The Kaohsiung journal of medical sciences最新文献

{"title":"GCKR Polymorphisms Increase the Risks of Low Bone Mineral Density in Young and Non-Obese Patients With MASLD and Hyperuricemia.","authors":"Tzu-Hao Li, Yu-Shin Huang, Chia-Chen Ma, Shin-Yu Tsai, Hung-Cheng Tsai, Hsiao-Yun Yeh, Hsiao-Chin Shen, Shiao-Ya Hong, Chien-Wei Su, Hwai-I Yang, Ying-Ying Yang, Ming-Chih Hou","doi":"10.1002/kjm2.70017","DOIUrl":"https://doi.org/10.1002/kjm2.70017","url":null,"abstract":"<p><p>Metabolic-associated steatotic liver disease (MASLD) encompasses common comorbidities including low bone mineral density (BMD) and hyperuricemia (HU), yet relevant genetic analyses are limited. This study aimed to investigate the genetic effects of risk single nucleotide polymorphisms (SNPs) on the occurrence of low BMD in patients with MASLD and HU, particularly focusing on relatively young or non-obese populations. We conducted a cross-sectional study utilizing data from the Taiwan Biobank, screening a total of 150,709 participants who were prospectively enrolled over a period of 13 years. The risk SNPs for MASLD were identified. Genotype analyses of HU and its effects on the occurrence of low BMD in the general population were evaluated, with further analyses of common SNPs focusing on patients with MASLD, including subgroup analyses on relatively young and non-obese populations. A total of 20,496 participants were eligible for analysis, including 7526 patients with MASLD. Several risk SNPs for MASLD were identified. Furthermore, MASLD patients carrying the PNPLA3-rs738409 C_C, PNPLA3-rs2896019 T_T, GCKR-rs780094 T_T, and GCKR-rs1260326 T_T genotypes exhibited an increased risk of comorbidity with HU. Trend analysis revealed that the T alleles in GCKR-rs780094 and GCKR-rs1260326 were associated with the occurrence of low BMD in MASLD individuals comorbid with HU, particularly among relatively young or non-obese populations. In relatively young, non-obese patients with MASLD and HU, genetic effects significantly increase the risk of occurrence of low BMD. Given the presence of genetic effects in these ostensibly low-risk groups, heightened awareness and close follow-up are recommended.</p>","PeriodicalId":94244,"journal":{"name":"The Kaohsiung journal of medical sciences","volume":" ","pages":"e70017"},"PeriodicalIF":0.0,"publicationDate":"2025-04-09","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143813280","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"RETRACTION: Paris Saponin VII Enhanced the Sensitivity of HepG2/ADR Cells to ADR via Modulation of PI3K/AKT/MAPK Signaling Pathway.","authors":"","doi":"10.1002/kjm2.70030","DOIUrl":"https://doi.org/10.1002/kjm2.70030","url":null,"abstract":"<p><strong>Retraction: </strong>G.-E. Tang, Y.-X. Niu, Y. Li, C.-Y. Wu, X.-Y. Wang and J. Zhang, \"Paris Saponin VII Enhanced the Sensitivity of HepG2/ADR Cells to ADR via Modulation of PI3K/AKT/MAPK Signaling Pathway,\" The Kaohsiung Journal of Medical Sciences 36, no. 2 (2020): 98-106, https://doi.org/10.1002/kjm2.12145. The above article, published online on 05 November 2019 in Wiley Online Library (wileyonlinelibrary.com), has been retracted by agreement between; the journal Editor-in-Chief, Wan-Long Chuang; Kaohsiung Medical University; and John Wiley and Sons Australia. The retraction has been agreed upon due to elements in Figures 4A and 6C, which were found duplicated in other articles published earlier elsewhere, and in some cases representing a different scientific context. The authors did not respond to the concerns raised. The editors have lost confidence in the data presented and consider the conclusions to be substantially compromised. The authors were informed of the retraction but were unavailable for comment.</p>","PeriodicalId":94244,"journal":{"name":"The Kaohsiung journal of medical sciences","volume":" ","pages":"e70030"},"PeriodicalIF":0.0,"publicationDate":"2025-04-08","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143813282","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Correction to \"Preventive Treatment Effects on Brain Structures and Functions in Patients With Chronic Migraine: A Multimodel Magnetic Resonance Imaging Study\".","authors":"","doi":"10.1002/kjm2.70016","DOIUrl":"https://doi.org/10.1002/kjm2.70016","url":null,"abstract":"","PeriodicalId":94244,"journal":{"name":"The Kaohsiung journal of medical sciences","volume":" ","pages":"e70016"},"PeriodicalIF":0.0,"publicationDate":"2025-04-08","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143805299","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Dose-response