Experimental cell research最新文献

{"title":"Novel Approaches to 3D Cancer Heterospheroid Culture and Assay Development for Immunotherapy Screening.","authors":"Natasha Helleberg Madsen, Boye Schnack Nielsen, Isabella Skandorff, Carlos Rodriguez-Pardo, Sine Reker Hadrup, Maria Ormhøj, Kim Holmstrøm, Jesper Larsen, Monika Gad","doi":"10.1016/j.yexcr.2025.114604","DOIUrl":"https://doi.org/10.1016/j.yexcr.2025.114604","url":null,"abstract":"<p><p>Advanced 3D heterospheroids, composed of cancer, fibroblast, and immune cells, serve as more physiologically relevant models for anticancer drug screening and immunotherapy research compared to traditional 2D cultures. This study aimed to optimize the culturing, dissociation, and analysis of heterospheroids, addressing limitations that restrict their broader use in immunotherapy research. Our study revealed significant effects of Human Plasma-Like culture medium on cell viability, necrotic core formation, and the spatial organization of cancer and fibroblast cells within heterospheroids compared to DMEM and RPMI media. In HT-29 heterospheroids, cell viability decreased from 75% in DMEM to 20% in HPLM, which was accompanied by increased necrotic core formation and elevated PD-L1 expression. TrypLE™ effectively dissociated heterospheroids but compromised immune cell viability and surface marker detection. In comparison, Accutase™ significantly reduced cell yield, while collagenase I preserved immune cell markers but affected those on cancer cells. Furthermore, we developed a luciferase-based assay to measure immune-mediated cancer cell killing in heterospheroids, excluding signals from non-target cells, such as dying fibroblasts and immune cells, without requiring spheroid lysis or dissociation. Our findings highlight the importance of tailoring experimental conditions to reflect specific tumor characteristics, thus enhancing the utility of heterospheroids in drug discovery and immunotherapy research.</p>","PeriodicalId":12227,"journal":{"name":"Experimental cell research","volume":" ","pages":"114604"},"PeriodicalIF":3.3,"publicationDate":"2025-05-14","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144086057","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Testicular aging: mechanism, management and future therapy.","authors":"Jing Zhou, Qiang Dong","doi":"10.1016/j.yexcr.2025.114603","DOIUrl":"https://doi.org/10.1016/j.yexcr.2025.114603","url":null,"abstract":"<p><p>Testicular aging results in degeneration in testicular function, including decreased testosterone production and quality of sperm. Decreased testosterone level is associated with a range of systemic diseases and comorbidities, including cardiovascular disease, cognitive decline, depression, osteoporosis, frailty, increased body fat, and metabolic syndrome. In addition, with the rapid development of industrialization and increasing environmental pollution, the quality of male semen continues to decline globally. Currently, the average age of first marriage and childbirth for men is delayed, and the birth rate has been declining year by year. At present, the therapies for testosterone level decline in clinical practice are relatively limited. Therefore, studying the triggering and delaying mechanisms of testicular aging is significant for improving male health and protecting male fertility. This review summarizes the mechanisms and treatment strategies for male reproductive aging.</p>","PeriodicalId":12227,"journal":{"name":"Experimental cell research","volume":" ","pages":"114603"},"PeriodicalIF":3.3,"publicationDate":"2025-05-13","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144076920","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Corrigendum to \"ANGPTL8/betatrophin alleviates insulin resistance via the Akt-GSK3βor Akt-FoxO1 pathway in HepG2 cells\" [Exp. Cell Res., 2016 Jul 15;345(2):158-67.doi: 10.1016/j.yexcr.2015.09.012. Epub 2015 Sep 24].","authors":"Xing Rong Guo, Xiao Li Wang, Yun Chen, Ya Hong Yuan, Yong Mei Chen, Yan Ding, Juan Fang, Liu Jiao Bian, Dong Sheng