Blood advances最新文献

{"title":"Poor Outcomes with BCMA-targeting bispecific antibodies following early relapse from ide-cel: a real-world French study.","authors":"Sarah Cayla, Lionel Karlin, Jerome Lambert, Anne Lazareth, Alexis Talbot, Mohamad Mohty, Florent Malard, Marie-Odile Petillon, Salomon Manier, Ibrahim Yakoub-Agha, Denis Caillot, Ingrid Lafon, Xavier Leleu, Niels Moya, Bruno Royer, Jean Marc Schiano de Colella, Gabriel Brisou, Cyrille Touzeau, Aurore Perrot, Pierre Bories, Laure Vincent, Hanane Guedon, Olivier Decaux, Benoît Ferment, Roch Houot, Steven Le Gouill, Noemie Bigot, Thierry Facon, Jill Corre, Hervé Avet-Loiseau, Philippe Moreau, Bertrand Arnulf","doi":"10.1182/bloodadvances.2025017597","DOIUrl":"https://doi.org/10.1182/bloodadvances.2025017597","url":null,"abstract":"<p><p>Idecabtagene vicleucel (ide-cel), an adoptive chimeric antigen receptor (CAR) T-cell therapy directed against B-cell maturation antigen (BCMA), has demonstrated high response rates and improved survival in patients with relapsed/refractory multiple myeloma. However, all patients eventually relapse, and data on salvage therapy outcomes remain limited. We conducted a national, real-world study of 154 patients relapsing after ide-cel, with a median time to progression of 6.0 months (interquartile range [IQR], 3.0-9.9). Salvage therapies included anti-BCMA bispecific antibodies (BsAbs) (n=79), non-BCMA BsAbs targeting GPRC5D or FcRH5 (n=12), combinations of immunomodulatory agent, proteasome inhibitor, and anti-CD38 monoclonal antibody (n=40), and others (n=23). Median overall survival (OS) was 12.12 months [95%CI, 6.6 to not-reached], and median progression-free survival (PFS) was 3.48 months [95%CI, 2.6-6.37]. The overall response rate (ORR) (≥ partial response) was higher in patients treated with BsAbs (36%) than others (13%, p=0.002). Treatment with non-BCMA BsAbs resulted in significantly higher ORR (67% vs. 30%, p=0.018), OS (19.48 vs. 8.41 months, p=0.034) and PFS (9.2 vs. 3.81 months, p=0.035) compared to anti-BCMA BsAbs. Early relapse after ide-cel (≤6 months) was associated with worse outcomes (OS: 5.95 vs. 12.58 months, p=0.040), as was extramedullary disease (OS: 13.8 vs 6.28 months, p=0.033) and exposure to >3 prior lines of therapy. In summary, anti-BCMA BsAbs offered limited efficacy whereas non-BCMA BsAbs may offer a promising therapeutic approach following ide-cel early-relapse. These results underscore the potential benefits of diversifying targets in relapse post-ide-cel treatment strategies. ClinicalTrials.gov identifier NCT04328298.</p>","PeriodicalId":9228,"journal":{"name":"Blood advances","volume":" ","pages":""},"PeriodicalIF":7.1,"publicationDate":"2025-09-18","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145085141","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Risk Biomarkers of Chronic Graft-versus-host disease in Children aged 10 years or younger and Children/adults Older than 10 years.","authors":"Anna Crawford Ferreira, Debjani Dutta, Courtney M Rowan, Jamie Renbarger, Kenneth R Cooke, Paul A Carpenter, Robert A Krance, Christine N Duncan, Conrad Russell Y Cruz, David A Jacobsohn, Catherine M Bollard, Elizabeth Hill, Sophie Paczesny","doi":"10.1182/bloodadvances.2025016624","DOIUrl":"https://doi.org/10.1182/bloodadvances.2025016624","url":null,"abstract":"<p><p>Assessment of risk biomarkers of chronic GVHD (cGVHD) after allogeneic hematopoietic cell transplantation (HCT) in pediatric patients is lacking. We conducted a prospective study of 318 patients: (129 children ≤10 years and 189 children/adults >10 years). Six plasma biomarkers [CXCL9, interleukin-1 receptor-like 1 (IL1RL1), regenerating-islet-derived-3-alpha (REG3α), matrix metallopeptidase-3 (MMP3), dickkopf-WNT signaling pathway inhibitor-3 (DKK3), and sCD163] were assessed at Day (D)100 post-HCT. We performed D100 landmark