The Kaohsiung journal of medical sciences最新文献

{"title":"Laparoscopic Modified One Anastomosis Gastric Bypass for Severe Obesity After Pancreaticoduodenectomy: A Safe Approach to the Hostile Abdomen, a First Case Report.","authors":"Chih-Kun Huang, Ming-Che Hsin, Long-Bin Jeng, Ting-Wei Chang","doi":"10.1002/kjm2.70233","DOIUrl":"https://doi.org/10.1002/kjm2.70233","url":null,"abstract":"","PeriodicalId":94244,"journal":{"name":"The Kaohsiung journal of medical sciences","volume":" ","pages":"e70233"},"PeriodicalIF":3.1,"publicationDate":"2026-05-07","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147848535","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":"Risk Factors Influencing Efficacy and Prognosis Evaluation of Neoadjuvant Systemic Therapy in Triple-Positive Breast Cancer.","authors":"Lin-Rui Miao, Hao Liu, Hai-Ying Yu, Jian Chen, Ming-Yu Yang, Ya-Lan Zhang, Gang Tu, Ling-Feng Tang","doi":"10.1002/kjm2.70228","DOIUrl":"https://doi.org/10.1002/kjm2.70228","url":null,"abstract":"<p><p>To identify the determinants of the response to neoadjuvant systemic therapy (NST) in triple-positive breast cancer (TPBC), we retrospectively enrolled 520 patients with human epidermal growth factor receptor 2 (HER2)-positive breast cancer who were treated at The First Affiliated Hospital of Chongqing Medical University between January 2015 and December 2021. The cohort comprised 299 cases of TPBC and 221 cases of hormone receptor (HR)-negative/HER2-positive breast cancer (HPBC). A comparative analysis revealed that the pathological complete response (pCR) rate was significantly lower in the TPBC group than in the HPBC group (30.1% vs. 50.2%; p < 0.001); however, this differential response did not translate into a significant difference in long-term survival. Within the TPBC cohort, pCR was identified as an independent prognostic factor for prolonged disease-free survival (DFS) (p = 0.014). Multivariate analysis further revealed that the NST regimen (p = 0.001), estrogen receptor (ER) status (p = 0.024), and Ki67 index (p = 0.018) were independent predictors of pCR. A nomogram incorporating these factors was developed using R software to estimate the individual probability of pCR in TPBC. The model was externally validated in an independent cohort of 143 TPBC patients treated between January 2022 and December 2024, and the results demonstrated robust predictive performance and good calibration. This model serves as a tool for early risk stratification in TPBC, thereby facilitating personalized treatment strategies and risk-adapted surveillance to improve patient outcomes.</p>","PeriodicalId":94244,"journal":{"name":"The Kaohsiung journal of medical sciences","volume":" ","pages":"e70228"},"PeriodicalIF":3.1,"publicationDate":"2026-05-07","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147848495","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":"Sporadic Hepatocellular Carcinoma in an Adolescent Harboring a Somatic CDH1 Mutation: A Case Report and Literature Review.","authors":"Chang-Wei Su, Peir-In Liang, Shih-Chang Chuang","doi":"10.1002/kjm2.70236","DOIUrl":"https://doi.org/10.1002/kjm2.70236","url":null,"abstract":"","PeriodicalId":94244,"journal":{"name":"The Kaohsiung journal of medical sciences","volume":" ","pages":"e70236"},"PeriodicalIF":3.1,"publicationDate":"2026-05-07","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147848449","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":"Predictive Value of Nutrition Indices in Advanced Hepatocellular Carcinoma Patients Treated With Lenvatinib.","authors":"Cheng-Wei Kuo, Wei-Chen Tai, Yen-Hao Chen, Ming-Chao Tsai, Jing-Houng Wang, Sheng-Nan Lu, Tsung-Hui Hu, Chao-Hung Hung, Chien-Hung Chen, Yuan-Hung Kuo","doi":"10.1002/kjm2.70230","DOIUrl":"https://doi.org/10.1002/kjm2.70230","url":null,"abstract":"<p><p>The prognostic nutritional index (PNI) and geriatric nutritional risk index (GNRI) are simple markers that reflect immune and nutritional status. This retrospective study evaluated their prognostic significance in 276 patients with advanced hepatocellular carcinoma (HCC) who received first-line lenvatinib. PNI and GNRI were calculated based on serum albumin, lymphocyte count, and body weight. Patients were classified into high and low groups for each index. Multivariate models were used to assess their prognostic value for progression-free survival (PFS) and overall survival (OS). Higher PNI (cut-off: 45) and GNRI (cut-off: 98) scores