Clinical and Experimental Medicine最新文献

{"title":"Increased glioblastoma risk in patients with myeloproliferative neoplasms and myelodysplastic syndromes.","authors":"Huaiyu Zhou, Shenghui Jin, Lei Huang, Wei Liu","doi":"10.1007/s10238-026-02296-z","DOIUrl":"https://doi.org/10.1007/s10238-026-02296-z","url":null,"abstract":"<p><p>Targeted therapies significantly extend the survival of patients with myeloproliferative neoplasms (MPNs) and myelodysplastic syndromes (MDS). This prolonged lifespan introduces an unintended clinical hazard. These patients face an elevated risk of developing primary central nervous system (CNS) tumors. The internal relationship between them remains to be explored. We integrated the Global Burden of Disease (GBD) and the Cancer Incidence in Five Continents (CI5) datasets to conduct spatial clustering mapping using Moran's I. Vector autoregression and Granger causality analysis were employed to examine the longitudinal incidence of these diseases in Sweden from 1990 to 2021. Bibliometric profiling was utilized to identify research frontiers, and two-sample Mendelian randomization (MR) was used to determine genetic correlation. Geospatial mapping indicated a dually dominant burden of MPN + MDS (MPN and MDS, not MPN/MDS) and CNS tumors in developed regions. Longitudinal data from Sweden exposed a strictly unidirectional predictive trajectory exclusive to females. Myeloid malignancies reliably preceded CNS tumors. Bibliometric analysis demonstrated a remarkable interdecadal convergence on neuroinflammation and the tumor microenvironment. Significantly, MR confirmed that MPN (odds ratio [OR] = 1.84, 95% confidence interval [CI]: 1.22-2.76) and MDS (OR = 2.54, 95% CI: 1.62-3.96) have definite positive effects on GBM susceptibility. We established the possible comorbidity relationship between MPN + MDS and GBM, and raised the myeloid-neuro-immune crosstalk theory. It lays a reliable foundation on the interactions between MPN + MDS and GBM for future research, and offers insights for building multidisciplinary team collaboration.</p>","PeriodicalId":10337,"journal":{"name":"Clinical and Experimental Medicine","volume":"26 1","pages":""},"PeriodicalIF":4.5,"publicationDate":"2026-08-22","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13633956/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149104938","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":"Retraction Note: Integrative multi-omics profiling for early diagnosis, stratification and personalized management of chronic kidney disease: a new paradigm.","authors":"Yue Li, Soroush Taherkhani, Khusniddin Saidov, Marhabo Matniyozova","doi":"10.1007/s10238-026-02289-y","DOIUrl":"https://doi.org/10.1007/s10238-026-02289-y","url":null,"abstract":"","PeriodicalId":10337,"journal":{"name":"Clinical and Experimental Medicine","volume":"26 1","pages":""},"PeriodicalIF":4.5,"publicationDate":"2026-08-19","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13490260/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148788937","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":"Radium - from discovery to the present day - narrative review.","authors":"Angelika Edyta Charkiewicz, Ivana Djuricic, Vanja Todorovic, Jacek Nikliński, Jaime Conceição, Brizita Djordjevic","doi":"10.1007/s10238-026-02292-3","DOIUrl":"10.1007/s10238-026-02292-3","url":null,"abstract":"<p><p>Following its discovery, radium was initially promoted as a therapeutic agent for a wide range of conditions, including skin disorders, allergies, visual problems, joint pain, and as a general health-enhancing remedy. However, subsequent research demonstrated its significant radiological toxicity and harmful effects on human health. Despite these risks, more than a century after its discovery, certain radium isotopes continue to have limited medical applications, particularly in the treatment of specific cancers. Following ingestion, radium is absorbed into the body and behaves similarly to calcium, resulting in its deposition in bone tissue. A proportion of absorbed radium is eliminated through feces and urine, while the remaining fraction may persist in the skeleton and contribute to long-term internal radiation exposure. The severity and onset of adverse health effects are closely related to the absorbed dose and duration of exposure. Chronic exposure to elevated radium levels has been associated with hematological abnormalities, cataracts, dental and jaw damage, bone cancer, and