Cell and Bioscience最新文献

{"title":"The relationship between abnormal glucose metabolism and chronic pain.","authors":"Lulin Ma, Yaoling Wang, Yi Zhao, Meng Sun, Tao Zhu, Cheng Zhou","doi":"10.1186/s13578-025-01430-w","DOIUrl":"10.1186/s13578-025-01430-w","url":null,"abstract":"<p><p>Chronic pain has a serious impact on the quality of patients' life. Currently, the mechanism of chronic pain has not been fully studied, and the treatments are often ineffective. Abnormal glucose metabolism plays an important role in the occurrence and development of chronic pain. It has been found that the abnormal glucose metabolism in anterior cingulate cortex (ACC), visual cortex, occipital cortex, brain stem, hippocampus, orbitofrontal cortex (OFC), thalamus and insula is involved in the primary headache (migraine); In addition, the abnormal glucose metabolism in the medial prefrontal cortex (mPFC), ACC, hippocampus, thalamus, primary somatosensory cortices (SI), OFC and cerebellum is involved in the neuropathic pain (NP); the abnormal glucose metabolism in the thalamus and brain stem is also involved in other types of chronic pain. Pain relieving therapies, such as transcranial magnetic stimulation (TMS), transcranial direct current stimulation (tDCS), electroacupuncture (EA) and acupuncture treatment can alleviate chronic pain by reversing abnormal glucose metabolism in some of the above brain regions. In conclusion, although further research is needed, the abnormal glucose metabolism and related treatment may be an important direction for the treatment of chronic pain, and relevant mechanisms still need to be further explored.</p>","PeriodicalId":49095,"journal":{"name":"Cell and Bioscience","volume":"15 1","pages":"86"},"PeriodicalIF":6.1,"publicationDate":"2025-06-21","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12182658/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144340522","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Programmed cell death in the cognitive impairment of obstructive sleep apnea.","authors":"Yanru Ou, Xiufang Wang, Dandan Zong, Ruoyun Ouyang","doi":"10.1186/s13578-025-01418-6","DOIUrl":"10.1186/s13578-025-01418-6","url":null,"abstract":"<p><p>Cognitive impairment (CI) is a significant and extraordinary complication of obstructive sleep apnea (OSA) patients. Programmed cell death (PCD) is an active and ordered process regulated by genes. A growing number of studies find that PCD is responsible for cognitive dysfunction and plays an important role in various neurological diseases, which involve apoptosis, necroptosis, pyroptosis, ferroptosis, and cell death associated with autophagy. However, the influence of PCD on OSA-CI remains unclear. We summarized the relevant studies that discussed the involvement of PCD in the CI of OSA and aimed to clarify the underlying mechanisms. Intermittent hypoxia (IH)-induced PCD had a critical effect on the mechanisms that produced the ultimate neurological deficit in OSA, and the PCD involved mainly included apoptosis, autophagy, ferroptosis, and pyroptosis. IH regulates PCD directly or through specific pathways, and drugs targeting related molecules have the potential to improve cognitive function. These findings enrich the pathogenesis of OSA-CI and provide new therapeutic insights.</p>","PeriodicalId":49095,"journal":{"name":"Cell and Bioscience","volume":"15 1","pages":"85"},"PeriodicalIF":6.1,"publicationDate":"2025-06-20","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12181853/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144337176","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Generation of a spontaneous murine HPV + oral cancer model with site-specific oncogene insertion using CRISPR-SONIC.","authors":"Julia Tao, Jason Murray, Hsin-Fang Tu, Darrell Fan, Ya-Chea Tsai, Ming-Hung Hu, Annie A Wu, Deyin Xing, Chien-Fu Hung, T-C Wu","doi":"10.1186/s13578-025-01427-5","DOIUrl":"10.1186/s13578-025-01427-5","url":null,"abstract":"<p><p>Human papillomavirus associated head and neck cancer (HPV + HNC) is rising globally, emphasizing the need for improved therapeutic and screening strategies. To test novel therapies and study HPV-related disease