International Journal of Medical Sciences最新文献

{"title":"Computed Tomography-Verified Deep Learning Model for Rib Fracture Prediction and Complication Association from Chest Radiographs.","authors":"Ting-Hsuan Chao, Chih-Chien Wang, Chin Lin, Chin-Sheng Lin, Teng-Wei Chen, Shih-Hua Lin, Dung-Jang Tsai","doi":"10.7150/ijms.131105","DOIUrl":"10.7150/ijms.131105","url":null,"abstract":"<p><strong>Background: </strong>Chest radiography (CXR) is the first-line imaging for suspected rib fractures but has limited sensitivity, potentially increasing the risk of thoracic complications. This study aimed to develop and validate a deep learning model (DLM) based on CT-verified labels to predict acute rib fractures on CXRs and evaluate its association with thoracic complications.</p><p><strong>Methods: </strong>This retrospective study included 14,758 patients who underwent chest CT and CXR within seven days. We used 10,818 CXRs for development, 4,377 for tuning, and 3,020 for validation. The DLM employed a Vision Transformer (ViT-B/32) architecture. Performance was assessed using AUC, sensitivity, and predictive values. Risk stratification was performed via Youden index and F-score optimization.</p><p><strong>Results: </strong>The DLM achieved an AUC of 0.874, sensitivity of 84.9%, and negative predictive value (NPV) of 99.4% in validation. Performance remained consistent across care settings (AUCs 0.819-0.853). Subgroup analysis showed the best performance in patients < 60 years (AUC 0.934), while comorbidities were associated with lower AUCs. High-risk patients exhibited significantly higher one-month and one-year incidences of pneumothorax (17.4% and 12.5%) and pulmonary contusion (9.8% and 8.0%) compared to low-risk patients (all p < 0.001). No significant difference was observed for pneumonia association.</p><p><strong>Conclusions: </strong>This CT-verified DLM demonstrated high diagnostic performance for predicting acute rib fractures and effectively stratified patients by associated complication risk. This model may assist clinicians with early prediction and triage, potentially enhancing clinical efficiency and patient outcomes in trauma workflows.</p>","PeriodicalId":14031,"journal":{"name":"International Journal of Medical Sciences","volume":"23 9","pages":"2796-2809"},"PeriodicalIF":3.7,"publicationDate":"2026-07-22","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13539916/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148887410","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Combined Effects of Vitamin D3 and Extracorporeal Shockwave Therapy on Osteoblast Differentiation via F-actin mediated Pdia3 Membrane Localization.","authors":"Jai-Hong Cheng, Chi-Hsiang Hsu, Meng-Lun Tsai, Jeng-Wei Chen, Shun-Wun Jhan, Suhyun Lee, Chien-Yiu Huang, Shan-Ling Hsu","doi":"10.7150/ijms.127831","DOIUrl":"10.7150/ijms.127831","url":null,"abstract":"<p><strong>Aim: </strong>1α,25(OH)₂D₃ (vitamin D3, VitD3) and extracorporeal shockwave therapy (ESWT) promote osteoblast differentiation and mineralization. Protein disulfide isomerase-associated 3 (Pdia3) mediates rapid membrane signaling of VitD3, but its interaction with ESWT remains unclear.</p><p><strong>Materials and methods: </strong>MC3T3-E1 cells were treated with VitD3, ESWT, or both. Alkaline phosphatase activity and Alizarin red staining assessed osteoblast differentiation and mineralization. Pdia3 expression and signaling were evaluated by Western blotting and ELISA. Pdia3 distribution was analyzed by immunofluorescence and flow cytometry.</p><p><strong>Results: </strong>The actin polymerization inhibitor latrunculin B tested the role of F-actin. Combined VitD3 and ESWT significantly increased ALP activity, mineral deposition, Pdia3 expression, and plasma membrane localization versus single treatments. These effects were mediated by Pdia3-dependent protein kinase C (PKC) activation. Disruption of F-actin reduced Pdia3 membrane localization and abolished the combined osteogenic effects. ESWT promoted F-actin repolymerization, facilitating Pdia3 trafficking to the membrane.