The Kaohsiung journal of medical sciences最新文献

Rhaponitin Reverses Cisplatin Resistance and Impairs Cancer Stemness Through HIF-1α/MCT4/Wnt Pathway in Tongue Squamous Cell Carcinoma. Rhaponitin通过HIF-1α/MCT4/Wnt通路逆转舌鳞状细胞癌顺铂耐药并损害癌干性

The Kaohsiung journal of medical sciences Pub Date : 2025-07-03 DOI: 10.1002/kjm2.70069

Yuan Wu, Xiao-Wen Wan, Lin Jiang, Wei Wang, Jia-Jun Zhu, Yi-Sen Shao

{"title":"Rhaponitin Reverses Cisplatin Resistance and Impairs Cancer Stemness Through HIF-1α/MCT4/Wnt Pathway in Tongue Squamous Cell Carcinoma.","authors":"Yuan Wu, Xiao-Wen Wan, Lin Jiang, Wei Wang, Jia-Jun Zhu, Yi-Sen Shao","doi":"10.1002/kjm2.70069","DOIUrl":"https://doi.org/10.1002/kjm2.70069","url":null,"abstract":"Rhaponitin (Rha) possesses anti-tumor activity and mediates the transcriptional activity of hypoxia-inducible factor (HIF)-1α that affects cisplatin (Cis) resistance. However, whether Rha can lessen Cis resistance in tongue squamous cell carcinoma (TSCC) by mediating HIF-1α activity is unclear. Cis-resistant SCC9 (SCC9-CisR) cells were treated with Cis, Rha, or Cis plus Rha to explore the effect of Rha on Cis resistance using a cell counting kit-8, flow cytometry, and tumor sphere formation assays. Stemness markers CD44 and SOX2 and HIF-1α mRNA levels were detected by quantitative PCR. The GSE115119 database and plugin iRegulon were employed to select target genes mediated by HIF-1α. Protein levels of HIF-1α, monocarboxylate transporter 4 (MCT4), and the Wnt/β-catenin pathway were measured by western blot. Subcutaneous xenograft models were constructed to explore the efficacy of Rha in combating Cis resistance. Rha repressed the growth and stemness of SCC9-CisR cells in vitro and in vivo. HIF-1α protein levels were markedly elevated in SCC9-CisR cells, yet Rha treatment attenuated the transcriptional activity of HIF-1α but not HIF-1α mRNA levels. Rha plus Cis repressed the viability and stemness of SCC9-CisR cells, but not HIF-1α-knockdown SCC9-CisR cells, compared with Cis alone. Rha-induced stemness inhibition and apoptosis in SCC9-CisR cells were overridden after HIF-1α overexpression. Rha inhibited the Wnt/β-catenin signaling by regulating the HIF-1α/MCT4 axis. In conclusion, Rha reduced cell stemness and enhanced Cis sensitivity in TSCC, which was achieved possibly via suppressing the Wnt/β-catenin signaling through mediation of the HIF-1α/MCT4 axis.","PeriodicalId":94244,"journal":{"name":"The Kaohsiung journal of medical sciences","volume":" ","pages":"e70069"},"PeriodicalIF":0.0,"publicationDate":"2025-07-03","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144562452","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}

引用次数: 0

Hypoxia-Enhanced Wharton's Jelly Mesenchymal Stem Cell Therapy for Liver Fibrosis: A Comparative Study in a Rat Model. 缺氧增强的沃顿果冻间充质干细胞治疗肝纤维化：大鼠模型的比较研究。

The Kaohsiung journal of medical sciences Pub Date : 2025-06-30 DOI: 10.1002/kjm2.70053

Wei-Ting Kuo, Chen-Yuan Hsiao, Sheng-Hao Chiu, Shu-Cheng Chou, Ching-Shu Chiang, Jui-Yu Chen, Solomon Chih-Cheng Chen, Tien-Hua Chen, Jia-Fwu Shyu, Chi-Hung Lin, Pei-Jiun Tsai