progression, it is vital to develop relevant preclinical models. However, many fail to address critical concerns, including generating a representative immune microenvironment and adequately modeling HPV-driven malignant transformation. Recent multi-omics studies reveal the significance of HPV integration location in HPV-related carcinogenesis and highlight the necessity of targeted treatment methods. Thus, we have developed a murine model of HPV16 + HNC modifying the published CRISPR-based Somatic Oncogene kNock-In for Cancer Modeling (CRISPR-SONIC) system for precise integration of HPV oncogenes. We showed that CRISPR-SONIC knock-in of Kras^G12D, HPV16 E6 and E7, and a luciferase reporter at the murine β-actin 3'-UTR locus could induce spontaneous buccal tumors with sarcomatous morphology under transient or selective immunosuppression. Both preventative and therapeutic pNGVL4a-CRT/E7(detox) DNA vaccination could induce HPV16 E7-specific immune response and reduce tumor growth. Furthermore, CRISPR-SONIC knock-in of HPV16 E6 and E7 with co-delivery of HNC-relevant oncogenes AKT and c-Myc produced tumors in NSG mice capturing the characteristic carcinomic morphology of HPV + HNC. Overall, our model offers a robust platform for evaluating new therapies and exploring HPV-related carcinogenesis.</p>","PeriodicalId":49095,"journal":{"name":"Cell and Bioscience","volume":"15 1","pages":"84"},"PeriodicalIF":6.2,"publicationDate":"2025-06-18","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12175459/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144327494","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"The indispensable role of Mediator complex subunit 27 during neurodevelopment.","authors":"Xiaocheng Li, Nuermila Yiliyaer, Tianyu Guo, Hui Zhao, Yong Lei, Shen Gu","doi":"10.1186/s13578-025-01425-7","DOIUrl":"10.1186/s13578-025-01425-7","url":null,"abstract":"<p><strong>Background: </strong>MED27 is a subunit of the Mediator complex, a highly conserved protein assembly that initiates transcription by bridging transcription factors bound at enhancers to RNA polymerase II transcription machinery at promoters. Recently, we identified an autosomal recessive neurodevelopmental disorder (NDD) caused by loss-of-function (LoF) variants in the MED27 gene. Affected individuals exhibit global developmental delay, intellectual disability, dystonia, and cerebellar atrophy, highlighting the neuronal system's vulnerability to MED27 disruptions.</p><p><strong>Results: </strong>To investigate the pathogenicity mechanisms and essential roles of this gene during neurodevelopment, we generated multiple zebrafish lines with LoF mutations in med27. Homozygous mutant zebrafish displayed severe developmental defects, motor deficits, and cerebellar atrophy, recapitulating the clinical phenotypes observed in MED27-NDD patients. Rescue experiments revealed that patient-specific mutant MED27 mRNA failed to restore normal phenotypes in mutant zebrafish, unlike wildtype MED27 mRNA, underscoring the clinical relevance of our models. Molecular analysis identified transcription factors foxo3a and fosab as direct downstream targets of med27. These genes are well-established master regulators in the central nervous system, providing mechanistic insights into how med27 disruption impairs neuronal and cerebellar development.</p><p><strong>Conclusion: </strong>Our findings establish med27 as a critical gene of embryogenesis and neurogenesis, shedding light on the disease mechanism underlying MED27-associated NDDs.</p>","PeriodicalId":49095,"journal":{"name":"Cell and Bioscience","volume":"15 1","pages":"83"},"PeriodicalIF":6.1,"publicationDate":"2025-06-16","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12172316/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144310714","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Alpha fetoprotein (AFP)-producing gastric cancer: clinicopathological features and treatment strategies.","authors":"Bixian Luo, Zelai Wu, Chengyu Hu, Weixun Xie, Jun He, Hongming Liu, Dong Cao, Yong Liu, Yuxin Zhong, Weihua Gong","doi":"10.1186/s13578-025-01424-8","DOIUrl":"10.1186/s13578-025-01424-8","url":null,"abstract":"<p><p>Alpha-fetoprotein (AFP) is a widely recognized tumor marker for hepatocellular carcinoma and yolk sac tumors. Alpha-fetoprotein-producing gastric cancer (AFPGC) is a rare but highly malignant subtype of gastric cancer associated with poor prognosis. It is characterized by AFP positivity detected in serum or immunohistochemical staining, may along with hepatocellular differentiation. In recent years, advancements in molecular biology and therapeutic agents have led to a deeper understanding of AFPGC. However, the mechanisms underlying its tumorigenesis and invasive metastasis remain unclear. This article summarizes the traits of AFP, its clinicopathological features, and therapeutic strategies for AFP-positive gastric cancer, providing a better understanding and reference for the clinical diagnosis and treatment of AFPGC.</p>","PeriodicalId":49095,"journal":{"name":"Cell and Bioscience","volume":"15 1","pages":"82"},"PeriodicalIF":6.1,"publicationDate":"2025-06-10","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12153134/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144267768","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Cilia at the crossroad: convergence of regulatory mechanisms to govern cilia dynamics during cell signaling and the cell cycle.","authors":"Lukáš Čajánek, Sindija Smite, Olha Ivashchenko, Martina Huranova","doi":"10.1186/s13578-025-01403-z","DOIUrl":"10.1186/s13578-025-01403-z","url":null,"abstract":"<p><p>Cilia are versatile, microtubule-based organelles that facilitate cellular signaling, motility, and environmental sensing in eukaryotic cells. These dynamic structures act as hubs for key developmental signaling pathways, while their assembly and disassembly are intricately regulated along cell cycle transitions. Recent findings show that factors regulating ciliogenesis and cilia dynamics often integrate their roles across other cellular processes, including cell cycle regulation, cytoskeletal organization, and intracellular trafficking, ensuring multilevel crosstalk of mechanisms controlling organogenesis. Disruptions in these shared regulators lead to broad defects associated with both ciliopathies and cancer. This review explores the crosstalk of regulatory mechanisms governing cilia assembly, disassembly, and maintenance during ciliary signaling and the cell cycle, along with the broader implications for development, tissue homeostasis, and disease.</p>","PeriodicalId":49095,"journal":{"name":"Cell and Bioscience","volume":"15 1","pages":"81"},"PeriodicalIF":6.1,"publicationDate":"2025-06-07","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12144771/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144250490","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Alkylglycerol monooxygenase represses prostanoid biosynthesis in a sex-dependent manner.","authors":"Zhigang Rao, Katharina Lackner, Ilaria Dorigatti, Natascha Brigo, Denise Kummer, Minh Bui Hoang, Christa Pfeifhofer-Obermair, Günter Weiss, Ernst R Werner, Andreas Koeberle, Katrin Watschinger","doi":"10.1186/s13578-025-01419-5","DOIUrl":"10.1186/s13578-025-01419-5","url":null,"abstract":"<p><strong>Background: </strong>Ether lipids are important constituents of biological membranes and harbor fatty alcohols attached via ether linkages to the sn-1 position of the glycerol backbone. Depending on the nature of the ether bond, they are subdivided into 1-O-alkyl (plasmanyl) and 1-O-alk-1'-enyl (plasmenyl) subclasses. They often contain polyunsaturated fatty acids at the sn-2 position, implicating them in cellular signaling and inflammatory processes including lipid mediator biosynthesis. Lipid mediators are produced by immune and non-immune cells, have diverse homeostatic and immunoregulatory functions and, together with other factors, orchestrate the initiation and resolution of inflammation. To date, alkylglycerol monooxygenase is the only known enzyme capable of cleaving alkylglycerols, one of two ether lipid subclasses. However, the exact role of alkylglycerol monooxygenase and that of its substrates in lipid mediator biosynthesis remains unclear.