Experimental cell research最新文献

{"title":"Tissue is the issue: overcoming limitations in lung cancer precision medicine through cryobiopsy-derived lung cancer organoids and organ-on-a-chip models","authors":"Yoonjoo Kim , Dongil Park , Dahye Lee, Chaeuk Chung","doi":"10.1016/j.yexcr.2025.114642","DOIUrl":"10.1016/j.yexcr.2025.114642","url":null,"abstract":"","PeriodicalId":12227,"journal":{"name":"Experimental cell research","volume":"450 2","pages":"Article 114642"},"PeriodicalIF":3.3,"publicationDate":"2025-06-16","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144293609","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":"The Scribble-Rac1 signaling axis drives epithelial cell motility and contributes to diffuse adenomyosis pathogenesis","authors":"Xiaoping He ,&nbsp;Yaoming Peng ,&nbsp;Haiou Liu ,&nbsp;Congjian Xu","doi":"10.1016/j.yexcr.2025.114654","DOIUrl":"10.1016/j.yexcr.2025.114654","url":null,"abstract":"<div><h3>Purpose</h3><div>The study was designed to investigate whether estrogen regulates cell migration through cell polarity signaling and contributes to adenomyosis development.</div></div><div><h3>Methods</h3><div>In vitro study, Ishikawa cells received different treatments, Western Blot was used to detect the expression of adhesion factors and cytoskeletal proteins. Pseudopodia formation was assessed by cell immunofluorescence staining. Scratch test and transwell invasion test were used to detect the changes in Ishikawa cell migration and invasion.</div></div><div><h3>Results</h3><div>Scribble expression in Ishikawa cells is down-regulated by estrogen, leading to reduced expression of adhesion factors, increased expression of cytoskeletal proteins, enhanced pseudopodia formation, and elevated cell motility and invasion. Molecular mechanism research suggests that reduced Scribble expression may promote cell motility and invasion through activation of the Rac1-IRSp53-WAVE2 signaling pathway.</div></div><div><h3>Conclusions</h3><div>Scribble downregulation may serve as an indicator of adenomyosis severity. Its reduction alters cytoskeletal protein expression, enhancing cell motility. Mechanistically, Scribble downregulation likely activates Rac1, triggering the Rac1/IRSp53/WAVE2 pathway, which promotes pseudopodia formation and increases cell migration. These insights provide a theoretical basis for understanding the pathogenesis of adenomyosis.</div></div>","PeriodicalId":12227,"journal":{"name":"Experimental cell research","volume":"450 2","pages":"Article 114654"},"PeriodicalIF":3.3,"publicationDate":"2025-06-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144307892","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":"Dysfunctional pericellular hyaluronan deposition contributes to attenuated CD44/EGFR co-localization and impaired myofibroblast differentiation in chronic wound fibroblasts","authors":"Nathaniel Glyn Morris ,&nbsp;Emma Louise Woods ,&nbsp;Jordanna Dally ,&nbsp;Adam Christopher Midgley ,&nbsp;Robert Steadman ,&nbsp;Ryan Moseley","doi":"10.1016/j.yexcr.2025.114646","DOIUrl":"10.1016/j.yexcr.2025.114646","url":null,"abstract":"<div><div>Non-healing chronic wounds, such as venous ulcers and pressure sores, represent significant causes of patient morbidity and financial burden to Healthcare Services worldwide. During normal healing, dermal fibroblasts (DFs) mediate numerous responses to promote wound closure. However, phenotypic changes induced within chronic wound environments lead to dysfunctional fibroblast functions, which facilitate non-healing. Although the processes underlying impaired proliferative and migratory responses in chronic wound fibroblasts (CWFs) are established, the mechanisms that mediate impaired CWF-myofibroblast differentiation remain poorly understood. Fibroblast-myofibroblast differentiation is induced by transforming growth factor-β₁ (TGF-β₁) and downstream classical Smad2/3 and non-classical epidermal growth factor receptor (EGFR)/ERK1/2 signaling, initiated through hyaluronan (HA) receptor (CD44) binding to EGFR and dependent on elevated HA synthesis and its