Central European Journal of Immunology最新文献

{"title":"Comments on: \"Long-term efficacy of mesenchymal stem cell treatment for complex perianal fistulas: A systematic review and meta-analysis\".","authors":"Lan Wang, Fang Cheng","doi":"10.5114/ceji.2025.149256","DOIUrl":"10.5114/ceji.2025.149256","url":null,"abstract":"<p><p>The meta-analysis by Wang et al. aimed to assess the long-term effects of mesenchymal stem cells on complex perianal fistula. The authors concluded that mesenchymal stem cell therapy has a long-term effect on the clinical response of complex perianal fistula and should be widely promoted not only in adults but also in infants and adolescents; however, more research on this topic is needed. We appreciate the authors' hard work, and we also agree with this argument. However, we have several concerns about the study. We think it is necessary to discuss the effect of anti-TNF and immunosuppressive therapy on the effcacy of mesenchymal stem cell treatment for perianal fistula in future trials, in order to optimize treatment strategies in perianal fistula patients and reduce the economic burden of patients. In the future, it will be interesting to assess the safety and feasibility of injection of fibrin glue combined with mesenchymal stem cells in perianal fistula.</p>","PeriodicalId":9694,"journal":{"name":"Central European Journal of Immunology","volume":"50 1","pages":"11-12"},"PeriodicalIF":1.5,"publicationDate":"2025-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12224247/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144574907","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Hsa_circ_0001445 regulates acne inflammation <i>via</i> sponging miR-1298-5p targeting ESR1.","authors":"Wenjun Zhong, Yuanyuan Li, Liqiao Chi, Dongmei Jia, Qiang Wang","doi":"10.5114/ceji.2025.149200","DOIUrl":"10.5114/ceji.2025.149200","url":null,"abstract":"<p><strong>Introduction: </strong>Acne is a prevalent inflammatory skin condition that occurs in adolescents and can persist into adulthood. CircRNA has been reported to be widely involved in a variety of human diseases. However, the regulatory mechanism of hsa_circ_0001445 in acne has rarely been reported. The purpose is to research the role of hsa_circ_0001445 in acne-induced inflammation and its molecular regulatory mechanism to provide a foundation for the exploration of acne-targeting drugs.</p><p><strong>Material and methods: </strong>We used the GEO, starBase, and GeneCards databases for bioinformatics analysis. The binding sequences of miR-1298-5p and hsa_circ_0001445 or ESR1 mRNA were predicted by the Circular RNA Interactome or starBase database. Double luciferase reporting assay was applied to verify the regulatory relationship between hsa_circ_0001445, miR-1298-5p, and ESR1. RT-qPCR was used to detect levels of hsa_circ_0001445, miR-1298-5p, and ESR1 mRNA. The secretion levels of interleukin (IL)-6, IL-8, and tumor necrosis factor <i>α</i> (TNF-<i>α</i>) were measured using an ELISA kit.</p><p><strong>Results: </strong>The luciferase activity was weakened by miR-1298-5p mimics in human keratinocytes and sebocytes transfected with wild-type (wt)-circ1445 and wt-ESR1, respectively. Moreover, the overexpression of hsa_circ_0001445 reduced the miR-1298-5p level and reversed the elevation of IL-6, IL-8, and TNF-<i>α</i> levels in Bio-C. acnes-stimulated keratinocytes and sebocytes. In turn, transfection of miR-1298-5p mimics partially eliminated the inflammatory inhibition of hsa_circ_0001445, which was reversed by co-transfection of pcDNA-ESR1.</p><p><strong>Conclusions: </strong>Hsa_circ_0001445 improved acne inflammation via sponging miR-1298-5p targeting ESR1.