analyses for cGVHD, stratifying at ≤10 years vs >10 yr and dichotomizing markers using Youden's index. IL1RL1 is associated with future cGVHD in both groups: ≤10 years [hazard ratio (HR) 95% confidence interval (CI): 2.35 (1.08, 5.12), p=0.03] and >10 years [HR (95% CI): 2.09 (1.22, 3.59), p=0.01], as is DKK3: ≤10 years [HR (95% CI): 2.39 (1.05, 5.42), p=0.04] and >10 years [HR (95% CI): 2.10 (1.20, 3.66), p=0.01]. CXCL9, REG3α, and MMP3 are associated with cGVHD in patients >10 years [HR (95% CI): CXCL9: 2.37 (1.08, 5.21), p=0.03; REG3α: 1.71 (1.03, 2.82), p=0.04; MMP3: 2.36 (1.33, 4.16), p=0.003]. This 5-marker panel has an AUC of 0.71 in children ≤10 years and 0.72 in children/adults >10 years for cGVHD risk, and 0.86 in children ≤10 years and 0.80 in children/adults >10 years for moderate/severe cGVHD risk. A 5-biomarker panel (IL1RL1, REG3α, MMP3, DKK3, and sCD163) was associated with TRM in both groups. Biomarkers measured 3 months post-HCT predict susceptibility and/or are prognostic for cGVHD and TRM in both children aged ≤10 years and children/adults >10 years, allowing for additional risk stratification.</p>","PeriodicalId":9228,"journal":{"name":"Blood advances","volume":" ","pages":""},"PeriodicalIF":7.1,"publicationDate":"2025-09-18","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145084614","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Artificial Intelligence Accelerates the Interpretation of Measurable Residual B Lymphoblastic Leukemia by Flow Cytometry.","authors":"Jansen N Seheult, Gregory E Otteson, Michael M Timm, Matthew J Weybright, Min Shi, Horatiu Olteanu, Dragan Jevremovic, Chuan Chen, April Chiu, Pedro Horna","doi":"10.1182/bloodadvances.2025016126","DOIUrl":"https://doi.org/10.1182/bloodadvances.2025016126","url":null,"abstract":"<p><p>Measurable residual disease (MRD) assessment by flow cytometry (FC) plays an essential role in prognosis and therapy escalation of B-cell acute lymphoblastic leukemia (B-ALL). However, the high degree of expertise and manual analysis time required limits the availability of this assay. To overcome this limitation, we developed a data-enhancing artificial intelligence (AI) pipeline that accelerates and simplifies MRD analysis. Unaltered FC files from 171 B-ALL MRD-positive and 89 MRD-negative cases were processed through an AI pipeline trained with 31 expert-gated negative controls. Cluster-informed downsampling reduced FC files from 1.2 million to 155,884 cells per case, on average (87% cellularity reduction), while preserving small MRD populations (median 100% retention for MRD <1%) and allowing for true %MRD estimates using a correction factor. A deep neural network (DNN) cell classifier automatically identified normal hematopoietic subsets (macro-averaged F1 score = 0.86); and an AI measure of anomaly discriminated B-ALL from benign mononuclear (area under the curve, AUC = 0.98) or B-lymphoid cells (AUC = 0.94). Manual analysis of AI-enhanced files was completed in only 1.01 minutes per case, on average (SD = 0.57); with 100% positive agreement with conventional analysis (for MRD ≥ 0.01%), 100% negative agreement, and excellent quantitative correlation (R2 = 0.92). Our cloud-based AI-enhancement solution accelerates B-ALL MRD identification without compromising test performance, and has the potential of facilitating BALL-MRD analysis by more clinical laboratories.