The Kaohsiung journal of medical sciences最新文献

{"title":"Intractable diarrhea caused by a rare rectal foreign body.","authors":"Qi Fan, Shuang Yu, De-Hai Xiong","doi":"10.1002/kjm2.12917","DOIUrl":"10.1002/kjm2.12917","url":null,"abstract":"","PeriodicalId":94244,"journal":{"name":"The Kaohsiung journal of medical sciences","volume":"41 3","pages":"e12917"},"PeriodicalIF":0.0,"publicationDate":"2025-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11924812/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143607642","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":"Effect of platelet-rich plasma and platelet-rich fibrin on healing of burn wound with dual-species biofilm.","authors":"Wen-Dan Li, Fang Lin, Yu Sun, Zi-Jing Zhu, Mei-Liang Luo, Yi-Qi Zeng, Zhen Lin, Mou Zhou","doi":"10.1002/kjm2.12940","DOIUrl":"10.1002/kjm2.12940","url":null,"abstract":"<p><p>This study evaluated the impact of platelet-rich plasma (PRP) and platelet-rich fibrin (PRF) on burn wound with dual-species biofilm. Pseudomonas aeruginosa (P. aeruginosa) and Staphylococcus aureus (S. aureus) were applied to infect the burn wound in rats to establish a dual-species biofilm model. After infection, the wound was treated with ionized silver (AG), PRF, and PRP. Silver scanning electron microscopy (SEM) was used to assess adhesion after infection. PRF and PRP reduced wound size from day 8 after burn injuries, while AG significantly promoted burn wound healing at day 12. New collagen was formed in the shortest time in PRF and PRP groups compared to AG and control groups. PRF and PRP greatly lowered the bacterial numbers in wounds with S. aureus and P. aeruginosa biofilm, whereas AG showed weak bacteriostatic effects. AG, PRF, and PRP treatments significantly reduced inflammatory mediators and induced VEGFA. However, AG treatment increased TNF-α. PRF and PRP accelerate wound healing in the presence of dual-species biofilm infection and show strong antibacterial activity against S. aureus and P. aeruginosa, indicating that PRF and PRP could be potential therapies for burn wounds with dual-species biofilm infection.</p>","PeriodicalId":94244,"journal":{"name":"The Kaohsiung journal of medical sciences","volume":" ","pages":"e12940"},"PeriodicalIF":0.0,"publicationDate":"2025-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11924799/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143019370","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":"Aptasensor-based point-of-care detection of cardiac troponin biomarkers for diagnosis of acute myocardial infarction.","authors":"Tharmaraj Vairaperumal, Ping-Yen Liu","doi":"10.1002/kjm2.12932","DOIUrl":"10.1002/kjm2.12932","url":null,"abstract":"<p><p>Acute myocardial infarction (AMI) represents a critical health challenge characterized by a significant reduction in blood flow to the heart, leading to high rates of mortality and morbidity. Cardiac troponins, specifically cardiac troponin I and cardiac troponin T, are essential proteins involved in cardiac muscle contraction and serve as vital biomarkers for the diagnosis of AMI. Aptasensors utilize synthetic aptamers or peptides with high affinity for specific biomarkers and offer a promising approach for integration into portable, user-friendly point-of-care (POC) applications. This review explores recent advances in POC aptasensor-based platforms for the rapid detection of cardiac troponin biomarkers. Furthermore, this review addresses current challenges and potential future directions in the development of aptasensor. Also, it highlights their potential to improve timely and accurate diagnosis in clinical and emergency settings.