Journal of cellular biochemistry最新文献

{"title":"The Role of Hsp72 in Handing Misfolded Proteins Metabolism in Heat-Stressed Cells: Mechanisms and Hypotheses","authors":"Yue Guo,&nbsp;Haotian Lan,&nbsp;Haoying Wang,&nbsp;Xiaoyu Sun,&nbsp;Benge Zou,&nbsp;Wei Zhang,&nbsp;Yu Wang,&nbsp;Xiaowei Wang,&nbsp;Chunying Li,&nbsp;Shiyong Zhu,&nbsp;Rongfeng Cao,&nbsp;Kaiqiang Fu","doi":"10.1002/jcb.70075","DOIUrl":"https://doi.org/10.1002/jcb.70075","url":null,"abstract":"<div>\u0000 \u0000 <p>The accumulation of misfolded proteins within cells, often induced by stress, is a major contributor to cellular dysfunction. Heat shock proteins, which serve as critical chaperone molecules in response to stress-related damage, are essential for maintaining protein homeostasis within cells. In this family of proteins, Heat Shock Protein 72 (Hsp72) stands out for its acute responsiveness to thermal stress. It can swiftly be produced in reaction to the surge of misfolded proteins caused by heat, thus maintaining the equilibrium of intracellular protein metabolism. This analysis explores the function of Hsp72 in maintaining protein homeostasis, focusing on its ability to assist in the refolding of incorrectly folded proteins and to guide their breakdown through the ubiquitin-proteasome and autophagy systems. Furthermore, the potential mechanisms through which cells may eliminate misfolded protein aggregates via the secretory autophagy pathway under heat stress conditions are explored. This study systematically analyzes the various mechanisms by which Hsp72 influences misfolded protein metabolism and discusses the relevance of each pathway in the context of heat stress. Integrating findings from prior laboratory research, it is concluded that Hsp72 plays a pivotal role in regulating misfolded protein metabolism through the secretory autophagy pathway, thereby sustaining intracellular protein homeostasis during heat stress. This investigation expands the functional network of Hsp72 in maintaining protein homeostasis and elucidates the molecular pathways involved in its regulation of misfolded protein metabolism under heat stress, providing a framework for future research on Hsp72's role in cellular recovery from heat stress.</p></div>","PeriodicalId":15219,"journal":{"name":"Journal of cellular biochemistry","volume":"126 11","pages":""},"PeriodicalIF":2.8,"publicationDate":"2025-11-27","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145619257","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":"Rescue of Aging-Dependent Reduction of Claudin-10b Expression by Glutamate in Mouse Intestinal MCE301 Cells","authors":"Miki Tanabe,&nbsp;Shunsuke Matsuda,&nbsp;Yuta Yoshino,&nbsp;Yoshiaki Tabuchi,&nbsp;Toshiyuki Matsunaga,&nbsp;Akira Ikari","doi":"10.1002/jcb.70077","DOIUrl":"10.1002/jcb.70077","url":null,"abstract":"<div>\u0000 \u0000 <p>Paracellular permeability of mineral ions and water in the intestines is restricted by claudins (CLDNs), which are key components of tight junctions (TJs). Glutamate (Glu) plays a role in regulating absorption mechanisms in the intestines, but the effect on paracellular permeability remains unclear. In mouse intestine-derived MCE301 cells, Glu treatment increased the mRNA levels of <i>CLDN10b</i>, while the levels of other CLDNs and zonula occludens-1, a scaffolding protein in TJs, remained unchanged. Similar results were obtained in rat intestine-derived IEC6 cells without CLDN1 and CLDN15. Glu also increased the protein level and TJ localization of CLDN10. The Glu-induced increase in <i>CLDN10b</i> mRNA expression was suppressed by knockdown of taste receptor type 1, T1R1 and T1R3. Glu treatment stimulated Ca²⁺ influx, which was inhibited by BAPTA, a Ca²⁺ chelator, and ebselen, a voltage-dependent Ca²⁺ channel inhibitor. Furthermore, the upregulation of <i>CLDN10b</i> mRNA by Glu was inhibited by BAPTA, ebselen, and rapamycin, an inhibitor of mammalian target of rapamycin (mTOR). These results suggest that Glu upregulates CLDN10b expression in MCE301 cells mediated by a T1R1/T1R3-Ca²⁺-mTOR signaling pathway. The mRNA levels of <i>CLDN10b</i> were decreased in the colon of aged mice and MCE301 cells treated with tenovin-1 (Ten-1), an inducer of cellular senescence. Glu reversed the Ten-1-induced reduction of <i>CLDN10b</i> mRNA and restored paracellular barrier function. These results suggest that Glu enhances the intestinal paracellular barrier function through the regulation of CLDN10b expression.