemostatic challenges. About 200 Mutations have been observed in <i>F13A</i> and <i>F13B</i> genes, with most being missense mutations, while large deletions are the rarest. There is no correlation between genotype and phenotype and a moderate to strong correlation between factor activity and clinical severity in FXIII-A deficiency, making it difficult to predict bleeding patterns based on genotype and FXIII activity levels. Primary prophylaxis is mandatory for all patients with severe FXIII-A deficiency, while those with heterozygous deficiency are generally asymptomatic and may require on-demand therapy during hemostatic challenges, most commonly in women. On the other hand, patients with severe FXIII-B deficiency may only require on-demand therapy, while heterozygotes are generally asymptomatic. Although there are general recommended therapeutic regimens for prophylaxis or on-demand therapy in different situations, personalized pharmacokinetic-based replacement therapy represents the optimal approach that can optimize intervention efficacy. In such an approach, several factors may affect the effectiveness of treatment and determine the dose and type of intervention, including the classification of FXIII deficiency, residual plasma levels of FXIII, clinical situation requiring intervention, age, weight, and also gender.</p>","PeriodicalId":21673,"journal":{"name":"Seminars in thrombosis and hemostasis","volume":" ","pages":"155-169"},"PeriodicalIF":3.6,"publicationDate":"2025-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142755450","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":"Clinical, Laboratory, Molecular, and Reproductive Aspects of Combined Deficiency of Factors V and VIII.","authors":"Elena Yakovleva, Bin Zhang","doi":"10.1055/s-0044-1789019","DOIUrl":"10.1055/s-0044-1789019","url":null,"abstract":"<p><p>Congenital combined deficiency of factor V (FV) and factor VIII (FVIII; F5F8D, OMIM 227300) is a rare hereditary coagulopathy and accounts for approximately 3% of cases of rare coagulation disorders. The prevalence of this disease in the general population is estimated to be 1:1,000,000 and is significantly higher in regions where consanguineous marriages are permitted, such as the Mideast and South Asia. The disease has an autosomal recessive mode of inheritance and therefore occurs with an equal incidence among males and females. Heterozygous mutation carriers usually do not have clinical manifestations. The molecular basis of this disease differs from that of stand-alone congenital deficiencies of FVIII and FV. F5F8D is caused by mutations in either <i>LMAN1</i> or <i>MCFD2</i>, which encode components of a cargo receptor complex for endoplasmic reticulum to Golgi transport of FV and FVIII, leading to defects in an intracellular transport pathway shared by these two coagulation factors. Congenital combined deficiency of FV and FVIII is characterized by decreased activities of both FV and FVIII in plasma, usually to 5 to 30% of normal. Clinical manifestations in most cases are represented by mild or moderate hemorrhagic syndrome. The simultaneous decreases of two coagulation factors present complications in the diagnosis and management of the disease. In female patients, the disease requires a special approach for family planning, pregnancy management, and parturition. This review summarizes recent progress in clinical, laboratory, and molecular understanding of this disorder.</p>","PeriodicalId":21673,"journal":{"name":"Seminars in thrombosis and hemostasis","volume":" ","pages":"116-127"},"PeriodicalIF":3.6,"publicationDate":"2025-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11839339/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142111609","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":"Bernard-Soulier Syndrome: A Review of Epidemiology, Molecular Pathology, Clinical Features, Laboratory Diagnosis, and Therapeutic Management.","authors":"Zühre Kaya","doi":"10.1055/s-0044-1789184","DOIUrl":"10.1055/s-0044-1789184","url":null,"abstract":"<p><p>Bernard-Soulier syndrome (BSS) is an inherited platelet function disorder caused by mutations in the genes that encode the glycoprotein (GP) Ibα and GPIbβ subunits, as well as the GPIX subunit in the GPIbIX complex, which is located on the platelet surface and has roles in platelet adhesion and activation. Patients with autosomal recessively inherited biallelic BSS have a homozygous or compound heterozygous expression in the GPIbα, GPIbβ, and GPIX subunits of the GPIbIX complex. Patients with autosomal dominantly inherited monoallelic BSS have a heterozygous expression in only the GPIbα and GPIbβ subunits of the GPIbIX complex. To date, no BSS mutations in the <i>GP5</i> gene have been reported. Patients with biallelic form are usually diagnosed at a young age, typically with mucocutaneous bleeding, whereas monoallelic forms are generally identified later in life and are frequently misdiagnosed with immune thrombocytopenic purpura (ITP). In biallelic BSS, giant platelets in the peripheral blood smear, absence of ristocetin-induced platelet aggregation (RIPA) using light transmission aggregometry (LTA), and complete loss of GPIbIX complex in flow cytometry are