👤 Xiaoping Hong

Chemotherapy-related cognitive impairment (CRCI) is a prevalent and distressing issue among older adults with cancer, affecting quality of life and treatment adherence. While its mechanisms remain unclear, biomarkers have emerged as promising tools for understanding CRCI. This systematic review aimed to explore the relationships between cognitive impairment following chemotherapy and biomarkers in older patients with cancer. A comprehensive search was conducted through December 2024 across PubMed, CINAHL, Embase, PsycINFO, and the Cochrane Library. An additional hand search was performed through July 2025. The focus was on patients over 60 years old with chemotherapy-related cognitive impairment and associated biomarkers. The review adhered to PRISMA 2020 guidelines, and the methodological quality of included studies was assessed using the Joanna Briggs Institute checklist to ensure rigor and reliability. Six of the initial 6,324 articles met the inclusion criteria, and seven additional studies were identified through manual searching. In total, 13 studies identified several biomarkers associated with CRCI in older patients with cancer. These included serum hemoglobin, brain-derived neurotrophic factor, percent cerebral oxyhemoglobin, functional network connectivity, and individual alpha peak frequency. This review highlights several biomarkers potentially associated with CRCI in older patients with cancer, though consistent and definitive biomarkers remain elusive. Further research is needed to clarify the biological mechanisms underlying CRCI and inform the development of interventions aimed at preventing cognitive decline in this vulnerable population. The identification of validated biomarkers will be critical for advancing personalized nursing and improving clinical outcomes in older adults with cancer. Show less

Premature ejaculation (PE) accompanied by anxiety or depression is a complex clinical condition at the intersection of male reproductive dysfunction and emotional disorders. Increasing evidence suggests that serotonin (5-HT) and brain-derived neurotrophic factor (BDNF) play central and interrelated roles in its pathogenesis. In this review we examine the bidirectional functions of 5-HT and BDNF in both the reproductive and nervous systems, highlighting their importance in regulating ejaculation, emotional stability, and synaptic plasticity. A comprehensive literature search (2010-2025) was conducted across multiple databases using relevant Medical Subject Headings (MeSH) terms, including pertinent original research and review articles, to synthesize the roles and regulatory pathways of 5-HT and BDNF in PE with comorbid anxiety or depression. We summarize the shared and distinct roles of 5-HT and BDNF in maintaining physiological balance across these systems and focus on their involvement in the major pathological processes underlying PE with anxiety or depression, including neurotransmitter imbalance, neuroendocrine dysregulation, inflammation, and oxidative stress. Furthermore, we outline the related signaling pathways through which 5-HT and BDNF exert their effects and interact. We also evaluate current pharmacological and non-pharmacological interventions targeting these molecules, demonstrating their potential to improve both ejaculatory control and emotional symptoms, and critically appraise selective serotonin reuptake inhibitor (SSRI)-related risks and highlighted the need for individualized dosing and monitoring. Emerging evidence suggests that Traditional Chinese Medicine formulations can extend intravaginal ejaculatory latency and mitigate mood symptoms and may serve as stand-alone or adjunctive options to reduce reliance on selective serotonin reuptake inhibitors (SSRIs). Overall, 5-HT and BDNF are not only deeply involved in the biological mechanisms of PE with comorbid psychological disorders, but also represent promising biomarkers and therapeutic targets, and their integrative neuro-reproductive regulatory functions provide new insights into the diagnosis and treatment of this multifaceted condition. Show less

Fatty acid-binding proteins (FABPs) influence cellular energy metabolism by regulating fatty acid kinetics. They also play a vital role in neuronal apoptosis following cerebral infarction. Resveratrol (RSV) has demonstrated neuroprotective effects in ischemic stroke; however, its regulatory impact on FABPs and associated pathways requires further investigation. This study aimed to explore the potential mechanisms by which RSV protects ischemic stroke neurons by regulating fatty acid metabolism. A weighted gene co-expression network analysis revealed significant enrichment of FABP5 in fatty acid metabolism-related pathways in rats with middle cerebral artery occlusion (MCAO). Modulating FABP5 expression level may influence post-infarction neuronal recovery. Molecular docking experiments demonstrated that RSV exhibited strong binding affinity with FABP5. In the MCAO-group of rats, administering different doses of RSV led to a significant decrease in cerebral infarct area and improved neurological function with increased RSV doses. Concurrently, the expression of FABP5 and neuron-specific enolase in brain tissue decreased, whereas the expression of the brain-derived neurotrophic factor increased and neuronal morphology improved. Further experiments using FABP5 overexpression and inhibition models revealed that FABP5 overexpression exacerbated neuronal apoptosis and suppressed the expression of adenosine monophosphate (AMP)-activated protein kinase (AMPK) protein, whereas FABP5 inhibition reduced neuronal apoptosis and enhanced AMPK protein expression. RSV downregulates FABP5 expression in cerebral infarction tissues and potentially mediates the AMPK-related pathways to ameliorate neuronal apoptosis. Show less

