Cell Biology and Toxicology最新文献

{"title":"Lamin A/C regulates cerebellar granule cell maturation.","authors":"Laura Vilardo, Ingrid Cifola, Marta Nardella, Paride Pelucchi, Maria Teresa Ciotti, Andrea Bianchi, Arianna Rinaldi, Ivan Arisi, Rossella Brandi, Mara d'Onofrio, Nicola Galvanetto, Giuliana Gatti, Myriam Catalano, Chiara Lanzuolo, Loredana Guglielmi, Igea D'Agnano","doi":"10.1007/s10565-025-10011-z","DOIUrl":"10.1007/s10565-025-10011-z","url":null,"abstract":"<p><p>Lamin A/C is a nuclear type V intermediate filament protein part of the meshwork structure underlying the inner nuclear membrane (nuclear lamina), which plays numerous roles, including maintenance of nuclear shape, heterochromatin organization, and transcriptional regulation. Our group has demonstrated the role of Lamin A/C in different pathophysiological conditions. Here, we investigated for the first time how Lamin A/C affects neuronal maturation in rat cerebellar granule cells (GCs). Primary rat cerebellar GCs where we silenced the Lmna gene constituted our key model; this provided a rather homogeneous cellular system showing a neuronal population in vitro. We then validated our findings in another in vivo murine model with knock-out of the Lmna gene and in an in vitro human neuronal model with silencing of the LMNA gene. We observed across three different models that Lamin A/C down-regulation affects neurons maturation by protecting the cells from glutamate-evoked excitotoxicity and correlates with an inhibition of calcium influxes and a down-regulation of pro-inflammatory cytokine pathways. Consistent with previous findings from our group, this study corroborates that Lamin A/C plays a key role in neural development and opens new significant implications for a better comprehension of the mechanisms involved in neurodegenerative diseases, where changes in the nuclear envelope are linked to neuroinflammatory processes and damage.</p>","PeriodicalId":9672,"journal":{"name":"Cell Biology and Toxicology","volume":"41 1","pages":"66"},"PeriodicalIF":5.3,"publicationDate":"2025-04-05","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143787780","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Targeting B4GALT3 in BMSCs-EVs for Therapeutic Control of HCC via NF-κB pathway inhibition.","authors":"Juncheng Guo, Kaiqiong Wang, Qigang Sun, Jun Liu, Jinfang Zheng","doi":"10.1007/s10565-025-10013-x","DOIUrl":"10.1007/s10565-025-10013-x","url":null,"abstract":"<p><p>Examining the communications in the tumor microenvironment (TME) specific to hepatocellular carcinoma (HCC), this exploration looks into the role played by beta-1,4-Galactosyltransferase III (B4GALT3) in bone marrow mesenchymal stromal cell-derived extracellular vesicles (BMSCs-EVs) regarding the NF-κB pathway and the triggering of cancer-associated fibroblasts (CAF). Through a multidisciplinary approach combining transcriptome sequencing, bioinformatic analysis, and various experimental models, the involvement of B4GALT3 in regulating CAF activity by modulating NF-κB signaling was brought to light in our study. The outcomes suggest that targeting B4GALT3 could impede HCC cell migration and invasion, promote apoptosis, and dampen tumor progression and metastasis, offering novel insights into potential therapeutic strategies for combating HCC.</p>","PeriodicalId":9672,"journal":{"name":"Cell Biology and Toxicology","volume":"41 1","pages":"67"},"PeriodicalIF":5.3,"publicationDate":"2025-04-05","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143787868","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Early endolysosomal dysfunction is a contributing factor to gadolinium-based contrast agent mouse renal proximal tubule epithelial cell injury.","authors":"Joshua DeAguero, Tamara Howard, G Patricia Escobar, Karol Dokladny, Brent Wagner","doi":"10.1007/s10565-025-10014-w","DOIUrl":"10.1007/s10565-025-10014-w","url":null,"abstract":"<p><p>The prevalence of contrast-enhanced magnetic resonance imaging (MRI) examinations and the absence of