Platelets最新文献

{"title":"Platelet-leukocyte aggregate formation and inflammation in patients with pulmonary arterial hypertension and CTEPH.","authors":"Mikael Åberg,&nbsp;Erik Björklund,&nbsp;Gerhard Wikström,&nbsp;Christina Christersson","doi":"10.1080/09537104.2022.2087867","DOIUrl":"https://doi.org/10.1080/09537104.2022.2087867","url":null,"abstract":"<p><p>Pulmonary hypertension (PH) is defined by increased mean pulmonary artery pressure, and the clinical classification includes five etiologies, of which we investigated subgroup 1, pulmonary arterial hypertension (PAH) and subgroup 4, chronic thrombotic and/or embolic disease (CTEPH). Platelets participate in both innate and adaptive immune responses and could possibly contribute to the suggested systemic inflammation associated with PAH. In this study, we utilized flow cytometry to analyze platelet activation and platelet-monocyte (PMA) and granulocyte (PGA) aggregates in PAH and CTEPH patients and healthy control subjects. The plasma concentration of proinflammatory cytokines was measured by multiplex electrochemiluminescence. Our main finding is that circulating platelets are activated in the circulation and form aggregates with both monocytes and granulocytes in patients with idiopathic PAH (IPAH), associated PAH (APAH) and pulmonary hypertension due to CTEPH. There was a strong correlation between the platelet activation, assessed as P-selectin, and the number of aggregates formed. IL-6, IL-8, IL-10 and TNF-α were increased in all PH subgroups as compared to healthy controls, and PMAs were associated with circulating IL-6, IL-8 and IL-10, whereas PGAs were associated with IL-6. The increased concentrations of platelet-leukocyte aggregates found in PAH/CTEPH patients might thus contribute to the inflammatory state in PH.</p>","PeriodicalId":20268,"journal":{"name":"Platelets","volume":null,"pages":null},"PeriodicalIF":3.3,"publicationDate":"2022-11-17","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"10445194","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":"The utility of flow cytometric platelet forward scatter as an alternative to mean platelet volume.","authors":"David Connor,&nbsp;David Rabbolini,&nbsp;Marie-Christine Morel-Kopp,&nbsp;Kate Fixter,&nbsp;Dea Donikian,&nbsp;Mayuku Kondo,&nbsp;Onki Chan,&nbsp;Susan Jarvis,&nbsp;Walter Chen,&nbsp;Timothy Brighton,&nbsp;Vivien Chen,&nbsp;Christopher Ward,&nbsp;Joanne Joseph","doi":"10.1080/09537104.2022.2052035","DOIUrl":"https://doi.org/10.1080/09537104.2022.2052035","url":null,"abstract":"<p><p>The use of mean platelet diameter (MPD) to classify inherited thrombocytopenia (IT) has been demonstrated in several studies. Alternatively, the mean platelet volume (MPV) may be used, but in macrothrombocytopenia this may not be available. We hypothesized that platelet forward scatter (FSC) measurements using flow cytometry may be used for the size-based classification of IT. The study aimed to assess the ability of platelet FSC to measure platelet size and whether it could be used as an alternative to the MPD or MPV.Blood samples were obtained from individuals undergoing investigation for inherited platelet function disorders (IPFD, n = 40) or platelet number disorders (IPND, n = 46). A hematology analyzer was used to obtain MPV and platelet counts, flow cytometry to measure platelet FSC and ImageJ software to measure MPD from stained blood smears. The International Society of Thrombosis and Hemostasis (ISTH) Bleeding Assessment Tool (BAT) was used to calculate bleeding scores.Twenty-nine(63%) of IPND patients had an MPV that could not be reported. A significant correlation to platelet FSC was found to the MPD (p < .0001) and MPV (p < .0001) and an inverse correlation with platelet count (p < .0001). No significant correlation was found between FSC and bleeding history. In conclusion, platelet FSC is an alternative to MPV and may be used in macrothrombocytopenia where the MPV is not recorded.