Immunobiology最新文献

{"title":"Clinical value of CTCs combined with serum tumor markers/inflammatory cytokines for the early diagnosis of non-small cell lung cancer","authors":"Xiuxue Gu ,&nbsp;Lingling Wan","doi":"10.1016/j.imbio.2026.153161","DOIUrl":"10.1016/j.imbio.2026.153161","url":null,"abstract":"<div><div>Objective: This study investigates the clinical utility of circulating tumor cells (CTCs) in combination with serum tumor markers/inflammatory cytokines for the diagnosis of early-stage non-small cell lung cancer (NSCLC). Methods: A retrospective analysis was conducted on the clinical data of 43 NSCLC patients (stage I-IIA) who underwent surgical treatment at the Fourth Hospital of Hebei Medical University between November 2021 and December 2022. A control group of 50 healthy individuals was also included. Comparative analyses of CTCs, serum tumor markers, and inflammatory cytokine levels were performed between the two groups. The clinical diagnostic value was assessed using receiver operating characteristic (ROC) curve analysis. Results: The median concentrations of CTCs, carcinoembryonic antigen (CEA), Cytokeratin 19 fragment (CYFRA21-1), neuron-specific enolase (NSE), interleukin-4 (IL-4), interleukin-6 (IL-6), interleukin-10 (IL-10), tumor necrosis factor-alpha (TNF-α), and interleukin-17 A (IL-17 A) were significantly elevated in the NSCLC cohort compared to the healthy control cohort, while interleukin-2 (IL-2) levels were reduced (<em>P</em> &lt; 0.05). ROC curve analysis revealed that CTCs exhibited a sensitivity of 65.12%, specificity of 100.00%, and an area under the curve (AUC) of 0.826 for the diagnosis of early-stage NSCLC. The combined diagnostic sensitivity of CTCs, CEA, CYFRA21-1, and NSE reached 86.05%, with 100.00% specificity and an AUC of 0.945. Among the seven inflammatory cytokines evaluated, IL-17 A exhibited the highest diagnostic efficacy for early-stage NSCLC, with an AUC of 0.871, sensitivity of 93.02%, and specificity of 75.00%. The combination of IL-17 A and CTCs achieved an AUC of 0.953, with a sensitivity of 86.05% and specificity of 90.00%. Conclusion: The integration of CTCs with serum tumor markers and/or inflammatory cytokines provides high sensitivity and specificity for the diagnosis of early-stage NSCLC, highlighting its significant clinical potential.</div></div>","PeriodicalId":13270,"journal":{"name":"Immunobiology","volume":"231 2","pages":"Article 153161"},"PeriodicalIF":2.3,"publicationDate":"2026-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"146131788","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":"BCL3 drives an immunosuppressive tumor microenvironment in esophageal cancer by promoting M2 macrophage polarization via STAT3 activation","authors":"Yushuai Geng ,&nbsp;Haowen Ma ,&nbsp;Minghang Liu ,&nbsp;Tairan Feng ,&nbsp;Yang Lv ,&nbsp;Zhiqiang Li ,&nbsp;Shujun Ma ,&nbsp;Hui Wang ,&nbsp;Yuna Niu","doi":"10.1016/j.imbio.2026.153164","DOIUrl":"10.1016/j.imbio.2026.153164","url":null,"abstract":"<div><h3>Introduction</h3><div>The progression of esophageal cancer is closely linked to the establishment of an immunosuppressive tumor microenvironment. Although B-cell leukemia/lymphoma 3 (BCL3) is dysregulated in various cancers, its specific role and mechanism in shaping the immune microenvironment of esophageal cancer, particularly in macrophage polarization, remain elusive.</div></div><div><h3>Results</h3><div>BCL3 was significantly overexpressed in esophageal cancer tissues, demonstrated good diagnostic value (AUC = 0.75, <em>P</em> &lt; 0.01), and its high expression was significantly associated with poor patient prognosis (<em>P</em> &lt; 0.05). Immune infiltration analysis revealed that high BCL3 expression correlated with increased M2 macrophage infiltration. In vitro experiments confirmed that knocking down BCL3 suppressed M2 macrophage polarization. Mechanistic studies indicated that BCL3 drives M2 polarization by enhancing the phosphorylation of STAT3.</div></div><div><h3>Conclusion</h3><div>Our study unveils a novel mechanism whereby BCL3 promotes an immunosuppressive tumor microenvironment in esophageal cancer by facilitating M2 macrophage polarization via the STAT3 signaling pathway. BCL3 represents a potential prognostic biomarker and a promising therapeutic target for immunotherapy in esophageal cancer.