Journal of Thrombosis and Haemostasis最新文献

{"title":"Internal lysis of contracted clots is accelerated by fiber alignment and bundling","authors":"Rebecca A. Risman,&nbsp;Eva Iungbliudt,&nbsp;Joshua Packard,&nbsp;Igor Novikov,&nbsp;Mason Lee Verhaeghe,&nbsp;John W. Weisel,&nbsp;Brittany E. Bannish,&nbsp;Valeri Barsegov,&nbsp;Nathan E. Hudson,&nbsp;Valerie Tutwiler","doi":"10.1016/j.jtha.2026.07.007","DOIUrl":"10.1016/j.jtha.2026.07.007","url":null,"abstract":"<div><h3>Background</h3><div>Clot contraction is the volume shrinkage of a blood clot due to action of platelet-driven contractile forces. Clot contraction is known to accelerate internal fibrinolysis (the physiological degradation of the fibrin network) but restrict external fibrinolysis (the exogenous delivery of thrombolytic agents) in whole blood. We previously showed that external fibrinolysis is limited in contracted clots due to the densified fibrin network in the periphery, but the mechanism of acceleration of internal lysis is unknown.</div></div><div><h3>Objectives</h3><div>We aimed to identify the driving mechanism that accelerated internal lysis of contracted clots.</div></div><div><h3>Methods</h3><div>A comprehensive array of wet-lab experiments at the micro- and macroscopic levels, as well as computational modeling, were used to systematically disentangle the dominating mechanism leading to faster fibrinolysis of contracted clots during internal fibrinolysis. Scanning electron microscopy and confocal microscopy were used to visualize clots made with platelet-rich plasma and platelet-poor plasma to study the fibrin network structure. Platelet-driven tension was mimicked by applying uniaxial tensile strain in both large clots and individual fibers.</div></div><div><h3>Results</h3><div>Clot contraction results in fibrin network structural changes—notably, a dense periphery and heterogeneous core. Internal lysis of clots made with platelet-rich plasma that contract normally was faster than all other clots tested. Tension delays lysis of individual fibers but accelerates lysis when fibers bundle with a high percent strain.</div></div><div><h3>Conclusion</h3><div>Apparent thickening of fibers due to fibrin bundling as a result of platelet-driven fibrin rearrangement and alignment, rather than platelet-driven tension on fibers, drives the acceleration of internal fibrinolysis of contracted clots.</div></div>","PeriodicalId":17326,"journal":{"name":"Journal of Thrombosis and Haemostasis","volume":"24 10","pages":"Pages 3771-3783"},"PeriodicalIF":5.2,"publicationDate":"2026-10-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148497796","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":"Beyond endothelial cells: mutant p53 drives de novo von Willebrand factor expression","authors":"Betül Ünlü,&nbsp;Jamie M. O’Sullivan","doi":"10.1016/j.jtha.2026.07.018","DOIUrl":"10.1016/j.jtha.2026.07.018","url":null,"abstract":"","PeriodicalId":17326,"journal":{"name":"Journal of Thrombosis and Haemostasis","volume":"24 10","pages":"Pages 3440-3442"},"PeriodicalIF":5.2,"publicationDate":"2026-10-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149078539","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 historical review of the biological, semantic and clinical aspects of aspirin resistance","authors":"Pierre Fontana,&nbsp;Jean-Luc Reny,&nbsp;Thomas Lecompte","doi":"10.1016/j.jtha.2026.06.027","DOIUrl":"10.1016/j.jtha.2026.06.027","url":null,"abstract":"<div><div>Aspirin is one of the most widely used antithrombotic agents worldwide. Nevertheless, the concept of aspirin resistance has generated sustained controversy for more than 2 decades. Initially introduced in the mid-1990s, the term was inconsistently applied to describe either recurrent ischemic events, despite aspirin therapy, or inadequate platelet inhibition, as measured using various laboratory assays. Reported prevalence estimates consequently varied widely, reflecting profound methodological and semantic heterogeneity rather than a uniform biological concept. This historical review retraced the evolution of knowledge about aspirin pharmacodynamics, from the earliest studies on bleeding