南方医科大学学报杂志最新文献

{"title":"[<i>Xiaohe</i> Granule improves breast hyperplasia in rats by promoting mammary epithelial cell apoptosis <i>via</i> activating the ASK1/MKK4/JNK signaling pathway].","authors":"Yu Zhang, Kang Sun, Juda Liu, Shuhan Wang, Jing Pei","doi":"10.12122/j.issn.1673-4254.2026.08.21","DOIUrl":"10.12122/j.issn.1673-4254.2026.08.21","url":null,"abstract":"<p><strong>Objectives: </strong>To explore the mechanism of <i>Xiaohe</i> Granule (XHG) for alleviating mammary hyperplasia in rats.</p><p><strong>Methods: </strong>A non-pregnant female SD rat model of mammary hyperplasia was established by intramuscular injections of estradiol benzoate (0.5 mg/kg) and progesterone (5 mg/kg). With untreated rats as the control group, the rat models were treated with saline (model group) or low-, medium- or high-dose XHG daily gavage, or with high-dose XHG plus oral administration of GS-444217. After the treatments, nipple height, diameter, and uterine index of the rats were measured, and histological changes in the mammary tissue were observed with HE staining. The expressions of Ki-67 and caspase-3 protein in the mammary tissue were detected using immunohistochemistry, and mammary epithelial cell apoptosis was examined using TUNEL staining. Serum levels of E2, P, PRL, FSH, IL-1β, and TNF-α were detected using ELISA, and the expressions of ASK1/MKK4/JNK and apoptosis-related proteins were analyzed using RT-qPCR and Western blotting.</p><p><strong>Results: </strong>Compared with the normal control rats, the rats in the model group showed significantly increased mammary diameter, nipple height, and uterine index with obvious acinar hyperplasia, ductal dilation, and inflammatory cell infiltration in the mammary tissue. The rat models also showed significantly increased Ki-67 expression and serum levels of E2, P, PRL, FSH, IL-1β and TNF-α, markedly increased Bcl-2 expression, and lowered protein levels of p-ASK1/ASK1, p-MKK4/MKK4, p-JNK/JNK, caspase-3, and Bax in the mammary tissue. Treatment with XHG significantly reversed these changes in a dose-dependent manner. Treatment with GS-444217 significantly attenuated the ameliorative effect of high-dose XHG on mammary hyperplasia in the rat models.</p><p><strong>Conclusions: </strong>XHG alleviates mammary hyperplasia in rats by promoting apoptosis of hyperplastic mammary epithelial cells <i>via</i> activating the ASK1/MKK4/JNK signaling pathway.</p>","PeriodicalId":18962,"journal":{"name":"南方医科大学学报杂志","volume":"46 8","pages":"1936-1946"},"PeriodicalIF":0.0,"publicationDate":"2026-08-20","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13458369/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148707091","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":"[Development and validation of a machine learning-based prediction model for fatty liver in Wilson disease].","authors":"Shiheng Shi, Daiping Hua, Shang Xiang, Lanting Sun, Qiaoyu Xuan, Wenming Yang, Han Wang","doi":"10.12122/j.issn.1673-4254.2026.08.13","DOIUrl":"10.12122/j.issn.1673-4254.2026.08.13","url":null,"abstract":"<p><strong>Objectives: </strong>To construct a machine learning-based predictive model for fatty liver in patients with Wilson disease (WD).</p><p><strong>Methods: </strong>Clinical data retrospectively collected from 1862 WD patients at the First Affiliated Hospital of Anhui University of Chinese Medicine were divided into a training set (70%) and a validation set (30%). The least absolute shrinkage and selection operator (LASSO) was employed to screen the key predictive variables. Seven algorithms, namely logistic regression (LR), decision tree (DT), random forest (RF), extreme gradient boosting (XGBoost), light gradient boosting machine (LightGBM), support vector machine (SVM), and artificial neural network (ANN), were compared for their performance using the area under the receiver-operating characteristic (ROC) curve (AUC), precision-recall (PR) curve, calibration curves, and decision curve analysis (DCA). The contribution of each feature to model prediction was assessed using SHAP analysis.