Experimental hematology最新文献

{"title":"Mechanistic insights into gene regulation driving normal and malignant hematopoietic development from embryonic and induced pluripotent stem cell differentiation.","authors":"Constanze Bonifer","doi":"10.1016/j.exphem.2026.105442","DOIUrl":"https://doi.org/10.1016/j.exphem.2026.105442","url":null,"abstract":"<p><p>The hematopoietic system originates from mesodermal cells of the vertebrate embryo giving rise to pluripotent hematopoietic stem cells (HSCs) from which all mature blood cell types originate for the entire lifespan of the organism. Due to the multitude of diseases of the blood system such as leukaemia and bone marrow failure it is of utmost importance to understand what regulates the initial formation of this system in the embryo and subsequent cell fate decisions occurring during the development of the different mature blood cell lineages. Research along these lines has been greatly facilitated by the development of embryonic and induced pluripotent stem (ESC and iPSC) cell-based methods. Such cells can be genetically altered and produce ample cell numbers thus being the ideal model to elucidate how our genome controls cell fate decisions. In this review, I will summarise our own work and that of others to highlight how ESC and iPSC based systems have been used to obtain global information enhancing our understanding of the genetic basis of hematopoiesis, how specific transcription factors interact with chromatin components to regulate differential gene expression and how signalling molecules and growth factors modulate this process. I will outline how such information can be used to optimise in vitro differentiation into specific cell types for regenerative medicine purposes. Last, but not least, I will describe how in vitro systems can inform about how blood cells development goes astray during disease processes. TEASER ABSTRACT: The hematopoietic system originates from mesodermal cells of the vertebrate embryo giving rise to pluripotent hematopoietic stem cells from which all mature blood cell types originate. Research into the molecular mechanisms regulating blood cell development is greatly facilitated by the development of embryonic and induced pluripotent stem (ESC and iPSC) cell-based methods. I will highlight how ESC and iPSC-based systems have been used to inform about the genetic basis of hematopoiesis, how transcription factors interact with chromatin to regulate differential gene expression, how signalling molecules modulate this process and how in vitro systems can be used to model disease.</p>","PeriodicalId":12202,"journal":{"name":"Experimental hematology","volume":" ","pages":"105442"},"PeriodicalIF":2.1,"publicationDate":"2026-04-29","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147812723","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"SiglecF-Expressing Neutrophils Differentiate from Mature Neutrophils Locally in the Heart after Myocardial Infarction.","authors":"Jonah K Stephan, Taylor Knerr, William S Isaacs, Yibing Nong, Marcin Wysoczynski","doi":"10.1016/j.exphem.2026.105429","DOIUrl":"https://doi.org/10.1016/j.exphem.2026.105429","url":null,"abstract":"<p><p>Myocardial infarction (MI) triggers an immune response marked by rapid infiltration of neutrophils. Though once considered a uniform population, neutrophils display remarkable heterogeneity post-MI, including a subset expressing SiglecF, a marker typically associated with eosinophils. In this study, we investigated the origin of SiglecF^Pos neutrophils following MI. We found that these cells appear early in the heart after MI, coinciding with the influx of CD101^Neg immature neutrophils. However, SiglecF^Pos neutrophils were absent in hematopoietic organs, suggesting their local differentiation. Interestingly, SiglecF^Pos neutrophils co-expressed CD101, indicating their maturity. Neutrophil stimulation in vitro with TGF-β and GM-CSF induced co-expression of SiglecF and CD101. When sorted CD101^Neg and CD101^Pos neutrophils were exposed to the same stimuli, only the mature (CD101^Pos) subset could acquire SiglecF expression, indicating maturation as a prerequisite for SiglecF induction. Using EdU labeling prior to MI to track neutrophil origins in vivo, we found that most SiglecF^Pos neutrophils in infarcted hearts were derived from mature circulating neutrophils existing prior to MI. SiglecF^Pos neutrophils emerge during heightened