</p>","PeriodicalId":9694,"journal":{"name":"Central European Journal of Immunology","volume":"50 1","pages":"109-118"},"PeriodicalIF":1.5,"publicationDate":"2025-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12224259/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144574909","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"PD-1/PD-L1 inhibitor treatment associated with cardiotoxicity regulated by macrophage polarization and SOCS3/JAK/STAT3 signaling pathway.","authors":"Jiding Fu, Ge Wang, Lisi Zeng, Jie Lin, Yier Wei, Wei Xu, Rui Xu, Lewu Xian","doi":"10.5114/ceji.2025.149377","DOIUrl":"10.5114/ceji.2025.149377","url":null,"abstract":"<p><p>Cardiotoxicity caused by immune checkpoint inhibitors is one of the most severe and potentially fatal side effects. Hence it is crucial from a therapeutic standpoint to understand the underlying processes and devise countermeasures. This study sought to determine whether the SOCS3/JAK/STAT3 signaling pathway, which controls macrophage polarization, contributes to the cardiotoxicity caused by PD-1/PD-L1 inhibitors. The PD-1/PD-L1 inhibitor BMS-1 (10 mg/kg) was used to create a mouse model of immune checkpoint inhibitor-related cardiotoxicity, and hematoxylin and Masson's trichome tests were used to measure cardiomyocyte apoptosis and cardiotoxicity. The production of M1 factors (tumor necrosis factor <i>α</i> [TNF-<i>α</i>] and interleukin [IL]-1 <i>b</i>), as well as the blood levels of myocardial enzymes (creatine kinase, aspartate transaminase, creatine kinase-MB, and lactate dehydrogenase), were evaluated by ELISA. Echocardiography was used to assess the heart's health. The processes were investigated using flow cytometric analysis, real-time PCR, Western blot, and chromatin immunoprecipitation. We found that the PD-1/PD-L1 inhibitor BMS-1 dramatically reduced tumor weight while considerably impairing cardiac function in melanoma-induced tumor-bearing mice. At the gene and protein levels, it was found that levels of SOCS3, JAK, STAT3, and the inflammatory mediators IL-6 and TNF-<i>α</i> had all significantly decreased. Immune checkpoint inhibitor-induced cardiotoxicity may be linked to major changes in the SOCS3/JAK/STAT3 signaling pathway, as indicated by the knockdown of SOCS3, JAK, and STAT3. Finally, immune checkpoint inhibitor intervention demonstrated a large elevation of CD86+ and MHCII+ as well as a considerable increase in macrophages. These data suggest that the SOCS3/JAK/STAT3 signaling pathway, which controls macrophage polarization, may be linked to cardiotoxicity caused by PD-1/PD-L1 inhibitor therapy.</p>","PeriodicalId":9694,"journal":{"name":"Central European Journal of Immunology","volume":"50 1","pages":"24-37"},"PeriodicalIF":1.5,"publicationDate":"2025-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12224271/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144574826","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Anifrolumab in the treatment of recurrent systemic lupus erythematosus: the first post-trial case report.","authors":"Przemysław Borowy, Alicja Kamińska, Patrycja Major, Jakub Smyk, Katarzyna Gołojuch, Bogdan Batko","doi":"10.5114/ceji.2025.148001","DOIUrl":"10.5114/ceji.2025.148001","url":null,"abstract":"<p><p>Systemic lupus erythematosus (SLE) is a chronic, multisystem autoimmune disease whose treatment is still a challenge. The latest registration of anifrolumab for the treatment of moderate-to-severe SLE raises hopes because of its novel anti-interferon mechanism of action. Anifrolumab, a human monoclonal antibody, selectively binds the interferon <i>α</i> (INF-<i>α</i>) receptor, inhibiting systemic inflammation moderated by interferon pathways. The article presents the first case of an 18-year-old man with severe, relapsing and repeatedly hospitalized SLE, successfully treated with anifrolumab. During a subsequent exacerbation with multi-organ involvement, which could not be controlled despite pulses and high doses of glucocorticoids (GCSs), treatment with anifrolumab was initiated. Clinical improvement was achieved 4 weeks after the first dose. The patient's dose of systemic GCSs was gradually reduced until complete withdrawal. No serious side effects were observed throughout the follow-up period, and the criteria for complete remission were achieved by the patient at month 3 of therapy. After 12 months, therapy was discontinued due to a payer decision. Nevertheless, the patient remains in follow-up 14 months after the completion of therapy on stable treatment with hydroxychloroquine and azathioprine. He is still not taking prednisone. This is the first case in Poland to show the fate of a \"real life patient\" after completion of anifrolumab therapy, an effective clinical remission of many months without the use of oral GCSs.