Analytical Cellular Pathology最新文献

{"title":"S1P, Generated by Sphingosine Kinase 1, Negatively Affects Corneal Wound Healing Process by Activating TGF-β/Smad Pathway.","authors":"Sandip K Basu, Sarah E Nicholas, Bradley P Hambly, Nataliya Lenchik, Richard C Grambergs, T J Hollingsworth, Amanda Prislovsky, Dimitrios Karamichos, Nawajes Mandal","doi":"10.1155/ancp/6404551","DOIUrl":"10.1155/ancp/6404551","url":null,"abstract":"<p><p>Abnormal healing of corneal injury can lead to corneal opacity, a leading cause of blindness. This process is extremely complex and involves precise interactions of multiple signaling pathways. A lack of understanding of these complex interactions provides a major challenge in developing therapeutic strategies. Both sphingosine-1-phosphate (S1P) and transforming growth factor beta (TGFβ) signaling have been associated with tissue fibrosis. The purpose of this study was to understand the interplay between S1P and TGFβ signaling in the process of corneal wound healing and fibrosis. Mice lacking the Sphingosine kinase 1 gene (Sphk1^-/-) and their wildtype littermates were subjected to corneal injury by alkali burn. The progress of wound healing and the expression and activation of TGFβ signaling intermediates and profibrotic proteins were measured at different days postinjury (DPI). We observed that reduction of S1P signaling in Sphk1^-/- mice induced the closure of corneal epithelial layer at a faster rate than its wildtype littermates following alkali burn. Reduced activation of profibrotic proteins Smad2 and 3, along with reduced expression of Smad4 and higher expression of antifibrotic protein Smad7, was also observed in the Sphk1^-/- mice as compared to the wildtype littermates following corneal injury. Inhibition of S1P signaling by exogenous delivery of a small-molecule inhibitor of sphingosine kinase 1 (SphK1) could accelerate corneal wound healing in similarly injured wildtype (Sphk1^+/+) mice. These results suggest that S1P signaling positively influences TGFβ signaling pathways that negatively affect corneal wound healing by delaying the process and inducing fibrotic development. Thus, inhibition of S1P signaling could be an effective therapeutic option to accelerate corneal wound healing and thereby prevent corneal fibrosis/scar formation.</p>","PeriodicalId":49326,"journal":{"name":"Analytical Cellular Pathology","volume":"2026 1","pages":"e6404551"},"PeriodicalIF":2.5,"publicationDate":"2026-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13387310/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148537425","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":"RETRACTION: Suppression of lncRNA OIP5-AS1 Attenuates Apoptosis and Inflammation, and Promotes Proliferation by Mediating miR-25-3p Expression in Lipopolysaccharide-Induced Myocardial Injury.","authors":"Analytical Cellular Pathology","doi":"10.1155/ancp/9805806","DOIUrl":"10.1155/ancp/9805806","url":null,"abstract":"","PeriodicalId":49326,"journal":{"name":"Analytical Cellular Pathology","volume":"2026 1","pages":"e9805806"},"PeriodicalIF":2.5,"publicationDate":"2026-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13253603/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148220564","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":"Midkine and CA9 Are Potential Cancer Stem Cell Biomarkers in Triple-Negative Breast Tumours.","authors":"Jorge Choque, Aparicio Aguilar, Javier Enciso-Benavides, Nancy Rojas-Moran, Nathaly Enciso, Carlos Castañeda Altamirano, Miluska Castillo, Luis Alfaro, Javier Enciso","doi":"10.1155/ancp/3265988","DOIUrl":"10.1155/ancp/3265988","url":null,"abstract":"<p><strong>Introduction: </strong>There is no specific therapy for triple-negative breast cancer (TNBC), and the recurrence rate is high. Cancer stem cells (CSCs) play an important role in cancer chemoresistance and metastasis, but there is no consensus marker in this type of cancer. The aim of this study was to identify CSC biomarkers in the plasma secretome of TNBC patients.