Journal of Gene Medicine最新文献

{"title":"Empagliflozin Ameliorates Angiotensin II-Induced Left Ventricular Diastolic Dysfunction by Suppressing EndoMT via PI3K/AKT/eNOS Signaling.","authors":"Dong-Li Shen, Zi-Mu Wang, Yan-Yan Wang, Zhong-Lei Xie, Shuai Yuan, Bao-Zhen Qi, Shun Yao, Xiao-Tong Cui, Yu Song, Xue-Ting Han, Jun-Bo Ge, Jing-Min Zhou","doi":"10.1002/jgm.70096","DOIUrl":"https://doi.org/10.1002/jgm.70096","url":null,"abstract":"<p><strong>Background: </strong>The SGLT2 inhibitor empagliflozin (EMPA) has been found to reduce the combined risk of cardiovascular death or hospitalization for heart failure in patients with or without reduced left ventricular ejection fraction, irrespective of diabetes status. The underlying mechanisms remain to be elucidated. Endothelial-to-mesenchymal transition (EndoMT) has been reported to play a pivotal role in the microvascular rarefaction. This study aimed to evaluate the effect of EMPA on angiotensin II (Ang II)-induced left ventricular dysfunction and to explore the underlying mechanism.</p><p><strong>Methods: </strong>In vivo, C57BL/6J mice were infused with saline or Ang II (1.5 mg/kg/day) and subsequently treated with or without EMPA (10 mg/kg) for 2 weeks. mRNA sequencing and gene set enrichment analysis (GSEA) indicated that the PI3K/AKT/eNOS signalling pathway may mediate the protective effects of empagliflozin in heart failure with preserved ejection fraction (HFpEF). Finally, in vitro, PI-103 was used to treat cells, and immunofluorescence, western blotting, qPCR, and other methods were used to verify whether empagliflozin exerts its effects through the PI3K/AKT/eNOS pathway.</p><p><strong>Results: </strong>In vivo, the mice treated with Ang II exhibited left ventricular dysfunction, increased microvascular rarefaction, and EndoMT, all of which were attenuated by EMPA treatment. In vitro, primary cardiac microvascular endothelial cells (CMECs) exposed to Ang II showed increased EndoMT, which was significantly inhibited by EMPA. EMPA also reversed the downregulation of PI3K/AKT/eNOS signalling and nitric oxide (NO) levels. PI-103 abrogated the anti-EndoMT effects of EMPA in CMECs.</p><p><strong>Conclusions: </strong>Our study suggested that EMPA can protect against Ang II-induced left ventricular dysfunction and microvascular rarefaction by suppressing EndoMT via PI3K/AKT/eNOS signalling.</p>","PeriodicalId":56122,"journal":{"name":"Journal of Gene Medicine","volume":"28 5","pages":"e70096"},"PeriodicalIF":2.2,"publicationDate":"2026-05-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147790275","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"CD74 Affects Ferroptosis in Traumatic Brain Injury by Modulating the Nrf2/HO-1 Signaling Pathway.","authors":"GuangWei Sun, Jie Li, Meng Wang, Kun Lu, DanDan Liu, ChangLong Hu, Tao Qiu","doi":"10.1002/jgm.70094","DOIUrl":"https://doi.org/10.1002/jgm.70094","url":null,"abstract":"<p><strong>Objective: </strong>This study aimed to explore whether CD74 participates in regulating ferroptosis and to clarify the related mechanisms in traumatic brain injury (TBI).</p><p><strong>Methods: </strong>A TBI rat model was generated using controlled cortical impact. The ferroptosis inducer RSL-3, the inhibitor Liproxstatin-1 (Lip-1), and lentiviral vectors targeting CD74 or Nrf2 were injected into the lateral ventricle. Knockdown efficiency of the lentiviral vectors was verified by RT-qPCR. Motor performance was evaluated using the foot fault test, neurobehavioral function via mNSS scoring, brain water content using the wet-dry method, iron deposition in cortical tissues by Perls' Blue staining, Fe²⁺ levels with an iron assay kit, degenerating neurons by Fluoro-Jade C staining, and Nrf2/HO-1 pathway protein expression via Western blot.