pericellular accumulation. Here, we demonstrate that these signaling pathways are dysregulated in venous ulcer- and pressure sore-derived CWFs, compared to DFs. CWFs exhibit increased susceptibilities to cellular senescence and impaired myofibroblast differentiation, accompanied by defective lysosomal/endosomal activities and dysfunctional activation of the HA/CD44/EGFR pathway. Irrespective of wound source, CWFs exhibited increased HAS1 versus HAS2 expression, altered HAS1 and HAS2 intracellular localization, and deregulated hyaladherin (CD44, TSG-6, and IαI heavy chain motifs, HC3, HC4 and HC5) induction, following TGF-β₁ stimulation. These events attenuated HA pericellular coat formation and CD44/EGFR co-localization within membrane lipid rafts, essential for myofibroblast development. Our findings suggest that aberrant HAS1 and HAS2 expression and distributions cause reduced pericellular hyaluronan deposition, leading to attenuated CD44/EGFR co-localization and dysfunctional CWF-myofibroblast differentiation, which contributes to the impaired closure and healing of chronic wounds.</div></div>","PeriodicalId":12227,"journal":{"name":"Experimental cell research","volume":"450 2","pages":"Article 114646"},"PeriodicalIF":3.3,"publicationDate":"2025-06-14","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144309789","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":"BMSC-derived exosomal CD73 mediated macrophage polarization promotes osteoblastic differentiation in diabetes","authors":"Yiping Dou ,&nbsp;Shujia Yu ,&nbsp;Shiyu Cao,&nbsp;Kang Gao,&nbsp;Menghao Lv,&nbsp;Yilin He,&nbsp;Ruihong Ma,&nbsp;Qian Zhu,&nbsp;Chenrui Li,&nbsp;Zhenhua Gao,&nbsp;Pan Ma","doi":"10.1016/j.yexcr.2025.114653","DOIUrl":"10.1016/j.yexcr.2025.114653","url":null,"abstract":"<div><div>Stem cell-derived exosomes have exhibited promise for applications in tissue regeneration. However, the osteogenic ability of exosomes derived from bone marrow mesenchymal stem cells(BMSCs) in diabetes is impaired. Exosomes play a role in intercellular communication and affect the functional status of many adjacent cells. The micro-inflammatory state in diabetes often leads to a higher proportion of M1/M2 macrophages in the tissue damage area than in non-diabetic individuals, which is unfavorable for tissue regeneration and delays wound healing. In the present study, we compared the macrophage polarization effect of exosomes secreted by BMSCs derived from type 2 diabetic rats(Exo(dm)) and derived from normal rats(Exo(wis)). The impact of Exo(dm) on regulating the polarization to M2 type in macrophages was weaker than that of Exo(wis), which brought less osteogenesis and was one of the reasons for poor regenerative repair of bone defects. To go a step further, Exo(dm) has lower expression of CD73, which could activate adenosine receptor A2b and cAMP/AKP pathway, leading to disorder of macrophage polarization in diabetes.</div></div>","PeriodicalId":12227,"journal":{"name":"Experimental cell research","volume":"450 2","pages":"Article 114653"},"PeriodicalIF":3.3,"publicationDate":"2025-06-14","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144309788","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":"CLEC5A suppresses cell growth and metastasis via interfering with the calcineurin/NFATc1 signaling pathway in osteosarcoma","authors":"Bin Hu ,&nbsp;Ruifeng Shi ,&nbsp;Xiang-an Kong ,&nbsp;Li Li ,&nbsp;Jie Gao ,&nbsp;Tao Xie ,&nbsp;Yong Hu","doi":"10.1016/j.yexcr.2025.114650","DOIUrl":"10.1016/j.yexcr.2025.114650","url":null,"abstract":"<div><div>Osteosarcoma (OS) is a prevalent primary bone malignancy characterized by a poor prognosis due to its high metastatic potential. Although the dysregulation of C-type lectin domain family 5, member A (CLEC5A) has been reported in various cancers, its role in OS progression and molecular pathogenesis remains elusive. We leveraged a comprehensive gene expression dataset (GSE21257) to elucidate the key genes in OS, both with and without metastatic involvement. Bioinformation analyses, Western blot, and RT-qPCR assays consistently