Journal of Cellular Physiology最新文献

{"title":"The Impact of Ageing on Skeletal Muscle: Roles of Mitochondrial Dysregulation, Systemic Communication, and Exercise","authors":"Juan Diego Hernández-Camacho,&nbsp;Marielle Saclier","doi":"10.1002/jcp.70212","DOIUrl":"10.1002/jcp.70212","url":null,"abstract":"<p>Ageing is a major risk factor for degenerative diseases, including sarcopenia, which is characterized by a progressive loss of skeletal muscle mass and function, frailty, and is associated with increased mortality. Skeletal muscle regeneration relies on muscle stem cells and efficient communication with cellular microenvironment. With ageing, skeletal muscle regenerative capacity declines, and sarcopenia results from complex, multitissue dysregulation involving mitochondrial dysfunction, immune ageing, chronic inflammation, senescence, extracellular matrix modification, disruption of neuromuscular junctions and muscle-specific vulnerability. This review summarizes current knowledge contributing to sarcopenia and inefficient muscle repair during ageing from cell-autonomous metabolic dysregulation to age-associated changes in the local and systemic cellular environment. We also explore recent insights into important role of exercise on muscle tissue health. Overall, emerging technologies, including human muscle atlases and spatial transcriptomics, together with exercise-based interventions, will help to identify of novel biomarkers and therapeutic targets to better prevent and treat sarcopenia.</p>","PeriodicalId":15220,"journal":{"name":"Journal of Cellular Physiology","volume":"241 8","pages":""},"PeriodicalIF":4.0,"publicationDate":"2026-07-26","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13402775/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148591438","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Arginine Methylation in Alternative Splicing: Implications for Cancer Therapy","authors":"Youyue Li,&nbsp;Shuyu Chen,&nbsp;Wenbo Ding,&nbsp;Bei Pan,&nbsp;Yujuan Yin,&nbsp;Xiaoqi Xin,&nbsp;Die Xia,&nbsp;Xueyang Wei,&nbsp;Siqi Bao,&nbsp;Mu Xu","doi":"10.1002/jcp.70206","DOIUrl":"10.1002/jcp.70206","url":null,"abstract":"<div>\u0000 \u0000 <p>Arginine methylation is a common post-translational modification that exists in three distinct forms—monomethylation, asymmetric dimethylation, and symmetric dimethylation—through which it regulates precursor RNA splicing and maintains cellular homeostasis. Dysregulation of the writing, reading, or erasure of arginine methylation promotes cancer development. Recent studies have identified PRMTs as key regulators of alternative splicing, and aberrant PRMT-driven splicing directly impacts multiple biological processes, including tumor proliferation, apoptosis resistance, metastasis, and immune evasion. This review focuses on the molecular mechanisms by which PRMTs regulate alternative splicing, their connections to oncogenic processes, and the therapeutic implications and challenges of targeting the PRMT-splicing axis in cancer.</p></div>","PeriodicalId":15220,"journal":{"name":"Journal of Cellular Physiology","volume":"241 7","pages":""},"PeriodicalIF":4.0,"publicationDate":"2026-07-23","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148562207","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"EXPRESSION OF CONCERN: Castration-Induced Prostate Epithelial Cell Apoptosis Results From Targeted Oxidative Stress Attack of M1142-Macrophages","authors":"","doi":"10.1002/jcp.70195","DOIUrl":"10.1002/jcp.70195","url":null,"abstract":"<p><b>EXPRESSION OF CONCERN</b>: G. O. Barbosa, J. A. F. Silva, A. Siqueira-Berti, U. Nishan, R. Rosa-Ribeiro, S. B. P. Oliveira, M. O. Baratti, D. Ferrucci, J. C. O. Santana, D. M. Damas-Souza, A. Bruni-Cardoso, T. M. Augusto, F. Corrêa-da-Silva, P. M. Moraes-Vieira, D. R. Stach-Machado, S. L. Felisbino, G. B. Menezes, C. L. Cesar, and H. F. Carvalho, “Castration-induced prostate epithelial cell apoptosis results from targeted oxidative stress attack of M1₁₄₂-macrophages,” <i>Journal of Cellular Physiology</i> 234, no. 10 (2019): 19048–19058, https://doi.org/10.1002/jcp.28544.