The FASEB Journal最新文献

{"title":"Liver-Specific Suppression of PLA2G6/iPLA₂β Improves Glucose and Lipid Metabolism in High-Fat Diet-Fed Mice.","authors":"Kahori Shimizu, Mana Nishibata, Katsuyuki Nagata, Sho Hori, Shotaro Michinaga, Miyuki Kanehara, Miho Hashimoto-Iwasaki, Fuminori Sakurai, Hideo Shindou, Koji Tomita, Toru Nishinaka, Hiroyuki Mizuguchi","doi":"10.1096/fj.202504753RR","DOIUrl":"10.1096/fj.202504753RR","url":null,"abstract":"<p><p>Phospholipase A2 group VI (PLA2G6, also called iPLA₂β) has been implicated in male fertility, neuronal disorders, and metabolic diseases. However, its therapeutic effects on metabolic disorders remain elusive. We investigated the effects of PLA2G6 suppression on glucose and lipid metabolism. Systemic inhibition of PLA2G6 in high-fat diet-fed mice reduced hepatic lipid droplet size without altering the levels of serum triglycerides and fasting blood glucose. Suppression of liver-specific Pla2g6 utilizing the short-hairpin RNA knockdown technique using an adenovirus vector (Ad-shPLA2G6) altered phospholipid and fatty acid metabolites and suppressed hepatic lipid accumulation, serum triglyceride, fasting glucose, and insulin levels. Additionally, Ad-shPLA2G6 treatment downregulated lipid biosynthesis-related genes but upregulated peroxisomal fatty acid oxidation-related genes. These findings indicate that targeting hepatic Pla2g6 modulates phospholipid and fatty acid metabolites and improves glucose and lipid metabolism, suggesting Pla2g6 as a potential therapeutic target in metabolic disorders, including type 2 diabetes mellitus and metabolic dysfunction-associated steatotic liver disease.</p>","PeriodicalId":50455,"journal":{"name":"The FASEB Journal","volume":"40 8","pages":"e71821"},"PeriodicalIF":4.2,"publicationDate":"2026-04-30","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13094463/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147730558","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":"Purification and Transcriptomic Characterization of Hypertrophied Hepatic Stellate Cells From CDAHFD Mouse Liver.","authors":"Marion Heckmann, Nour-El-Houda Djerir, Keola Greliche, Pierre-Henri Commere, Julien Fernandes, Guillaume Sarrabayrouse, Bernard Hainque, Pascal Bigey, Virginie Escriou, Céline Hoffmann","doi":"10.1096/fj.202502655RR","DOIUrl":"https://doi.org/10.1096/fj.202502655RR","url":null,"abstract":"<p><p>Hepatic stellate cells (HSC) are known for their major role in hepatic fibrosis. It is well established that upon liver injury, they undergo a transition from a quiescent state to an activated state and transdifferentiate into proliferative, fibrogenic myofibroblasts. Recently, it has been shown that different subpopulations of HSC co-exist during fibrogenesis and play different roles in the establishment of fibrosis. We previously highlighted, in murine model and human biopsies, a specific subpopulation of hypertrophied HSC (hypHSC) which exhibits exacerbated retinoid droplets and were closely associated with collagen fibers. The present study focuses on the molecular characterization of hypHSCs isolated from a murine model of metabolic liver fibrosis thanks to an experimental strategy we developed and described here. Liver dissociation followed by density gradient and fluorescence assisted cell sorting allowed us to obtain highly pure hypHSC preparations. Then, a transcriptomic analysis (bulk RNAseq) of hypHSCs versus quiescent HSCs purified from healthy mouse liver was performed. This showed that hypHSCs' molecular signature differs from HSC subtypes already described in the literature, with a \"hybrid\" profile involved in the regulation of the immune system, the remodeling of extracellular matrix and exhibiting a deregulation of lipid metabolism. Our study highlights that a phenotype-to-molecular approach can provide complementary elements to single-cell molecular approaches and provides additional insights into the plasticity of hepatic stellate cells in a context of hepatic fibrosis.