南方医科大学学报杂志最新文献

{"title":"[<i>Qihuang Jianpi Zishen</i> Granules improves thrombocytopenia in mice with systemic lupus erythematosus by suppressing platelet autophagy <i>via</i> the Ca²⁺/CaMKK2/AMPK/mTOR signaling pathway].","authors":"Yunfei Li, Lijun Pang, Longwu Shu, Ming Li, Chuanbing Huang","doi":"10.12122/j.issn.1673-4254.2024.12.08","DOIUrl":"10.12122/j.issn.1673-4254.2024.12.08","url":null,"abstract":"<p><strong>Objectives: </strong>To explore the mechanism of <i>Qihuang Jianpi Zishen</i> Granules (QJZG) for improving thrombocytopenia in a mouse model of systemic lupus erythematosus (SLE).</p><p><strong>Methods: </strong>Twenty-four MRL/lpr lupus mice were randomized equally into 4 groups for treatment with daily gavage of saline, QJZG or prednisone (Pred) or intraperitoneal injection (twice a week) of CaMKK2 activator, with 6 C57BL/6 mice with saline gavage as the control group. After 8 weeks of treatment, the mice were examined for PLT, PCT, PDW, MPV, serum levels of TPO, IL-6, IL-10, TNF-α and IFN-γ, and calcium ion fluorescence intensity using ELISA or flow-through assay. RT-qPCR was used to detect platelet CaMKK2, AMPK2α, mTOR, Beclin1 and p62 mRNA expression levels, and the protein expressions of CaMKK2, p-CaMKK2, AMPK, p-AMPK, mTOR, p-mTOR, LC3, Beclin1 and p62 were detected using Western blotting.</p><p><strong>Results: </strong>The saline-treated MRL/lpr lupus mice showed significantly lowered levels of PLT, PCT, IL-10, mTOR, p62 mRNA, p-mTOR and P62 with increased PDW, MPV, serum TPO, IL-6, TNF-α and IFN-γ levels, and platelet expressions of CaMKK2, AMPK, Bcl-1 mRNA, p-CaMKK2, p-AMPK, LC3II and Beclin1. These abnormalities were significantly improved in QJZG group and Pred group but worsened after treatment with the CaMKK2 activator.</p><p><strong>Conclusions: </strong>QJZG can ameliorate thrombocytopenia in mouse models of SLE by reducing inflammation and inhibiting platelet autophagy via regulating the Ca²⁺/CaMKK2/AMPK/mTOR signaling pathways.</p>","PeriodicalId":18962,"journal":{"name":"南方医科大学学报杂志","volume":"44 12","pages":"2327-2334"},"PeriodicalIF":0.0,"publicationDate":"2024-12-20","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11683354/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142896213","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":"[Electroacupuncture improves learning and memory function and promotes hippocampal synaptic regeneration in rats with cerebral ischemia-reperfusion injury].","authors":"Ruhui Lin, Jinyan Xia, Xiaohan Ma, Zuanfang Li","doi":"10.12122/j.issn.1673-4254.2024.12.07","DOIUrl":"10.12122/j.issn.1673-4254.2024.12.07","url":null,"abstract":"<p><strong>Objectives: </strong>To explore the neuroprotective mechanism of electroacupuncture at the acupoints <i>Baihui</i> and <i>Shenting</i> in rats with cerebral ischemia-reperfusion (IR) injury.</p><p><strong>Methods: </strong>Forty-eight male SD rats were equally randomized into sham operation group, cerebral IR model group, acupoint electroacupuncture group and non-acupoint acupuncture group. In the latter 3 groups, cerebral focal ischemic injury was induced using the Longa method; in the two electroacupuncture groups, electroacupuncture was performed either at the acupoints <i>Baihui</i> and <i>Shenting</i> or at non-acupoint sites for 7 days. The changes in neurological deficit scores, cerebral infarction volume, learning and memory function, pathologies in hippocampal CA1 area, neuronal and synaptic ultrastructures, and synaptic density of the rats were observed, and serum GABA level and mRNA and protein expressions of GABA_AR α1, CaMK II, SYN1 and PSD-95 in the hippocampal tissue were detected.</p><p><strong>Results: </strong>Compared with those in cerebral IR model group, the rats receiving electroacupuncture at the acupoints, but not those with electroacupuncture at the non-acupoints, showed significantly decreased neurological deficit scores and cerebral infarction volume with shortened escape latency and increased platform crossings. Electroacupuncture at the acupoints significantly increased neuronal cell number, decreased the width of the synaptic gaps and increased density of synaptic bodies in the ischemic hippocampal CA1 area, resulting also in increased serum GABA levels and hippocampal expressions of GABA_ARα1, SYN1 and PSD-95 and lowered expression level of CaMK II.