</p><p><strong>Results: </strong>Among the 1862 WD patients, 1296 (69.60%) were complicated with fatty liver. LASSO regression identified platelet count (PLT), red cell distribution width (RDW), alanine aminotransferase (ALT), total bile acids (TBA), type IV collagen (CIV), and indirect bilirubin (IBIL) as the key predictive variables. The LightGBM model demonstrated optimal overall performance, with a training set AUC of 0.826 (95% <i>CI</i>: 0.801-0.849) and good calibration (Brier score 0.143); its validation set AUC was 0.815 (95% <i>CI</i>: 0.776-0.852), and the PR curve showed a high average precision (AP=0.903) with good calibration (Brier score 0.138) and significant clinical net benefit across all the diagnostic thresholds as confirmed by DCA. SHAP analysis indicated that ALT, IBIL, TBA, and CIV all had significant positive effects on model outputs, while RDW and PLT contributed minimally to the cumulative predictive outcomes.</p><p><strong>Conclusions: </strong>Among the 7 predictive models for fatty liver in WD patients, the LightGBM model demonstrates superior performance to potentially facilitate early screening and risk stratification of WD patients at high risk of fatty liver.</p>","PeriodicalId":18962,"journal":{"name":"南方医科大学学报杂志","volume":"46 8","pages":"1861-1869"},"PeriodicalIF":0.0,"publicationDate":"2026-08-20","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13458563/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148707123","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>Wuyou</i> Decoction alleviates hippocampal neuronal injury and improves synaptic plasticity in rats with chronic sleep deprivation by inhibiting ferroptosis <i>via</i> activating the Nrf2/HO-1 pathway].","authors":"Liling He, Dan Wu, Bixuan Lai, Qixuan Niu, Junhua Chen, Jianhong Gao, Qinghua Long, Zhengyu Wang","doi":"10.12122/j.issn.1673-4254.2026.08.04","DOIUrl":"10.12122/j.issn.1673-4254.2026.08.04","url":null,"abstract":"<p><strong>Objectives: </strong>To investigate the mechanism of <i>Wuyou</i> Decoction (WYD) for ameliorating hippocampal neuron damage and protecting synaptic plasticity in rats with chronic sleep deprivation (CSD).</p><p><strong>Methods: </strong>Fifty SD rats were randomly divided into normal control group, CSD model group, and low-, medium-, and high-dose WYD treatment groups (<i>n</i>=10). Except for those in the control group, all the rats were subjected to CSD modeling using the horizontal platform method. Cognitive function of the rats was assessed with Morris water mazetest, and hippocampal pathology, synaptic structure, iron content, oxidative stress markers, and ferroptosis-related protein expressions were evaluated. Molecular docking study was performed to explore the interactions between WYD components and ferroptosis-related proteins.</p><p><strong>Results: </strong>CSD induced significant cognitive impairment and neuronal and synaptic damage in the rat models, causing also increased oxidative stress and iron deposition and upregulated Nrf2 and HO-1 expressions. Treatment with WYD, especially at the medium dose, significantly improved learning and memory abilities of the rat models, alleviated neuronal degeneration, restored synaptic structure, reduced iron accumulation and oxidative stress, and upregulated ferroptosis-related markers as well as Nrf2 and HO-1 expressions.</p><p><strong>Conclusions: </strong>WYD, optimally at the medium dose, alleviates CSD-induced cognitive impairment in rats by inhibiting ferroptosis, reducing neuronal damage, and enhancing synaptic repair via activation of the Nrf2/HO-1 signaling pathway.