inflammation, which drives emergency granulopoiesis in the bone marrow. Neutrophils from mice treated with G-CSF to stimulate emergency granulopoiesis exhibited enhanced capacity for SiglecF expression. Neutrophils exposed to G-CSF in vitro exhibited enhanced SiglecF induction by TGF-β, indicating that G-CSF primes neutrophils for SiglecF expression in vivo and ex vivo. These findings support a model in which SiglecF^Pos neutrophils originate from mature CD101^Pos precursors following MI, and emergency granulopoiesis enhancing their capacity to acquire this phenotype and contributing to neutrophil heterogeneity in cardiac injury. Teaser Abstract: Myocardial infarction provokes neutrophil infiltration and the emergence of a SiglecF^Pos subset. Using in vivo EdU labeling and in vitro assays, we demonstrate that SiglecF is acquired by circulating mature neutrophils within the infarcted myocardium, rather than by local maturation of immature precursors. G-CSF and emergency granulopoiesis prime neutrophils with an enhanced capacity to upregulate SiglecF, highlighting a stress-induced program that reshapes neutrophil fate and function after cardiac injury.</p>","PeriodicalId":12202,"journal":{"name":"Experimental hematology","volume":" ","pages":"105429"},"PeriodicalIF":2.1,"publicationDate":"2026-04-20","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147766778","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Stem11 score: toward rapid clinical prognostication for acute myeloid leukemia.","authors":"Tomoya Isobe, Manja Meggendorfer, Sebastian Wolf, Thomas Oellerich, Nicola K Wilson, Berthold Göttgens","doi":"10.1016/j.exphem.2026.105441","DOIUrl":"10.1016/j.exphem.2026.105441","url":null,"abstract":"<p><p>Acute myeloid leukemia (AML) is an aggressive form of myeloid malignancy with high relapse and poor survival rates. Despite recent advances in genomics-based risk classification, accurate prediction of patient outcomes remains a challenge, posing the need for complementary molecular information to enable precise treatment stratification. In the current study, we assessed the prognostic value of the recently developed 11-gene Stem11 signature in a uniformly treated cohort of 107 patients with de novo AML and showed that Stem11 classification stratifies overall survival and response to allogeneic hematopoietic cell transplantation across the European LeukemiaNet risk groups. We further developed a NanoString-based Stem11 scoring platform and validated its high concordance with RNA-sequencing-based scoring and its retained prognostic power to identify the most refractory AML subgroup. With its rapid turnaround time and standardized built-in analysis pipeline, our NanoString-based Stem11 scoring panel represented a faster yet reliable alternative to RNA sequencing, providing preclinical proof of concept for Stem11-based clinical decision support. Acute myeloid leukemia (AML) is an aggressive hematological malignancy with a poor prognosis. Current genetic risk stratification remains insufficient for accurately predicting patient outcomes, and additional information that can refine and improve prospective risk prediction is urgently needed. Here, we developed a NanoString-based diagnostic assay measuring the prognostic Stem11 score. Our assay provided highly concordant Stem11 scores with RNA-sequencing-based quantification, thereby establishing a rapid and reliable transcriptional prognostication system for time-sensitive clinical decision support for AML.</p>","PeriodicalId":12202,"journal":{"name":"Experimental hematology","volume":" ","pages":"105441"},"PeriodicalIF":2.1,"publicationDate":"2026-04-17","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147722265","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"The rise of bone marrow organoids as next-generation models for blood formation and failure.","authors":"Anne Stolz, Lauren M Harmon, Jingjing Li, Jasmin Rettkowski, Alba Rodriguez-Meira, Kohei Shiroshita, Vu L Tran, Abdullah Khan, Christoph Klein","doi":"10.1016/j.exphem.2026.105428","DOIUrl":"10.1016/j.exphem.2026.105428","url":null,"abstract":"<p><p>Bone marrow organoids (BMOs) are three-dimensional (3D) cell culture models that recapitulate key structural and functional features of the bone marrow (BM) niche. BMOs offer important advantages in hematopoietic research by modeling key aspects of human hematopoiesis compared with classical in vitro 2D and 