</p><p><strong>Conclusion: </strong>VitD3 and ESWT exert enhanced combined effects on osteoblast differentiation and mineralization by promoting F-actin mediated Pdia3 membrane localization and activating the PKC pathway. The integrity of the actin cytoskeleton is essential for these effects.</p>","PeriodicalId":14031,"journal":{"name":"International Journal of Medical Sciences","volume":"23 9","pages":"2767-2779"},"PeriodicalIF":3.7,"publicationDate":"2026-07-22","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13539911/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148887451","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"WISP-3 promotes tumor-monocyte adhesion through a MEK/ERK-dependent miR-12131/ICAM-4 axis in lung adenocarcinoma.","authors":"Chia-Chia Chao, Syuan-Ling Lin, Yu-Chen Chen, Ching-Yuan Cheng, En-Ming Chang, Chih-Hsin Tang, Chih-Yang Lin","doi":"10.7150/ijms.136597","DOIUrl":"10.7150/ijms.136597","url":null,"abstract":"<p><p>Tumor-immune cell interactions critically contribute to the progression of non-small cell lung cancer (NSCLC). In this study, we investigated the role of WNT1-inducible signaling pathway protein 3 (WISP-3) in regulating tumor cell adhesion and the underlying molecular mechanisms in lung adenocarcinoma cells. Treatment with recombinant WISP-3 significantly increased intercellular adhesion molecule-4 (ICAM-4) expression at both mRNA and protein levels in A549 and H1299 cells in a dose-dependent manner. Consistently, WISP-3 enhanced tumor-monocyte adhesion, indicating its involvement in tumor-immune cell interactions. Mechanistically, WISP-3 stimulated rapid activation of the MEK/ERK signaling cascade, as demonstrated by increased phosphorylation of MEK and ERK. Pharmacological inhibition of MEK using PD98059 or U0126, as well as direct inhibition of ERK with SCH772984, markedly attenuated WISP-3-induced ICAM-4 expression and THP-1 adhesion. These findings were further supported by siRNA-mediated knockdown of MEK or ERK, confirming the essential role of this pathway. In addition, WISP-3 suppressed the expression of hsa-miR-12131, which was identified as a negative regulator of ICAM-4. Restoration of hsa-miR-12131 significantly reduced ICAM-4 expression and impaired tumor-monocyte adhesion, indicating that miR-12131 functions downstream of MEK/ERK signaling. Collectively, these results demonstrate that WISP-3 promotes ICAM-4-dependent monocyte adhesion through activation of the MEK/ERK pathway and subsequent suppression of hsa-miR-12131. This WISP-3/MEK/ERK/miR-12131/ICAM-4 axis provides new insight into tumor-immune interactions in NSCLC and highlights potential therapeutic targets.</p>","PeriodicalId":14031,"journal":{"name":"International Journal of Medical Sciences","volume":"23 8","pages":"2637-2646"},"PeriodicalIF":3.7,"publicationDate":"2026-07-13","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13410858/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148619972","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Multi-Omics and Clinical Data Analyses of Protein Arginine Methyltransferases in Pan-Cancer and Colorectal Cancer.","authors":"Jialing Xie, Qihui Wu, Yuanyuan Xu, Jiaxin Liu, Yan Wang, Xuan Wang, Xiaodan Fu, Yimin Li","doi":"10.7150/ijms.129345","DOIUrl":"10.7150/ijms.129345","url":null,"abstract":"<p><strong>Objective: </strong>Arginine methylation, catalyzed by protein arginine methyltransferases (PRMTs), is a critical post-translational modification that modulates gene expression and signal transduction. Although the involvement of PRMTs in malignancy is increasingly recognized, a comprehensive pan-cancer synthesis of this family remains elusive. We sought to elucidate the multi-omic landscape of PRMTs and define their biological contributions to colorectal cancer (CRC) progression.