</p>","PeriodicalId":18962,"journal":{"name":"南方医科大学学报杂志","volume":"46 8","pages":"1754-1763"},"PeriodicalIF":0.0,"publicationDate":"2026-08-20","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13458619/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148707145","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>Liuwei Dihuang</i> Pill regulate osteoclast membrane fusion to improve postmenopausal osteoporosis in mice: the CLCF1/NFATc1 signaling axis as a therapeutic target].","authors":"Ruoxi Zheng, Lihua Xie, Xiaobin Huang, Jirong Ge","doi":"10.12122/j.issn.1673-4254.2026.08.03","DOIUrl":"10.12122/j.issn.1673-4254.2026.08.03","url":null,"abstract":"<p><strong>Objectives: </strong>To explore the mechanism of <i>Liuwei Dihuang</i> Pill (LWDHW) for improving postmenopausal osteoporosis (PMOP).</p><p><strong>Methods: </strong>Thirty female C57BL/6 mice were randomized equally into sham-operated group, PMOP model group, and LWDHW treatment group. The mice in the latter two groups underwent ovariectomy to simulate PMOP, followed by gavage of normal saline and LWDHW (twice daily) for 60 days, respectively. Bone mineral density (BMD) of the mice was detected, and TRAP staining was used to observe osteoclast and osteoclast maturation in the tibia tissue. In RANKL-induced RAW264.7 cells with or without lentivirus-mediated CLCF1 knockdown, the effects of incubation with normal rat serum or LWDHW-medicated rat serum on cell membrane fusion rate and F-actin loop formation were observed using immunofluorescence staining with phalloidin peptide; the mRNA and protein expressions of CLCF1, NFATc1, DC-STAMP, OC-STAMP and ATP6V0D2 were detected using RT-qPCR and Western blotting.</p><p><strong>Results: </strong>In PMOP mice, LWDHW treatment significantly increased BMD, reduced osteoclast maturation, osteoclast membrane fusion rate, and F-actin ring formation, upregulated the mRNA and protein expressions of CLCF1 in tibial tissues, and lowered the expressions of NFATc1, DC-STAMP, OC-STAMP and ATP6V0D2. In RANKL-induced RAW264.7 cells with CLCF1 knockdown, treatment with LWDHW-medicated rat serum significantly decreased osteoclast membrane fusion rate, F-actin ring formation, and the expressions of NFATc1, DC-STAMP, OC-STAMP and ATP6V0D2.</p><p><strong>Conclusions: </strong>LWDHW improves PMOP in mice by regulating osteoclast membrane fusion through upregulating CLCF1 expression and downregulating NFATc1, DC-STAMP, OC-STAMP and ATP6V0D2 expressions.</p>","PeriodicalId":18962,"journal":{"name":"南方医科大学学报杂志","volume":"46 8","pages":"1743-1753"},"PeriodicalIF":0.0,"publicationDate":"2026-08-20","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13458560/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148707129","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":"[Reflections on surgical management strategies for locally advanced gastric cancer after neoadjuvant immunotherapy].","authors":"Yijie Xi, Yuxuan Li, Lifan Lin, Lu Chen, Xin Yuan, Liying Zhao, Hao Liu, Tian Lin, Mingli Zhao, Wu Zhong, Yanfeng Hu, Weihong Guo","doi":"10.12122/j.issn.1673-4254.2026.08.25","DOIUrl":"10.12122/j.issn.1673-4254.2026.08.25","url":null,"abstract":"<p><p>Neoadjuvant immunotherapy is reshaping the treatment landscape of locally advanced gastric cancer (GC). The central clinical challenge has expanded from whether immunotherapy can enhance treatment efficacy to accurate identification of patients who are most likely to benefit and optimization of the subsequent surgical intervention. Accumulating evidence indicates that perioperative immunotherapy-based regimens can improve pathological complete response (pCR) rates and event-free survival (EFS) of the patients, promoting a shift from conventional chemotherapy plus radical surgery toward biomarker-guided, integrated precision treatment. For therapeutic stratification, microsatellite instability (MSI) status, programmed death-ligand 1 (PD-L1) expression, and refined human epidermal growth factor receptor 2 (HER2) classification have emerged as key indicators for predicting treatment response and selecting eligible