Chronic neuroinflammation is associated with comorbidities in people with HIV (PWH) on antiretroviral therapy (ART). While cannabis use is associated with reduced neuroinflammation and neurocognitive impairment (NCI) in PWH, the underlying mechanisms are unknown. To address this gap in knowledge, we analyzed monocyte-derived macrophages (MDMs) from a cohort of 50 PWH and 33 people without HIV (mean age: 61.9 years), categorized by frequency of cannabis use (naïve/low, moderate, daily). We performed immunocytochemistry, RNA sequencing, and qPCR on MDMs and quantified related biomarkers in donor plasma. In this cohort study, daily cannabis use in PWH was associated with less global neurocognitive deficits, and with an anti-inflammatory immunometabolic-phenotype in MDMs characterized by (1) a metabolic shift from glycolysis to oxidative phosphorylation, (2) higher mitochondrial numbers, (3) altered cytokine profiles (pro-inflammatory downregulation, anti-inflammatory upregulation), and (4) higher brain-derived neurotrophic factor (BDNF) expression. These cellular changes were corroborated by a plasma biomarker profile in PWH including (1) lower levels of growth differentiation factor 15 and soluble triggering receptor expressed on myeloid cells 2, and (2) higher mature BDNF/precursor BDNF ratios that correlated with better cognition. Thus, cannabis use may mitigate NCI in PWH by immunometabolically reprogramming MDM function towards an anti-inflammatory and neuroprotective state. Show less

Valproic acid (VPA) is recognized for its neurotrophic properties and is widely used in psychiatric and peripheral disorders, while dextromethorphan (DM) has demonstrated anti-inflammatory and neuroprotective effects. This study examined whether adjunctive DM provides additional benefits on cognitive or immunomodulatory beyond standard VPA treatment in bipolar disorder (BD). BD aged 20-65 received open-label VPA (500-2500 mg/day; target blood level 50-100 μg/dl) for one week and were then randomized to VPA plus placebo (BDVPA) or VPA plus extended-release DM (BDVPA + DM; 30 or 60 mg/day) for twelve weeks. Neuropsychological measures (Continuous Performance Test, CPT; Wechsler Memory Scale-Revised, WMS-R), symptom severity, cytokines, and BDNF were assessed at baseline and post-treatment. A total of 109 participants (mean age 31.04 years, SD = 10.04) were enrolled; 96 completed cognitive testing and blood sampling (66 BD Show less

Alzheimer's disease (AD) is characterized by progressive cognitive decline and memory dysfunction, with prominent roles in cholinergic deficits and synaptic plasticity impairments. Vitisin B, a resveratrol tetramer derived from Vitis vinifera, exhibits potent antioxidant and neuroprotective properties. However, its potential to influence cognitive function in AD models remains inadequately explored. In this study, we first tested vitisin B in an in vitro model using SH-SY5Y cells exposed to scopolamine-induced cytotoxicity, where vitisin B significantly enhanced cell viability and promoted cell survival. We evaluated its therapeutic potential in vivo using both systemic administration and direct delivery into the third ventricle of the brain in a scopolamine-induced AD mouse model. Across both administration routes, vitisin B exerted a broad pro-cognitive effect, restoring multiple domains of learning and memory disrupted by scopolamine. Vitisin B recovered spatial working memory in the Y-maze, normalized exploratory activity in the open field, improved recognition memory in the novel object recognition (NOR) test, and enhanced long-term memory retention in the passive avoidance assay. This treatment restored cognitive function, alleviated cholinergic deficits, increased hippocampal brain-derived neurotrophic factor (BDNF) levels, and enhanced synaptic plasticity. These results suggest that vitisin B exerts reliable cognitive and neuroprotective effects through both systemic and cerebral administration, highlighting its potential as a promising therapeutic compound for restoring cholinergic function and enhancing hippocampal synaptic plasticity in AD. Show less

Computerized cognitive training allows real-time tracking of performance metrics that may serve as digital biomarkers. This study investigated the value of a novel in-game digital biomarker, RTACC (Reaction Time-Accuracy Correlation), the correlation between reaction time and accuracy, using data from 130 participants with mild cognitive impairment enrolled in the intervention arm of the SUPERBRAIN-MEET randomized controlled trial. Participants underwent a 24-week multi-domain intervention, consisting of computerized cognitive training, physical exercise, nutritional education, vascular/metabolic risk management, and motivation enhancement. RTACC was derived from task-level RT and accuracy and examined in relation to cognitive and biomarker outcomes. Linear regression analysis revealed a significant association between RTACC and changes in Repeatable Battery for the Assessment of Neuropsychological Status scores from baseline to 24 weeks (beta coefficient = -11.90 ± 3.78, T = - 3.14, P = 0.002). RTACC also showed a marginal effect on changes in brain-derived neurotrophic factor levels (beta coefficient = - 3.13 ± 1.64, P = 0.057). Logistic regression analysis demonstrated that RTACC combined with clinical information identified good responders with an area under the receiver operating characteristic curve of 0.73 (95% CI: 0.62-0.84). These findings suggest that this in-game digital biomarker (RTACC) may help identify individuals likely to benefit from multi-domain intervention. Show less