</p>","PeriodicalId":9694,"journal":{"name":"Central European Journal of Immunology","volume":"50 1","pages":"105-108"},"PeriodicalIF":1.5,"publicationDate":"2025-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12224262/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144574906","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Paeoniflorin inhibits degranulation of mast cells through suppressing the cGAS/STING signaling pathway.","authors":"Guanli Song, Guanbo Song, Xiaji Zhou, Lei Zhang","doi":"10.5114/ceji.2025.153658","DOIUrl":"10.5114/ceji.2025.153658","url":null,"abstract":"<p><strong>Introduction: </strong>Allergic rhinitis is an allergic disease that affects the nasal mucosa, and its incidence has been increasing significantly in recent years. Paeoniflorin (PF) is the main chemical component of total glucosides of paeony and is reported to have an excellent effect on anti-allergic inflammation. In this study, we aimed to investigate the mechanism of PF regulating the degranulation of mast cells induced by dinitrophenol (DNP)-human serum albumin (DNP-HSA).</p><p><strong>Material and methods: </strong>The effect of PF on the degranulation of mast cells was evaluated through the measurement of histamine, <i>β</i>-hexosaminidase, and intracellular calcium level, and the signaling pathway was screened through western blot assay and molecular docking.</p><p><strong>Results: </strong>The results showed that PF treatment reduced the release of histamine and <i>β</i>-hexosaminidase, and reduced the intracellular calcium level in mast cells with DNP-HSA treatment. In addition, PF downregulated the protein levels of cGAS and STING to inactivate the cGAS/STING signaling pathway, in which the inhibitory effects of PF on mast cells were reversed by 5,6-imethylxanthenone-4-acetic acid (DMXAA, a STING agonist).</p><p><strong>Conclusions: </strong>In conclusion, PF inhibits degranulation of mast cells through the cGAS/STING signaling pathway, which provides a theoretical basis for the application of PF in allergic rhinitis therapy.</p>","PeriodicalId":9694,"journal":{"name":"Central European Journal of Immunology","volume":"50 4","pages":"331-340"},"PeriodicalIF":1.5,"publicationDate":"2025-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13100591/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147763610","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Pan-cancer analysis of polycomb repressive complex 1 (PRC1) in relation to prognosis and immunotherapy response.","authors":"Bobin Ning, Qingyu Meng, Baoqing Jia","doi":"10.5114/ceji.2025.151960","DOIUrl":"10.5114/ceji.2025.151960","url":null,"abstract":"<p><strong>Introduction: </strong>Polycomb repressive complex 1 (PRC1) is a crucial epigenetic modification complex that plays significant roles in embryonic development, cell differentiation, and tumorigenesis. However, its predictive value and role in immunotherapy remain unclear.</p><p><strong>Material and methods: </strong>Expression of the PRC1 complex was analyzed through RNA-seq, quantitative PCR, and immunohistochemistry. Then, we utilized the TCGA and GEO databases to cross-validate the prognostic risk. A pan-cancer analysis was conducted, including clinical traits, tumor microenvironment (TME), tumor mutational burden (TMB), stemness indices, and drug sensitivity. Furthermore, we cross-validated the effect of PRC1 on immunotherapy through ROC Plotter and Kaplan-Meier Plotter databases. The immune cell infiltration and signaling pathways were further identified.</p><p><strong>Results: </strong>The expression of PRC1 differed between tumor and normal tissue in most cases. In particular, the whole group exhibited consistent high abundance in gastric, colorectal, and liver cancer. In addition, the expression of PRC1 can serve as a marker of survival prognosis. The members of PRC1 were also associated with clinical characteristics, immune cell infiltration, immune checkpoint inhibitor (ICI)-related immune indexes, and drug sensitivity. Moreover, high expression of BMI1 can increase resistance to immunotherapy, with a worse prognosis. The expression level of BMI1 can affect the immune-related pathways, as indicated by the gene set enrichment analysis (GSEA).