FEBS Open BioPub Date : 2026-09-04Epub Date: 2026-06-27DOI: 10.1002/2211-5463.70280
Otmane Lamrabet, Pierre Cosson
{"title":"How phagocytic cells kill bacteria: Lessons from a professional killer","authors":"Otmane Lamrabet, Pierre Cosson","doi":"10.1002/2211-5463.70280","DOIUrl":"10.1002/2211-5463.70280","url":null,"abstract":"<p>Professional phagocytic cells such as neutrophils and macrophages, as well as free-living soil amoebae like <i>Dictyostelium discoideum</i>, employ evolutionarily conserved mechanisms to ingest and kill bacteria. Ingested bacteria are killed in phagosomes by four main antibacterial systems: production of reactive oxygen and nitrogen species, accumulation of bactericidal ions, deployment of lysosomal enzymes, and release of membrane-permeabilizing peptides. Despite extensive studies, important questions persist. How complete is the list of known antibacterial mechanisms? What is their relative contribution to bacterial destruction? How specific are they for different bacterial species? This review examines how <i>D. discoideum</i> amoebae and mammalian phagocytes ingest and eliminate non-pathogenic bacteria, focusing on three specific elements: the dual role of lysozyme, the specificity of antibacterial mechanisms, and the redundancy of the antibacterial arsenal. Overall, our current knowledge highlights the sophisticated strategies employed by phagocytes against diverse microorganisms. It also provides a framework to study the more complex interactions between phagocytic cells and pathogenic bacteria.</p>","PeriodicalId":12187,"journal":{"name":"FEBS Open Bio","volume":"16 9","pages":"1637-1644"},"PeriodicalIF":2.7,"publicationDate":"2026-09-04","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13399256/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148338345","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
{"title":"Identifying gene expression signatures for risk stratification of postoperative adjuvant chemotherapy in colorectal cancer","authors":"Mayuko Otomo, Keisuke Okuno, Shuichi Watanabe, Sakiko Oba, Hiroyasu Kagawa, Masanori Tokunaga, Daisuke Ban, Yusuke Kinugasa","doi":"10.1002/2211-5463.70243","DOIUrl":"10.1002/2211-5463.70243","url":null,"abstract":"<p>Clinical risk stratification for postoperative recurrence in patients with pathological stage II (pStage II) colorectal cancer (CRC) is essential for guiding the use of postoperative adjuvant chemotherapy (ACT). In this study, we identified novel prognostic gene expression biomarkers in patients with pStage II CRC and developed a new risk stratification framework for ACT decision-making. First, genome-wide biomarker discovery was conducted to identify prognostic gene expression biomarkers associated with recurrence risk in pStage II CRC. This analysis identified 10 differentially expressed genes as potential biomarkers for recurrence. The efficacy of these biomarkers was then tested using 188 clinical surgical specimens obtained from patients with pStage II CRC. A predictive panel was developed using qRT-PCR and used to assess 93 clinical specimens with an area under the curve (AUC) of 0.82, and its performance was further validated in an independent cohort (<i>n</i> = 95). By incorporating key clinicopathological features, a Gene expression-based Prediction of Recurrence in pStage II CRC (GPRSC) signature was developed, which robustly predicted postoperative recurrence (AUC: 0.80). Finally, combining the GPRSC signature, microsatellite instability status, and conventional criteria, we developed a novel risk stratification system for postoperative ACT decision-making in pStage II CRC. Overall, we identified novel gene expression biomarkers and developed a prognostic signature that informs clinical decision-making regarding postoperative ACT in patients with pStage II CRC.</p>","PeriodicalId":12187,"journal":{"name":"FEBS Open Bio","volume":"16 9","pages":"1813-1824"},"PeriodicalIF":2.7,"publicationDate":"2026-09-04","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13398948/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147581090","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