safer alternatives to gadolinium-based contrast agents (GBCAs) make the associated adverse effects of GBCAs much more concerning. Safety concerns arise from the toxic behavior of heavy metal gadolinium (Gd³⁺) and the potential release of the metal from the chelating ligand. Renal insufficiency and other patient factors increase the susceptibility to the toxic effects of GBCAs. It is, therefore, imperative that the molecular and cellular mechanisms underlying GBCA toxicity be defined. This study aims to determine GBCA-induced endolysosomal dysfunction in mouse renal proximal tubule epithelial cells. Loss of cell viability was agent- and time-dependent, and proximal tubule injury was detectable following 24 h linear GBCA exposure. Both classes of GBCAs displayed lysosomotropic behaviors, characterized by early lysosomal enlargement and lysosomal injury. Hijacking of the endolysosomal system by these agents inhibited cathepsin processing by blocking the transport and maturation of cathepsin B (CTSB) and cathepsin D (CTSD). Lysosomal enlargement coincided with the translocation of CTSB and CTSD from the lysosomal lumen to the cytosol, suggesting lysosomal membrane destabilization. Even though both agents displayed a similar response, linear exposures appeared to exhibit a greater effect. Disturbance of mitochondrial activity and loss of cell viability occurs downstream of early lysosome damage. This effect was partially restored by lysosomal protease inhibitor co-treatment. This data suggests that GBCA exposures induce a lysosomal stress response, and partial LMP occurs upstream of mitochondrial dysfunction and resultant cellular injury.</p>","PeriodicalId":9672,"journal":{"name":"Cell Biology and Toxicology","volume":"41 1","pages":"65"},"PeriodicalIF":5.3,"publicationDate":"2025-04-03","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11965215/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143771509","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Sodium fluoride promotes myopia progression via the activation of the ferroptosis pathway by PIEZO1 and pharmacological targeting PIEZO1 represents an innovative approach for myopia treatment.","authors":"Bo Liu, Xueting Yao, Qinying Huang, Zehui Shi, Jinfei Wei, Shijia Li, Min Li, Xiuping Chen, Jinhui Dai","doi":"10.1007/s10565-025-10020-y","DOIUrl":"10.1007/s10565-025-10020-y","url":null,"abstract":"<p><p>Sodium fluoride-induced ocular damage constitutes a significant public health concern globally; however, the precise molecular mechanisms underlying this issue remain obscure. This study aims to investigate the effects of sodium fluoride on myopia and to offer novel theoretical foundations for future strategies in myopia prevention and control. The experimental data showed that sodium fluoride could promote myopia progression, and through bioinformatics analysis, we found that sodium fluoride could affect the ferroptosis pathway. Western blotting and redox kit assays further confirmed that sodium fluoride activates the ferroptosis pathway. We also demonstrated that PIEZO1 plays a crucial role in sodium fluoride-induced myopia, and that the PIEZO1 inhibitor (GsMTx4) can inhibit the ferroptosis pathway. Subsequently, we identified PIEZO1 as a potential target of baicalin, which inhibited PIEZO1 expression in vivo and in vitro, as confirmed by molecular docking modeling and CETSA assays. Finally, we found that baicalin inhibited sodium fluoride-induced myopia via PIEZO1. Taken together, our findings indicate that sodium fluoride can promote myopia progression by activating the ferroptosis pathway through PIEZO1, and that targeting PIEZO1 expression can delay myopia progression, which may provide a new drug target for myopia treatment in the future.