</p>","PeriodicalId":20268,"journal":{"name":"Platelets","volume":null,"pages":null},"PeriodicalIF":3.3,"publicationDate":"2022-11-17","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"40313853","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":"Platelet index on admission as a predictor of bacteremia in acute cholangitis: a 7-year retrospective observational study.","authors":"XiaoYing Chen,&nbsp;Fu Wei,&nbsp;Dan Zhang,&nbsp;Shijing Tian","doi":"10.1080/09537104.2022.2123466","DOIUrl":"https://doi.org/10.1080/09537104.2022.2123466","url":null,"abstract":"<p><p>Bacteremia frequently occurs in patients with acute cholangitis, which could increase the risk of mortality. This single-center retrospective observational study was conducted from July 2013 to July 2020 to evaluate the predictive value of platelet index for bacteremia at admission for acute cholecystitis. A total of 285 patients with acute cholangitis were divided into bacteremia group and non-bacteremia group. The incidence of bacteremia in acute cholangitis was 48.42%. The bacteremia group had more grade III patients, higher 30d mortality rate [17(12.32%) vs 8(5.44%), p = .040] and higher incidence of thrombocytopenia [76(55.07%) vs 35(23.81%), p < .001]. Platelet counts and plateletcrit were significantly lower in the bacteremia group [84.5(60, 180) vs 162(102,225) ×10⁹/L and 0.10(0.07, 0.21)% vs 0.18(0.12, 0.25) %, both p < .001]. ROC analysis indicated a high predictive value of platelet count and plateletcrit for bacteremia in patients with acute cholangitis and the area under the ROC curve (AUC) were 0.649 and 0.655, respectively. These results support the value of platelet count and plateletcrit in early prediction of bacteremia at admission for acute cholangitis.</p>","PeriodicalId":20268,"journal":{"name":"Platelets","volume":null,"pages":null},"PeriodicalIF":3.3,"publicationDate":"2022-11-17","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"40366469","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":"Evidence for a PI3-kinase independent pathway in the regulation of Rap1b activation downstream of the P2Y12 receptor in platelets.","authors":"Carol Dangelmaier, Satya P Kunapuli","doi":"10.1080/09537104.2022.2071855","DOIUrl":"10.1080/09537104.2022.2071855","url":null,"abstract":"<p><p>Platelet activation by adenosine diphosphate (ADP) is mediated through two G-protein-coupled receptors, P2Y1 and P2Y12, which signal through Gq and Gi, respectively. P2Y1 stimulation leads to phospholipase C activation and an increase in cytosolic calcium necessary for CalDAG-GEF1 activation. Engagement of P2Y12 inhibits adenylate cyclase, which reduces cAMP, and activation of PI3-kinase, which inhibits RASA3 resulting in sustained activated Rap1b. In this study we activated human platelets with 2-MeSADP in the presence of LY294002, a PI3-kinase inhibitor, AR-C69931MX, a P2Y12 antagonist or MRS2179, a P2Y1 antagonist. We measured the phosphorylation of Akt on Ser473 as an indicator of PI3-kinase activity. As previously shown, LY294002 and ARC69931MX abolished 2MeSADP-induced Akt phosphorylation. MRS2179 reduced ADP-induced Akt phosphorylation but did not abolish it. Rap1b activation, however, was only reduced, but not ablated, using LY294002 and was completely inhibited by ARC69931MX or MRS2179. Furthermore, 2MeSADP-induced Rap1b activation was abolished in either P2Y1 or P2Y12 null platelets. These data suggest that ADP-induced Rap1b activation requires both P2Y1 and P2Y12. In addition, although stimulation of P2Y12 results in PI3-kinase activation leading to Akt phosphorylation and Rap1b activation, Rap1b activation can occur independently of PI3-kinase downstream of P2Y12. Thus, we propose that the P2Y12 receptor can regulate Rap1b, possibly through RASA3, in a pathway independent of PI3-kinase.</p>","PeriodicalId":20268,"journal":{"name":"Platelets","volume":null,"pages":null},"PeriodicalIF":3.3,"publicationDate":"2022-11-17","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9547944/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"43075825","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":"Clopidogrel versus ticagrelor in East Asian patients aged 75 years or older with acute coronary syndrome: observations from the GF-APT registry.","authors":"Ziwei Xi,&nbsp;Zifeng Qiu,&nbsp;Jianan Li,&nbsp;Hong Qiu,&nbsp;Tingting Guo,&nbsp;Yong Wang,&nbsp;Jianfeng Zheng,&nbsp;Yanan Gao,&nbsp;Runlin