increased mortality. Advances in radiobiology, radiation protection, and personalized medicine continue to improve the safety and effectiveness of radiation-based treatments. Modern radiotherapy, including selected applications involving targeted radionuclide therapy, requires a detailed understanding of radiation dose distribution, biological responses, and patient-specific factors. The optimization of re-irradiation strategies remains an important clinical challenge that requires careful assessment of previous radiation exposure, tissue tolerance, and potential risks. Because radium exposure can occur through ingestion, inhalation, or dermal contact, continued monitoring, appropriate regulatory frameworks, and access to specialized analytical methods remain essential components of public health protection. International cooperation and strengthened surveillance programs are needed to ensure the safe management of radium-containing materials and minimize potential health risks.</p>","PeriodicalId":10337,"journal":{"name":"Clinical and Experimental Medicine","volume":"26 1","pages":""},"PeriodicalIF":4.5,"publicationDate":"2026-08-18","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13486116/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148788857","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":"Trajectory of preserved ratio impaired spirometry (PRISm): patterns, predictors, and potential interventions.","authors":"Tian Li, Ximing Liao, Huiling Dai, Kun Wang, Yin Wu, Rongzhang Chen, Wei Gao, Wujian Xu","doi":"10.1007/s10238-026-02288-z","DOIUrl":"10.1007/s10238-026-02288-z","url":null,"abstract":"<p><p>Preserved ratio impaired spirometry (PRISm), an abnormal spirometry condition characterized by a decreased forced expiratory volume at the first second (FEV₁), is recognized as a precursor of chronic obstructive pulmonary disease (COPD). Growing studies demonstrate that PRISm is associated with an increased risk of the development of fixed airflow obstruction (FAO) and cardiovascular mortality. However, there is still a lack of comprehensive understanding of the patterns and predictors of lung function trajectories in PRISm. Furthermore, standardized interventions that can prevent the deterioration of lung function in PRISm remain unclear. The purpose of this narrative review is to examine the natural history of PRISm by summarizing current evidence on its progression over time, key determinants, and modifiable factors, thereby identifying opportunities for early intervention. In this review, three main patterns of PRISm trajectories were reported, including PRISm to normal spirometry, persistent PRISm, and PRISm to FAO. In accordance, several important factors, such as body mass index (BMI), smoking status, baseline lung function values, comorbid respiratory symptoms and various diseases, and PRISm subtypes, were identified as predictors for the transition of PRISm to other lung function status. Additionally, several potential intervention strategies were developed to slow down the decline of lung function in PRISm and reduce PRISm-related mortality, including early screening and regular monitoring, non-pharmacological interventions, pharmacological interventions, and hierarchical management.</p>","PeriodicalId":10337,"journal":{"name":"Clinical and Experimental Medicine","volume":"26 1","pages":""},"PeriodicalIF":4.5,"publicationDate":"2026-08-13","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13654867/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149164957","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":"Real-world cardiovascular safety profile of bexarotene for the treatment of mycosis fungoides.","authors":"Charalampos Filippatos, Despina Fotiou, Peggy Kostakou, Maria Gavriatopoulou, Evangelos Terpos, Meletios-Athanasios Dimopoulos, Alexandros Briasoulis","doi":"10.1007/s10238-026-02282-5","DOIUrl":"10.1007/s10238-026-02282-5","url":null,"abstract":"<p><p>Bexarotene has been established as an effective therapeutic agent for mycosis fungoides (MF), both in early, refractory disease and in advanced stages. It has a predictable, albeit significant, metabolic toxicity profile, raising concerns regarding long-term cardiovascular safety. We conducted a retrospective cohort study utilizing TriNetX to identify adults with MF. Patients were stratified by bexarotene exposure and 1:1 propensity score matched (PSM) for demographics, lifestyle factors, comorbidities, and baseline