observed, whereas in monoallelic forms, genetic diagnosis is recommended due to the presence of large platelets in the peripheral blood smear, decreased or normal RIPA response in LTA, and partial loss or normal GPIbIX complex in flow cytometry. Platelet transfusion is the main therapy but recombinant factor VIIa is advised in alloimmunized patients, and allogeneic stem cell transplantation is suggested in refractory cases. Antifibrinolytics and oral contraceptives are utilized as supplementary treatments. Finally, differentiation from ITP is critical due to differences in management. Thus, BSS should be kept in mind in the presence of individuals with chronic persistent thrombocytopenia, positive family history, unresponsive ITP treatment, macrothrombocytopenia, and absence of RIPA response.</p>","PeriodicalId":21673,"journal":{"name":"Seminars in thrombosis and hemostasis","volume":" ","pages":"209-218"},"PeriodicalIF":3.6,"publicationDate":"2025-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142081397","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":"Clinical, Laboratory Aspects and Management of Factor X Deficiency.","authors":"Marzia Menegatti, Flora Peyvandi","doi":"10.1055/s-0044-1789595","DOIUrl":"10.1055/s-0044-1789595","url":null,"abstract":"<p><p>Coagulation factor X (FX), originally named Stuart-Prower factor, plays a pivotal role in the coagulation cascade, activating thrombin to promote platelet plug formation and prevent excess blood loss. Genetic variants in <i>F10</i> may lead to FX deficiency and to impaired coagulation. FX variants are phenotypically classified as being type I, with the concomitant reduction of FX coagulant activity and FX antigen levels or type II, corresponding to a reduction in activity with normal antigen plasma levels. Patients affected with FX deficiency tend to be one of the most seriously affected among those with rare bleeding disorders. They show a variable bleeding tendency strongly associated with FX coagulant activity levels in plasma and may present, in the severe form of the deficiency, life-threatening symptoms such as gastrointestinal and umbilical stump bleeding and intracranial hemorrhages or central nervous system bleeding. Treatment of FX deficiency was originally based on the replacement of the missing factor using fresh frozen plasma, cryoprecipitate and prothrombin complex concentrates; however, a plasma-derived concentrate, shown to be safe and effective in clinical trials, is now available. In addition, novel nonreplacement therapy such as small interference RNA, gene therapy, drug repurposing, and gene editing may also represent novel therapeutic approaches for FX deficiency, but further, much focused studies are needed before considering this emerging therapy in such patients.</p>","PeriodicalId":21673,"journal":{"name":"Seminars in thrombosis and hemostasis","volume":" ","pages":"138-144"},"PeriodicalIF":3.6,"publicationDate":"2025-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142111607","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":"Clinical, Laboratory, and Molecular Aspects of Factor VII Deficiency.","authors":"Francesco Bernardi, Guglielmo Mariani","doi":"10.1055/s-0044-1788792","DOIUrl":"10.1055/s-0044-1788792","url":null,"abstract":"<p><p>Congenital factor VII (FVII) deficiency, the most frequent among the recessively inherited disorders of blood coagulation, is characterized by a wide range of symptoms, from mild mucosal bleeds to life-threatening intracranial hemorrhage. Complete FVII deficiency may cause perinatal lethality. Clinically relevant thresholds of plasma levels are still uncertain, and modest differences in low FVII levels are associated with large differences in clinical phenotypes. Activated FVII (FVIIa) expresses its physiological protease activity only in a complex with tissue factor (TF), which triggers clotting at a very low concentration. Knowledge of the FVIIa-TF complex helps to interpret the clinical findings associated with low FVII activity as compared with other rare bleeding disorders and permits effective management, including prophylaxis, with recombinant FVIIa, which, however, displays a short half-life. Newly devised substitutive and nonsubstitutive treatments, characterized by extended half-life properties, may further improve the quality of life of patients. Genetic diagnosis has been performed in thousands of patients with FVII deficiency, and among the heterogeneous <i>F7</i> mutations, mostly missense changes, several recurrent variants show geographical distribution and identity by descent. In the general population, common <i>F7</i> polymorphisms explain a large proportion of FVII level variance in plasma through FVII-lowering effects. Their combination with pathogenic variants may impact on the frequent detection of FVII coagulant levels lower than normal, as well as on mild bleeding conditions. In the twenties of this century, 70 years after the first report of FVII deficiency, more than 200 studies/reports about FVII/FVII deficiency have been published, with thousands of FVII-deficient patients characterized all over the world.