</p>","PeriodicalId":9228,"journal":{"name":"Blood advances","volume":" ","pages":""},"PeriodicalIF":7.1,"publicationDate":"2025-09-18","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145085133","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"mTOR activity and metabolic reprogramming of CD8+ T cells is impaired under hypoxia and within the multiple myeloma bone marrow.","authors":"Taylor Fulton-Ward, Nancy Gudgeon, Isaac Thirlwell, Emma Louise Bishop, Bryan Marzullo, Hannah Victoria Giles, Graham McIlroy, Paul Ferguson, Bhuvan Kishore, Kate Rogers, Nuri Nuri Alfasi, Timothy Wong, Satnam Aytain, Daniel A Tennant, Guy Pratt, Sarah Dimeloe","doi":"10.1182/bloodadvances.2025016439","DOIUrl":"https://doi.org/10.1182/bloodadvances.2025016439","url":null,"abstract":"<p><p>Novel therapies for multiple myeloma aim to engage anti-tumour functions of T cells. However, evidence indicates these functions are limited within the bone marrow environment. This is relatively hypoxic in health and studies indicate widespread hypoxia in multiple myeloma. In this study, CD8+ T cell responses to stimulation were assessed under hypoxia, which identified that activation, proliferation and interferon-gamma (IFN-γ) secretion were profoundly suppressed, whilst cytotoxicity and tumour necrosis factor-alpha (TNF-α) expression were unaffected. These changes occurred alongside decreased mTOR activity and expression of c-Myc, which drives T cell metabolic reprogramming upon stimulation. Consistently, hypoxic CD8+ T cells demonstrated decreased activation-induced glycolysis and mitochondrial glutamine oxidation. Mechanistically, this was linked to elevated BNIP3 expression under hypoxia and reciprocally decreased abundance of its interaction partner, Rheb, an important mTOR activator. Assessment of BCMAxCD3 bispecific antibody activity confirmed impaired capacity to elicit CD8+ T cell activation, IFN-γ expression, proliferation and altered memory differentiation under hypoxia, although initial target cell killing was unaffected. Finally, assessment of bone marrow CD8+ T cells from multiple myeloma patients identified decreased proliferation, c-Myc and Rheb expression compared to peripheral blood cells, alongside elevated BNIP3, confirming mechanistic features of hypoxic exposure in this environment. Taken together, the findings indicate potential for bone marrow hypoxia to influence efficacy of T cell-directed therapies for multiple myeloma.</p>","PeriodicalId":9228,"journal":{"name":"Blood advances","volume":" ","pages":""},"PeriodicalIF":7.1,"publicationDate":"2025-09-12","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145051783","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Overall survival, conditioning, and MRD in MORPHO.","authors":"Gege Gui, Christopher S Hourigan","doi":"10.1182/bloodadvances.2025017937","DOIUrl":"https://doi.org/10.1182/bloodadvances.2025017937","url":null,"abstract":"","PeriodicalId":9228,"journal":{"name":"Blood advances","volume":" ","pages":""},"PeriodicalIF":7.1,"publicationDate":"2025-09-12","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145051866","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Abatacept Improves Post-Transplant Survival and Reduces Endothelial Injury Syndromes in Beta-Thalassemia major.","authors":"Pooja Khandelwal, Azada Ibrahimova, Adam Lane, Michael Grimley, Stella M Davies, Sonata Jodele","doi":"10.1182/bloodadvances.2025017197","DOIUrl":"https://doi.org/10.1182/bloodadvances.2025017197","url":null,"abstract":"<p><p>Iron overload in transfusion-dependent beta thalassemia (TDT) generates reactive oxygen species, predisposing to post hematopoietic stem cell transplant (HSCT) endothelial activation. Abatacept prevents acute graft versus host disease (GVHD) by inhibiting CD80/CD86 on T-cells, but CD80 is also expressed on neutrophils. Elevated neutrophil extracellular traps (NETs) at day+14 are associated with thrombotic microangiopathy (TMA) after HSCT, mechanistically linking endothelial activation to complement activation. We wanted to compare post HSCT survival and incidence of endothelial injury syndromes in children with TDT with and without addition of abatacept to standard acuteGVHDprophylaxis. We performed a retrospective review of children with TDT who underwent HSCT at our center. All received intravenous busulfan, fludarabine and