</p><p><strong>Conclusions: </strong>Electroacupuncture at <i>Baihui</i> and <i>Shenting</i> improves learning and memory function of rats with cerebral IR injury possibly through a mechanism that promotes synaptic regeneration, upregulates hippocampal expressions of GABAAR α 1, SYN1 and PSD-95 and downregulates the expression of CaMK II.</p>","PeriodicalId":18962,"journal":{"name":"南方医科大学学报杂志","volume":"44 12","pages":"2317-2326"},"PeriodicalIF":0.0,"publicationDate":"2024-12-20","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11683340/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142896217","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":"[FER-1 inhibits methylglyoxal-induced ferroptosis in mouse alveolar macrophages <i>in vitro</i>].","authors":"Qi Zhang, Zezhao Ji, Abai Jiashaer, Youda Wang, Abuduxukuer Abulimiti","doi":"10.12122/j.issn.1673-4254.2024.12.21","DOIUrl":"10.12122/j.issn.1673-4254.2024.12.21","url":null,"abstract":"<p><strong>Objectives: </strong>To investigate the inhibitory effect of FER-1 on methylglyoxal-induced ferroptosis in cultured mouse alveolar macrophages.</p><p><strong>Methods: </strong>MH-S cells derived from mouse alveolar macrophages treated with 90 μg/mL methylglyoxal, 10 μmol/mL FER-1MG+FER-1, or both were examined for intracellular reactive oxygen species (ROS), malondialdehyde (MDA) and ferrous ion (Fe²⁺) levels and changes in mitochondrial membrane potential. Western blotting was performed to detect the protein expression levels of glutathione peroxidase 4 (GPX4) and long-chain acyl-CoA synthase 4 (ACSL4).</p><p><strong>Results: </strong>Methylglyoxal treatment of MH-S cells for 24 h significantly decreased the protein expression level of GPX4, upregulated the protein expression of ACSL4, increased intracellular concentrations of ferrous ions, ROS and MDA, caused loss of mitochondrial membrane potential, and decreased cell viability. Treatment of the cells with FER-1 effectively attenuated these detrimental effects of methylglyoxal in MH-S cells by increasing GPX4 expression, reducing ACSL4 expression and intracellular ferrous ions, ROS and MDA levels, and restoring the mitochondrial membrane potential.</p><p><strong>Conclusions: </strong>Methylglyoxal can induce ferroptosis in MH-S cells in a dose-dependent manner, and FER-1 can rescue the cells from methylglyoxal-induced ferroptosis.</p>","PeriodicalId":18962,"journal":{"name":"南方医科大学学报杂志","volume":"44 12","pages":"2443-2448"},"PeriodicalIF":0.0,"publicationDate":"2024-12-20","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11683347/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142896219","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":"[Holliday junction-recognizing protein is a potential predictive and prognostic biomarker for kidney renal clear cell carcinoma].","authors":"Huahua Zhang, Qingyin Ta, Yun Feng, Jiming Han","doi":"10.12122/j.issn.1673-4254.2024.12.10","DOIUrl":"10.12122/j.issn.1673-4254.2024.12.10","url":null,"abstract":"<p><strong>Objectives: </strong>To investigate the role of Holliday cross-recognition protein (HJURP) in tumorigenesis, progression, and immunotherapy responses.</p><p><strong>Methods: </strong>Bioinformatics approaches were used to analyze the expression level of <i>HJURP</i> in various cancers and its association with prognosis, clinical stage, and immune cell infiltration using TCGA, GTEx, SangerBox and TIMER 2.0 databases. LinkedOmics database was employed to investigate <i>HJURP</i>-related genes and their potential functions in kidney renal clear cell carcinoma (KIRC). The expression of <i>HJURP</i> in KIRC samples was examined with immunohistochemistry, Western blotting and qRT-PCR, and the effect of <i>HJURP</i> silencing on cell proliferation and migration was tested in cultured KIRC cells.