</p><p>This Expression of Concern is for the above article, published online on 28 March 2019 in Wiley Online Library (wileyonlinelibrary.com), and has been issued by agreement between the journal Editor-in-Chief, Robert Heath, and Wiley Periodicals LLC. The Expression of Concern has been agreed due to concerns raised by third parties. The article was found to present overstated and misleading conclusions regarding the identification of a putative novel macrophage subpopulation based on ZNF142 expression. In addition, the antibody reported to have been used for this identification was determined to be incorrect in the published article. In their subsequent clarification, the authors state that a different antibody was used (Prestige Antibodies, Sigma-Aldrich; catalog number HPA049594); however, this antibody is reported to be reactive against the human protein, and the study does not provide evidence validating its cross-species reactivity. Therefore, the journal has decided to issue an Expression of Concern to inform and alert the readers.</p>","PeriodicalId":15220,"journal":{"name":"Journal of Cellular Physiology","volume":"241 7","pages":""},"PeriodicalIF":4.0,"publicationDate":"2026-07-23","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13392841/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148562220","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"EXPRESSION OF CONCERN: Intelligent TAT-Coupled Anti-HER2 Immunoliposomes Knock Downed MDR1 to Produce Chemosensitize Phenotype of Multidrug Resistant Carcinoma","authors":"","doi":"10.1002/jcp.70201","DOIUrl":"10.1002/jcp.70201","url":null,"abstract":"<p><b>EXPRESSION OF CONCERN:</b> N. Gholamian Dehkordi, F. Elahian, P. Khosravian, and S. A. Mirzaei, “Intelligent TAT‑Coupled Anti‑HER2 Immunoliposomes Knock Downed MDR1 to Produce Chemosensitize Phenotype of Multidrug Resistant Carcinoma,” <i>Journal of Cellular Physiology</i> 234, no. 11 (2019): 20769–20778, https://doi.org/10.1002/jcp.28683.</p><p>This Expression of Concern is for the above article, published online on 18 April 2019 in Wiley Online Library (wileyonlinelibrary.com), and has been published by agreement between the journal Editor-in-Chief, Robert Heath; and Wiley Periodicals LLC. The Expression of Concern has been agreed due to concerns raised by a third party, which identified overlapping Western blot images in Figures 4(c) and 4(d). The authors stated that the figure legend requires correction. However, further review of the article revealed substantial inconsistencies in Section 3.5, Table 1, and Figure 2 regarding the reported size of the nanocarriers. The authors were unable to provide the original raw data of the Western blot images or offer a satisfactory explanation for these issues. The authors plan to further investigate and characterize particle morphology and have reported to the editor that their results should be forthcoming. However, the Editor-in-Chief and the publisher have decided to publish this Expression of Concern to inform readers that questions regarding the reliability of the reported results remain.</p>","PeriodicalId":15220,"journal":{"name":"Journal of Cellular Physiology","volume":"241 7","pages":""},"PeriodicalIF":4.0,"publicationDate":"2026-07-23","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13392978/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148562154","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Zhenwu Decoction Alleviates Renal Fibrosis by Disrupting the Bidirectional Crosstalk Between TGF-β/Smad and Notch Signaling","authors":"Meiqi Hong,&nbsp;Ruolan Wu,&nbsp;Fugen Li,&nbsp;Xue Xiao,&nbsp;Xin Huang,&nbsp;Qinqiang Long,&nbsp;Shasha Li","doi":"10.1002/jcp.70209","DOIUrl":"10.1002/jcp.70209","url":null,"abstract":"<div>\u0000 \u0000 <p>Zhenwu