</p>","PeriodicalId":9672,"journal":{"name":"Cell Biology and Toxicology","volume":"41 1","pages":"64"},"PeriodicalIF":5.3,"publicationDate":"2025-04-02","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11965261/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143771510","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Insights into emerging mechanisms of ferroptosis: new regulators for cancer therapeutics.","authors":"Si-Yi Xu, Shuang-Shuang Yin, Lei Wang, Hao Zhong, Hong Wang, Hai-Yang Yu","doi":"10.1007/s10565-025-10010-0","DOIUrl":"10.1007/s10565-025-10010-0","url":null,"abstract":"<p><p>Ferroptosis is an iron-dependent form of regulated cell death characterized by the accumulation of iron-dependent lipid peroxides, which has been implicated in the pathogenesis of various diseases, and therapeutic agents targeting ferroptosis are emerging as promising tools for cancer treatment. Current research reveals that ferroptosis-targeted therapies can effectively inhibit tumor progression or delay cancer development. Notably, natural product-derived compounds-such as artemisinin, baicalin, puerarin, quercetin, kaempferol, and apigenin-have demonstrated the ability to modulate ferroptosis, offering potential anti-cancer benefits. Mechanistically, ferroptosis exhibits negative glutathione peroxidase 4 (GPX4) regulation and demonstrates a positive correlation with plasma membrane polyunsaturated fatty acid (PUFA) abundance. Moreover, the labile iron pool (LIP) serves as the redox engine of ferroptosis. This review systematically analyzes the hallmarks, signaling pathways, and molecular mechanisms of ferroptosis, with a focus on how natural product-derived small molecules regulate this process. It further evaluates their potential as ferroptosis inducers or inhibitors in anti-tumor therapy, providing a foundation for future clinical translation.</p>","PeriodicalId":9672,"journal":{"name":"Cell Biology and Toxicology","volume":"41 1","pages":"63"},"PeriodicalIF":5.3,"publicationDate":"2025-03-25","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11937073/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143708760","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Myeloid cells are involved in tumor immunity, metastasis and metabolism in tumor microenvironment.","authors":"Chenbo Zhang, Ying Song, Huanming Yang, Kui Wu","doi":"10.1007/s10565-025-10012-y","DOIUrl":"10.1007/s10565-025-10012-y","url":null,"abstract":"<p><p>Bone marrow-derived cells in the tumor microenvironment, including macrophages, neutrophils, dendritic cells, myeloid-derived suppressor cells, eosinophils and basophils, participate in the generation, development, invasion and metastasis of tumors by producing different cytokines and interacting with other cell types, and play a pro-tumor or anti-tumor role in regulating tumor immunity. Due to the complexity of cell types in the tumor microenvironment and the unknown process of tumor development and metastasis, cancer treatment to achieve better survival status remains challenging. In this article, we summarize the effects of myeloid cells in tumor microenvironment on tumor immunity, cancer migration, and crosstalk with metabolism (including glucose metabolism, lipid metabolism, and amino acid metabolism), which will help to further study the tumor microenvironment and seek targeted therapeutic strategies for patients.</p>","PeriodicalId":9672,"journal":{"name":"Cell Biology and Toxicology","volume":"41 1","pages":"62"},"PeriodicalIF":5.3,"publicationDate":"2025-03-25","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11937113/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143708765","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"CUL1-neddylation contributes to K29-linked ubiquitination on p27 for autophagic degradation in sorafenib-resistant liver cancer.","authors":"Haitao Xu, Shaoyue Zheng, Qiuqi Zhang, Ying Xu, Hanbo Zhang, Tianming Hu, Xiaoling Zhang, Jiaoting E, Xuedong Li, Ruitao Wang, Hongyan Liu, Rui Xie","doi":"10.1007/s10565-025-10008-8","DOIUrl":"10.1007/s10565-025-10008-8","url":null,"abstract":"<p><p>Sorafenib has demonstrated great efficacy in liver cancer, however, its application as first-line treatment has been hampered due to the emerging drug resistance. This study is