</div></div>","PeriodicalId":13270,"journal":{"name":"Immunobiology","volume":"231 2","pages":"Article 153164"},"PeriodicalIF":2.3,"publicationDate":"2026-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"146197513","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":"Preface to the special issue for the 30th International Complement Workshop Brisbane 2025","authors":"Barbara E. Rolfe ,&nbsp;John D. Lee ,&nbsp;Trent M. Woodruff","doi":"10.1016/j.imbio.2025.153149","DOIUrl":"10.1016/j.imbio.2025.153149","url":null,"abstract":"<div><div>This <em>Immunobiology</em> special issue commemorates the 30th International Complement Workshop, held for the first time in Australia. Reflecting the global reach of complement research, the Workshop brought together delegates from 24 countries and showcased a diverse range of topics including: Structural insight into complement function; Mechanisms of activation and regulation; Cell-autonomous and intracellular complement; Novel and non-canonical roles; Complement in infection and disease; and Biomarkers, diagnostics and therapeutics<em>.</em> In addition to invited reviews and an original research article, this issue includes all accepted abstracts from the Workshop. Together, these contributions provide a compelling snapshot of a rapidly evolving field, one that continues to expand in scope and deepen mechanistic understanding. They highlight the dynamic, interdisciplinary and collaborative nature of complement research, and set the stage for future discoveries that will translate into clinical benefit.</div></div>","PeriodicalId":13270,"journal":{"name":"Immunobiology","volume":"231 2","pages":"Article 153149"},"PeriodicalIF":2.3,"publicationDate":"2026-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145827669","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":"Unraveling SLAN+/− monocytes transcriptomics in lupus and extracellular vesicles effects","authors":"Paula X. Losada ,&nbsp;Juan Antonio Villatoro-García ,&nbsp;Julio Jaramillo ,&nbsp;Lina Serrato ,&nbsp;Karen Álvarez ,&nbsp;Daniel Rodriguez ,&nbsp;Juan Camilo Diaz ,&nbsp;Ricardo Pineda ,&nbsp;Pedro Carmona-Saez ,&nbsp;Mauricio Rojas ,&nbsp;Gloria Vásquez","doi":"10.1016/j.imbio.2025.153153","DOIUrl":"10.1016/j.imbio.2025.153153","url":null,"abstract":"<div><h3>Objective</h3><div>Lupus Nephritis (LN) is a common and serious complication in patients with Systemic Lupus Erythematosus (SLE), an immune complex-mediated disease. Extracellular Vesicles (EVs) can carry autoantigens recognized by circulating antibodies, forming immune complexes (ICs) that may deposit in the kidney and be detected by inflammatory cells like monocytes in LN class III/IV. The SLAN marker identifies a subset of non-classical monocytes considered highly inflammatory and migratory. However, the interactions between these blood components in the context of LN remain incompletely understood. We aimed to analyze the transcriptional profiles of circulating SLAN+/− monocytes from LN patients and assess the influence of patient-derived EVs on SLAN− monocyte gene expression.</div></div><div><h3>Methods</h3><div>SLAN+/− monocytes were isolated from female LN patients, and controls were matched by similar age. Plasma-derived EVs from LN patients were co-incubated with SLAN-monocytes from controls. Next-generation RNA sequencing was employed to evaluate gene expression profiles and changes induced by EVs, followed by bioinformatic analysis to identify differential gene expression and functional pathways.</div></div><div><h3>Results</h3><div>Monocytes from LN patients exhibited an inflammatory profile characterized by elevated interferon response genes. The SLAN+ fraction displayed biological processes relevant to renal pathology, including cellular stress response, differentiation, and migration pathways. EVs elicited an inflammatory response with differentiation potential in non-SLAN monocytes.