were associated with significantly better outcomes: the high PNI and low PNI groups achieved median PFS of 7.5 vs. 4.0 months (p = 0.002) and OS of 19.3 vs. 9.8 months (p < 0.001), respectively. Similarly, the high GNRI and low GNRI groups achieved median PFS of 7.3 versus 4.7 months (p = 0.001) and OS of 21 versus 9.8 months (p < 0.001), respectively. Patients with higher indices also had higher objective response rates, lower rates of severe treatment-related adverse events, and were more likely to receive posttreatment therapies. The PNI (hazard ratio [HR]: 0.678, p = 0.018), GNRI (HR: 0.679, p = 0.031), and the combined indices (HR: 0.655, p = 0.013) independently demonstrated prognostic value for mortality in multivariate models. PNI and GNRI, both individually and in combination, are simple yet powerful tools that predict survival and treatment tolerance in patients with HCC receiving lenvatinib. Routine assessment of these indices may enhance patient stratification and guide therapeutic strategies.</p>","PeriodicalId":94244,"journal":{"name":"The Kaohsiung journal of medical sciences","volume":" ","pages":"e70230"},"PeriodicalIF":3.1,"publicationDate":"2026-05-07","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147848467","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":"Proteomic and Metabolomic Profiling Reveal Mitochondrial Transplantation-Mediated Reprogramming in Gastric Cancer Cells.","authors":"Ping-Chen Chen, Chen-Kai Liu, Ching-Chung Tsai, Erna Sulistyowati, Fu-An Li, Chung-Jung Liu, Deng-Chyang Wu, Shih-Hsuan Chou, Fu-Chen Kuo, Bin Huang","doi":"10.1002/kjm2.70232","DOIUrl":"https://doi.org/10.1002/kjm2.70232","url":null,"abstract":"<p><p>Mitochondria provide multiple functions for cellular physiology. Transplantation of mitochondria isolated from gastric epithelial cells GES-1 reducing the malignancy of gastric cancer cells AGS was previously reported. To elucidate the underlying mechanisms, TMT-based proteomic analysis coupling ingenuity pathway software prediction revealed that 257 upregulated and 34 downregulated proteins were implicated in 14 signaling pathways, including mitochondrial cell dysfunction (data became available from ProteomeXchange with identifier PXD061705). The upregulation of p53, Bax, p-Akt^S473, p-mTOR^S2448 and the downregulation of Sirt 3, p-NRF2^S40, and HO-1 were further verified by western blotting. In the metabolomic analysis, 3 upregulated and 8 downregulated metabolites involved in glycolysis, TCA cycle, pentose phosphate pathway (PPP) and ATP production were identified. Aligning the catalytic step of these metabolites in glycolysis and TCA cycle, the lower fructose 1,6-bisphosphate, 2-phosphoglyceric acid and phosphoenolpyruvate was coupled with higher isocitrate while the reduced α-ketoglutarate, malate, ATP and NADH all implied an accumulation of pyruvate in the cytosol. Western blotting, along with pyruvate and lactate assays, showed decreased extracellular lactate due to upregulated MCT1 (lactate importer) and downregulated MCT4 (lactate exporter). The higher pyruvate was caused by increased LDHB (lactate-to-pyruvate conversion) and a decrease in mitochondrial pyruvate carrier (MPC). With the finding that transplanted GES-1 mitochondria led to an accumulation of pyruvate, the inhibitory effect of elevated pyruvate on migrated AGS cells was observed. In conclusion, combining proteomic and metabolomic analysis revealed the underlying mechanisms for understanding how transplanted GES-1 mitochondria attenuate AGS gastric cancer malignancy.</p>","PeriodicalId":94244,"journal":{"name":"The Kaohsiung journal of medical sciences","volume":" ","pages":"e70232"},"PeriodicalIF":3.1,"publicationDate":"2026-05-07","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147848503","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":"Ginsenoside Rg1 Ameliorates LPS-Induced Sepsis-Associated Lung Injury in Mice via VEGFC/D-VEGFR3 Signaling-Mediated Lymphangiogenesis and Lymphatic Remodeling.","authors":"He Wang, Lan Hu, Chun-Pan Zhang, Wen-Jie Qi, Yu-Guo Song","doi":"10.1002/kjm2.70229","DOIUrl":"https://doi.org/10.1002/kjm2.70229","url":null,"abstract":"<p><p>Sepsis-induced acute lung injury (ALI) remains challenging to treat, with conventional anti-inflammatory therapies offering limited efficacy. The lymphatic system is crucial for removing edema and inflammatory mediators, and its impairment can exacerbate lung injury. Ginsenoside Rg1, a bioactive