relationship and predictive value of soluble B7-DC in bronchoalveolar lavage fluid and risk of refractory Mycoplasma pneumoniae pneumonia in children.","authors":"Xue-Hua Li, Jun-Mei Xu","doi":"10.1002/kjm2.12944","DOIUrl":"10.1002/kjm2.12944","url":null,"abstract":"<p><p>This study was to investigate the clinical significance of soluble B7-dendritic cell (sB7-DC) concentration in bronchoalveolar lavage fluid (BALF) of children with Refractory Mycoplasma pneumoniae pneumonia (RMPP). A total of 298 patients with Mycoplasma pneumoniae pneumonia (MPP) were enrolled. Patients were divided into general MPP (GMPP) (n = 213) and RMPP groups (n = 85). Detection of sB7-DC and serum inflammatory factors in BALF was performed by ELISA. The relationship between sB7-DC and the risk of RMPP was assessed using restricted cubic spline (RCS) model. A base model for predicting RMPP was constructed using logistic regression analysis, and a compound model was created with the addition of sB7-DC in the base model. ROC curves were plotted to evaluate the predictive value of the model. Column line plots were plotted to assess the contribution of each variable to the outcome event. Calibration curves were plotted and the Hosmer-Lemeshow test (HL test) was performed to assess the calibration performance of the model. Decision curve analysis (DCA) plots were plotted to assess determine whether sB7-DC has clinical value. There was no statistical difference between sB7-H3 and sB7-H4 in the two groups (both p > 0.05). sB7-DC levels were higher in the RMPP group than in the GMPP group (91.66 [77.36, 122.5] pg/ml vs. 64.87 [47.07, 86.46] pg/ml, p < 0.001). RCS analysis showed that the risk of RMPP gradually increased with the increase of sB7-DC when sB7-DC > 76.505 pg/ml. Both the base model and the compound model constructed with independent correlates of RMPP had some predictive value, and the models were well-fitted. The column line graphs showed that the models had discriminative ability. Notably, the compound model had a higher predictive value, with a higher AUC value than the base model: 0.76 (0.65-0.87) versus 0.68 (0.54-0.81). The highest net benefit was close to 0.15 (only 0.1 in the base model). When the net benefit was >0, the high-risk threshold took on a wide range of values. sB7-DC in children with RMPP is an independent predictor of RMPP. sB7-DC helps to improve quantitative prediction of RMPP risk and accurately guide medical decisions.</p>","PeriodicalId":94244,"journal":{"name":"The Kaohsiung journal of medical sciences","volume":" ","pages":"e12944"},"PeriodicalIF":0.0,"publicationDate":"2025-04-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143412242","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Identification of diagnostic and therapeutic biomarkers for attention-deficit/hyperactivity disorder.","authors":"Sheng-Yu Lee, Liang-Jen Wang, Cheng-Fang Yen","doi":"10.1002/kjm2.12931","DOIUrl":"https://doi.org/10.1002/kjm2.12931","url":null,"abstract":"<p><p>Attention-deficit/hyperactivity disorder (ADHD) is a common psychiatric condition among children and adolescents, often associated with a high risk of psychiatric comorbidities. Currently, ADHD diagnosis relies exclusively on clinical presentation and patient history, underscoring the need for clinically relevant, reliable, and objective biomarkers. Such biomarkers may enable earlier diagnosis and lead to improved treatment outcomes. Our research team has focused on identifying potential biomarkers for ADHD by investigating its possible pathomechanisms, with consideration of the aforementioned criteria. Given the significant sex-related differences in ADHD prevalence (male predominance) and the age-related variability in its symptomatology, we explored the role of neuroendocrine systems in ADHD. Specifically, we examined the epigenetic regulation mechanism involved in ADHD pathogenesis and developed a diagnostic model based on peripheral microRNA. Additionally, we investigated the role of microbiota dysbiosis in the pathophysiology of ADHD and provided novel insights into its management. This paper presents a summary of our findings on potential biomarkers for ADHD. By analyzing blood, salivary, and fecal samples, we identified several promising biomarkers that may serve as objective parameters for improving the diagnostic accuracy for ADHD. Further research involving larger cohort studies is required to confirm the reliability of these biomarkers.