Critical Reviews in Eukaryotic Gene Expression最新文献

{"title":"SPIB Modulates Macrophage Polarization and Correlates with Prognosis in Breast Cancer.","authors":"Le Cui, Yun Li, Zhengjun Cui","doi":"10.1615/CritRevEukaryotGeneExpr.2025060230","DOIUrl":"https://doi.org/10.1615/CritRevEukaryotGeneExpr.2025060230","url":null,"abstract":"<p><p>Breast cancer (BC) is the leading malignancy affecting women globally, characterized by significant heterogeneity. Therefore, our objective was to explore potential targets within the context of intra-tumor heterogeneity (ITH) to modulate the response of tumor-associated macrophages (TAMs) to treatment in BC patients. The TCGA database was used to integrate and analyze human BC samples, from which the ITH score was extracted to identify genetic differences. Using non-negative matrix factorization clustering analysis, we successfully identified two distinct molecular subtypes, referred to as C1 and C2. Notably, subtype C1 exhibited a significantly more favorable prognosis compared with subtype C2. Further investigation of immune cell infiltration using the CIBERSORT algorithm revealed a significant correlation between both subtypes and the infiltration of TAMs. Additionally, we identified SPIB as a key factor influencing TAM infiltration within the model. Notably, SPIB is expressed at low levels in BC and is associated with an unfavorable prognosis for patients. Interestingly, overexpression of SPIB led to increased infiltration of M1 macrophages. In conclusion, this study sheds light on the characteristics of BC and immune cell infiltration within its microenvironment. SPIB emerges as a promising therapeutic candidate, with potential to modulate the immunosuppressive nature of the BC microenvironment and improve patient outcomes.</p>","PeriodicalId":56317,"journal":{"name":"Critical Reviews in Eukaryotic Gene Expression","volume":"35 7","pages":"51-63"},"PeriodicalIF":1.6,"publicationDate":"2025-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145369334","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":"Epigenetic Signatures and Prognostic Biomarkers Analysis of Methylation-Driven Genes in Uterine Endometrial Carcinosarcoma.","authors":"Na Zhang, Wangshu Li, Fang Wang, Cailing Han, Guijun Li, Liyun Ren, Chen Hua","doi":"10.1615/CritRevEukaryotGeneExpr.2024055577","DOIUrl":"10.1615/CritRevEukaryotGeneExpr.2024055577","url":null,"abstract":"<p><p>Uterine corpus endometrial carcinoma (UCEC) is one of the most common gynecological malignancies, and understanding the molecular mechanisms underlying its development is essential for improving diagnosis and treatment. However, the role of DNA methylation, a key epigenetic modification, in UCEC prognosis prediction and clinical treatment strategies has rarely been studied. This study utilized publicly available datasets from The Cancer Genome Atlas (TCGA) and online bioinformatics tools to analyze the differential methylation and expression of six selected genes: TP53, PTEN, PTX3, TNK1, PPP2R1A, and KLRG2. These genes were chosen based on their known roles in cancer-related pathways, previous associations with oncogenic processes, and preliminary data showing significant changes in methylation and expression in UCEC compared with normal tissues. We integrated mRNA expression and DNA methylation data with the MethylMix method to identify genes with methylation-driven expression changes. Our analysis revealed that these genes exhibit distinct differential expression and methylation patterns in UCEC, suggesting potential regulatory mechanisms. The expression patterns across the six genes were observed, and TP53, TNK1, PPP2R1A, and KLRG2 were upregulated in tumors, and PTX3 was downregulated in tumors. At the same time, there was no significant change in the expression of PTEN gene. The differential expression correlates with changes in methylation, providing insights into the gene regulation occurring in UCEC. Additionally, Kaplan-Meier survival analysis revealed that the expression levels of specific genes, particularly PTX3, TNK1, and KLRG1, are significantly associated with overall survival in UCEC patients. Higher