Journal of Thrombosis and Haemostasis最新文献

{"title":"Annoucements","authors":"","doi":"10.1016/S1538-7836(25)00179-5","DOIUrl":"10.1016/S1538-7836(25)00179-5","url":null,"abstract":"","PeriodicalId":17326,"journal":{"name":"Journal of Thrombosis and Haemostasis","volume":"23 4","pages":"Pages 1458-1459"},"PeriodicalIF":5.5,"publicationDate":"2025-04-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143767491","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":"“Estimation of gestational age-specific reference intervals for coagulation assays in a neonatal intensive care unit using real-world data”: reply","authors":"Natasha Lalos , Zachary Vesoulis , Carly Maucione , Nicholas C. Spies","doi":"10.1016/j.jtha.2025.01.017","DOIUrl":"10.1016/j.jtha.2025.01.017","url":null,"abstract":"","PeriodicalId":17326,"journal":{"name":"Journal of Thrombosis and Haemostasis","volume":"23 4","pages":"Pages 1454-1455"},"PeriodicalIF":5.5,"publicationDate":"2025-04-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143768017","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":"Basics of diagnosis and treatment of venous thromboembolism","authors":"Catrin Cox ,&nbsp;Lara N. Roberts","doi":"10.1016/j.jtha.2025.01.009","DOIUrl":"10.1016/j.jtha.2025.01.009","url":null,"abstract":"<div><div>Venous thromboembolism (VTE), comprising deep vein thrombosis and pulmonary embolism (PE), is common and associated with significant morbidity and mortality. The symptoms and signs of VTE are nonspecific. Well-established integrated diagnostic strategies combining clinical probability scores and D-dimer are used to identify patients with a low probability of VTE, where the diagnosis can be safely excluded without imaging. In patients with confirmed VTE, anticoagulation is the mainstay of treatment. However, patients with high-risk features at presentation may benefit from advanced reperfusion therapies such as thrombolysis and/or interventional approaches to reduce early mortality and/or long-term morbidity. The advent of direct oral anticoagulants has greatly simplified the treatment of VTE for most patients, with a persisting role for low molecular weight heparin and vitamin K antagonists in select patient groups. Following an initial 3 to 6 months of anticoagulation, those with major transient provoking factors can safely discontinue anticoagulation. Balancing the risk of recurrent VTE and bleeding risk is central to decisions regarding long-term anticoagulation, and patients should be included in shared decision-making. Assessment and recognition of common long-term complications such as postthrombotic syndrome and post-PE syndrome are also essential, given they are associated with significant adverse impact on long-term quality of life, with a significant risk of mortality associated with the less frequent complication of chronic thromboembolic pulmonary hypertension. This review provides a basic overview and framework for the diagnostic approach to deep vein thrombosis and PE, risk stratification of confirmed diagnoses, and management.</div></div>","PeriodicalId":17326,"journal":{"name":"Journal of Thrombosis and Haemostasis","volume":"23 4","pages":"Pages 1185-1202"},"PeriodicalIF":5.5,"publicationDate":"2025-04-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143408911","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":"Therapeutic plasma exchange for fibrinogen-associated hyperviscosity: results of the COVID-19 PLasma EXchange (COPLEX) randomized controlled trial","authors":"Cheryl L. Maier ,&nbsp;Hirotomo Nakahara ,&nbsp;Nicholas A. Barker ,&nbsp;Sara C. Auld ,&nbsp;Alexander D. Truong ,&nbsp;Sarah Friend ,&nbsp;Mark Caridi-Scheible ,&nbsp;Michael Connor ,&nbsp;Manila Gaddh ,&nbsp;Jason Cobb ,&nbsp;Derek M. Polly ,&nbsp;Jeannette Guarner ,&nbsp;Cindy Powell ,&nbsp;Christine L. Kempton ,&nbsp;Lisa Daniels ,&nbsp;A. Thanushi Wynn ,&nbsp;Roman Sniecinski ,&nbsp;Alexander Duncan ,&nbsp;John Roback ,&nbsp;Tahsun Masud ,&nbsp;Sean R. Stowell","doi":"10.1016/j.jtha.2024.12.021","DOIUrl":"10.1016/j.jtha.2024.12.021","url":null,"abstract":"<div><h3>Background</h3><div>Therapeutic plasma exchange (TPE) is the primary intervention for treating symptomatic hyperviscosity from hypergammaglobulinemia, yet its efficacy for treating hyperviscosity related to hyperfibrinogenemia is unclear.