Alzheimer's disease (AD) and osteoporosis are common age-related degenerative diseases. Emerging evidence suggests that amyloid-β (Aβ) deposition may contribute to the pathogenesis of both conditions. This study investigated whether probucol could alleviate AD-associated bone loss and Aβ42-induced osteoblast dysfunction, and further explored the underlying mechanisms. Female mice were divided into four groups (n = 5 per group): C57BL/6 wild-type (WT), WT treated with probucol (WT + PBC), APP/PS1 transgenic (AD) mice, and AD treated with probucol (AD+PBC). Bone mineral density (BMD) was assessed by micro-CT. Levels of pro-inflammatory cytokines (IL-1β, IL-6, TNF-α) along with bone metabolism markers including fibroblast growth factor 23 (FGF23), sclerostin, and brain-derived neurotrophic factor (BDNF) in bone and brain tissues were measured by ELISA. FOXO3a was knocked down in the bone marrow of APP/PS1 mice via stereotactic injection of lentiviral vectors. Expression of APP and FOXO3a in bone tissue was evaluated using RT-qPCR and Western blotting (WB). Mitochondrial damage in osteoblasts and neuronal cells was assessed by transmission electron microscopy (TEM). In vitro study, osteoblast differentiation and mineralization deficits were evaluated using Alizarin Red staining. WB was used to measure the expression of AKT, FOXO3a, autophagy and apoptosis related proteins. Probucol attenuated bone loss and mitochondrial damage in both APP/PS1 and FOXO3a-knockdown APP/PS1 mice, and improved cognitive impairment and neuronal ultrastructure in APP/PS1 mice. Furthermore, probucol attenuated Aβ42-induced osteoblast differentiation and mineralization via the AKT/FOXO3a signaling pathway in vitro. These findings demonstrate that probucol ameliorates AD-associated bone loss and Aβ42-induced osteoblast impairments by regulating AKT/FOXO3a signaling pathway. Show less

Reliable prediction of reproductive toxicity remains a critical challenge in drug development and environmental safety. Here, a biomarker-integrated, fluorescent reporter-based reproductive organ-on-a-chip platform that recapitulates the multicellular composition, 3D architecture, endocrine signaling, and cyclic dynamics of the human menstrual cycle, is presented. The system is constructed using primary human theca, granulosa, endometrial stromal and stem cells, vascular endothelial cells, uterine macrophages, and myometrial smooth muscle cells, compartmentalized within collagen-hyaluronic acid hydrogels. Early-response toxicity biomarkers-ANGPTL4 (ovary) and SERPINB2 (endometrium)-are genetically linked to mCherry or GFP fluorescent reporters, enabling real-time, cell-type-specific visualization of toxicant-induced stress. Transcriptomic profiling, KEGG pathway enrichment, and gene knockdown studies confirm ANGPTL4 and SERPINB2 as functional mediators of toxic injury, not just passive indicators. Upon exposure to dioxin and other reproductive toxicants, the platform shows strong, region-specific fluorescent responses that preceded changes detected by conventional cytotoxicity assays. This system demonstrates high sensitivity, temporal precision, and mechanistic insight, offering a scalable and physiologically relevant tool for high-content reproductive toxicology screening. Furthermore, it supports endocrine crosstalk between the ovary and uterus, and dynamic responses across the menstrual cycle, enabling future applications in personalized toxicity prediction and preclinical safety evaluation. Show less

Breast cancer is the most frequently diagnosed cancer, with metastasis accounting for the majority of cancer-related deaths. The mechanisms of early-stage breast cancer metastasis to regional immune sites like lymph nodes remain elusive. Here, we performed an in-depth proteomic and phosphoproteomic analysis of a substantial series of breast cancer samples, alongside genomic and transcriptomic evaluations. This cohort encompasses 195 specimens: 65 primary breast tumors, their corresponding normal tissues, and metastatic axillary lymph nodes. We offer an overview of the molecular alterations at the transcriptomic, proteomic, and phosphoproteomic levels during lymph node metastasis. Notably, the findings indicate that regional lymph node metastasis is primarily influenced by proteomic and phosphoproteomic alterations, rather than genomic or transcriptomic changes. We found the ANGPTL4 and HMGB1 could serve as the biomarker of lymph node metastasis. Data analysis and cell experiments involving silencing of the alternative splicing factor HNRNPU demonstrated that alternative splicing plays a significant role in modulating protein expression, phosphorylation profiles and cell proliferation. The key phosphorylation sites, including MARCKSL1-S104 and FKBP15-S320, as well as the upstream kinase PRKCB, were identified as playing crucial roles in breast cancer lymph node metastasis. Targeted intervention of the kinase PRKCB resulted in effectively suppressing the proliferation and metastasis of breast cancer tumor cells. Immune profiling analysis and experimental validation of breast cancer cell cocultured with CD8+ T cell reveals correlations between phosphorylation of MARCKSL1-S104 and FKBP15-S320 with immune checkpoint PD-L1 expression, and their impact on tumor cell apoptosis, suggesting a potential mechanism of immune evasion in metastasis. This study systematically characterizes the molecular landscape and features of primary breast tumors and their matched metastatic lymph nodes. These insights enhance our understanding of early-stage breast cancer metastasis and may pave the way for improved diagnostic tools and targeted therapeutic strategies. Show less

