{"title":"Identification of BMX as a Potential Biomarker for Rheumatoid Arthritis Based on WGCNA, Machine Learning, and Experimental Validation.","authors":"Xinmin Huang, Xu Cai, Zhenbo Yan, Xian Wu, Xinpeng Chen, Jianwei Xiao","doi":"10.1080/08820139.2026.2674702","DOIUrl":"10.1080/08820139.2026.2674702","url":null,"abstract":"<p><strong>Background: </strong>Rheumatoid arthritis (RA) is a chronic autoimmune disease needing reliable biomarkers. This study aimed to identify potential RA biomarkers using WGCNA and machine learning, and analyze their correlation with disease activity and STAT3.</p><p><strong>Methods: </strong>GEO datasets were used. WGCNA and three machine learning methods (LASSO, SVM, Boruta) screened common core genes. Correlation with STAT3 was analyzed. RT-qPCR validated core gene expression in RA patients. Correlation with clinical parameters (DAS28, CCP, RF, ESR) and ROC curves were assessed.</p><p><strong>Results: </strong>WGCNA identified 11 modules; the black module correlated most with RA. LASSO, SVM, and Boruta identified 16, 35, and 46 key genes respectively, with one overlapping core gene: BMX. BMX expression positively correlated with STAT3. RT-qPCR confirmed BMX upregulation in RA, which positively correlated with DAS28 and RF. ROC analysis gave an AUC of 0.789.</p><p><strong>Conclusion: </strong>BMX expression is upregulated in RA patients, correlates with disease activity, and represents a potential diagnostic biomarker. The BMX‑STAT3 correlation suggests its possible involvement in RA pathogenesis, but the regulatory relationship requires further functional validation.</p>","PeriodicalId":13387,"journal":{"name":"Immunological Investigations","volume":" ","pages":"1229-1246"},"PeriodicalIF":2.3,"publicationDate":"2026-08-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148042096","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":"TFEB Activator Curcumin Analog C1 Downregulates PKM2 and Alleviates Inflammatory Injury in Endotoxemic Mice.","authors":"Yanliuying Zhu, Xinyan Zan, Kerui Fan, Jiao Wang, Ying Zhi, Jinlin Liu, Yongqiang Yang, Li Zhang","doi":"10.1080/08820139.2026.2663149","DOIUrl":"10.1080/08820139.2026.2663149","url":null,"abstract":"<p><strong>Objective: </strong>Autophagy dysfunction results in the accumulation of pro-inflammatory components and drives inflammatory injury. Transcription factor EB (TFEB) is a master regulator of autophagy and a novel target for controlling inflammatory injury. Curcumin analog C1 directly binds to and activates TFEB, but its anti-inflammatory effects remain unclear.</p><p><strong>Methods: </strong>The anti-inflammatory and protective effects of curcumin analog C1 were investigated in lipopolysaccharide (LPS)-induced endotoxemia mice.</p><p><strong>Results: </strong>Curcumin analog C1 reversed LPS-induced autophagy dysfunction, downregulated pyruvate kinase M2 (PKM2), and reduced pro-inflammatory cytokines including TNF-α, IL-6, and MCP-1. It also attenuated systemic abnormalities, alleviated lung injury, and decreased blood urea nitrogen (BUN), brain-type natriuretic peptide (BNP), and extracellular DNA levels.</p><p><strong>Conclusions: </strong>Curcumin analog C1 exhibits potential pharmacological value in the control of inflammatory injury.Thank you for your assistance.</p>","PeriodicalId":13387,"journal":{"name":"Immunological Investigations","volume":" ","pages":"1146-1160"},"PeriodicalIF":2.3,"publicationDate":"2026-08-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147769761","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":"Mechanisms and Therapeutic Targeting of the Gut Microbiota-Immune-Brain Axis in Alzheimer's Disease.","authors":"Siwen Wang, Xu Yuan, Tiantian Wang, Meng Yang, Peiliang Dong, Hua Han","doi":"10.1080/08820139.2026.2669375","DOIUrl":"10.1080/08820139.2026.2669375","url":null,"abstract":"<p><strong>Background: </strong>Alzheimer's disease (AD) is a highly prevalent neurodegenerative disease globally. The main pathological features of AD are amyloid-β (Aβ) deposition and tau hyperphosphorylation. Recent studies suggest that the gut microbiota-immunity-brain axis plays an important role in the onset and progression of AD. Gut microbiota dysbiosis may impair intestinal barrier integrity and promote the entry of pro-inflammatory mediators into the circulation. Pro-inflammatory signals in the bloodstream may further activate the central immune system, drive microglial polarization, and increase the release of inflammatory factors in the brain. The resulting neuroinflammatory cascade may aggravate Aβ accumulation, tau phosphorylation, and cognitive impairment, although this mechanism has not been conclusively established in humans.