patients. Meanwhile, treatment response assessment has evolved beyond conventional radiological evaluation to a multimodal framework incorporating pathological assessment, liquid biopsy, endoscopy, functional imaging, and artificial intelligence (AI)-assisted analysis, thereby providing more comprehensive support for individualized therapeutic decision-making. However, improved treatment efficacy has also raised new questions for surgical management. In particular, discordant responses between primary tumors and regional lymph nodes have challenged whether D2 radical gastrectomy planned according to pretreatment clinical staging remains the optimal surgical strategy. This review systematically summarizes the evolution of neoadjuvant treatment strategies for locally advanced GC, comprehensive response assessment, and redefinition of gastrectomy extent and lymphadenectomy strategy. Looking forward, with the clinical translation of emerging therapeutic targets such as Claudin 18.2 (CLDN18.2) and fibroblast growth factor receptor 2 (FGFR2), together with the maturation of AI-driven multimodal assessment systems, GC surgery may move beyond traditional anatomical boundaries. This transition potentially enables \"maximally tolerated radical resection\" to \"function-preserving surgery guided by biological radicality\", ultimately providing truly individualized precision surgical treatment for patients with locally advanced GC.</p>","PeriodicalId":18962,"journal":{"name":"南方医科大学学报杂志","volume":"46 8","pages":"1981-1992"},"PeriodicalIF":0.0,"publicationDate":"2026-08-20","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13458701/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148707159","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":"[Overexpression of miR-183-5p enhances malignant phenotype and inhibits ferroptosis of triple-negative breast cancer cells by negatively regulating KLHL24].","authors":"Kun Wang, Shunfu Hou, Yong Li, Qinghua Liu, Chonggao Yin, Hongli Li","doi":"10.12122/j.issn.1673-4254.2026.08.07","DOIUrl":"10.12122/j.issn.1673-4254.2026.08.07","url":null,"abstract":"<p><strong>Objectives: </strong>To investigate the effects of miR-183-5p overexpression on proliferation, invasion, migration, and ferroptosis of triple-negative breast cancer (TNBC) cells and the role of Kelch-like protein 24 (KLHL24) in mediating these effects.</p><p><strong>Methods: </strong>Bioinformatics analyses were conducted to screen differentially expressed genes in breast cancer (BRCA) and predict the target gene of miR-183-5p. RT-qPCR was used to verify miR-183-5p expression in normal breast epithelial and TNBC cell lines. Dual-luciferase reporter assay was performed to confirm direct binding of miR-183-5p to 3'-UTR of KLHL24. Western blotting was used to detect KLHL24 expression in different TNBC cells after transfection with miR-183-5p-overexpressing plasmids. MDA-MB-231 cells were co-transfected with NC-miR and NC-KLHL24, oe-miR-183-5p and NC-KLHL24, NC-miR and oe-KLHL24, or oe-miR-183-5p and oe-KLHL24 plasmids, and the changes in cell proliferation, migration and invasion were examined using EdU, Transwell, and wound healing assays. Western blotting was used to detect the changes in expressions of ferroptosis-related proteins (GPX4, SLC7A11, and Nrf2), and ROS, LPO, MDA, and GSH levels in the transfected cells were determined.</p><p><strong>Results: </strong>The expression of miR-183-5p was significantly elevated in BRCA tissues and TNBC cell lines, and MDA-MB-231 cells showed the highest miR-183-5p expression. Dual-luciferase reporter assay confirmed the direct binding of miR-183-5p to 3'-UTR of KLHL24. Overexpression of miR-183-5p significantly downregulated KLHL24 expression. In TNBC cells, miR-183-5p overexpression obviously promoted cell proliferation, invasion, and migration, upregulated the expressions of GPX4, SLC7A11 and Nrf2, reduced the levels of ROS, LPO and MDA, and increased the level of GSH (<i>P</i><0.0001); these effects were significantly reversed by co-transfection of the cells with KLHL24-overexpressing plasmids.