demonstrated significantly lower CLEC5A expression levels in human OS cell lines and tissues. Notably, OS tissues from patients with metastasis exhibited lower CLEC5A levels compared to those without metastasis. We generated stable CLEC5A-deficient MG-63 and 143B cells with short hairpin RNA. Our findings revealed that CLEC5A knockdown enhanced OS cell proliferation and metastasis. Additionally, CLEC5A-deficient cells displayed increased calcineurin activity, which promoted the nuclear translocation of NFATc1, leading to elevated expression of MMPs. Conversely, CLEC5A overexpression suppressed OS cells growth and invasion and concurrently inhibited calcineurin activity. In summary, our study uncovers a suppressive role for CLEC5A in OS tumorigenesis and metastasis through the modulation of the calcineurin/NFATc1 signaling pathway. The deregulation of this pathway significantly impacts OS progression, highlighting its potential as a predicted and therapeutic target for metastatic OS.</div></div>","PeriodicalId":12227,"journal":{"name":"Experimental cell research","volume":"450 2","pages":"Article 114650"},"PeriodicalIF":3.3,"publicationDate":"2025-06-14","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144279740","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":"Medication targeting to subcellular organelles: Emphasizing mitochondria as a therapeutic marvel—Current situation and future prospects","authors":"Riyad F. Alzhrani ,&nbsp;Adel Ali Alhowyan ,&nbsp;Ehab I. Taha ,&nbsp;Sabry M. Attia ,&nbsp;Samir A. Salama ,&nbsp;Gamaleldin I. Harisa","doi":"10.1016/j.yexcr.2025.114647","DOIUrl":"10.1016/j.yexcr.2025.114647","url":null,"abstract":"<div><div>Subcellular disorders are linked with several diseases, specifically mitochondrial dysfunction linked to age, metabolic disorders, cancer, cardiovascular disease, and other mitochondrial diseases (MDs). Intracellular medication delivery is a promising option for effective therapy. This study aims to highlight subcellular delivery with focus on mitochondrial pharmacology, gene therapy, transplantation, and drug targeting. PubMed, Google Scholar, Scopus, and other scholarly sources were leveraged to prepare this narrative review. According to current studies, intermittent fasting, consistent exercise, well-balanced diets, and proper sleep can all help to increase mitochondrial quality. Molecular therapies improve mitochondrial bioenergetics, redox status, biogenesis, dynamics, mitophagy, bioenergetic, and sirtuins. The antioxidant supplementation restores endogenous antioxidants such as alpha-lipoic acid, tocopherols, L-carnitine, and coenzyme Q10 to prevent mitochondrial damage. Mdivi-1, melatonin, resveratrol, PGC-1α agonists, metformin, and Opa1 activators modify the dynamics and biogenesis of mitochondria. Bioactive phytochemicals, including curcumin, berberine, quercetin, and capsaicin, affect OXPHOS and mitochondrial sirtuins. These agents affect gene expression, antioxidant defenses, inflammation, and mitochondrion functions. Therefore, bioactive phytochemicals limit oxidative damage, increase insulin sensitivity, and improve extended cell longevity. Mitochondrial transplantation and gene therapy using mRNA and gene editing technologies are promising treatment options for MDs. Mitoquidone, triphenylphosphine, mitochondrial-targeting peptides, and nanocarriers localize medicines within mitochondrial compartments. In conclusion, a good lifestyle and bioactive materials, alongside mitochondrial medications, gene therapy, transplantation, and drug targeting, could restore overall cellular health.