thiotepa for conditioning and calcineurin inhibitor-based acute GVHD prophylaxis. Patients without abatacept served as controls. Abatacept was administered intravenously at 10 mg/kg on days -1, +5, +14 and +28 after HSCT. Sixty-four children underwent HSCT for TDT. Fifty received abatacept while 14 did not. No differences were observed between rates of neutrophil or platelet engraftment, rates of bacteremia or viral reactivation. Acute grade II-IV GVHD was lower in the abatacept cohort (0%) compared to no abatacept cohort (35%) p=0.0003. Incidence of any endothelial injury syndromes (TA-TMA, SOS, PRES, DAH) was lower in the abatacept cohort (16%) compared to no abatacept (64%) p=0.0009. Day+14 dsDNA( surrogate of NETs) and sC5b-9 values were lower in the abatacept cohort compared to no abatacept cohort (p=0.04 and p<0.001 respectively). All patients in the abatacept cohort had full donor myeloid chimerism and remained transfusion-independent at a median last follow up of 1915 days (range 266-3464 days) post HSCT. Thalassemia-free survival was 100% in the abatacept cohort and 71% in the no abatacept cohort. Addition of abatacept to calcineurin inhibitor based acute GVHD prophylaxis resulted in excellent thalassemia-free survival and lower endothelial injury syndromes.</p>","PeriodicalId":9228,"journal":{"name":"Blood advances","volume":" ","pages":""},"PeriodicalIF":7.1,"publicationDate":"2025-09-12","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145051868","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Induction of Moderate DNA Damage Enhances Megakaryopoiesis and Platelet Production.","authors":"Virginia Camacho, Roelof Bekendam, Andrew P Stone, Maria N Barrachina, Siobhan Branfield, Estelle Carminita, Isabelle C Becker, Dong H Lee, Ethan Walsey, Clementine Payne, Jakub Piotr Kaplan, Julia Tilburg, Sharmistha Pal, Luis Francisco Zirnberger Batista, Joseph E Italiano, Kellie R Machlus","doi":"10.1182/bloodadvances.2025017375","DOIUrl":"10.1182/bloodadvances.2025017375","url":null,"abstract":"<p><p>Megakaryocytes (MKs) are large, hematopoietic cells with a polyploid, multi-lobulated nucleus. While DNA replication in MKs (endomitosis) is well studied, limited investigations have examined the impact of DNA instability on megakaryopoiesis. Poly-ADP ribose polymerase (PARP) inhibitors are chemotherapeutics that result in accumulation of DNA damage and are commonly associated with thrombocytopenia, presumably mediated through platelet progenitors, MKs. To explore PARP inhibitor-induced thrombocytopenia, we treated mice with the PARP inhibitor Niraparib. While high dose Niraparib treatment led to thrombocytopenia, consistent with clinical observations, lower dosage treatment led to a significant increase in bone marrow MKs, MK progenitors, and circulating platelets. This increase was accompanied by elevated DNA damage in both MKs and MK progenitors, as measured by gH2AX accumulation and comet assays. Notably, platelets from Niraparib-treated mice were functionally normal in their response to ADP, TRAP, and collagen. Treatment of mice with low-dose gamma-irradiation similarly led to DNA damage in MKs and resulted in increased MK and platelet counts, suggesting that moderate DNA damage is a common mechanism that enhances megakaryopoiesis and platelet counts. These data reveal a previously unknown relationship between MKs and DNA damage and present a novel target for triggering enhanced platelet production in vivo.