The Kaohsiung journal of medical sciences最新文献

{"title":"Regulatory factor X-5/SCL/TAL1 interruption site axis promotes aerobic glycolysis and hepatocellular carcinoma cell stemness.","authors":"Zhi-Zhong Zhang, Zi-Ming Wang, Hao-Wen Zhang, Yan-Xin Gong, Hao-Ran Sun, Wei Zhang","doi":"10.1002/kjm2.12922","DOIUrl":"10.1002/kjm2.12922","url":null,"abstract":"<p><p>The incidence and development of various tumors, such as hepatocellular carcinoma (HCC), are linked to tumor stem cells. Although research has revealed how important SCL/TAL1 interruption site (STIL) is in many human tumors, the impact of STIL on HCC stem cells is poorly understood. This study aimed to examine the regulatory mechanisms and the function of STIL in the stemness of HCC tumor cells. Bioinformatics analysis was applied to determine the STIL and regulatory factor X-5 (RFX5) expression in HCC tissues. Immunohistochemistry (IHC) was used to detect the expression of STIL and RFX5 in HCC tissues. Quantitative real-time polymerase chain reaction was utilized to measure the STIL and RFX5 expression levels in HCC cells. The viability of the cells was assessed by the Cell Counting Kit-8 assay. The sphere formation assay was used to evaluate the sphere-forming capacity. The expression levels of the stem cell markers SOX2, Oct-4, CD133, CD44, the glycolysis-related proteins LDHA, HK2, AKT, p-AKT, and β-catenin were assessed by Western blot. Lactate production, oxygen consumption rate, and extracellular acidification rate were measured to assess the glycolytic capacity of HCC cells. Chromatin immunoprecipitation and dual-luciferase experiments were performed to validate the connection between RFX5 and STIL. Bioinformatics analysis determined that STIL exhibited high expression in HCC tissues and was enriched in the glycolysis pathway. In addition, the expression of glycolysis marker genes was positively correlated with STIL expression. Cell experiments verified that the activation of the glycolysis pathway by overexpression of STIL promoted stemness in HCC. Molecular experiments also revealed the binding relationship between STIL and RFX5. IHC detected high expression of STIL and RFX5 in HCC tissues. Cell functional experiments revealed that RFX5 could influence the HCC cells stemness by activating the STIL transcription via the glycolysis pathway. This study identified a novel role for the RFX5/STIL axis in HCC progression, which may offer treatment targets for HCC.</p>","PeriodicalId":94244,"journal":{"name":"The Kaohsiung journal of medical sciences","volume":" ","pages":"e12922"},"PeriodicalIF":0.0,"publicationDate":"2025-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11724169/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142883945","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":"A study of specific immunoglobulin G4 expression in allergic rhinitis and its value in assessing efficacy and in predicting prognosis of sublingual immunotherapy.","authors":"Ting-Ting Wei, Kai Gao, Jun-Hu Tai, Yong-Jun Wei, Bin Zhan","doi":"10.1002/kjm2.12916","DOIUrl":"10.1002/kjm2.12916","url":null,"abstract":"<p><p>Allergic rhinitis (AR) is a widespread health issue with a rising global prevalence, and sublingual immunotherapy (SLIT) has shown efficacy in AR treatment. We examined specific immunoglobulin G4 (sIgG4) expression in AR and its role in evaluating SLIT efficacy and predicting patient prognosis. We compared total nasal symptom score (TNSS), total medication score (TMS), visual analogue scale (VAS) score, inflammatory cytokines, and immune function markers in AR patients before and after SLIT. SLIT reduced TNSS, TMS, VAS scores, IL-4, IL-17, eosinophilia percentage (EOS%), and specific immunoglobulin E (sIgE) levels, while increasing INF-γ, IL-10, and sIgG4. The sIgG4 level at pre-treatment and 12 months post-treatment was negatively correlated with TNSS, TMS, VAS score, IL-4, IL-17, EOS%, and sIgE, and positively correlated with IFN-γ and IL-10. Most patients showed symptomatic improvement. After 12 months, sIgG4 level demonstrated an area under the curve (AUC) of 0.867 for assessing SLIT as effective. Pre-treatment sIgG4 level showed an AUC of 0.869 for predicting SLIT as effective. Collectively, sIgG4 has strong potential assessing SLIT efficacy and prognosis in AR patients, with correlations to TNSS, TMS, VAS score, and IL-4, IL-10, IL-17, INF-γ, EOS% and sIgE levels.