expression of these genes correlated with poorer survival outcomes, suggesting their potential as prognostic markers. In contrast, the expression of TP53, PTEN, and PPP2R1A did not show a significant impact on patient survival. The functional importance of these genes was investigated utilizing pathway enrichment and protein-protein interaction networks. Additionally, pathway enrichment analysis indicated these genes are involved in critical cancer pathways. The findings highlight the importance of integrating epigenetic and transcriptomic data to understand UCEC pathogenesis and suggest that the identified genes could serve as potential biomarkers for early diagnosis and treatment strategies.</p>","PeriodicalId":56317,"journal":{"name":"Critical Reviews in Eukaryotic Gene Expression","volume":"35 2","pages":"27-47"},"PeriodicalIF":1.5,"publicationDate":"2025-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143434419","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":"Propofol Protects against Pyroptosis of Photoreceptors in Subretinal Hemorrhage via Regulating SIRT6/NLRP3 Signaling.","authors":"Huihui Wang, Limei Zhang, Xiaoli Bai, Hao Wang, Hao Sun","doi":"10.1615/CritRevEukaryotGeneExpr.2024056605","DOIUrl":"10.1615/CritRevEukaryotGeneExpr.2024056605","url":null,"abstract":"<p><p>Subretinal hemorrhage-induced neurotoxicity is a key cause of vision loss in age-related macular degeneration (AMD). The purpose of this study is to investigate the effects of Propofol on neurotoxicity. Oxygen glucose deprivation (OGD) was used to establish in vitro subretinal hemorrhage model. Gene expression was determined using reverse transcription-quantitative polymerase chain reaction and western blot. Cytokine release was determined using enzyme-linked immunosorbent assay. The interaction between sirtuin 6 (SIRT6) and NLR family pyrin domain containing 3 (NLRP3) was detected using co-immunoprecipitation assay. Cellular function was determined using cell counting kit-8 assay, lactate dehydrogenase assay, and terminal deoxynucleotidyl transferase dUTP nick end labeling assay. Propofol suppressed the inflammatory response induced by OGD. Moreover, Propofol inhibited the neurotoxicity and pyroptosis of photoreceptors. Propofol mediated the overexpression of SIRT6, which was downregulated in AMD. Inhibition of SIRT6 alleviated its deacetylation of NLRP3. Additionally, SIRT6 deficiency antagonized the effects of Propofol and promoted the neurotoxicity and pyroptosis of photoreceptors. Taken together, Propofol protects against subretinal hemorrhage-induced neurotoxicity and pyroptosis of photoreceptors via promoting SIRT6-mediated deacetylation of NLRP3.</p>","PeriodicalId":56317,"journal":{"name":"Critical Reviews in Eukaryotic Gene Expression","volume":"35 2","pages":"75-85"},"PeriodicalIF":1.5,"publicationDate":"2025-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143434426","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-143-3p Inhibits the Differentiation of Th1 Cells in Rhinosinusitis by Regulating TET1/IFN-γ Signaling.","authors":"Peiyuan Tang, Peng Zhang, Yiping Wang, Yuxi Qin, Tong Mi, Geng Zhang, Ying Guo","doi":"10.1615/CritRevEukaryotGeneExpr.2025059784","DOIUrl":"https://doi.org/10.1615/CritRevEukaryotGeneExpr.2025059784","url":null,"abstract":"<p><p>Dysregulated microRNAs (miRNAs) are a hallmark of chronic rhinosinusitis, especially chronic rhinosinusitis with nasal polyps (CRSwNP). This study aimed to investigate the role of miR-143-3p in chronic rhinosinusitis. miR-143-3p and mRNA levels were calculated by reverse transcription quantitative polymerase chain reaction (RT-qPCR). Protein expressed was determined by Western blot. The infiltration of CD4 cells and eosinophils was analyzed using immunohistochemistry and hematoxylin and eosin staining. The binding sites between miR-143-3p and TET1 were predicted with TargetScan and verified using luciferase assay. The DNA methylation of interferon-gamma (IFN-γ) was predicted using DNA methylation-specific RT-qPCR assay. The interaction between TET1 and IFN-γ was confirmed using the chromatin immunoprecipitation assay. CD4+ T cell polarization was analyzed using flow cytometry. miR-143-3p was downregulated in CRSwNP patients, mediating nasal polyp presence. Overexpressed miR-143-3p promoted the differentiation of T helper 1 (Th1) cells. miR-143-3p targeted and downregulated the expression of TET1, which was upregulated in CRSwNP patients. TET1-mediated DNA methylation of IFN-γ, inducing its downregulation. Overexpressed TET1 inhibited Th1 differentiation and promoted the Th1 cell to Th2 polarization. miR-143-3p promotes the differentiation of anti-inflammatory Th1 cells in CRSwNP via regulating TET1/IFN-γ axis.