Li","doi":"10.1016/j.yexcr.2025.114601","DOIUrl":"https://doi.org/10.1016/j.yexcr.2025.114601","url":null,"abstract":"","PeriodicalId":12227,"journal":{"name":"Experimental cell research","volume":" ","pages":"114601"},"PeriodicalIF":3.3,"publicationDate":"2025-05-13","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144076906","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"URB597 downregulates DJ-1 expression in the mouse striatum and induces neurodegeneration","authors":"Haoran Wu ,&nbsp;Jiarui Zhang ,&nbsp;Fei Song ,&nbsp;Xuejin Zhang ,&nbsp;Dong Sun ,&nbsp;Hui Wu ,&nbsp;Li Zhao ,&nbsp;Hang Cai ,&nbsp;Tuoxian Tang ,&nbsp;Zhenjiang Liu","doi":"10.1016/j.yexcr.2025.114602","DOIUrl":"10.1016/j.yexcr.2025.114602","url":null,"abstract":"<div><div>DJ-1 is a multifunctional protein involved in diverse cellular processes, including defense against oxidative stress, regulation of gene transcription, and maintenance of mitochondrial function. Mutations in the <em>DJ-1</em> gene are closely associated with early-onset Parkinson's disease, and loss of DJ-1 function increases the susceptibility of dopaminergic neurons to oxidative damage, potentially driving neurodegeneration. Therefore, DJ-1 represents an attractive therapeutic target for PD. In this study, we screened a library of blood-brain barrier-permeable small molecules to identify compounds that modulate DJ-1 expression in the mouse brain. Through molecular docking, we discovered that URB597, a selective fatty acid amide hydrolase inhibitor, binds to DJ-1 and forms a stable complex. URB597 treatment markedly reduced DJ-1 protein levels in SH-SY5Y cells, leading to decreased cell survival and impaired mitochondrial function under oxidative stress conditions. In addition, URB597-treated mice exhibited motor deficits and dopaminergic neuron loss, indicating that suppressing DJ-1 expression may adversely affect neuronal function. Gene expression and pathway enrichment analyses revealed that URB597 targets DJ-1 in the mouse striatum and regulates the expression of genes involved in protein acetylation. Collectively, these findings underscore the critical role of DJ-1 in protecting dopaminergic neurons from oxidative damage and uncover its potential implications in regulating protein acetylation.</div></div>","PeriodicalId":12227,"journal":{"name":"Experimental cell research","volume":"449 2","pages":"Article 114602"},"PeriodicalIF":3.3,"publicationDate":"2025-05-13","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144067941","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"GLUT1 maintains esophageal cancer stem cell-like characteristics by inhibiting autophagy-dependent ferroptosis via EGFR","authors":"Xin Sui ,&nbsp;Haining Zhou ,&nbsp;Tingting Wang","doi":"10.1016/j.yexcr.2025.114600","DOIUrl":"10.1016/j.yexcr.2025.114600","url":null,"abstract":"<div><div>Esophageal cancer, a highly malignant tumor with poor prognosis, is characterized by the presence of cancer stem cells (CSCs) that drive tumor initiation, metastasis, and recurrence. This study investigates the molecular mechanism by which glucose transporter 1 (GLUT1) maintains esophageal CSC-like properties through regulation of autophagy-dependent ferroptosis via epidermal growth factor receptor (EGFR). Using shRNA to knock down GLUT1 or EGFR and constructing a GLUT1 overexpression vector in KYSE520 cells, we employed western blotting, qRT-PCR, flow cytometry, sphere formation, Transwell assays, and xenograft models to assess stemness markers (NANOG, OCT4, SOX2), autophagic flux (LC3B, P62, Beclin1), and ferroptosis-related parameters (ROS, Fe²⁺, GSH, GPX4, COX2). Mechanistic analyses included co-immunoprecipitation to validate the GLUT1-EGFR interaction, chloroquine to inhibit autophagy, and cycloheximide/MG132 to evaluate EGFR protein stability. Results showed that GLUT1 depletion reduced CSC marker expression, increased ROS and Fe²⁺ levels, depleted GSH, and induced lipid peroxidation, sensitizing cells to ferroptosis while activating autophagy (elevated LC3 II/I, Beclin1; reduced P62); autophagy inhibition exacerbated cell death, indicating a