3D cellular models including bioreactors, BM-on-a-chip platforms, 2D models or BM ossicles by better recreating the 3D architecture, cellular heterogeneity, and spatial organization of the BM microenvironment. They offer a scalable and cost-effective alternative to animal models and reduce the need for animal experiments. Induced pluripotent stem cell (iPSC)-derived BMOs can be generated from a patient's own cells, enabling personalized disease modeling and drug testing and are highly amenable to gene editing technologies allowing precise modifications to study gene function or model diseases. Recent landmark studies from Christoph Klein and Abdullah Khan have established protocols for the generation of BMOs and demonstrated their applications in disease modeling. Here, we reviewed the critical steps in BMO generation, their structural/functional validation, and discussed how BMOs can be applied to model inflammatory responses, rare genetic bone marrow failure syndromes, and multiple myeloma. These advancements demonstrate BMOs' growing potential as powerful tools in hematopoietic research and will pave the way for further innovation and increasingly refined systems in future studies.</p>","PeriodicalId":12202,"journal":{"name":"Experimental hematology","volume":" ","pages":"105428"},"PeriodicalIF":2.1,"publicationDate":"2026-04-02","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147618598","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Evaluation of dual BCL-2/BCL-XL inhibition in acute myeloid leukemia preclinical models with and without prior venetoclax therapy","authors":"Reecha Shah ,&nbsp;Nathan Kingston ,&nbsp;Giulia Fabbri ,&nbsp;Jamal Saeh ,&nbsp;Courtney Andersen ,&nbsp;Patricia Cheung","doi":"10.1016/j.exphem.2026.105379","DOIUrl":"10.1016/j.exphem.2026.105379","url":null,"abstract":"<div><div>Acute myeloid leukemia (AML) is an aggressive hematologic malignancy that relies heavily on the antiapoptotic protein B-cell lymphoma 2 (BCL-2) for survival. Venetoclax, a BCL-2 inhibitor, exploits this dependency and is currently approved for treatment of elderly patients with AML. BCL-XL, another prosurvival protein in the BCL-2 family, has been identified as a key driver of both intrinsic and acquired resistance to venetoclax. Patients often develop resistance to BCL-2 inhibition through upregulation of BCL-XL. This study investigates the efficacy of a dual BCL-2/BCL-XL inhibitor and its combination with standard-of-care (SOC) agents. Dual BCL-2/BCL-XL inhibitor demonstrates robust activity in AML cell lines and patient-derived models, including activity in samples from patients who relapsed following venetoclax therapy. Its combination with SOC agents deepens the antileukemic activity both in vitro and in vivo. Among the combination regimens tested, cytarabine or hypomethylating agents (HMAs) drive strong blast reduction in patient samples previously exposed to venetoclax and yield improved survival in xenograft models derived from patients with AML who underwent prior venetoclax/5-azacytidine treatment. These preclinical findings support the clinical evaluation of dual BCL-2/BCL-XL inhibition in patients with AML, particularly, those who do not respond to venetoclax.</div></div>","PeriodicalId":12202,"journal":{"name":"Experimental hematology","volume":"156 ","pages":"Article 105379"},"PeriodicalIF":2.1,"publicationDate":"2026-04-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145984639","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Anti-IL-18 immunotherapy decreases inflammatory and vaso-occlusive responses in mice with sickle cell disease","authors":"Érica M.F. Gotardo ,&nbsp;Lidiane S. Torres ,&nbsp;Irmgard Förster ,&nbsp;Lucas F.S. Gushiken ,&nbsp;Pâmela L. Brito ,&nbsp;Flavia C. Leonardo ,&nbsp;Bruna Cunha Zaidan ,&nbsp;Andreas Bruederle ,&nbsp;Sergei Agoulnik ,&nbsp;Jiri Kovarik ,&nbsp;John Millholland ,&nbsp;Fernando F. Costa ,&nbsp;Nicola Conran","doi":"10.1016/j.exphem.2025.105366","DOIUrl":"10.1016/j.exphem.2025.105366","url":null,"abstract":"<div><div>Sickle cell disease (SCD) is characterized by inflammatory and vaso-occlusive processes that drive acute crises and progressive organ damage. Interleukin-18 (IL-18), elevated in patients with SCD and mouse models, contributes to these pathological mechanisms. We evaluated the effects of acute and prolonged IL-18 blockade using the SK113AE-4 monoclonal antibody in Townes and Berkeley SCD