</p>\u0000 </div>","PeriodicalId":15219,"journal":{"name":"Journal of cellular biochemistry","volume":"126 11","pages":""},"PeriodicalIF":2.8,"publicationDate":"2025-11-26","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145604208","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":"In Silico Study of Molecular Docking Between Lactoferrin and Autophagy-apoptosis Genes ATG3, ATG5, and ATG12 and In Vitro Study of Lactoferrin Effect on These Gene Expressions in Breast Cancer","authors":"Seyedeh Fatemeh Noorani,&nbsp;Fatemeh Moradian,&nbsp;Havva Mehralitabar,&nbsp;Mohammed Kuddus","doi":"10.1002/jcb.70072","DOIUrl":"https://doi.org/10.1002/jcb.70072","url":null,"abstract":"<div>\u0000 \u0000 <p>Cancer is a major global health problem. Considering the special role of lactoferrin (Lf) in inhibiting the growth of cancer cells, a new approach has emerged for cancer treatment. The present study aimed to investigate the effect of Lf on the expression level of autophagy-apoptotic genes ATG5, ATG3, and ATG12 in breast cancer cell line MCF7 and an <i>in silico</i> study of the interaction between lactoferrin and the promoter of these genes and their proteins. The survival percentage of MCF7 cells in concentrations of 200, 300, and 500 µg was 94.4%, 91.64%, and 52%, respectively. The expression level of the ATG3 gene in treatment with different concentrations of Lf was increased, but for the ATG5 gene, it decreased. The expression level of the ATG12 gene in cancer cells treated with Lf concentrations of 200 and 300 µg/ml was increased; however, it decreased at the concentration of 500 μg/ml. All concentrations significantly differed from the control (<i>p</i> &lt; 0.05). The interaction of lactoferrin with ATG3, ATG5, and ATG12 proteins showed that the N-lobe region of the lactoferrin interacted with the N-lobe, catalytic domain, and the HR domain of the ATG3 protein, with the HR domain and the UblB domain of the ATG5 protein, and with the C domain of the ATG12 protein. Analysis of HADDOCK data showed that Lf interacted with the promoter of the genes. Lf, in addition to its effect on the expression of the genes, also interacts with the promoter of genes and their protein.</p>\u0000 </div>","PeriodicalId":15219,"journal":{"name":"Journal of cellular biochemistry","volume":"126 11","pages":""},"PeriodicalIF":2.8,"publicationDate":"2025-11-26","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145626643","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":"Potential Mechanisms of Lipid-Soluble Vitamins Alleviate Brain Damage in Preterm Infants: Integration of Network Pharmacology and Molecular Docking","authors":"Xiao Li,&nbsp;Li Liu","doi":"10.1002/jcb.70068","DOIUrl":"10.1002/jcb.70068","url":null,"abstract":"<div>\u0000 \u0000 <p>Vitamin A, E, and other vitamins have been demonstrated to potentially be used in the treatment of brain injury in preterm infants; however, whether all types of vitamins can be utilized for this purpose remains unclear. In this study, we systematically investigated the therapeutic mechanisms of vitamins in preterm infant brain injury using network pharmacology and molecular docking techniques. A total of 23 potential targets for four vitamin components against preterm infant brain injury were identified through public databases. Key genes mediating preterm infant brain injury were obtained via transcriptome analysis of human cells from the GEO database. The intersection of therapeutic targets for brain injury and