medications. After PSM, two well-balanced cohorts of 2,242 patients each were formed with a median follow-up of 4.0 years for both groups. Bexarotene treatment demonstrated no significant increase in the risk of the composite adapted-MACE endpoint (HR = 0.93, 95% CI: 0.78-1.11, p = 0.425). Similarly, no significant differences were observed for individual cardiovascular components, including acute myocardial infarction (HR = 0.95, p = 0.730), stroke (HR = 0.90, p = 0.514), or heart failure (HR = 0.93, p = 0.455). Conversely, bexarotene was associated with a significantly increased risk of metabolic and endocrine abnormalities, including hypertriglyceridemia (RR = 6.98, p < 0.001), hypothyroidism (RR = 4.93, p < 0.001), hyperlipidemia (RR = 2.18, p < 0.001), and hypercholesterolemia (RR = 1.99, p < 0.001). In the largest real-world cohort of MF patients treated with bexarotene to date, the substantial metabolic and endocrine abnormalities associated with treatment did not translate into an observed increase in cardiovascular events during a median follow-up of 4 years. These findings provide reassurance regarding the short- to intermediate-term cardiovascular profile of bexarotene when appropriate monitoring and management of lipid and thyroid abnormalities are maintained. However, longer follow-up is required to determine whether these metabolic effects influence long-term cardiovascular risk.</p>","PeriodicalId":10337,"journal":{"name":"Clinical and Experimental Medicine","volume":"26 1","pages":""},"PeriodicalIF":4.5,"publicationDate":"2026-08-10","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13457487/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148705580","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":"Neural regulation in lung cancer: from mechanisms to new therapeutic perspectives.","authors":"Junfeng Zhao, Yiming Han, Yongxue Li, Ying Li, Yiheng Sun, Yingrui Bai, Jiaxuan Chen, Chuankun Han, Yifei Yan, Chen Zhou, Chengxin Liu","doi":"10.1007/s10238-026-02278-1","DOIUrl":"https://doi.org/10.1007/s10238-026-02278-1","url":null,"abstract":"<p><p>Lung cancer remains a leading cause of cancer-related deaths worldwide. Despite advances in targeted therapy and immunotherapy, treatment outcomes are often constrained by tumor heterogeneity and the complex tumor microenvironment. Recent studies highlight the critical role of the nervous system in lung cancer pathogenesis through bidirectional interactions between the central/peripheral nervous system and cancer cells. This review systematically explores how psychological stress, sleep disorders, and smoking influence the initiation and progression of lung cancer via neuroendocrine-immune networks. We further detail the dual roles of key neurotransmitters-including catecholamines, GABA, serotonin, dopamine, glutamate, histamine, and acetylcholine-in regulating tumor proliferation, epithelial-mesenchymal transition, angiogenesis, and immune evasion, with an emphasis on their context-dependent and receptor subtype-specific effects. Emerging evidence indicates that neurotransmitters remodel the tumor microenvironment by modulating immune cell function and receptor-mediated signaling pathways. We also discuss the therapeutic potential of neuromodulatory agents, particularly β-blockers and neurotransmitter receptor-targeted drugs, and their possible synergistic effects with conventional therapies, while critically distinguishing between strategies supported by clinical evidence and those remaining at the preclinical stage. Challenges persist, including neurotransmitter concentration gradients, receptor subtype specificity, and limitations of preclinical models. The convergence of neuroscience and oncology offers promising avenues for innovative lung cancer therapies, underscoring the necessity for interdisciplinary collaboration to translate these discoveries into clinical practice.