Platelets最新文献

{"title":"Complement C3 inhibition reduces complement activation in clinical platelet concentrates but does not counteract platelet storage lesions.","authors":"Linnea I Andersson, Per Sandgren, Dick J Sjöström, Camilla Mohlin, Kim Hägerström, Ivar Tjernberg, Tom Eirik Mollnes, Per H Nilsson","doi":"10.1080/09537104.2025.2513298","DOIUrl":"https://doi.org/10.1080/09537104.2025.2513298","url":null,"abstract":"<p><p>Platelet storage is associated with storage lesions, including platelet morphological changes and a gradual functional loss. We investigated the impact of complement C3 inhibition on complement activation and platelet storage lesions in clinical platelet concentrates. Platelet concentrates (<i>n</i> = 8) were prepared in PAS-E and stored for seven days at 22°C. Each concentrate was split in two, with the C3 inhibitor compstatin Cp40 added to one part, and the other serving as the control. Complement and platelet activation markers, platelet function, and metabolic measures were analyzed every second day. Cp40 significantly reduced C3bc and sC5b-9 levels, but not C4c, indicating inhibition of complement activation at the level of C3. However, Cp40 did not affect platelet-specific or metabolic measures. Surface expression of CD62P and NAP-2 release increased significantly over the storage time, whereas CD63 expression and PF4 and TSP-1 release remained stable. Platelet responses to TRAP-6 mediated PAR-1 activation and U46619 mediated TXA₂R stimulation decreased over time, recorded as CD62P and CD63 expression and release of soluble factors. No drop in platelet count was observed, and metabolic markers remained within their critical limits. While C3 inhibition effectively reduced complement activation in stored platelet concentrates, it did not mitigate platelet storage lesions.</p>","PeriodicalId":20268,"journal":{"name":"Platelets","volume":"36 1","pages":"2513298"},"PeriodicalIF":2.5,"publicationDate":"2025-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144497794","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":"Pharmacodynamic effects of early aspirin withdrawal after percutaneous coronary intervention in patients with atrial fibrillation treated with ticagrelor or prasugrel.","authors":"Mark A Sammut, Mohammed E F Rahman, Claire Bridge, Jessica Hanson, Heather Judge, Bethany Lynch, Emily Maz, Hannah McMellon, Janet Middle, Georgia Williamson, William A E Parker, Justin Lee, Robert F Storey","doi":"10.1080/09537104.2025.2507037","DOIUrl":"https://doi.org/10.1080/09537104.2025.2507037","url":null,"abstract":"<p><p>Dual antithrombotic therapy (DAT) without aspirin reduces bleeding compared with triple antithrombotic therapy (TAT) in patients with atrial fibrillation who have undergone percutaneous coronary intervention, without apparently increasing ischemic events. A prospective pharmacodynamic study was performed to investigate the impact of aspirin on bleeding time, platelet function and fibrin clot analysis in this population. Patients receiving TAT (<i>n</i> = 16), comprising aspirin, ticagrelor/prasugrel and a direct-acting oral anticoagulant (DOAC), were compared with those receiving DAT without aspirin (<i>n</i> = 18). Bleeding time was reduced with DAT compared with TAT (median 27.8 vs 30.0 minutes, <i>p</i> = .005). Assessed by light transmission aggregometry, median platelet aggregation was significantly increased with DAT compared with TAT in response to arachidonic acid (63 vs 3%, <i>p</i> = .002) and collagen (72 vs 37%, <i>p</i> < .001) but not 5-μmol/L adenosine diphosphate (25 vs 27%, <i>p</i> = .966) or thrombin-receptor-activating peptide (37 vs 24%, <i>p</i> = .086). VerifyNow P2Y₁₂ assay showed > 70% inhibition in all patients. Fibrin clot lysis time and maximum turbidity were similar between groups. Using P2Y₁₂ inhibitors of consistent potency, DAT improves hemostasis through sparing cyclooxygenase-1-mediated platelet activation but has a comparable effect to TAT on other pathways and fibrin clot properties. DAT with ticagrelor/prasugrel and DOAC may provide sufficient antithrombotic effect without excessive anti-hemostatic effect.