</p>","PeriodicalId":50455,"journal":{"name":"The FASEB Journal","volume":"40 8","pages":"e71754"},"PeriodicalIF":4.2,"publicationDate":"2026-04-30","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13104797/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147787600","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":"Causal Associations Between Immune Cell-Specific Gene Expression and Major Depressive Disorder: A Single-Cell Transcriptome-Wide Mendelian Randomization Study.","authors":"Xin Mo, Dongren Sun, Fangfang Li, Danqi Wang, Yiwei Liao","doi":"10.1096/fj.202504837R","DOIUrl":"https://doi.org/10.1096/fj.202504837R","url":null,"abstract":"<p><p>Major depressive disorder (MDD) is a prevalent psychiatric disorder, and its pathophysiology is related to immune dysregulation. The use of genetic evidence to identify molecular targets of specific immune cell types will provide new directions for the development of precision immunotherapy. We integrated single-cell cis-eQTL data for 14 immune cell subtypes from the OneK1K cohort with MDD GWAS summary statistics. We assessed the causal effect of genetically predicted immune cell-specific gene expression on depression using single-cell transcriptome-wide Mendelian randomization (scTWMR), followed by Bayesian colocalization. Functional analyses included enrichment, protein-protein interaction, phenome-wide association, and druggability assessment. We identified six significant gene-cell associations across CD4⁺ T cells, immature B cells, and plasma cells. Three genes showed strong colocalization evidence (PPH₄ > 80%): PTCH1 (CD4 NC, OR = 1.17, P-FDR = 3.78 × 10^-4), MTHFD1L (plasma cells, OR = 1.11, P-FDR = 5.20 × 10^-7), and RP11-293M10.2 (CD4 NC, OR = 0.91, P-FDR = 7.96 × 10^-8). Enrichment implicated Hedgehog signaling and folate metabolism. Drug repurposing highlighted metabolites targeting MTHFD1L and approved drugs targeting PTCH1 warranting further investigation. This study provides evidence for a genetically predicted causal relationship between immune cell-specific gene expression and MDD, which not only constructs a screening framework for candidate gene drug targets but also validates and finds potential drug targets.</p>","PeriodicalId":50455,"journal":{"name":"The FASEB Journal","volume":"40 8","pages":"e71823"},"PeriodicalIF":4.2,"publicationDate":"2026-04-30","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147788042","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Correction to \"Nur77 Regulates the Phosphorylation of Smad3, Thereby Influencing Skeletal Muscle Fibrosis Caused by Obesity\".","authors":"","doi":"10.1096/fj.202601694","DOIUrl":"10.1096/fj.202601694","url":null,"abstract":"","PeriodicalId":50455,"journal":{"name":"The FASEB Journal","volume":"40 8","pages":"e71802"},"PeriodicalIF":4.2,"publicationDate":"2026-04-30","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147678550","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Analgesic Effects of Olfactory Stimulation: A Systematic Review of Clinical and Experimental Evidence.","authors":"Yunhe Zhu, Shan Wang, Jingping Sun, Qidong Zhang, Guobi Chai, Qingzhao Shi, Jian Mao, Wu Fan, Jianping Xie","doi":"10.1096/fj.202504977R","DOIUrl":"https://doi.org/10.1096/fj.202504977R","url":null,"abstract":"<p><p>Pain perception is a multidimensional process encompassing sensory, affective, and cognitive components. In recent years, accumulating evidence suggests that olfactory stimulation can modulate pain perception through neurophysiological and emotional mechanisms. However, systematic understanding of how olfactory processing contributes to analgesia across different experimental and clinical contexts remains limited. This review aims to provide an integrative overview of current evidence regarding the role of olfactory pathways in pain modulation, summarizing findings from human and animal studies that investigated the analgesic potential of volatile compounds. A systematic literature search was conducted across PubMed, Web of Science, OVID, Cochrane Reviews, Embase, CNKI, and WanFang databases. A total of 4360 records were retrieved, screened for relevance, and refined to 147 studies, including 138 human-based and 9 animal-based investigations. Lavender, peppermint, chamomile, bergamot, and citrus-derived oils were most frequently associated with analgesic outcomes. Olfactory stimulation was found to modulate pain via central integrative circuits involving affective, autonomic, and sensory processing, engaging conserved pathways that support descending pain inhibition. Olfactory stimulation by specific flavor and fragrance compounds holds translational potential for non-pharmacological pain management. Nevertheless, methodological standardization and mechanistic validation are necessary to advance this emerging field.