</p><p><strong>Conclusions: </strong>Overexpression of miR-183-5p enhances TNBC cell proliferation, invasion, migration and inhibits ferroptosis by negatively regulating KLHL24.</p>","PeriodicalId":18962,"journal":{"name":"南方医科大学学报杂志","volume":"46 8","pages":"1790-1798"},"PeriodicalIF":0.0,"publicationDate":"2026-08-20","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13458494/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148706954","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>LCN2</i> knockout protects endothelial barrier function in mice with sepsis-induced acute lung injury by regulating the NF-κB signaling pathway].","authors":"Mengjie Yu, Anbo Zhao, Yixuan Hao, Yiren Wang, Yuexian Liu, Hongwei Ye, Qin Gao","doi":"10.12122/j.issn.1673-4254.2026.08.06","DOIUrl":"10.12122/j.issn.1673-4254.2026.08.06","url":null,"abstract":"<p><strong>Objectives: </strong>To investigate the protective effect of lipocalin-2 (LCN2) gene knockout against sepsis-induced acute lung injury (ALI) and vascular endothelial dysfunction in mice and the mediating role of the nuclear factor-κB (NF-κB) signaling pathway.</p><p><strong>Methods: </strong>Wild-type (WT) C57BL/6 mice receiving sham operation or cecal ligation and puncture (CLP) to induce sepsis were randomized into 3 subgroups for intraperitoneal injections of saline, PDTC, or Bay 11-7082 (<i>n</i>=10). Twenty LCN2 knockout (LCN2KO) mice were randomized for sham operation or CLP modeling. Pulmonary histopathological changes, lung wet-to-dry (W/D) ratio, lung index, Evans blue extravasation, and serum TNF-α and IL-6 levels in the mice were assessed. The colocalization of NF-κB, ICAM-1, and VCAM-1 with CD31 were analyzed using immunofluorescence staining, and endothelial cell apoptosis was examined with TUNEL/CD31 double staining. Western blotting and co-immunoprecipitation assay were performed to analyze the protein expressions of LCN2, p-P65/P65, ICAM-1, VCAM-1 and VE-cadherin and the interaction between LCN2 and P65.</p><p><strong>Results: </strong>The WT mice receiving CLP showed severe lung structural damage with obvious edema and inflammation. In contrast, both the LCN2KO mouse and PDTC-treated WT mouse models of CLP showed milder lung injury with lower W/D ratio, lung index, Evans blue leakage, serum TNF‑α and IL-6 levels and markedly reduced colocalization signals of NF-κB, ICAM-1, and VCAM-1 with CD31. CLP resulted in significantly increased expression levels of LCN2, p-P65/P65, ICAM-1, and VCAM-1, lowered VE-cadherin levels, and enhanced endothelial cell apoptosis, and all these changes were significantly ameliorated in LCN2KO mice and WT mice with NF‑κB inhibitor treatment. Co-immunoprecipitation results suggested the interaction between lung LCN2 and P65. Bay 11-7082 significantly reduced inflammatory cytokine production, downregulated p-P65 expression and its downstream adhesion molecules, and restored VE-cadherin expression.</p><p><strong>Conclusions: </strong>LCN2 knockout alleviates sepsis-induced ALI and vascular endothelial dysfunction in mice by inhibiting NF-κB signaling.</p>","PeriodicalId":18962,"journal":{"name":"南方医科大学学报杂志","volume":"46 8","pages":"1779-1789"},"PeriodicalIF":0.0,"publicationDate":"2026-08-20","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13458366/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148707097","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 ameliorates cognitive impairment and suppresses TLR4/MyD88/NF-κB pathway-mediated astrocyte activation in rats with vascular dementia].","authors":"Jianhong Gao, Ce Shi, Weiran Li, Xiang Shang, Fei Wang, Qiqi Yang, Fei Li","doi":"10.12122/j.issn.1673-4254.2026.08.09","DOIUrl":"10.12122/j.issn.1673-4254.2026.08.09","url":null,"abstract":"<p><strong>Objectives: </strong>To investigate the effects of electroacupuncture (EA) on cognitive function and neuroinflammation in a rat model of vascular dementia (VD) and the underlying mechanism.