</p>","PeriodicalId":20268,"journal":{"name":"Platelets","volume":"36 1","pages":"2507037"},"PeriodicalIF":2.5,"publicationDate":"2025-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144128529","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":"Differential effects of dual antiplatelet and dual antithrombotic therapy on hemostasis in chronic coronary syndrome patients: the DEFINE CCS study.","authors":"Tony Haddad, Osama Elkhateeb, Lawrence Title, Ata Quraishi, Wan Cheol Kim, Ali Hillani, Scott Grandy, Stefan S Heinze, Finn Eichhorn, Hannah Harquail, John Sapp, William Parker, Shamir R Mehta, Robert F Storey, Wael Sumaya","doi":"10.1080/09537104.2025.2524624","DOIUrl":"10.1080/09537104.2025.2524624","url":null,"abstract":"<p><p>Optimal long term antithrombotic treatment in high-risk chronic coronary syndrome (CCS) patients remains uncertain. Both ticagrelor (60 mg BID) and low-dose rivaroxaban (2.5 mg BID) in addition to low-dose aspirin resulted in significant reductions in major cardiovascular events in high-risk patients at the expense of increased bleeding risk. We aimed to compare the effects of both strategies on bleeding time, fibrin clot lysis time and inflammatory biomarkers in CCS patients with history of acute coronary syndrome. Twenty aspirin-treated patients were recruited into a randomized crossover study to receive ticagrelor 60 mg BID in 1 week and rivaroxaban 2.5 mg BID in the other with a 2-week washout period in between. Outcome measures were determined at the start and end of each treatment week. Two-way ANOVA was used to determine difference in treatment effect. Data are presented as mean ± SD. At baseline, there was no significant difference in any studied outcome measure. Bleeding time was significantly longer with ticagrelor compared to rivaroxaban (Ticagrelor: 897 ± 481secs vs. Rivaroxaban: 440 ± 184 secs; <i>p</i> = .0001). Fibrin clot lysis time was not impacted by ticagrelor but significantly dropped post treatment with rivaroxaban (Ticagrelor: 5743 ± 2590 secs vs. Rivaroxaban: 4309 ± 2308 secs; <i>p</i> = .0049). Neither treatment had an impact on levels of high-sensitivity CRP or white cell count. In conclusion, ticagrelor 60 mg BID has greater impact on bleeding time compared to rivaroxaban 2.5 mg BID. Whereas rivaroxaban, positively modulates fibrin clots, rendering them more prone to lysis.</p>","PeriodicalId":20268,"journal":{"name":"Platelets","volume":"36 1","pages":"2524624"},"PeriodicalIF":2.5,"publicationDate":"2025-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144554275","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":"CD39-Diannexin alleviates the platelet storage lesion by protecting platelets from activation, a new attempt from a traditional perspective.","authors":"Cheng Liu, Peng Wang, Yafei Gao, Xiaolong Ma, Yang Su, Yao Wei, Rui Qiao","doi":"10.1080/09537104.2025.2517108","DOIUrl":"https://doi.org/10.1080/09537104.2025.2517108","url":null,"abstract":"<p><p>Due to platelet storage lesions (PSL), transfused platelets are unable to function properly in the prevention and treatment of bleeding in critically ill patients. It is a traditional assumption that PSL is closely related to platelet activation during storage because of the exposure of CD62P, phosphatidylserine (PS), etc. In this standpoint, activated platelets in <i>vitro</i> cannot be reactivated in <i>vivo</i> to exert their hemostatic function and exposed PS accelerates platelet clearance. Therefore, reducing platelet activation is helpful to alleviate PSL. Diannexin is the dimer of annexin that has a higher affinity for PS. CD39 is an ADP hydrolase produced by the vascular endothelium. As a result, we construct CD39-Diannexin (CD39-DA) fusion protein and hypothesize that CD39-DA can reduce platelet activation during storage to alleviate PSL. CD39-DA can bind to the exposed PS on the surface of stored platelets by immunofluorescence. Compared to the control groups, CD39-DA reserves part of stored platelets' aggregation function confirmed by platelet aggregation assay, induced by AA, ADP and collagen. Additionally, CD39-DA reduces lactic dehydrogenase (LDH) levels and CD62P-positive events after three-day storage. Interestingly, we preliminarily discover that CD39-DA may reduce stored platelets' apoptosis and increase aggregatory platelets after activation by thrombin, collagen and calcium, which is marked by GSAO. In conclusion, we confirm that CD39-DA can alleviate PSL by reducing platelet activation.