</p>","PeriodicalId":94244,"journal":{"name":"The Kaohsiung journal of medical sciences","volume":" ","pages":"e12916"},"PeriodicalIF":0.0,"publicationDate":"2025-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11724161/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142911360","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":"ULK1 methylation promotes TGF-β1-induced endometrial fibrosis via the FOXP1/DNMT1 axis.","authors":"Yuhua Zeng, Qing Feng","doi":"10.1002/kjm2.12915","DOIUrl":"10.1002/kjm2.12915","url":null,"abstract":"<p><p>Intrauterine adhesion (IUA) is the second most common cause of secondary infertility in women and can also lead to menstrual abnormalities and multiple adverse pregnancy outcomes. Therefore, elucidating the mechanism of its development is crucial for the prevention and treatment of IUA. This study will investigate the function and mechanism of forkhead box P1 (FOXP1)/DNA methyltransferase 1 (DNMT1)/unc-51-like autophagy activating kinase 1 (ULK1) in IUA. Expression levels of key genes were detected using western blot and quantitative - real time reverse transcription polymerase chain reaction. Cell proliferation was detected by CCK-8 and EdU staining. Transcriptional regulation relationships were detected by dual luciferase reporter gene and chromatin immunoprecipitation (ChIP) assay. Methylation station of ULK1 was detected by methylmion specific PCR (MSP). Fibrosis and pathological changes in the uterine cavity tissues were detected by Masson and hematoxylin and eosin staining. It was observed that the expression of FOXP1 and DNMT1 increased in transforming growth factor (TGF)-β1-induced cells, while ULK1 expression decreased. Downregulation of FOXP1 could inhibit human endometrial stromal cells proliferation and autophagy, as well as decrease the expression of fibrogenic factors (collagen type I alpha 1 chain [COL1A1], fibronectin [FN], and alpha-smooth muscle actin [α-SMA]). The results of MSP and ChIP experiments showed that DNMT1 promotes methylation of the ULK1 promoter region and inhibits its transcription. In an animal model, knockdown of FOXP1 alleviated pathological fibrosis and uterine adhesions. Knockdown of FOXP1 can inhibit endometrial fibrosis in IUA rats; FOXP1 could be a potential target for the treatment of IUA.</p>","PeriodicalId":94244,"journal":{"name":"The Kaohsiung journal of medical sciences","volume":" ","pages":"e12915"},"PeriodicalIF":0.0,"publicationDate":"2025-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11724166/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142776150","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":"Expression of serum miR-135a in patients with allergic rhinitis and its relationship with Treg/Th17 balance.","authors":"Jing Cai, Fang Wang, Sheng-Liu Shi","doi":"10.1002/kjm2.12918","DOIUrl":"10.1002/kjm2.12918","url":null,"abstract":"<p><p>The dysregulation of microRNA (miRNA) expression contributes to the development of allergic rhinitis (AR). This study investigates serum miR-135a levels and their association with regulatory T cell (Treg) and T helper cell 17 (Th17) balance in AR patients. A total of 93 AR patients and 76 healthy controls were retrospectively recruited. Levels of serum miR-135a, peripheral blood Th17 and Treg cells, and Treg/Th17-related cytokines were measured. We assessed the diagnostic value of serum miR-135a for AR and its relationship with Treg/Th17 balance. AR patients showed significantly elevated immunoglobulin E (IgE), peripheral blood Th17 cells, and IL-17 and IL-6 levels, alongside reduced serum miR-135a, Treg cells, IL-10, TGF-β1, and Treg/Th17 ratios. A serum miR-135a of ≤0.536 demonstrated diagnostic potential for AR. Patients with higher serum miR-135a levels displayed increased Treg cell level and Treg/Th17 ratios, reduced Th17 cell, and lower total nasal symptom score (TNSS). Serum miR-135a levels in AR patients negatively correlated with TNSS, IL-17, IL-6, and Th17 cell percentages, and positively correlated with IL-10, TGF-β1, Treg cell percentages, and Treg/Th17 ratios. Collectively, decreased serum miR-135a levels in AR patients are associated with Treg/Th17 balance, supporting miR-135a as a potential biomarker for AR diagnosis.</p>","PeriodicalId":94244,"journal":{"name":"The Kaohsiung journal of medical sciences","volume":" ","pages":"e12918"},"PeriodicalIF":0.0,"publicationDate":"2025-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11724171/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142815439","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":"SIRT5-mediated HOXA5 desuccinylation inhibits ferroptosis to alleviate sepsis induced-lung injury.","authors":"Lei Wang, Heng Fan, Min Sun, Ji-Hui Ye","doi":"10.1002/kjm2.12921","DOIUrl":"10.1002/kjm2.12921","url":null,"abstract":"<p><p>Acute lung injury (ALI) is a common and severe complication of sepsis with a high mortality rate. Ferroptosis, an iron-dependent form of cell death, contributes to lung injury. Homeobox A5 (HOXA5) is involved in the regulation of septic acute kidney damage; however, its function on ferroptosis in septic ALI remains unclear. An in vitro model of septic lung