The Kaohsiung journal of medical sciences最新文献_第6页

Novel Endoscopic-Assisted Long Plate Approach for Mandibular Condylar Fracture Reconstruction-A Preliminary Study. 新型内窥镜辅助下长钢板入路下颌髁突骨折重建的初步研究。

IF 3.1

The Kaohsiung journal of medical sciences Pub Date : 2025-08-01 Epub Date: 2025-05-19 DOI: 10.1002/kjm2.70033

Chao-Hsin Huang, Chia-Chen Lee, Yi-Chia Wu, Hsiao-Chen Lee, Yur-Ren Kuo, Su-Shin Lee

{"title":"Novel Endoscopic-Assisted Long Plate Approach for Mandibular Condylar Fracture Reconstruction-A Preliminary Study.","authors":"Chao-Hsin Huang, Chia-Chen Lee, Yi-Chia Wu, Hsiao-Chen Lee, Yur-Ren Kuo, Su-Shin Lee","doi":"10.1002/kjm2.70033","DOIUrl":"10.1002/kjm2.70033","url":null,"abstract":"Mandibular condylar fractures can lead to facial asymmetry, malocclusion, and temporomandibular joint instability. To minimize the risk of these issues, endoscopic-assisted reduction techniques were developed. Nevertheless, the confined working space inherent in endoscopic procedures poses challenges, especially in cases with unstable fracture sites, movable plates, and screws. To solve this dilemma, we developed a novel surgical technique using long plate for condylar fracture fixation. \"Long Plate Technique\" involves a long plate being stabilized via the submandibular incision site, with screws inserted through the trocar to affix the titanium plate onto the superior condylar segment from the tragus incision site. A total of 98 patients were included in this study. The overall average operation time was 365 min. Specifically, the average operation time for the group treated with closed reduction and intermaxillary fixation was 250 min, for Group B cases treated with short plate open reduction and intermaxillary fixation was 429 min, and for Group C treated with long plate open reduction and intermaxillary fixation was 413 min. The utilization of the Long Plate Technique provides a secure and efficient operation technique that can lessen the stress on surgeons during the operation.","PeriodicalId":94244,"journal":{"name":"The Kaohsiung journal of medical sciences","volume":" ","pages":"e70033"},"PeriodicalIF":3.1,"publicationDate":"2025-08-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12407336/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144096572","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}

引用次数: 0

Monotropein Induced Ferroptosis to Alleviate the Progression of Hepatocellular Carcinoma via Regulating Nrf2/HO-1/GPX4 Axis. 单肌蛋白诱导铁下垂通过调控Nrf2/HO-1/GPX4轴缓解肝癌进展

IF 3.1

The Kaohsiung journal of medical sciences Pub Date : 2025-08-01 Epub Date: 2025-05-29 DOI: 10.1002/kjm2.70034