</p><p><strong>Results: </strong>TBI rats displayed increased foot faults, elevated mNSS scores, increased brain water content, higher Fe²⁺ levels, more iron-positive cells, and greater numbers of degenerating neurons in the cerebral cortex. Lip-1 or CD74 downregulation alleviated TBI-related changes, whereas RSL-3 or CD74 upregulation worsened them. Downregulating CD74 enhanced Nrf2/HO-1 pathway activity, and Nrf2 knockdown counteracted the benefits of CD74 downregulation.</p><p><strong>Conclusion: </strong>Reducing CD74 expression ameliorates ferroptosis in TBI by activating the Nrf2/HO-1 signaling axis.</p>","PeriodicalId":56122,"journal":{"name":"Journal of Gene Medicine","volume":"28 5","pages":"e70094"},"PeriodicalIF":2.2,"publicationDate":"2026-05-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147823798","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Correction to “De Novo Missense Variant in TP63 Gene: Insights on Clinical and Molecular Investigations”","authors":"","doi":"10.1002/jgm.70093","DOIUrl":"10.1002/jgm.70093","url":null,"abstract":"<p>\u0000 <span>J. Chen</span>, <span>X. Xi</span>, <span>X. Xu</span>, and <span>Y. Lin</span>, “ <span>De Novo Missense Variant in <i>TP63</i> Gene: Insights on Clinical and Molecular Investigations</span>,” <i>Journal of Gene Medicine</i> <span>27</span>, no. <span>11</span> (<span>2025</span>): e70055, https://doi.org/10.1002/jgm.70055.\u0000 </p><p>In the originally published version of this article, Figure 2A contained a facial photograph in which the patient's eyes were inadvertently left unobscured. In addition, visual markers (arrows) intended to indicate specific clinical features in Figure 2B and Figure 2D were not consistently displayed in the earlier version of the figure. Furthermore, because the pedigree was simplified to a two-generation presentation in the final revised version, the proband identifier in the Figure 2 legend should be updated from (Ⅲ:12) to (II:3).</p><p>To address these issues, Figure 2 has been replaced with an updated version in which the patient's eyes in Figure 2A are appropriately obscured and the intended visual markers (arrows) in Figure 2B and Figure 2D are correctly shown. In addition, the proband identifier in the Figure 2 legend should be updated from (III:12) to (II:3). The corrected Figure 2 is provided below.</p><p>We apologize for this error.</p>","PeriodicalId":56122,"journal":{"name":"Journal of Gene Medicine","volume":"28 4","pages":""},"PeriodicalIF":2.2,"publicationDate":"2026-04-14","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1002/jgm.70093","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147678872","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"CRISPR–Cas Systems in Human Disease Therapy: Advances, Clinical Applications, Limitations, and Future Directions","authors":"Gedion Mengistu","doi":"10.1002/jgm.70091","DOIUrl":"10.1002/jgm.70091","url":null,"abstract":"<div>\u0000 \u0000 <p>CRISPR–Cas systems have emerged as versatile platforms for targeted genome and transcriptome engineering, enabling precise manipulation of disease-associated genetic pathways. Continued advances in CRISPR technologies including base editing, prime editing, and epigenome modulation have expanded therapeutic possibilities beyond nuclease-mediated DNA cleavage, allowing programmable gene correction and regulation. Early clinical studies demonstrate sustained therapeutic benefit in selected monogenic disorders and highlight the feasibility of both ex vivo and in vivo editing strategies. However, clinical translation remains constrained by challenges such as off-target activity, delivery inefficiency, immune responses to Cas proteins, editing heterogeneity, and uncertainties regarding long-term safety. This review critically synthesizes recent advances in CRISPR–Cas systems for human disease therapy, integrating molecular innovations, delivery strategies, clinical progress, and ethical considerations. By evaluating both technological achievements and unresolved limitations, this article outlines key priorities for advancing CRISPR-based therapeutics toward safe, effective, and equitable precision medicine.