</p>","PeriodicalId":56317,"journal":{"name":"Critical Reviews in Eukaryotic Gene Expression","volume":"35 7","pages":"1-10"},"PeriodicalIF":1.6,"publicationDate":"2025-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145369363","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":"Helicobacter pylori Suppress the Ferroptosis of Gastric Cancer via Inhibiting NAE1-Mediated Neddylation of TFR1.","authors":"Xinguo Wang, Xingting Ma, Lazati Baheti, Juan Dong, Jie Xu","doi":"10.1615/CritRevEukaryotGeneExpr.2025060632","DOIUrl":"10.1615/CritRevEukaryotGeneExpr.2025060632","url":null,"abstract":"<p><p>Helicobacter pylori (H. pylori) infection promotes the progression of gastric cancer. The purpose of this study is to investigate the effects of H. pylori infection on gastric cancer and the underlying mechanisms. mRNA levels were determined by reverse transcription quantitative PCR (RT-qPCR). Protein expression was detected by Western blot. Cell viability was detected by Cell Counting Kit-8 assay. Cell proliferation was detected by colony formation assay. Cell mobility was detected by transwell assay. The co-localization of NEDD8 activating enzyme E1 subunit 1 (NAE1) and transferrin receptor 1 (TFR1) was determined by fluorescence in situ hybridization (FISH) assay. TFR1 neddylation was determined using in vitro neddylation assay. H. pylori infection contributed to the proliferation, migration, and invasion of gastric cancer. Moreover, H. pylori infection inhibited erastin-induced ferroptosis of gastric cancer cells. H. pylori infection downregulated NAE1, which promoted the neddylation and protein stability of TFR1. Intriguingly, overexpressed NAE1 inhibited the metastasis as well as promoted the ferroptosis of gastric cancer. H. pylori infection mediates malignant behaviors of gastric cancer via inactivating NAE1/TFR1 signaling. Therefore, targeting NAE1/TFR1 signaling may provide a novel strategy for gastric cancer.</p>","PeriodicalId":56317,"journal":{"name":"Critical Reviews in Eukaryotic Gene Expression","volume":"35 7","pages":"39-49"},"PeriodicalIF":1.6,"publicationDate":"2025-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145369306","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":"Specific Non-Coding RNAs Involve in and Regulate the Transcriptional Network during Keloid Formation.","authors":"Xun Zhang, Linlin Song, Yong Ma, Zifu Zhou, Qiyun Luo, Juan Zhang, Yaozhu Yang, Lei Liu, Lifeng Guan","doi":"10.1615/CritRevEukaryotGeneExpr.2025056805","DOIUrl":"10.1615/CritRevEukaryotGeneExpr.2025056805","url":null,"abstract":"<p><p>Keloid formation is an undesirable outcome of wound healing and is detrimental to patients' physical and mental health, while the molecular regulators of its pathogenesis, especially non-coding RNAs (ncRNAs), are largely unknown. In this study, we integrated and analyzed RNA-seq and miRNA microarray datasets of skin samples from keloid-prone and healthy normal individuals to detect the dysregulated long ncRNAs (lncRNAs) and miRNAs. We excavated 583 and 104 keloid-specific lncRNAs and miRNAs, respectively. Moreover, the molecular functions of these ln-cRNAs and miRNAs are all related to ossification. Next, we constructed the relationship between lncRNAs and immune cell infiltration, and found the macrophages, NK cells, and dendritic cells were specifically dysregulated in keloid-prone or normal groups during wound healing. We constructed the potential regulatory network between these cell types and 20 dysregulated lncRNAs, suggesting their regulatory function in keloid formation. At last, we constructed the competitive endogenous RNA network and found two hub lncRNAs and five miRNAs, including DLEU1 and SLC25A21-AS1, miR-197-5p, miR-940, miR-6765-5p, miR-711, and miR-4284, which were highly dysregulated during keloid formation. In summary, these results demonstrate that lncRNAs and miRNAs play important roles and form a regulatory network in the pathogenesis, immune infiltration, and development of keloid formation.