Decoction (ZWD) is a traditional Chinese medicine prescription with well-documented renoprotective effects, though its precise mechanism of action against renal fibrosis remains to be elucidated. This study aimed to explore whether ZWD mitigates renal fibrosis by modulating the loop of transforming growth factor-β (TGF-β)/Smad and Notch signaling pathways. In vivo and in vitro experiments were conducted using unilateral ureteral obstruction (UUO) rat models and TGF-β1-stimulated NRK-49F fibroblast cells, respectively. The study's findings revealed that ZWD significantly improved renal function, mitigated pathological damage, and decreased extracellular matrix deposition in UUO rats. Treatment with ZWD led to a marked downregulation of TGF-β1, Notch1, and Jagged1 expression, as well as a reduction in Smad2/3 phosphorylation, both in vivo and in vitro. Gain- and loss-of-function experiments demonstrated that overexpression of TGF-β1 enhanced Notch signaling, whereas TGF-β1 knockdown inhibited it. Similarly, Notch1 overexpression increased TGF-β/Smad signaling, while Notch1 silencing suppressed TGF-β/Smad activity, thus confirming the existence of a positive bidirectional feedback loop in the context of renal fibrosis. Importantly, Notch1 overexpression directly induced a fibrotic phenotype in NRK 49F cells. In summary, the TGF-β/Smad and Notch pathways constitute a bidirectional positive feedback loop that promotes renal fibrosis. ZWD alleviates renal fibrosis by disrupting this crosstalk, highlighting its potential as a therapeutic strategy for chronic kidney disease (CKD).</p></div>","PeriodicalId":15220,"journal":{"name":"Journal of Cellular Physiology","volume":"241 7","pages":""},"PeriodicalIF":4.0,"publicationDate":"2026-07-23","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148578734","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Cover Image, Volume 241, Number 7, July 2026","authors":"","doi":"10.1002/jcp.70210","DOIUrl":"https://doi.org/10.1002/jcp.70210","url":null,"abstract":"<p>\u0000 <figure>\u0000 <div><picture>\u0000 <source></source></picture><p></p>\u0000 </div>\u0000 </figure></p>","PeriodicalId":15220,"journal":{"name":"Journal of Cellular Physiology","volume":"241 7","pages":""},"PeriodicalIF":4.0,"publicationDate":"2026-07-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1002/jcp.70210","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148533394","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Primary Cilia as Integrative Hubs of Metabolic Signaling in Type 2 Diabetes: Inter-Organ Evidence From Central, Peripheral, and Pancreatic Islet Tissues","authors":"Meifang Liang,&nbsp;Chenxin Wen,&nbsp;Li Deng,&nbsp;Youqin Li,&nbsp;Fengru Lv,&nbsp;Zhengmin Feng,&nbsp;Ergan Li,&nbsp;Jingyi Li,&nbsp;Jiayu Zhou,&nbsp;Hai Liao,&nbsp;Shanshan Feng,&nbsp;Zhonghui Feng","doi":"10.1002/jcp.70208","DOIUrl":"10.1002/jcp.70208","url":null,"abstract":"<div>\u0000 \u0000 <p>Primary cilia are highly specialized, solitary microtubule-based organelles widely present on the surface of mammalian cells. Acting as integrative platforms for membrane-associated signaling and intracellular pathways, primary cilia regulate Hedgehog (Hh), Wnt, G protein–coupled receptor (GPCR), and mTOR signaling and are closely implicated in metabolic dysregulation associated with type 2 diabetes (T2D). This review systematically summarizes current methodological approaches for studying primary cilia and delineates their pathogenic roles in T2D from multiple dimensions. In the central nervous system, hypothalamic primary cilia regulate appetite and energy expenditure through ADCY3/MC4R and BBSome modules. In peripheral metabolic organs, primary cilia in adipose tissue, liver, and bone influence cellular differentiation, lipid metabolism, and insulin sensitivity. In pancreatic islets, primary cilia on α, β, and δ cells coordinate hormone secretion and vascular remodeling via GPCR–cAMP, Somatostatin–SSTR3–GLI2, and