To evaluate the lipid-lowering efficacy, safety, and adherence of switching from moderate- or low-intensity statin monotherapy to ezetimibe 10 mg/rosuvastatin 2.5 mg in Korean patients with type 2 diabetes mellitus (T2DM) and dyslipidaemia. This multicentre, open-label, single-arm, prospective study enrolled adults with T2DM and LDL-C ≥70 mg/dL despite ≥12 weeks of moderate or low-intensity statin therapy. Participants received ezetimibe 10 mg/rosuvastatin 2.5 mg once daily for 12 weeks. The primary endpoint was the proportion achieving LDL-C <70 mg/dL at Week 12. Secondary endpoints included changes in lipid and glycaemic parameters, subgroup analyses, and safety outcomes. Of 639 screened patients, 586 were included in the full analysis set (FAS). At Week 12, 62.3% (95% CI 58.4-66.2) achieved LDL-C <70 mg/dL. Mean LDL-C decreased by 26.0% from 90.9 ± 17.2 to 67.3 ± 19.3 mg/dL (p < 0.001). Total cholesterol, non-HDL-C, and apoB decreased significantly (all p < 0.001); HDL-C and triglycerides were unchanged (p = 0.914 and p = 0.393, respectively). HbA1c increased by 0.15 ± 0.53% and fasting glucose by 3.6 ± 24.7 mg/dL (both p < 0.001). HOMA-IR decreased by -0.22 ± 3.09, not significant (p = 0.085). Subgroup analyses showed greater LDL-C reductions in patients with BMI <23 kg/m Switching to ezetimibe 10 mg/rosuvastatin 2.5 mg achieved substantial LDL-C reductions, high goal attainment, excellent adherence, and good tolerability in Korean T2DM patients with dyslipidaemia. Show less

Alzheimer's disease (AD) is one of the most pressing public health challenges in an aging world. However, effective therapeutic strategies are still lacking. Imbalance in lipid homeostasis is a key driver of AD. Given the established link between dysregulated lipid metabolism and amyloid-beta (Aβ) aggregation, we investigated whether chicoric acid (CA), a dietary polyphenol with reported lipid-modulating properties, could mitigate Aβ pathology by modulating lipid metabolism in 5xFAD transgenic mice. In the brain, we found that CA upregulated the expression of liver X receptor Beta (LXR-β) and ATP-binding cassette transporter A1 (ABCA1) in 5xFAD mice. Through this pathway, it promoted apolipoprotein E (ApoE) lipidation and enhanced the expression of Aβ-clearance proteins (IDE and LRP1). Notably, in the periphery, CA reshaped the gut microbiota in 5xFAD mice, which reduced serum neurotoxic bile acid levels and preserved the integrity of the peripheral Aβ clearance system. Together, our study first demonstrated that CA globally regulated lipid homeostasis to alleviate Aβ pathology by coordinating cerebral cholesterol efflux with peripheral bile acid metabolism. The findings facilitated exploring active compounds from traditional Chinese medicine that may reduce Aβ deposition by targeting lipid metabolism pathways. Show less

Vascular graft fibrosis can cause a decrease in cellular infiltration and capillary ingrowth in vascular walls. It can also lead to vascular stiffening. As such, there are still no vascular grafts that can be used in blood vessels where their diameters are less than 6 mm in patients. Although various approaches have been evaluated to mitigate implant-associated fibrosis, effective treatments remain quite limited. In this study, we demonstrated that Apolipoprotein E (APOE) significantly increased during vascular regeneration after graft implantation Show less