</p><p><strong>Methods: </strong>Using multi-omic data from TCGA and GTEx, we performed an integrative pan-cancer analysis of PRMT expression, genetic alterations, epigenetic modifications, and their associations with prognosis, genomic heterogeneity, stemness, the tumor microenvironment, and oncogenic pathways. After validating PRMT expression patterns across multiple independent CRC cohorts from the GEO database, PRMT1 was prioritized for further investigation. Its expression was assessed in a real-world CRC cohort using immunohistochemistry, while its oncogenic potential was scrutinized through <i>in vitro</i> proliferation assays.</p><p><strong>Results: </strong>PRMT family genes exhibit heterogeneous molecular profiles across cancers, which correlate significantly with genomic instability, stemness, immune infiltration, and oncogenic pathway activation. Clinical validation demonstrated that PRMT1 is markedly upregulated in CRC, where its overexpression correlates with larger tumor size, advanced T stage, and lymph node metastasis. Loss-of-function experiments demonstrated that PRMT1 is essential for maintaining CRC cell proliferation.</p><p><strong>Conclusion: </strong>Our study highlights the multifaceted roles of PRMTs across the pan-cancer spectrum. By identifying PRMT1 as a key driver of CRC progression, this work provides a rationale for the development of PRMT-targeted therapies and personalized diagnostic biomarkers.</p>","PeriodicalId":14031,"journal":{"name":"International Journal of Medical Sciences","volume":"23 8","pages":"2621-2636"},"PeriodicalIF":3.7,"publicationDate":"2026-07-13","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13411392/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148620038","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Licoricidin triggers reactive oxygen species-mediated PANoptosis in human hepatocellular carcinoma cells.","authors":"Ming-Chun Hung, Hui-Ling Chiou, Yi-Hsien Hsieh, Pei-Ni Chen, Yung-Luen Yu, Hsiang-Lin Lee","doi":"10.7150/ijms.132175","DOIUrl":"10.7150/ijms.132175","url":null,"abstract":"<p><p>Licoricidin (LCD), a natural isoflavonoid compound extracted from Glycyrrhiza species, has been extensively demonstrated to possess diverse biological activities, including anti-inflammatory and potent anti-cancer effects. However, the precise mechanism underlying LCD action against hepatocellular carcinoma (HCC) remains unclear, particularly regarding its regulation of cell death. In this study, we comprehensively explored the effects of LCD on HCC cells <i>in vitro</i> and investigated its role and mechanism of action in the induction of PANoptosis. Our results reveal that LCD exhibited potent anti-HCC activities by decreasing cell viability and significantly inhibiting clonogenic survival in HCC cell lines. Our results demonstrate that LCD triggered a substantial accumulation of reactive oxygen species and induced depolarization of the mitochondrial membrane, leading to profound mitochondrial dysfunction. We further confirmed that LCD activated a comprehensive PANoptosis program by synchronously upregulating the expression of apoptotic proteins (Bax, c-CASP3, and c-PARP1), pyroptotic proteins (c-CASP 1 and c-GSDMD), and the phosphorylation of necroptotic executioners (p-MLKL and p-RIPK1). Treatment with the ROS inhibitor (NAC), apoptosis inhibitor (ZVAD), or necroptosis inhibitor (Nec-1) significantly reduced the expression of PANoptosis-related proteins in LCD-treated cells. Furthermore, molecular docking simulations and cellular thermal shift assay (CETSA) assay confirmed the direct and stable binding of LCD to PANoptosis-related proteins. In summary, we show for the first time that LCD exerts favorable anti-HCC activities via the induction of PANoptosis through a ROS-dependent mechanism and potntial direct modulation of core executive proteins. This multi-target action suggests that LCD could be a novel candidate for the management of hepatocellular carcinoma.