</p><p><strong>Conclusions: </strong>Our study revealed the expression, prognostic value and mechanism of PRC1 in pan-cancer. Its core member BMI1 can be used as a biomarker for the prognosis of tumor patients and the efficacy of ICIs. It provides a theoretical basis for the implementation of individualized immunotherapy.</p>","PeriodicalId":9694,"journal":{"name":"Central European Journal of Immunology","volume":"50 2","pages":"149-167"},"PeriodicalIF":1.6,"publicationDate":"2025-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12512113/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145278936","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Glutaminase-mediated glutamate metabolism is critical for maintaining Th17/Treg balance.","authors":"Xiaohan Jin, Jinglong Tao","doi":"10.5114/ceji.2025.155429","DOIUrl":"10.5114/ceji.2025.155429","url":null,"abstract":"<p><p>Autoimmune diseases are severe disorders that affect populations worldwide. Their occurrence is considered to be multifactorial: genetic, hormonal and immunological factors all contribute to the development of autoimmune diseases. CD4 T cells differentiate into different subtypes, among which Th17 and Treg cells are the two most important in regulation of immune response balance. The Th17/Treg equilibrium is crucial in the pathogenesis of autoimmune diseases. Glutamate, an excitatory neurotransmitter in the nervous system, induces multiple effects. It activates normal T cells, enhancing cell adhesion, migration, secretion and gene expression. However, the effect of glutamate on T cell fate remains unclear. Here, we found that glutamate promotes Treg differentiation but suppresses Th17 differentiation. Further results showed that the rate-limiting enzyme of glutamate metabolism, glutaminase (GLS), is the key regulator for Treg cell generation. These findings suggest that GLS-mediated glutamate metabolism is critical for Treg cell differentiation, and may represent a potential therapeutic target for autoimmune disease.</p>","PeriodicalId":9694,"journal":{"name":"Central European Journal of Immunology","volume":"50 4","pages":"341-352"},"PeriodicalIF":1.5,"publicationDate":"2025-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13100586/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147763650","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Role of <i>TLR2</i> rs5743708 and dectin-1 rs16910526 polymorphisms in susceptibility to fungal infections in COVID-19 patients.","authors":"Karzan Abdulmuhsin Mohammad, Hero M Ismael, Shukur Wasman Smail, Taban Kamal Rasheed, Mohammed O Rahman, Niaz Albarzinji, Rebaz Hamza Salih, Kalthum Othman Taha, Khawlah Salah KHAleel, Kawa Amin, Christer Janson","doi":"10.5114/ceji.2025.149165","DOIUrl":"10.5114/ceji.2025.149165","url":null,"abstract":"<p><strong>Introduction: </strong>The progression of fungal co-infection with COVID-19 depends on the patient's genetic innate immunity. Our goal is to understand the connection between the single nucleotide polymorphisms (SNPs) rs5743708 and rs16910526 in the toll-like receptor 2 (TLR2) and dectin-1 (CLEC7A) genes, respectively, and fungal infection in COVID-19 patients.</p><p><strong>Material and methods: </strong>This study assessed the SNPs rs5743708 from the TLR2 gene and rs16910526 from dectin-1 by Sanger sequencing. Two groups of COVID-19 patients participated in this study: 110 COVID-19 patients free from fungal infection (COVID-19 FFI), and 77 COVID-19 patients with fungal infection (COVID-19 WFI).</p><p><strong>Results: </strong>The AG genotype of the TLR2 SNP rs5743708 showed no significant association with fungal infection in COVID-19 compared to the AA genotype. However, the GG genotype and G allele were significantly associated with decreased vulnerability to fungal co-infections. Similarly, regarding the dectin-1 SNP rs16910526, the TG genotype did not show a significant association with fungal infection compared to the TT genotype, but the GG genotype and G allele were significantly related to decreased susceptibility to fungal co-infections in COVID-19. The TLR2 protein levels in the serum of COVID-19 patients with GG genotypes of TLR2 rs5743708 were elevated. Variations in the dectin-1 genotypes (specifically GG genotype) can also raise the levels of dectin-1 serum protein.