{"title":"Hypoxia-Enhanced Wharton's Jelly Mesenchymal Stem Cell Therapy for Liver Fibrosis: A Comparative Study in a Rat Model.","authors":"Wei-Ting Kuo, Chen-Yuan Hsiao, Sheng-Hao Chiu, Shu-Cheng Chou, Ching-Shu Chiang, Jui-Yu Chen, Solomon Chih-Cheng Chen, Tien-Hua Chen, Jia-Fwu Shyu, Chi-Hung Lin, Pei-Jiun Tsai","doi":"10.1002/kjm2.70053","DOIUrl":"https://doi.org/10.1002/kjm2.70053","url":null,"abstract":"Liver fibrosis is a progressive disease that can lead to cirrhosis and liver failure, with limited treatment options. Wharton's jelly-derived MSCs (WJ-MSCs) have immunomodulatory and antifibrotic potential. Hypoxia preconditioning enhances MSC survival and paracrine activity, but its effects in liver fibrosis remain unclear. This study compares hypoxia and normoxia WJ-MSCs in a CCl4-induced liver fibrosis rat model. Sprague-Dawley rats received chronic CCl4 to induce fibrosis. At Week 8, normoxia or hypoxia WJ-MSCs were injected via the portal vein. Liver function was assessed using biochemical markers (ALT, AST, T-Bil, albumin), PET/MR imaging, and qPCR for IL-1β and IL-6. Fibrosis regression was evaluated via ultrasound, histology, and collagen quantification. Regeneration was analyzed through Ki67 immunostaining and qPCR for Ki67 and HGF. MSC engraftment was determined by hNA immunohistochemistry. Both normoxia and hypoxia WJ-MSCs improved liver function, with hypoxia WJ-MSCs showing greater AST and T-Bil reductions. PET/MR imaging demonstrated superior metabolic recovery in the hypoxia group, with greater 18F-FDG uptake reduction. Histological analysis confirmed more significant fibrosis regression and collagen reduction in the hypoxia group. Gene expression analysis showed stronger suppression of TGF-β, α-SMA, and collagen I. Liver regeneration markers Ki67 and HGF were significantly upregulated with a greater HGF increase in the hypoxia group. Additionally, hypoxia WJ-MSCs exhibited higher engraftment and reduced pulmonary entrapment, indicating improved liver homing. Both normoxia and hypoxia WJ-MSCs improved liver fibrosis, but hypoxia preconditioning further enhanced liver function, fibrosis regression, and metabolic recovery, supporting its therapeutic superiority.","PeriodicalId":94244,"journal":{"name":"The Kaohsiung journal of medical sciences","volume":" ","pages":"e70053"},"PeriodicalIF":0.0,"publicationDate":"2025-06-30","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144532198","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}

引用次数: 0

Integration of the Comprehensive Physical Examination and Diagnostic Tools in Clinical Cardiology. 综合体格检查和诊断工具在临床心脏病学中的整合。

The Kaohsiung journal of medical sciences Pub Date : 2025-06-30 DOI: 10.1002/kjm2.70074

Regina Wilson, Halil Tekiner, Steven H Yale, Eileen S Yale

引用次数: 0

Astragaloside IV Alleviates Ulcerative Colitis Progression by Inhibiting WDR5-Mediated ENO1 H3K4me3 Modification. 黄芪甲苷通过抑制wdr5介导的ENO1 H3K4me3修饰缓解溃疡性结肠炎进展。

The Kaohsiung journal of medical sciences Pub Date : 2025-06-30 DOI: 10.1002/kjm2.70064