</p><p><strong>Methods and results: </strong>Based on relevant literature on AD, gut microbiota, immunity, neuroinflammation, and the gut-brain axis, this article systematically reviews the mechanism of action of the microbiota-immunity-brain axis in AD. Current intervention strategies targeting this axis, including probiotics, fecal microbiota transplantation, dietary interventions, and traditional Chinese medicine, were also discussed. Such intervention measures have the potential to regulate the balance of the gut microbiota, reduce neuroinflammation, and slow the progression of AD pathology.</p><p><strong>Conclusion: </strong>It is essential to integrate multi-omics approaches in future research to deepen the understanding of AD pathogenesis and support the development of more precise and personalized treatment strategies.</p>","PeriodicalId":13387,"journal":{"name":"Immunological Investigations","volume":" ","pages":"1296-1326"},"PeriodicalIF":2.3,"publicationDate":"2026-08-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147874122","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}
Ming Li, Tingting Zhao, Jing Sun, Yunhui Wang, Lin Shen
{"title":"Screening of Sepsis Diagnostic Biomarkers Based on Fumarate Metabolism-Related Genes with Analysis of Immune Infiltration and Subtype Identification.","authors":"Ming Li, Tingting Zhao, Jing Sun, Yunhui Wang, Lin Shen","doi":"10.1080/08820139.2026.2667875","DOIUrl":"10.1080/08820139.2026.2667875","url":null,"abstract":"<p><strong>Background: </strong>Sepsis is a major global health challenge characterized by a complex pathogenesis involving an early hyperinflammatory phase followed by a subsequent immunosuppressive state. Recent studies have revealed that dysregulation of fumarate metabolism plays a central role in immune dysregulation during sepsis, making related genes promising candidates as novel diagnostic biomarkers and therapeutic targets.</p><p><strong>Methods: </strong>Three sepsis datasets (GSE65682, GSE95233, GSE131761) were analyzed to identify differentially expressed fumarate metabolism-related genes. Key genes were selected via machine learning (Least Absolute Shrinkage and Selection Operator, Support Vector Machine, Boruta) to construct a diagnostic model, validated by Receiver Operating Characteristic, nomogram, and Decision Curve Analysis. Immune infiltration, functional enrichment, subtype analysis, and a ceRNA network were further explored.</p><p><strong>Results: </strong>This study identified four core diagnostic genes for sepsis related to fumarate metabolism (EPHX2, S100A8, TXN, ANXA3). Immune analysis revealed increased infiltration of neutrophils and M1 macrophages in sepsis patients, alongside a reduction in adaptive immune cells such as CD8<sup>+</sup> T cells. Molecular subtyping based on these genes identified two sepsis subtypes with distinct immune characteristics, and a relevant ceRNA regulatory network was constructed.</p><p><strong>Conclusion: </strong>This study constructs a diagnostic model for sepsis based on fumarate metabolism-related genes, linking metabolic reprogramming to immune dysregulation and offering biomarkers and theoretical support for personalized treatment.</p>","PeriodicalId":13387,"journal":{"name":"Immunological Investigations","volume":" ","pages":"1209-1228"},"PeriodicalIF":2.3,"publicationDate":"2026-08-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147868101","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":"Molecular Mechanisms of Polysaccharides in Regulating Immune Function and Treating Rheumatoid Arthritis Through Modulation of Gut Microbiota.","authors":"Kunqin Huang, Jianlei Xie, Fang Zhang","doi":"10.1080/08820139.2026.2615701","DOIUrl":"10.1080/08820139.2026.2615701","url":null,"abstract":"<p><strong>Objective: </strong>To clarify the core mechanisms by which polysaccharides treat rheumatoid arthritis (RA) via gut microbiota modulation, and to systematically summarize their regulatory network and therapeutic potential. Methods: This study adopted a systematic review approach to synthesize existing evidence on polysaccharides in RA, focusing on their structural features, interactions with the gut microbiota, and downstream effects on host immunity and metabolism.