</p>","PeriodicalId":10337,"journal":{"name":"Clinical and Experimental Medicine","volume":"26 1","pages":""},"PeriodicalIF":4.5,"publicationDate":"2026-08-08","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13481421/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148788803","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":"Application of a machine learning model integrating T cell subsets and clinical markers in 28-Day mortality prediction of sepsis patients.","authors":"Ruiqi Li, Haiqi Wang, Junyu Wang, Shubin Guo, Jun Lu","doi":"10.1007/s10238-026-02227-y","DOIUrl":"10.1007/s10238-026-02227-y","url":null,"abstract":"<p><p>To develop a machine learning-based prediction model that integrating T cell subset data with clinical features to predict the 28-day mortality risk in sepsis patients. A retrospective cohort study was conducted using the MIMIC-IV database. Collected data included demographics, T cell subsets, laboratory results, SOFA score, GCS, and 28-day mortality. Feature selection was performed using LASSO regression combined with 10-fold cross-validation. We compared the performance of six machine learning models, namely RF, SVM, XGB, GLM, GBM, and LASSO logistic regression. Model performance was evaluated using the AUROC, calibration curves, and DCA, while the SHAP method was employed to interpret the optimal model. A total of 781 sepsis patients were included in our study, with a 28-day mortality rate of 18.5%. LASSO regression identified 12 key features: Age, CD + 4 Count, CD8 + T cell count, lactate, platelet, albumin, Na+, Bun, heart rate, anion gap, eosinophil count, monocyte count. Among the six compared machine learning models, GLM achieved the best comprehensive performance in the testing set, with an AUROC of 0.720, good calibration (Brier score: 0.134). SHAP analysis clarified the contribution degree and direction of each predictive factor to the model output. A GLM model integrating T cell subsets (notably CD8 + T cell count) and clinical features was successfully constructed. The model showed moderate discriminative ability and potential clinical application value in predicting the 28-day mortality risk of sepsis. SHAP-based interpretability clarifies individual risk factors, serving as an auxiliary prognostic tool for clinicians.</p>","PeriodicalId":10337,"journal":{"name":"Clinical and Experimental Medicine","volume":"26 1","pages":""},"PeriodicalIF":4.5,"publicationDate":"2026-08-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13499742/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148788763","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":"The TAF3/SREBP2/cholesterol axis drives tumor progression in hepatocellular carcinoma.","authors":"Jiali Qiu, Lei Cao, Yi Li, Yan Li, Zhiqi Yin, Dejun Kong, Na Chen, Zhenglu Wang","doi":"10.1007/s10238-026-02267-4","DOIUrl":"10.1007/s10238-026-02267-4","url":null,"abstract":"<p><p>TATA-binding protein-associated factor 3 (TAF3), a member of the TAF family, plays a crucial role in safeguarding finely balanced transcriptional programs. Previous research identified TAF3 as a critical prognostic marker in hepatocellular carcinoma (HCC). This study aimed to elucidate TAF3's functional role and mechanistic underpinnings in liver cancer progression. Through the establishment of stable TAF3-knockdown and overexpression cell lines in human HCC cells (HepG2 and MHCC97H), comprehensive functional analyses revealed that TAF3 knockdown significantly inhibited cancer cell proliferation, migration, and invasion, while its overexpression promoted these malignant phenotypes. Clinically, elevated TAF3 expression correlated with aggressive clinicopathological features and poor prognosis in HCC patients. Mechanistic investigations demonstrated that TAF3 transcriptionally activates sterol regulatory element-binding protein 2 (SREBP2), a master regulator of cholesterol synthesis, leading to increased intracellular cholesterol accumulation. This cholesterol elevation functionally contributed to oncogenic processes, as exogenous cholesterol supplementation reversed the impaired malignancy in TAF3-deficient cells. In vivo validation using a subcutaneous xenograft mouse model confirmed that TAF3 knockdown suppressed tumor growth, an effect effectively counteracted by high-cholesterol dietary intervention. Collectively, these findings establish that TAF3 promotes liver cancer progression through transcriptional activation of SREBP2 and subsequent enhancement of cholesterol biosynthesis. The study identifies a novel TAF3/SREBP2/cholesterol axis as a promising therapeutic target in TAF3-overexpressing hepatocellular carcinomas, providing mechanistic insights into the interplay between transcriptional regulation and metabolic reprogramming in cancer progression.