Thrombosis research最新文献

{"title":"Suboptimal CT pulmonary angiography for PE diagnosis, is it worth further study? A retrospective 7.5-year evaluation in a large academic medical center","authors":"Pedro Parra Caballero , Fernando Ruiz Berraco , Ana Salvador Rodríguez , Ángela Sánchez Juez , Nuria Ruiz-Giménez Arrieta , Jaime Bustos Carpio , Ana Rodríguez Revillas , Isabel López Villar , María del Carmen de Benavides Bernaldo de Quirós , María Jesús Delgado Heredia","doi":"10.1016/j.thromres.2025.109324","DOIUrl":"10.1016/j.thromres.2025.109324","url":null,"abstract":"","PeriodicalId":23064,"journal":{"name":"Thrombosis research","volume":"250 ","pages":"Article 109324"},"PeriodicalIF":3.7,"publicationDate":"2025-04-21","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143873582","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Disseminated Intravascular Coagulopathy and Persistent Inflammation, Immunosuppression, and Catabolism Syndrome: Pathophysiology, shared pathways, and clinical implications","authors":"Nicole Ann Gunn ,&nbsp;Yukei Oo ,&nbsp;Christy Whei Lynn Lee ,&nbsp;Edward Heaney ,&nbsp;Nichole Yue Ting Tan ,&nbsp;Yan Zhi Chan ,&nbsp;Samuel Sherng Young Wang","doi":"10.1016/j.thromres.2025.109321","DOIUrl":"10.1016/j.thromres.2025.109321","url":null,"abstract":"<div><h3>Background</h3><div>Disseminated Intravascular Coagulopathy (DIC) and Persistent Inflammation, Immunosuppression, and Catabolism Syndrome (PICS) are critical care syndromes that frequently coexist in critically ill patients, but mechanisms underlying their shared pathways are not well understood.</div></div><div><h3>Objective</h3><div>This review discusses the pathophysiology of DIC and PICS and explores the shared mechanisms behind DIC and PICS and their implications for clinical management.</div></div><div><h3>Findings</h3><div>DIC and PICS share a common pathophysiological foundation of endothelial dysfunction, coagulation dysregulation, and inflammation, leading to a vicious cycle of microvascular injury and systemic inflammation, culminating in organ dysfunction. DIC has also been identified as an independent risk factor for PICS. Anticoagulation therapies such as antithrombin, recombinant human soluble thrombomodulin (rhTM), and heparin attenuates inflammation, a mechanism underlying both syndromes, thereby improving outcomes in PICS.</div></div><div><h3>Conclusion</h3><div>DIC and PICS share critical pathophysiological pathways that exacerbate outcomes in critically ill patients. Recognizing these interconnections is essential for developing targeted therapies. Standardizing PICS definitions and advancing research to clarify mechanisms, interplay, and causality between DIC and PICS are crucial next steps.</div></div>","PeriodicalId":23064,"journal":{"name":"Thrombosis research","volume":"250 ","pages":"Article 109321"},"PeriodicalIF":3.7,"publicationDate":"2025-04-21","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143873511","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Disulfide bond control of platelet αIIbβ3 integrin","authors":"Aster E. Pijning,&nbsp;Philip J. Hogg","doi":"10.1016/j.thromres.2025.109320","DOIUrl":"10.1016/j.thromres.2025.109320","url":null,"abstract":"<div><div>The platelet αIIbβ3 integrin is the most abundant platelet receptor, orchestrating platelet adhesion, activation, and mechano-sensing during hemostasis and thrombosis. Disulfide bonds are the covalent links between the sulfur atoms of two cysteine residues and their role in the functioning of αIIbβ3 has been a topic of investigation for over two decades. The advent of differential cysteine alkylation using isotopic alkylators and mass spectrometry has led to the identification of multiple partially disulfide-bonded states of αIIbβ3 that are constitutively produced by megakaryocytes and reside in the platelet surface membrane, and an allosteric disulfide that is cleaved in the mature receptor to control function. One of the disulfide-bonded integrin states has reduced capacity due to particular clustering, internalisation, and recycling dynamics and lower avidity for fibrinogen, suggesting that other states may also have specific properties. Cleavage of an allosteric disulfide bond in the activated integrin uncouples the receptor from its ligand, and it is likely that other allosteric disulfides are yet to be identified. This review presents the current knowledge of the role of specific disulfide bonds in the regulation of αIIbβ3 integrin and perspectives on the future.