</p><p><strong>Results: </strong>Polysaccharides with specific structural features (e.g., plant-derived polysaccharides containing β-1,4 glycosidic bonds) selectively enhanced the abundance of gut probiotics (e.g., <i>Bifidobacterium</i> and <i>Lactobacillus</i>) by 15%-30%. They also promoted the production of short-chain fatty acids (SCFAs, such as acetate and propionate) through microbial degradation, increasing intestinal concentrations of these metabolites by more than 20%. These changes further regulated host metabolism and immune function, including restoring the balance between regulatory T cells (Treg) and T helper 17 cells (Th17), and inhibiting the nuclear factor-kappa B (NF-κB) signaling pathway to alleviate joint inflammation.</p><p><strong>Limitations: </strong>Current research has critical clinical translation barriers: most evidence relies on in vitro experiments and animal models (e.g., collagen-induced arthritis (CIA) mice), while human clinical trials are restricted by small sample sizes and a lack of long-term follow-up data.</p><p><strong>Conclusions: </strong>Targeted interactions between polysaccharides and the gut microbiota represent a crucial pathway for RA intervention. Future research should focus on optimizing polysaccharide structural modification technologies, conducting large-scale multicenter clinical trials, and exploring personalized therapeutic strategies to promote the clinical translation of polysaccharides in RA treatment.</p>","PeriodicalId":13387,"journal":{"name":"Immunological Investigations","volume":" ","pages":"1327-1352"},"PeriodicalIF":2.3,"publicationDate":"2026-08-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148204738","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":"mRNA-Based Vaccines and Immunomodulatory Strategies for Muscle Regeneration and Recovery: A Comprehensive Review.","authors":"Yunchang Yang, XiangXiang Cao, Yongdong Li, Xinyao Kang, Yuping Huang, Huigen Feng, Changchun Li","doi":"10.1080/08820139.2026.2667884","DOIUrl":"10.1080/08820139.2026.2667884","url":null,"abstract":"<p><strong>Background: </strong>The convergence of vaccinology and immunotherapy with regenerative medicine provides a novel approach to therapeutic strategies for skeletal muscle repair.</p><p><strong>Methods: </strong>This review critically examines the application of mRNA-based platforms and immunomodulatory interventions, systematically bifurcating these strategies into two distinct pathophysiological domains: acute mechanical trauma (sports injuries) and senescence-driven, chronic age-related sarcopenia.</p><p><strong>Results: </strong>We detail how engineered mRNA can precisely control the expression of myogenic factors and immune modulators to overcome satellite cell dysfunction and inflammatory dysregulation. Furthermore, we critically evaluate current and emerging therapeutic paradigms - ranging from advanced biomaterial delivery systems to next-generation RNA platforms (e.g. circRNA and saRNA). Finally, we analyze their translational progress, the readiness of diagnostic modalities, and the profound ethical challenges of clinical integration, including the emerging threat of 'gene doping.'</p><p><strong>Conclusions: </strong>This comprehensive reference bridges microscopic molecular insights with macroscopic clinical practice for researchers in immunology, sports medicine, and geriatrics.