</p>","PeriodicalId":9228,"journal":{"name":"Blood advances","volume":" ","pages":""},"PeriodicalIF":7.1,"publicationDate":"2025-09-12","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145051839","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Developing an AI-Generated Peptide Targeting Platelet-type von Willebrand Disease.","authors":"Thomas David Daniel Kazmirchuk, Jiashu Wang, Loredana Bury, Emanuela Falcinelli, Calvin Bradbury-Jost, Anastasiia Koziar, Mustafa Al-Gafari, Sarah Takallou, William G Willmore, Frank Dehne, Paolo Gresele, Maha Othman, Ashkan Golshani","doi":"10.1182/bloodadvances.2025017674","DOIUrl":"https://doi.org/10.1182/bloodadvances.2025017674","url":null,"abstract":"<p><p>Platelet-type von Willebrand disease (PT-VWD) is a rare bleeding disorder caused by gain-of-function mutations in platelet glycoprotein Ib alpha (GPIbα). These mutations lead to a hyperactive protein-protein interaction (PPI) with von Willebrand factor (VWF) and pathological platelet aggregation. Counterintuitively, PT-VWD patients suffer from bleeding diathesis as opposed to thrombosis. Despite well-defined genetic etiology, no targeted therapy yet exists for PT-VWD. Here, we sought to develop a peptide inhibitor that selectively targets the aberrant interaction in PT-VWD. Using the In-Silico Protein Synthesizer, we designed and screened 10,000 peptides for predicted affinity and specificity towards GPIbαMet239Val. Functional validation of top-ranked peptides included a combination of in-vitro functional assays using GPIbαGly233Val, Met239Val and ex-vivo PT-VWD patient platelet assays. One peptide, G14, emerged as a potent and selective inhibitor of the GPIbαGly233Val, Met239Val-VWF PPI. Functional assays demonstrated that G14 disrupts this interaction without binding GPIbαWT or VWF alone. The peptide also displays picomolar affinity (6.6 pM) for GPIbαGly233Val, Met239Val. Structural modeling predicted G14 binds the β-switch region of GPIbαGly233Val, Met239Val involving the disease-associated Val239 residue. In PT-VWD patient-derived platelet-rich plasma, G14 selectively inhibited VWF binding and ristocetin-induced agglutination with no measurable effect on healthy samples. The G14 peptide appears to be a highly specific inhibitor of the GPIbαGly233Val, Met239Val-VWF interaction, providing proof-of-concept data for therapeutic development in PT-VWD. Further, the protein and platelet specificity these data suggest that G14 may be a potential diagnostic tool for PT-VWD. The approach highlights the utility of artificial intelligence in targeting disease-specific PPIs with high precision.</p>","PeriodicalId":9228,"journal":{"name":"Blood advances","volume":" ","pages":""},"PeriodicalIF":7.1,"publicationDate":"2025-09-12","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145051819","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Debunking Myths: Sickle Cell Trait, Crises & Sudden Death.","authors":"Michael R DeBaun, Corey J Hebert, Yvette Marie Miller","doi":"10.1182/bloodadvances.2025016736","DOIUrl":"https://doi.org/10.1182/bloodadvances.2025016736","url":null,"abstract":"","PeriodicalId":9228,"journal":{"name":"Blood advances","volume":" ","pages":""},"PeriodicalIF":7.1,"publicationDate":"2025-09-10","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145190954","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Patterns of progression among 427 patients with smoldering myeloma diagnosed after 2014: importance of monitoring.","authors":"Efstathios Kastritis, Irene Solia, Panagiotis Malandrakis, Foteini Theodorakakou, Ioannis Ntanasis-Stathopoulos, Nikolaos Kanellias, Despina Fotiou, Magdalini Migkou, Evangelos Eleutherakis-Papaiakovou, Vassiliki Spiliopoulou, Nikoleta Kokkali, Asimina Papanikolaou, Stavroula Giannouli, Maria Gavriatopoulou, Evangelos Terpos, Meletios A Dimopoulos","doi":"10.1182/bloodadvances.2025016083","DOIUrl":"10.1182/bloodadvances.2025016083","url":null,"abstract":"","PeriodicalId":9228,"journal":{"name":"Blood advances","volume":" ","pages":"4444-4447"},"PeriodicalIF":7.1,"publicationDate":"2025-09-09","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12410520/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143751273","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}