Su-Xiao Wu, Zi-Lan Chen, Xiao-Hong Wang, Jie Gu

{"title":"Astragaloside IV Alleviates Ulcerative Colitis Progression by Inhibiting WDR5-Mediated ENO1 H3K4me3 Modification.","authors":"Su-Xiao Wu, Zi-Lan Chen, Xiao-Hong Wang, Jie Gu","doi":"10.1002/kjm2.70064","DOIUrl":"https://doi.org/10.1002/kjm2.70064","url":null,"abstract":"Ulcerative colitis (UC) has become a prevalent global health concern. This study scrutinized the influence of Astragaloside IV (ASI) on DSS-induced UC, with particular emphasis on the role of WDR5 in mediating ENO1 expression. The therapeutic efficacy of ASI was assessed in a mouse model of UC by evaluating disease activity index, pathology, colon length, and inflammatory factor contents. Through bioinformatics analysis, the UC-related differentially expressed genes were predicted using the GSE38713 database and intersected with the lists of ASI targets and transcription factors, and the protein-protein network was constructed to screen the key target transcription factors. ASI inhibited the shortening of colon length, reduced histological damage scores, ameliorated pathology, and the overproduction of pro-inflammatory cytokines. After ASI treatment, DSS-stimulated human NCM460 cells showed increased cell viability, decreased levels of pro-inflammatory cytokines and cleaved-Caspase-3, and enhanced ZO-1 and claudin-3 expression. WDR5 was a target of ASI in UC, and overexpression of WDR5 compromised the effects of ASI. WDR5 promoted the H3K4me3 modification of the ENO1 promoter and thereby regulated ENO1 transcriptional activation. Silencing of ENO1, again, repressed NCM460 cell apoptosis and alleviated UC-like symptoms in mice. In conclusion, ASI mitigated UC by inhibiting WDR5 and reducing H3K4me3-mediated ENO1 activation.","PeriodicalId":94244,"journal":{"name":"The Kaohsiung journal of medical sciences","volume":" ","pages":"e70064"},"PeriodicalIF":0.0,"publicationDate":"2025-06-30","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144532197","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}

引用次数: 0

Recurrent Self-Limiting Acute Pancreatitis: Intraductal Papillary Mucinous Neoplasm Requiring Surgery. 复发性自限性急性胰腺炎：导管内乳头状粘液瘤需要手术治疗。

The Kaohsiung journal of medical sciences Pub Date : 2025-06-30 DOI: 10.1002/kjm2.70073

Chia-Hsin Chang, Yu-Chun Ma, Shih-Chang Chuang, Chih-Wen Wang

引用次数: 0

Morroniside Improves Diabetic Osteoporosis via the AGE/RAGE/Wnt/β-Catenin Signaling Pathway. Morroniside通过AGE/RAGE/Wnt/β-Catenin信号通路改善糖尿病骨质疏松症

The Kaohsiung journal of medical sciences Pub Date : 2025-06-26 DOI: 10.1002/kjm2.70063

Lu Yang, Kai Wang, Zhao-Hui Zeng, Hai-En Zhao, Li-Min Bai

{"title":"Morroniside Improves Diabetic Osteoporosis via the AGE/RAGE/Wnt/β-Catenin Signaling Pathway.","authors":"Lu Yang, Kai Wang, Zhao-Hui Zeng, Hai-En Zhao, Li-Min Bai","doi":"10.1002/kjm2.70063","DOIUrl":"https://doi.org/10.1002/kjm2.70063","url":null,"abstract":"Morroniside has been shown to possess various pharmacological activities, including anti-inflammatory and antioxidative effects. This study investigates the potential mechanisms by which morroniside ameliorates diabetic osteoporosis (DOP). In vivo experiments were conducted to evaluate biochemical parameters in rats under different treatment conditions. Bone tissues underwent HE staining, and bone mineral density (BMD) along with key bone metabolism markers (β-CTX, OC, SOST) were measured. The activities of antioxidant enzymes (SOD, GPX, CAT), oxidative stress indicators (MDA), and levels of inflammatory factors (MCP-1, IL-6, IL-1, TNF-α) were also assessed. Western blot was used to analyze the expression of proteins associated with AGE/RAGE signaling and the Wnt/β-catenin pathway. Morroniside increased trabecular bone quantity and quality, upregulated the bone formation markers OC and SOST, downregulated the bone resorption marker β-CTX, and significantly increased BMD. Additionally, it modulated the systemic metabolic status by reducing fasting blood glucose (FBG), glycated hemoglobin (HbA1c), free fatty acids (FFA), triglycerides (TG), and total cholesterol (TC). Further research indicated that morroniside inhibited AGE/RAGE signaling, mitigated oxidative stress and inflammatory responses, and enhanced Wnt/β-catenin pathway activity, thereby promoting osteoblast proliferation, differentiation, and mineralization. The introduction of DKK1 significantly attenuated these beneficial effects of morroniside, confirming its protective role through activation of the Wnt/β-catenin pathway. Morroniside exerts beneficial effects on bone metabolism and quality in DOP rats by regulating the AGEs/RAGE/Wnt/β-catenin signaling pathway, while also alleviating oxidative stress and inflammatory responses. These findings provide novel insights and potential therapeutic targets for the treatment of DOP.","PeriodicalId":94244,"journal":{"name":"The Kaohsiung journal of medical sciences","volume":" ","pages":"e70063"},"PeriodicalIF":0.0,"publicationDate":"2025-06-26","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144510193","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}