FEBS Open BioPub Date : 2026-09-04Epub Date: 2026-04-06DOI: 10.1002/2211-5463.70244
Tokio Takaji, Yurika Nakanishi, Nobuhiro Nakamura
{"title":"YIPFα1A expression is regulated by multilayered molecular mechanisms","authors":"Tokio Takaji, Yurika Nakanishi, Nobuhiro Nakamura","doi":"10.1002/2211-5463.70244","DOIUrl":"10.1002/2211-5463.70244","url":null,"abstract":"<p>Yip domain family (YIPF) proteins are five-pass transmembrane proteins that localize primarily to the Golgi apparatus. These proteins assemble into higher-order complexes with each <i>α</i>-subunit pairing specifically with a <i>β</i>-subunit to form a dimer which then assemble into complexes with two to four dimers. Notably, <i>β</i>-subunit expression depends on the corresponding <i>α</i>-subunit partner, and conventional transient overexpression of <i>α</i>-subunits has been extremely inefficient, hindering deeper analysis of YIPF complexes. To identify the cause of poor exogenous expression, we examined YIPF gene features and found two properties correlated with low expression: (i) rare-codon enrichment in the CDS and (ii) extended 3′ UTRs. Experimental analyses focusing on YIPFα1A revealed that rare-codon enrichment suppresses expression mainly at the mRNA level, consistent with translation-coupled mRNA decay, whereas inclusion of the native 3′ UTR enhances expression by increasing mRNA abundance. Deletion mapping further showed that a proximal 3′ UTR segment (51–150) is necessary and sufficient for mRNA stabilization, thereby elevating both mRNA and protein levels. Conversely, a distal 3′ UTR fragment (1116–2230) increased mRNA but not protein levels, suggesting translational repression resulting in a reduced protein-to-mRNA ratio. Together, these findings explain the discrepancy between endogenous and exogenous YIPFα1A expression and propose a multilayered regulatory model in which rare codons decrease mRNA, the proximal 3′ UTR stabilizes mRNA, and the distal 3′ UTR reduces translation.</p><p>\u0000 </p>","PeriodicalId":12187,"journal":{"name":"FEBS Open Bio","volume":"16 9","pages":"1669-1690"},"PeriodicalIF":2.7,"publicationDate":"2026-09-04","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13398756/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147622151","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
FEBS Open BioPub Date : 2026-09-04Epub Date: 2026-04-24DOI: 10.1002/2211-5463.70246
Daniella Beiner, Hainan Zhu, Carol Christine Bosholm, Heuy-Ching Wang, Tracy Criswell, Anthony Atala, Jian-Xing Ma, Yuanyuan Zhang
{"title":"Derivation and characterization of retinal pigment epithelium from urine-derived iPSCs","authors":"Daniella Beiner, Hainan Zhu, Carol Christine Bosholm, Heuy-Ching Wang, Tracy Criswell, Anthony Atala, Jian-Xing Ma, Yuanyuan Zhang","doi":"10.1002/2211-5463.70246","DOIUrl":"10.1002/2211-5463.70246","url":null,"abstract":"<p>Age-related macular degeneration (AMD), particularly its dry form, is a leading cause of irreversible vision loss due to retinal pigment epithelium (RPE) dysfunction and loss. Addressing this unmet therapeutic need requires non-invasive strategies for generating patient-specific RPE cells. This study reports the successful generation and initial characterization of RPE cells derived from urine-derived induced pluripotent stem cells (u-iPSC-RPE). Urine-derived stem cells (USCs) were isolated from healthy individuals and comprehensively characterized, confirming strong expression of renal progenitor makers and mesenchymal stem cell markers, while lacking standard hematopoietic markers. USCs were reprogrammed into iPSCs using the integration-free Sendai virus expressing the Yamanaka factors. The reprogrammed u-iPSC clones displayed characteristic pluripotency marker expression and demonstrated clearance of the Sendai virus by later passages. Subsequently, these u-iPSCs were efficiently differentiated into RPE cells, exhibiting characteristic hexagonal morphology and pigmentation which was confirmed by the expression of key RPE-specific proteins. Our findings demonstrate the feasibility and reliability of generating patient-specific u-iPSC-RPE cells from readily accessible USCs providing a foundation for future studies to investigate their functional potential for retinal disease modeling and therapeutic applications for AMD.</p>","PeriodicalId":12187,"journal":{"name":"FEBS Open Bio","volume":"16 9","pages":"1691-1707"},"PeriodicalIF":2.7,"publicationDate":"2026-09-04","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13398809/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147766770","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