</p>\u0000 </div>","PeriodicalId":56122,"journal":{"name":"Journal of Gene Medicine","volume":"28 4","pages":""},"PeriodicalIF":2.2,"publicationDate":"2026-04-08","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147640918","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Vitamin D Mitigates Klebsiella pneumoniae-Induced Pneumonia by Regulating Macrophage Polarization Through miR-223/ACSL3 Axis-Mediated Lipid Metabolism Reprogramming.","authors":"Jiajia Hu, Yushen Lin, Wanrong Guo, Jingcong Zhang, Benquan Wu, Yanhong Wang","doi":"10.1002/jgm.70092","DOIUrl":"10.1002/jgm.70092","url":null,"abstract":"<p><strong>Background: </strong>Pneumonia caused by Klebsiella pneumonia (Kp) poses a significant risk to global public health. Vitamin D may reduce Kp infection risk and improve prognosis through immunomodulation. This study aimed to validate the treatment effects of Vitamin D and explore its regulatory mechanism in Kp-pneumonia.</p><p><strong>Methods: </strong>In this study, a murine model of Kp-induced pneumonia and the MH-S alveolar macrophage cell line were used. Experimental assays included RT-qPCR, Western blot, TUNEL assay, ELISA, flow cytometry, dual-luciferase reporter assay, and metabolic analyses (FAO activity, Seahorse XF Glycolysis Stress Test).</p><p><strong>Results: </strong>The results showed that vitamin D administration mitigated Kp-induced lung injury in mice. Mechanically, vitamin D alleviated inflammation by inhibiting macrophage M1 polarization. Vitamin D exerted its effects by upregulating miR-223, which directly targeted and suppressed ACSL3 expression. In macrophages, miR-223 overexpression alleviated macrophage apoptosis and M1 polarization by downregulating ACSL3. Knockdown of ACSL3 induced a shift to M2 polarization by enhancing FAO and suppressing glycolysis. In vivo, miR-223 overexpression alleviated Kp-induced lung injury by downregulating ACSL3.</p><p><strong>Conclusion: </strong>In conclusion, vitamin D induces macrophage M2 polarization by upregulating miR-223, which inhibits ACSL3, leading to lipid metabolism reprogramming. This novel axis represents a potential therapeutic strategy for Kp-induced pneumonia.</p>","PeriodicalId":56122,"journal":{"name":"Journal of Gene Medicine","volume":"28 4","pages":"e70092"},"PeriodicalIF":2.2,"publicationDate":"2026-04-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147724723","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Further Evidence for LRRC7 Gene Involvement in Neurodevelopmental Disorder: A Novel Variant","authors":"Shazia Khan,&nbsp;Muhammad Bilal,&nbsp;Hammal Khan,&nbsp;Qamre Alam,&nbsp;Ali Bin Thani,&nbsp;Muhammad Umair","doi":"10.1002/jgm.70090","DOIUrl":"10.1002/jgm.70090","url":null,"abstract":"<div>\u0000 \u0000 \u0000 <section>\u0000 \u0000 <h3> Background</h3>\u0000 \u0000 <p>Neurodevelopmental disorders (NDDs) are clinically heterogeneous conditions with complex etiologies and limited therapeutic options. Here, we investigated a proband presenting global developmental delay (GDD), tonic seizures, failure to thrive, mild microcephaly, intellectual disability (ID), and hypotonia.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Methods</h3>\u0000 \u0000 <p>Exome sequencing (ES), followed by Sanger sequencing, was performed for molecular diagnosis. Gene expression was assessed by reverse-transcriptase quantitative PCR (RT-qPCR), and 3D protein modeling was performed.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Results</h3>\u0000 \u0000 <p>ES revealed a novel de novo (heterozygous) missense variant [c.2660C&gt;T; p.