protective role for autophagy in this context. GLUT1 directly bound to EGFR, stabilizing the receptor by blocking ubiquitin-proteasome-mediated degradation, whereas EGFR knockdown enhanced autophagic flux and reversed GLUT1-overexpression-induced ferroptosis resistance and stemness maintenance. In vivo, GLUT1 knockdown suppressed tumor growth and lung metastasis, and clinical samples revealed a positive correlation between GLUT1 and EGFR expression, linked to advanced TNM stages and poor survival. Collectively, these findings demonstrate that GLUT1 preserves esophageal CSC-like characteristics by stabilizing EGFR to inhibit autophagy-dependent ferroptosis, highlighting targeting GLUT1 as a potential therapeutic strategy to eliminate CSCs and combat esophageal cancer progression.</div></div>","PeriodicalId":12227,"journal":{"name":"Experimental cell research","volume":"449 2","pages":"Article 114600"},"PeriodicalIF":3.3,"publicationDate":"2025-05-12","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144076918","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Magnesium Promoting OVX Rats' Rotator Cuff Tear Repair With Relieving Stem Cell Senescence Effect.","authors":"Minghui Sun, Weijiao Zhang, Xin Sun, Kaixu Yu, Xiangming He, Liming Zheng, Ziao Ling, Kaikai Duan, Xiling Qi, Yan Liu, Xin Zhao, Hui Wang, Jiankun Xu, Yifeng Zhang","doi":"10.1016/j.yexcr.2025.114593","DOIUrl":"https://doi.org/10.1016/j.yexcr.2025.114593","url":null,"abstract":"<p><p>The rotator cuff tear (RCT) repairing of tendon-to-bone junction (enthese) after surgery in osteoporotic patients is mainly hindered by poor bone formation at the damaged humeral tuberosity region. We found that long-term oral supplementation of Magnesium ions (Mg²⁺) can significantly promote humeral tuberosity bone formation and enthese regeneration after RCT surgery in ovariectomized (OVX) rats, attributing to the promotive effect of Mg²⁺ on the osteogenic differentiation of bone marrow mesenchymal stem cells (BMSCs) and its inhibition of new bone mineralization. Meanwhile, the in vitro replicative senescent markers of BMSCs are significantly relieved by Mg²⁺. The BMSCs' RNA-seq data analysis and cell energy metabolism results indicate that Mg²⁺ significantly increase senescent BMSCs' mitochondrial transmembrane potential and intracellular ATP content, and reduce reactive oxygen species production.</p>","PeriodicalId":12227,"journal":{"name":"Experimental cell research","volume":" ","pages":"114593"},"PeriodicalIF":3.3,"publicationDate":"2025-05-08","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143981440","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Research progress of connexin 43 mediated gap junction communication regulating bone metabolism in glucocorticoid-induced osteonecrosis of the femoral head","authors":"Yang Gao ,&nbsp;Changjun Chen ,&nbsp;Rongxing Liu ,&nbsp;Zhongkai Zhang ,&nbsp;Xin Zhao ,&nbsp;Huanzhi Ma","doi":"10.1016/j.yexcr.2025.114598","DOIUrl":"10.1016/j.yexcr.2025.114598","url":null,"abstract":"<div><div>Osteonecrosis of the femoral head (ONFH) is a refractory orthopedic disease that commonly affects young and middle-aged individuals. Long-term and high-dose use of glucocorticoids (GCs) is one of the main causes. Currently, the pathological mechanism of GCs-induced ONFH remains unclear, which poses difficulties for clinical prevention and treatment. This article focuses on reviewing the roles of gap junctions (GJs) and connexin 43 (Cx43) in GCs-induced ONFH. Under normal circumstances, cells in bone tissue form a network structure through GJs to maintain bone metabolic balance. However, GCs can obstruct the normal connections and signal transmission between bone tissue cells, leading to bone metabolic imbalance and triggering ONFH. As a key component of GJs in bone tissue, Cx43 is of great significance in bone metabolism. It not only participates in the construction of the osteocyte network but also regulates osteocyte activity, osteoblast differentiation, and osteogenic activities. Meanwhile, in vascular endothelial cells, Cx43 plays an important role