{"title":"Establishing an assay to evaluate d-amino acid oxidase enzyme kinetics and inhibition using WST-8 redox dye","authors":"Kahoko Miyake, Yuki Enoki, Yuka Nakazawa, Kazuaki Taguchi, Kazuaki Matsumoto","doi":"10.1002/2211-5463.70217","DOIUrl":"10.1002/2211-5463.70217","url":null,"abstract":"<p><span>d</span>-Amino acid oxidase (DAO) inhibitors are novel candidate therapeutic agents for neurodegenerative diseases. In this study, a novel inhibition assay using WST-8 as a detection reagent was developed and its effectiveness for evaluating redox-based enzyme kinetics was tested. Furthermore, using this assay, we also investigated the inhibitory activities of uremic toxins and endogenous amino acid metabolites. Briefly, a mixture of DAO, WST-8, and <span>d</span>-amino acids was allowed to react in phosphate buffer and DAO activity was detected as an increase in absorbance when both <span>d</span>-serine and DAO were present. However, as reducing compounds could potentially cause false-positive results, we confirmed that the detection of DAO activity in this system was mediated by the redox reaction of WST-8. Critically, we verified that this assay could be used to evaluate the inhibitory activity of known DAO inhibitors, including uremic toxins which showed weak DAO inhibition. This study establishes an alternative assay system that can be utilized for assessing DAO-inhibitory activity and other enzymatic reactions mediated by redox reactions.</p>","PeriodicalId":12187,"journal":{"name":"FEBS Open Bio","volume":"16 9","pages":"1645-1656"},"PeriodicalIF":2.7,"publicationDate":"2026-09-04","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13398905/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147276080","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
FEBS Open BioPub Date : 2026-09-04Epub Date: 2026-03-24DOI: 10.1002/2211-5463.70237
Hana Nopia, Masahiro Kimura, Daisuke Kurimoto, Atsushi Sato
{"title":"Suppression of lung adenocarcinoma migration through organelle alkalization by human lactoferrin – albumin fusion","authors":"Hana Nopia, Masahiro Kimura, Daisuke Kurimoto, Atsushi Sato","doi":"10.1002/2211-5463.70237","DOIUrl":"10.1002/2211-5463.70237","url":null,"abstract":"<p>The fusion of human serum albumin with human lactoferrin (hLF-HSA) exerts strong anti-migratory effects in human lung adenocarcinoma cells through matrix metalloproteinase 1 (MMP1) downregulation. We demonstrate that hLF-HSA disrupts organelle pH homeostasis via Na<sup>+</sup>/H<sup>+</sup> exchanger 7 (NHE7) upregulation, inducing organelle alkalization in the Golgi apparatus. This organelle dysfunction alters the Golgi-mediated secretome, leading to MMP1 downregulation and suppression of cell migration. hLF-HSA-induced MMP1 downregulation also reverses epithelial-mesenchymal transition (EMT), further suppressing migration. Additionally, hLF-HSA-driven activation of caveolae-mediated endocytosis (CavME) signaling downregulated MMP1 expression without NHE7 upregulation. These findings highlight that hLF-HSA–mediated disruption of organelle pH regulation and CavME activation represents a potential strategy to suppress cancer cell migration.</p><p>\u0000 </p>","PeriodicalId":12187,"journal":{"name":"FEBS Open Bio","volume":"16 9","pages":"1786-1800"},"PeriodicalIF":2.7,"publicationDate":"2026-09-04","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13399163/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147503469","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