</p>","PeriodicalId":50455,"journal":{"name":"The FASEB Journal","volume":"40 8","pages":"e71827"},"PeriodicalIF":4.2,"publicationDate":"2026-04-30","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147787869","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Integration of Single-Cell RNA Sequencing and Machine Learning to Identify and Validate Prognostic Genes With Lymph Node Metastasis and Immune Cell Signatures in Lung Adenocarcinoma.","authors":"Chuan Lin, Xuan Chen, Yong Sun, Xiaomei Tang, Yi Jiang","doi":"10.1096/fj.202503871R","DOIUrl":"10.1096/fj.202503871R","url":null,"abstract":"<p><p>The poor prognosis of lung adenocarcinoma (LUAD) remains unimproved. This study aimed to identify lymph node metastasis (LNM)-related and cellular immunity-related prognostic genes in LUAD and propose novel strategies to improve its prognosis. LUAD-related datasets were obtained from public databases. Prognostic genes and a prognostic model were obtained through various bioinformatics analyzes, and the immunotherapy response in risk groups was assessed. Subsequently, the expression levels of prognostic genes and the intercellular communication relationships were explored at the single-cell level. Moreover, malignant cells were identified, and their differentiation mechanisms were explored via inferCNV analysis. Additionally, FURIN was silenced and overexpressed to investigate its effects on the invasion, metastasis, and lymphangiogenesis of LUAD cells in vitro. RGS20, KYNU, RAET1E, FGF12, GJB2, CACNA2D2, FURIN, and GDF10 were identified as prognostic genes with LNM. In 4 datasets, LUAD patients with the high LNM and immune cell-related risk scores exhibited higher mortality rates compared to those in the low-risk group. Furthermore, individuals in the low-risk group demonstrated a greater propensity to derive advantages from immunotherapeutic interventions. Epithelial cells were identified as key cells, with CACNA2D2 being significantly up-regulated during their late-stage differentiation. Basal cells, the malignant subset within epithelial cells, showed elevated FURIN expression in the pre-differentiation phase, which declined in the middle and late phases. Functionally, FURIN was found to enhance the migratory and proliferative capacities of LUAD cells. Moreover, we demonstrated that FURIN accelerated lymphatic metastasis and lymphangiogenesis in vitro. In this paper, we identified LUAD prognostic genes with LNM and immune cell signatures, emphasized treating LUAD patients according to LNM- and immune cell-related risk scores, and provided novel ideas on how to improve poor prognosis and develop targeted therapy for LUAD.</p>","PeriodicalId":50455,"journal":{"name":"The FASEB Journal","volume":"40 8","pages":"e71783"},"PeriodicalIF":4.2,"publicationDate":"2026-04-30","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147678562","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Multi-Omics Integration Identifies the CBS-CTH-GSH Axis as a Critical Regulator of β-Cell Ferroptosis in Type 2 Diabetes.","authors":"Xiaotong Li, Fengdan Wang, Di Zhao, Yang Xu, Shoumeng Yan, Bo Li","doi":"10.1096/fj.202600188R","DOIUrl":"10.1096/fj.202600188R","url":null,"abstract":"<p><p>Ferroptosis, an iron-dependent form of regulated cell death, has been implicated in the pathogenesis of type 2 diabetes (T2DM), but its underlying mechanisms remain unclear. Here, we identify cystathionine β-synthase (CBS), a rate-limiting enzyme in the trans-sulfuration pathway, as a critical metabolic regulator linking glutathione (GSH) homeostasis to ferroptosis sensitivity in T2DM. Multi-omics integration revealed marked disruption of the ferroptosis pathway and