</p><p><strong>Methods: </strong>CD44+/CD24- CSCs were isolated from MDA-MB-436 and MDA-MB-231 (ATCC) lines by magnetic immunoselection. The extracellular vesicles (EVs) of CSCs were isolated by size exclusion chromatography (SEC) of conditioned medium (CM) without fetal bovine serum (FBS) and blood plasma from TNBC and healthy women. Tetraspanins CD9 and CD81 identified the EVs, while electron microscopy determined the morphology and tunable resistive pulse sensing (TRPS) established particle size. Luminex technology was used to determine the presence of L1 cell adhesion molecule (L1CAM), carbonic anhydrase IX (CA9), mesothelin, midkine, hepsin, kallikrein-6 (KLK6), transglutaminase 2 (TGM2), aldehyde dehydrogenase 1a1 (ALDH1A1), epithelial cell adhesion molecule (EpCAM), and differentiation cluster 44 (CD44).</p><p><strong>Results: </strong>Particles of 0-200 nm in size were more frequent in CSC-MDA-MB-436, while particles of 201-500 nm were more frequent in CSC-MDA-MB-231. In blood plasma, the particle size was 150-250 nm in TNBC patients and 150-300 nm in healthy individuals. Particle concentrations were 1.3 × 10¹⁰ in CSCs of the MDA-MB-231 (CSC-MDA-MB-231) cell line and 3.8 × 10⁷ in the MDA-MB-231 cell line (L-MDA-MB-231). The concentration of CSCs in MDA-MB-436 was 2.7 × 10⁸ compared to 9.4 × 10⁷ in L-MDA-MB-436. Midkine and CA9 were present in the EVs of both CSC lines and in the plasma of women with TNBC but absent in the blood plasma of healthy women. Midkine showed better statistical discrimination.</p><p><strong>Conclusions: </strong>The size and concentration of EVs are heterogeneous. Midkine and CA9 are produced by CSCs in women with TNBC and may be possible biomarkers of these cells in this tumour type.</p>","PeriodicalId":49326,"journal":{"name":"Analytical Cellular Pathology","volume":"2026 1","pages":"e3265988"},"PeriodicalIF":2.5,"publicationDate":"2026-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13527379/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148867269","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 \"Inhibition of miR-182-5p Targets FGF9 to Alleviate Osteoarthritis\".","authors":"","doi":"10.1155/ancp/9879754","DOIUrl":"10.1155/ancp/9879754","url":null,"abstract":"","PeriodicalId":49326,"journal":{"name":"Analytical Cellular Pathology","volume":"2026 1","pages":"e9879754"},"PeriodicalIF":2.5,"publicationDate":"2026-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13502284/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148809252","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":"THBS2 Promotes Prostate Cancer Malignancy via INHBA-Dependent FAK/PI3K/AKT Signaling Activation.","authors":"Yifeng Yao, Yiyang Guo, Shoulei Liu, Yaojun Li, Shanmiao Chen","doi":"10.1155/ancp/3503659","DOIUrl":"10.1155/ancp/3503659","url":null,"abstract":"<p><p>Prostate cancer (PCa) is a leading malignancy among men, with a growing incidence and mortality rate worldwide. There is a pressing need to identify novel molecular biomarkers and therapeutic targets to improve prognosis and treatment strategies for PCa. We analyzed thrombospondin 2 (THBS2) expression patterns in PCa using The Cancer Genome Atlas (TCGA) datasets and validated findings in clinical tissues and cell lines. Functional assays, including Cell Counting Kit (CCK)-8 proliferation, flow cytometry apoptosis, wound healing, and Transwell invasion, were performed on PCa cell lines with altered THBS2 expression. Bioinformatic analyses were conducted to explore THBS2-related pathways, and protein interactions were examined via STRING and Western blot. THBS2 expression was significantly upregulated in PCa tissues and cell lines and correlated with advanced clinicopathological features and poor prognosis. Overexpression of THBS2 promoted PCa cell proliferation, migration, invasion, and epithelial-mesenchymal transition (EMT), while inhibiting apoptosis. Mechanistically, THBS2 interacted with INHBA to activate the focal adhesion kinase (FAK)/PI3K/AKT signaling pathway, facilitating malignant progression. INHBA knockdown reversed the oncogenic effects of THBS2, indicating a synergistic interaction between THBS2 and INHBA in PCa pathogenesis. THBS2 acts as an oncogene in PCa by promoting proliferation, invasion, and EMT via the FAK/PI3K/AKT pathway in cooperation with INHBA. These findings highlight THBS2 as a promising biomarker for PCa.