Seminars in hematology最新文献

Autologous gene therapy versus allogeneic transplantation for sickle cell disease and transfusion-dependent β-thalassemia: Choosing between 2 definitive therapies. 自体基因治疗与异体移植治疗镰状细胞病和输血依赖性β-地中海贫血：两种确定治疗方法的选择

IF 4.3 3区医学

Seminars in hematology Pub Date : 2026-09-22 DOI: 10.1053/j.seminhematol.2026.09.004

Urvi Kapoor, Monica Bhatia

{"title":"Autologous gene therapy versus allogeneic transplantation for sickle cell disease and transfusion-dependent β-thalassemia: Choosing between 2 definitive therapies.","authors":"Urvi Kapoor, Monica Bhatia","doi":"10.1053/j.seminhematol.2026.09.004","DOIUrl":"https://doi.org/10.1053/j.seminhematol.2026.09.004","url":null,"abstract":"<p><p>Autologous hematopoietic stem and progenitor cell (HSPC) gene therapy and allogeneic hematopoietic cell transplantation (allo-HCT) can both provide durable hematologic and clinical correction for sickle cell disease (SCD) and transfusion-dependent β-thalassemia (TDT). Allo-HCT has decades of follow-up and established rescue pathways, but outcomes depend on donor type, HLA matching, graft source, conditioning, and graft-versus-host disease (GVHD) prophylaxis. Gene therapy removes donor dependence, alloreactive graft rejection, and GVHD, but requires adequate HSPC collection, successful manufacturing and product release, myeloablative conditioning, and long-term genomic surveillance. In SCD, 29/30 efficacy-evaluable exagamglogene autotemcel recipients were free of severe vaso-occlusive crises for at least 12 consecutive months, and 28/32 efficacy-evaluable lovotibeglogene autotemcel recipients were free of vaso-occlusive events during months 6-18. In TDT, transfusion independence occurred in 32/35 efficacy-evaluable exagamglogene autotemcel recipients and 32/36 efficacy-evaluable betibeglogene autotemcel recipients. These percentages are conditional on reaching infusion and the prespecified assessment window. Among 1000 HLA-identical sibling HCT recipients with SCD, 5-year event-free survival was 91.4% and overall survival was 92.9%. In 823 prospectively studied patients with TDT, 2-year event-free survival was 97.2%, 92.9%, and 94.7% after matched-sibling, matched-unrelated, and haploidentical HCT. No randomized trial directly compares these platforms. Treatment selection should therefore compare the specific gene-therapy product with the available donor-graft-regimen option, accounting for disease urgency, organ reserve, conditioning exposure, time to treatment, fertility preservation, failure and rescue pathways, center-specific outcomes, and patient priorities.</p>","PeriodicalId":21684,"journal":{"name":"Seminars in hematology","volume":" ","pages":""},"PeriodicalIF":4.3,"publicationDate":"2026-09-22","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149224824","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}

引用次数: 0

Defects in ribosomes and translational control in lymphoid leukemia and lymphoma. 淋巴性白血病和淋巴瘤的核糖体缺陷和翻译控制。

IF 4.3 3区医学

Seminars in hematology Pub Date : 2026-09-16 DOI: 10.1053/j.seminhematol.2026.09.002