</p>","PeriodicalId":94244,"journal":{"name":"The Kaohsiung journal of medical sciences","volume":" ","pages":"e12932"},"PeriodicalIF":0.0,"publicationDate":"2025-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11924801/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142924413","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":"Telocinobufagin suppresses malignant metastasis of undifferentiated thyroid carcinoma via modulation of the LARP1-mTOR pathway.","authors":"Li-Zhi Qiang, Shi-Zhi Fang","doi":"10.1002/kjm2.12934","DOIUrl":"10.1002/kjm2.12934","url":null,"abstract":"<p><p>Metastasis is the trigger of death in anaplastic thyroid cancer (ATC) patients, yet the specific mechanisms at play are still largely enigmatic. While the involvement of LARP1 in the metastatic process of various cancers has been documented, there is a noticeable gap in the literature regarding its potential influence on ATC metastasis. Molecular studies probed LARP1 expression within ATC cells, with subsequent in vitro experiments examining the effects of LARP1 on ATC cell metastasis and the mTOR signaling cascade. A suite of assays, including colony formation, scratch wound healing, transwell invasion, and cell adhesion, was used to assess cell growth, movement, invasion, and attachment. Western Blot determined the expression levels of epithelial-mesenchymal transition (EMT) markers (E-cadherin, Vimentin, N-cadherin) and proteins implicated in metastasis (MMP-2, MMP-9), along with mTOR and p-mTOR. The affinity of Telocinobufagin (TBG) from Yuanhua Toad Essence for LARP1 was investigated through molecular docking, with CETSA assays providing subsequent validation. Further cellular experiments substantiated the influence of TBG on ATC cell metastasis and modulation in the mTOR pathway. LARP1 levels were heightened in ATC cells, and its depletion effectively curbs their proliferative, migratory, invasive, and adhesive activities. With LARP1 knockdown, we also observed that the onset of EMT and metastatic processes was thwarted, as was the mTOR pathway. Subsequent research has uncovered that TBG formed a physical complex with LARP1, allowing it to target and suppress the mTOR pathway, thus preventing the metastasis of ATC. The simultaneous overexpression of LARP1, however, lessened the ability of TBG to inhibit ATC metastasis. This study highlights the importance of TBG binding to LARP1 in the mediation of the mTOR signaling pathway, a key process in the inhibition of ATC cell metastasis. This discovery introduces a new target for the diagnosis of ATC and enlightens the consideration of TBG as a treatment for ATC metastasis.</p>","PeriodicalId":94244,"journal":{"name":"The Kaohsiung journal of medical sciences","volume":" ","pages":"e12934"},"PeriodicalIF":0.0,"publicationDate":"2025-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11924809/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142960919","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":"Dapagliflozin combined with metformin improves blood glucose, bone metabolism and bone mineral density in elderly patients with type 2 diabetes mellitus complicated with osteoporosis.","authors":"Haiyan Zheng, Qian Wang, Min Si","doi":"10.1002/kjm2.12937","DOIUrl":"10.1002/kjm2.12937","url":null,"abstract":"<p><p>The incidence of type 2 diabetes mellitus (T2DM) complicated with osteoporosis (OP) (T2DM-OP) is growing. Dapagliflozin and metformin are commonly prescribed to manage glycemic levels in T2DM patients. We investigated the clinical efficacy of combining dapagliflozin with metformin in elderly patients with T2DM-OP. Totally 144 T2DM-OP patients were prospectively enrolled and allocated into two groups: the Metformin and Dapagliflozin + Metformin groups. Each group received treatment for 12 months. Fasting peripheral blood samples were collected before and after 12 months of treatment. Glycemic parameters and bone metabolic parameters were measured using oral glucose tolerance test, automatic biochemical analyzers, or liquid chromatography. Bone mineral density (BMD) changes at lumbar vertebrae (L1-4), femoral neck (FN) and total hip (TH) were assessed using dual-energy X-ray bone mineral densitometry. Pain severity was evaluated using the visual analog scale (VAS). The total effective rate, fracture incidence, and adverse reaction rate were also evaluated. After 12 months, both groups showed improvements in glycemic parameters, bone metabolic parameters, and BMD at L1-4, FN, and TH, and reductions in VAS scores. The Dapagliflozin + Metformin group exhibited more significant improvements. The overall effective rate was higher and fracture incidence, was lower in Dapagliflozin + Metformin group, with comparable rates of adverse reactions and safety profiles between the two groups. Taken together, treatment with a combination of dapagliflozin and metformin led to improvements in blood glucose levels, bone metabolism, and BMD in elderly patients with T2DM-OP, demonstrating superior efficacy and safety compared to metformin monotherapy.