</p>","PeriodicalId":94244,"journal":{"name":"The Kaohsiung journal of medical sciences","volume":"41 4","pages":"e12931"},"PeriodicalIF":0.0,"publicationDate":"2025-04-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143757109","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Photocarcinogenesis of the skin: Current status and future trends.","authors":"Ting-Ting Yang, Cheng-Che E Lan","doi":"10.1002/kjm2.12946","DOIUrl":"10.1002/kjm2.12946","url":null,"abstract":"<p><p>Solar radiation is essential for life on Earth but is also a major contributor to skin carcinogenesis. Solar radiation, particularly ultraviolet (UV) B (280-320 nm) and UVA (320-400 nm), induces photocarcinogenesis via various pathways. UV light can directly cause DNA damage, resulting in genetic mutations if not repaired correctly. UV light can also induce photocarcinogenesis by generating reactive oxygen species, inducing immunosuppression and inflammation. Recently, visible light (400-760 nm) has been shown to contribute to photocarcinogenesis by activating oxidative pathways. In addition to the irradiation dose (fluence, J/m²), UVB irradiance (W/m²) is also considered a factor influencing photocarcinogenesis. In this review, we summarize the mechanisms of photocarcinogenesis and provide strategies to prevent skin cancer.</p>","PeriodicalId":94244,"journal":{"name":"The Kaohsiung journal of medical sciences","volume":" ","pages":"e12946"},"PeriodicalIF":0.0,"publicationDate":"2025-04-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143191198","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Antithrombotic use in retinal artery occlusion: A narrative review.","authors":"Wan-Yu Liu, Yun-Hsin Tang, Yi-Hsing Chen","doi":"10.1002/kjm2.12938","DOIUrl":"10.1002/kjm2.12938","url":null,"abstract":"<p><p>Retinal artery occlusion (RAO) is a critical ophthalmic emergency with a high risk of significant visual impairment. While traditional treatment aims to promptly restore blood flow to the retina, recent research has investigated the potential benefits of anticoagulation therapy for managing this condition. This paper reviews current literature and clinical trials investigating the efficacy and safety of anticoagulant and antiplatelet therapies, such as systemic heparinization and direct oral anticoagulants and aspirin, in treating RAO. The mechanism of action involves preventing thrombus propagation and platelet aggregation to promote microvascular circulation, potentially mitigating ischemic damage and improving visual outcomes. However, controversies exist regarding the optimal timing, duration, and selection of antithrombotic agents due to the risk of hemorrhagic complications. Further large-scale prospective studies are warranted to establish evidence-based guidelines for incorporating antithrombotic into the standard management of RAO. This paper underscores the evolving landscape of antithrombotic therapy as a promising adjunctive treatment strategy in the management of retinal artery occlusion.</p>","PeriodicalId":94244,"journal":{"name":"The Kaohsiung journal of medical sciences","volume":" ","pages":"e12938"},"PeriodicalIF":0.0,"publicationDate":"2025-04-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143019369","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"LINC01871 facilitates cervical cancer cell migration and immune escape by targeting miR-873-3p/MAP3K2 axis.","authors":"Yan Li, Li Wei, Hui-Hui Zhang, Hong-Fei Ci, Duo-Jie Li","doi":"10.1002/kjm2.12948","DOIUrl":"10.1002/kjm2.12948","url":null,"abstract":"<p><p>Cervical cancer (CC) poses a significant threat to women's health and lives worldwide. Emerging evidence indicates that long noncoding RNA LINC01871 is closely associated with immune regulation in CC patients. However, its specific role and underlying mechanisms in CC remain poorly understood. In this study, we examined the expression levels and subcellular localization of LINC01871 in CC cell lines. Functional assays, including transwell migration and invasion assays as well as macrophage phagocytosis assays, were conducted to estimate CC cell invasiveness, migration, and immune response. Western blotting was performed to assess the protein expression of markers associated with epithelial-mesenchymal transition (EMT), immunity, and MAPK signaling. A luciferase reporter assay was used to confirm the interactions between LINC01871, miR-873-3p, and MAP3K2. Additionally, a xenograft mouse model was employed to investigate the in vivo effects of LINC01871 on CC progression. Our results revealed that LINC01871 is highly expressed and predominantly localized in the cytoplasm of CC cell lines. LINC01871 knockdown significantly suppressed CC cell invasion, migration, EMT, and immune escape in vitro and reduced tumor growth in vivo. Mechanistically, LINC01871 was found to interact with miR-873-3p, leading to the upregulation of MAP3K2 and subsequent activation of MAPK signaling. Furthermore, MAP3K2 overexpression rescued the inhibitory effects of LINC01871 silencing on the malignant behaviors of CC cells. In conclusion, LINC01871 facilitates CC metastasis by driving EMT and modulating the immune response via the miR-873-3p/MAP3K2/MAPK signaling pathway.