</p>","PeriodicalId":49326,"journal":{"name":"Analytical Cellular Pathology","volume":"2026 1","pages":"e3503659"},"PeriodicalIF":2.5,"publicationDate":"2026-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13580850/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147437183","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":"Mechanisms of Action and Biomarker Potential of ncRNAs in Hepatocellular Carcinoma and Liver Fibrosis: A Review.","authors":"Eun Jung Sohn, Sae-Ock Oh","doi":"10.1155/ancp/2283163","DOIUrl":"10.1155/ancp/2283163","url":null,"abstract":"<p><p>Liver diseases constitute a major global health burden, contributing substantially to morbidity and mortality worldwide. Although effective therapeutic strategies have been developed for key risk factors, such as hepatitis C infection, therapeutic options for most other liver diseases remain limited. Noncoding RNAs (ncRNAs), which regulate diverse cellular and molecular processes, have emerged as promising therapeutic targets and biomarkers in liver diseases. In this study, we summarize the mechanisms of action and functional roles of ncRNAs, such as long ncRNAs (lncRNAs), circular RNAs (circRNAs), and PIWI-interacting RNAs (piRNAs), to improve therapeutic strategies and diagnostic precision in liver diseases, such as liver fibrosis and hepatocellular carcinoma (HCC).</p>","PeriodicalId":49326,"journal":{"name":"Analytical Cellular Pathology","volume":"2026 1","pages":"e2283163"},"PeriodicalIF":2.5,"publicationDate":"2026-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13580803/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147437136","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":"The m6A Reader YTHDF3 Promotes Glioma Progression by Regulating the m6A Modification of lncRNA-PAR5.","authors":"LiuFei Xu, Yuan Xu, YongBin Duan, Bo Wang, YiYu Luo, XiangPeng Wang","doi":"10.1155/ancp/8467384","DOIUrl":"10.1155/ancp/8467384","url":null,"abstract":"<p><strong>Background: </strong>Long non-coding RNA PAR5 (lncRNA-PAR5) is downregulated in glioma and has been confirmed to inhibit glioma progression; however, the specific regulatory mechanism underlying its downregulation remains unclear.</p><p><strong>Objective: </strong>This study aimed to investigate the key molecular mechanism by which PAR5 inhibits glioma progression, with a focus on the regulatory role of m6A modification.</p><p><strong>Methods: </strong>Potential m6A modification sites in the PAR5 sequence were predicted using the SRAMP online tool. The expression profiles of m6A regulatory genes in glioblastoma were analyzed via the GEPIA database. RNA pull-down, RIP-qPCR, and MeRIP-qPCR were employed to validate the specific binding of YTHDF3 to PAR5 and its effect on the m6A modification level of PAR5. The expression of PAR5 and YTHDF3 was modulated by cell transfection, and cell proliferation, invasion, and migration were assessed using CCK-8, Transwell, and wound healing assays, respectively. Further in vivo functional validation was performed using a subcutaneous xenograft tumor model in nude mice.