</p>","PeriodicalId":13387,"journal":{"name":"Immunological Investigations","volume":" ","pages":"1247-1263"},"PeriodicalIF":2.3,"publicationDate":"2026-08-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147837613","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":"Lactylation-Mediated METTL14 Promotes Glycolysis Through Facilitating PGAM1 m6A Methylation in Non-Small Cell Lung Cancer.","authors":"Qibin Wang, Guangjun Liu","doi":"10.1080/08820139.2026.2662683","DOIUrl":"10.1080/08820139.2026.2662683","url":null,"abstract":"<p><strong>Objective: </strong>Non-small cell lung cancer (NSCLC) accounts for the highest proportion of lung cancers. METTL14 is a m6A methyltransferase affects the development of NSCLC. Lactylation can induced by glycolysis production lactate, but whether it modulates NSCLC through m6A methylation remains unclear. We aimed to determine whether METTL14 mediates NSCLC through glycolysis.</p><p><strong>Methods: </strong>METTL14 expression was validated in NSCLC clinical samples. Effects of METTL14 knockdown in NSCLC cells were evaluated by cell viability, colony formation and glycolysis. Lactylation was detceted by IP and western blotting.</p><p><strong>Results: </strong>We observed elevated METTL14 in NSCLC tissues and cells. METTL14 knockdown reduced cell viability, cell proliferation and glycolysis in NSCLC cells and tumor development <i>in vivo</i>. PGAM1 was the downstream target of METTL14, and METTL14 knockdown inhibited m6A level and mRNA stability of PGAM1. PGAM1 overexpression reversed the effect on METTL14 knockdown in NSCLC cells. Moreover, pan-lactylation, METTL14 expression and lactylation were upregulated in NSCLC tumor tissues, and exogenous promotion or inhibition of overall lactylation can promote or inhibit the lactylation level and protein stability of METTL14, respectively.</p><p><strong>Conclusion: </strong>Lactylation enhanced METTL14 expression, thereby promoting PGAM1 m6A methylation to facilitate glycolysis in NSCLC. This finding uncovers a novel metabolic regulatory axis and offers a potential therapeutic target for NSCLC intervention.</p>","PeriodicalId":13387,"journal":{"name":"Immunological Investigations","volume":" ","pages":"1127-1145"},"PeriodicalIF":2.3,"publicationDate":"2026-08-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147769688","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}
Marcio José Concepción-Zavaleta, Jean Pierre Villanueva-De La Cruz, Jenyfer Fuentes Mendoza, Luis Concepción-Urteaga, Cristian D Armas, Arturo Basurto-Ayala, José Paz-Ibarra
{"title":"Precision Medicine in Autoimmune Thyroid Diseases: Decoding Biomarkers, Targeted Therapies and Digital Innovation.","authors":"Marcio José Concepción-Zavaleta, Jean Pierre Villanueva-De La Cruz, Jenyfer Fuentes Mendoza, Luis Concepción-Urteaga, Cristian D Armas, Arturo Basurto-Ayala, José Paz-Ibarra","doi":"10.1080/08820139.2026.2663365","DOIUrl":"10.1080/08820139.2026.2663365","url":null,"abstract":"<p><strong>Introduction: </strong>Autoimmune thyroid diseases (AITDs), including Graves' disease and Hashimoto's thyroiditis, arise from genetic, epigenetic, and environmental disruption of immune tolerance. These conditions represent the extremes of thyroid autoimmunity and contribute substantially to global endocrine morbidity.</p><p><strong>Areas covered: </strong>Recent advances in precision medicine have identified novel biomarkers, such as circulating microRNAs (miR-22, miR-375) and exosomal proteins (VAMP8, hsa_circRNA_000102), which enhance early detection and disease monitoring. Immunogenetic profiling highlights polymorphisms in HLA-DR, CTLA4, and PTPN22 as susceptibility loci. Emerging therapies, including rituximab (anti-CD20), teprotumumab (anti-IGF-1 R), and SYD5115 (TSH-R antagonist), target specific immune pathways. Artificial intelligence improves diagnostic accuracy through radiomics and wearable biosensors, while epigenetic studies and microbiota research further refine pathophysiological understanding.</p><p><strong>Expert opinion: </strong>Despite these advances, major challenges remain in predicting phenotypic conversion and personalizing long-term therapy. Integration of multi-omics with digital health tools is expected to transform patient stratification and management. Within the next decade, precision medicine will likely redefine treatment algorithms, enabling individualized, dynamic care in AITDs.