Bing Shi, Yan-Ping Li, Zhuo Gan, Pan Chen

{"title":"Monotropein Induced Ferroptosis to Alleviate the Progression of Hepatocellular Carcinoma via Regulating Nrf2/HO-1/GPX4 Axis.","authors":"Bing Shi, Yan-Ping Li, Zhuo Gan, Pan Chen","doi":"10.1002/kjm2.70034","DOIUrl":"10.1002/kjm2.70034","url":null,"abstract":"Hepatocellular carcinoma (HCC) exhibits a high global morbidity rate and ranks as the fourth leading cause of cancer-related mortality worldwide. In response to the urgent need for effective HCC treatments, naturally occurring, botanical-driven compounds have gained increasing attention. Notably, the anti-tumor properties of some compounds might be linked to the induction of ferroptosis. The present study aimed to evaluate the capacity of Monotropein (Mon) to induce ferroptosis in HCC and elucidate its underlying mechanisms. First, Mon was found to play an anti-tumor role in HCC cells by inhibiting cell proliferation and invasion, elevated the expression of E-cadherin, and decreased N-cadherin and Vimentin expression. Furthermore, Mon activated ferroptosis in HCC cells, characterized by elevated levels of Fe2+, reactive oxygen species (ROS), and malondialdehyde (MDA), alongside a reduction in glutathione (GSH) content and downregulation of nuclear factor E2-related factor 2 (Nrf2), heme oxygenase-1 (HO-1), and glutathione peroxidase 4 (Gpx-4). These in vitro findings were confirmed by in vivo tumorigenicity experiments. With regard to the mechanism, the suppression of Nrf2 signaling played a significant role in facilitating ferroptosis induced by Mon, ultimately slowing down the progression of HCC cells. In conclusion, this study revealed that Mon suppressed the progression of HCC both in vitro and in vivo, which was closely associated with ferroptosis induction via inhibiting Nrf2 signaling. These results suggest that Mon represents a promising alternative for HCC treatment.","PeriodicalId":94244,"journal":{"name":"The Kaohsiung journal of medical sciences","volume":" ","pages":"e70034"},"PeriodicalIF":3.1,"publicationDate":"2025-08-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12407331/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144176173","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}

引用次数: 0

Kussmaul's Sign Provoked by Intracardiac Metastasis of Endometrial Neuroendocrine Tumor. 子宫内膜神经内分泌肿瘤心内转移引起的Kussmaul征象。

IF 3.1

The Kaohsiung journal of medical sciences Pub Date : 2025-08-01 Epub Date: 2025-04-14 DOI: 10.1002/kjm2.70026

Yi-Hsun Chen, Chin-Chuan Chang, Yao-Kuang Wang, I-Chen Wu

引用次数: 0

Investigating the Impact of hsa_circ_0005255 on Proliferation and Autophagy in Crohn's Disease Intestinal Epithelial Cells Through miR-23a-3p-Mediated NCOA3 Expression. 通过mir -23a-3p介导的NCOA3表达研究hsa_circ_0005255对克罗恩病肠上皮细胞增殖和自噬的影响

IF 3.1

The Kaohsiung journal of medical sciences Pub Date : 2025-08-01 Epub Date: 2025-05-07 DOI: 10.1002/kjm2.70035

Dong Liu, De-Run Kong

{"title":"Investigating the Impact of hsa_circ_0005255 on Proliferation and Autophagy in Crohn's Disease Intestinal Epithelial Cells Through miR-23a-3p-Mediated NCOA3 Expression.","authors":"Dong Liu, De-Run Kong","doi":"10.1002/kjm2.70035","DOIUrl":"10.1002/kjm2.70035","url":null,"abstract":"Crohn's Disease (CD), an inflammatory bowel disorder, is influenced by genetic, immune, and environmental factors. The present study highlights the pioneering role of circular RNAs (circRNAs) in the etiology of CD, with a specific focus on hsa_circ_0005255 and its regulatory role. Utilizing both bioinformatic and experimental approaches, we exposed the mechanistic and therapeutic significance of hsa_circ_0005255 within the pathophysiological framework of CD. Our findings revealed a significant underexpression of hsa_circ_0005255 in tissue samples from CD patients and in DSS-induced CD mouse models. The overexpression of hsa_circ_0005255 markedly mitigated inflammatory responses, as indicated by decreased serum levels of tumor necrosis factor-alpha, interleukin-1 beta, and interleukin-6, and reduced histopathological indications of inflammation in colonic tissues. It substantially improved the integrity of the epithelial barrier, evidenced by the upregulation of Zonula Occludens-1 expression and the reduction of apoptosis in colonic epithelial cells. Furthermore, this regulatory effect extended to the enhancement of epithelial cell proliferation and autophagy, characterized by the elevated expression of Ki-67, microtubule-associated protein 1A/1B-light chain 3 II, and Beclin-1, along with the suppression of cleaved caspase-3 and sequestosome 1. Mechanistically, hsa_circ_0005255 functioned as a competitive endogenous RNA, absorbing miR-23a-3p and thereby regulating Nuclear Receptor Coactivator 3. This investigation not only broadens our understanding of the involvement of circRNAs in CD pathogenesis but also identifies hsa_circ_0005255 as a potent biomarker and therapeutic target.","PeriodicalId":94244,"journal":{"name":"The Kaohsiung journal of medical sciences","volume":" ","pages":"e70035"},"PeriodicalIF":3.1,"publicationDate":"2025-08-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12407262/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144059397","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}