</div></div>","PeriodicalId":23064,"journal":{"name":"Thrombosis research","volume":"250 ","pages":"Article 109320"},"PeriodicalIF":3.7,"publicationDate":"2025-04-16","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143881425","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Antiplatelet-anticoagulant, APAC, a mimic of endogenous heparin, is an antithrombotic with von Willebrand factor-mediated characteristics","authors":"Annukka Jouppila ,&nbsp;Ilja Nevola ,&nbsp;Marja Lemponen ,&nbsp;Tomi Mattila ,&nbsp;Riitta Lassila","doi":"10.1016/j.thromres.2025.109318","DOIUrl":"10.1016/j.thromres.2025.109318","url":null,"abstract":"<div><h3>Background</h3><div>We have conjugated selected number of unfractionated heparin (UFH) chains to human albumin core to mimic mast-cell heparin proteoglycans (HEP-PG). Indeed, APAC, dual antiplatelet and anticoagulant, as HEP-PG, has inhibited collagen- (CIPA) and thrombin-induced platelet aggregation, being simultaneously an anticoagulant. In several animal models of arterial thrombosis, APAC has provided vascular-injury-associated local antithrombotic properties mediated by von Willebrand factor (VWF).</div></div><div><h3>Aims</h3><div>We compared the structure-function effects of APAC with those of UFH <em>in vitro</em>, and when supplemented in blood studied platelet and VWF-dependency and anticoagulation.</div></div><div><h3>Methods</h3><div>We assessed the total thrombosis formation analysis system (T-TAS) and coagulation (rotational thromboelastometry, ROTEM) in blood, and thrombin generation and aggregation in platelet-rich plasma. We studied aggregation responses of APAC to collagen, ristocetin, ADP, and potential synergism with cangrelor, P2Y12 receptor antagonist. Finally, heparin-neutralizing role of platelet factor 4 (PF4) on antiplatelet and anticoagulant functions of APAC was investigated.</div></div><div><h3>Results</h3><div>APAC concentration-dependently exceeded the anticoagulant and antithrombotic action of UFH in ROTEM, and platelet thrombus formation under arterial blood flow over collagen/tissue factor. APAC uniquely inhibited CIPA. While ADP- and ristocetin-induced aggregation were unaffected by APAC, we detected synergism with cangrelor for CIPA. Disruption of the tertiary structure of APAC reverted its mode of action to anticoagulation only, alike UFH. PF4 neutralized antithrombotic actions of APAC.</div></div><div><h3>Conclusion</h3><div>The structure-function of APAC conveys dual and unique antiplatelet and anticoagulant actions in flowing blood over collagen and beyond. Our studies confirmed the inhibitory role of APAC on VWF functions and fibrin formation.</div></div>","PeriodicalId":23064,"journal":{"name":"Thrombosis research","volume":"250 ","pages":"Article 109318"},"PeriodicalIF":3.7,"publicationDate":"2025-04-12","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143844945","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Splanchnic vein thrombosis (2003−2022): a Swiss nationwide epidemiological study","authors":"Silvia Cardi ,&nbsp;Simon Wolf ,&nbsp;Riccardo M. Fumagalli ,&nbsp;Corrado Lodigiani ,&nbsp;Fabian Rössler ,&nbsp;Alice Trinchero ,&nbsp;Luca Valerio ,&nbsp;Walter Ageno ,&nbsp;Nils Kucher ,&nbsp;Stefano Barco","doi":"10.1016/j.thromres.2025.109319","DOIUrl":"10.1016/j.thromres.2025.109319","url":null,"abstract":"<div><h3>Background</h3><div>Splanchnic vein thrombosis (SVT) is a rare form of venous thromboembolism with limited epidemiological data. This study aims to provide a detailed overview in Switzerland using administrative records.