</p><p><strong>Results: </strong>Using a knockout mouse model, we demonstrate a sex- and cell type-dependent role of alkylglycerol monooxygenase in limiting prostanoid formation without affecting polyunsaturated fatty acid release, as revealed by metabololipidomics profiling of lipid mediators using ultra-performance liquid chromatography‒tandem mass spectrometry. This female-specific effect is driven by the suppression of prostaglandin G/H synthase 2 transcription, as deficiency in alkylglycerol monooxygenase significantly elevated prostaglandin G/H synthase 2 gene expression in female bone marrow-derived macrophages of the M1 phenotype. Furthermore, this regulatory role of alkylglycerol monooxygenase extends to visceral white adipose tissue, where elevated prostaglandin G/H synthase 2 expression and enhanced prostaglandin E₂ production were observed in female samples following alkylglycerol monooxygenase knockout.</p><p><strong>Conclusion: </strong>Our results expand the immunomodulatory functions of ether lipid metabolism and highlight the sex- and cell type-dependent role of alkylglycerol monooxygenase in controlling lipid mediator production and maintaining tissue homeostasis.</p>","PeriodicalId":49095,"journal":{"name":"Cell and Bioscience","volume":"15 1","pages":"80"},"PeriodicalIF":6.1,"publicationDate":"2025-06-05","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12143016/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144235688","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Post-translational modifications in the pathophysiological process of metabolic dysfunction‑associated steatotic liver disease.","authors":"Yiyang Min, Yiqiao Zhang, Yu Ji, Shanshan Liu, Chengjian Guan, Luyang Wei, Huajing Yu, Zhongtao Zhang","doi":"10.1186/s13578-025-01411-z","DOIUrl":"10.1186/s13578-025-01411-z","url":null,"abstract":"<p><p>In recent years, the prevalence of metabolic dysfunction‑associated steatotic liver disease (MASLD), which was called non-alcoholic fatty liver disease (NAFLD), has been progressively increasing in populations. The progression of MASLD encompasses a spectrum from simple steatosis to metabolic dysfunction-associated steatohepatitis (MASH), and ultimately to cirrhosis or even hepatocellular carcinoma. During the early stages of the disease, lipid accumulation and endoplasmic reticulum stress may lead to abnormalities in hepatic DNA expression, protein synthesis, and post-translational modifications (PTMs). PTMs play a crucial role in the progression of MASLD and include histone and non-histone modifications, with major types including methylation, acetylation, ubiquitination, and phosphorylation. Numerous studies indicate that within MASLD-related signaling pathways, PTMs can modulate protein activity, localization, folding, and interactions by altering their physicochemical properties. This review summarizes various significant PTMs involved in MASLD progression to elucidate the regulatory mechanisms and pathogenesis associated with the disease.</p>","PeriodicalId":49095,"journal":{"name":"Cell and Bioscience","volume":"15 1","pages":"79"},"PeriodicalIF":6.1,"publicationDate":"2025-06-05","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12143077/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144235689","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"WNT3 promotes chemoresistance to oxaliplatin in oral squamous cell carcinoma via regulating ABCG2 expression.","authors":"Kairui Sun, Xuyang Zhang, Ruihuan Gan, Shuoqi Lin, Yu Chen, Dali Zheng, Youguang Lu","doi":"10.1186/s13578-025-01414-w","DOIUrl":"10.1186/s13578-025-01414-w","url":null,"abstract":"<p><p>Oxaliplatin (OXA) is a frontline therapeutic agent used in the treatment of oral squamous cell carcinoma (OSCC). However, the development of chemoresistance has emerged as a significant challenge, compromising the effectiveness of treatment strategies. Therefore, there is a critical need to unravel the mechanisms underpinning drug resistance and to identify potential therapeutic targets. In recent years, there has been a growing interest in understanding the role of drug efflux in cancer chemoresistance mechanisms. Despite this, the contribution of ABCG2, a member of the ATP-binding