Conversion of cholesterol into bile acids is a central pathway for cholesterol disposal, which was mainly controlled by cholesterol 7alpha-hydroxylase (Cyp7a1). In present study, we aimed to investigate the effect and the potential underlying mechanism of microRNA-96 (miR-96) on atherosclerosis development. The anti-atherosclerosis effects of a miR-96 inhibitor (miR-96i) were evaluated using ApoE KO mice fed a high-fat diet, which was treated with miR-96i for 8 weeks. The regulatory mechanism was revealed and validated by RNA-seq transcriptomics, quantitative PCR and western blotting analyses in hepatic cells. The authors identified that miR-96i significantly decreased serum cholesterol and bile acid levels and attenuated arterial plaque in mice. We further revealed that miR-96 regulated Cyp7a1 via a FOXO1-involved indirect pathway, in which miR-96 directly modulated FOXO1 in a posttranscriptional manner. A coordinated regulatory effect of miR-96 and miR-185 on FOXO1 was also observed. The full spectrum of mechanisms underlying the antiatherosclerotic activity beside miR-96-FOXO1-CYP7A1 axis remains to be elucidated. This study provides convincing evidence for the pivotal role of miR-96 in FOXO1 modulation and CYP7A1-involved cholesterol-bile acid metabolism, suggesting that miR-96 is a novel therapeutic target for the discovery and development of drugs against ACVD. Show less

Aberrant deposition of β-amyloid (Aβ) and hyperphosphorylated tau, along with neuroinflammation, are key drivers of Alzheimer's disease (AD) pathology. Here, we identify ramalin, a natural antioxidant, as a promising therapeutic agent that alleviates AD pathology by modulating β-site APP cleaving enzyme 1 (BACE1), histone deacetylase 6 (HDAC6), and the mitogen-activated protein kinases (MAPK) pathway. Ramalin reduced BACE1 protein levels, independently of its transcription, translation, or enzymatic activity, an effect mediated by inhibition of HDAC6. Consistently, HDAC6 knockout similarly decreased BACE1 levels, highlighting HDAC6 as a key regulator of BACE1. Ramalin further suppressed neuroinflammatory responses by downregulating inducible nitric oxide synthase (iNOS) and the NLR family pyrin domain containing 3 (NLRP3) inflammasome. In AD mouse models, ramalin treatment significantly attenuated neuroinflammation, Aβ plaque burden, and tau hyperphosphorylation, while improving cognitive performance. Notably, ramalin reversed Aβ oligomer-induced synaptic transmission impairment and restored synaptic vesicle recycling in hippocampal neurons. Transcriptomic analysis identified modulation of the MAPK pathway, with reduced phosphorylation of c-Jun N-terminal kinase (JNK) and extracellular signal-regulated kinase (ERK) implicated in tau pathology. These findings establish ramalin as a disease-modifying intervention that provides neuroprotection through concurrent regulation of BACE1, HDAC6, and MAPK signaling pathway. Collectively, our findings highlight ramalin as a compelling disease-modifying candidate with the potential to drive a breakthrough approach targeting AD pathology. Show less

Prostate cancer (PCa) is the most common male cancer and the second leading cause of cancer death in men. Androgen deprivation therapy (ADT) has been widely used as the first-line treatment for PCa. However, most PCa will progress to castration-resistant PCa (CRPC) that resists ADT 1 to 3 years after the treatment. Steroidogenesis from cholesterol is one of the mechanisms leading to ADT resistance. In PCa cells, low-density lipoprotein (LDL) mediated uptake is the major venue to acquire cholesterol. However, the mechanism of regulating this process is not fully understood. Fibroblast growth factor receptor 1 (FGFR1) is a receptor tyrosine kinase (RTK) that is ectopically expressed in PCa cells and promotes PCa progression by activating downstream signaling pathways. To comprehensively determine the roles of FGFR1 in PCa, we generated FGFR1-null DU145 cells and compared the transcriptomes of FGFR1-null and wild-type cells. We found that ablation of FGFR1 reduced the expression of genes promoting LDL uptake and de novo synthesis of cholesterol, thereby reducing the overall cholesterol pool in PCa cells. Detailed mechanistic studies further revealed that FGFR1 boosted the activation of sterol regulatory element-binding protein 2 (SREBP2) through ERK-dependent phosphorylation and cleavage, which, in turn, increased the expression of low-density lipoprotein receptor (LDLR) and enzymes involved in de novo cholesterol synthesis. Furthermore, in silico analyses demonstrated that high expression of FGFR1 was associated with high LDLR expression and clinicopathological features in PCa. Collectively, our data unveiled a previously unrecognized therapeutic avenue for CRPC by targeting FGFR1-driven cholesterol uptake and de novo synthesis. Show less