</p>","PeriodicalId":13387,"journal":{"name":"Immunological Investigations","volume":" ","pages":"1161-1193"},"PeriodicalIF":2.3,"publicationDate":"2026-08-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147769763","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":"Dual Faces of Immune Regulation: The Roles of Tregs and Bregs in <i>Helicobacter pylori</i> Infection and Therapeutic Implications.","authors":"Wathiqah Wahid, Barathan Muttiah, Alfizah Hanafiah","doi":"10.1080/08820139.2026.2707166","DOIUrl":"10.1080/08820139.2026.2707166","url":null,"abstract":"<p><p><b>Background:</b> <i>Helicobacter pylori</i> maintains life-long colonization even though it triggers a strong immune response. This phenomenon is mainly related to regulatory immune responses involving regulatory T cells (Tregs) and regulatory B cells (Bregs). These help in maintenance of immune tolerance but allow bacteria to survive.<b>Methods:</b> In this mini-review, existing data on immunoregulatory role of Tregs and Bregs in <i>H. pylori</i> infection are discussed, considering the cellular interactions, cytokine-mediated processes, impact on immune response and treatment prospects.<b>Results:</b> The FOXP3 Tregs down-regulate Th1 and Th17 immune responses through IL-10 and TGF-β production resulting in reduction of inflammatory response but blocking bacterial eradication. The IL-10 producing Bregs induce immune tolerance via inhibition of antigen presentation and expansion of Tregs, including Tr1 cells induction. Some new data suggest that regulation of the mentioned pathways, IL-10, TGF-β, PD-1/PD-L1 can increase chances of bacterial eradication and reduce adverse effects. Vaccines that target regulatory pathways in Tregs and Bregs also hold promise for the improvement of protective immunity.<b>Conclusion:</b> The Tregs and Bregs complement each other in the balance between the protection and tolerance during <i>H. pylori</i> infection. Better knowledge of this regulatory network will lead to targeted immunotherapy and improved vaccines.</p>","PeriodicalId":13387,"journal":{"name":"Immunological Investigations","volume":" ","pages":"1-20"},"PeriodicalIF":2.3,"publicationDate":"2026-07-30","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148630335","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":"SKAP1, FYN and CD3E Are Potential Biomarkers and Therapeutic Targets of Sepsis.","authors":"Xingkai Shen, Jian Guo, Kaili Yang, Yuhong Jin","doi":"10.1080/08820139.2026.2701227","DOIUrl":"https://doi.org/10.1080/08820139.2026.2701227","url":null,"abstract":"<p><strong>Background: </strong>Sepsis is a systemic inflammatory response caused by pathogen infection, leading tomultiple organ failure. This study aims to identify potential sepsis biomarkers.</p><p><strong>Methods: </strong>Differentially expressed genes in sepsis-related datasets GSE57065 and GSE95233 were analyzed, and sepsis-associated genes were identified using weighted gene co-expression network analysis. Protein-protein interaction network was further analyzed to screen the core genes, which were verified using external datasets GSE65682 and GSE9960. An <i>in vitro</i> septic cardiomyopathy model was constructed by inducing H9c2 cells with lipopolysaccharide (LPS).</p><p><strong>Results: </strong>TCF7, LEF1, FYN, IL7R, CD3E, SKAP1 and FCER1G showed significant differences between sepsis and the control samples, and were related with immune cells infiltration. Sepsis patients with high expression of SKAP1, FYN and CD3E had better prognosis. Overexpression of SKAP1, FYN and CD3E could significantly inhibit the levels of inflammatory counterfactors TNF-α, IL-6 and IL-8 induced by LPS, and reduce the apoptosis rate of H9c2 cardiomyocytes, the ratio of cleaved caspase 3 and Bax/Bcl-2. Additionally, SKAP1 and FYN exerted these biological functions partially via activating PI3K/Akt pathway.</p><p><strong>Conclusion: </strong>SKAP1, FYN and CD3E are potential sepsis biomarkers associsted with favorable prognosis, protecting against inflammation and cardiomyocyte apoptosis.</p>","PeriodicalId":13387,"journal":{"name":"Immunological Investigations","volume":" ","pages":"1-25"},"PeriodicalIF":2.3,"publicationDate":"2026-07-30","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148620003","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}