The Kaohsiung journal of medical sciences最新文献

{"title":"Impact of Hepatitis C Virus Clearance on Cardiovascular Risk: A Real-World Experience From the Nationwide Taiwan Hepatitis C Virus Registry.","authors":"Ping-Jen Hu, Pei-Chien Tsai, Chi-Yi Chen, Hsing-Tao Kuo, Chao-Hung Hung, Kuo-Chih Tseng, Hsueh-Chou Lai, Cheng-Yuan Peng, Jing-Houng Wang, Jyh-Jou Chen, Pei-Lun Lee, Rong-Nan Chien, Chi-Chieh Yang, Gin-Ho Lo, Jia-Horng Kao, Chun-Jen Liu, Chen-Hua Liu, Sheng-Lei Yan, Chun-Yen Lin, Wei-Wen Su, Cheng-Hsin Chu, Chih-Jen Chen, Shui-Yi Tung, Chi-Ming Tai, Chih-Wen Lin, Ching-Chu Lo, Pin-Nan Cheng, Yen-Cheng Chiu, Chia-Chi Wang, Jin-Shiung Cheng, Wei-Lun Tsai, Han-Chieh Lin, Yi-Hsiang Huang, Ming-Lun Yeh, Chung-Feng Huang, Meng-Hsuan Hsieh, Jee-Fu Huang, Chia-Yen Dai, Wan-Long Chung, Yen-Hsiange Wang, Ming-Lung Yu, Ming-Jong Bair","doi":"10.1002/kjm2.70036","DOIUrl":"10.1002/kjm2.70036","url":null,"abstract":"<p><p>Hepatitis C virus (HCV) infection is associated with an increased risk of cardiovascular disease (CVD); however, the impact of interferon (IFN)-based therapy on cardiovascular outcomes remains unclear. This nationwide cohort study included 7411 patients with HCV from The Taiwanese Chronic Hepatitis C Cohort registry who received IFN-based therapy between 2003 and 2014. Patients were categorized into sustained virological response (SVR) (n = 5785) and non-SVR (n = 1676) groups. The incidence of new-onset CVD events, including stroke, coronary artery disease, heart failure, and arrhythmia, was assessed using three Cox proportional hazard models adjusted for different sets of confounding factors. The cumulative CVD incidence was comparable in the SVR and non-SVR groups (11.2% vs. 10.2%, p = 0.609). SVR was not significantly associated with a reduced overall CVD risk among the three models [hazards ratio (HR) = 0.88, 95% confidence interval (CI): 0.71-1.05, p = 0.158]. However, a lower risk of stroke was observed in patients who achieved an SVR, although the difference was not significant (HR = 0.84, 95% CI: 0.74-0.94). The results of the sensitivity analyses confirmed these findings. An SVR following IFN-based therapy did not substantially reduce the overall CVD risk; however, a potential reduction in stroke risk was observed. These results emphasize the importance of long-term cardiovascular risk assessments and highlight the need for further research, particularly in the direct-acting antiviral era in which increased cardiovascular benefits may be expected.</p>","PeriodicalId":94244,"journal":{"name":"The Kaohsiung journal of medical sciences","volume":" ","pages":"e70036"},"PeriodicalIF":3.1,"publicationDate":"2025-08-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12407379/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144136637","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"RETRACTION: Comparison of the Postoperative Analgesic Effects of Paracetamol-Codeine Phosphate and Naproxen Sodium-Codeine Phosphate for Lumbar Disk Surgery.","authors":"","doi":"10.1002/kjm2.12945","DOIUrl":"10.1002/kjm2.12945","url":null,"abstract":"<p><p>Retraction: R. Polat , K. Peker , Ç. T. Gülöksüz , J. Ergil , T. Akkaya , \"Comparison of the Postoperative Analgesic Effects of Paracetamol-Codeine Phosphate and Naproxen Sodium-Codeine Phosphate for Lumbar Disk Surgery,\" Kaohsiung Journal of Medical Sciences 31, no. 9 (2015): 468-472. https://doi.org/10.1016/j.kjms.2015.07.001. The above article, published online on 06 August 2015, in Wiley Online Library (wileyonlinelibrary.com), and has been retracted by agreement between the journal Editor-in-Chief, Wan-Long Chuang; Kaohsiung Medical University; and John Wiley and Sons Australia, Ltd. In 2021, a third party raised concerns regarding evidence of unlikely similarity in the standard deviation values presented in Figures 1 and 2. The journal contacted the authors, who provided original data for evaluation by the journal. Following further correspondence, the journal and publisher concluded that the authors' response satisfied their concerns and that the investigation should be closed without further action. In 2024, the complainant appealed to the journal and publisher to re-open the investigation based on the substantial evidence of errors. The publisher accepted this appeal and re-opened the investigation. The editors have conducted a review of the evidence and the provided dataset and found that the data includes substantial numbers of duplicated values across pairs of patients. The editors have determined that the substantial quantity of duplicated values is incompatible with a genuine randomized controlled trial and that the evidence compromises the conclusions of the article. As such, the parties agree that a retraction is necessary. The authors disagree with the retraction.