</div></div><div><h3>Conclusions</h3><div>These findings suggest that EVs transport antigenic molecules and induce transcriptional changes in monocytes toward inflammatory and migratory states, implicating them in LN pathogenesis and highlighting their potential as therapeutic targets.</div></div>","PeriodicalId":13270,"journal":{"name":"Immunobiology","volume":"231 2","pages":"Article 153153"},"PeriodicalIF":2.3,"publicationDate":"2026-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145976249","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":"Chlamydia psittaci inclusion membrane protein CPSIT_0844 elicits inflammatory IL-6 and IL-8 production in human monocytes via TLR2/TLR4 signaling pathways","authors":"Xiaoliang Yan ,&nbsp;Buwei Wang ,&nbsp;Kang Zheng ,&nbsp;Dan Luo ,&nbsp;Yumeng Li ,&nbsp;Jian Xiao ,&nbsp;Yuqing Chen ,&nbsp;Zhangping He ,&nbsp;Yating Wen ,&nbsp;Chuan Wang ,&nbsp;Yimou Wu","doi":"10.1016/j.imbio.2026.153160","DOIUrl":"10.1016/j.imbio.2026.153160","url":null,"abstract":"<div><div>The respiratory disease caused by <em>Chlamydia psittaci</em> (<em>C. psittaci</em>) infection is often characterized by significant inflammation. In the present study, we demonstrated that the <em>C. psittaci</em> inclusion membrane protein CPSIT_0844 induced THP-1 cells to express IL-6 and IL-8. However, silencing of the Toll-like receptor 2 (TLR2) and Toll-like receptor 4 (TLR4) genes by using small interfering RNA (siRNA) and transfection with the dominant negative plasmid encoding MyD88 (pDeNy-hMyD88) were found to reduce the expression of IL-6 and IL-8 in THP-1 cells stimulated with CPSIT_0844. Furthermore, CPSIT_0844 induces IL-6 and IL-8 production by signaling pathways involving JNK, p38, and NF-κB in monocytes. Collectively, our findings identify CPSIT_0844 as a proinflammatory virulence factor that triggers IL-6 and IL-8 expression via a TLR2/TLR4-MyD88-dependent mechanism, culminating in the activation of MAPK and NF-κB pathways. This work provides crucial molecular insight into the inflammatory pathogenesis of <em>C. psittaci</em> infection.</div></div>","PeriodicalId":13270,"journal":{"name":"Immunobiology","volume":"231 2","pages":"Article 153160"},"PeriodicalIF":2.3,"publicationDate":"2026-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"146036477","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":"Unveiling a novel NBAS mutation in common variable immunodeficiency: Expanding the genetic landscape of immunodeficiency disorders","authors":"Theresia Risa Davita ,&nbsp;Deepti Naruka ,&nbsp;Harry Lesmana ,&nbsp;James Fernandez","doi":"10.1016/j.imbio.2025.153144","DOIUrl":"10.1016/j.imbio.2025.153144","url":null,"abstract":"<div><div><em>NBAS</em>, neuroblastoma-amplified sequence, mutations have been linked to multisystem disorders, including immunodeficiency. Common variable immunodeficiency (CVID) represents a heterogeneous group of primary immunodeficiency disorders characterized by hypogammaglobulinemia, lack of functional antibodies, and frequent sinopulmonary or gastrointestinal infections. The exact cause of CVID is often unknown; however, recent studies using gene sequencing have identified disease-causing genes underlying this heterogeneous immune defect. Here, we present a case of a novel <em>NBAS</em> mutation identified in a patient with CVID, revealing the genetic basis of immunodeficiency disorders and emphasizing the importance of comprehensive genetic analysis in clinical practice. This case underscores the need for further investigation into the functional consequences of <em>NBAS</em> mutations and their implications for the management of CVID and related immune conditions.</div></div>","PeriodicalId":13270,"journal":{"name":"Immunobiology","volume":"231 2","pages":"Article 153144"},"PeriodicalIF":2.3,"publicationDate":"2026-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147490895","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":"Screening of kinase-related genes as diagnostic biomarkers and immune infiltration analysis in sepsis","authors":"Bingqiang Su ,&nbsp;Yingwei Ding ,&nbsp;Xiuqi Zhu ,&nbsp;Laifa Kong","doi":"10.1016/j.imbio.2026.153158","DOIUrl":"10.1016/j.imbio.2026.153158","url":null,"abstract":"<div><h3>Background</h3><div>Sepsis is a systemic inflammatory syndrome that can lead to loss of organ function. Kinase-related genes (KRGs) modulate immune diseases by regulating inflammation, immune metabolism, and apoptosis. However, their specific role in Sepsis remains unexplored.