引用次数: 0

RETRACTION: Role of miR-490-3p in Blocking Bladder Cancer Growth Through Targeting the RNA-Binding Protein PCBP2. 撤回：miR-490-3p通过靶向rna结合蛋白PCBP2在阻断膀胱癌生长中的作用

IF 3.1

The Kaohsiung journal of medical sciences Pub Date : 2025-08-01 Epub Date: 2025-03-04 DOI: 10.1002/kjm2.70009

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。

IF 3.1

The Kaohsiung journal of medical sciences Pub Date : 2025-08-01 Epub 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":"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":3.1,"publicationDate":"2025-08-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12412489/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144478353","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}

引用次数: 0

Correction to "Long non-coding RNA MALAT1 triggers ferroptosis via interaction with FUS to enhance ACSF2 mRNA stabilization in septic acute kidney injury". 更正“在脓毒性急性肾损伤中，长链非编码RNA MALAT1通过与FUS相互作用触发铁下垂，增强ACSF2 mRNA的稳定性”。

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The Kaohsiung journal of medical sciences Pub Date : 2025-08-01 Epub Date: 2025-02-13 DOI: 10.1002/kjm2.12947

引用次数: 0

Circ_0006646 Promotes the Progression of Osteoarthritis via Upregulating CDH11 Expression in an IGF2BP2-Dependent Manner. Circ_0006646通过igf2bp2依赖性方式上调CDH11表达促进骨关节炎的进展。

IF 3.1

The Kaohsiung journal of medical sciences Pub Date : 2025-08-01 Epub Date: 2025-05-19 DOI: 10.1002/kjm2.70031

Ming-Yu Hua, Guo-Liang Wang, Wen-Hao Duan, Xiao-Heng Tang

{"title":"Circ_0006646 Promotes the Progression of Osteoarthritis via Upregulating CDH11 Expression in an IGF2BP2-Dependent Manner.","authors":"Ming-Yu Hua, Guo-Liang Wang, Wen-Hao Duan, Xiao-Heng Tang","doi":"10.1002/kjm2.70031","DOIUrl":"10.1002/kjm2.70031","url":null,"abstract":"Osteoarthritis (OA) is a common degenerative osteoarthropathy with an unclear pathogenesis. Circular RNA (circRNA) has been reported to be associated with OA progression. This study aims to explore the role and potential mechanism of hsa_circ_0006646 in OA. Interleukin-1β (IL-1β)-induced human chondrocytes were used as the cell model of OA. RT-qPCR and western blotting were used to detect the expression of circ_0006646, IGF2BP2, and cadherin 11 (CDH11). Cell counting kit-8 assay, 5-ethynyl-2'-deoxyuridine assay, and flow cytometry were performed to assess chondrocyte cell proliferation and apoptosis, respectively. Western blot assay was performed to determine the levels of proliferation-related proteins, apoptosis-related proteins, and extracellular matrix (ECM) proteins. RNA immunoprecipitation (RIP) assay was performed to verify the interaction between IGF2BP2 and circ_0006646 or CDH11. In OA patients and IL-1β-stimulated chondrocytes, circ_0006646 and CDH11 were upregulated. IL-1β suppressed proliferation and induced apoptosis, inflammation, and ECM degradation in chondrocytes, and circ_0006646 knockdown protected chondrocytes from IL-1β-induced damage. IGF2BP2 was proved to interact with both circ_0006646 and CDH11. The overexpression of IGF2BP2 or CDH11 enhanced IL-1β-induced apoptosis, inflammation, and ECM degradation in chondrocytes. Moreover, circ_0006646 absence-mediated effects in IL-1β-treated chondrocytes could be largely overturned by the overexpression of IGF2BP2 or CDH11. In conclusion, circ_0006646 knockdown protected chondrocytes from IL-1β-induced injury by regulating CDH11 in an IGF2BP2-dependent manner, suggesting a novel potential target for OA treatment.","PeriodicalId":94244,"journal":{"name":"The Kaohsiung journal of medical sciences","volume":" ","pages":"e70031"},"PeriodicalIF":3.1,"publicationDate":"2025-08-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12407339/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144096569","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}