cassette (ABC) transporter family, to oxaliplatin resistance in OSCC remains unclear. In the current study, we aimed to investigate the involvement of ABCG2 in oxaliplatin resistance in OSCC and to elucidate the molecular mechanisms through which the Wingless and Int-1 (WNT) canonical signaling pathway upregulates ABCG2 to promote chemoresistance. To achieve this, we established oxaliplatin-resistant (OXA-R) OSCC cells as a model system. Our investigations revealed that the efflux ability of resistant cells was enhanced and the ABCG2 expression was up-regulated. Genetic silencing of ABCG2 significantly attenuated both efflux activity and chemoresistance in these resistant cells. Notably, we observed aberrant activation of the WNT canonical signaling pathway in resistant cells, accompanied by heightened expression of the WNT3 ligand. Additionally, overexpression of WNT3 in parental cells recapitulated the activation of the WNT canonical signaling cascade, resulting in increased chemoresistance, enhanced efflux function, and elevated ABCG2 expression levels. Conversely, inhibition of WNT3 in resistant cells resulted in reduced chemoresistance, suppression of efflux activity, and decreased ABCG2 expression. Finally, treatment with the WNT/β-catenin pathway inhibitor methyl 3-benzoate (MSAB) effectively reversed chemoresistance in resistant cells. Mechanistically, our studies revealed that the abnormal activation of the WNT canonical pathway promotes the recruitment of the transcription factor lymphoid enhancer-binding factor 1 (LEF1) to the ABCG2 promoter, thereby enhancing its transcriptional activity. In summary, our findings underscore the critical role of WNT3-mediated activation of the WNT canonical signaling pathway in upregulating ABCG2 expression, which enhances oxaliplatin efflux and contributes to the development of oxaliplatin resistance in OSCC.</p>","PeriodicalId":49095,"journal":{"name":"Cell and Bioscience","volume":"15 1","pages":"77"},"PeriodicalIF":6.1,"publicationDate":"2025-06-04","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12139312/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144227314","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Domain acquisition enabled functional expansion of the TFIIS transcription factor family.","authors":"Kateryna Matveyeva, Ainhoa Sánchez de Diego, María Ángeles García-López, Julio Gutiérrez, Thierry Fischer, Karel H M van Wely","doi":"10.1186/s13578-025-01423-9","DOIUrl":"10.1186/s13578-025-01423-9","url":null,"abstract":"<p><p>TFIIS and its homologs were long considered a delimited family of transcription factors, for the ability to induce RNA Polymerase II backtracking and nascent RNA cleavage. Recent studies however show that the relevant domains, which correspond to the TFIIS middle and carboxyterminal regions, are used to control transcription by additional protein architectures. The TFIIS middle region is paired with a SPOC domain in BYE1, the founder protein of the subfamily, and in its homologs; this combination of domains accommodates additional features such as a small zinc finger resembling the TFIIS carboxyterminal region. In metazoans, the architecture has evolved additional extensions to act on downstream RNA processing. Here, we argue in favor of a single protein superfamily encompassing TFIIS, BYE1, and their metazoan homologs. We conclude that the TFIIS middle domain comprises a common Pol2-interacting domain, shared by various generic protein functions. Domain composition of the vertebrate BYE1 homologs indicates a role in transcription elongation. Depending on the combination with other structures, the TFIIS middle domain may promote mutually exclusive activities, for example backtracking versus RNA synthesis and splicing. In this way, exchange of TFIIS for other superfamily members supports the separate Pol2 actions.</p>","PeriodicalId":49095,"journal":{"name":"Cell and Bioscience","volume":"15 1","pages":"78"},"PeriodicalIF":6.1,"publicationDate":"2025-06-04","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12139180/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144227300","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}