引用次数: 0

Deletion of NFIA Leads to Activation of S100A7 and Inflammatory Response-Induced Apoptosis of Keratinocytes in Oral Lichen Planus Progression. NFIA缺失导致口腔扁平苔藓进展中S100A7激活和炎症反应诱导的角化细胞凋亡

The Kaohsiung journal of medical sciences Pub Date : 2025-06-25 DOI: 10.1002/kjm2.70052

Maimaiti Tudi, Zumulaiti Aierken, Maihebubaimu Tuerxun, Maimaitituxun Tuerdi

{"title":"Deletion of NFIA Leads to Activation of S100A7 and Inflammatory Response-Induced Apoptosis of Keratinocytes in Oral Lichen Planus Progression.","authors":"Maimaiti Tudi, Zumulaiti Aierken, Maihebubaimu Tuerxun, Maimaitituxun Tuerdi","doi":"10.1002/kjm2.70052","DOIUrl":"https://doi.org/10.1002/kjm2.70052","url":null,"abstract":"S100 calcium-binding protein A7 (S100A7) has been implicated in psoriasis and other inflammatory diseases. However, the function of S100A7 in oral lichen planus (OLP), a chronic inflammatory disease, remains unclear. OLP was induced in mice by transplanting human OLP lesions into the backs of thymus-free mice, and an in vitro cell model was constructed using LPS-stimulated HaCaT cells. Gene intervention was performed using shRNA lentiviral vectors. The secretion of the pro-inflammatory factors IL-6 and TNF-α, as well as the rate of apoptosis in HaCaT cells, was also assessed. ChIP assay and dual-luciferase assay were used to validate the transcriptional regulation of S100A7 by nuclear factor 1 A-type (NFIA). The expression of S100A7 was significantly elevated in the lesion tissues of OLP-induced mice. Knockdown of S100A7 alleviated inflammation and reduced keratinocyte apoptosis. The transcription factor NFIA repressed S100A7 expression by binding to the S100A7 promoter. The overexpression of NFIA ameliorated inflammation in vivo and reduced apoptosis in vitro, which was abrogated by further overexpression of S100A7. Overall, our results indicate that NFIA reduces inflammatory response-induced keratinocyte apoptosis in OLP by inhibiting S100A7 transcription.","PeriodicalId":94244,"journal":{"name":"The Kaohsiung journal of medical sciences","volume":" ","pages":"e70052"},"PeriodicalIF":0.0,"publicationDate":"2025-06-25","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144500001","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}

引用次数: 0

RNA Binding Protein YTHDF2 Inhibits Synovial Fibroblast Inflammation and Bone Injury in Rheumatoid Arthritis by Reducing the mRNA Stability of IL-6R. RNA结合蛋白YTHDF2通过降低IL-6R mRNA稳定性抑制类风湿关节炎滑膜成纤维细胞炎症和骨损伤。

The Kaohsiung journal of medical sciences Pub Date : 2025-06-23 DOI: 10.1002/kjm2.70010