FEBS Open BioPub Date : 2026-09-04Epub Date: 2026-04-19DOI: 10.1002/2211-5463.70253
Heyong Yin, Ziyang Yuan, Wenli Jiang, Ai Guo
{"title":"Early-life high-fat diet exposure increases Achilles tendon stiffness and induces transcriptomic alterations","authors":"Heyong Yin, Ziyang Yuan, Wenli Jiang, Ai Guo","doi":"10.1002/2211-5463.70253","DOIUrl":"10.1002/2211-5463.70253","url":null,"abstract":"<p>High-fat diet (HFD) exposure is a recognized risk factor for tendinopathy and impaired tendon healing in adults, yet its effects on baseline tendon properties following early-life exposure remain poorly understood. In this study, we investigated the structural, biomechanical, and transcriptomic characteristics of Achilles tendons in 12-week-old rat offspring born to dams fed an HFD or a normal diet during gestation. Compared with controls, HFD-exposed tendons exhibited a significant reduction in anteroposterior diameter on sagittal ultrasound imaging. However, histological assessment revealed comparable cellular density and collagen fiber organization between groups. Biomechanically, HFD exposure was associated with a significant increase in tendon stiffness, while the maximum tensile load was not significantly altered. Transcriptomic profiling identified 980 differentially expressed genes, including a marked downregulation of key tenogenic markers such as Scx and Eya2, along with an enrichment of pathways related to extracellular matrix remodeling and inflammation. Gene set enrichment further revealed an upregulation of inflammatory response, adipogenesis, and osteoblast differentiation signatures. Together, these findings demonstrate that early-life HFD exposure induces biomechanical and molecular alterations in intact Achilles tendons, suggesting compromised tendon quality that may increase susceptibility to mechanical overload and injury later in life.</p>","PeriodicalId":12187,"journal":{"name":"FEBS Open Bio","volume":"16 9","pages":"1741-1751"},"PeriodicalIF":2.7,"publicationDate":"2026-09-04","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13398776/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147722235","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
FEBS Open BioPub Date : 2026-09-04DOI: 10.1002/2211-5463.70335
Sara Fuentes, Miguel A. De la Rosa
{"title":"Early Career Reviewer Hub: Paving the way for the next generation of peer reviewers","authors":"Sara Fuentes, Miguel A. De la Rosa","doi":"10.1002/2211-5463.70335","DOIUrl":"https://doi.org/10.1002/2211-5463.70335","url":null,"abstract":"<p><i>FEBS Open Bio</i> is pleased to announce the launch of the Early Career Reviewer Hub, a new initiative designed to provide professional training and first-hand experience to Early Career Researchers (ECRs) interested in taking part in the peer-review process. We hope that, through this new programme and our focus on Research Protocols, we will continue to support and contribute to the professional development of early career molecular life scientists.</p>","PeriodicalId":12187,"journal":{"name":"FEBS Open Bio","volume":"16 9","pages":"1634-1636"},"PeriodicalIF":2.7,"publicationDate":"2026-09-04","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1002/2211-5463.70335","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148878225","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
FEBS Open BioPub Date : 2026-09-04Epub Date: 2026-03-26DOI: 10.1002/2211-5463.70239
Saira Munshani, Eiman Y. Ibrahim, Rozalyn L. Rodwin, Leah M. Ferrucci, Kim Blenman, Maryam Lustberg, Barbara E. Ehrlich