mice. Acute IL-18 neutralization reduced tumor necrosis factor-alpha (TNF-α)-induced microvascular leukocyte recruitment and prevented hypoperfusion, indicating that modulation of inflammatory signaling improves physiological responses in SCD. Prolonged anti-IL-18 immunotherapy for 6 weeks decreased circulating TNF-α and IL-10 and reduced hepatic macrophage infiltration, but did not prevent liver fibrosis, iron deposition, or alter biochemical markers of hemolysis or hepatic/renal injury. As such, IL-18 blockade attenuates vascular inflammation and vaso-occlusive-like events but may be insufficient to prevent SCD-related liver injury under the conditions tested. In contrast, in our previous study, anti-IL-1β immunotherapy provided added liver protection, highlighting potentially divergent cytokine pathways in SCD. Collectively, these results support IL-18 as a therapeutic target to reduce vascular inflammation and vaso-occlusive processes, and suggest that combined inflammasome cytokine-targeted or multiapproach strategies may be required to prevent organ damage in SCD.</div></div>","PeriodicalId":12202,"journal":{"name":"Experimental hematology","volume":"156 ","pages":"Article 105366"},"PeriodicalIF":2.1,"publicationDate":"2026-04-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145892358","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Gene therapy acceptance in a high-consanguinity sickle cell disease population: bridging genetic literacy to therapeutic innovation in Saudi Arabia","authors":"Khaled Essawi","doi":"10.1016/j.exphem.2026.105380","DOIUrl":"10.1016/j.exphem.2026.105380","url":null,"abstract":"<div><div>The Jazan region of Saudi Arabia has a high prevalence of sickle cell disease (SCD), compounded by consanguineous marriages. The Jazan region exemplifies a population that is markedly underrepresented in genomic medicine research, distinguished by distinctive sociocultural factors, including consanguinity rates surpassing one half. Although gene therapy (GT) offers a potential cure, its implementation requires an understanding of local awareness and acceptance. A cross-sectional online survey of 357 Jazan residents, including 104 individuals/families affected with SCD, assessed genetic literacy, clinical burden, and GT attitudes. Multivariate logistic regression identified predictors of GT awareness and acceptance. Despite high genetic literacy (84.0% knew SCD inheritance; 72.5% were aware of consanguinity risks), only 45.4% were aware of GT. Graduate education (odds ratio [OR], 3.54; 95% confidence interval [CI], 1.80–6.95) and personal SCD status (OR, 1.97; 95% CI, 1.15–3.37) independently predicted GT awareness. Among affected individuals, GT acceptance was independently predicted by awareness of consanguinity risk (OR, 3.51; 95% CI, 1.25–9.80) and personal SCD status (OR, 2.89; 95% CI, 1.08–7.74). This educated cohort exhibits a significant gap between genetic knowledge and GT awareness. Acceptance is strongly driven by an understanding of inheritance patterns, highlighting the need for genetic counseling that links consanguinity risks to therapeutic advances to facilitate equitable GT implementation.</div></div>","PeriodicalId":12202,"journal":{"name":"Experimental hematology","volume":"156 ","pages":"Article 105380"},"PeriodicalIF":2.1,"publicationDate":"2026-04-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"146043761","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Taking the direct route: menin inhibitors go straight to the frontline in KMT2A-rearranged acute leukemia","authors":"Anjum B. Khan ,&nbsp;Brian J.P. Huntly","doi":"10.1016/j.exphem.2026.105386","DOIUrl":"10.1016/j.exphem.2026.105386","url":null,"abstract":"<div><div>Menin inhibitors disrupt oncogenic transcription in KMT2A-rearranged leukemias, but responses are heterogeneous. A previous study highlighted the role of nongenetic resistance driven by altered chromatin context, including loss of KMT2C/D-UTX activity, underscoring the need for broader epigenetic profiling to guide therapy timing and combination strategy selection.