</div></div><div><h3>Objectives</h3><div>Define the safety and efficacy of TPE for critically ill COVID-19 patients with elevated blood viscosity from hyperfibrinogenemia.</div></div><div><h3>Methods</h3><div>We performed a prospective randomized controlled trial in critically ill COVID-19 patients in a single US healthcare system. Patients with hyperfibrinogenemia (&gt;800 mg/dL) or elevated plasma viscosity (2.3-3.5 centipoise [cP]) were randomized to receive TPE on 2 consecutive days or continued standard of care (SOC).</div></div><div><h3>Results</h3><div>Twenty participants were enrolled, with 10 receiving TPE and 10 receiving SOC alone. Mean (±SEM) plasma viscosity decreased significantly from 2.35 cP (±0.12) to 1.61 cP (±0.03) in the TPE group and was unchanged in the SOC group (2.47 cP [±0.11] to 2.47 cP [±0.15]). Mean fibrinogen decreased from 934.0 mg/dL (±25.1) to 359.1 mg/dL (±22.5) after TPE vs from 859.6 mg/dL (±57.6) to 807.3 mg/dL (±63.1) in SOC. There was no significant difference in 28-day all-cause mortality between groups, with 2 deaths in the TPE cohort and 5 deaths in the SOC cohort (<em>P</em> = .13). No serious safety events related to TPE were reported. TPE significantly decreased biomarkers of inflammation (erythrocyte sedimentation rate and C-reactive protein) and endothelial activation (von Willebrand factor and factor VIII) but not hemostatic activation (prothrombin fragment 1.2, thrombin-antithrombin complex, and fibrin monomer) or immunoglobulin (IgG and IgM) levels.</div></div><div><h3>Conclusion</h3><div>TPE is safe and effective for normalizing elevated blood viscosity from hyperfibrinogenemia in COVID-19 patients. Additional studies are needed to determine the impact of TPE on overall patient outcomes, including in those with non–COVID-19 conditions associated with hyperfibrinogenemia.</div></div>","PeriodicalId":17326,"journal":{"name":"Journal of Thrombosis and Haemostasis","volume":"23 4","pages":"Pages 1393-1400"},"PeriodicalIF":5.5,"publicationDate":"2025-04-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142922035","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":"Systematic analysis of the design, methodology, and patient population characteristics of the pediatric direct oral anticoagulant trials of venous thromboembolism treatment","authors":"Marisol Betensky ,&nbsp;Manuela Albisetti ,&nbsp;Tina Biss ,&nbsp;Rukhmi V. Bhat ,&nbsp;Leonardo R. Brandão ,&nbsp;Thomas Diacovo ,&nbsp;Paul Monagle ,&nbsp;Leslie Raffini ,&nbsp;Shoshana Revel-vilk ,&nbsp;C. Heleen van Ommen ,&nbsp;Hilary Whitworth ,&nbsp;Neil A. Goldenberg ,&nbsp;Christoph Male ,&nbsp;Antithrombotic Trials Working Party of the ISTH SSC Subcommittee on Pediatric and Neonatal Thrombosis and Hemostasis","doi":"10.1016/j.jtha.2024.12.035","DOIUrl":"10.1016/j.jtha.2024.12.035","url":null,"abstract":"<div><h3>Background</h3><div>The pediatric direct oral anticoagulation (DOAC) trials provide an opportunity to evaluate and characterize challenges in their design and execution to inform future antithrombotic trials.</div></div><div><h3>Objectives</h3><div>To perform a systematic review of pediatric DOAC trials for the treatment of venous thromboembolism to critically appraise their methodology and understand the feasibility and challenges.</div></div><div><h3>Methods</h3><div>We performed a systematic search of MEDLINE, EMBASE, the Cochrane Library, and <em>ClinicalTrials.gov</em> (January 2002 to December 2022). Studies reporting the results of interventional trials of a DOAC for the <em>treatment of acute venous thromboembolism</em> in children and their respective design papers were included. Trial registration information was reviewed in <em>ClinicalTrials.gov.