</p><p><strong>Results: </strong>lncRNA-PAR5 significantly inhibited the proliferation, invasion, and migration of glioma cells. Bioinformatics analysis and experimental validation revealed that the m6A reader protein YTHDF3 is highly expressed in glioma, specifically recognizes and binds to PAR5, and promotes PAR5 degradation by enhancing its m6A modification level, thereby negatively regulating PAR5 expression. Functional experiments demonstrated that YTHDF3 plays a pro‑oncogenic role, while knockdown of YTHDF3 suppressed malignant phenotypes of glioma, an effect that could be partially reversed by simultaneous knockdown of PAR5. In vivo experiments further confirmed that YTHDF3 knockdown inhibits tumor growth by upregulating PAR5.</p><p><strong>Conclusion: </strong>YTHDF3 promotes glioma cell proliferation, invasion, and migration by inhibiting PAR5 expression through enhancing its m6A modification. This study reveals the critical role of the YTHDF3/PAR5 axis in glioma progression and provides a potential novel target for glioma‑targeted therapy.</p>","PeriodicalId":49326,"journal":{"name":"Analytical Cellular Pathology","volume":"2026 1","pages":"e8467384"},"PeriodicalIF":2.5,"publicationDate":"2026-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13580842/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147700510","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":"Colorectal Adenocarcinoma: A Comprehensive Narrative Review of Molecular Pathogenesis, Metabolic Vulnerabilities, and Therapeutic Potential of Sorghum Polyphenols.","authors":"Birhanemaskal Malkamu","doi":"10.1155/ancp/5527243","DOIUrl":"10.1155/ancp/5527243","url":null,"abstract":"<p><p>Colorectal cancer (CRC) remains a formidable global health challenge, characterized by uncontrolled cell proliferation and significant socioeconomic burden. Projections anticipate a substantial increase in new cases, straining healthcare systems worldwide. CRC, the most common histological subtype, originates from gland cells lining the colon and rectum, often preceded by benign polyps. Its development is complex, influenced by sporadic, familial, and inherited factors. Sporadic cases, accounting for 70%-80%, are linked to genetic mutations and epigenetic alterations, with lifestyle factors like physical inactivity, diet, obesity, smoking, and alcohol consumption playing significant roles. Familial cases (25%) suggest shared environmental influences, while inherited conditions (5%) like familial adenomatous polyposis (FAP) and Lynch syndrome involve germline mutation with high lifetime CRC risk. The molecular pathogenesis of CRC involves genomic instability, notably chromosomal instability (CIN), microsatellite instability (MSI), and the CpG island methylator phenotype (CIMP). Mitochondria, beyond ATP production, critically influence cellular processes. The mitochondrial metabolic theory (MMT) proposes impaired oxidative phosphorylation (OxPhos) drives genomic instability. While the Warburg effect is recognized, many tumors retain functional oxidative metabolism, often relying heavily on OxPhos. Key genetic mutations like KRAS and BRAF significantly impact CRC, influencing mitochondrial metabolism and tumor progression, and are associated with different prognostic outcomes. Emerging therapeutic strategies target metabolic vulnerabilities to overcome chemoresistance. Inhibition of mitochondrial genes and key enzymes, along with modulating calcium homeostasis, shows promise. Preclinical research highlights sorghum extracts as potential therapeutic agents. High-phenolic sorghum bran extracts demonstrate anticancer action by suppressing proliferation, inducing apoptosis, and inhibiting migration and invasion. These effects involve targeting specific cancer pathways and influencing proteins like those in the Ras-ERK pathway, β-catenin, cMyc, cyclin D1, and surviving. Specific sorghum compounds like anthocyanidins, luteolin, and quercetin exhibit cytotoxicity against CRC cells, including those with KRAS and BRAF mutations. Further research is crucial to translate these preclinical findings into clinical applications, understand bioavailability, and account for individual differences in gut microbiota.