key genes revealed potential targets for vitamin action in the treatment of preterm infant brain injury. Protein-protein interaction (PPI) analysis identified two key targets (PFKFB3 and PDGFRB). KEGG pathway and GO enrichment analyses elucidated the critical pathways. Molecular docking results indicated that the key targets effectively bind with vitamin components (E and Vitamin K) through hydrogen bonds and hydrophobic interactions. This study theoretically explores the potential mechanisms of vitamin therapy for preterm infant brain injury and provides a preliminary theoretical basis for the development and application of vitamins as potential functional therapeutic agents for preventing brain injury in preterm infants.</p>\u0000 </div>","PeriodicalId":15219,"journal":{"name":"Journal of cellular biochemistry","volume":"126 11","pages":""},"PeriodicalIF":2.8,"publicationDate":"2025-11-24","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145587621","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":"Correction to “Sweet Science: Exploring the Impact of Fructose and Glucose on Brown Adipocyte Differentiation Using Optical Diffraction Tomography”","authors":"","doi":"10.1002/jcb.70074","DOIUrl":"10.1002/jcb.70074","url":null,"abstract":"<p>Journal of Cellular Biochemistry, 2025; 126:e70052, https://doi.org/10.1002/jcb.70052</p><p>In Figure 3, the images we provided were incorrect. The correct images are provided here.</p><p>We apologize for this error.</p>","PeriodicalId":15219,"journal":{"name":"Journal of cellular biochemistry","volume":"126 11","pages":""},"PeriodicalIF":2.8,"publicationDate":"2025-11-18","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1002/jcb.70074","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145541165","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Extracellular Ubiquitin Drives M2 Macrophage Polarization in Multiple Myeloma Through JAK1/STAT3-mediated Transcriptional Activation of CXCR4","authors":"Xi Chen,&nbsp;Nan Hou,&nbsp;Tiancheng Luo,&nbsp;Xinyi Zhou,&nbsp;Dongjian Chen,&nbsp;Wanting Qiang,&nbsp;Jin Liu,&nbsp;Pei Guo,&nbsp;Jing Lu,&nbsp;Juan Du,&nbsp;Haiyan He","doi":"10.1002/jcb.70073","DOIUrl":"10.1002/jcb.70073","url":null,"abstract":"<div>\u0000 \u0000 <p>Macrophage polarization engenders an immunosuppressive microenvironment, thereby facilitating the survival and epithelial-mesenchymal transition (EMT)-like changes of malignant plasma cells. Ubiquitin (Ub), a short polypeptide predominantly involved in proteasome-mediated protein degradation, has been detected extracellularly in body fluids. In certain diseases, it exerts immune-regulatory functions, including the modulation of macrophage polarization. Nevertheless, its immune-regulatory role in multiple myeloma (MM) remains undetermined. This study investigated the role of extracellular ubiquitin (eUb) in macrophage polarization and MM progression. We demonstrated that serum eUb levels were significantly higher in MM patients than in healthy volunteers. Elevated eUb levels were closely associated with a poor prognosis in MM patients. Exposure to eUb induced M2 macrophage polarization, which in turn promoted MM cell proliferation and EMT via the CXCR4/JAK1/STAT3 pathway. Notably, STAT3 was identified as a transcription factor that directly binds to the CXCR4 promoter, enhancing its expression and establishing a positive-feedback loop. Collectively, eUb promotes MM cell proliferation and EMT-like changes by driving M2 macrophage polarization through activation of the CXCR4/JAK1/STAT3 positive-feedback pathway. These findings underscore the pathological significance of eUb in the MM tumor microenvironment and suggest that targeting this pathway may provide novel therapeutic strategies for MM.