</p>","PeriodicalId":56317,"journal":{"name":"Critical Reviews in Eukaryotic Gene Expression","volume":"35 3","pages":"63-74"},"PeriodicalIF":1.5,"publicationDate":"2025-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143451137","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":"Cancer Network Macromolecules.","authors":"George L Eliceiri","doi":"10.1615/CritRevEukaryotGeneExpr.2025055921","DOIUrl":"10.1615/CritRevEukaryotGeneExpr.2025055921","url":null,"abstract":"<p><p>The members of the network (interactome) that controls cancer needs to be known. This network consists of proteins and non-coding, single-stranded RNAs, such as microRNAs (miRNAs), long non-coding RNAs (lncRNAs), circular RNAs (circRNAs), and transfer RNAs (tRNAs). miRNAs are 21-23 nucleotides-long, and degrade messenger RNAs (mRNAs) and lncRNAs. lncRNAs are longer than 200 nucleotides, and sponge (sequester) miRNAs.</p>","PeriodicalId":56317,"journal":{"name":"Critical Reviews in Eukaryotic Gene Expression","volume":"35 3","pages":"75-84"},"PeriodicalIF":1.5,"publicationDate":"2025-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143451131","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":"CircCNKSR2 Facilitates NSCLC Tumorigenesis and Warburg Effect via miRNA-138-5p/PLEK2 Axis.","authors":"Dongxiao Ding, Ke Shi, Junjie Ying, Wenjun Shang, Chengli Du","doi":"10.1615/CritRevEukaryotGeneExpr.2024055827","DOIUrl":"10.1615/CritRevEukaryotGeneExpr.2024055827","url":null,"abstract":"<p><p>Non-small cell lung cancer (NSCLC) has a high global incidence and mortality rate. Although circRNAs have significant attention in tumor research, it's role in NSCLC is uncertain. QRT-PCR and Western blotting were utilized to quantify the expression of circCNKSR2, miR-138-5p, and PLEK2 in NSCLC tissues and cells. The characteristics and subcellular localization of circCNKSR2 were determined using RNase R analysis and qRT-PCR. In vitro functional experiments determined the biological functions of circCNKSR2. The specific binding interactions among circCNKSR2, miR-138-5p, and PLEK2 were evaluated through bioinformatics analysis, luciferase reporter, and rescue assays. In vivo xenograft model was established to examine the impact of circCNKSR2, which was significantly increased in NSCLC tissues and cells. Functional studies demonstrated that silencing circCNKSR2 significantly inhibited NSCLC malignant phenotype and Warburg effect. Bioinformatics analysis and rescue experiments verification indicated circCNKSR2 functioned as a miR-138-5p sponge, and inhibiting miR-138-5p reversed the suppressive effect of silencing circCNKSR2 in NSCLC. Additionally, PLEK2 identified as a miR-138-5p target gene. The potential regulatory role of circCNKSR2 in NSCLC progression and Warburg effect via the miR-138-5p/PLEK2 pathway was demonstrated.</p>","PeriodicalId":56317,"journal":{"name":"Critical Reviews in Eukaryotic Gene Expression","volume":"35 2","pages":"49-63"},"PeriodicalIF":1.5,"publicationDate":"2025-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143434417","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":"HECW1 Gene's Role in Gastric Cancer Prognosis and Its Suppressive Effect on Cell Progression after Knockdown.","authors":"Jinchuan Wang, Baozhen Wang, Yichen Yin, Nan Tian, Tao Li","doi":"10.1615/CritRevEukaryotGeneExpr.2025058112","DOIUrl":"https://doi.org/10.1615/CritRevEukaryotGeneExpr.2025058112","url":null,"abstract":"<p><strong>Background: </strong>The HECT, C2, and WW domain-containing E3 ubiquitin protein ligase 1 (HECW1) gene is a member of the HECT family of E3 ubiquitin ligases. While HECW1 has been implicated in various cancers, its role in gastric cancer (GC) remains unclear.