(Pro887Leu)], in <i>LRRC7</i> (NM_001370785.2) gene, located in exon 18, which may contribute to the proband's phenotype. The identified variant was classified as variant of uncertain significant (VUS) according to the American College of Medical Genetics and Genomics Guidelines (ACMG). RT-qPCR showed reduced <i>LRRC7</i> mRNA expression in the proband compared to control samples, while and 3D protein modeling revealed substantial changes in the LRRC7-secondary structure.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Conclusion</h3>\u0000 \u0000 <p>Using genetic, molecular, in silico, and expression analysis, we characterize a novel de novo-<i>LRRC7</i> variant and describe its association with an NDD phenotype.</p>\u0000 </section>\u0000 </div>","PeriodicalId":56122,"journal":{"name":"Journal of Gene Medicine","volume":"28 4","pages":""},"PeriodicalIF":2.2,"publicationDate":"2026-03-31","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147596081","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Development of CpG-Depleted CFTR Plasmid-Based Nanoparticles for Nonviral Gene Therapy in Lung Cystic Fibrosis Disease","authors":"Bei Qiu,&nbsp;Maryann Lorino,&nbsp;Yinghao Li,&nbsp;Zhonglei He,&nbsp;Xianqing Wang,&nbsp;Wenxin Wang,&nbsp;Irene Lara-Sáez","doi":"10.1002/jgm.70087","DOIUrl":"10.1002/jgm.70087","url":null,"abstract":"<p>Nonviral gene therapy holds promise as a potential treatment for lung cystic fibrosis (CF). However, the transient expression of the CF transmembrane conductance regulator (CFTR) protein has limited its clinical application. To circumvent this challenge, a CpG-depleted CFTR plasmid was developed. The CpG-depleted CFTR plasmid could be compacted into DNA nanoparticles and modified with the addition of highly branched poly(β-amino ester)s (HPAEs), leading to an improved and sustained CFTR protein expression. Using a CpG-depleted and codon-optimized CFTR sequence, around 20-fold increase in CFTR protein production was achieved 48 h after treatment, compared with healthy human bronchial epithelial cells (16HBE14o-). To evaluate the duration of CFTR protein expression induced by the plasmid based on human elongation factor 1α (hEFIα) and cytomegalovirus (CMV) promoters, a time course study was conducted in human CF bronchial epithelial (CFBE14o-) cells. hEFIα promoter revealed a remarkable 2.26-fold increase in CFTR protein expression at 7 days after transfection compared with 16HBE14o- cells. This level of CFTR protein expression outperformed the commonly used CMV promoter. The in vitro results demonstrated that CpG-depleted CFTR plasmid could be used to achieve high efficacy in subsequent in vivo evaluations, which, if validated, may provide promising prospects for the development of a novel and effective treatment for lung cystic fibrosis.</p>","PeriodicalId":56122,"journal":{"name":"Journal of Gene Medicine","volume":"28 3","pages":""},"PeriodicalIF":2.2,"publicationDate":"2026-03-23","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13006820/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147500592","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Correction to “NLRC4-Mediated Pyroptosis Was Involved in Coagulation Disorders of Acute Pancreatitis”","authors":"","doi":"10.1002/jgm.70089","DOIUrl":"10.1002/jgm.70089","url":null,"abstract":"<p>\u0000 <span>Hu, S</span>, <span>Lin, T</span>, <span>Chen, Y</span>, <span>Guo, Y</span>, <span>Sun, X</span>, <span>Shi, L</span>, <span>Pan, J</span>. <span>NLRC4-Mediated Pyroptosis Was Involved in Coagulation Disorders of Acute Pancreatitis</span>. <i>J. Gene Med.</i> <span>2024</span>; <span>26</span>(<span>4</span>):e3683.\u0000 </p><p>The second affiliation in the published article is incomplete. It should read:</p><p>²Key Laboratory of Intelligent Treatment and Life Support for Critical Diseases of Zhejiang Province, The First Affiliated Hospital of Wenzhou Medical University, Wenzhou, China.</p><p>We apologize for this error.