</p>","PeriodicalId":20268,"journal":{"name":"Platelets","volume":"36 1","pages":"2517108"},"PeriodicalIF":2.5,"publicationDate":"2025-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144258820","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":"Extracellular thiol isomerase ERp5 regulates integrin αIIbβ3 activation by inhibition of fibrinogen binding.","authors":"Kaifei Sun, Yaqiong Zhang, Aizhen Yang, Yuxin Zhang, Zhenzhen Zhao, Xiaofeng Yan, Yi Lu, Yue Han, Depei Wu, Freda Passam, Jingyu Zhang, Yi Wu","doi":"10.1080/09537104.2025.2455743","DOIUrl":"10.1080/09537104.2025.2455743","url":null,"abstract":"<p><p>Recent studies have shown that anti-ERp5 antibodies inhibit platelet activation and thrombus formation; Moreover, ERp5-deficient platelets exhibit enhanced platelet reactivity via regulation of endoplasmic reticulum (ER) stress. In this study, we used a new ERp5-knockout mouse model as well as recombinant ERp5 (rERp5) protein, to examine the role of ERp5 in platelet function and thrombosis. Although platelet-specific ERp5-deficient mice had decreased platelet count, the mice had shortened tail-bleeding times and enhanced platelet accumulation in FeCl₃-induced mesenteric artery injury, compared with wild-type mice. Using platelet-specific ERp5-deficient mice, we found that ERp5 deficiency increased platelet aggregation, granule secretion, and integrin αIIbβ3 activation. Wild-type recombinant ERp5 protein (rERp5-wt) and inactive mutant ERp5 protein (rERp5-mut) both inhibited human platelet aggregation and the binding of fibrinogen to human platelets, indicating that ERp5 protein interferes with the interaction between integrin αIIbβ3 and its ligand fibrinogen, and its enzymatic activity is not required for this process. Consistently, wild-type mice injected with rERp5-wt or rERp5-mut protein had prolonged tail-bleeding times. Our results provide important evidence that platelet ERp5 negatively regulates platelet activation and thrombus formation, via steric hindrance interfering with integrin αIIbβ3 ligation.</p>","PeriodicalId":20268,"journal":{"name":"Platelets","volume":"36 1","pages":"2455743"},"PeriodicalIF":2.5,"publicationDate":"2025-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143067537","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":"Transcriptomic and functional characterization of megakaryocytic-derived platelet-like particles: impaired aggregation and prominent anti-tumor effects.","authors":"Kaitlin Garofano, Vera Mariani, Kameron Rashid, Sumanun Suwunnakorn, Alfateh Sidahmed, Anelia Horvath, Sanjay B Maggirwar, Travis J O'Brien, Minoli A Perera, Michael Whalen, Norman H Lee","doi":"10.1080/09537104.2024.2449344","DOIUrl":"10.1080/09537104.2024.2449344","url":null,"abstract":"<p><p>Platelet-like particles (PLPs), derived from megakaryocytic cell lines MEG-01 and K-562, are widely used as a surrogate to study platelet formation and function. We demonstrate by RNA-Seq that PLPs are transcriptionally distinct from platelets. Expression of key genes in signaling pathways promoting platelet activation/aggregation, such as the PI3K/AKT, protein kinase A, phospholipase C, and α-adrenergic and GP6 receptor pathways, was missing or under-expressed in PLPs. Functionally, PLPs do not aggregate following epinephrine, collagen, or ADP stimulation. While PLPs aggregated in response to thrombin, they did not display enhanced expression of surface markers P-selectin and activated α_2bβ₃, in contrast to platelets. We have previously demonstrated that platelets physically couple to MDA-PCa-2b and RC77T/E prostate cancer (PCa) cells via specific ligand-receptor interactions, leading to platelet-stimulated cell invasiveness and apoptotic resistance, and reciprocal cell-induced platelet aggregation. In contrast, PLP interactions with PCa cells inhibited both cell invasion and apoptotic resistance while failing to promote PLP aggregation. Moreover, PLPs reduced platelet-PCa cell interactions and antagonized platelet-stimulated oncogenic effects in PCa cells. RNA-Seq analysis identified candidate ligand-transmembrane protein combinations involved in anti-tumorigenic signaling of PLPs to PCa cells. Antibody neutralization of the TIMP3-MMP15 and VEGFB-FGFR1 signaling axes reversed PLP-mediated anti-invasion and apoptotic sensitization, respectively. In summary, PLPs lack many transcriptomic, molecular and functional features of platelets and possess novel anti-tumorigenic properties. These findings indicate that PLPs may have a potential therapeutic role in targeting and disrupting the oncogenic signaling between platelets and cancer cells, offering a new avenue for anti-cancer strategies.