</p><p><strong>Methods: </strong>Bioinformatics approaches were employed to investigate HECW1's role in GC. Functional assays, including the CCK-8, transwell migration, and wound healing assays, were performed to assess its impact on GC cell proliferation, invasion, and migration.</p><p><strong>Results: </strong>HECW1 expression was significantly upregulated in GC tissues compared to normal controls, correlating with specific clinical characteristics. Cox regression analyses identified HECW1 as an independent prognostic factor for GC. Prognostic nomograms accurately predicted 1-, 3-, and 5-year survival rates, with calibration curves closely aligned with the ideal diagonal line. Elevated HECW1 expression was associated with poorer overall survival and disease progression outcomes. ROC analyses demonstrated that HECW1 had strong predictive power for outcomes (AUC = 0.746, CI = 0.683-0.808) and five-year survival rates (AUC = 0.734, CI = 0.600-0.869). Enrichment analysis suggested HECW1's involvement in protein processing and interactions with substrates such as SMAD4, TTF1, DVL1, and NEDD4. Functional assays showed that HECW1 knockdown significantly reduced GC cell proliferation, invasion, and migration.</p><p><strong>Conclusions: </strong>HECW1 acts as an oncogene in GC and represents a potential prognostic indicator. Targeting HECW1 may inhibit GC progression, providing a promising therapeutic strategy.</p>","PeriodicalId":56317,"journal":{"name":"Critical Reviews in Eukaryotic Gene Expression","volume":"35 5","pages":"1-16"},"PeriodicalIF":1.5,"publicationDate":"2025-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144327807","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":"Clinical characteristics and gene analysis in 7 Chinese children with cystic fibrosis.","authors":"Chunyan Guo, Xing Chen, Fengqin Liu, Yan Liang, Juan Yang, Fangfang Dai, Ning Ding, Ke Wang, Jing Zhang","doi":"10.1615/CritRevEukaryotGeneExpr.2025057731","DOIUrl":"10.1615/CritRevEukaryotGeneExpr.2025057731","url":null,"abstract":"<p><strong>Background: </strong>Cystic fibrosis (CF) is common genetic disorder in Europe and North America but rarer in Asian populations.</p><p><strong>Objective: </strong>To explore the clinical manifestations and gene mutations of cystic fibrosis.</p><p><strong>Methods: </strong>This case series study enrolled children with CF diagnosed in the pediatric respiratory department of Shandong Provincial Hospital affiliated to Shandong First Medical University between June 2016 and August 2022.</p><p><strong>Results: </strong>Seven children, including 6 girls and 1 boy, were enrolled. All 7 patients had recurrent wet cough and (chronic) pneumonia. Six patients suffered from chronic sinusitis, 4 patients had recurrent wheezing; 2 patients had chronic diarrhea, malnutrition and growth lag; 2 patients were complicated by allergic bronchopulmonary aspergillosis; and 1 patient had pancreatic insufficiency. Bronchiectasis, thickening of bronchial wall and mucous impaction, were seen in the chest CT of 7 children. Six patients showed a large amount of viscous sputum adhered to the bronchial wall by bronchoscopy. Infection of Pseudomonas aeruginosa was found in 6 cases, Staphylococcus aureus in 2 cases, and Aspergillus fumigatus in 2 cases by bronchoalveolar lavage fluid or sputum culture. Sweat sodium chloride test was performed in 3 cases, and the result showed that Cl-> 60 mmol/L. CFTR gene mutations were found in 7 cases, which were rare mutations of Caucasians, including 2 cases with new mutation sites (c.325T>G and 326A>G).</p><p><strong>Conclusions: </strong>The major clinical presentations of CF could be chronic and recurrent upper and lower respiratory tract infections, malnutrition, and digestive tract diseases. The rare and even new mutations of Caucasians on CFTR gene may occur in Chinese children.</p>","PeriodicalId":56317,"journal":{"name":"Critical Reviews in Eukaryotic Gene Expression","volume":"35 4","pages":"55-64"},"PeriodicalIF":1.6,"publicationDate":"2025-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144000448","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}