</p>","PeriodicalId":21673,"journal":{"name":"Seminars in thrombosis and hemostasis","volume":" ","pages":"128-137"},"PeriodicalIF":3.6,"publicationDate":"2025-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142111608","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":"Correlation between Phenotype and Coagulation Factor Activity Level in Rare Bleeding Disorders: A Systematic Review.","authors":"Behnaz Tavasoli, Alireza Zangooie, Seyed Mehrab Safdari, Taraneh Hoseinnezhad, Ashkan Shabannezhad, Amirreza Alikhani, Zahra Salehi, Akbar Dorgalaleh","doi":"10.1055/s-0044-1800832","DOIUrl":"10.1055/s-0044-1800832","url":null,"abstract":"&lt;p&gt;&lt;p&gt;Rare bleeding disorders (RBDs) represent 3 to 5% of congenital bleeding disorders and are primarily inherited in an autosomal recessive manner, with increased prevalence in consanguineous populations. Clinically, RBDs can be accompanied by mild to severe bleeding episodes, often assessed using bleeding assessment tools (BATs) such as the International Society on Thrombosis and Hemostasis (ISTH)-BAT. However, the correlation between bleeding severity and coagulation factor activity levels remains inconsistent. This systematic review investigates this relationship to enhance understanding and improve management strategies for patients with RBD. This review adhered to Preferred Reporting Items for Systematic Reviews and Meta-Analyses (PRISMA) guidelines and was registered with the International Prospective Register for Systematic Reviews (PROSPERO) (CRD42024504537). Using the PICO (Population, Intervention, Comparator, and Outcomes) framework, the study focused on RBD patients to explore the correlation between coagulation factor activity levels and bleeding severity. A comprehensive search was conducted across PubMed, Scopus, and Web of Science until April 1, 2024, with data extracted on bleeding severity, phenotype, and coagulation factor activity levels. The analysis highlights complex and often inconsistent relationships between coagulation factor levels and the severity of bleeding. In cases of fibrinogen deficiency, three out of four studies (&lt;i&gt;n&lt;/i&gt; = 73 of 111 cases, 66%) demonstrated a moderate to strong correlation between fibrinogen levels and bleeding severity. In prothrombin deficiency, one of two studies (&lt;i&gt;n&lt;/i&gt; = 16 of 29 cases, 55%) found a strong correlation between FII levels and bleeding severity. Four of six studies (&lt;i&gt;n&lt;/i&gt; = 106 of 139 cases, 76%) in FV deficiency found a weak or no correlation between factor activity and bleeding severity. In combined FV and FVIII deficiency, two of three studies (&lt;i&gt;n&lt;/i&gt; = 26 of 60 cases, 43%) found a significant correlation between factor activity and bleeding severity. In FVII deficiency, four (of nine) studies with a study population of 325 patients (65%) found a weak correlation between factor activity and severity of bleeding. Almost all studies (five of six studies, &lt;i&gt;n&lt;/i&gt; = 114 of 118 patients, 97%) in FX deficiency revealed a strong correlation between FX levels and bleeding severity. In FXI deficiency, most studies (five of seven studies, &lt;i&gt;n&lt;/i&gt; = 254 patients, 93%) found a weak or no correlation between factor activity and bleeding severity or symptoms. For FXIII deficiency, there was a moderate to strong correlation between FXIII activity and bleeding severity in all three studies (&lt;i&gt;n&lt;/i&gt; = 61 patients). In conclusion, despite current controversies, this review highlights a moderate or strong correlation between factor activity and bleeding severity in fibrinogen, FX, and FXIII deficiencies, but no correlation or weak correlation for FV, FVII, and FXI deficiencies.","PeriodicalId":21673,"journal":{"name":"Seminars in thrombosis and hemostasis","volume":" ","pages":"180-195"},"PeriodicalIF":3.6,"publicationDate":"2025-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142787020","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":"Clinical, Laboratory, and Molecular Aspects of Factor V Deficiency.","authors":"Massimo Franchini, Daniele Focosi","doi":"10.1055/s-0044-1789021","DOIUrl":"10.1055/s-0044-1789021","url":null,"abstract":"<p><p>Factor V (FV) is a glycoprotein that plays a pivotal role in hemostasis, being involved in coagulant and anticoagulant pathways. Congenital FV deficiency is a rare bleeding disorder with an incidence of 1 per million live births, considering the most severe homozygous form. FV deficiency is diagnosed using routine coagulation tests and FV activity assays. Several mutations, including missense, nonsense, and frameshift, have been detected in the <i>F5</i> gene. Clinical symptoms are variable, ranging from mild ecchymoses and mucosal bleeding to life-threatening intracranial hemorrhage. The mainstay of treatment includes fresh-frozen plasma, preferentially virus-inactivated. In this narrative review, we provide an update of the main laboratory, molecular, clinical, and therapeutic features of inherited FV deficiency.</p>","PeriodicalId":21673,"journal":{"name":"Seminars in thrombosis and hemostasis","volume":" ","pages":"111-115"},"PeriodicalIF":3.6,"publicationDate":"2025-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142081398","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}