aimed to investigate the mechanism underlying acquired sorafenib resistance in liver cancer. Based on GSE109211 and TCGA datasets, bioinformatics analysis was conducted to find the potential genes implicated in the sorafenib resistance in liver cancer. mCherry-/eGFP-LC3B dual-fluorescent system was used to assess autophagic state. Wild and mutant types of HA-labeled ubiquitin (K27, K29, K33, K48, K63, K29R and K48R) were used to identify the type of polyubiquitin chains added to p27 by CUL1. Herein, we identified that F-box protein (SCF) ubiquitin ligase complexes (CUL1 and SKP2) and NEDD8 were highly expressed in sorafenib-resistant tissues using both the public data and clinical samples. NEDD8-mediated CUL1 neddylation enhanced SCF ubiquitin ligase complex to target p27 and subsequently linked K29-linked polyubiquitin chains to p27. Furthermore, NBR1 facilitated the degradation of ubiquitinated p27 protein by enhancing autophagy flux. Knocking down of CUL1 could prevent ubiquitination- and autophagy-mediated p27 protein degradation. The resistance to sorafenib was suppressed with CUL1 knockdown both in vitro and in vivo. In conclusion, our findings indicated that blocking neddylation or autophagy can restore drug sensitivity, thus providing a potential strategy for overcoming sorafenib resistance in the future.</p>","PeriodicalId":9672,"journal":{"name":"Cell Biology and Toxicology","volume":"41 1","pages":"61"},"PeriodicalIF":5.3,"publicationDate":"2025-03-20","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11926008/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143669215","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Olfactory mucosal mesenchymal stem cell-derived exosome Lnc A2M-AS1 ameliorates oxidative stress by regulating TP53INP1-mediated mitochondrial autophagy through interacting with IGF2BP1 in Parkinson's diseases.","authors":"Jiangshan Zhang, Chuang Wang, Guoshuai Yang, Yanhui Zhou, Dan Hou, Ying Xia","doi":"10.1007/s10565-025-10009-7","DOIUrl":"10.1007/s10565-025-10009-7","url":null,"abstract":"<p><strong>Background: </strong>Exosome Lnc A2M-AS1 from olfactory mucosa mesenchymal stem cells (OM-MSCs) can ameliorate oxidative stress by improving mitophagy in cardiomuscular cells; however, it remains unclear whether this effect exists in the brain tissues of patients with Parkinson's disease (PD).</p><p><strong>Methods: </strong>OM-MSC-Exosomes were isolated and verified based on morphology and specific biomarkers. The effects of OM-MSC-Exo on mitochondrial autophagy, oxidative stress, and lncRNA A2M-AS1 were detected in MPP⁺-treated HT22 cells. The effects of OM-MSC-Exos on mitochondrial autophagy and oxidative stress were detected in an MPTP-induced Parkinson's disease (PD) model in C57BL/6 mice. The interaction between IGF2BP1, A2M-AS1, and TP53INP1 was assessed via RNA pull-down/RNA Immunoprecipitation and RNA stability assays. The effects of lnc A2M-AS1 on IGF2BP1/TP53INP1-mediated mitochondrial autophagy and oxidative stress were verified in MPP⁺-treated HT22 cells and MPTP-induced PD mouse models.</p><p><strong>Results: </strong>Exosomes isolated from olfactory mucosa mesenchymal stem cells were found to be rich in Lnc A2M-AS1. Lnc A2M-AS1 was proved to be able to ameliorate oxidative stress induced by MPP⁺ in HT22 cells. lncRNA A2M-AS1 regulates oxidative stress by enhancing mitophagy in HT22 cells. In addition, lncRNA A2M-AS1 induced mitophagy through TP53INP1 and mediated TP53INP1 expression by binding to IGF2BP1. Furthermore, OM-MSC-Exo and Lnc A2M-AS1 treatment improved symptoms and ameliorated oxidative stress in MPTP-induced PD mouse models.</p><p><strong>Conclusion: </strong>Collectively, lncRNA A2M-AS1 from OM-MSC-derived exosomes regulates TP53INP1 expression by targeting IGF2BP1 to induce mitophagy and ameliorate oxidative stress. OM-MSC-derived exosomes could potentially serve as promising candidates for new treatment methods for PD.