</p></div>","PeriodicalId":15219,"journal":{"name":"Journal of cellular biochemistry","volume":"126 11","pages":""},"PeriodicalIF":2.8,"publicationDate":"2025-11-12","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145495613","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":"Bmpr2 Loss in the Vascular Endothelium Enhances Neoangiogenesis and Growth of Lung Metastatic Lesions in a Mouse Model of Breast Cancer","authors":"Jordan A. Harry,&nbsp;Sofia I. Skebo,&nbsp;Devon V. Cole,&nbsp;Vincent Dinh,&nbsp;M. Martin VandenBroek,&nbsp;Abby K. Lee,&nbsp;Natasha Camacho,&nbsp;Hollie N. Piepjohn,&nbsp;Victoria Hoskin,&nbsp;Kimberly J. Laverty,&nbsp;Yan Gao,&nbsp;Douglas Quilty,&nbsp;Peter A. Greer,&nbsp;Mark L. Ormiston","doi":"10.1002/jcb.70071","DOIUrl":"10.1002/jcb.70071","url":null,"abstract":"<p>Bone morphogenetic protein-9 (BMP9) has been implicated as a regulator of metastasis and tumor angiogenesis, with contrasting studies demonstrating both pro- and antiangiogenic roles for BMP9 across different cancer cell lines and animal models. However, these works have yet to define the contribution of the type-II BMP receptor (BMPR-II) to these processes, or assess whether the effects of BMP9 are mediated via actions on the endothelium, the tumor, or its microenvironment. Here, we demonstrate that the heterozygous (<i>Bmpr2</i>^{<i>EC+/−</i>}) or homozygous (<i>Bmpr2</i>^{<i>EC−/−</i>}) deletion of BMPR-II in the pulmonary endothelium is associated with increased overall burden and vascularization of metastases in the lungs of mice subjected to the EO771 orthotopic engraftment model of metastatic breast cancer. These increases, relative to <i>Bmpr2</i>^<i>EC+/+</i> littermates, were observed despite equivalent primary mammary tumor growth across mice of all genotypes. <i>In vitro</i>, secreted factors or extracellular matrix components from BMPR-II-silenced human pulmonary arterial endothelial cells (HPAECs) did not alter EO771 proliferation relative to controls. However, endothelial BMPR-II depletion did eliminate the capacity of BMP9 to suppress both HPAEC migration to VEGF₁₆₅ and EO771 transmigration across an HPAEC monolayer. In a tail vein injection model, the short-term establishment of EO771 cell metastatic lesions was equivalent in the lungs of female <i>Bmpr2</i>^{<i>EC+/−</i>} and <i>Bmpr2</i>^{<i>EC−/−</i>} mice, relative to <i>Bmpr2</i>^<i>EC+/+</i> controls, suggesting that the enhanced lung tumor burden observed in orthotopically implanted mice with endothelial <i>Bmpr2</i> deletion is likely a consequence of enhanced tumor vascularization, rather than altered lung retention and engraftment. Our findings identify an important role for endothelial BMPR-II signaling in regulating the vascularization of metastatic lesions in the lungs.</p>","PeriodicalId":15219,"journal":{"name":"Journal of cellular biochemistry","volume":"126 11","pages":""},"PeriodicalIF":2.8,"publicationDate":"2025-11-12","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12606701/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145495648","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"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: Kaempferol Induces Apoptosis in Two Different Cell Lines via Akt Inactivation, Bax and SIRT3 Activation, and Mitochondrial Dysfunction†","authors":"","doi":"10.1002/jcb.70070","DOIUrl":"https://doi.org/10.1002/jcb.70070","url":null,"abstract":"<p><b>EXPRESSION OF CONCERN</b>: G. Marfe, M. Tafani, M. Indelicato, P. Sinibaldi-Salimei, V. Reali, B. Pucci, M. Fini and M. A. Russo “Kaempferol Induces Apoptosis in Two Different Cell Lines via Akt Inactivation, Bax and SIRT3 Activation, and Mitochondrial Dysfunction†,” <i>Journal of Cellular Biochemistry</i> 106, no. 4 (2009): 643–650, https://doi.org/10.1002/jcb.22044.</p><p>This Expression of Concern is for the above article, published online on 21 January 2009 in Wiley Online Library (wileyonlinelibrary.com), and has been issued by agreement between the journal Editor-in-Chief, Christian Behl; and Wiley Periodicals LLC. The Expression of Concern has been issued due to the identification of duplicated β-actin bands for the K562 and U937 cell lines in Figure 6 A. The authors agree that the bands appear very similar and believe this resulted from figure mismanagement. Due to the time that has elapsed since the study was conducted, the authors were unable to produce the original blots. The editors are satisfied that the article's conclusions are not affected but have decided to issue an Expression of Concern to inform and alert readers to the duplication.