</p>","PeriodicalId":14031,"journal":{"name":"International Journal of Medical Sciences","volume":"23 8","pages":"2610-2620"},"PeriodicalIF":3.7,"publicationDate":"2026-07-13","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13411510/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148619991","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"ZDHHC-Mediated Protein S-Palmitoylation in Cancer: Epigenetic Interfaces, Structural Logic and Therapeutic Targeting.","authors":"Xinyi Chen, Duo Xu, Yongbiao Huang, Xianglin Yuan","doi":"10.7150/ijms.130609","DOIUrl":"10.7150/ijms.130609","url":null,"abstract":"<p><p>Protein S-palmitoylation, the reversible thioesterification of cysteine side chains, is emerging as a druggable post-translational modification that couples membrane topology to oncogenic, metabolic, immune, and epigenetic networks in cancer. ZDHHC palmitoyltransferases and depalmitoylating enzymes, including acyl-protein thioesterases and palmitoyl-protein thioesterase 1, constitute a dynamic circuitry that governs the localization, stability, and signaling competence of key regulators of tumor growth, metabolic adaptation, and immune phenotype. Here, we synthesize recent structural and chemical biology advances that clarify how human ZDHHC enzymes achieve acyl-chain recognition and substrate engagement. Structural studies show that these enzymes adopt a four-transmembrane, \"tent-like\" fold, in which the helices create a membrane-embedded cavity for acyl-chain accommodation. We also discuss how ankyrin-repeat domains and accessory partners shape substrate recruitment and subcellular localization, and we highlight emerging high-throughput platforms that enable quantitative profiling of isoform- and site-selective modulators. We then discuss how ZDHHC-substrate circuits rewire canonical growth-factor signaling and epithelial-mesenchymal transition programs, metabolic and ferroptotic control nodes, innate immune sensing, and chromatin-linked regulation. These convergent mechanisms position ZDHHC-mediated S-palmitoylation as a context-dependent regulator of tumor progression, therapy response, ferroptosis sensitivity, and immune phenotype. Finally, we outline a translational framework encompassing clinical-stage PPT1 inhibitors, selective ABHD17 blockade, emerging ZDHHC modulators, substrate-competitive strategies targeting checkpoint palmitoylation, and selected comparator approaches affecting Wnt and Hedgehog ligand lipidation. Current evidence positions ZDHHC-mediated S-palmitoylation as a regulatory layer with potential biomarker and therapeutic relevance; however, not all reported ZDHHC-substrate associations carry equivalent evidentiary weight. Mechanisms supported by convergent site-directed, genetic, biochemical, functional, and in vivo evidence should be distinguished from associations inferred mainly from expression profiling, overexpression systems, single-model observations, or broad pharmacological perturbation. Clinical translation remains preliminary and is constrained by isoform selectivity, substrate redundancy, incomplete pharmacodynamic read-outs, and the absence of validated biomarker-guided patient stratification.</p>","PeriodicalId":14031,"journal":{"name":"International Journal of Medical Sciences","volume":"23 8","pages":"2679-2714"},"PeriodicalIF":3.7,"publicationDate":"2026-07-13","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13411175/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148620057","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Inhibition of UBE2N enhances TRAIL-mediated apoptosis through upregulation of DR5 in cancer cells.","authors":"Yu Jin Jeong, Seon Min Woo, Seung Un Seo, So Rae Song, Taeg Kyu Kwon","doi":"10.7150/ijms.130235","DOIUrl":"10.7150/ijms.130235","url":null,"abstract":"<p><p>Tumor necrosis factor-related apoptosis-induced ligand (TRAIL) selectively induces apoptosis in cancer cells. However, many cancer cells are resistant to TRAIL because of downregulation of death receptors (DRs) and overexpression of anti-apoptotic proteins. Ubiquitin-conjugating enzyme E2N (UBE2N), also known as