</p>","PeriodicalId":9672,"journal":{"name":"Cell Biology and Toxicology","volume":"41 1","pages":"60"},"PeriodicalIF":5.3,"publicationDate":"2025-03-20","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11926059/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143669217","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Exosome-mediated effects of BRCA1 on cardiovascular artery disease.","authors":"Hairui Yu, Dong Wei, Weiqian Liao, Xiaoming Shang, Dandan Li, Chunzhao Liu, Qimei Deng, Haiquan Huangfu","doi":"10.1007/s10565-025-09996-4","DOIUrl":"10.1007/s10565-025-09996-4","url":null,"abstract":"<p><p>The progression of coronary artery disease atherosclerosis (CAD) is closely associated with cardiomyocyte apoptosis and inflammatory responses. This study focused on investigating the impact of BRCA1 in exosomes (Exo) derived from M1 macrophages on CAD. Through the analysis of single-cell RNA-seq datasets, significant communication between macrophages and cardiomyocytes in CAD patients was observed. BRCA1, identified as a significant apoptosis-related gene, was pinpointed through the assessment of differential gene expression and weighted gene co-expression network analysis (WGCNA). Experimental procedures involved BRCA1 lentivirus transfection of M1 macrophages, isolation of Exo for application to cardiomyocytes and smooth muscle cells, cell viability assessments, and characterization of Exo. The results showed that BRCA1-Exo from M1 macrophages induced cardiomyocyte apoptosis and affected smooth muscle cell behavior. In vivo studies further supported the exacerbating effects of BRCA1-Exo on CAD progression. Overall, the involvement of Exo carrying BRCA1 from M1 macrophages is evident in the induction of cardiomyocyte apoptosis and the regulation of smooth muscle cell behaviors, thereby contributing to CAD atherosclerosis progression. These findings unveil novel molecular targets that could have potential implications for CAD treatment strategies.</p>","PeriodicalId":9672,"journal":{"name":"Cell Biology and Toxicology","volume":"41 1","pages":"59"},"PeriodicalIF":5.3,"publicationDate":"2025-03-13","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11906578/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143623720","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Targeted nanoparticle delivery system for tumor-associated macrophage reprogramming to enhance TNBC therapy.","authors":"Xiaoshen Dong, Xiaoou Wang, Xinyu Zheng, Haiyang Jiang, Lu Liu, Ningye Ma, Shuo Wang","doi":"10.1007/s10565-025-10001-1","DOIUrl":"10.1007/s10565-025-10001-1","url":null,"abstract":"<p><p>Triple-negative breast cancer (TNBC) poses as a daunting and intricate manifestation of breast cancer, highlighted by few treatment options and a poor outlook. The crucial element in fostering tumor growth and immune resistance is the polarization of tumor-associated macrophages (TAMs) into the M2 state within the tumor microenvironment (TME). To address this, we developed M2 targeting peptide-chitosan-curcumin nanoparticles (M2pep-Cs-Cur NPs), a targeted delivery system utilizing chitosan (Cs) as a carrier, curcumin (Cur) as a therapeutic agent, and targeting peptides for specificity. These NPs effectively inhibited TNBC cell proliferation (~ 70%) and invasion (~ 70%), while increasing the responsiveness of tumors to anti-PD-L1 treatment (~ 50% survival enhancement) in vitro and in vivo. Bioinformatics analysis suggested that Cur modulates TAM polarization by influencing key genes such as COX-2, offering insights into its underlying mechanisms. This study highlights the potential of M2pep-Cs-Cur NPs to reverse M2 polarization in TAMs, providing a promising targeted therapeutic strategy to overcome immunotherapy resistance and improve TNBC outcomes.</p>","PeriodicalId":9672,"journal":{"name":"Cell Biology and Toxicology","volume":"41 1","pages":"58"},"PeriodicalIF":5.3,"publicationDate":"2025-03-08","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11890257/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143582195","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}