</div></div><div><h3>Methods</h3><div>We analysed nationwide patient-level data on SVT-related hospitalizations, including portal, splenic, and hepatic (Budd-Chiari syndrome) vein thrombosis from 2003 to 2022. We assessed trends in crude and age-standardized incidence rates, proportion of SVT-related hospitalizations, readmission rates as well as gender differences, comorbidities, clinical features, and in-hospital outcomes. Multivariable logistic regression was used to identify predictors of in-hospital death.</div></div><div><h3>Results</h3><div>SVT was recorded in 17,966 hospitalizations (35 % women) involving 13,689 patients. Portal vein thrombosis was the most frequent manifestation, followed by splenic, hepatic and multisegmental thrombosis. Age-standardized incidence rate increased from 0.4 (95 % CI: 0.3–0.4) per 10,000 general population in 2003 to 1.5 (95 % CI: 1.4–1.6) in 2022, with rising proportions of SVT-related hospitalizations and readmission rates. Case fatality rate remained steady at 13 % and was highest for portal vein thrombosis. For most SVT subtypes, incidence rate was higher in males and case fatality rate in females. Predictors of in-hospital death included liver failure, intestinal infectious diseases, cancer. Common comorbidities included non-neoplastic abdominal diseases (14,010; 78 %), cardiovascular diseases (11,214; 62 %), and cancer (8510; 47 %). Diagnostic or therapeutic procedures involved 56 % of cases, intensive care stay 19 %, and median length of stay was 11 days (Q1-Q3 5–19).</div></div><div><h3>Conclusion</h3><div>Despite its rarity, SVT is characterized by substantial morbidity and in-hospital mortality. Further research is needed to validate these findings and improve patient management.</div></div>","PeriodicalId":23064,"journal":{"name":"Thrombosis research","volume":"250 ","pages":"Article 109319"},"PeriodicalIF":3.7,"publicationDate":"2025-04-12","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143864601","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Phenotype, genotype, and laboratory assessment of congenital fibrinogen disorders: Data from the Rare Bleeding disorders in the Netherlands study","authors":"Bauke Haisma ,&nbsp;Sanna R. Rijpma ,&nbsp;Marjon H. Cnossen ,&nbsp;Paul L. den Exter ,&nbsp;Ilmar C. Kruis ,&nbsp;Karina Meijer ,&nbsp;Laurens Nieuwenhuizen ,&nbsp;Nick van Es ,&nbsp;Joline L. Saes ,&nbsp;Nicole M.A. Blijlevens ,&nbsp;Waander L. van Heerde ,&nbsp;Saskia E.M. Schols","doi":"10.1016/j.thromres.2025.109317","DOIUrl":"10.1016/j.thromres.2025.109317","url":null,"abstract":"<div><h3>Introduction</h3><div>Congenital fibrinogen disorders (CFDs), encompassing quantitative (hypo−/afibrinogenemia) and qualitative (dysfibrinogenemia) defects, can result in bleeding or thrombotic events. This study aimed to enhance understanding of the clinical and genetic characteristics of CFD patients.</div></div><div><h3>Methods</h3><div>The Dutch cross-sectional RBiN study included 47 CFD patients (median age 38, 55 % women), categorized into (hypo)dysfibrinogenemia, severe (&lt;500 mg/L), moderate (500–1000 mg/L) and mild hypofibrinogenemia (1000–1800 mg/L) as well as carriers with pathogenic variants but normal fibrinogen levels (&gt;1800 mg/L). Clinical assessments included bleeding phenotype, thrombosis history, fibrinogen activity and antigen levels, thrombin and plasmin generation assays and genotypic analysis.