time and platelet aggregation to the identification of platelet cyclo-oxygenase-1 as aspirin’s molecular target and the recognition of serum thromboxane B₂ as a specific biomarker of target inhibition. We examined how reliance on integrative platelet-function tests fostered the concept of apparent resistance, later recognized, in many cases, as pseudo-resistance related to assay choice or pharmacokinetic factors. We then reviewed the clinical, genetic and disease-related determinants of variability in aspirin response, highlighting conditions characterized by accelerated platelet production and turnover, such as essential thrombocythaemia, as a notable exception in which target-guided dosing has influenced practice. Finally, we summarized the outcome studies and guideline statements that uniformly discourage routine testing and aspirin dose escalation. Taken together, the historical evidence supports abandoning the term aspirin resistance in favor of recognizing the variability in platelet reactivity found among patients treated with aspirin.</div></div>","PeriodicalId":17326,"journal":{"name":"Journal of Thrombosis and Haemostasis","volume":"24 10","pages":"Pages 3761-3770"},"PeriodicalIF":5.2,"publicationDate":"2026-10-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148339047","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":"Diagnostic utility of the von Willebrand factor collagen-binding activity assay in patients with mild-to-moderate bleeding: results from the Vienna Bleeding Biobank","authors":"Dino Mehic,&nbsp;Daniel Kraemmer,&nbsp;Tim Dreier,&nbsp;Justin Oosterlee,&nbsp;Peter Quehenberger,&nbsp;Cihan Ay,&nbsp;Ingrid Pabinger,&nbsp;Johanna Gebhart","doi":"10.1016/j.jtha.2026.07.020","DOIUrl":"10.1016/j.jtha.2026.07.020","url":null,"abstract":"","PeriodicalId":17326,"journal":{"name":"Journal of Thrombosis and Haemostasis","volume":"24 10","pages":"Pages 3801-3805"},"PeriodicalIF":5.2,"publicationDate":"2026-10-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148620627","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":"RNA sequencing indicates distinct platelet transcriptomic changes in immune thrombocytopenia","authors":"Julia-Annabell Georgi,&nbsp;Marita Hartwig,&nbsp;Ulrike Anne Friedrich,&nbsp;Maximilian Krause,&nbsp;Andreas Dahl,&nbsp;Heidi Altmann,&nbsp;Thomas Stauch,&nbsp;Jan Moritz Middeke,&nbsp;Martin Bornhäuser,&nbsp;Peter Bugert,&nbsp;Christian Thiede,&nbsp;Karolin Trautmann-Grill","doi":"10.1016/j.jtha.2026.06.034","DOIUrl":"10.1016/j.jtha.2026.06.034","url":null,"abstract":"<div><h3>Background</h3><div>In immune thrombocytopenia (ITP), platelet-intrinsic alterations and their potential contribution to disease pathogenesis remain incompletely understood. Since platelets, although anucleate, retain a functional transcriptome, transcriptomic profiling may provide insight into disease-associated changes.</div></div><div><h3>Objectives</h3><div>To investigate platelet-intrinsic transcriptomic changes in ITP and to determine whether these alterations are disease-specific compared with non-ITP.</div></div><div><h3>Methods</h3><div>Total RNA sequencing was performed on purified platelets from patients with active ITP (<em>n</em> = 6), chemotherapy-induced thrombocytopenia as a non-ITP control (<em>n</em> = 6), ITP in treatment-free remission (<em>n</em> = 6), and healthy controls (<em>n</em> = 8).</div></div><div><h3>Results</h3><div>Platelets from patients with active ITP exhibited higher total RNA content, consistent with enrichment of young, recently released platelets. Transcriptomic analysis identified a profile dominated by platelet activation pathways, including integrin- and calcium-dependent signaling, cytoskeletal remodeling, and vesicle trafficking. In contrast, genes involved in mitochondrial biogenesis and oxidative phosphorylation were downregulated, accompanied by a reduced proportion of mitochondrial-derived RNA. Although both active ITP and chemotherapy-induced thrombocytopenia showed elevated RNA content relative to healthy controls, reflecting enhanced platelet turnover, the coordinated upregulation of activation-associated transcripts was unique to active ITP. Platelets from ITP patients in treatment-free remission showed partial normalization of the transcriptional profile, with loss of the activation signature and intermediate expression patterns between active ITP and healthy controls.