</div></div><div><h3>Methods</h3><div>mRNA and single-cell sequencing data in sepsis were obtained from the Gene Expression Omnibus. Weighted gene co-expression network analysis (WGCNA) was used to identify gene modules associated with sepsis, which were intersected with KRGs to determine candidate genes. Functional enrichment analyses (GO, KEGG, GSVA) were conducted, followed by biomarker selection using Least Absolute Shrinkage and Selection Operator (LASSO) regression and the Boruta algorithm. Model performance was assessed via receiver operating characteristic (ROC) curves, and immune infiltration was assessed using CIBERSORT and ssGSEA. Consensus clustering defined kinase-associated molecular subtypes of sepsis, while CellChat analysis of single-cell data characterized intercellular communication patterns.</div></div><div><h3>Results</h3><div>This study employed WGCNA and machine learning analyses to identify four key diagnostic genes for sepsis—ZAP70, TXK, TRRAP, and TRIM28—and constructed a highly accurate diagnostic model (AUC = 0.986). Immune infiltration analysis revealed significant associations with T cells, NK cells, and other cell types. Single-cell data analysis demonstrated increased proportions of platelets and neutrophils in sepsis, highlighted the prominent role of monocytes in intercellular communication, and showed widespread expression of TRIM28 in monocyte subsets. Additionally, two distinct molecular subtypes with significant immune differences were identified.</div></div><div><h3>Conclusion</h3><div>This study systematically analyzed KRGs in sepsis and identified four clinically valuable biomarkers. By integrating single-cell transcriptomic data, it offers novel insights into the pathogenesis of sepsis and proposes potential biomarkers and therapeutic targets.</div></div>","PeriodicalId":13270,"journal":{"name":"Immunobiology","volume":"231 2","pages":"Article 153158"},"PeriodicalIF":2.3,"publicationDate":"2026-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"146029464","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":"Advances in research on the complement system and cognitive impairment","authors":"Jie Gao ,&nbsp;Zhe Li ,&nbsp;Xinyue Zhang,&nbsp;Wenshu Huang,&nbsp;Zhiyu Tian,&nbsp;Chuyu Xiao,&nbsp;Yuanyang Zhen,&nbsp;Fang Yu ,&nbsp;Xuezhao Cao","doi":"10.1016/j.imbio.2026.153157","DOIUrl":"10.1016/j.imbio.2026.153157","url":null,"abstract":"<div><div>Cognitive impairment is a global health problem with increasing prevalence and mortality rates. The complement system plays a key role in the underlying pathological mechanisms. To explore potential strategies for ameliorating and preventing cognitive impairment through targeted therapies involving the complement system, it is crucial to understand the relationship between the complement system and neuroinflammation, as well as its role in the development of cognitive dysfunction. In recent years, the mechanisms involving the complement system and its targeted treatments have become a major focus of research. This review provides an overview of the physiological functions of the complement system, its association with to neuroinflammation, the mechanisms by which it contributes to cognitive impairment, and the potential applications of complement inhibitors in the treatment of cognitive dysfunction.