{"title":"Blood-based proteomic profiling reveals context-dependent changes in BCL2-associated signaling during taxane therapy in breast cancer patients","authors":"Saira Munshani, Eiman Y. Ibrahim, Rozalyn L. Rodwin, Leah M. Ferrucci, Kim Blenman, Maryam Lustberg, Barbara E. Ehrlich","doi":"10.1002/2211-5463.70239","DOIUrl":"10.1002/2211-5463.70239","url":null,"abstract":"<p>The quality of life for many cancer survivors is compromised due to severe, long-lasting side effects of chemotherapy. As part of a pilot, prospective, non-interventional study to examine the side effects of chemotherapy in breast cancer patients, we examined the change in protein expression in blood collected from patients before and after treatment with taxanes for 12 weeks. Protein expression was measured with reverse phase proteomic arrays (RPPA), which revealed divergent changes in apoptosis, senescence, and calcium signaling-related proteins depending on treatment setting (neoadjuvant vs. adjuvant). The largest change identified was BCL2 (B-cell lymphoma 2), a founding member of the BCL2 family of proteins that regulate apoptosis. Other proteins regulated by BCL2, including RB1 (retinoblastoma protein 1) and NLRP3 (NLR family pyrin domain containing 3) changed significantly over the course of treatment. These differences are consistent with intracellular calcium signaling dysregulation and activation of stress-response pathways that overlap with senescent-associated secretory phenotype (SASP)-like signaling, which has been implicated in cancer recurrence. To contextualize these observations, we generated Kaplan–Meier survival curves using publicly available proteomics data from The Cancer Proteome Atlas (TCPA). This work aims to demonstrate how blood-based proteomics can serve as a non-invasive method to monitor systemic physiological shifts during cancer therapy, offering a framework for generating hypotheses about chemotherapy timing and long-term outcomes.</p>","PeriodicalId":12187,"journal":{"name":"FEBS Open Bio","volume":"16 9","pages":"1801-1812"},"PeriodicalIF":2.7,"publicationDate":"2026-09-04","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13398688/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147510754","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
FEBS Open BioPub Date : 2026-09-04Epub Date: 2026-04-07DOI: 10.1002/2211-5463.70245
Debora Singer, Angelique Kragl, Katrin Ziems, Juliane Glaubitz, Sophie Grammbauer, Susanne Hildebrandt, Mladen V. Tzvetkov, Gabriele Jedlitschky
{"title":"Identifying transcription factors controlling the basal expression of human MRP4 highlights a substantial role for Sp1","authors":"Debora Singer, Angelique Kragl, Katrin Ziems, Juliane Glaubitz, Sophie Grammbauer, Susanne Hildebrandt, Mladen V. Tzvetkov, Gabriele Jedlitschky","doi":"10.1002/2211-5463.70245","DOIUrl":"10.1002/2211-5463.70245","url":null,"abstract":"<p>The multidrug resistance protein 4 (MRP4/ABCC4) is a versatile efflux pump, known to transport several drugs but also signaling molecules such as cyclic nucleotides and lipid mediators. Based on this substrate spectrum and its broad tissue distribution, MRP4 plays a significant physiological and pathophysiological role in both the cardiovascular and oncological fields. However, the determinants of its gene expression are still incompletely defined. This study aimed to identify key regulatory elements and transcription factors that are essential for basal <i>MRP4</i> expression. Using luciferase reporter assays with a series of 5′-deletion constructs, we identified a region upstream of the transcription start site as crucial for basal expression across diverse cell types. This region is evolutionary highly conserved and contains putative binding sites for Sp1 and Ets transcription factors. Site-directed mutagenesis of both binding elements resulted in a significant decrease in the promoter activity in HeLa and megakaryoblastic M07e cells. The binding of Sp1 to this region was further confirmed by electrophoretic mobility shift and chromatin immunoprecipitation assays. Finally, siRNA knockdown of Sp1 led to a significant decrease in MRP4 protein levels and function. In summary, we show that Sp1 binds to the <i>MRP4</i> promoter and plays an essential role in the basal expression of <i>MRP4</i>, with Ets factors also potentially cooperating in this regulation.</p>","PeriodicalId":12187,"journal":{"name":"FEBS Open Bio","volume":"16 9","pages":"1825-1839"},"PeriodicalIF":2.7,"publicationDate":"2026-09-04","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13398795/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147627612","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}