To describe the network structure and heterogeneity of symptom burden in patients with acute coronary syndrome (ACS) after percutaneous coronary intervention (PCI), and to examine factors associated with different symptom burden profiles to inform risk-stratified management after PCI. A convenience sample of 261 patients with ACS who underwent PCI at a tertiary hospital in Chongqing between November 2024 and August 2025 was recruited. Data were collected using a demographic questionnaire, the Cardiac Symptom Survey, and the Seattle Angina Questionnaire. Network analysis was conducted to identify inter-symptom associations and the structural characteristics of the symptom network. Latent profile analysis (LPA) was performed to classify symptom burden patterns, and multinomial logistic regression analysis was used to explore factors associated with profile membership. Network analysis indicated that depression was the most central symptom (strength Symptom burden in patients with ACS after PCI demonstrates substantial individual heterogeneity. Depression occupies a central position within the symptom network, and BMI is associated with moderate and high symptom burden profiles. These findings suggest that integrating symptom network characteristics and BMI status into post-PCI assessment may facilitate risk-stratified management and targeted psychological and weight-related interventions to improve recovery outcomes. Show less

Child maltreatment measurement has been a longstanding issue, with discrepancies across administrative records, parent-reports, and self-reports. One proposed solution is "triangulation," or integrating data from multiple reporters and sources. However, it remains unclear how best to operationalize this concept. This study examines the concept of "triangulation" by employing different analytic methods to determine whether these methods reveal a common underlying construct of physical abuse and whether they predict adult depression. Data come from the Lehigh Longitudinal Study, a 40+ year prospective study that began in the 1970s with children ages 18 months to 6 years of age. Data were collected in early childhood, middle childhood, adolescence, and adulthood (ages 36 and 46, on average). We applied five analytic approaches - network analysis, ordinary least squares (OLS) regression, structural equation modeling (SEM), latent profile analysis (LPA), and a cumulative index regression - to assess the relationships among multiple reporters of childhood physical abuse and adult depression. SEM best modeled the latent construct of physical abuse and significantly predicted adult depression, with adult self-reports playing a particularly strong role. Network analysis also highlighted strong intercorrelations among self-reports and meaningful links with depression. SEM and network analysis were the most informative for triangulation and prediction of adult depression. Adult self-reports of abuse were most related and most predictive of adult depression. Show less

To investigate the association between vaginal microbiota structure in early pregnancy and gestational diabetes mellitus (GDM) and to characterize microbial signatures for early screening for GDM. The present study was a nested case-control study recruiting pregnant women from the Nanjing Gulou Maternal-Child Health Center, China. Vaginal swabs were collected before 20 weeks of gestation for 16S rRNA sequencing. Following 1:3 propensity score matching, 45 GDM cases and 135 controls were enrolled. The final analysis included 42 GDM cases and 121 controls. A random forest model was used to explore the genera of vaginal differential microbiota associated with GDM. Based on these findings, latent profile analysis (LPA) was conducted to explore potential types of vaginal microbiota, and logistic regression was used to analyze the association between vaginal microbiota types and GDM. The GDM group exhibited elevated alpha diversity (Chao1 index, The composition and structure of vaginal microbiota in early pregnancy are different in the two groups. The vaginal microbiota in early pregnancy, which is characterized by co-dominated by The online version contains supplementary material available at 10.1186/s12866-026-04910-2. Show less

Through the selective breeding of superior strains, livestock and poultry can achieve enhanced disease resistance and production performance, thereby improving farming efficiency and increasing chicken meat yield. This study analyzed the expression of gut health-related genes, cecal microbiota, and untargeted serum metabolomics in Wenchang chickens from the NS strain (Normal strain) and the AFS strain (Antibiotic-free strain), and explored the relationships between their cecal microbiota and serum metabolites. Our results show that in the ileum, antioxidant-related indicators T-AOC (P < 0.05), T-SOD (P < 0.05), and GSH-PX (P < 0.05) were significantly higher in the AFS strain than in the NS strain, while MDA (P < 0.05) was significantly lower in the AFS strain than in the NS strain. The mRNA expression level of RORγt/FoxP3, which is related to immune regulation, was significantly lower in the AFS strain than in the NS strain (P < 0.05). The differential microorganisms in the cecum primarily included Muribaculum, Cryptobacteroides, Blautia, Enterocloster, Lachnoclostridium, Hydrogenoanaerobacterium, Ruminococcus, Subdoligranulum, Clostridioides, and Evtepia. The main differential metabolites in serum included folinic acid, biotin, lysophosphatidic acid (LPA), 3-hydroxy-3-methylbutanoic acid, 3-hydroxybutyric acid, and others. The differential metabolites are primarily enriched in the following metabolic pathways: gap junction, glycolipid metabolism, and fatty acid biosynthesis. In addition, the Pearson correlation analysis between the gut microbiota and serum metabolites showed that Blautia was positively correlated with folinic acid (P < 0.05) and biotin (P < 0.05); Lachnoclostridium was positively correlated with biotin (P < 0.01); and Ruminococcus was positively correlated with 3-hydroxybutyric acid (P < 0.05). This study mainly elucidates the metabolic characteristics of the antibiotic-free Wenchang chicken strain by analyzing gut microbiota and serum metabolites. Show less