</div></div>","PeriodicalId":12227,"journal":{"name":"Experimental cell research","volume":"450 2","pages":"Article 114647"},"PeriodicalIF":3.3,"publicationDate":"2025-06-13","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144298479","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":"PKR inhibition reduces high glucose and H2O2-induced injury in rat renal epithelial cells by suppressing the sonic hedgehog pathway","authors":"Ganesh Panditrao Lahane ,&nbsp;Dishank Arondekar ,&nbsp;Audesh Bhat ,&nbsp;Arti Dhar","doi":"10.1016/j.yexcr.2025.114652","DOIUrl":"10.1016/j.yexcr.2025.114652","url":null,"abstract":"<div><div>Double-stranded RNA-dependent protein kinase (PKR) is involved in signaling pathways that mediate responses to oxidative and endoplasmic reticulum (ER) stress and has been linked to various cardiovascular diseases. However, the role of PKR in renal cells under chronic oxidative stress and the direct impact of PKR inhibitor treatment on such stress-induced damage remain unexplored. This study aimed to investigate the effect of PKR inhibition on oxidative stress-induced injury in renal epithelial cells using an in vitro model. Oxidative stress was induced in NRK-52E renal epithelial cells using a combination of high glucose (HG) and hydrogen peroxide (H₂O₂). Cell viability, immunofluorescence, and gene expression were analyzed using MTT assay, confocal microscopy, and RT-PCR respectively. Moreover, ROS levels were assessed by FACS. Exposure to HG and H₂O₂ significantly increased PKR expression in renal epithelial cells compared to control cells. Co-treatment with the PKR inhibitor C16 and gene silencing reduced elevated levels of reactive oxygen species (ROS), malondialdehyde (MDA), nitric oxide, and myeloperoxidase (MPO) in NRK-52E cells. Additionally, HG and H₂O₂ treatment upregulated Shh, Smo, and Gli1 mRNA while downregulated Ptch1 mRNA compared to control cells. All these altered mRNA was reversed by C16 co-treatment and PKR gene silencing. Furthermore, C16 co-treatment supressed fibrosis and EMT related markers, including TGF-β, α-SMA, fibronectin, vimentin, and type-1 collagen while, increased E-cadherin level in NRK-52E cells. In summary, PKR expression was increased in renal epithelial cells under stress-induced conditions. C16 co-treatment under stress-induced conditions protects the renal epithelial cells via inhibition of oxidative stress, fibrosis, EMT, and modulating Sonic hedgehog signaling pathway.</div></div>","PeriodicalId":12227,"journal":{"name":"Experimental cell research","volume":"450 2","pages":"Article 114652"},"PeriodicalIF":3.3,"publicationDate":"2025-06-12","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144279742","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":"Estradiol inhibits endometrial injury by promoting the stability of the KLF15 protein and the recovery of mitochondrial function","authors":"Jianghong Zhou ,&nbsp;Zhenghua Xiong ,&nbsp;Xicui Long ,&nbsp;Lijuan Yang ,&nbsp;Wenjiao Jin ,&nbsp;Xuesong Han","doi":"10.1016/j.yexcr.2025.114651","DOIUrl":"10.1016/j.yexcr.2025.114651","url":null,"abstract":"<div><h3>Background</h3><div>Endometrial injury (EI) is an important factor leading to infertility, which seriously affects women's fertility and reproductive health. Research indicates that estradiol (E2) therapy can promote the repair of EI, but the specific mechanism of E2 action in EI remains unclear.</div></div><div><h3>Methods</h3><div>The research involved creating an EI model for human endometrial epithelial cells (hEECs) using lipopolysaccharide (LPS), and constructing a rat intrauterine adhesion (IUA) model through simulating mechanical injury of human endometrial. Western blot, immunohistochemistry and RT-qPCR were used to detect the expression of key proteins and genes; endometrial damage was detected by HE, TUNEL and Masson staining; mitochondrial function changes were detected by detecting ROS, ATP levels and mitochondrial membrane potential.</div></div><div><h3>Results</h3><div>Our research revealed a reduced expression of E2 and Krüppel-like factor 15 (KLF15) in IUA rats. Exogenous E2 treatment inhibited EI by activating the expression of KLF15, inhibited the expression of apoptosis-related proteins Bax and cleaved caspase-3, and promoted the expression of Bcl-2 protein. Additionally, our findings revealed that treatment with E2 decreased mitochondrial ROS (mROS) levels, enhanced mitochondrial membrane potential, and promoted ATP production in EI model cells, whereas KLF15 interference weakens the therapeutic effect of E2, suggesting that E2 treatment alleviates EI by promoting the expression of KLF15 and restoring mitochondrial function. In addition, E2 promotes PGC-1α expression by inhibiting WWP1-mediated ubiquitination degradation of KLF15, thereby restoring mitochondrial function and easing the development of EI.