injury was established in the pulmonary epithelial cell line (MLE-12) via lipopolysaccharide (LPS) stimulation. Cell viability, ferrous iron (Fe²⁺) level, and cellular lipid reactive oxygen species (ROS) were determined with Cell Counting Kit-8 assay, iron assay kit, and BODIPY™ 665/676 molecular probe, respectively. HOXA5, ferroptosis suppressor protein 1 (FSP1), sirtuin 5 (SIRT5), and glutathione peroxidase 4 (GPX4) expressions were measured using western blotting and Real-Time Quantitative Polymerase Chain Reaction (RT-qPCR. Chromatin immunoprecipitation and luciferase reporter assays were performed to validate HOXA5 binding to the FSP1/GPX4 promoter, and regulation of SIRT5 on HOXA5 desuccinylation was confirmed through co-immunoprecipitation. LPS stimulation induced ferroptosis (reduced cell viability, elevated Fe²⁺ and lipid ROS levels, and decreased GPX4 levels) and downregulated FSP1 and HOXA5 protein levels. HOXA5 overexpression neutralized LPS-induced ferroptosis. Moreover, LPS exposure inhibited HOXA5 binding to the FSP1 promoter, which was counteracted via HOXA5 overexpression. Furthermore, SIRT5 overexpression suppressed LPS-induced ferroptosis. In LPS-challenged MLE-12 cells, SIRT5-mediated HOXA5 desuccinylation was reduced. HOXA5 depletion neutralized the suppressive role of SIRT5 overexpression in LPS-induced ferroptosis. SIRT5-mediated HOXA5 desuccinylation inhibited LPS-induced ferroptosis by upregulating FSP1, which may offer a prospective therapeutic strategy for septic lung injury.</p>","PeriodicalId":94244,"journal":{"name":"The Kaohsiung journal of medical sciences","volume":" ","pages":"e12921"},"PeriodicalIF":0.0,"publicationDate":"2025-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11724168/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142879244","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":"Mitochondrial DNA copy number as a mediator of the relationship between insulin resistance and cognitive function in patients with euthymic bipolar disorder.","authors":"Tsung Han Tsai, Cheng Ying Wu, Cheng Chen Chang, Ta Tsung Lin, Chin San Liu, Po See Chen","doi":"10.1002/kjm2.12914","DOIUrl":"10.1002/kjm2.12914","url":null,"abstract":"<p><p>Persistent cognitive challenges in bipolar disorder (BD) may be tied to insulin resistance, which crucially affects both metabolism and brain health. Additionally, mitochondrial DNA (mtDNA) copy number has emerged as an indicator of cognitive performance and response to treatment in BD. However, it remains unclear whether and how this indicator might serve as a bridge between metabolic dysfunction and cognitive capacity. In 68 study participants with euthymic BD, insulin resistance was assessed according to fasting glucose and insulin levels. mtDNA copy number was quantified from leukocytes, and executive function was measured with the Wisconsin card-sorting test (WCST). Mediation models were applied to explore the statistical relationship between insulin resistance, mtDNA copy number, and executive function. Both linear regression and Poisson distribution approaches with robust bootstrap simulations were used for significance testing. The results indicated that insulin resistance indirectly affects executive function via mtDNA copy number. This mediation relationship was statistically significant for both preservation errors and completion of categories in the WCST, although there were no significant direct effects of insulin resistance on the executive functions. We therefore concluded that insulin resistance is associated with reduced mtDNA copy number in blood, which may negatively impact executive functions in patients with euthymic BD. Further work is warranted to determine if improving metabolic and mitochondrial health may lead to better cognitive outcomes in BD.</p>","PeriodicalId":94244,"journal":{"name":"The Kaohsiung journal of medical sciences","volume":" ","pages":"e12914"},"PeriodicalIF":0.0,"publicationDate":"2025-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11724167/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142696296","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":"Radiofrequency ablation for primary hyperparathyroidism and benign thyroid nodules.","authors":"Yu-Hsiang Lin, Tzu-Yen Huang","doi":"10.1002/kjm2.12919","DOIUrl":"10.1002/kjm2.12919","url":null,"abstract":"","PeriodicalId":94244,"journal":{"name":"The Kaohsiung journal of medical sciences","volume":" ","pages":"e12919"},"PeriodicalIF":0.0,"publicationDate":"2025-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11724159/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142809025","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":"E3 ubiquitination ligase XIAP lightens diabetes-induced cognitive impairment by inactivating TXNIP-ERS-mediated