</p>","PeriodicalId":94244,"journal":{"name":"The Kaohsiung journal of medical sciences","volume":" ","pages":"e12937"},"PeriodicalIF":0.0,"publicationDate":"2025-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11924806/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142985907","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":"Targeting SETDB1 in cancer and immune regulation: Potential therapeutic strategies in cancer.","authors":"Bo-Syong Pan, Cheng-Yu Lin, Gilbert Aaron Lee, Hui-Kuan Lin","doi":"10.1002/kjm2.12933","DOIUrl":"10.1002/kjm2.12933","url":null,"abstract":"<p><p>SET domain bifurcated histone lysine methyltransferase 1 (SETDB1/ESET), a pivotal H3K9 methyltransferase, has been extensively studied since its discovery over two decades ago. SETDB1 plays critical roles in immune regulation, including B cell maturation, T-cell activity modulation, and endogenous retrovirus (ERV) silencing. While essential for normal immune cell function, SETDB1 overexpression in cancer cells disrupts immune responses by suppressing tumor immunogenicity and facilitating immune evasion. This is achieved through the repression of anti-tumor immune cell production, ERV silencing, and interference with the type I interferon pathway leading to inhibiting immune checkpoint blockade (ICB) efficacy. Beyond its immunological implications, SETDB1 overexpression fosters tumor growth and metastasis via transcriptional silencing of tumor suppressor genes through histone regulation and activating oncogenic signaling by non-histone regulation. These multifaceted roles make SETDB1 an attractive epigenetic target for novel cancer therapies. This review explores SETDB1's dual function in immune regulation and tumor progression, emphasizing its potential in the development of innovative cancer treatments targeting epigenetic dysregulation and oncogenic signaling.</p>","PeriodicalId":94244,"journal":{"name":"The Kaohsiung journal of medical sciences","volume":"41 3","pages":"e12933"},"PeriodicalIF":0.0,"publicationDate":"2025-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11924802/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143598690","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":"hnRNPA2B1 drives colorectal cancer progression via the circCDYL/EIF4A3/PHF8 axis.","authors":"Yu-Kai Sun, Jin-Fu Wang, Xi-Wen Sun, Ming Zhang","doi":"10.1002/kjm2.12943","DOIUrl":"10.1002/kjm2.12943","url":null,"abstract":"<p><p>The RNA-binding protein hnRNPA2B1 acts as an m6A reader and plays a role in tumor development. This study investigates the potential mechanism of hnRNPA2B1 in colorectal cancer (CRC) progression. The expression profiles of hnRNPA2B1, circCDYL, and PHF8 in CRC cell lines were analyzed. Following si-hnRNPA2B1 transfection, CRC cell proliferation, invasion, and migration were evaluated by CCK-8 and Transwell. CDYL expression was detected after actinomycin D and RNase R treatment. RIP was conducted to assess the enrichment of hnRNPA2B1 and m6A on circCDYL. RIP and RNA pull-down assays established the interaction between circCDYL and EIF4A3/PHF8. EIF4A3 expression was evaluated using RT-qPCR and Western blot techniques. hnRNPA2B1 and PHF8 displayed high expression levels, whereas circCDYL showed low expression levels in colorectal cancer cells. Inhibition of hnRNPA2B1 reduced CRC cell proliferation, migration, and invasion. hnRNPA2B1 mechanistically elevated the m6A level of circCDYL while decreasing its expression, which in turn reduced the binding of circCDYL to EIF4A3 and enhanced PHF8 expression. In summary, hnRNPA2B1-mediated m6A modification decreases circCDYL expression, which inhibits the interaction of circCDYL with EIF4A3, enhances PHF8 expression, and ultimately facilitates CRC progression.