</p>","PeriodicalId":94244,"journal":{"name":"The Kaohsiung journal of medical sciences","volume":" ","pages":"e12945"},"PeriodicalIF":3.1,"publicationDate":"2025-08-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12407323/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142985916","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","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":"10.1002/kjm2.70016","url":null,"abstract":"","PeriodicalId":94244,"journal":{"name":"The Kaohsiung journal of medical sciences","volume":" ","pages":"e70016"},"PeriodicalIF":3.1,"publicationDate":"2025-08-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12407372/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143805299","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Multiple Metastases to the Lungs 14 Years After Surgery for Adult-Type Granular Cell Tumor of the Ovary.","authors":"Di-Ping Yu, Liu-Qing Yang","doi":"10.1002/kjm2.70032","DOIUrl":"10.1002/kjm2.70032","url":null,"abstract":"","PeriodicalId":94244,"journal":{"name":"The Kaohsiung journal of medical sciences","volume":" ","pages":"e70032"},"PeriodicalIF":3.1,"publicationDate":"2025-08-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12407370/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144059398","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Y-Box-Binding Protein 1 Facilitates the Proliferation and Osteogenic Differentiation of Periodontal Ligament Stem Cells Through the Transcriptional Activation of FGF2-Mediated Akt/GSK3β/β-Catenin Signaling.","authors":"Yun-Hao Xi, Chang-Shun Li, Pin-Lin Wu, Xiao-Yang Zhou, Qian-Wen Li, Cheng-Hui Shen","doi":"10.1002/kjm2.70079","DOIUrl":"https://doi.org/10.1002/kjm2.70079","url":null,"abstract":"<p><p>Periodontal ligament stem cells (PDLSCs) are derived from periodontal tissue and can differentiate into osteoblasts, which are ideal materials for alveolar bone repair and periodontal tissue regeneration. In this study, we aimed to explore the effects of Y-box binding protein 1 (YB-1) on the osteogenic differentiation and proliferation of PDLSCs and its underlying mechanism. hPDLSC proliferation was detected by CCK-8 and EdU assays. The osteogenic differentiation of hPDLSCs was clarified using alkaline phosphatase (ALP) activity detection and Alizarin red S (ARS) staining. The expression levels of osteogenic differentiation-related factors, Akt/GSK3β/β-catenin pathway-related factors, YB-1, and fibroblast growth factor 2 (FGF2) were evaluated using qPCR and Western blotting. The interplay between YB-1 and FGF2 was clarified using ChIP and dual-luciferase reporter gene assays. YB-1 expression was markedly decreased in periodontitis clinical tissues but increased in hPDLSCs during osteogenic differentiation. Moreover, silencing YB-1 suppressed the osteogenic differentiation and proliferation of hPDLSCs. In addition, YB-1 promotes hPDLSC proliferation and osteogenic differentiation in a manner dependent on the activation of the Akt/GSK3β/β-catenin signaling pathway, which is mediated by FGF2 transcriptional activation. Furthermore, the inhibitory effects of YB-1 knockdown on the osteogenic differentiation and proliferation of hPDLSCs were antagonized by human recombinant FGF2. Taken together, our findings revealed that YB-1 facilitates hPDLSC proliferation and osteogenic differentiation through increasing the level of FGF2 via transcriptional regulation, thereby activating the Akt/GSK3β/β-catenin pathway.