</p><p><strong>Results: </strong><i>HJURP</i> was highly expressed in 26 cancers with negative correlations with the patients' survival outcomes in 5 cancers including KIRC (<i>P</i><0.05). <i>HJURP</i> expression levels was strongly correlated with clinical stages and immune cell infiltration in the tumors. In KIRC, <i>HJURP</i> expression was significantly elevated (<i>P</i><0.0001) and showed a positive correlation with TNM stage (<i>P</i><0.05), overall stage (<i>P</i><0.01) and immune cell infiltration. Gene Ontology (GO) functional analysis showed that <i>HJURP</i> is predominantly enriched in biological processes such as biological regulation and metabolic processes. Concerning cellular components, <i>HJURP</i> is primarily localized to the cell membrane and nucleus. In terms of molecular functions, it is chiefly enriched in activities related to protein binding and ion binding. <i>HJURP</i> was highly expressed in both clinical KIRC tissues and KIRC cell lines (<i>P</i><0.001). In cultured KIRC cells, silencing of <i>HJURP</i> significantly inhibited cell proliferation and migration abilities.</p><p><strong>Conclusions: </strong><i>HJURP</i> may serves as an indicator of prognosis and immunotherapy response of KIRC, and its high expression enhances malignant behaviors of KIRC cells.</p>","PeriodicalId":18962,"journal":{"name":"南方医科大学学报杂志","volume":"44 12","pages":"2347-2358"},"PeriodicalIF":0.0,"publicationDate":"2024-12-20","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11683356/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142896224","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":"[Parameter estimation using time-dependent Weibull proportional hazards model for survival analysis with partly interval censored data].","authors":"Shuying Wang, Xinyu Liu, Rundong Li, Yang Li","doi":"10.12122/j.issn.1673-4254.2024.12.23","DOIUrl":"10.12122/j.issn.1673-4254.2024.12.23","url":null,"abstract":"<p><p><b>OBJECTIVE</b>: To assess the validity and effectiveness of parameter estimation using a time-dependent Weibull proportional hazards model for survival analysis containing partly interval censored data and explore the impact of different covariates on the results of analysis. <b>METHODS</b>: We established a time-dependent Weibull proportional hazards model using the Weibull distribution as the baseline hazard function of the model which incorporated time-varying covariates. Maximum likelihood estimation was employed to estimate the model parameters, which were obtained by optimization of the likelihood function. <b>RESULTS AND CONCLUSION</b>: Numerical simulation results showed that with higher proportions of precise observations across different sample sizes and parameter settings, the proposed model resulted in improved accuracy of parameter estimation with coverage probabilities approximating the theoretical expectation of 95%. As the sample sizes increased, the parameter biases of the model tended to decrease. Experiments with empirical data further validated the effectiveness of the model. Compared with the failure time data for each precisely observed individual, additional interval-censored data helped to obtain more effective estimates of the regression parameters. Comparison with the Cox model that included time-varying covariates further demonstrated the effectiveness of the time-dependent Weibull proportional hazards model for parameter estimation in survival analysis with partly interval censored data.</p>","PeriodicalId":18962,"journal":{"name":"南方医科大学学报杂志","volume":"44 12","pages":"2461-2468"},"PeriodicalIF":0.0,"publicationDate":"2024-12-20","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11683352/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142896228","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":"[Parkin deletion affects PINK1/Parkin-mediated mitochondrial autophagy to exacerbate neuroinflammation and accelerate progression of Parkinson's disease in mice].","authors":"Chengcheng Jiang, Yangyang Li, Kexin Duan, Tingting Zhan, Zilong Chen, Yongxue Wang, Rui Zhao, Caiyun Ma, Yu Guo, Changqing Liu","doi":"10.12122/j.issn.1673-4254.2024.12.11","DOIUrl":"10.12122/j.issn.1673-4254.2024.12.11","url":null,"abstract":"<p><strong>Objectives: </strong>To investigate the role of mitochondrial autophagy disorder caused by deletion of E3 ubiquitin ligase Parkin in neuroinflammation in a mouse model of MPTP-induced Parkinson's disease (PD).