</p>","PeriodicalId":49326,"journal":{"name":"Analytical Cellular Pathology","volume":"2026 1","pages":"e5527243"},"PeriodicalIF":2.5,"publicationDate":"2026-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13580860/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148139523","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":"Expression Levels of DNMT1, HDAC1, and MT1E Genes as Diagnostic Biomarkers for Breast Cancer Clinicopathological Features: In Vitro and In Silico Analyses.","authors":"Sedigheh Akhtartavan, Hamid Madanchi, Raheb Ghorbani, Abolfazl Khalafi-Nezhad, Ahmad Abdullahi, Fahimeh Shamsi, Hossein Heli","doi":"10.1155/ancp/9606190","DOIUrl":"10.1155/ancp/9606190","url":null,"abstract":"<p><strong>Background: </strong>Breast cancer (BC) is the second leading cause of cancer-related deaths worldwide and has a high recurrence rate. This study aimed to evaluate the expression levels of three biomarkers: DNA methyltransferase 1 (DNMT1), histone deacetylase 1 (HDAC1), and metallothionein 1E (MT1E) in BC patients.</p><p><strong>Methods: </strong>Peripheral blood and tissue samples from 95 female BC patients and 50 age-matched (±5 years) healthy female controls were analyzed using an enzyme-linked immunosorbent assay (ELISA). Diagnostic potential was assessed through receiver operating characteristic (ROC) curve analysis. In silico analyses identified differentially expressed genes (DEGs), Gene Ontology (GO) terms, pathway enrichment, correlation analysis, miRNA-mRNA interactions, and drug-gene networks.</p><p><strong>Results: </strong>Both experimental and computational results revealed significantly higher levels of DNMT1 and HDAC1 but lower levels of MT1E in BC patients compared to controls (p-value < 0.0001). Furthermore, tumor expression of these genes correlated with molecular subtypes, showing distinct expression patterns in triple-negative BC (TNBC). Advanced-stage tumors also exhibited increased HDAC1 and DNMT1 expression. GO enrichment analysis indicated that these DEGs are involved in cell division, differentiation, and nuclear functions. Kyoto Encyclopedia of Genes and Genomes (KEGG) pathway analysis linked DNMT1 to the p53 pathway, HDAC1 to mismatch repair, and MT1E to cytokine receptor interactions. The strongest gene correlations were DNMT1-ILF3, HDAC1-RBBP4, and MT1E-MT2A. Additionally, miRNA-mRNA interaction analysis revealed that DNMT1, HDAC1, and MT1E are targeted by multiple miRNAs, with the top interacting miRNAs being hsa-miR-103a-3p for DNMT1, hsa-miR-34a-5p for HDAC1, and hsa-miR-126-3p for MT1E. DNMT1 showed the highest number of miRNA interactions among the three genes. Moreover, 98 drugs were found to interact with these three genes. ROC analysis demonstrated promising diagnostic performance, with areas under the curve (AUC) of 0.916 for DNMT1, 0.792 for HDAC1, and 0.683 for MT1E (95% confidence interval [CI]).</p><p><strong>Conclusion: </strong>These findings suggest that DNMT1, HDAC1, and MT1E show potential as complementary biomarkers in BC diagnosis. However, further validation in larger cohorts and functional studies are warranted.</p>","PeriodicalId":49326,"journal":{"name":"Analytical Cellular Pathology","volume":"2026 1","pages":"e9606190"},"PeriodicalIF":2.5,"publicationDate":"2026-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13386243/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148537420","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":"RETRACTION: Numb Promotes Autophagy through p53 Pathway in Acute Kidney Injury Induced by Cisplatin.","authors":"Analytical Cellular Pathology","doi":"10.1155/ancp/9803403","DOIUrl":"10.1155/ancp/9803403","url":null,"abstract":"","PeriodicalId":49326,"journal":{"name":"Analytical Cellular Pathology","volume":"2026 1","pages":"e9803403"},"PeriodicalIF":2.5,"publicationDate":"2026-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13580780/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147718730","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}