GSH metabolism in patients with T2DM and highlighted CBS as a ferroptosis-associated gene strongly correlated with glycemic traits. Population-level analyses revealed that CBS expression was positively associated with GSH and negatively with plasma ferritin, and Mendelian randomization supported a causal protective effect of CBS on T2DM risk. In vitro, high glucose reduced CBS expression in MIN6 cells, whereas CBS overexpression increased GSH, restored antioxidant capacity, suppressed Fe²⁺ accumulation, and shifted ferroptosis markers toward an anti-ferroptotic profile, accompanied by improved β-cell functional gene expression. Notably, inhibition of GSH synthesis largely abolished the protective effects of CBS, indicating that the anti-ferroptotic function is GSH dependent. Mechanistically, cystathionine γ-lyase (CTH) was identified as an essential coregulator of CBS. Disruption of CTH greatly weakened CBS-driven improvements in GSH maintenance, iron-redox homeostasis, and β-cell function, establishing a functional CBS-CTH-GSH axis. In summary, our findings identify that CBS can protect β-cells from ferroptotic injury and functional decline under glucotoxic stress and highlight the CBS-CTH-GSH axis as a promising β-cell-targeted intervention point for delaying or preventing T2DM progression.</p>","PeriodicalId":50455,"journal":{"name":"The FASEB Journal","volume":"40 8","pages":"e71792"},"PeriodicalIF":4.2,"publicationDate":"2026-04-30","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147718736","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Defined Microbiota Modulates Host Metabolome and Skeletal Adaptation to Diet-Induced Obesity.","authors":"Melanie Cristine Scalise, Mathieu Simon, Jasmin Bernhardt, Ora Trümpi, Timm Hettich, Stefan Gaugler, Nikola Saulacic, Benjamin Gantenbein, Philippe Zysset, Maria Luisa Balmer","doi":"10.1096/fj.202600564RR","DOIUrl":"https://doi.org/10.1096/fj.202600564RR","url":null,"abstract":"<p><p>The gut microbiota is increasingly recognized as a regulator of host metabolism and bone physiology. However, how microbial colonization integrates systemic metabolic cues with skeletal remodeling under metabolic stress remains unclear. We used germ-free (GF) and gnotobiotic C57BL/6J mice colonized with the defined 12-member Oligo-Mouse-Microbiota (Oligo-MM¹²) to dissect microbiota-dependent bone adaptation during high-fat diet (HFD)-induced obesity. Micro-CT analysis revealed that only colonized mice exhibited structural adaptations, namely increased cortical thickness and trabecular area, in response to HFD, whereas GF mice failed to remodel their skeleton despite broadly comparable weight gain trajectories and adiposity. Serum metabolomics uncovered distinct microbiota-specific metabolic signatures. GF mice accumulated bone-relevant metabolites including lysine, uridine, DHA, and pyruvate, suggesting altered systemic handling of bone-relevant metabolites, whereas colonized mice displayed reduced circulating levels associated with skeletal remodeling. These metabolic patterns correlated with reduced β-CTX levels in colonized mice, indicative of microbiota-mediated suppression of bone resorption. Our findings identify the gut microbiota as a key determinant of skeletal adaptation to diet-induced obesity, presumably acting through systemic metabolic reprogramming and modulation of bone turnover. The defined-microbiota mouse model provides a powerful framework to disentangle the gut-bone axis at a systems and metabolic level.</p>","PeriodicalId":50455,"journal":{"name":"The FASEB Journal","volume":"40 8","pages":"e71831"},"PeriodicalIF":4.2,"publicationDate":"2026-04-30","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13098627/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147787995","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 Critical Role of GALNTs-Regulated O-GalNAc Glycosylation in Cancer Malignancy.","authors":"Jiahao Liu, Sihan Wu, Ge Zhang, Jiehan Li, Yuhan Yin, Aman Uiiah, Sanfei Peng, Yang Fu","doi":"10.1096/fj.202504815R","DOIUrl":"https://doi.org/10.1096/fj.202504815R","url":null,"abstract":"<p><p>Aberrant mucin-type O-glycosylation, mediated by the