Postoperative symptoms in lung cancer patients are complex and dynamic, yet recovery is highly heterogeneous. Traditional analyses often fail to capture individual recovery trajectories, limiting the ability to provide personalized care. This study aimed to identify distinct postoperative symptom trajectories and their clinical predictors using a person-centered approach. We conducted a prospective longitudinal study with 394 patients undergoing uniportal video-assisted thoracoscopic surgery (uniportal VATS) for early-stage non-small cell lung cancer. Patient-reported symptoms were collected at 1, 7, 14, and 30 days postoperatively. Latent Profile Analysis (LPA) was used to identify distinct symptom profiles, and Latent Transition Analysis (LTA) modeled the transitions between these profiles over time. Multinomial logistic regression was used to identify predictors of these transitions. LPA identified two distinct recovery profiles: a "Rapid Recovery" group (C1) and a "High-Symptom, Slow Recovery" group (C2). The first postoperative week was a critical window, with 73.0% of patients in the High-Symptom, Slow Recovery group transitioning to the Rapid Recovery group. This transition rate slowed significantly in subsequent weeks. A higher ASA classification, use of a thicker chest tube, and extensive lymph node dissection predicted a slower recovery. Conversely, better pulmonary function (FEV1%, MVV%) facilitated a faster transition, while postoperative complications were associated with a negative trajectory shift. Postoperative recovery in lung cancer patients follows predictable, heterogeneous trajectories. This person-centered approach enables the early identification of high-risk patients based on preoperative and surgical factors. Understanding these distinct pathways allows for a shift from a one-size-fits-all model to staged, personalized interventions designed to optimize symptom management and enhance patient recovery. Show less

Organic afterglow materials are garnering increasing attention due to their great potential in practical applications. To date, most organic afterglow materials can achieve only millisecond- or second-scale afterglow lifetimes, while realizing long persistent luminescence (LPL) lasting for hours or even days remains a significant challenge. Since 2017, when Adachi and Kabe first achieved LPL lasting over an hour in a purely organic system, LPL materials have undergone a decade of development, with polymer-based LPL materials exhibiting rapid progress in recent years. The energy level alignment in exciplex polymers and the resulting charge separation characteristics are closely associated with their unique LPL functional properties, primarily stemming from the well-designed donor and acceptor organic structures. This article provides a systematic review of the design strategies for LPL polymers and summarizes their current application advances in optical anti-counterfeiting, night-time illumination, smart textiles, and other related fields. Show less

The primary renal complication of diabetes mellitus is diabetic kidney disease (DKD). The precise pathogenic mechanisms of DKD remain poorly elucidated. The aim of this study was to identify potential energy metabolism-related genes associated with DKD. The GSE30529 and GSE30528 datasets were retrieved from the Gene Expression Omnibus, and energy metabolism-related genes were obtained from the GeneCards database. Differentially expressed genes (DEGs) between DKD and control groups were analyzed. The biological functions and signaling pathways of these DEGs were evaluated using Gene Ontology (GO), the Kyoto Encyclopedia of Genes and Genomes (KEGG), and gene set enrichment analysis (GSEA). The diagnostic performance of hub genes for DKD was assessed using receiver operating characteristic (ROC) curve analysis. Expression levels of five significant energy metabolism-related genes were validated through immunohistochemistry. The Nephroseq V5 tool was used to evaluate gene expression in DKD and to determine correlations between gene expression and renal function in patients with DKD. A total of 17 energy metabolism-related DEGs were identified. Five hub genes-ALB, IGF1, CD36, LPL, and UCP2-were identified. Among these, CD36 and LPL demonstrated relatively high diagnostic accuracy for DKD. The findings suggest that CD36, IGF1, LPL, and UCP2 may serve as potential biomarkers for DKD. The genes CD36, IGF1, LPL, and UCP2 represent potential energy metabolism-related biomarkers with possible applications in the diagnosis and treatment of DKD. Show less

Norethindrone (NET) and levonorgestrel (LNG) are synthetic progestins frequently detected in aquatic environments, have unclear effects on lipid metabolic homeostasis during the early life stages of aquatic organisms. Although progestins commonly occur as mixtures, their combined impacts remain unclear. In this study, we investigated the individual and combined impacts of NET and LNG at environmentally relevant concentrations (2-200 ng/L) on lipid metabolism in zebrafish larvae. NET and LNG significantly disrupted early development in zebrafish. It also altered lipid profiles, as indicated by elevated triglyceride (TG) levels, reduced total cholesterol (TC), as well as alterations in key metabolic enzymes (FASN, LPL) and lipid-regulatory genes (pparγ, fasn, lpl, pparα). Co-exposure with LNG resulted in non-additive responses across multiple endpoints. Antagonistic interactions were predominant at medium and high concentrations, while occasional synergism was observed at low doses. These complex patterns were further supported by Bliss independence model analysis. Notably, combined exposure suppressed both lipid synthesis and degradation pathways more strongly than individual treatments, leading to lipid accumulation and altered energy regulation. This study advanced understanding of the ecological risks caused by progestins in aquatic environments and highlighted the necessity of mixture-based risk assessment of endocrine-disrupting compounds. Show less