</div></div><div><h3>Results</h3><div>Patients with severe hypofibrinogenemia displayed the highest median ISTH-BAT score (16), followed by moderate hypofibrinogenemia (11), (hypo)dysfibrinogenemia (6), mild hypofibrinogenemia (4) and carriers (0). Female-specific bleeding (postpartum hemorrhage, heavy menstrual bleeding) was prevalent across all CFD subtypes, with moderate hypofibrinogenemia showing high average scores on these ISTH-BAT items (3.0 and 2.3). Postoperative bleeding was common in moderate and severe hypofibrinogenemia (average ISTH-BAT item scores of 2.5 and 2.8, respectively). Patients with biallelic variants had lower fibrinogen activity levels (median 200 mg/L) than those with monoallelic variants (935 mg/L, <em>p</em> &lt; 0.001). Fibrinogen activity levels correlated positively with plasmin peak height (<em>R</em> = 0.74, p &lt; 0.001) and inversely with thrombin potential (R = –0.55, <em>p</em> = 0.002). Thrombin potential was 1.77-fold higher in patients with a venous thrombosis history (<em>n</em> = 5, <em>p</em> = 0.03) than in healthy controls.</div></div><div><h3>Conclusions</h3><div>In patients with CFDs, postoperative bleeding correlates with fibrinogen activity, while female-specific bleeding affects all CFD subtypes. Elevated thrombin generation might explain thrombosis risk in these patients.</div></div>","PeriodicalId":23064,"journal":{"name":"Thrombosis research","volume":"249 ","pages":"Article 109317"},"PeriodicalIF":3.7,"publicationDate":"2025-04-04","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143800691","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Loss of von Willebrand factor large multimers in patients undergoing hemodialysis: A single-center, retrospective study","authors":"Yoshinari Fujii ,&nbsp;Satomi Nagaya ,&nbsp;Taro Kanno ,&nbsp;Shinya Yamada ,&nbsp;Misako Suzuki ,&nbsp;Kota Goto ,&nbsp;Hisanori Horiuchi ,&nbsp;Masanori Matsumoto ,&nbsp;Eriko Morishita","doi":"10.1016/j.thromres.2025.109316","DOIUrl":"10.1016/j.thromres.2025.109316","url":null,"abstract":"<div><h3>Introduction</h3><div>Von Willebrand factor (VWF) is produced by vascular endothelial cells as large multimers and is cleaved by ADAMTS13 into an appropriate size in a shear stress-dependent manner. Excessive shear stress enhances VWF cleavage, leading to a hemorrhagic disease known as acquired von Willebrand syndrome. No clear reports on the prevalence of the loss of VWF large multimers in patients receiving hemodialysis are currently available. Therefore, this study investigated the prevalence of the loss of VWF large multimers in patients undergoing hemodialysis.</div></div><div><h3>Methods</h3><div>This single-center, retrospective study involved 90 patients undergoing hemodialysis and 32 healthy participants as controls. VWF antigen levels (VWF:Ag), VWF activity (VWF:RCo), and ADAMTS13 activity were measured. VWF multimer analysis was performed by modified western blotting with an agarose gel electrophoresis, followed by densitometric evaluation of band intensities to calculate the VWF large multimer index (VWF-LMI). A VWF-LMI &lt;80 % was defined as the loss of VWF large multimers, and the prevalence of the loss of VWF large multimers was calculated.</div></div><div><h3>Results</h3><div>VWF:Ag and VWF:RCo levels in patients undergoing hemodialysis were significantly higher than those in healthy individuals (<em>p</em> &lt; 0.01 both) and were negatively correlated with ADAMTS13 activity (<em>p</em> &lt; 0.01, R = −0.353 and <em>p</em> &lt; 0.01, R = −0.392, respectively). A VWF-LMI &lt;80 % was present in 24 of 90 patients.</div></div><div><h3>Conclusions</h3><div>The loss of VWF large multimers was identified in 26.7 % of patients receiving hemodialysis. However, the prevalence of the loss of VWF multimers in these patients may be underestimated, as their relatively high VWF activity makes significant bleeding manifestations less likely.