Marino Caruso, Naomy Pasau, Óscar Herranz, Kim De Keersmaecker

{"title":"Defects in ribosomes and translational control in lymphoid leukemia and lymphoma.","authors":"Marino Caruso, Naomy Pasau, Óscar Herranz, Kim De Keersmaecker","doi":"10.1053/j.seminhematol.2026.09.002","DOIUrl":"https://doi.org/10.1053/j.seminhematol.2026.09.002","url":null,"abstract":"<p><p>Translational control has emerged as a critical layer of gene expression reprogramming in cancer, with the ribosome functioning as a central regulatory node rather than a passive protein synthesis machinery. This review provides an integrated overview of how defects in ribosomes and translational regulation contribute to the pathogenesis of lymphoid leukemias and lymphomas. We focus on 3 major axes: mutations in ribosomal proteins, alterations in ribosomal RNA, and dysregulation of translation initiation mediated by the eukaryotic initiation factor 4F complex. Recurrent mutations in ribosomal proteins, such as RPL10 in T-cell acute lymphoblastic leukemia and RPS15 in chronic lymphocytic leukemia, alter ribosome function, leading to selective changes in mRNA translation, impaired translational fidelity, and increased oxidative stress that promotes genomic instability. In parallel, emerging evidence indicates that alterations in ribosomal RNA, including changes in ribosomal DNA copy number, biogenesis, and epigenetic modifications, contribute to ribosome heterogeneity and oncogenic transformation, although their precise roles in hematologic malignancies remain incompletely understood. Furthermore, aberrant activation of translation initiation pathways-often driven by the AKT/mTOR/MYC signaling axis-enhances both global protein synthesis and selective translation of oncogenic transcripts, reinforcing malignant phenotypes. Together, these ribosome-intrinsic and -extrinsic defects converge to reprogram the translatome, promote tumor progression, and create therapeutic vulnerabilities. Targeting translational control mechanisms therefore represents a promising strategy for the treatment of lymphoid malignancies.</p>","PeriodicalId":21684,"journal":{"name":"Seminars in hematology","volume":" ","pages":""},"PeriodicalIF":4.3,"publicationDate":"2026-09-16","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149184194","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}

引用次数: 0

Making space for cures: Conditioning for autologous hematopoietic stem cell gene therapies. 为治愈创造空间：自体造血干细胞基因治疗的条件。

IF 4.3 3区医学

Seminars in hematology Pub Date : 2026-09-09 DOI: 10.1053/j.seminhematol.2026.09.001

Zachary D Crees, John F DiPersio, Stephen P Persaud

{"title":"Making space for cures: Conditioning for autologous hematopoietic stem cell gene therapies.","authors":"Zachary D Crees, John F DiPersio, Stephen P Persaud","doi":"10.1053/j.seminhematol.2026.09.001","DOIUrl":"https://doi.org/10.1053/j.seminhematol.2026.09.001","url":null,"abstract":"<p><p>Although allogeneic hematopoietic stem cell transplantation has long been the only curative therapy for nonmalignant blood diseases, recent clinical successes have demonstrated the transformative potential of autologous gene therapies as definitive treatments for these disorders. By providing durable life-changing clinical benefit while reducing the need for suitable allogeneic donors and avoiding immunologic complications like graft rejection and graft-versus-host disease, autologous transplantation with genetically modified hematopoietic stem cells provides a potentially safer and, in some respects, more accessible pathway to cure. However, several formidable barriers still prevent broader use of autologous gene therapy, including the risk of adverse acute and chronic effects from the busulfan-based conditioning regimens used to deplete host hematopoietic stem cells before transplant. In this article, we define the role transplant conditioning regimens play in autologous gene therapy, including contrasting the goals of care in this setting with those for stem cell transplantation for malignancies. We also discuss the conditioning strategies that are used by approved and select investigational autologous gene therapies to date, while highlighting exciting preclinical and clinical advances aimed at making transplant conditioning safer for myriad nonmalignant and malignant disease applications.</p>","PeriodicalId":21684,"journal":{"name":"Seminars in hematology","volume":" ","pages":""},"PeriodicalIF":4.3,"publicationDate":"2026-09-09","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149148668","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}

引用次数: 0

The current state of cerebral complications of sickle cell disease. 镰状细胞病脑并发症的现状

IF 4.3 3区医学

Seminars in hematology Pub Date : 2026-08-09 DOI: 10.1053/j.seminhematol.2026.08.001