in angiogenesis and maintaining vascular homeostasis, and is closely related to the vascularization of bone tissue. In addition, Cx43 is associated with the release of prostaglandin E2 (PGE2). GCs can inhibit the activity of Cx43, reduce the release of PGE2, and disrupt the balance of bone metabolism. Studies have shown that measuring changes in the expression level of Cx43 is expected to become an early diagnostic biomarker for GCs-induced ONFH. Enhancing its expression through small - molecule drugs, biological agents, and gene therapy may be potential treatment approaches for ONFH. This article proposes the PI3K/Akt/GSK3β/β-catenin pathway and conducts research on the regulatory mechanism of Cx43-mediated GJ-based intercellular communication, aiming to provide new ideas for the treatment of ONFH and bone metabolism-related diseases.</div></div>","PeriodicalId":12227,"journal":{"name":"Experimental cell research","volume":"449 1","pages":"Article 114598"},"PeriodicalIF":3.3,"publicationDate":"2025-05-06","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143936462","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Nuciferine alleviates non-alcoholic steatohepatitis by restoring endoplasmic reticulum stress","authors":"Zhiqiang Zhao ,&nbsp;Yunlong Zong ,&nbsp;Wenchao Zhang,&nbsp;Kai Wang,&nbsp;Yang Yang,&nbsp;Fenghua Li","doi":"10.1016/j.yexcr.2025.114599","DOIUrl":"10.1016/j.yexcr.2025.114599","url":null,"abstract":"<div><h3>Background</h3><div>Nuciferine(NF) has been shown to alleviate Non-alcoholic steatohepatitis (NASH), however, the exact mechanism of action remains to be explored. In this study we evaluated the pharmacological impact of NF on NASH models in vitro and in vivo, with a particular focus on its roles in regulating lipid metabolism, mitigating endoplasmic reticulum stress(ERS), and safeguarding mitochondrial function.</div></div><div><h3>Methods</h3><div>In vivo, Male C57BL/6J mice were fed a methionine and choline-deficient(MCD) diet to induce NASH, and then given NF orally for four weeks. NASH indexes were evaluated by histopathological analysis and biochemical parameters. In vitro, we established a free fatty acid (FFA)-induced NASH model in HepG2 cells and evaluated NASH by detecting cellular lipids and inflammatory factors.</div></div><div><h3>Results</h3><div>We found that NF had the potential ability to counteract the weight loss triggered by the MCD diet and to dose-dependently ameliorate liver steatosis and inflammatory responses as observed histopathologically. It was further found that NF was able to reduce hepatic malondialdehyde (MDA) levels, and elevate superoxide dismutase (SOD) and glutathione peroxidase (GSH-PX) activities. An in vitro model of FFA-induced steatotic HepG2 cells was established, and it was found that NF was able to reduce cellular lipid accumulation, lower triglyceride (TG) levels, and reduce MDA levels and restore mitochondrial respiratory function. In vitro and in vivo studies showed that NF was able to downregulate ERS-related protein expression.</div></div><div><h3>Conclusion</h3><div>In conclusion, NF played a multifaceted role by reducing oxidative stress, decreasing the levels of inflammatory cytokines, and mitigating ERS, which are pivotal in the pathogenesis of NASH.</div></div>","PeriodicalId":12227,"journal":{"name":"Experimental cell research","volume":"449 1","pages":"Article 114599"},"PeriodicalIF":3.3,"publicationDate":"2025-05-06","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143917444","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Astrocyte lactoferrin deficiency affects the construction and function of spinal neurons by regulating cholesterol metabolism","authors":"Xin Tong ,&nbsp;Xin Liu ,&nbsp;Yu-Xuan Jiang,&nbsp;Jia-Rui Su,&nbsp;Jun-Qi Luan,&nbsp;Chuang Guo","doi":"10.1016/j.yexcr.2025.114595","DOIUrl":"10.1016/j.yexcr.2025.114595","url":null,"abstract":"<div><div>Astrocytes play pivotal roles in central nervous system (CNS) homeostasis, with emerging evidence implicating astrocyte-derived lactoferrin (Lf) in neurodevelopmental and