Ubc13, plays a central role in ubiquitin-mediated cellular activities. In this study, we aimed to explore the sensitization effect of UBE2N inhibition in TRAIL-mediated apoptosis in cancer cells. NSC697923 (a potent inhibitor of UBE2N) alone and TRAIL alone did not induce apoptosis in renal carcinoma Caki cells. However, combined treatment with NSC697923 and TRAIL significantly enhanced apoptotic cell death in cancer cells, but not in normal cells. Mechanistically, NSC697923 induced upregulation of DR5 mRNA and protein levels through CHOP-mediated DR5 transcriptional activation and ubiquitin-mediated DR5 stabilization. NSC697923-mediated DR5 mRNA upregulation was regulated by upregulation of CHOP expression, a key transcriptional factor of DR5. CHOP siRNA treatment inhibited NSC697923-mediated DR5 protein expression. Moreover, NSC697923 generated ROS, and pretreatment with ROS scavengers inhibited DR5 upregulation and NSC697923 plus TRAIL-mediated cell death. These findings suggest that UBE2N inhibitor enhances TRAIL-induced apoptosis by DR5 upregulation and UBE2N inhibition may serve as a potential strategy to overcome TRAIL resistance in cancer therapy.</p>","PeriodicalId":14031,"journal":{"name":"International Journal of Medical Sciences","volume":"23 8","pages":"2647-2656"},"PeriodicalIF":3.7,"publicationDate":"2026-07-13","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13411021/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148619930","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Cyr61 Promotes Oral Squamous Cell Carcinoma Cell Motility via an Integrin αvβ3/αvβ5-PLC/PKC/c-Src-AP-1-ICAM-1 Signaling Axis.","authors":"Kuan-Chou Lin, Pei-Wen Peng, Tsung-Ming Chang, Ying-Sui Sun, Chih-Hsin Tang, Ju-Fang Liu, Chia-Jung Lee","doi":"10.7150/ijms.133127","DOIUrl":"10.7150/ijms.133127","url":null,"abstract":"<p><p>Oral squamous cell carcinoma (OSCC) frequently metastasizes, leading to poor patient outcomes. Cysteine-rich angiogenic inducer 61 (Cyr61/CCN1) has been implicated in cancer progression; however, the downstream mechanism driving OSCC motility remains incompletely defined. Cyr61 expression was elevated in OSCC and associated with advanced clinicopathological features. In OSCC cell lines, recombinant Cyr61 enhanced wound closure and Transwell migration and increased intercellular adhesion molecule-1 (ICAM-1) expression at both the mRNA and protein levels. ICAM-1 silencing significantly attenuated Cyr61-induced cell motility, indicating that ICAM-1 is an important downstream effector. Mechanistically, Cyr61 signaling was initiated through integrin αvβ3 and αvβ5, as neutralizing antibodies and siRNAs targeting these integrins suppressed Cyr61-induced migration and ICAM-1 expression. Cyr61 also induced phosphorylation of PLC, PKC, and c-Src, and pharmacological or siRNA-mediated inhibition of these kinases attenuated ICAM-1 upregulation and cell migration. Moreover, Cyr61 enhanced AP-1 activity via c-Jun phosphorylation, increased c-Jun occupancy at the ICAM-1 promoter, and inhibition of AP-1 signaling diminished Cyr61-driven ICAM-1 expression and motility. Together, these data define an integrin αvβ3/αvβ5-PLC-PKC-c-Src-AP-1 axis that transcriptionally upregulates ICAM-1, promoting OSCC migration and providing a mechanistic basis for targeting Cyr61-driven migratory programs in OSCC.</p>","PeriodicalId":14031,"journal":{"name":"International Journal of Medical Sciences","volume":"23 8","pages":"2657-2669"},"PeriodicalIF":3.7,"publicationDate":"2026-07-13","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13411012/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148619940","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Eosinophilic Esophagitis and Risk of Non-Alcoholic Fatty Liver Disease and Cirrhosis: A Multi-Center Retrospective Study.","authors":"Shuo-Yan Gau, Yu-Jung Su, Shih-Chi Yang, Chih-Lung Wu, Solomon Chih-Cheng Chen, Hui-Chin Chang, Meng-Che Wu","doi":"10.7150/ijms.123768","DOIUrl":"10.7150/ijms.123768","url":null,"abstract":"<p><strong>Background and aim: </strong>Eosinophilic esophagitis (EoE) is a chronic Th2-mediated inflammatory disease. Given its systemic immune activation and eosinophil-rich pathology, this study aimed to evaluate the longitudinal risk of non-alcoholic fatty liver disease (NAFLD) and cirrhosis among patients with EoE.