Danielle Cicka, Tanatuch Tiratrakoonseree, Melanie E Fields

{"title":"The current state of cerebral complications of sickle cell disease.","authors":"Danielle Cicka, Tanatuch Tiratrakoonseree, Melanie E Fields","doi":"10.1053/j.seminhematol.2026.08.001","DOIUrl":"https://doi.org/10.1053/j.seminhematol.2026.08.001","url":null,"abstract":"<p><p>Cerebral complications are among the most devastating manifestations of sickle cell disease (SCD), affecting children and adults with a spectrum that includes overt ischemic and hemorrhagic stroke, silent cerebral infarcts, vasculopathy, and long-term neurocognitive impairment. Advances in screening, primary and secondary stroke prevention, and acute stroke care have reduced risk for some patients, yet cerebrovascular injury remains common and likely underdiagnosed. The pathophysiology of cerebral injury in SCD is multifactorial, resulting from chronic hemolytic anemia, vaso-occlusion, large- and small-vessel vasculopathy, endothelial dysfunction, inflammation, and altered cerebral hemodynamics. Emerging data suggest stabilization or reduced incidence of new infarcts and preservation of neurocognitive function after successful hematopoietic cell transplantation (HCT), although some neurodevelopmental deficits may persist. This review synthesizes contemporary epidemiology, pathophysiology, diagnostic strategies, prevention and treatment, in the context of HCT. Key gaps for future research include optimizing screening strategies, quantifying neurocognitive benefit of curative therapy, and improving access to prevention in resource-limited settings.</p>","PeriodicalId":21684,"journal":{"name":"Seminars in hematology","volume":" ","pages":""},"PeriodicalIF":4.3,"publicationDate":"2026-08-09","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148888596","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}

引用次数: 0

Alloimmunization in sickle cell disease: Addressing an ongoing clinical challenge. 镰状细胞病的同种异体免疫：解决一个持续的临床挑战。

IF 4.3 3区医学

Seminars in hematology Pub Date : 2026-06-05 DOI: 10.1053/j.seminhematol.2026.06.002

Alistair Murray, Sean R Stowell

引用次数: 0

Clonal hematopoiesis in the setting of sickle cell disease and its relevance to curative therapies. 镰状细胞病的克隆造血及其与治疗的相关性

IF 4.3 3区医学

Seminars in hematology Pub Date : 2026-06-03 DOI: 10.1053/j.seminhematol.2026.05.008

Lachelle D Weeks

{"title":"Clonal hematopoiesis in the setting of sickle cell disease and its relevance to curative therapies.","authors":"Lachelle D Weeks","doi":"10.1053/j.seminhematol.2026.05.008","DOIUrl":"10.1053/j.seminhematol.2026.05.008","url":null,"abstract":"<p><p>Sickle cell disease (SCD) is an inherited hemoglobinopathy characterized by chronic hemolytic anemia, painful vaso-occlusive episodes, and end-organ damage. Population-level studies indicate individuals with SCD are at an increased risk for myeloid neoplasia (MN). While the absolute risk of MN remains low, fatal cases of myelodysplastic syndrome and acute myeloid leukemia suggest MN risk is enhanced in the setting of curative cellular therapies for SCD, including allogeneic hematopoietic cell transplantation and autologous gene therapy. Clonal hematopoiesis (CH), the expansion of a genetically related population of hematopoietic stem or progenitor cells, is commonly caused by mutations in myeloid leukemia driver genes and is a recognized precursor state for MNs, including myelodysplastic syndrome and acute myeloid leukemia. This review synthesizes current data on MN incidence in SCD populations, prevalence of adverse-risk CH in SCD, and clustering of high-risk subtypes of MN among cases involving SCD patients. CH emerges as a potential biological mechanism linking SCD to increased susceptibility to MN with implications for clinical research and counseling of patients with SCD.</p>","PeriodicalId":21684,"journal":{"name":"Seminars in hematology","volume":" ","pages":""},"PeriodicalIF":4.3,"publicationDate":"2026-06-03","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13418573/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148353430","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}

引用次数: 0

Ten years of clinical genetic therapies for sickle cell disease: Current and future directions. 镰状细胞病的十年临床基因治疗：当前和未来的方向。

IF 4.1 3区医学

Seminars in hematology Pub Date : 2026-04-17 DOI: 10.1053/j.seminhematol.2026.03.013