</div></div><div><h3>Conclusion</h3><div>Our study reveals that E2 alleviates EI progression by stabilizing KLF15 protein and restoring mitochondrial function, providing potential targets for EI treatment.</div></div>","PeriodicalId":12227,"journal":{"name":"Experimental cell research","volume":"450 2","pages":"Article 114651"},"PeriodicalIF":3.3,"publicationDate":"2025-06-11","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144279739","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":"Retraction notice to \"Silenced long non-coding RNA activated by DNA damage elevates microRNA-495-3p to suppress atherosclerotic plaque formation via reducing Krüppel-like factor 5\" [Exp. Cell Res. 401 (2021) 112519].","authors":"Dan-Ni Fu, Yu Wang, Li-Jun Yu, Ming-Jie Liu, Dong Zhen","doi":"10.1016/j.yexcr.2025.114633","DOIUrl":"10.1016/j.yexcr.2025.114633","url":null,"abstract":"","PeriodicalId":12227,"journal":{"name":"Experimental cell research","volume":" ","pages":"114633"},"PeriodicalIF":3.3,"publicationDate":"2025-06-10","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144274550","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":"EZH2 in digestive system cancers: Epigenetic regulation, oncogenic interactions, and therapeutic potential","authors":"Ahmed Hjazi ,&nbsp;Ahmed Hussn ,&nbsp;A.K. Kareem ,&nbsp;Mohammad Y. Alshahrani ,&nbsp;H. Malathi ,&nbsp;Priya Priyadarshini Nayak ,&nbsp;Ashish Singh Chauhan ,&nbsp;Jatin Sharma","doi":"10.1016/j.yexcr.2025.114648","DOIUrl":"10.1016/j.yexcr.2025.114648","url":null,"abstract":"<div><div>EZH2 (enhancer of zeste homolog 2) is an important component of the Polycomb Repressive Complex 2 (PRC2) and is essential for the epigenetic regulation of gene expression. EZH2 primarily methylates histone H3 at lysine 27 (H3K27me3) to repress target gene transcription, particularly concerning tumor suppressor genes. The silencing of these genes ultimately promotes cancer by facilitating several important processes, a notable one being epithelial-mesenchymal transition (EMT), which promotes the invasiveness and metastatic potential of cancer cells, particularly in digestive system cancers. In addition to its role in histone modification, EZH2 interacts with diverse noncoding RNA species, including long noncoding RNAs (lncRNAs) and microRNAs, which can influence expression and activity. These interactions form elaborate regulatory pathways through which EZH2 enhances its oncogenic abilities. For example, lncRNAs recruit EZH2 to specific gene promoters and promote EZH2's repressive function to repress important tumor suppressor genes seen in colon, gastric, and esophageal cancers. Also, EZH2 overexpression has been associated with poor prognosis in several cancers, including gastrointestinal cancers. EZH2 overexpression is linked with aggressive tumor behavior and contributes to therapeutic resistance as cancer cells adapt to avoid the effects of traditional cancer therapy. EZH2 allows cancer cells to persist and proliferate in response to therapy by silencing genes that control apoptosis and the cell cycle. Since EZH2 is strongly associated with poor prognosis and therapeutic resistance in digestive cancers, targeting EZH2 will be a highly effective therapeutic strategy. This in-depth review suggests that further efforts will be required to thoroughly characterize the complex molecular networks that involve EZH2, especially with the hope of generating new therapeutic pathways in malignant cancers of the digestive system.</div></div>","PeriodicalId":12227,"journal":{"name":"Experimental cell research","volume":"450 2","pages":"Article 114648"},"PeriodicalIF":3.3,"publicationDate":"2025-06-10","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144271642","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}