</div></div><div><h3>Conclusion</h3><div>RNA sequencing data show distinct platelet transcriptomic changes in ITP, marked by coordinated upregulation of platelet activation pathways and reduced mitochondrial gene expression. This profile is consistent with an activation-primed, metabolically altered platelet state and may reflect disease-related changes in platelet biology in ITP.</div></div>","PeriodicalId":17326,"journal":{"name":"Journal of Thrombosis and Haemostasis","volume":"24 10","pages":"Pages 3723-3731"},"PeriodicalIF":5.2,"publicationDate":"2026-10-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148387805","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":"Safety and emergency dose-response evaluation of lyophilized synthetic platelets in a rat model of traumatic hemorrhage.","authors":"Norman F Luc, Dante Disharoon, Selvin Hernandez, Ujjal Didar Singh Sekhon, Baylee Traylor, Emily Gahagan, Emma Quill, Kristin Aldridge, Michael A Bruckman, Christa L Pawlowski, Anirban Sen Gupta","doi":"10.1016/j.jtha.2026.09.033","DOIUrl":"10.1016/j.jtha.2026.09.033","url":null,"abstract":"<p><strong>Background: </strong>Early hemostatic resuscitation with platelets can significantly improve survival in patients with hemorrhage. Here, platelet-mimicking technologies can serve as surrogates when donor-derived platelets are unavailable. We have developed a synthetic platelet (SP) technology that mimics platelets' primary hemostatic mechanisms and have previously reported its efficacy. Recently, we have advanced SP into a lyophilized product (Lyo-SP) that preserves functional equivalence to SP while allowing long shelf life, easy portability, and rapid reconstitution for on-demand use.</p><p><strong>Objective: </strong>We evaluated Lyo-SP in an emergency setting in a rat model of liver injury hemorrhage.</p><p><strong>Methods: </strong>First, Lyo-SP was tested ex vivo in 2 complementary microfluidic assays (BioFlux and total thrombus formation analysis system) to establish functionality in rat blood. Subsequently, Lyo-SP was administered in rats at escalating doses to determine safety. Finally, Lyo-SP hemostatic efficacy was evaluated in the rat liver hemorrhage model, given at 2 different doses at 2 different time points post injury, simulating emergency treatment.</p><p><strong>Results: </strong>Ex vivo, Lyo-SP demonstrated significant hemostatic capability in a rat blood-based hemodilution model. In vivo, Lyo-SP was well tolerated in rats up to 20 mg/kg and showed no clotting risks in clearance organs, confirmed by histology. In the liver hemorrhage model, rats dosed with 0.5 mg/kg Lyo-SP immediately (∼1 minute) or at 5 minutes post injury minimally reduced blood loss and mortality compared with controls. In contrast, rats dosed with 5 mg/kg Lyo-SP immediately (∼1 minute) or at 5 minutes post injury significantly reduced blood loss and mortality.</p><p><strong>Conclusions: </strong>The results indicate significant promise of Lyo-SP as an on-demand therapy for emergency management of hemorrhage to improve survival.</p>","PeriodicalId":17326,"journal":{"name":"Journal of Thrombosis and Haemostasis","volume":" ","pages":""},"PeriodicalIF":5.2,"publicationDate":"2026-09-30","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149111315","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":"Biomarker changes after surgical left atrial appendage occlusion: a substudy of the Left Atrial Appendage Occlusion Study III.","authors":"Mandy N Lauw, John W Eikelboom, Qilong Yi, Emilie P Belley-Cote, Jeffrey I Weitz, Richard P Whitlock","doi":"10.1016/j.jtha.2026.09.031","DOIUrl":"10.1016/j.jtha.2026.09.031","url":null,"abstract":"<p><strong>Background: </strong>The Left Atrial Appendage Occlusion Study (LAAOS) III showed that surgical left atrial appendage occlusion (LAAO) reduced ischemic stroke or systemic embolism (SE) in patients with atrial fibrillation (AF) undergoing cardiac surgery.