</p>","PeriodicalId":94244,"journal":{"name":"The Kaohsiung journal of medical sciences","volume":" ","pages":"e70079"},"PeriodicalIF":3.1,"publicationDate":"2025-07-30","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144746629","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":"GNPAT/USP30 Stabilizes DRP1 Protein to Promote Mitochondrial Fission and Functional Damage in COPD Progression.","authors":"Xin-Gui Cheng, Yun-Chan Liu, Fei Chen, Ji-Wei Li, Xiao-Zhou Yao, Qing-Yun Chen","doi":"10.1002/kjm2.70080","DOIUrl":"https://doi.org/10.1002/kjm2.70080","url":null,"abstract":"<p><p>Our previous study revealed the role of glycerol phosphate O-acyltransferase (GNPAT) in regulating chronic obstructive pulmonary disease (COPD). However, its further mechanisms remained unclear. In this study, COPD models were established by exposing mice to cigarette smoke particulates. H&E staining and immunohistochemistry assays were performed on COPD tissue. A549 cells were stimulated with 5% cigarette smoke extract (CSE) and transfected with GNPAT, ubiquitin-specific protease 30 (USP30), and dynamin-related protein 1 (DRP1) plasmids. Cell viability, cell apoptosis, lactate dehydrogenase (LDH) release, ATP production, and reactive oxygen species (ROS) levels were determined using commercial kits. Quantitative real-time PCR and western blotting were used to evaluate mRNA and protein expression. Mitochondrial morphology was examined by transmission electron microscopy. A co-immunoprecipitation assay determined the binding relationships among GNPAT, USP30, and DRP1. Our results showed that GNPAT and DRP1 were highly expressed in the COPD model mice. CSE promoted mitochondrial fission, mitochondrial dysfunction, and cell apoptosis, which were further enhanced by treatment with a mitochondrial fission inducer (TA9). GNPAT promoted mitochondrial fission, mitochondrial dysfunction, and cell apoptosis by enhancing DPR1 protein stability, which depended on USP30. DRP1 enhanced mitochondrial fission, mitochondrial dysfunction, and cell apoptosis, which were both reversed by GNPAT/USP30 inhibition. Collectively, our present study found that GNPAT recruited USP30 and stabilized DRP1, thereby mediating mitochondrial fission and mitochondrial dysfunction that contributed to cell apoptosis in COPD. This study suggests a promising therapeutic biomarker for COPD.</p>","PeriodicalId":94244,"journal":{"name":"The Kaohsiung journal of medical sciences","volume":" ","pages":"e70080"},"PeriodicalIF":0.0,"publicationDate":"2025-07-25","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144710354","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":"Long Noncoding RNA TOB1-AS1 Represses Cervical Cancer Cell Proliferation, Invasion, and Migration via the MicroRNA-27a-3p/Thioredoxin-Interacting Protein Molecular Axis.","authors":"Yang Wang, You-Xiang Hou, Li Xie, Yi-La Xia, Yi-Na Wang","doi":"10.1002/kjm2.70076","DOIUrl":"https://doi.org/10.1002/kjm2.70076","url":null,"abstract":"<p><p>Cervical cancer (CC) remains a major global health concern, particularly due to its aggressive nature and limited treatment options in advanced stages. Long noncoding RNA (lncRNA) TOB1-AS1 has been proposed as a tumor suppressor, yet its regulatory mechanism in CC remains unclear. This study aimed to elucidate the role of TOB1-AS1 in CC progression through the miR-27a-3p/thioredoxin-interacting protein (TXNIP) molecular axis. Functional gain- and loss-of-function assays were conducted to assess the effects of TOB1-AS1, miR-27a-3p, and TXNIP on cell proliferation, invasion, migration, and apoptosis. RT-qPCR, Western blotting, dual-luciferase reporter assays, and in vivo xenograft models were used to validate interactions and phenotypic outcomes. TOB1-AS1 was found to be downregulated in CC cells. Its overexpression suppressed proliferation, invasion, and migration, while enhancing apoptosis. Mechanistically, TOB1-AS1 functioned as a competing endogenous RNA (ceRNA) by sponging miR-27a-3p, thereby restoring TXNIP expression. Modulating miR-27a-3p or TXNIP levels partially reversed the effects of TOB1-AS1. In vivo, TOB1-AS1 overexpression significantly inhibited tumor growth and altered miR-27a-3p and TXNIP expression profiles. These findings suggest that lncRNA TOB1-AS1 acted as a ceRNA of miR-27a-3p to upregulate TXNIP, thereby suppressing CC cell proliferation, invasion and migration.</p>","PeriodicalId":94244,"journal":{"name":"The Kaohsiung journal of medical sciences","volume":" ","pages":"e70076"},"PeriodicalIF":0.0,"publicationDate":"2025-07-16","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144644495","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":"Response to Integration of the Comprehensive Physical Examination and Diagnostic Tools in Clinical Cardiology.","authors":"Yu-Shien Kao, Yi-Hsun Chen, I-Chen Wu","doi":"10.1002/kjm2.70075","DOIUrl":"https://doi.org/10.1002/kjm2.70075","url":null,"abstract":"","PeriodicalId":94244,"journal":{"name":"The Kaohsiung journal of medical