Eph/Ephrin signaling pathways. Ciliopathy-associated genetic disorders and defects in centrosomal proteins further substantiate the pathological association between primary ciliary dysfunction and T2D. In addition, the identification of primary cilia–related biomarkers, together with therapeutic explorations involving MC4R agonists, GLP-1 receptor agonists, and mutation-targeted repair strategies, provides a rationale for the clinical translation of cilium-targeted interventions. Collectively, primary cilia may function as central hubs for integrating metabolic signals, regulating intercellular communication, and maintaining energy homeostasis. Future studies should further elucidate cell type–specific differences in primary ciliary receptor localization, signal integration, and secretory regulation; clarify the temporal dynamics of primary ciliary function during development, metabolic stress, and disease progression; and evaluate the structural and functional plasticity of primary cilia, as well as potential therapeutic windows, to facilitate the translation of cilia biology from mechanistic insights to clinical applications in T2D.</p>\u0000 </div>","PeriodicalId":15220,"journal":{"name":"Journal of Cellular Physiology","volume":"241 7","pages":""},"PeriodicalIF":4.0,"publicationDate":"2026-07-12","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148421123","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Mt1–Ca2+–Mitochondrial Metabolic Axis Maintains Temporomandibular Joint Condylar Cartilage Homeostasis Under Low Oxygen and Hypoxic Condition","authors":"Yuwei Yan,&nbsp;Fangwen Jia,&nbsp;Zhenhua Gao,&nbsp;Chao Liang,&nbsp;Wei Geng","doi":"10.1002/jcp.70203","DOIUrl":"10.1002/jcp.70203","url":null,"abstract":"<div>\u0000 \u0000 <p>The adaptive capacity of chondrocytes to fluctuating oxygen levels during the process of osteoarthritis remains poorly understood. This study aimed to investigate the role and underlying mechanisms of the Mt1–Ca²⁺–mitochondrial metabolic axis in chondrocyte function and cartilage homeostasis. Primary rat condylar chondrocytes were cultured under physiological low oxygen (5% O₂) and hypoxia (&lt;1% O₂) with Mt1 knockdown or overexpression. The role of Mt1 in chondrocyte functions were investigated. Transcriptomic analysis identified intracellular Ca²⁺ and metabolism-related pathways regulated by Mt1. Mitochondrial respiration and glycolytic capacity were evaluated by Seahorse XF assays, while intracellular Ca²⁺ concentration was quantified by Calcium Assay Kit. The effects of extracellular Ca²⁺ supplementation were analyzed to clarify the Mt1–Ca²⁺ interaction in metabolic regulation. In vivo, a rat model with intra-articular Mt1 knockdown and chronic sleep deprivation-induced hypoxia was established to verify the role of Mt1 in condylar cartilage homeostasis. Mt1 expression was significantly upregulated under hypoxia and positively correlated with chondrocyte viability, migration, and extracellular matrix synthesis. RNA-seq and enrichment analyses revealed that Mt1 regulates genes associated with mitochondrial respiration and Ca²⁺ binding. Mt1 knockdown significantly downregulated intracellular Ca²⁺, which were restored by extracellular Ca²⁺ supplementation. Seahorse analysis demonstrated that Mt1 knockdown significantly suppressed mitochondrial respiration and glycolytic capacity, whereas extracellular Ca²⁺ supplementation restored these deficits. In vivo, Mt1 knockdown aggravated condylar cartilage degeneration, which was further exacerbated under chronic sleep deprivation-induced hypoxia, as evidenced by surface erosion, matrix loss, and histological disorganization. Mt1 preserves TMJ condylar chondrocyte homeostasis under low oxygen and hypoxic conditions by coordinating mitochondrial and glycolytic metabolism through Ca²⁺ regulation. The Mt1–Ca²⁺–mitochondrial metabolic axis serves as a key adaptive mechanism sustaining cellular energy homeostasis and represents a potential therapeutic target for preventing temporomandibular joint osteoarthritis.