</em> Discrepancies in study design, targeted populations, sample size, and analyses between planned and actual trial conduct were examined qualitatively.</div></div><div><h3>Results</h3><div>Five published studies and unpublished data for 2 additional trials were included. All trials had modifications to their design or methodology and discrepancies between the trial’s registration and the final published study, suggesting feasibility challenges. Modifications to the eligibility criteria, changes in sample size, challenges with the recruitment of younger patients, and an enrolled population not matching the clinical target population were identified for all trials. Discrepancies in outcome reporting, particularly for secondary endpoints, were also common.</div></div><div><h3>Conclusion</h3><div>DOAC trials experienced feasibility challenges that led to design or methodology modifications. Future pediatric antithrombotic trials will need to be adaptive in their design, prioritize enrollment of younger children and input from clinicians providing care to target populations, ensure that enrolled populations match the clinical population, and select clinically meaningful endpoints.</div></div>","PeriodicalId":17326,"journal":{"name":"Journal of Thrombosis and Haemostasis","volume":"23 4","pages":"Pages 1315-1331"},"PeriodicalIF":5.5,"publicationDate":"2025-04-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142971503","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":"Tolerance to factor VIII in the era of nonfactor therapies: immunologic perspectives and a systematic review of the literature","authors":"Lilianne Esmée van Stam ,&nbsp;Sébastien Lacroix-Desmazes ,&nbsp;Karin Fijnvandraat ,&nbsp;Samantha Claudia Gouw","doi":"10.1016/j.jtha.2024.12.039","DOIUrl":"10.1016/j.jtha.2024.12.039","url":null,"abstract":"<div><div>Persons with hemophilia A lack clotting factor (F)VIII (FVIII) due to a genetic mutation in the <em>F8</em> gene. The administration of FVIII concentrate leads to the development of neutralizing anti-FVIII antibodies (inhibitors) in about 30% of children with severe hemophilia A. The other 70% of children do not mount a detectable antibody response, suggesting that they may have developed tolerance toward FVIII. Our knowledge on the underlying immunologic mechanisms that determine formation of inhibitors or apparent tolerance to FVIII is limited. Up to recently, FVIII concentrates were regularly used as prophylaxis. In the last years, nonfactor therapy for prophylaxis is increasingly used, in which case FVIII concentrate administration is limited to treatment for bleeding or perioperative hemostasis. As nonfactor therapy is very effective in the prevention of bleeds, patients may not be exposed to the deficient FVIII protein for periods up to a year or longer. Thus, while in the past persons with severe hemophilia were frequently exposed to the deficient antigen, exposure is now reduced to incidental treatment moments. It is currently not known how this will affect the tolerance for FVIII. In this review, we will discuss tolerance to FVIII from a clinical, immunologic, and epidemiologic perspective. We aimed to provide an outlook on the effect of reduced FVIII exposure on tolerance for FVIII in persons with hemophilia A.