</div></div>","PeriodicalId":13270,"journal":{"name":"Immunobiology","volume":"231 1","pages":"Article 153157"},"PeriodicalIF":2.3,"publicationDate":"2026-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145973287","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":"MiR-210 suppresses Candida albicans-derived β-glucan-induced inflammation in THP-1-derived macrophages via the Syk-NF-κB pathway","authors":"Junsheng Hou ,&nbsp;Min Li","doi":"10.1016/j.imbio.2026.153156","DOIUrl":"10.1016/j.imbio.2026.153156","url":null,"abstract":"<div><div>In immunocompromised individuals, infections due to <em>Candida albicans (C. albicans)</em> can be life-threatening. Recognition of the insoluble β-glucan derived from the <em>C. albicans</em> cell wall <em>(CaIG)</em> by Dectin-1 in macrophages initiates an inflammatory reaction that is critical for clearing the fungal infection. However, uncontrolled inflammation may lead to septic shock. Research has established that miR-210 is strongly upregulated in THP-1-derived macrophages (THP-1 macrophages) following <em>CaIG</em> stimulation. MiR-210 has been implicated in the metabolic and immunological responses of macrophages in various infectious and inflammatory disease models. Nevertheless, whether miR-210 modulates Dectin-1-activated inflammation remains unclear. An in vitro inflammation model was established using <em>CaIG</em>-stimulated THP-1 macrophages in the current research. By using miR-210 mimic and inhibitor transfection approaches, we observed that miR-210 overexpression significantly reduced <em>CaIG</em>-induced IL-6 and TNF-α expression, whereas inhibition of endogenous miR-210 enhanced their production. Furthermore, by inhibiting <em>CaIG</em>-triggered spleen tyrosine kinase (Syk) activation and subsequent IκBα phosphorylation, miR-210 effectively prevents the accumulation of NF-κB p65 in the nucleus in THP-1 macrophages. These findings demonstrate that miR-210 participates in negative feedback to limit <em>CaIG</em>-triggered inflammation, primarily through downregulating the Syk-NF-κB signaling cascade. In summary, our findings reveal that miR-210 acts as a precise inflammatory modulator in macrophages, highlighting its therapeutic potential.</div></div>","PeriodicalId":13270,"journal":{"name":"Immunobiology","volume":"231 1","pages":"Article 153156"},"PeriodicalIF":2.3,"publicationDate":"2026-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145973288","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":"Single-cell transcriptome reveals that immune cells inhibit the repairment of IGFBP3 + stromal cells in thin endometrium","authors":"Haijiao Zou ,&nbsp;Dongmei Zhou ,&nbsp;Shaodan Fang ,&nbsp;Han Lin ,&nbsp;Hanzhen Xiong ,&nbsp;Qingping Jiang ,&nbsp;Mingxing Liu ,&nbsp;Xiujie Sheng ,&nbsp;Miaoxian Ou","doi":"10.1016/j.imbio.2025.153152","DOIUrl":"10.1016/j.imbio.2025.153152","url":null,"abstract":"<div><div>Thin endometrium (TE), affecting 1.5 %–9.1 % of reproductive-aged women, emerges as a disturbed decidua microenvironment underpinning implantation failure and recurrent pregnancy loss. Through integrated single-cell transcriptomics with histopathology and multiplex immunofluorescence (TSA) validation, we delineated TE as a disease of coordinated repairment impairment and pro-fibrotic remodeling across stromal and immune compartments. Key findings revealed a pathological imbalance in stromal subsets, including the decrease of regenerative IGFBP3 + Stromal_1 cells and expansion of fibrogenic Stromal_2 populations, driving collagen-dominant extracellular matrix remodeling. Concurrently, immune dysfunction was unmasked. NK cells decreased and shifted from immune surveillance to a pro-inflammatory phenotype, T cells transitioned from immune regulation to extracellular matrix remodeling effectors and macrophages adopted a pro-fibrotic phenotype with lipid metabolic collapse. CellChat analysis pinpointed suppression of GZMA-PARD3 and APOE-TREM2 axes as drivers of stromal dysfunction, while the hyperactivated adhesion (LAMA3) and collagen pathways served as central mediators of the fibro-inflammatory cascade. These findings, based on single-cell RNA-seq and spatial verification, suggest therapeutic targets for restoring endometrial homeostasis in TE. These findings suggested that TE as a disease of progressive stromal-immune fibrosis dysregulation, offering novel therapeutic targets to restore endometrial repairment and microenvironmental homeostasis.</div></div>","PeriodicalId":13270,"journal":{"name":"Immunobiology","volume":"231 1","pages":"Article 153152"},"PeriodicalIF":2.3,"publicationDate":"2026-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145911098","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}