</p>","PeriodicalId":20268,"journal":{"name":"Platelets","volume":"36 1","pages":"2449344"},"PeriodicalIF":2.5,"publicationDate":"2025-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11890189/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142984432","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":"Platelet parameters for distinguishing between inherited macrothrombocytopenia and acquired thrombocytopenia: a retrospective case-control study.","authors":"Wenlan Chen, Yajie Ding, Li Cai, Mei Xue, Abdul Rehman Arif, Heng Mei, Yadan Wang","doi":"10.1080/09537104.2025.2489025","DOIUrl":"https://doi.org/10.1080/09537104.2025.2489025","url":null,"abstract":"<p><p>Inherited macrothrombocytopenia (IMT) is characterized by increased platelet volume. Using platelet parameters, including platelet count, mean platelet volume (MPV), platelet-large cell ratio (P-LCR), and platelet distribution width, to differentiate IMT from acquired thrombocytopenia (AT) in the Chinese population is unclear. This study aimed to evaluate these parameters and determine optimal thresholds for early IMT identification. This single-center, retrospective case-control study included IMT patients from 1 January 2022 to 31 January 2024. Age- and sex-matched AT patients and healthy individuals were selected (1:3 ratio). Platelet parameters were compared using a one-way analysis of variance and the Kruskal-Wallis test. The ability of platelet parameters to identify IMT was assessed using the receiver operating characteristic curve, with the optimal threshold determined using the Youden index. This study included 13 IMT patients, 39 AT patients, and 39 controls. The MPV and P-LCR were significantly higher in IMT than in AT patients (<i>P</i> < 0.05) and strongly differentiated between groups. The area under the curve (95% confidence interval) for MPV and P-LCR were 0.865 (0.724-1.000) and 0.860 (0.719-1.000), respectively. The optimal MPV and P-LCR thresholds for IMT were 14.55 fL and 58%, respectively. The MPV was most important for distinguishing IMT from patients with thrombocytopenia.</p>","PeriodicalId":20268,"journal":{"name":"Platelets","volume":"36 1","pages":"2489025"},"PeriodicalIF":2.5,"publicationDate":"2025-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144041596","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":"Regulation of lipid metabolism: a new strategy for platelet storage.","authors":"Jieyun Shi, Wenting Wang, Jinmei Xu, Wen Yin","doi":"10.1080/09537104.2025.2465321","DOIUrl":"10.1080/09537104.2025.2465321","url":null,"abstract":"<p><p>Transfusions of platelets are often used as prophylaxis in patients with hematologic malignancies and as treatment for active bleeding. However, platelets are in short supply due to the fact that they could only be kept for 5-7 days in vitro and they lose some of their functionality as a result of platelet storage lesions. To address this issue, refrigeration, cryopreservation and platelet additive solutions have been researched to determine their abilities to extend platelet storage duration. However, refrigerated platelets are quickly cleared after transfusion, while platelets in platelet additive solutions still present issues such as platelets quality and the risk of allergic reactions. Recent studies showed that changes in lipid metabolites during platelet storage and inadequate of fatty acid metabolism may also limit platelet shelf life and function. In this review, we address the principles of lipid metabolism during platelet storage and discuss the strategies for effective platelet storage systems. The findings of this review highlight the role of lipid metabolism during platelet storage, providing insights into future research focused on extending the preservation period and function of platelet.