Alexis Leonard

{"title":"Ten years of clinical genetic therapies for sickle cell disease: Current and future directions.","authors":"Alexis Leonard","doi":"10.1053/j.seminhematol.2026.03.013","DOIUrl":"https://doi.org/10.1053/j.seminhematol.2026.03.013","url":null,"abstract":"<p><p>Gene therapy for sickle cell disease (SCD) has advanced rapidly over the past decade, beginning with the first clinical trial 10 years ago and culminating in FDA approval of ex vivo lentiviral and CRISPR-based therapies in 2023. Investment and scientific interest remain high, with both academia and industry actively pursuing next-generation strategies. The field is also shaped by complex economic realities, the discontinuation of otherwise promising programs, and the shifting role of academia as industry pivots toward in vivo platforms. Emerging in vivo gene therapies offer the potential to simplify delivery, reduce conditioning toxicity, and expand global accessibility, but remain preclinical or early-stage, leaving patients and clinicians to navigate difficult trade-offs between current ex vivo options and waiting on experimental in vivo therapies. Manufacturing, mobilization, and long-term durability continue to pose practical and clinical challenges, while real-world outcomes remain largely unmeasured outside clinical trials. This review synthesizes recent developments in ex vivo and in vivo gene therapy for SCD, highlighting the scientific, regulatory, and economic forces shaping the field. Ongoing challenges, future directions, and the critical importance of long-term follow-up and real-world registries are discussed. By providing a contemporary snapshot, the review contextualizes therapeutic progress, clarifies the trajectory of research, and illuminates how patients are affected by the rapid evolution of gene therapy for individuals with SCD.</p>","PeriodicalId":21684,"journal":{"name":"Seminars in hematology","volume":" ","pages":""},"PeriodicalIF":4.1,"publicationDate":"2026-04-17","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147942882","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}

引用次数: 0

Germline predisposition in myeloproliferative neoplasms 骨髓增生性肿瘤的种系易感性。

IF 4.3 3区医学

Seminars in hematology Pub Date : 2026-04-01 Epub Date: 2026-07-03 DOI: 10.1053/j.seminhematol.2026.06.006

Meytal Chernoff, Michael W. Drazer

{"title":"Germline predisposition in myeloproliferative neoplasms","authors":"Meytal Chernoff, Michael W. Drazer","doi":"10.1053/j.seminhematol.2026.06.006","DOIUrl":"10.1053/j.seminhematol.2026.06.006","url":null,"abstract":"<div><div>Myeloproliferative neoplasms (MPNs) were previously thought to result solely from somatic mutations; however, familial clustering and germline genetic testing have revealed hereditary MPNs. These hereditary MPNs are one type of hereditary hematopoietic malignancy (HHM) syndrome, or hereditary blood cancer, and generally display an autosomal-dominant inheritance pattern within families. Point estimates of the prevalence of hereditary MPNs vary with testing methodology and the patient population sampled, but diagnostic yields for pathogenic/likely pathogenic variants in patients with MPNs range from 8% to 27% across all seemingly sporadic MPN cases. We discuss the history and current state of emerging knowledge regarding the genetic basis of hereditary MPNs. We use the broader HHM framework as a lens to identify and manage patients at risk for, and those who have developed, an MPN. This review discusses the selection of rigorous diagnostic assays, the need for personalized stem cell transplant care, and the lack of “precision” therapies for hereditary MPNs. Finally, we appraise hereditary MPNs in the context of existing criteria for genetic testing and discuss evidence pertaining to the potential benefits of universal germline genetic testing for patients with MPNs more broadly.</div></div>","PeriodicalId":21684,"journal":{"name":"Seminars in hematology","volume":"63 2","pages":"Pages 71-80"},"PeriodicalIF":4.3,"publicationDate":"2026-04-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148607256","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}

引用次数: 0

Blood or marrow transplantation and cellular therapies in myeloproliferative neoplasms: A comprehensive review 骨髓增殖性肿瘤的血液或骨髓移植和细胞治疗：综合综述。

IF 4.3 3区医学

Seminars in hematology Pub Date : 2026-04-01 Epub Date: 2026-07-31 DOI: 10.1053/j.seminhematol.2026.07.003