neuronal injury.","authors":"Qin Zhang, Hai-Jin Huang, Jing-Ling Zhang, Ying Tian, Ying Hu","doi":"10.1002/kjm2.12913","DOIUrl":"10.1002/kjm2.12913","url":null,"abstract":"<p><p>Diabetes-induced cognitive dysfunction (DCD) is a neurological disorder associated with diabetes, characterized by cognitive impairment driven by neuronal injury from chronic high glucose (HG) exposure. This study aims to elucidate the role and mechanisms of the X-linked inhibitor of apoptosis protein (XIAP)/thioredoxin-interacting protein (TXNIP) in hippocampal neuron cell death and cognitive function within DCD models. A diabetic rat model was established using a high-fat/sucrose diet and streptozotocin injection. Primary hippocampal neurons were stimulated with HG to mimic diabetic conditions. Cognitive and memory functions were assessed using the Morris water maze (MWM) and novel object recognition test (ORT).</p>","PeriodicalId":94244,"journal":{"name":"The Kaohsiung journal of medical sciences","volume":" ","pages":"e12913"},"PeriodicalIF":0.0,"publicationDate":"2025-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11724162/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142776146","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":"ELAVL1-dependent SOAT2 exacerbated the pancreatitis-like cellular injury of AR42J cells induced by hyperstimulation with caerulein.","authors":"Yu-Jing Sun, Hua-Ying Chen, Xiao-Qin Lai","doi":"10.1002/kjm2.12911","DOIUrl":"10.1002/kjm2.12911","url":null,"abstract":"<p><p>Pancreatitis is a severe inflammatory condition characterized by damage to the pancreas. Sterol o-acyltransferase 2 (SOAT2) has been reported to aggravate acute pancreatitis, however, the underlying mechanism remains to be elucidated. Rat pancreatic exocrine cells (AR42J) were treated with caerulein to induce pancreatitis-like cellular injury. Cell viability was determined using a cell counting kit-8 (CCK-8) assay, while cell proliferation was analyzed through a 5-Ethynyl-2'-deoxyuridine assay. Cell apoptosis was measured using flow cytometry, and enzyme-linked immunosorbent assays were performed to detect levels of pro-inflammatory cytokines IL-6 and TNF-α. Additionally, Fe²⁺ levels were analyzed using a colorimetric assay kit, reactive oxygen species (ROS) levels were assessed with a Cellular ROS Assay kit, and lipid peroxidation was measured using a malondialdehyde assay kit. Glutathione levels were analyzed with a detection assay. Protein and mRNA expression were evaluated through western blotting and quantitative real-time polymerase chain reaction, respectively. Furthermore, an RNA immunoprecipitation assay was conducted to investigate the association between ELAV-like RNA binding protein 1 (ELAVL1) and SOAT2. Actinomycin D assay was performed to explore the effect of ELAVL1 depletion on the transcript stability of SOAT2 mRNA. SOAT2 and ELAVL1 expression were upregulated in caerulein-exposed AR42J cells. Caerulein treatment induced pancreatitis-like cellular apoptosis, inflammatory response, ferroptosis, and cell proliferation inhibition. Silencing of SOAT2 protected against caerulein-induced AR42J cell injury. Moreover, ELAVL1 stabilized SOAT2 mRNA expression in AR42J cells. SOAT2 overexpression attenuated the effects induced by ELAVL1 silencing in caerulein-exposed AR42J cells. Additionally, ELAVL1 knockdown activated the NRF2/HO-1 pathway by downregulating SOAT2 expression in caerulein-exposed AR42J cells. SOAT2 silencing protected AR42J cells from caerulein-induced injury by inactivating the NRF2 pathway. In conclusion, ELAVL1-dependent SOAT2 exacerbated pancreatic exocrine cell injury by inactivating the NRF2/HO-1 pathway in pancreatitis. These findings provide new insights into the molecular mechanisms underlying pancreatitis and offer potential therapeutic targets for the treatment of this condition.</p>","PeriodicalId":94244,"journal":{"name":"The Kaohsiung journal of medical sciences","volume":" ","pages":"e12911"},"PeriodicalIF":0.0,"publicationDate":"2025-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11724160/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142718035","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":"A rare case of Listeria monocytogenes bacteremia complicated by severe hyperbilirubinemia and liver failure.","authors":"Yuan-Ai Tseng, Sheau-Fang Yang, Tyng-Yuan Jang","doi":"10.1002/kjm2.12920","DOIUrl":"10.1002/kjm2.12920","url":null,"abstract":"","PeriodicalId":94244,"journal":{"name":"The Kaohsiung journal of medical sciences","volume":" ","pages":"e12920"},"PeriodicalIF":0.0,"publicationDate":"2025-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11724158/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142809018","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}