</div></div>","PeriodicalId":12202,"journal":{"name":"Experimental hematology","volume":"156 ","pages":"Article 105386"},"PeriodicalIF":2.1,"publicationDate":"2026-04-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"146131683","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"A roadmap for systematic humanization of a chimeric antigen receptor: preclinical validation of a humanized CD22 scFv as a model.","authors":"Narcís Fernández, Paolo Petazzi, Vladimir Mulens-Arias, Laura García Pérez, Pablo Menéndez, Víctor M Díaz","doi":"10.1016/j.exphem.2026.105424","DOIUrl":"10.1016/j.exphem.2026.105424","url":null,"abstract":"<p><p>The humanization of chimeric antigen receptor (CAR) T-cell constructs is essential for reducing immunogenicity while preserving optimal antigen-binding affinity. However, this process poses significant challenges, as alterations within the single-chain variable fragments (scFvs) can adversely affect specificity, stability, and functional efficacy. In this study, we presented a structure-guided humanization strategy for the development of CD22-targeted CAR T cells to treat relapsed or refractory B-cell malignancies. Our approach involved rational grafting of murine complementarity-determining regions (CDRs) onto human antibody frameworks, followed by comprehensive in silico and biophysical evaluations to identify and mitigate potential liabilities, including aberrant glycosylation sites and structural instability. The resulting humanized CD22-CAR constructs retained antigen recognition, specificity, and cytotoxic potency comparable with their murine counterparts, as demonstrated in extensive in vitro and in vivo validation studies. Collectively, these findings established a robust, structure-informed humanization pipeline that supports the translation of next-generation CAR-T therapies with reduced immunogenicity and sustained therapeutic efficacy.</p>","PeriodicalId":12202,"journal":{"name":"Experimental hematology","volume":" ","pages":"105424"},"PeriodicalIF":2.1,"publicationDate":"2026-03-23","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147510676","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Inhibition of activated protein C anticoagulant function enhances coagulation but does not interrupt downstream mechanisms driving hemophilic arthropathy.","authors":"Clotilde Martin, Leonard A Valentino, Salomé Farny-Quentin, Alexandre Leuci, Yesim Dargaud","doi":"10.1016/j.exphem.2026.105421","DOIUrl":"10.1016/j.exphem.2026.105421","url":null,"abstract":"<p><p>Hemophilic arthropathy results from recurrent joint bleeding driven by impaired thrombin generation and a synovial environment favoring bleeding and chronic inflammation. Activated protein C (APC), abundant in hemophilic joints, may exacerbate cartilage degradation through enhanced matrix metalloproteinase activity. APC inhibition has emerged as a potential therapeutic strategy that may improve hemostasis and possibly protect joint tissues. The aim of the present work was to evaluate whether systemic inhibition of APC anticoagulant activity provides superior protection of cartilage compared with standard factor (F) VIII prophylaxis in a murine model of hemophilic arthropathy. FVIII-deficient mice underwent two induced knee hemarthroses. Animals received either extended-half-life FVIII, an APC-inhibitory peptide, or saline for three weeks. Plasma APC activity was measured using a chromogenic assay. Magnetic resonance imaging (MRI) scan assessed joint bleeding, and histopathology was evaluated using Valentino and standardized microscopic arthritis scoring of histologic sections (SMASH) scoring systems, with blinded analysis of synovitis, vascularity, and cartilage integrity. Both FVIII and APC inhibitor treatments reduced MRI scan-detected intra-articular bleeding compared with untreated controls. Histology confirmed synovial hypertrophy in all injured knees. Total Valentino and SMASH synovitis scores did not differ significantly between groups. Neither FVIII replacement nor APC inhibition resulted in measurable joint protection compared with untreated FVIII-deficient controls. Systemic inhibition of APC anticoagulant activity rebalanced coagulation but did not yield superior joint preservation. Differences from prior antibody-based APC inhibition studies likely reflect inhibitor design, dosing strategies, and the limited impact of systemic inhibition on synovial APC activity. Further work should explore targeted APC modulation within the joint microenvironment.</p>","PeriodicalId":12202,"journal":{"name":"Experimental hematology","volume":" ","pages":"105421"},"PeriodicalIF":2.1,"publicationDate":"2026-03-20","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147497920","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}