Yan Zhang, Xu-Qing Cao, Xiao-Li Ma, Yin-Yan Guo, Tao Zhang, Li-Li Wu, Ya-Shan Yang, Chun-Fang Hao, Wei-Li Liu, Jiang-Tao Guo

{"title":"RNA Binding Protein YTHDF2 Inhibits Synovial Fibroblast Inflammation and Bone Injury in Rheumatoid Arthritis by Reducing the mRNA Stability of IL-6R.","authors":"Yan Zhang, Xu-Qing Cao, Xiao-Li Ma, Yin-Yan Guo, Tao Zhang, Li-Li Wu, Ya-Shan Yang, Chun-Fang Hao, Wei-Li Liu, Jiang-Tao Guo","doi":"10.1002/kjm2.70010","DOIUrl":"https://doi.org/10.1002/kjm2.70010","url":null,"abstract":"This study examined YTHDF2's role in modulating IL-6R signaling to regulate synovial fibroblast inflammation and bone damage in rheumatoid arthritis (RA). Synovial tissues of RA patients were collected. Human fibroblast-like synoviocyte (FLS), MH7A cell line, was induced with TNF-α and transfected. Cell proliferation was assessed using MTT and EdU assays; apoptosis was measured with flow cytometry, and migration and invasion were evaluated through scratch and Transwell assays. Lentiviral vectors designed to overexpress YTHDF2 or IL-6R were created to study their effects in mice with collagen-induced arthritis (CIA). Pathological changes of ankle joints in mice were observed, and TNF-α, IL-1β, and IL-6 contents were determined. MMP3 and MMP9 levels were detected by Western blot, while YTHDF2 and IL-6R were detected by RT-qPCR and Western blot. The binding relationship between YTHDF2 and IL-6R was studied. YTHDF2 in synovial tissues of RA patients was down-regulated. Elevating YTHDF2 inhibited TNF-α-induced MH7A cell proliferation, migration, invasion, and pro-inflammatory factors; Knocking down YTHDF2 showed the opposite effect. Upregulating YTHDF2 improved synovial inflammation and bone damage in CIA mice. IL-6R in synovial tissues of patients was significantly up-regulated and negatively correlated with YTHDF2 expression. YTHDF2 reduced IL-6R mRNA stability in a m6A-dependent manner. Overexpressing IL-6R impaired the anti-proliferating and anti-inflammatory effect of YTHDF2 on TNF-α-induced MH7A cells. In CIA mice, overexpression of IL-6R reversed the benefits on synovial inflammation and bone injury mediated by up-regulating YTHDF2. YTHDF2 inhibits inflammation and bone damage in RA synovial fibroblasts by reducing the mRNA stability of IL-6R.","PeriodicalId":94244,"journal":{"name":"The Kaohsiung journal of medical sciences","volume":" ","pages":"e70010"},"PeriodicalIF":0.0,"publicationDate":"2025-06-23","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144478353","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}

引用次数: 0

Cystoid Macular Edema Secondary to Hyperviscosity Syndrome in Waldenström Macroglobulinemia: A Case Report of Multimodal Treatment Response and the Adjunctive Role of Acetazolamide. Waldenström巨球蛋白血症继发于高粘滞综合征的囊样黄斑水肿：多模式治疗反应和乙酰唑胺辅助作用的一例报告。

The Kaohsiung journal of medical sciences Pub Date : 2025-06-20 DOI: 10.1002/kjm2.70066

Yu-Mei Yang, Chuan-Cheng Wang, San-Ni Chen, Jian-Sheng Wu

引用次数: 0

Psychological Capital Moderates the Association Between Social Participation and Depressive Symptoms in Taiwanese University Students. 心理资本调节台湾大学生社会参与与抑郁症状的关系。

The Kaohsiung journal of medical sciences Pub Date : 2025-06-20 DOI: 10.1002/kjm2.70072

Yi-Lung Chen, Agata Chudzicka-Czupała, Cheng-Fang Yen

引用次数: 0