</p><p><strong>Methods: </strong>Wild-type (WT) male C57BL/6 mice and Parkin^-/- mice were given intraperitoneal injections with MPTP or PBS for 5 consecutive days, and the changes in motor behaviors of the mice were observed using open field test. The effects of Parkin deletion on PD development and neuroinflammation were evaluated using immunofluorescence and Western blotting. The changes of the PINK 1/Parkin signaling pathway in the midbrain substantia nigra of the mice were examined to explore the molecular mechanism of Parkin-mediated regulation of mitochondrial autophagy and its effect on neuroinflammation in PD mice.</p><p><strong>Results: </strong>Compared with their WT counterparts, the Parkin^-/- mice with MPTP injections exhibited significant impairment of motor function with decreased TH⁺ neurons, increased α-synuclein (α-syn) accumulation, and increased numbers of GFAP⁺ and I-ba1⁺ cells in the midbrain substantia nigra. Parkin deletion obviously affected PINK1/Parkin-mediated mitochondrial autophagy to result in significantly increased mtDNA and upregulated expressions of STING and NLRP3 inflammatosomes in the midbrain substantia nigra of MPTP-treated transgenic mice.</p><p><strong>Conclusions: </strong>Parkin deletion causes mitochondrial autophagy disorder to accelerate PD progression and exacerbates neuroinflammation in mice by affecting the PINK1/Parkin signaling pathway, suggesting the important role of Parkin in early pathogenesis of PD.</p>","PeriodicalId":18962,"journal":{"name":"南方医科大学学报杂志","volume":"44 12","pages":"2359-2366"},"PeriodicalIF":0.0,"publicationDate":"2024-12-20","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11683357/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142896229","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":"[<i>Liangxue Jiedu Huayu</i> Formula improves liver function of mice with acute-on-chronic liver failure by inhibiting excessive activation of the cGAS-STING signaling pathway].","authors":"Qiao Tang, Chao Zhou, Zhaofang Bai, Qing Yao, Simin Chen, Xinru Wen, Zhaoyun He, Jin Zhang, Ruisheng Li, Man Gong","doi":"10.12122/j.issn.1673-4254.2024.12.04","DOIUrl":"10.12122/j.issn.1673-4254.2024.12.04","url":null,"abstract":"<p><strong>Objectives: </strong>To explore the role of the cGAS-STING signaling pathway in the therapeutic mechanism of <i>Liangxue Jiedu Huayu</i> Formula (LXJDHYF) for acute-on-chronic liver failure (ACLF) in mice.</p><p><strong>Methods: </strong>Thirty C57BL/6 mice were randomly divided into blank control group, model group, low- and high-dose LXJDHYF groups, and H151 (a specific cGAS-STING pathway inhibitor) group (<i>n=</i>6). In all but the control group, the mice were treated with CCl₄ to induce liver cirrhosis followed by intraperitoneal injections of lipopolysaccharide and D-amino galactose to establish mouse models of ACLF. After the treatments, the mouse livers were collected for HE and TUNEL staining, and serum levels of ALT, AST and TBil were determined. In bone marrow-derived macrophages (BMDMs) and liver tissues of ACLF mice, the expressions of cGAS-STING signaling pathway-related mRNAs including IFN‑β, ISG15, IL-6 and TNF-α were determined with RT-qPCR, and the phosphorylation levels of IRF3 and STING proteins were investigated using Western blotting.</p><p><strong>Results: </strong>Compared with the mice in the model group, the LXJDHYF-treated mice exhibited milder hepatocyte necrosis and inflammatory cell infiltration in the liver with significantly reduced hepatocyte apoptosis. LXJDHYF treatment also significantly lowered serum levels of ALT, AST, TBil, IL-6 and TNF-α in ACLF mice and effectively suppressed the expressions of cGAS-STING signaling pathway-related mRNA in both the BMDMs and the liver tissues and the phosphorylation of IRF3 and STING proteins in the BMDMs.