</div></div>","PeriodicalId":23064,"journal":{"name":"Thrombosis research","volume":"249 ","pages":"Article 109316"},"PeriodicalIF":3.7,"publicationDate":"2025-03-31","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143748278","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Efficacy and safety of low-dose acetylsalicylic acid for the prevention of thromboembolic events in individuals positive for antiphospholipid antibodies: A systematic review and meta-analysis","authors":"Alessandro Squizzato ,&nbsp;Federica De Pascali ,&nbsp;Vittorio Pengo ,&nbsp;Marco P. Donadini","doi":"10.1016/j.thromres.2025.109313","DOIUrl":"10.1016/j.thromres.2025.109313","url":null,"abstract":"","PeriodicalId":23064,"journal":{"name":"Thrombosis research","volume":"249 ","pages":"Article 109313"},"PeriodicalIF":3.7,"publicationDate":"2025-03-29","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143773370","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Investigation of the impact of antithrombin deficiency on the inflammatory response: Results from a single centre cohort study","authors":"Katarzyna Mayger ,&nbsp;Johanna Young ,&nbsp;Rui Leite ,&nbsp;Kiran Parmar ,&nbsp;Beverley J. Hunt","doi":"10.1016/j.thromres.2025.109315","DOIUrl":"10.1016/j.thromres.2025.109315","url":null,"abstract":"<div><h3>Background</h3><div>Antithrombin signalling may exert an anti-inflammatory effect; therefore we hypothesised that individuals with inherited antithrombin deficiency (ATD) may have an altered inflammatory state.</div></div><div><h3>Aims</h3><div>To assess the inflammatory state in those with ATD compared with healthy controls (HCs), by measuring inflammatory markers.</div></div><div><h3>Methods</h3><div>A case-control study of age- and sex-matched HCs (<em>n</em> = 51) with ATD patients (n = 51). Seven inflammatory makers were selected. ELISA assays quantified: high-sensitivity C-reactive protein (hsCRP), intercellular adhesion molecule-1 (ICAM-1), vascular adhesion molecule-1 (VCAM-1) and complement C3a-des-Arg. Circulating nucleosomes were measured using a chemiluminescence immunoassay (Nu.Q®NETs). Clauss fibrinogen and HemosIL VWF activity were also measured. Results are expressed as median (range).</div></div><div><h3>Results</h3><div>Overall analysis of ATD vs HCs showed elevated circulating nucleosomes 29.3 ng/mL [0.5–309.3] vs 21.3 ng/mL [3.7–86.3], <em>p</em> = 0.012 but no differences were observed for C3a, VCAM-1, ICAM-1, VWF and fibrinogen. ATD patients were separated into two groups based on the history of VTE. PF1 + 2 levels were decreased in ATD with previous VTE due to anticoagulation. Increased circulating nucleosomes 38.4 ng/mL [11.6–309.3] vs 24.2 ng/mL [9.3–46.5], <em>p</em> = 0.003 and VCAM-1858.3 ng/mL [564.4–2483.2] vs 746.2 ng/mL [460.6–1034.8], <em>p</em> = 0.016 was observed in ATD with previous VTE vs HCs, respectively. Decreased ICAM-1 and VWF levels were noted in the ATD with no history of VTE when compared to HCs. No significant relationships between AT activity and inflammatory markers were found.</div></div><div><h3>Conclusion</h3><div>Those with ATD did not have an altered inflammatory state as measured by a group of biomarkers except for increased circulating nucleosomes and VCAM-1 compared to paired healthy controls which can be attributed to previous VTE; while those with no personal history of VTE had reduced ICAM-1 and VWF. No correlation was observed between AT activity and levels of inflammatory markers.</div></div>","PeriodicalId":23064,"journal":{"name":"Thrombosis research","volume":"249 ","pages":"Article 109315"},"PeriodicalIF":3.7,"publicationDate":"2025-03-28","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143783694","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Comment on: “Efficacy and safety of low-dose acetylsalicylic acid for the prevention of thromboembolic events in individuals positive for antiphospholipid antibodies: A systematic review and meta-analysis”","authors":"Shubham Kumar ,&nbsp;Nosaibah Razaqi ,&nbsp;Rachana Mehta ,&nbsp;Ranjana Sah","doi":"10.1016/j.thromres.2025.109312","DOIUrl":"10.1016/j.thromres.2025.109312","url":null,"abstract":"","PeriodicalId":23064,"journal":{"name":"Thrombosis research","volume":"249 ","pages":"Article 109312"},"PeriodicalIF":3.7,"publicationDate":"2025-03-27","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143748279","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}