</p><p><strong>Objectives: </strong>To explore whether LAAO changes levels of circulating biomarkers of coagulation activation, inflammation, hemodynamic stress, or myocardial injury after surgical LAAO.</p><p><strong>Methods: </strong>In this single-center biomarker substudy of LAAOS III, D-dimer, C-reactive protein, interleukin-6, N-terminal pro-B-type natriuretic peptide, high-sensitivity cardiac troponin T, and heart-type fatty acid-binding protein were measured at baseline and at 30 days and/or 1 year in patients randomized to LAAO or no LAAO. Biomarker levels and changes from baseline were compared by treatment group. Exploratory landmark Cox models assessed associations between biomarker changes and subsequent stroke/SE after the 30-day and 1-year landmarks.</p><p><strong>Results: </strong>Baseline samples were available for 208 participants, 30-day samples for 170, and 1-year samples for 123. Baseline biomarker levels were similar between groups. At 30 days, all measured biomarkers increased without between-group differences. At 1 year, most biomarkers had returned toward baseline. Too few events occurred after the 30-day and 1-year landmarks to support reliable analyses on biomarker changes and subsequent stroke/SE.</p><p><strong>Conclusion: </strong>Despite its clinical benefit in patients with AF, surgical LAAO was not associated with consistent changes in circulating biomarkers over 1 year in this exploratory substudy. The lack of a detectable effect on the circulating biomarkers evaluated in this study does not provide a mechanistic explanation for the clinical benefit of surgical LAAO.</p>","PeriodicalId":17326,"journal":{"name":"Journal of Thrombosis and Haemostasis","volume":" ","pages":""},"PeriodicalIF":5.2,"publicationDate":"2026-09-29","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149081468","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 C-terminal amidation on platelet activation by protease-activated receptors 1 and 4 activating peptides: communication from the ISTH SSC Subcommittee on Platelets in Health and Disease.","authors":"Imane Boukhatem, Jessica Blais, Dianne E van der Wal, Hanna Baloch, Tea Jerlström, Marie Lordkipanidzé, Sofia Ramström","doi":"10.1016/j.jtha.2026.09.030","DOIUrl":"10.1016/j.jtha.2026.09.030","url":null,"abstract":"<p><strong>Background: </strong>Platelet protease-activated receptor (PAR)1 or PAR4 can be specifically activated with thrombin receptor-activating peptides (APs), available with either amide (-NH₂) or free acid (-OH) in their C-terminus.</p><p><strong>Objectives: </strong>To assess differences in potency on platelet activation and aggregation induced by PAR1- and PAR4-APs with either C-terminal amide or free-acid groups.</p><p><strong>Methods: </strong>Platelet aggregation was evaluated using light transmission aggregometry in platelet-rich plasma and washed platelets. Platelet activation markers CD62P (P-selectin), CD63, and PAC-1 binding were evaluated by flow cytometry in blood anticoagulated with citrate or hirudin and in washed platelets. Platelet responses were recorded following stimulation with PAR1-AP (SFLLRN) or PAR4-AP (AYPGKF), in either their free acid or amidated forms. EC₅₀ values were calculated from concentration-response curves.</p><p><strong>Results: </strong>Amidated peptides displayed consistently higher potency than their free-acid counterparts. Median EC₅₀ values for PAR1-AP-NH₂ were 2.6 to 12.6 times lower than for PAR1-AP-OH, and median EC₅₀ values for PAR4-AP-NH₂ were 4.7 to 10 times lower than for PAR4-AP-OH. PAR4-AP-OH showed low potency and did not reach maximal platelet activation for several activation markers.</p><p><strong>Conclusions: </strong>The amidated forms of either PAR1-AP or PAR4-AP agonists were significantly more potent compared with their free-acid counterparts. Results obtained with one form should not be assumed to apply to the other, as structural differences can substantially affect biological activity. Thus, the SSC recommends that the complete peptide structure be reported in studies using these agonists.