</p>\u0000 </div>","PeriodicalId":15220,"journal":{"name":"Journal of Cellular Physiology","volume":"241 6","pages":""},"PeriodicalIF":4.0,"publicationDate":"2026-06-30","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148352041","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Correction to “IRE1α/NOX4 Signaling Pathway Mediates Ros-Dependent Activation of Hepatic Stellate Cells in NaAsO2-Induced Liver Fibrosis”","authors":"","doi":"10.1002/jcp.70204","DOIUrl":"10.1002/jcp.70204","url":null,"abstract":"<p>Y. Tao, Qiu T., Yao X., et al. 2021. “IRE1α/NOX4 Signaling Pathway Mediates Ros-Dependent Activation of Hepatic Stellate Cells in NaAsO₂-Induced Liver Fibrosis.” <i>Journal of Cellular Physiology</i> 236, no. 2: 1469–1480.</p><p>An incorrect DCFH-DA staining image for the 0 group in Figure 6b was used inadvertently during compilation. The corrected figure is shown below.</p><p></p><p>We apologize for this error.</p>","PeriodicalId":15220,"journal":{"name":"Journal of Cellular Physiology","volume":"241 6","pages":""},"PeriodicalIF":4.0,"publicationDate":"2026-06-29","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1002/jcp.70204","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148345329","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Lipocalin-2 Restores Mitochondrial and Antioxidant Adaptation in a Strain-Specific Manner During LPS Induced Sepsis","authors":"Vinita Kushwaha,&nbsp;Mrunmayee R. Kandalgaonkar,&nbsp;Sukhvinder Singh,&nbsp;Piu Saha,&nbsp;Ashok Kumar,&nbsp;Beng San Yeoh,&nbsp;Matam Vijay-Kumar","doi":"10.1002/jcp.70205","DOIUrl":"10.1002/jcp.70205","url":null,"abstract":"<p>Sepsis induces profound metabolic and mitochondrial dysfunction, contributing to multiple organ injury and mortality. Lipocalin-2 (Lcn2), an acute-phase protein, regulates iron homeostasis and oxidative stress, but its impact on mitochondrial resilience remains poorly understood. Here, we investigated the role of Lcn2 in modulating mitochondrial function and hepatic stress responses in C57BL/6 J (BL6) and BALB/c mice in LPS-induced endotoxemia. Lcn2-deficient (Lcn2KO) mice exhibited reduced basal respiration, maximal respiration, and spare respiratory capacity, indicating impaired mitochondrial oxidative phosphorylation. Administration of recombinant Lcn2 (rLcn2) restored mitochondrial respiration in both mouse strains under basal conditions; however, during LPS challenge, only BL6 mice partially preserved mitochondrial function, whereas BALB/c mice remained compromised. To explore underlying mechanisms, we assessed hepatic gene expression by qRT-PCR. LPS induced Acyl-CoA synthetase long-chain family member 4 (ACSL4) and suppressed lysophosphatidylcholine acyltransferase 3 (LPCAT3), markers associated with lipid remodeling, as well as altered antioxidant genes glutathione peroxidase 4 (GPX4) and superoxide dismutase 2 (SOD2) in both strains. rLcn2 treatment in BL6 mice normalized ACSL4 and LPCAT3 expression and enhanced antioxidant gene transcription, whereas BALB/c mice showed minimal recovery. In BL6 mice, Lcn2 supports oxidative phosphorylation while simultaneously modulating lipid metabolism and antioxidant defenses, highlighting its integrated role in cellular adaptation to endotoxemia. Our results reveal that differential Lcn2 responsiveness contributes to inter-strain variation in susceptibility to sepsis-induced mitochondrial dysfunction and identify Lcn2 as a potential therapeutic target for enhancing metabolic resilience during sepsis.</p>","PeriodicalId":15220,"journal":{"name":"Journal of Cellular Physiology","volume":"241 6","pages":""},"PeriodicalIF":4.0,"publicationDate":"2026-06-28","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1002/jcp.70205","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148345372","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}