</p><p><strong>Methods: </strong>A retrospective cohort study was conducted using the TriNetX US Collaborative Network. Adults (≥18 years) with an EoE diagnosis were matched 1:1 with EoE-free controls based on demographics, comorbidities, and healthcare utilization. Patients with prior liver disease or malignancy were excluded. Incident NAFLD and cirrhosis were evaluated excluding diagnoses within 3 months of the index date. Sensitivity analyses explored alternative EoE definitions (proton pump inhibitor use, topical corticosteroids, endoscopy records) and longer wash-out periods.</p><p><strong>Results: </strong>Compared with matched controls, EoE patients had a significantly elevated risk of NAFLD (HR = 1.409, 95% CI: 1.277-1.555) and cirrhosis (HR = 1.529, 95% CI: 1.176-1.988). Elevated risks persisted using PPI-based (NAFLD: HR = 1.705, 95% CI: 1.535-1.894; cirrhosis: HR = 1.962, 95% CI: 1.478-2.605), steroid-based (NAFLD: HR = 1.746, 95% CI: 1.561-1.953; cirrhosis: HR = 2.101, 95% CI: 1.557-2.837), and endoscopy-based definitions (NAFLD: HR = 1.951, 95% CI: 1.506-2.528).</p><p><strong>Conclusions: </strong>EoE is associated with higher long-term risks of NAFLD and cirrhosis. These findings underscore the importance of hepatic surveillance and immune-metabolic research in EoE patients. However, potential residual confounder caused by comedications should be cautiously interpreted.</p>","PeriodicalId":14031,"journal":{"name":"International Journal of Medical Sciences","volume":"23 8","pages":"2670-2678"},"PeriodicalIF":3.7,"publicationDate":"2026-07-13","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13411181/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148619927","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Migration of Cardiac Cells: Hot Topics that have not Attracted Clinical Attention.","authors":"Jie Ma, Yaping Xu, Yali Wang, Zhikun Guo","doi":"10.7150/ijms.130458","DOIUrl":"10.7150/ijms.130458","url":null,"abstract":"<p><p>Cell migration plays a critical role in various physiological and pathological processes, particularly in the development and repair of cardiac diseases. It is a complex, multi-step process involving different mechanisms and cell types. This review summarizes the roles of cardiac cell migration in cardiac immune responses, myocardial regeneration, and chronic inflammation. Specifically, we explore how cardiac cells promote repair and regeneration following myocardial injury through migration. In addition, the article reviews the impact of cell migration on processes such as angiogenesis and fibrosis, which are crucial for myocardial repair and pathological states. Due to the complexity of intercellular interactions, signaling pathways, and microenvironmental factors, understanding cardiac cell migration remains a significant challenge. Further research into these migratory mechanisms will help uncover their pathological roles in cardiac diseases and provide new therapeutic approaches for cardiac repair and regeneration. This review also highlights the migratory mechanisms of major cardiac cell types and examines the regulatory roles of chemokines in these processes. Furthermore, we discuss how cardiac cells engage in localized migration under different disease conditions, thereby contributing to the heart's self-repair.</p>","PeriodicalId":14031,"journal":{"name":"International Journal of Medical Sciences","volume":"23 8","pages":"2587-2609"},"PeriodicalIF":3.7,"publicationDate":"2026-07-11","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13411177/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148620012","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}