</p><p><strong>Conclusions: </strong>LXJDHYF can significantly improve liver function and attenuate inflammation in ACLF mice possibly by inhibiting excessive activation of the cGAS-STING signaling pathway.</p>","PeriodicalId":18962,"journal":{"name":"南方医科大学学报杂志","volume":"44 12","pages":"2291-2299"},"PeriodicalIF":0.0,"publicationDate":"2024-12-20","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11683336/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142896212","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":"[Exocarpium Citri Grandis formula granules alleviate fatty liver disease in Zebrafish by maintaining iron homeostasis and suppressing lipid peroxidation and ferroptosis].","authors":"Yuxue Zahng, Jieying Lan, Xinyi Ma, Qiong Zhou, Mengchen Qin, Lei Gao","doi":"10.12122/j.issn.1673-4254.2024.12.01","DOIUrl":"10.12122/j.issn.1673-4254.2024.12.01","url":null,"abstract":"<p><strong>Objectives: </strong>To investigate the therapeutic effect of Exocarpium Citri Grandis formula granules (ECGFG) on fatty liver disease (FLD) in zebrafish and explore the underlying mechanism.</p><p><strong>Methods: </strong>Nonalcoholic fatty liver disease (NAFLD) and alcoholic fatty liver disease (ALD) models were established in zebrafish larvae at 3 days post fertilization (dpf), in which the treatment efficacy of 16, 32, or 64 μg/mL ECGFG was evaluated by examining zebrafish survival and liver pathologies and using whole-fish oil red O staining and RT-qPCR. The therapeutic mechanism of ECGFG for FLD was investigated using Prussian blue staining, DCFH-DA probe, MDA content detection, RT-qPCR assay and immunohistochemical staining for CAV1.</p><p><strong>Results: </strong>In zebrafish models of NAFLD and ALD, treatment with ECGFG significantly reduced lipid accumulation and the expression levels of FASN, SREBP1, HMGCRA, TNF-α and IL-6, increased the expressions of Apoa1 and PPARα, and reduced iron deposition and the contents of MDA and ROS in the liver. In zebrafish models of NAFLD, treatment with ECGFG at the 3 doses significantly increased hepatic expressions of Tf, TfR, FPN and SLC7A11, and at the doses of 32 and 64 μg/mL, ECGFG obviously increased hepatic expression of GPX4. ALD fish models showed significantly increased hepatic expressions of Tf, TfR and FPN, which were effectively lowered by treatment with ECGFG at the 3 doses. ECGFG did not obviously affect the expression of SLC7A11, but its high dose (64 μg/mL) caused significant elevation of GPX4 expression. Both zebrafish models of NAFLD and ALD showed obviously increased CAV1 expression level in the liver, which was significantly reduced by treatment with 32 and 64 μg/mL ECGFG.</p><p><strong>Conclusions: </strong>In zebrafish models of NAFLD and ALD, ECGFG can alleviate lipid accumulation and inflammatory response and lower the expression level of CAV1 to restore iron homeostasis and suppress lipid peroxidation and ferroptosis in the liver.</p>","PeriodicalId":18962,"journal":{"name":"南方医科大学学报杂志","volume":"44 12","pages":"2265-2275"},"PeriodicalIF":0.0,"publicationDate":"2024-12-20","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11683359/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142896218","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":"[Performance of multi-modality and multi-classifier fusion models for predicting radiation-induced oral mucositis in patients with nasopharyngeal carcinoma].","authors":"Yue Hu, Yu Zeng, Linjing Wang, Zhiwei Liao, Jianming Tan, Yanhao Kuang, Pan Gong, Bin Qi, Xin Zhen","doi":"10.12122/j.issn.1673-4254.2024.12.20","DOIUrl":"10.12122/j.issn.1673-4254.2024.12.20","url":null,"abstract":"<p><strong>Objectives: </strong>To evaluate the performance of different multi-modality fusion models for predicting radiation-induced oral mucositis (RIOM) following radiotherapy in patients with nasopharyngeal carcinoma (NPC).