</div></div>","PeriodicalId":17326,"journal":{"name":"Journal of Thrombosis and Haemostasis","volume":"23 4","pages":"Pages 1169-1184"},"PeriodicalIF":5.5,"publicationDate":"2025-04-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142971507","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":"“Estimation of gestational age-specific reference intervals for coagulation assays in a neonatal intensive care unit using real-world data”: comment from Karlaftis et al.","authors":"Vasiliki Karlaftis ,&nbsp;Chantal Attard ,&nbsp;Vera Ignjatovic ,&nbsp;Paul Monagle","doi":"10.1016/j.jtha.2024.12.019","DOIUrl":"10.1016/j.jtha.2024.12.019","url":null,"abstract":"","PeriodicalId":17326,"journal":{"name":"Journal of Thrombosis and Haemostasis","volume":"23 4","pages":"Pages 1452-1453"},"PeriodicalIF":5.5,"publicationDate":"2025-04-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143768016","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":"Impact of coincident lower extremity deep vein thrombosis on symptomatic and incidental pulmonary embolism outcomes. A single-center prospective cohort study","authors":"Steven Callori ,&nbsp;Waldemar Wysokinsk ,&nbsp;Danielle Vlazny ,&nbsp;Damon E. Houghton ,&nbsp;David A. Froehling ,&nbsp;David O. Hodge ,&nbsp;Ana I. Casanegra ,&nbsp;Robert D. McBane II","doi":"10.1016/j.jtha.2024.12.025","DOIUrl":"10.1016/j.jtha.2024.12.025","url":null,"abstract":"<div><h3>Background</h3><div>The prognostic implications of co-incident DVT at the time of PE diagnosis remains unclear.</div></div><div><h3>Objectives</h3><div>Study aims were to assess the impact of co-incident lower extremity (LE) deep vein thrombosis (DVT) on clinical outcomes of pulmonary embolism (PE) including venous thromboembolism (VTE) recurrence and mortality.</div></div><div><h3>Methods</h3><div>Consecutive patients with confirmed acute symptomatic or incidental PE (March 1, 2013 to June 30, 2021) who underwent ultrasound imaging were divided into two groups depending on the presence or absence of LE DVT. Patients were followed prospectively for VTE recurrence, bleeding, and all-cause mortality.</div></div><div><h3>Results</h3><div>Over the study period, 1907 patients with PE were stratified into groups based on the presence (<em>n</em> = 920) or absence (<em>n</em> = 987) of LE DVT. Patients with co-incident LE DVT were older, heavier, and had a significantly greater frequency of trauma, confinement, thrombophilia, and VTE. Those without LE DVT had a higher prevalence of active cancer, metastatic disease, and active systemic therapy use. All-cause mortality rates (per 100 person-years) were significantly higher for patients without vs with co-incident LE DVT (42.4/100 person-years vs 29.6/100 person- years; <em>P</em> &lt; .001) with no differences in VTE recurrence or bleeding outcomes. After stratification by cancer status, mortality in those without vs. with co-incident DVT only remained significant among noncancer patients (15.2/100 person-years vs 12.1/100 person-years, <em>P</em> = .046).</div></div><div><h3>Conclusions</h3><div>Among patients with acute PE, the absence of co-incident lower extremity DVT is associated with significantly higher mortality rates. Mortality rate differences were only observed for those without cancer. No differences in VTE recurrence or bleeding were observed.</div></div>","PeriodicalId":17326,"journal":{"name":"Journal of Thrombosis and Haemostasis","volume":"23 4","pages":"Pages 1260-1268"},"PeriodicalIF":5.5,"publicationDate":"2025-04-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142922030","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":"Joint effects of atrial fibrillation and prothrombotic genotypes on the risk of ischemic stroke","authors":"Erin Mathiesen Hald ,&nbsp;Maja-Lisa Løchen ,&nbsp;Ellisiv B. Mathiesen ,&nbsp;Kristian Hveem ,&nbsp;Sigrid K. Brækkan ,&nbsp;John-Bjarne Hansen","doi":"10.1016/j.jtha.2024.12.022","DOIUrl":"10.1016/j.jtha.2024.12.022","url":null,"abstract":"<div><h3>Background</h3><div>Atrial fibrillation (AF) is a major risk factor for ischemic stroke. Whether prothrombotic single nucleotide polymorphisms (SNPs) impact stroke risk in AF is not well known.</div></div><div><h3>Objectives</h3><div>To investigate the joint effects of 5 prothrombotic SNPs and AF on ischemic stroke risk.</div></div><div><h3>Methods</h3><div>A subcohort (<em>n</em> = 14 583) was randomly sampled from the Tromsø (1994-2012) and the Trøndelag Health (1995-2008) studies. DNA was genotyped for rs8176719 (ABO blood type), rs6025 (factor [F]V Leiden), rs1799963 (prothrombin G20210A), rs2066865 (fibrinogen-γ), and rs2036914 (F11). Hazard ratios (HRs) with 95% CIs for incident ischemic stroke were estimated by AF status for individual SNPs and by categories of a genetic risk score.