</p>","PeriodicalId":15219,"journal":{"name":"Journal of cellular biochemistry","volume":"126 11","pages":""},"PeriodicalIF":2.8,"publicationDate":"2025-11-11","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1002/jcb.70070","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145479865","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"SIRT1 in Aging and Diseases","authors":"Altaf A. Abdulkhaliq,&nbsp;Glowi Alasiri,&nbsp;Johra Khan,&nbsp;Amir Ajoolabady,&nbsp;Jaakko Tuomilehto,&nbsp;Nils Henninger,&nbsp;Suhad Bahijri,&nbsp;Domenico Pratico,&nbsp;Anwar Borai,&nbsp;Bahauddeen M. Alrfaei,&nbsp;Bonglee Kim,&nbsp;Jun Ren","doi":"10.1002/jcb.70069","DOIUrl":"10.1002/jcb.70069","url":null,"abstract":"<div>\u0000 \u0000 <p>Sirtuin 1 (SIRT1) is a NAD⁺-dependent deacetylase belonging to the sirtuin family, which regulates a broad spectrum of cellular processes through deacetylation of both histones in the nucleus and non-histone proteins in the cytosol. Accumulating evidence indicates that biological aging is associated with a marked decline in the expression and activation of <i>SIRT1</i>/SIRT1, which contributes to the onset and progression of various age-related diseases. Conversely, activation of SIRT1 has been shown to mitigate aging-associated cellular anomalies including mitochondrial dysfunction, oxidative stress, and cellular senescence. In this review, we summarize recent advances in understanding the role of SIRT1 in aging and age-associated diseases across various experimental models, and we also discuss current limitations in the field as well as potential future research direction.</p></div>","PeriodicalId":15219,"journal":{"name":"Journal of cellular biochemistry","volume":"126 10","pages":""},"PeriodicalIF":2.8,"publicationDate":"2025-10-16","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145300595","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":"Ferroptosis in Spinal Cord Injury: Research Progress and Novel Insights","authors":"Shizhe Li,&nbsp;Shutao Gao,&nbsp;Yukun Hu,&nbsp;Guangxu Sun,&nbsp;Jingsheng Feng,&nbsp;Weibin Sheng","doi":"10.1002/jcb.70067","DOIUrl":"https://doi.org/10.1002/jcb.70067","url":null,"abstract":"<div>\u0000 \u0000 <p>Spinal cord injury (SCI) is a severe condition affecting the central nervous system that often leads to varying degrees of motor and sensory impairment. Acute primary SCI is often managed with early surgical intervention; however, secondary SCI generally has a poor prognosis owing to the lack of effective drug therapy, complex pathophysiological processes, and inherent challenges of neural repair. Ferroptosis, a novel form of programmed cell death, is characterised by oxidative damage resulting from iron-mediated accumulation of reactive oxygen species (ROS) and lipid peroxidation (LPO) within cells. This type of cell death is prevalent in various pathological processes. Although research on ferroptosis in SCI is still emerging, some inhibitors (such as target proteins and natural compounds) have shown promising results in preclinical studies. Targeting ferroptosis may be a potential strategy for treating SCI. This paper reviews the current state of research on ferroptosis in SCI by analysing recent literature and proposes future research directions, aiming to provide new insights into SCI treatment.</p></div>","PeriodicalId":15219,"journal":{"name":"Journal of cellular biochemistry","volume":"126 10","pages":""},"PeriodicalIF":2.8,"publicationDate":"2025-10-03","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145204730","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}