sciences","volume":" ","pages":"e70075"},"PeriodicalIF":0.0,"publicationDate":"2025-07-13","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144628465","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":"Dynamics of Cardiometabolic Risk Factors Are Linked to the Risk of Hypertension and Diabetes in MASLD.","authors":"Chin-I Shih, Ming-Lun Yeh, Yi-Hung Lin, Ping-Tsung Shih, Kuan-Ta Wu, Meng-Hsuan Hsieh, Jeng-Fu Yang, Yi-Yu Chen, Po-Cheng Liang, Yu-Ju Wei, Pei-Chien Tsai, Ya-Yun Cheng, Ming-Yen Hsieh, Chih-Wen Wang, Chung-Feng Huang, Jee-Fu Huang, Chia-Yen Dai, Chi-Kung Ho, Wan-Long Chuang, Vincent Wai-Sun Wong, Wei-Ting Chang, Ming-Lung Yu","doi":"10.1002/kjm2.70077","DOIUrl":"https://doi.org/10.1002/kjm2.70077","url":null,"abstract":"<p><p>This study investigates the impact of cardiometabolic risk factors (CMRF) on the prevalence and incidence of hypertension (HTN) and diabetes mellitus (DM) in individuals with metabolic dysfunction-associated steatotic liver disease (MASLD) and nonsteatotic liver disease (non-SLD), using both cross-sectional and longitudinal data. A total of 32,569 Taiwanese adults without viral hepatitis or significant alcohol consumption who underwent health checkups from 1999 to 2013 were analyzed cross-sectionally. Among them, 27,109 individuals free of HTN and DM at baseline and within 1 year of enrollment were followed longitudinally. Participants were classified into four groups based on hepatic steatosis assessed by ultrasound and presence of CMRF: healthy control (non-SLD/CMRF-), simple SLD (SLD/CMRF-), non-SLD/CMRF+, and MASLD. MASLD patients exhibited markedly higher annual incidence rates of HTN and DM (19.7 and 6.3 per 1000 person-years) compared to non-SLD individuals (HTN: 9.0; DM: 0.6 per 1000 person-years). The risk of incident HTN and DM increased progressively with the number of CMRF, with adjusted hazard ratios (aHR) ranging from 2.02 to 15.53 for HTN and from 2.92 to 82.38 for DM. Regression of cardiometabolic dysfunction decreased the risk of HTN and/or DM, and vice versa. The presence of CMRF significantly increased the likelihood of developing HTN and DM in both SLD and non-SLD groups, with aHRs up to 7.48 for HTN and 15.38 for DM. In conclusion, MASLD is strongly associated with increased prevalence and incidence of HTN and DM, and the burden and trajectory of CMRF critically modulate these risks.</p>","PeriodicalId":94244,"journal":{"name":"The Kaohsiung journal of medical sciences","volume":" ","pages":"e70077"},"PeriodicalIF":0.0,"publicationDate":"2025-07-12","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144621599","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":"GATA1 Transcriptionally Upregulates LMCD1, Promoting Ferroptosis in Sepsis-Associated Acute Kidney Injury Through the Hippo/YAP Pathway.","authors":"You-Qi Zhang, Wei-Xia Peng, You-Fu Li, Peng Lu, Hui Liu, Wen-Guang Liu","doi":"10.1002/kjm2.70071","DOIUrl":"https://doi.org/10.1002/kjm2.70071","url":null,"abstract":"<p><p>Sepsis-associated acute kidney injury (SA-AKI) is associated with morbidity and mortality. Ferroptosis is associated with the pathophysiology of SA-AKI. Here, we investigated the role of LIM and cysteine-rich domain 1 (LMCD1) in the regulation of ferroptosis during SA-AKI progression. SA-AKI models were established by CLP and LPS treatments. Hematoxylin and eosin (HE) and (PAS) staining were conducted to examine renal pathological changes. ELISA was used to measure serum creatinine and BUN levels. Lipid ROS levels in cells were examined using flow cytometry. MDA, GSH, SOD, and Fe²⁺ levels in the cells were measured using appropriate kits. Molecular interactions were analyzed using ChIP, a dual-luciferase reporter gene, and Co-IP assays. GATA1 knockdown inhibits LPS-induced cell injury, oxidative stress, and ferroptosis in HK-2 cells by transcriptionally inhibiting LMCD1 expression. Moreover, LMCD1 activates the Hippo/YAP pathway by promoting CUL3-mediated Nrf2 ubiquitination degradation. LMCD1 knockdown alleviates CLP-induced AKI in mice by inhibiting ferroptosis. Taken together, LMCD1 transcriptionally activated by GATA1 promotes ferroptosis during SA-AKI progression by activating the Hippo/YAP pathway and facilitating CUL3-mediated Nrf2 ubiquitination degradation.</p>","PeriodicalId":94244,"journal":{"name":"The Kaohsiung journal of medical sciences","volume":" ","pages":"e70071"},"PeriodicalIF":0.0,"publicationDate":"2025-07-12","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144621600","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}