</p>","PeriodicalId":17326,"journal":{"name":"Journal of Thrombosis and Haemostasis","volume":" ","pages":""},"PeriodicalIF":5.2,"publicationDate":"2026-09-29","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149081508","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":"Preserving expertise in vitamin K antagonists in the era of direct oral anticoagulants: avoiding therapeutic segregation.","authors":"Céline Everard, Catherine Lambert, Cédric Hermans","doi":"10.1016/j.jtha.2026.08.020","DOIUrl":"10.1016/j.jtha.2026.08.020","url":null,"abstract":"<p><p>The rapid uptake of direct oral anticoagulants has sharply reduced the prescribing of vitamin K antagonists (VKAs), giving rise to an underappreciated risk: the progressive loss of the clinical expertise required to manage them. Yet, several populations remain dependent on VKAs, including patients with mechanical heart valves, high-risk antiphospholipid syndrome, and advanced renal disease, as well as patients in resource-limited settings. These patients face both the intrinsic complexity of VKA therapy and a health care environment in which practical experience with these agents is becoming scarce. Preserving this competence is a matter of patient safety and professional responsibility. We argue for a structured response combining education, the maintenance of specialized anticoagulation clinics, patient empowerment, and anticoagulation stewardship with artificial intelligence remaining, for now, only a prospect.</p>","PeriodicalId":17326,"journal":{"name":"Journal of Thrombosis and Haemostasis","volume":" ","pages":""},"PeriodicalIF":5.2,"publicationDate":"2026-09-25","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148851044","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":"Intravenous Immunoglobulin (IVIG) use in HIT and efficacy of early IVIG compared to standard of care treatment.","authors":"Jivtesh Singh, Grace Gorecki, Prabhsimrat Gill, Samantha Maples, Irina Chibisov, Angela Verdoni, Robert A Kaplan, Rama Ganesh, Deep Shah, Arjun Lakshman","doi":"10.1016/j.jtha.2026.09.029","DOIUrl":"https://doi.org/10.1016/j.jtha.2026.09.029","url":null,"abstract":"<p><strong>Background: </strong>Heparin-induced thrombocytopenia (HIT) is an immune-mediated prothrombotic complication of heparin exposure. Intravenous immunoglobulin (IVIG) has been proposed as an adjunctive therapy for refractory or autoimmune HIT. Real-world utilization patterns and impact of early administration on clinical outcomes remain unclear.</p><p><strong>Methods: </strong>We performed a retrospective chart review across the Allegheny Health Network (2015-2025). We described clinical characteristics and outcomes among all HIT patients who received IVIG (n=29). We also compared early IVIG recipients (n=24) to controls (n=129) using 1:2 propensity score matching. The primary outcome was time to platelet recovery, analyzed using Kaplan-Meier estimation and Cox proportional hazards regression.</p><p><strong>Results: </strong>IVIG was used in a cohort of patients with a median platelet count nadir of 26 × 10⁹/L (IQR of 16 - 35 ×10⁹/L) and thrombosis was present at diagnosis in 75.8% of patients. Platelet recovery was achieved in 93.1% at a median of 6 days (IQR 3 - 9 Days) days from first dose of IVIG administration, with a favorable safety profile. Early IVIG (within 3 days of HIT diagnosis) was associated with significantly faster platelet recovery in the matched cohort (median 3 vs. 5 days; HR 2.15, 95%CI 1.09-4.26, p=0.028). Higher platelet nadir predicted faster recovery (HR 2.247 per 10 × 10⁹/L, p < 0.001). No significant differences in thrombosis, bleeding, or mortality were observed.</p><p><strong>Conclusions: </strong>At our institution, IVIG use in HIT was confined to severely ill patients with high thrombotic burden. Early IVIG administration accelerated platelet recovery compared to standard-of-care alone. Prospective multicenter studies are needed to confirm these findings.</p>","PeriodicalId":17326,"journal":{"name":"Journal of Thrombosis and Haemostasis","volume":" ","pages":""},"PeriodicalIF":5.2,"publicationDate":"2026-09-24","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149039737","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}