</p><p><strong>Methods: </strong>We retrospectively collected the data from 198 patients with locally advanced NPC who experienced RIOM following radiotherapy at the Affiliated Tumor Hospital of Guangzhou Medical University from September, 2022 to February, 2023. Based on oral radiation dose-volume parameters and clinical features of NPC, basic classification models were developed using different combinations of feature selection algorithms and classifiers and integrated using a multi-criterion decision-making (MCDM)-based classifier fusion (MCF) strategy and its variant, the H-MCF model. The basic classification models, MCF model, the H-MCF model with a single modality or multiple modalities and other ensemble classifiers were compared for performances for predicting RIOM by assessing the area under the ROC curve (AUC), accuracy, sensitivity, and specificity.</p><p><strong>Results: </strong>The H-MCF model, which integrated multi-modality features, achieved the highest accuracy for predicting severe RIOM with an AUC of 0.883, accuracy of 0.850, sensitivity of 0.933, and specificity of 0.800.</p><p><strong>Conclusions: </strong>Compared with each of the individual classifiers, the multimodal multi-classifier fusion algorithm combining clinical and dosimetric modalities demonstrates superior performance in predicting the incidence of severe RIOM in NPC patients following radiotherapy.</p>","PeriodicalId":18962,"journal":{"name":"南方医科大学学报杂志","volume":"44 12","pages":"2434-2442"},"PeriodicalIF":0.0,"publicationDate":"2024-12-20","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11683337/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142895389","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":"[High expression of AURKB promotes malignant phenotype of osteosarcoma cells by activating nuclear factor-κB signaling <i>via</i> DHX9].","authors":"Yanxin Zhong, Yu Liu, Weilai Tong, Xinsheng Xie, Jiangbo Nie, Feng Yang, Zhili Liu, Jiaming Liu","doi":"10.12122/j.issn.1673-4254.2024.12.06","DOIUrl":"10.12122/j.issn.1673-4254.2024.12.06","url":null,"abstract":"<p><strong>Objectives: </strong>To investigate the regulatory mechanism of aurora kinase B (AURKB) for promoting malignant phenotype of osteosarcoma cells.</p><p><strong>Methods: </strong>HA-Vector or HA-AURKB was transfected in 293T cells to identify the molecules interacting with AURKB using immunoprecipitation combined with liquid chromatography-tandem mass spectrometry followed by verification with co-immunoprecipitation and Western blotting. In cultured osteosarcoma cells with lentivirus-mediated RNA interference of AURKB or DHX9 or their overexpression, the changes in cell proliferation, migration, and invasion activities were observed with EDU and Transwell assays. Mechanistic analysis was performed using Co-IP and <i>in vivo</i> ubiquitination experiments to detect the interaction between AURKB and DHX9 and the phosphorylation and ubiquitination levels of DHX9. Western blotting was used to detect the effect of AURKB and DHX9 on activation of nuclear factor-κB (NF-κB) signaling.</p><p><strong>Results: </strong>AURKB was highly expressed in osteosarcoma cell lines, and in osteosarcoma 143B cells, AURKB silencing significantly reduced cell proliferation, migration and invasion abilities. Interactions between AURKB and DHX9 were detected, and they were both highly expressed in osteosarcoma tissues; silencing AURKB reduced the protein expression of DHX9, and AURKB overexpression increased DHX9 phosphorylation. Silencing AURKB did not significantly affect the transcription and translation of DHX9 but accelerated its degradation and ubiquitination. Overexpression of DHX9 effectively reversed the effects of AURKB silencing on IKBα protein and phosphorylated p65, promoted nuclear translocation of p65 to activate the NF-κB signaling pathway, and enhanced the proliferation, migration, and invasion abilities of cultured osteosarcoma cells.</p><p><strong>Conclusions: </strong>AURKB overexpression promotes the malignant phenotype of osteosarcoma cells by activating the NF-κB signaling pathway via regulating DHX9.</p>","PeriodicalId":18962,"journal":{"name":"南方医科大学学报杂志","volume":"44 12","pages":"2308-2316"},"PeriodicalIF":0.0,"publicationDate":"2024-12-20","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11683349/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142896221","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}