</p>","PeriodicalId":94244,"journal":{"name":"The Kaohsiung journal of medical sciences","volume":" ","pages":"e12948"},"PeriodicalIF":0.0,"publicationDate":"2025-04-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143544978","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"ELK4 transcription promotes MSI2-mediated progression of non-small cell lung cancer through the TGF-β/SMAD3 pathway.","authors":"Guo-Cui Shi, Yu-Qing Teng, Jin-Song Zhu, Jia-Wei Sun, Cui Liu, Yi-Wei Zhang","doi":"10.1002/kjm2.12952","DOIUrl":"10.1002/kjm2.12952","url":null,"abstract":"<p><p>Non-small cell lung cancer (NSCLC) is a primary contributor to global cancer-related mortality. Musashi-2 (MSI2), an RNA-binding protein (RBP), is upregulated in specific NSCLC tumor subgroups. The current investigation evaluated the role and underlying mechanism of MSI2 in NSCLC. The expression levels of ELK4, MSI2, SMAD3, p-SMAD3 and TGFβR1 were assessed via RT-qPCR or Western blot. Chromatin immunoprecipitation (ChIP) and dual luciferase reporter assays were used to confirm the interaction between ELK4 and MSI2. The proliferation, migration and invasion of NSCLC cells were determined via MTT, colony formation, and transwell assays, respectively. A xenograft tumor model was established in BALB/c nude mice. Immunohistochemical (IHC) staining was used to test Ki67 expression. We found that MSI2 and ELK4 expression levels were increased in NSCLC tissues and cells. ELK4 depletion suppressed the proliferation, migration and invasion of NSCLC cells. ELK4 acts as a transcription factor and promotes the transcription of MSI2. MSI2 depletion repressed NSCLC cell proliferation, migration and invasion through the TGF-β/SMAD3 pathway. Overexpression of ELK4 reversed the inhibitory effect of MSI2 repression on NSCLC progression. These results confirmed that ELK4 is a direct regulator of MSI2 expression and that MSI2 promotes NSCLC progression through TGF-β/SMAD3 activation, suggesting the potential clinical value of inhibiting MSI2 in NSCLC.</p>","PeriodicalId":94244,"journal":{"name":"The Kaohsiung journal of medical sciences","volume":" ","pages":"e12952"},"PeriodicalIF":0.0,"publicationDate":"2025-04-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143451352","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Circular RNA circCD44 targets methyltransferase-like 3/homeobox containing 1 to facilitate esophageal squamous cell carcinoma progression.","authors":"Wei-Wen Zou, Yan-Fang Liao, Xi-Rui Huang, Wen-Song Lin, Shan-Ming Lu","doi":"10.1002/kjm2.12950","DOIUrl":"10.1002/kjm2.12950","url":null,"abstract":"<p><p>Esophageal squamous cell carcinoma (ESCC) is a prevalent gastrointestinal malignancy with unclear functional mechanisms of circular RNAs. This study focused on investigating the role of circCD44 in ESCC progression. The expression of circCD44 and homeobox containing 1 (HMBOX1) was found to be elevated in ESCC cell lines. The overexpression of circCD44 or HMBOX1 enhanced proliferation and invasion, while inhibiting apoptosis in ESCC cells, whereas knockdown of these genes had inverse effects. METTL3 was observed to bind to circCD44 and HMBOX1 mRNA, promoting m⁶A modification in HMBOX1 mRNA and subsequent HMBOX1 protein expression. Knockdown of METTL3 or HMBOX1 attenuated the oncogenic effects of circCD44 overexpression both in vitro and in vivo. These findings suggest that circCD44 promotes ESCC progression by facilitating HMBOX1 mRNA m⁶A modification and protein expression through METTL3 binding, providing insights into the molecular mechanisms underlying ESCC pathogenesis.</p>","PeriodicalId":94244,"journal":{"name":"The Kaohsiung journal of medical sciences","volume":" ","pages":"e12950"},"PeriodicalIF":0.0,"publicationDate":"2025-04-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143506729","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}