引用次数: 0

RETRACTION: Paris Saponin VII Enhanced the Sensitivity of HepG2/ADR Cells to ADR via Modulation of PI3K/AKT/MAPK Signaling Pathway. 撤回：巴黎皂苷VII通过调节PI3K/AKT/MAPK信号通路增强HepG2/ADR细胞对ADR的敏感性。

IF 3.1

The Kaohsiung journal of medical sciences Pub Date : 2025-08-01 Epub Date: 2025-04-08 DOI: 10.1002/kjm2.70030

引用次数: 0

A Preliminary Study on the Therapeutic Role of γδT Cells in Triple-Negative Breast Cancer. γδT细胞治疗三阴性乳腺癌的初步研究。

IF 3.1

The Kaohsiung journal of medical sciences Pub Date : 2025-08-01 Epub Date: 2025-04-28 DOI: 10.1002/kjm2.70029

Shi Qiu, Qin-Yu Han, Xian Zhao, Wen-Jing Li, Xiang-Qi Li

{"title":"A Preliminary Study on the Therapeutic Role of γδT Cells in Triple-Negative Breast Cancer.","authors":"Shi Qiu, Qin-Yu Han, Xian Zhao, Wen-Jing Li, Xiang-Qi Li","doi":"10.1002/kjm2.70029","DOIUrl":"10.1002/kjm2.70029","url":null,"abstract":"This study was aimed to elucidate the cytotoxic effects of γδT cells on triple-negative breast cancer (TNBC) cells and assess their antitumor efficacy in a mouse xenograft model. Furthermore, the underlying mechanisms of γδT cell action on TNBC were explored. The study utilized three TNBC cell lines (MDA-MB-231, MDA-MB-468, and BT-549) as target cells, with γδT cells serving as effector cells. Cytotoxicity was assessed in different effector-to-target ratios (E:T) at 5:1, 10:1, and 20:1 subsequent to coculture. To evaluate the antitumor effects of γδT cells in vivo, a xenograft mice model was established by inoculating MDA-MB-231 cells into the mammary fat pad of B-NDG mice. The mice received tail vein injections of γδT cells at different doses. The effects on tumor growth, mouse body weight, and γδT cell accumulation in the spleen were then determined. γδΤ cells at E:T of 10:1 exhibited significant cytotoxicity against all three TNBC cell lines, indicating a statistically significant difference compared to the control group (p < 0.0001). The cytotoxic effect at this ratio was superior to that at 20:1 and 5:1 effector-to-target ratios, as evidenced by statistical significance (p < 0.05). Following 21 days of adoptive transfer via tail vein injection, γδΤ cells at both low and high doses significantly reduced tumor volume and mass compared to the PBS control group (p < 0.001). This reduction was accompanied by an increased accumulation of γδΤ cells in the spleen. In conclusion, γδΤ cells exert significant cytotoxic effects on TNBC cells and effectively inhibit the growth of breast cancer xenografts in mice while also promoting the accumulation of γδΤ cells in the mouse spleen.","PeriodicalId":94244,"journal":{"name":"The Kaohsiung journal of medical sciences","volume":" ","pages":"e70029"},"PeriodicalIF":3.1,"publicationDate":"2025-08-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12407383/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144035353","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}

引用次数: 0