</p>","PeriodicalId":20268,"journal":{"name":"Platelets","volume":"36 1","pages":"2465321"},"PeriodicalIF":2.5,"publicationDate":"2025-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143414952","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":"Megakaryocyte phenotyping in response to SARS-CoV-2 variants.","authors":"Marcin A Sowa, Michael Tuen, Florencia Schlamp, Yuhe Xia, Marie I Samanovic, Mark J Mulligan, Tessa J Barrett","doi":"10.1080/09537104.2025.2532459","DOIUrl":"https://doi.org/10.1080/09537104.2025.2532459","url":null,"abstract":"<p><p>SARS-CoV-2 infection is associated with platelet hyperreactivity and increased rates of arterial and venous thrombosis. SARS-CoV-2 mutations have resulted in several variants with differences in transmissibility, infectivity, and patient outcomes. This study investigates the effects of the ancestral strain of SARS-CoV-2 (WA1) and two variants of concern, Delta and Omicron, on the human megakaryocyte (MK) phenotype and transcriptome. Human CD34⁺-derived MKs were incubated with WA1, Delta or Omicron SARS-CoV-2 variants for 24 hours. MK activation markers were measured under resting and thrombin-stimulated conditions. RNA-seq and cytokine release in response to the viruses were assessed. Plasma cytokines were measured in hospitalized COVID-19 patients. Treatment of MKs with WA1, Delta or Omicron variants of SARS-CoV-2 resulted in similar increases in classical activation markers. However, SARS-CoV-2 variants mediated distinct transcriptomic changes. Across variants, 60 genes overlapped, including <i>CXCL8</i>. Consistent with transcriptomic changes, SARS-CoV-2-incubated MKs secreted significantly elevated levels of IL-8. Among hospitalized COVID-19 patients, plasma IL-8 levels were highest in COVID-19 patients who subsequently experienced thrombotic events or died. In conclusion, WA1, Delta, and Omicron similarly induce classical MK activation responses while mediating distinct transcriptomic changes. Increased IL-8 levels may serve as a biomarker to inform platelet hyperreactivity and thrombotic events associated with COVID-19.</p>","PeriodicalId":20268,"journal":{"name":"Platelets","volume":"36 1","pages":"2532459"},"PeriodicalIF":2.5,"publicationDate":"2025-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144699344","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":"Immune-induced thrombocytopenia by pembrolizumab: case report and review of literature.","authors":"Nathan El-Ghazzi, Anna Monier, Antoine Italiano, Aude Besson, Eurydice Angeli","doi":"10.1080/09537104.2025.2487767","DOIUrl":"10.1080/09537104.2025.2487767","url":null,"abstract":"<p><p>Immune-checkpoint blockades (ICBs) are now used in early-stage diseases like triple-negative breast cancer (TNBC). While effective, they can cause severe toxicities. We report the first case of life-threatening immune thrombocytopenia (ITP) induced by pembrolizumab during neoadjuvant chemo-immunotherapy for early TNBC. A 42-year-old woman with early-stage TNBC developed grade 4 thrombocytopenia, diagnosed as ITP, after 107 days of pembrolizumab treatment. She required intensive care unit (ICU) admission and high-dose steroids, and intravenous immunoglobulin therapy, leading to a rapid recovery. ITP is a rare but potentially fatal complication of immunotherapy, with an incidence of less than 1% and a mortality rate of up to 20% in affected patients. Immediate recognition and steroid therapy are critical, as platelet transfusion is usually ineffective. Diagnosis is often delayed due to its similarity to chemotherapy-induced marrow toxicity. Immunotherapy-induced ITP generally contraindicates further use of the treatment. ITP, although uncommon, is a serious complication of immunotherapy requiring immediate intervention. The growing use of immunotherapy necessitates increased awareness of its potential toxicities among healthcare providers.</p>","PeriodicalId":20268,"journal":{"name":"Platelets","volume":"36 1","pages":"2487767"},"PeriodicalIF":2.5,"publicationDate":"2025-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143773088","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}