Gao","doi":"10.1080/09537104.2022.2118250","DOIUrl":"https://doi.org/10.1080/09537104.2022.2118250","url":null,"abstract":"<p><p>The benefits of potent antithrombotic therapy usually come at the expense of a higher risk of bleeding. The efficacy and safety of ticagrelor in elderly East Asian populations remains debated due to the concerns about the imbalance of ischemic and bleeding risks. This study aimed to compare the impact of clopidogrel with ticagrelor on clinical outcomes in East Asian patients aged ≥75 years with acute coronary syndrome (ACS) using data from an institutional registry. We assessed the treatment effect of ticagrelor versus clopidogrel based on propensity scores and multivariate Cox proportional hazards models. A total of 2775 ACS patients were included, of which 235 (8.5%) were treated with ticagrelor. The primary efficacy outcome occurred in 11.9% of patients treated with ticagrelor versus 8.8% treated with clopidogrel. There was no significant association between treatment with ticagrelor and a lower risk of the primary efficacy outcome (p = .156). However, the incidences of all-cause death (hazard ratio [HR] 1.69, 95% confidence interval [CI] 1.02 to 2.79) and major bleeding (adjusted HR 2.20, 95% CI 1.06 to 4.56) were significantly higher in patients treated with ticagrelor than clopidogrel. In elderly patients with ACS from East Asia, the efficacy of clopidogrel was comparable to ticagrelor, while ticagrelor is associated with an increased risk of mortality and major bleeding.</p>","PeriodicalId":20268,"journal":{"name":"Platelets","volume":null,"pages":null},"PeriodicalIF":3.3,"publicationDate":"2022-11-17","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"40341501","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":"In vitro evaluation of platelet extracellular vesicles (PEVs) for corneal endothelial regeneration.","authors":"Rifa Widyaningrum,&nbsp;Yu-Wen Wu,&nbsp;Liling Delila,&nbsp;Deng-Yao Lee,&nbsp;Tsung-Jen Wang,&nbsp;Thierry Burnouf","doi":"10.1080/09537104.2022.2105829","DOIUrl":"https://doi.org/10.1080/09537104.2022.2105829","url":null,"abstract":"<p><p>Corneal endothelial cells (CECs) slowly decrease in number with increasing age, which is a clinical issue as these cells have very limited regenerative ability. Therapeutic platelet biomaterials are increasingly used in regenerative medicine and cell therapy because of their safety, cost-effective manufacture, and global availability from collected platelet concentrates (PCs). Platelet extracellular vesicles (PEVs) are a complex mixture of potent bioactive vesicles rich in molecules believed to be instrumental in tissue repair and regeneration. In this study we investigated the feasibility of using a PEVs preparation as an innovative regenerative biotherapy for corneal endothelial dysfunction. The PEVs were isolated from clinical-grade human PC supernatants by 20,000 × <i>g</i> ultracentrifugation and resuspension. PEVs exhibited a regular, fairly rounded shape, with an average size of <200 nm and were present at a concentration of approximately 10¹¹ /mL. PEVs expressed cluster of differentiation 41 (CD41) and CD61, characteristic platelets membrane markers, and CD9 and CD63. ELISA and LC-MS/MS proteomic analyses revealed that the PEVs contained mixtures of growth factors and multiple other trophic factors, as well as proteins related to extracellular exosomes with functional activities associated with cell cadherin and adherens pathways. CECs treated with PEVs showed increased viability, an enhanced wound-healing rate, stronger proliferation markers, and an improved adhesion rate. PEVs did not exert cellular toxicity as evidenced by the maintenance of cellular morphology and preservation of corneal endothelial proteins. These findings clearly support further investigations of PEV biomaterials in animal models for translation as a new CEC regeneration biotherapy.