</p>","PeriodicalId":10337,"journal":{"name":"Clinical and Experimental Medicine","volume":"26 1","pages":""},"PeriodicalIF":4.5,"publicationDate":"2026-07-31","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13538215/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148879375","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":"Prognostic factor analysis of CD19 CAR-T therapy followed by hematopoietic stem cell transplantation in relapsed/refractory B-ALL.","authors":"Xin Wang, Linlin Liu, Yuanyuan Zhai, Jianmei Xu, Jile Liu, Hairong Lyu, Mingfeng Zhao","doi":"10.1007/s10238-026-02273-6","DOIUrl":"https://doi.org/10.1007/s10238-026-02273-6","url":null,"abstract":"<p><p>To evaluate the long-term prognosis of patients with relapsed/refractory B-cell acute lymphoblastic leukemia (R/R B-ALL) who received sequential allogeneic hematopoietic stem cell transplantation (allo-HSCT) following CD19 Chimeric Antigen Receptor T-cell (CAR-T) therapy, and to identify the risk factors influencing overall survival (OS) and the severity of acute graft-versus-host disease (aGVHD). A retrospective analysis was conducted on 63 patients with R/R B-ALL who received sequential allo-HSCT after CD19 CAR-T therapy. Cox regression analysis was used to identify factors influencing OS. Patients were stratified according to the severity of aGVHD (low-grade vs. high-grade). Logistic regression was employed to identify predictors of severe aGVHD, and a nomogram was constructed based on these predictors. The model was internally validated using receiver operating characteristic (ROC) curves, calibration plots, and decision curve analysis (DCA). The two-year OS and progression-free survival (PFS) rates were 67.7% and 55.6%, respectively.The time interval from CAR-T therapy to transplantation, along with high-grade aGVHD, were identified as independent risk factors for OS, whereas low-grade aGVHD exerted a protective effect. A longer time interval from CAR-T therapy to transplantation and pre-transplant minimalresidual disease (MRD)-positive status were independent predictors of severe aGVHD. The nomogram developed for predicting the severity of aGVHD demonstrated good discrimination (areaunder the curve [AUC] = 0.827), satisfactory calibration, and clinical utility upon internal validation. We identified key prognostic factors and developed a validated nomogram that enables early, individualized prediction of severe aGVHD in this setting. This model can assist in early risk stratification and targeted intervention to improve outcomes.</p>","PeriodicalId":10337,"journal":{"name":"Clinical and Experimental Medicine","volume":"26 1","pages":""},"PeriodicalIF":4.5,"publicationDate":"2026-07-30","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13481590/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148788929","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":"Fatty acids metabolic reprogramming and tumor microenvironment in pancreatic cancer: targeting pathways.","authors":"Bassant Ehab, Ekram Saleh","doi":"10.1007/s10238-026-02235-y","DOIUrl":"10.1007/s10238-026-02235-y","url":null,"abstract":"<p><p>Pancreatic ductal adenocarcinoma (PDAC) represents a highly aggressive form of pancreatic cancer. It is distinguished by a profound metabolic plasticity that supports its survival in a hypoxic and nutrient deprived microenvironment. Among the metabolic pathways altered in PDAC, fatty acid metabolism including synthesis, uptake, storage and β-oxidation serves as a key metabolic process that supports tumor growth, progression, and therapeutic resistance. This review discusses emerging evidence on fatty acid metabolic reprogramming and its relevance to the development and progression of pancreatic ductal adenocarcinoma. Key dysregulated enzymes as well as critical metabolic regulators are highlighted. Also, we discuss how genetic alterations drive lipogenic and oxidative pathways to sustain proliferation, redox balance, and adaptation to metabolic stress. Additionally, this review integrates current evidence to illustrate how the tumor microenvironment influences enhancing lipid availability and promoting metabolic symbiosis. Finally, this review outlines current pharmacological approaches that interfere with fatty acid metabolism, emphasizing lipid metabolism as a promising potential intervention strategy to inhibit tumor growth and sensitize cancer cells to existing treatments.</p>","PeriodicalId":10337,"journal":{"name":"Clinical and Experimental Medicine","volume":"26 1","pages":""},"PeriodicalIF":4.5,"publicationDate":"2026-07-29","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13421207/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148618712","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}