</p>","PeriodicalId":94244,"journal":{"name":"The Kaohsiung journal of medical sciences","volume":" ","pages":"e12943"},"PeriodicalIF":0.0,"publicationDate":"2025-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11924810/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142985913","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":"EZH2-mediated downregulation of miR-155-5p contributes to prostate cancer cell malignancy through SMAD2 and TAB2.","authors":"Zhi-Jie Bai, Jia-Yi Liu, Wen-Zhou Xing, Hai-Feng Wang","doi":"10.1002/kjm2.12936","DOIUrl":"10.1002/kjm2.12936","url":null,"abstract":"<p><p>miR-155 exhibits variable expression in different tumors and fulfills diverse biological roles. However, specific molecular mechanisms by which miR-155-5p, which is under-expressed in prostate cancer (PCa), operates are yet to be elucidated. The role of the enhancer of zeste 2 (EZH2)/miR-155-5p axis in PCa was determined by using bioinformatics tools and performing luciferase reporter assay, chromatin immunoprecipitation PCR, CCK-8 assays, cell migration and invasion assays, RNA isolation, reverse transcription quantity (RT-qPCR) and Western blot. miR-155-5p expression would be reduced and promoter methylation would increase in PCa. After 5-Aza-CdR treatment and the integration of the upstream promoter of miR-155-5p into a pGL3-basic/luciferase construct, fluorescence reporter analysis showed that promoter hypermethylation mediated the suppression of miR-155-5p in PCa. Furthermore, EZH2 attached to the miR-155-5p promoter and modulated its expression. EZH2 facilitated the suppression of miR-155-5p through enhanced H3K27me3 methylation, considerably affecting its expression. Through dual-luciferase assays, SMAD2 and TAB2 were confirmed as downstream targets of miR-155-5p, regulating the PCa cellular phenotype governed by miR-155-5p. Lastly, 5-Aza-CdR regulated miR-155-5p expression by modulating its promoter methylation and influenced the malignant behavior of PCa cells. EZH2 promotes H3K27me3 methylation, repressing miR-155-5p expression, which subsequently upregulates the downstream targets SMAD2 and TAB2 and promotes PCa cell proliferation, epithelial-mesenchymal transition (EMT), migration and invasion.</p>","PeriodicalId":94244,"journal":{"name":"The Kaohsiung journal of medical sciences","volume":" ","pages":"e12936"},"PeriodicalIF":0.0,"publicationDate":"2025-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11924804/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142960917","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":"Successful treatment of a mixed candidal and bacterial skull base osteomyelitis with antimicrobial agents and hyperbaric oxygen therapy-A rare case report.","authors":"Yu-Hsin Liu, Chun-Chieh Wu, Yen-Hsu Chen, Chun-Yu Lin","doi":"10.1002/kjm2.12939","DOIUrl":"10.1002/kjm2.12939","url":null,"abstract":"","PeriodicalId":94244,"journal":{"name":"The Kaohsiung journal of medical sciences","volume":" ","pages":"e12939"},"PeriodicalIF":0.0,"publicationDate":"2025-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11924805/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142985919","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 \"Long non-coding RNA MALAT1 triggers ferroptosis via interaction with FUS to enhance ACSF2 mRNA stabilization in septic acute kidney injury\".","authors":"","doi":"10.1002/kjm2.12947","DOIUrl":"https://doi.org/10.1002/kjm2.12947","url":null,"abstract":"","PeriodicalId":94244,"journal":{"name":"The Kaohsiung journal of medical sciences","volume":" ","pages":"e12947"},"PeriodicalIF":0.0,"publicationDate":"2025-02-13","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143412241","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}