botanical compound, has diverse pharmacological properties, but its ability to modulate lymphangiogenesis in septic ALI is unclear. This study investigated whether Ginsenoside Rg1 can alleviate lipopolysaccharide (LPS)-induced ALI in mice by promoting lymphangiogenesis via the vascular endothelial growth factor C (VEGFC)/D-VEGF receptor 3 (VEGFR3) signaling pathway. ALI was induced in C57BL/6 mice by intraperitoneal injection of LPS (10 mg/kg). Mice were treated with Rg1 at low (30 mg/kg) or high (60 mg/kg) doses. Lung injury was assessed by wet-to-dry weight ratios, vascular permeability, histopathology, and lymphatic vessel density. Levels of inflammatory cytokines, VEGFC/D, VEGFR3, and downstream signaling molecules were measured by enzyme-linked immunosorbent assay, western blotting, and qPCR. Ginsenoside Rg1 treatment dose-dependently reduced pulmonary edema, vascular leakage, and histological damage. It also reversed LPS-induced decreases in VEGFC/D and increased VEGFR3 expression, resulting in enhanced lymphatic vessel density. Rg1 activated VEGFR3 downstream pathways (ERK/Prox-1, AKT) and upregulated lymphatic function genes (CCL21a, ACKR2). Ginsenoside Rg1 can attenuate septic ALI by stimulating the VEGFC/D-VEGFR3 axis to promote functional lymphangiogenesis, thereby facilitating clearance of edema and inflammatory mediators. This mechanism offers a novel therapeutic strategy focused on enhancing clearance rather than only on suppressing inflammation, potentially reducing tissue damage and the side effects associated with conventional treatments.</p>","PeriodicalId":94244,"journal":{"name":"The Kaohsiung journal of medical sciences","volume":" ","pages":"e70229"},"PeriodicalIF":3.1,"publicationDate":"2026-05-07","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147848515","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":"Knockdown of CREB3L4 Inhibits Autophagy and Reduces Cisplatin Resistance in Gastric Cancer Cells by Downregulating BAG3.","authors":"Wen-Ke Yin, Xue-Mei Xie, Xiao-Yan Song, Yue Xiang","doi":"10.1002/kjm2.70231","DOIUrl":"https://doi.org/10.1002/kjm2.70231","url":null,"abstract":"<p><p>Cisplatin resistance remains a major obstacle in the treatment of gastric cancer (GC), and autophagy has been increasingly recognized as a key cytoprotective mechanism contributing to chemoresistance. CREB3L4 is an endoplasmic reticulum membrane-bound transcription factor that has been shown to regulate the expression of Bcl-2 associated athanogene 3 (BAG3), a co-chaperone protein involved in autophagy and survival signaling in various cancers. However, whether the CREB3L4/BAG3 axis regulates autophagy and contributes to cisplatin resistance in gastric cancer cells remains unclear. In the present study, we investigated the roles of CREB3L4 and BAG3 in cisplatin-resistant GC cell lines and found that CREB3L4 and BAG3 were overexpressed. Furthermore, BAG3 expression was inhibited following CREB3L4 knockdown in gastric cancer cells. Notably, knockdown of CREB3L4 inhibited autophagy and alleviated cisplatin resistance in gastric cancer cells by down-regulating BAG3. In addition, silencing of CREB3L4 promoted apoptosis and inhibited cell proliferation, which was also associated with decreased BAG3 expression. Taken together, these findings indicate that depletion of CREB3L4 suppressed autophagy and reduced cisplatin resistance in GC cells by downregulating BAG3.</p>","PeriodicalId":94244,"journal":{"name":"The Kaohsiung journal of medical sciences","volume":" ","pages":"e70231"},"PeriodicalIF":3.1,"publicationDate":"2026-05-07","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147848457","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":"Multi-Site Hymenoptera Stings Mark a High-Risk Subgroup in the Emergency Department.","authors":"Shih-Fen Tseng, Shum-Shin Lin, Che-Cheng Su, Yu-Jang Su","doi":"10.1002/kjm2.70220","DOIUrl":"https://doi.org/10.1002/kjm2.70220","url":null,"abstract":"","PeriodicalId":94244,"journal":{"name":"The Kaohsiung journal of medical sciences","volume":" ","pages":"e70220"},"PeriodicalIF":3.1,"publicationDate":"2026-05-07","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147848540","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":"Role of ZNF652 in Regulating Hepatocellular Carcinoma Cell Proliferation and Apoptosis via the circRHOT1/SLC38A6 Axis.","authors":"Kang Chen, Fei-Hu Sun, Chen Fan, Wei Ding, Hao-Huan Tang, Lei Sun, Wei-Tao Wang, Wei-Dong