</p><p><strong>Methods: </strong>Sixty male SD rats were randomly assigned to sham-operated group (<i>n</i>=10) and VD model group (<i>n</i>=50) receiving bilateral common carotid artery occlusion. Thirty rats with successful VD modeling were randomized into model group, EA group, and donepezil treatment group (<i>n</i>=10). EA treatment was administered at the acupoints Baihui (GV20) and Shenting (GV24) with a disperse-dense wave (2/15 Hz, 1 mA, 30 min/day), and donepezil was given by gavage at 0.45 mg/kg. Both interventions lasted 28 days. Cognitive function of the rats was assessed using Morris water maze test, and neuronal pathologies were observed using HE and Nissl staining. GFAP-labeled astrocyte activation was assessed by immunohistochemistry, and astrocytic ultrastructure was examined with transmission electron microscopy. GFAP/p-NF-κB colocalization was detected by immunofluorescence staining. Hippocampal IL-1β, IL-6, and TNF-α levels were measured by ELISA, and the protein expression levels of C3, S100A10, TLR4, and MyD88 and the p-NF-κB/NF‑κB ratio were detected by Western blotting.</p><p><strong>Results: </strong>Compared with the sham-operated rats, VD rats showed significant cognitive impairment, obvious neuronal disorganization and pyknosis in the hippocampus, excessive astrocyte activation, increased GFAP/p-NF‑κB colocalization, inflammatory cytokine levels and expressions of C3 and TLR4/MyD88/NF-κB pathway proteins, and decreased expression of S100A10. Treatment with EA and donepezil significantly improved the performance of the rats in Morris water maze test, alleviated neuronal injury, inhibited astrocyte overactivation and ultrastructural damage, reduced inflammatory cytokine levels, expressions of C3, TLR4, and MyD88 proteins and the p-NF-κB/NF-κB ratio, and increased the expression of S100A10 in the hippocampus.</p><p><strong>Conclusions: </strong>EA at GV20 and GV24 improves cognitive impairment and attenuate neuroinflammation in VD rats possibly by inhibiting TLR4/MyD88/NF-κB signaling and regulating astrocytic A1/A2-like phenotypic imbalance.</p>","PeriodicalId":18962,"journal":{"name":"南方医科大学学报杂志","volume":"46 8","pages":"1814-1822"},"PeriodicalIF":0.0,"publicationDate":"2026-08-20","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13458684/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148706707","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":"[Early mean arterial pressure variability and in-hospital mortality from severe subarachnoid hemorrhage: a U-shaped association based on MIMIC-IV and eICU-CRD data].","authors":"Haiyan Xiang, Xiujuan Chen, Laiyou Wang, Weihua Lai","doi":"10.12122/j.issn.1673-4254.2026.08.05","DOIUrl":"10.12122/j.issn.1673-4254.2026.08.05","url":null,"abstract":"<p><strong>Objectives: </strong>To explore the association between mean arterial pressure variability (MBPV) and in-hospital mortality in patients with non-traumatic subarachnoid hemorrhage (NSAH).</p><p><strong>Methods: </strong>This study was conducted using the data of NSAH patients from the Medical Information Mart for Intensive Care IV (MIMIC-IV) database and the eICU-CRD, with the final sample size ranging from 1345 to 1820 subjects across different MBPV indicators. Mean arterial pressure (MAP) data within 24, 48, and 72 h after admission were extracted, and the standard deviation (SD), average real variability (ARV), range, and successive variability (SV) of MBPV were calculated. Restricted cubic spline (RCS) combined with Cox regression analysis was adopted to evaluate the nonlinear correlation and determine the risk inflection point using piecewise regression. Time-dependent Cox regression was performed only for variables violating the proportional hazards assumption. Two sensitivity analyses were conducted (excluding patients with surgery within 72 h of admission and those with missing data of medication) to validate the robustness of the results. The primary outcome was all-cause in-hospital mortality.