</p>","PeriodicalId":20268,"journal":{"name":"Platelets","volume":null,"pages":null},"PeriodicalIF":3.3,"publicationDate":"2022-11-17","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"40600453","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":"Romiplostim for PARP inhibitor-induced thrombocytopenia in solid tumor malignancies.","authors":"Abraham Z Cheloff,&nbsp;Hanny Al-Samkari","doi":"10.1080/09537104.2022.2117293","DOIUrl":"https://doi.org/10.1080/09537104.2022.2117293","url":null,"abstract":"TO THE EDITOR: PARP (poly-adenosine diphosphate-ribose polymerase) inhibitors are a series of drugs designed to inhibit DNA repair mechanisms, preventing DNA repair in cancer cells and inducing cell death [1]. Currently approved for the treatment of breast, ovarian, pancreatic, and prostate cancers [2], indications for PARP inhibitor therapy continue to expand. However, patients undergoing PARP inhibitor treatment may encounter multiple hematologic toxicities, including anemia, neutropenia, and thrombocytopenia [3,4]. Based on recent results describing success in the use of romiplostim to treat chemotherapy-induced thrombocytopenia (CIT) in patients receiving traditional myelosuppressive chemotherapy [5–8] we sought to understand whether a similar approach could be used for PARP inhibitor induced thrombocytopenia, for which there are little published data. A case series of 5 patients with PARP inhibitor-induced thrombocytopenia treated with avatrombopag suggests potential effectiveness of thrombopoietin receptor agonists in these patients; however, no data to date has been published evaluating romiplostim for PARP inhibitorinduced thrombocytopenia. Given that none of these agents are FDAapproved for CIT but that the majority of safety and efficacy data for use of TPO-RAs to treat CIT generally is for romiplostim (thereby resulting in its specific inclusion as a treatment option for CIT in recent NCCN guidelines) [9,10], we sought to examine romiplostim use in patients with PARP inhibitor-induced thrombocytopenia. This study was approved by the Institutional Review Board of Mass General Brigham (protocol #2015P000152). An electronic patient data registry at Mass General Brigham was used to identify patients who had received both romiplostim and a PARP inhibitor (niraparib, olaparib, rucaparib, or talazoparib) at any time. This resource was used specifically to identify the study population; patients identified by the query then underwent manual chart review by the authors to determine which patients met inclusion criteria (defined as a patient diagnosed with cancer, prescribed a PARP inhibitor, who developed thrombocytopenia requiring support and was treated with romiplostim). Clinical data regarding patients’ oncologic treatment course, platelet counts, and any adverse events were collected manually from charts by investigators and analyzed. The database query returned 32 patients who met initial criteria (had received romiplostim and a PARP inhibitor). Manual review of each chart found 5 patients who met inclusion criteria, all of whom were prescribed niraparib. Baseline characteristics and parameters for these patients can be found in Table I. Platelet counts for each patient were collected prior to niraparib prescription (baseline platelet count), prior to romiplostim initiation, and during romiplostim therapy (on-romiplostim counts defined as platelet counts drawn one week after each romiplostim administration until one week after the last do","PeriodicalId":20268,"journal":{"name":"Platelets","volume":null,"pages":null},"PeriodicalIF":3.3,"publicationDate":"2022-11-17","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"10690440","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":"Prevalence and natural history of variants in the <i>ANKRD26</i> gene: a short review and update of reported cases.","authors":"Hrushikesh Vyas,&nbsp;Ahmad Alcheikh,&nbsp;Gillian Lowe,&nbsp;William S Stevenson,&nbsp;Neil V Morgan,&nbsp;David J Rabbolini","doi":"10.1080/09537104.2022.2071853","DOIUrl":"https://doi.org/10.1080/09537104.2022.2071853","url":null,"abstract":"<p><p><i>ANKRD26</i> is a highly conserved gene located on chromosome 10p12.1 which has shown to play a role in normal megakaryocyte differentiation. <i>ANKRD26</i>-related thrombocytopenia, or thrombocytopenia 2, is an inherited thrombocytopenia with mild bleeding diathesis resulting from point mutations the 5'UTR of the <i>ANKRD26</i> gene. Point mutations in the 5'UTR region have been shown to prevent transcription factor-mediated downregulation of <i>ANKRD26</i> in normal megakaryocyte differentiation. Patients with <i>ANKRD26</i>-related thrombocytopenia have a predisposition to developing hematological malignancies, with acute myeloid leukemia and myelodysplastic syndrome most commonly described in the literature. We review the clinical features and biological mechanisms of <i>ANKRD26</i>-related thrombocytopenia and summarize known cases in the literature.