</p><p><strong>Conclusions: </strong>The relationship between TLR2 rs5743708 and dectin-1 rs16910526 SNPs and susceptibility to fungal infection in COVID-19 patients was found to be significant, highlighting the im- portance of investigating their connection to infection progression for personalized patient care. The variation in genotypes also affects the levels of corresponding serum TLR2 and dectin-1.</p>","PeriodicalId":9694,"journal":{"name":"Central European Journal of Immunology","volume":"50 1","pages":"77-86"},"PeriodicalIF":1.5,"publicationDate":"2025-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12224246/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144574829","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Dexmedetomidine inhibits the Wnt/β-catenin pathway, regulates ferroptosis in bladder cancer cells and the tumor immune microenvironment, and suppresses tumorigenesis in a mouse bladder cancer model.","authors":"Zhi Wang, Weina Bai","doi":"10.5114/ceji.2025.155276","DOIUrl":"10.5114/ceji.2025.155276","url":null,"abstract":"<p><strong>Introduction: </strong>This study aimed to explore the antitumor effects of dexmedetomidine (Dex) in bladder cancer, focusing on its role in modulating ferroptosis and the tumor immune microenvironment.</p><p><strong>Material and methods: </strong>Bladder cancer cell lines (T24 and RT4) were treated with various concentrations of Dex, followed by analysis of cell proliferation, ferroptosis markers, and immune evasion factors. In vivo, a mouse xenograft model of bladder cancer was used to assess tumor growth and related molecular mechanisms. Western blotting, flow cytometry, immunohistochemistry, and ELISA were used to evaluate protein expression levels, immune cell activity and cytokine production.</p><p><strong>Results: </strong>Dex significantly inhibited bladder cancer cell proliferation and promoted ferroptosis by increasing intracellular Fe²⁺ and ROS levels. Dex also downregulated the ferroptosis-related proteins GPX4 and SLC7A11, disrupting the antioxidant defenses of bladder cancer cells. Furthermore, Dex inhibited immune evasion by reducing PD-L1 expression and enhancing CD8⁺ T-cell activity. Additionally, Dex suppressed the Wnt/<i>β</i>-catenin pathway by reducing active <i>β</i>-catenin, cyclin D1, and c-Myc levels. Dexmedetomidine significantly reduced tumor volume and weight in a T24 xenograft mouse model, reduced GPX4 and PD-L1 expression, increased IFN-<i>γ</i> levels, and suppressed Wnt/<i>β</i>-catenin pathway components.</p><p><strong>Conclusions: </strong>Dexmedetomidine exerted antitumor effects in bladder cancer by inducing ferroptosis and modulating the tumor immune microenvironment through suppression of the Wnt/<i>β</i>-catenin signaling pathway. These findings suggested that Dex could be a promising therapeutic agent for bladder cancer, particularly in combination with immunotherapy strategies.</p>","PeriodicalId":9694,"journal":{"name":"Central European Journal of Immunology","volume":"50 4","pages":"435-448"},"PeriodicalIF":1.5,"publicationDate":"2025-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13100589/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147763607","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Glucose metabolism and immune dysregulation - a metabolic lens on lupus pathogenesis.","authors":"Urszula Radzikowska, Marlena Tynecka, Andrzej Eljaszewicz","doi":"10.5114/ceji.2025.151334","DOIUrl":"10.5114/ceji.2025.151334","url":null,"abstract":"","PeriodicalId":9694,"journal":{"name":"Central European Journal of Immunology","volume":"50 1","pages":"1"},"PeriodicalIF":1.5,"publicationDate":"2025-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12224240/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144574908","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}