</p><p><strong>Results: </strong>MBPV at all time windows showed a U-shaped nonlinear association with in-hospital mortality of the patients (all <i>P</i><0.05), and the strongest association was found at 24 h. The inflection point of MBP SD was 8.9, and either excessively low or high fluctuation increased the mortality risk. Time-dependent analysis showed that ARV and SV of MBPV became more hazardous after 4-7 days, while its SD and range were risky mainly within the first 14 days. Both sensitivity analyses confirmed the robustness of the main results.</p><p><strong>Conclusions: </strong>Early MBPV presents a U-shaped association with in-hospital mortality from NSAH, and moderate fluctuation predicts better prognosis. MBP SDs within 24 and 72 h are the most robust indicators, and the former can serve as the preferred indicator for early blood pressure monitoring.</p>","PeriodicalId":18962,"journal":{"name":"南方医科大学学报杂志","volume":"46 8","pages":"1764-1778"},"PeriodicalIF":0.0,"publicationDate":"2026-08-20","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13458493/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148707117","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":"[Association between 473 gut microbiota and Alzheimer's disease: a Mendelian randomization mediation analysis of 233 circulating metabolites].","authors":"Dechen Li, Yanjie Li, Xinyu Yang, Yawen Wang, Yanfei Qu","doi":"10.12122/j.issn.1673-4254.2026.08.20","DOIUrl":"10.12122/j.issn.1673-4254.2026.08.20","url":null,"abstract":"<p><strong>Objectives: </strong>To investigate the causal associations between gut microbiota (GM) and Alzheimer's disease (AD) and the mediating role of circulating metabolites using Mendelian randomization (MR) analysis.</p><p><strong>Methods: </strong>A two-sample MR analysis was conducted based on genome-wide association study (GWAS) summary data. Valid instrumental variables for 473 GM taxa and 233 circulating metabolites were selected, and the inverse-variance weighted (IVW) method was used as the primary analytical approach, with MR-Egger regression and weighted median method as the complementary analyses. Multiple sensitivity analyses were conducted to assess the robustness of the results, and reverse MR analyses were used to verify the direction of causality. Mediation MR analyses were performed to determine the mediating effects of the circulating metabolites.</p><p><strong>Results: </strong>A positive causal association was identified between the abundance of <i>Negativibacillus massiliensis</i> and the risk of AD (OR=1.204, 95% <i>CI</i>: 1.020-1.421,<i>P</i>=0.028), and the results were stable and reliable as confirmed by sensitivity analyses (<i>P</i>>0.05). Reverse MR analysis revealed no significant causal effect of AD on the abundance of <i>Negativibacillus massiliensis</i> (<i>P</i>=0.678). Mediation MR analysis showed that the indirect effect mediated by free cholesterol to total lipid ratio in very small very-low-density lipoprotein (v-VLDL FC/TL) accounted for 6.63% of the total effect of <i>Negativibacillus massiliensis</i> on AD.</p><p><strong>Conclusions: </strong>From a genetic causal inference perspective, <i>Negativibacillus massiliensis</i> is likely associated with an increased risk of AD, and v-VLDL FC/TL may partially mediate this association, suggesting their potential as targets for AD prevention and treatment.</p>","PeriodicalId":18962,"journal":{"name":"南方医科大学学报杂志","volume":"46 8","pages":"1926-1935"},"PeriodicalIF":0.0,"publicationDate":"2026-08-20","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13458591/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148707152","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}