</p>","PeriodicalId":56122,"journal":{"name":"Journal of Gene Medicine","volume":"28 3","pages":""},"PeriodicalIF":2.2,"publicationDate":"2026-03-23","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1002/jgm.70089","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147505560","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Correction to “Chronic Granulomatous Disease: Clinical and Molecular Characterization of Brazilian Patients”","authors":"","doi":"10.1002/jgm.70088","DOIUrl":"10.1002/jgm.70088","url":null,"abstract":"<p>\u0000 <span>L. M. Rosa</span>, <span>M. B. Rosa</span>, <span>M. S. L. J. Wilson</span>, <span>I. V. D. Schwartz</span>, and <span>F. Sperb-Ludwig</span>, “ <span>Chronic Granulomatous Disease: Clinical and Molecular Characterization of Brazilian Patients</span>,” <i>Journal of Gene Medicine</i> <span>28</span>, no. <span>2</span> (<span>2026</span>): e70086, https://doi.org/10.1002/jgm.70086.\u0000 </p><p>We apologize for this error.</p>","PeriodicalId":56122,"journal":{"name":"Journal of Gene Medicine","volume":"28 3","pages":""},"PeriodicalIF":2.2,"publicationDate":"2026-03-20","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1002/jgm.70088","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147492292","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Chronic Granulomatous Disease: Clinical and Molecular Characterization of Brazilian Patients","authors":"Leonardo Martinello da Rosa,&nbsp;Martha Braun da Rosa,&nbsp;Mariana de Sampaio Leite Jobim Wilson,&nbsp;Ida Vanessa Doederlein Schwartz,&nbsp;Fernanda Sperb-Ludwig","doi":"10.1002/jgm.70086","DOIUrl":"10.1002/jgm.70086","url":null,"abstract":"<p>Chronic granulomatous disease (CGD) is a rare inborn error of immunity caused by defects in components of the NADPH oxidase that impair the elimination of infectious microorganisms. Individuals affected by CGD become more susceptible to recurrent and severe infections. Six male patients from Southern Brazil were clinically and genetically analyzed through data collection from medical records and massively parallel sequencing by a panel for the following genes: <i>CYBB</i>, <i>CYBA</i>, <i>NCF1</i>, <i>NCF2</i>, and <i>NCF4</i> and whole genome sequencing analysis. The gene-scan technique was used to identify the GT deletion in <i>NCF1</i>. The most common affected organs were the lungs, skin, and lymph nodes; the most common clinical manifestations were recurrent pneumonia, cutaneous involvement, lymph node manifestations, and failure to thrive. Four patients were identified with variants in <i>CYBB</i>: p.Cys257Ser, which is novel; p.Cys257Arg; p.Arg157Ter; and p.Trp483Ter. Both missense variants damage the loop E in gp91^phox, a region with functional and structural relevance for the protein. Functional studies show the expression absence of the protein in patients with the variant p.Arg157Ter. The variant p.Trp483Ter is predicted to undergo nonsense mRNA-mediated decay. The GT deletion in <i>NCF1</i> was identified in two siblings from consanguineous parents: one homozygous and the other apparently heterozygous for the deletion, both with a clinical diagnosis of CGD. Variant analysis in this gene is particularly challenging due to the presence of pseudogenes. A hypothesis for this genotypic discrepancy is the occurrence of a second type of pseudogene lacking the GT deletion, which may have arisen in one parent and been transmitted to the patient observed as heterozygous, being misinterpreted in the analyses as a functional <i>NCF1</i> sequence.</p>","PeriodicalId":56122,"journal":{"name":"Journal of Gene Medicine","volume":"28 2","pages":""},"PeriodicalIF":2.2,"publicationDate":"2026-02-06","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12880906/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"146133533","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}