</p>","PeriodicalId":20268,"journal":{"name":"Platelets","volume":null,"pages":null},"PeriodicalIF":3.3,"publicationDate":"2022-11-17","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9555274/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"9371148","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":"Apolipoprotein A-I, elevated in trauma patients, inhibits platelet activation and decreases clot strength.","authors":"Wilbert L Jones, Christopher R Ramos, Anirban Banerjee, Ernest E Moore, Kirk C Hansen, Julia R Coleman, Marguerite Kelher, Keith B Neeves, Christopher C Silliman, Jorge Di Paola, Brian Branchford","doi":"10.1080/09537104.2022.2078488","DOIUrl":"10.1080/09537104.2022.2078488","url":null,"abstract":"<p><p>Apolipoprotein A-I (ApoA-I) is elevated in the plasma of a subgroup of trauma patients with systemic hyperfibrinolysis. We hypothesize that apoA-I inhibits platelet activation and clot formation. The effects of apoA-I on human platelet activation and clot formation were assessed by whole blood thrombelastography (TEG), platelet aggregometry, P-selectin surface expression, microfluidic adhesion, and Akt phosphorylation. Mouse models of carotid artery thrombosis and pulmonary embolism were used to assess the effects of apoA-I <i>in vivo</i>. The ApoA-1 receptor was investigated with transgenic mice knockouts (KO) for the scavenger receptor class B member 1 (SR-BI). Compared to controls, exogenous human apoA-I inhibited arachidonic acid and collagen-mediated human and mouse platelet aggregation, decreased P-selectin surface expression and Akt activation, resulting in diminished clot strength and increased clot lysis by TEG. ApoA-I also decreased platelet aggregate size formed on a collagen surface under flow. <i>In vivo</i>, apoA-I delayed vessel occlusion in an arterial thrombosis model and conferred a survival advantage in a pulmonary embolism model. SR-BI KO mice significantly reduced apoA-I inhibition of platelet aggregation versus wild-type platelets. Exogenous human apoA-I inhibits platelet activation, decreases clot strength and stability, and protects mice from arterial and venous thrombosis via the SR-BI receptor.</p>","PeriodicalId":20268,"journal":{"name":"Platelets","volume":null,"pages":null},"PeriodicalIF":3.3,"publicationDate":"2022-11-17","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9547822/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"46109440","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":"Reply to \"Peripheral versus central venous blood sampling does not influence the assessment of platelet activation in cirrhosis\".","authors":"Sarah Shalaby,&nbsp;Alberto Zanetto,&nbsp;Elena Campello,&nbsp;Sabrina Gavasso,&nbsp;Giulio Barbiero,&nbsp;Michele Battistel,&nbsp;Paolo Feltracco,&nbsp;Debora Bizzaro,&nbsp;Patrizia Burra,&nbsp;Paolo Simioni,&nbsp;Marco Senzolo","doi":"10.1080/09537104.2022.2060499","DOIUrl":"https://doi.org/10.1080/09537104.2022.2060499","url":null,"abstract":"Gastroenterology/Multivisceral Transplant Unit, Department of Surgery, Oncology and Gastroenterology, Padua University Hospital, Padua, Italy; Health Care Provider of the European Reference Network on Rare Liver Disorders (ERN-Liver), Padua, Italy, General Internal Medicine, Hemorrhagic and Thrombotic Diseases Unit, Department of Medicine (DIMED), University of Padua Medical School, Padua, Italy, Institute of Radiology, Department of Medicine (DIMED), Padua University Hospital, Padua, Italy, and Section of Anesthesiology and Intensive Care, Department of Medicine (DIMED), Padua University Hospital, Padua, Italy","PeriodicalId":20268,"journal":{"name":"Platelets","volume":null,"pages":null},"PeriodicalIF":3.3,"publicationDate":"2022-10-03","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"10707267","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}