Kanishka Uttam Chandani, Tania Jain

{"title":"Blood or marrow transplantation and cellular therapies in myeloproliferative neoplasms: A comprehensive review","authors":"Kanishka Uttam Chandani, Tania Jain","doi":"10.1053/j.seminhematol.2026.07.003","DOIUrl":"10.1053/j.seminhematol.2026.07.003","url":null,"abstract":"<div><div>Philadelphia-negative myeloproliferative neoplasms (Ph-negative MPNs) are clonal malignancies, with a complex interaction of the malignant clone, extramedullary haematopoiesis, and chronic inflammation. In high-risk disease, transformation to blast phase remains a constant risk and outcomes are usually dismal. Allogeneic blood or marrow transplantation (BMT) remains the only potentially curative treatment to date. In this narrative review, we summarize the evidence available to date on the role of BMT in MPNs and the ongoing investigations exploring the use of mutant CALR-targeted immune-based therapies, including engineered cellular therapeutics. BMT aims at the eradication of the malignant clone, although not without risks. To balance the risk vs benefit, BMT is usually considered in patients with higher risk features of disease. Historically, matched related or unrelated donors were preferred, but with the emergence of post-transplantation cyclophosphamide (PTCy), mismatched, family or unrelated, donors are increasingly used. Reduced-intensity conditioning regimens and peripheral blood graft sources are commonly employed but can vary by individual patient and institutional practice. Post-transplantation monitoring remains critical because engraftment is often delayed, contributing to nonrelapse mortality. Molecular evidence of disease post-transplantation increases the risk of relapse, but optimal timing of monitoring and interventions thereafter remain elusive. We also review the BMT landscape in MDS/MPN overlap neoplasms. Prevention and effective management of relapse remains an unmet need in both MPN and MDS/MPN. The role of cellular therapies in MPN is investigational. Progress in target identification in <em>CALR</em>-mutated MPN has resulted in the development of Fc-silent antibodies, T cell redirecting antibodies, and engineered cellular therapies which are advancing in clinical development.</div></div>","PeriodicalId":21684,"journal":{"name":"Seminars in hematology","volume":"63 2","pages":"Pages 136-144"},"PeriodicalIF":4.3,"publicationDate":"2026-04-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148832104","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}

引用次数: 0

The thrombopoietin receptor in myeloproliferative neoplasms: A unifying mechanism of disease pathogenesis and therapeutic targeting 骨髓增殖性肿瘤中的血小板生成素受体：疾病发病机制和治疗靶向的统一机制。

IF 4.3 3区医学

Seminars in hematology Pub Date : 2026-04-01 Epub Date: 2026-07-17 DOI: 10.1053/j.seminhematol.2026.07.001

Khaled Elhusseiny, Brandi N. Reeves

{"title":"The thrombopoietin receptor in myeloproliferative neoplasms: A unifying mechanism of disease pathogenesis and therapeutic targeting","authors":"Khaled Elhusseiny, Brandi N. Reeves","doi":"10.1053/j.seminhematol.2026.07.001","DOIUrl":"10.1053/j.seminhematol.2026.07.001","url":null,"abstract":"<div><div>The Philadelphia chromosome negative myeloproliferative neoplasms (MPNs), essential thrombocythemia, polycythemia vera, and primary myelofibrosis, are clonal hematopoietic stem cell disorders unified by constitutive thrombopoietin receptor (MPL) signaling. All 3 MPN driver mutations, JAK2, CALR, and MPL, converge on enhanced MPL signaling, establishing the thrombopoietin (TPO)/MPL axis as the central molecular hub linking clonal hematopoiesis to the cardinal manifestations of MPN, including thrombosis, hemorrhage, and fibrotic progression. As the principal regulator of hematopoietic stem cell maintenance and megakaryopoiesis and a key mediator of platelet priming, the TPO/MPL axis links stem cell biology to thromboinflammation and disease progression. This review summarizes the physiologic functions of the TPO/MPL axis, its dysregulation in MPN, and the downstream mechanisms linking aberrant MPL signaling to thrombosis, hemorrhage, and fibrotic progression. We further highlight recent advances in our understanding of TPO/MPL signaling in platelet biology, including its roles in platelet activation, metabolism, and thromboinflammation, and discuss emerging therapeutic strategies targeting the TPO/MPL pathway with the goal of simultaneously reducing thrombohemorrhagic complications, limiting fibrotic progression, and diminishing the malignant stem cell clone.</div></div>","PeriodicalId":21684,"journal":{"name":"Seminars in hematology","volume":"63 2","pages":"Pages 81-90"},"PeriodicalIF":4.3,"publicationDate":"2026-04-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148697852","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}

引用次数: 0