neurodegenerative processes. This study investigates Lf's functional significance in spinal cord integrity using astrocyte-specific Lf knockout (cKO) mice. Behavioral analyses of 1-month-old male cKO mice revealed impaired motor coordination (increased balance beam scores and prolonged pole-climbing latency) and delayed nociceptive responses (increased thermal withdrawal latency). Morphological assessments demonstrated neuron-specific pathology: motor neurons exhibited atrophy and reduced Nissl substance staining, spinal ganglion cells showed quantitative depletion with vacuolar degeneration, and protein expression analyses confirmed declines in neuronal markers (NeuN), synaptic components (SNAP25, PSD95), axonal and myelin related proteins (NF-L, MBP), and neurotransmitter transporters (AChE). Notably, glial cell populations remained unaffected. Mechanistic investigations identified reduced spinal cholesterol content accompanied by downregulation of cholesterol biosynthesis and transport regulators (Srebp2, HMGCR, ApoE, ABCA1) and activation of AMP-activated protein kinase (AMPK). These findings establish astrocytic Lf as a critical modulator of cholesterol metabolism essential for maintaining neuronal structural and functional integrity in the spinal cord. The discovered Lf-cholesterol regulatory axis provides novel insights into the pathogenesis of spinal cord disorders and highlights potential therapeutic targets for neurodegenerative conditions.</div></div>","PeriodicalId":12227,"journal":{"name":"Experimental cell research","volume":"449 1","pages":"Article 114595"},"PeriodicalIF":3.3,"publicationDate":"2025-05-05","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143911487","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Low concentration of quercetin promotes BDNF expression and osteoblast differentiation during fracture healing via TrkB-ERK1/2 signaling pathway","authors":"Xiao Meng ,&nbsp;Xi Chen ,&nbsp;Weihao Meng ,&nbsp;Chenghua Han ,&nbsp;Xiwen Qian ,&nbsp;Zitao Zhang","doi":"10.1016/j.yexcr.2025.114569","DOIUrl":"10.1016/j.yexcr.2025.114569","url":null,"abstract":"<div><div>Quercetin (Que), one of the flavonoids, plays a role in fracture healing, while brain-derived neurotrophic factor (BDNF) and tyrosine kinase receptor kinase B (TrkB) have also been shown to be involved. Que and BDNF signaling pathways are interrelated in the nervous system, but their reciprocal regulatory mechanisms in fracture healing and osteoblast differentiation have not yet been studied. We conducted cellular experiments and fracture animal models to preliminarily clarify the roles and signaling mechanisms of Que and BDNF in osteoblast differentiation and fracture healing. Cellular experiments confirmed that low concentrations of Que (0.01–5 μM) promoted osteoblast differentiation and the expression of osteogenesis-related markers, including COL1A1, ALP and Runx2; activated EKR1/2 and promoted the expression of BDNF (P &lt; 0.05); and that the combination of Que and exogenous BDNF had the strongest effect on promoting osteogenic differentiation (P &lt; 0.05); further mechanistic studies revealed that, the ERK1/2-specific chemical inhibitor PD98059 significantly inhibited the expression of BDNF and osteogenic differentiation markers under the action of Que (P &lt; 0.05), whereas the TrkB-specific chemical inhibitor K252a inhibited the activation of ERK1/2, the expression of BDNF, and the expression of osteoblast differentiation markers under the effect of Que (P &lt; 0.05). In fracture animal models, Que (100 mg/kg) significantly promoted fracture healing and increased BDNF expression at the bone callus. Thus, low concentrations of Que promote osteogenic differentiation through the TrkB-ERK1/2-BDNF signaling pathway, which in turn affects fracture healing.</div></div>","PeriodicalId":12227,"journal":{"name":"Experimental cell research","volume":"449 1","pages":"Article 114569"},"PeriodicalIF":3.3,"publicationDate":"2025-05-05","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143911467","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}