</div></div><div><h3>Results</h3><div>A total of 1091 participants developed AF during follow-up, of whom 169 (15.5%) subsequently had a stroke. Having ≥1 risk allele in prothrombin, FV Leiden, F11, or fibrinogen-γ was not associated with excess stroke risk in AF. In the absence of AF, ≥1 risk allele(s) in ABO was not associated with stroke (HR, 1.03; 95% CI, 0.85-1.25), whereas those with AF and ≥1 risk allele(s) in ABO had a 1.4-fold increased stroke risk compared with those with AF and no risk allele (HR, 1.42; 95% CI, 0.99-2.04). There was no linear increase in stroke risk across categories of the genetic risk score in participants either with or without AF.</div></div><div><h3>Conclusion</h3><div>Most prothrombotic SNPs were not associated with ischemic stroke risk, regardless of AF status. The ABO SNP was associated with ischemic stroke risk in those with AF only.</div></div>","PeriodicalId":17326,"journal":{"name":"Journal of Thrombosis and Haemostasis","volume":"23 4","pages":"Pages 1401-1406"},"PeriodicalIF":5.5,"publicationDate":"2025-04-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142922033","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":"Progesterone regulates gut microbiota mediating bone marrow mesenchymal stem cell injury in immune thrombocytopenia patients during pregnancy","authors":"Qi Chen ,&nbsp;Fengqi Liu ,&nbsp;Gaochao Zhang ,&nbsp;Qingyuan Qu ,&nbsp;Yuxiu Chen ,&nbsp;Menglin Li ,&nbsp;Qiusha Huang ,&nbsp;Haixia Fu ,&nbsp;Xiaolu Zhu ,&nbsp;Yun He ,&nbsp;Xiaojun Huang ,&nbsp;Xiaohui Zhang","doi":"10.1016/j.jtha.2024.12.027","DOIUrl":"10.1016/j.jtha.2024.12.027","url":null,"abstract":"<div><h3>Background</h3><div>Immune thrombocytopenia during pregnancy (PITP) is the most common cause of platelet reduction in early and mid-pregnancy. However, the pathogenesis of PITP is still unclear.</div></div><div><h3>Objectives</h3><div>To determine the characteristics of bone marrow mesenchymal stem cells (BM-MSCs) in PITP patients and to explore the associations between metabolites, the gut microbiota, and BM-MSCs in PITP.</div></div><div><h3>Methods</h3><div>The characteristics of BM-MSCs were detected through <em>in vitro</em> and <em>in vivo</em> experiments. Nontargeted metabolomics was used to screen metabolites. The features of the gut microbiota were analyzed by 16S rDNA sequencing. PITP and fecal microbiota transplantation (FMT) mouse model were established to explore the associations between metabolites, gut microbiota, and BM-MSCs.</div></div><div><h3>Results</h3><div>BM-MSCs from PITP patients had significant senescence and apoptosis, as well as impaired immunoregulatory function. Metabolomic analysis indicated that progesterone was the most significant specific metabolite in PITP patients. <em>In vivo</em> studies showed that progesterone mediated MSC injury. Further analysis of the gut microbiota and FMT experiments revealed that progesterone mediated BM-MSCs injury by regulating the composition of the gut microbiota in PITP. RNA sequencing analysis of BM-MSCs from FMT mice revealed abnormal expression of genes related to cell aging and the NOD-like receptor signaling pathway.</div></div><div><h3>Conclusion</h3><div>In conclusion, BM-MSCs in the PITP were significantly impaired, which was associated with increased progesterone and changes in the gut microbiota regulated by progesterone. Intervening with the gut microbiota may become a new treatment for PITP.</div></div>","PeriodicalId":17326,"journal":{"name":"Journal of Thrombosis and Haemostasis","volume":"23 4","pages":"Pages 1428-1441"},"PeriodicalIF":5.5,"publicationDate":"2025-04-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142932190","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}