Polypeptide N-acetylgalactosaminyltransferase (GALNT) family of enzymes, is a defining feature of many cancers and has also been strongly linked to non-neoplastic conditions, including developmental disorders and metabolic abnormalities. Mucin-type O-GalNAc glycosylation, a prevalent and highly specific form of post-translational modification, is centrally involved in key processes underlying cancer progression, such as cell signaling, invasion, angiogenesis, and metastasis. It is intricately linked to a diverse array of human diseases, with a particular association with cancer. Ongoing research endeavors to elucidate the functional mechanisms by which GALNT enzymes regulate O-GalNAc glycosylation, thereby enhancing our understanding of their pivotal roles in cancer biology. Although significant advances have been made in understanding their contributions to cancer initiation and progression, a comprehensive characterization of both the GALNT family and O-GalNAc glycosylation in oncology remains lacking. This review aims to summarize the structure of the GALNT family and its regulatory roles in the initiation and elongation of O-GalNAc glycans, providing an in-depth exploration of the functions of GALNT-mediated O-GalNAc glycosylation in cancer. Ultimately, these insights will help uncover underlying oncogenic mechanisms and may offer new potential directions for the development of anticancer therapeutics and diagnostic biomarkers.</p>","PeriodicalId":50455,"journal":{"name":"The FASEB Journal","volume":"40 8","pages":"e71790"},"PeriodicalIF":4.2,"publicationDate":"2026-04-30","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13098630/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147787616","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":"Cathepsin G Promotes Hepatic Lipid Deposition by Regulating Key Genes Related to Lipid Metabolism.","authors":"Weili Yang, Jiaqi Lin, Qiuyue Pan, Yan Jiang, Tingting Shi, Xi Cao","doi":"10.1096/fj.202600042R","DOIUrl":"10.1096/fj.202600042R","url":null,"abstract":"<p><p>Cathepsins play critical roles in various physiopathological processes, with several reported to be associated with nonalcoholic fatty liver disease (NAFLD). Herein, we investigated the expression patterns of the cathepsin family in human and mouse livers, cultured hepatocytes, and their roles in NAFLD. Public datasets of NAFLD patients and controls were analyzed to examine hepatic cathepsin expression in human livers. RT-qPCR assessed these genes in mouse livers, HepG2, Hepa1-6, and mouse primary cells. Despite different expression patterns, CTSA, CTSB, CTSD, CTSH, and CTSL were consistently highly expressed across all samples. Notably, steatosis patients and diabetic mice exhibited significantly increased hepatic expression of four cathepsins. Among these, we first observed elevated CTSG and CTSW, with CTSG showing the most pronounced increase. Moreover, hepatic CTSG was increased and positively correlated with disease severity in NASH patients. CTSG was also upregulated in HepG2 cells treated with high glucose or free fatty acids. In vitro, CTSG overexpression promoted, while its knockdown reduced lipid accumulation. In vivo, hepatic CTSG overexpression significantly induced lipid deposition, impaired glucose tolerance, and elevated HOMA-IR. Mechanistically, CTSG upregulated key lipid synthesis genes (ACC, SCD1) and downregulated those involved in lipid oxidation (PPARα, Lcad) and secretion (MTTP) by suppressing Akt. Furthermore, Akt activation alleviated lipid deposition induced by CTSG overexpression, while Akt inhibition abolished the beneficial effect of CTSG knockdown. This study is the first to reveal the expression patterns of the cathepsin family in human and mouse livers, and identifies that hepatic CTSG is elevated in NAFLD and can promote lipid deposition, supporting CTSG as a novel potential therapeutic target for NAFLD.</p>","PeriodicalId":50455,"journal":{"name":"The FASEB Journal","volume":"40 8","pages":"e71788"},"PeriodicalIF":4.2,"publicationDate":"2026-04-30","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147718770","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}