Wang","doi":"10.1002/kjm2.70129","DOIUrl":"10.1002/kjm2.70129","url":null,"abstract":"<p><p>Hepatocellular carcinoma (HCC) is a heterogeneous malignancy characterized by high mortality rates. This article presents a discussion of the role of ZNF652 in HCC cell proliferation and apoptosis, thereby identifying a new target for HCC treatment. The expression levels of ZNF652, circRHOT1, and SLC38A6 in HCC and healthy cells were analyzed. Cell proliferation and apoptosis were subsequently validated. The binding relationships between ZNF652 and the circRHOT1 promoter and between circRHOT1 and KAT5 were validated. The recruitment of KAT5 and H3K27ac to the SLC38A6 promoter was assessed via ChIP. Combined experiments were carried out to verify the role of the circRHOT1/SLC38A6 pathway in HCC cell proliferation and apoptosis. ZNF652, circRHOT1, and SLC38A6 were upregulated in HCC cells. ZNF652 silencing inhibited HCC cell proliferation but promoted apoptosis. Mechanistically, ZNF652 increased circRHOT1 expression at the transcriptional level and recruited KAT5 to the SLC38A6 promoter to increase H3K27ac enrichment and activate SLC38A6 expression. Combined experiments revealed that overexpression of circRHOT1 or SLC38A6 could alleviate the effects of ZNF652 silencing on HCC cell proliferation and apoptosis. In conclusion, ZNF652 transcriptionally activated circRHOT1 expression, recruited KAT5 to the SLC38A6 promoter, increased H3K27ac enrichment, and activated SLC38A6 expression, thus promoting HCC cell proliferation and inhibiting apoptosis.</p>","PeriodicalId":94244,"journal":{"name":"The Kaohsiung journal of medical sciences","volume":" ","pages":"e70129"},"PeriodicalIF":3.1,"publicationDate":"2026-05-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145644331","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":"MiR-145-5p Attenuates Doxorubicin-Induced Heart Injury Through Targeting Cardiomyocyte Pyroptosis.","authors":"Xing-Tao Chen, Yong-Hong Yu, Yan-Hua Du, Lin Xu, Xiang-Ping Meng","doi":"10.1002/kjm2.70126","DOIUrl":"10.1002/kjm2.70126","url":null,"abstract":"<p><p>Doxorubicin (DOX), a potent anthracycline chemotherapeutic, exhibits dose-dependent cardiotoxicity that limits its clinical utility. Although miR-145-5p demonstrates cardioprotective properties in cardiovascular diseases, its role in DOX-induced cardiomyopathy remains undefined. This study investigated the therapeutic potential of miR-145-5p against DOX-induced cardiotoxicity and its underlying mechanism. Wistar rats received cumulative DOX dosing (15 mg/kg total) to establish cardiotoxicity, with miR-145-5p overexpression achieved via adeno-associated virus serotype 9 (AAV9) delivery. Cardiac function was assessed by echocardiography and serum biomarkers, including creatine kinase-MB isoenzyme (CK-MB), cardiac troponin T (c-TnT), C-reactive protein (CRP), and N-terminal pro-B-type natriuretic peptide (NT-proBNP). Histopathology (Hematoxylin & Eosin/Masson's Trichrome staining), apoptosis (TUNEL), oxidative stress (dihydroethidium staining/malondialdehyde/glutathione), and NLRP3 inflammasome activation (ELISA/Western blot/immunohistochemistry) were evaluated. Clinical relevance was determined by quantifying serum miR-145-5p and SOX9 mRNA in healthy controls and breast cancer patients before and after DOX treatment. DOX significantly downregulated miR-145-5p and upregulated SOX9 in rat myocardium and H9C2 cells. DOX-treated patients displayed reduced serum miR-145-5p and increased SOX9 mRNA compared with pre-chemotherapy baselines. AAV9-miR-145-5p attenuated DOX-induced systolic dysfunction, reduced serum biomarkers, ameliorated histopathological injury and fibrosis, suppressed apoptosis and oxidative stress, and inhibited NLRP3 inflammasome activation (decreased NLRP3, ASC, caspase-1, IL-1β, and IL-18). miR-145-5p directly targeted the SOX9 3'UTR, and SOX9 overexpression reversed miR-145-5p-mediated reductions in CK release, ROS production, apoptosis, and NLRP3 expression in H9C2 cells. These findings demonstrate that miR-145-5p protects against DOX cardiotoxicity by targeting SOX9 to inhibit NLRP3 inflammasome-mediated pyroptosis, offering a potential therapeutic strategy.</p>","PeriodicalId":94244,"journal":{"name":"The Kaohsiung journal of medical sciences","volume":" ","pages":"e70126"},"PeriodicalIF":3.1,"publicationDate":"2026-05-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145508556","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}