Snail (SNAI1), a central transcription factor driving epithelial-mesenchymal transition (EMT), is pivotal in cancer metastasis and tissue remodeling. Owing to its labile nature, Snail activity is tightly controlled by post-translational modifications that dictate its stability. Here this review summarizes how the ubiquitin-proteasome system orchestrates Snail degradation through coordinated phosphorylation and ubiquitination, mediated by diverse E3 ligases and regulated by kinases, acetyltransferases and deubiquitinases. These mechanisms dynamically adjust Snail levels in both the cytoplasm and nucleus, thereby modulating EMT outcomes. In parallel, emerging studies reveal that chaperone-mediated autophagy (CMA) provides an additional layer of regulation. Through recognition of KFERQ-like motifs, CMA selectively directs cytoplasmic Snail to lysosomes for LAMP2A-dependent degradation, functioning as a quality control system. Impairment of CMA leads to nuclear accumulation of Snail, enhancing its EMT-inducing and prometastatic potential. Together, the ubiquitin-proteasome system and CMA represent complementary, context-dependent axes that maintain Snail homeostasis. Their disruption facilitates EMT activation and metastatic progression. By integrating recent findings, this review highlights the dual degradative control of Snail and its implications for cancer biology, providing a conceptual framework for therapeutic approaches aimed at restoring degradative balance and limiting metastasis. Show less

Ischemia-reperfusion (I/R) injury, resulting from transient or permanent cerebral vessel occlusion, triggers oxidative stress, neuroinflammation, and blood-brain barrier (BBB) disruption, leading to progressive neuronal damage and cognitive decline. The hippocampus, due to its high metabolic demand and susceptibility to oxidative stress, is particularly vulnerable to I/R-induced injury. This study evaluated the neuroprotective effects of α-lipoic acid (α-LA), a potent antioxidant, using bilateral common carotid arteries occlusion/reperfusion (BCCAO/R) mouse model and an oxygen-glucose deprivation/reoxygenation in vitro model. In BCCAO/R mice, α-LA improved spatial memory without affecting motor activity and restored hippocampal tight junction proteins (Claudin-5 and Occludin) and antioxidant enzyme expression, indicating BBB stabilization and oxidative stress reduction. Although synaptic proteins (BDNF and PSD-95) were not restored, cognitive improvements suggest alternative protective mechanisms. In HT22 cells, α-LA decreased intracellular reactive oxygen species levels, enhanced viability, and inhibited apoptosis via decreased PARP cleavage and caspase-3 activation. These protective effects were linked to the activation of the Nrf2/ARE signaling pathway and the upregulation of its downstream antioxidant targets. Overall, α-LA demonstrated marked neuroprotective effects in ischemic models by reducing oxidative stress, preserving BBB integrity, and restoring hippocampal function, positioning it as a promising therapeutic candidate for ischemic brain injury. Show less

Insulin resistance (IR) is a key mechanism underlying type 2 diabetes mellitus and is closely associated with obesity. Although numerous genome-wide association studies (GWASs) have identified variants that influence IR-related traits, it remains unclear whether the genetic architecture of IR differs according to obesity status. We conducted a stratified GWAS of the Homeostasis Model Assessment of Insulin Resistance (HOMA-IR) in 8906 Korean individuals from the Korean Genome and Epidemiology Study. Participants were categorized into a normal-weight group (Body Mass Index (BMI) ≤ 23 kg/m Show less

To investigate the effect of tannic acid (TA) on the growth, disease resistance, and intestinal health of Chinese soft-shelled turtles, individual turtles were fed with 0 g/kg (CG), 0.5 g/kg, 1 g/kg, 2 g/kg, and 4 g/kg TA diets for 98 days. Afterwards, the turtles' disease resistance was tested using Show less

Metabolic diseases such as high blood lipids, high blood sugar, and disrupted gut microbiota pose a serious threat to people's physical health. The occurrence of these diseases is closely related to the lack of nutrients in daily rice staple foods, but there is a lack of comprehensive analysis of the underlying mechanisms. This study used fully nutritious brown rice as raw material, and after germination under various stress conditions, it significantly increased the levels of gamma aminobutyric acid (GABA, four carbon non protein amino acid), resistant starch, flavonoids, and other components that regulate metabolic diseases. Using rats as experimental subjects, a model of hyperlipidemia and hyperglycemia was constructed, with rice consumption as the control. The experimental period was 8 weeks. Research has found that feeding sprouted brown rice can significantly improve the accumulation of white fat in the liver caused by a high-fat diet, significantly reduce TC, TG, LDL-C, apoB, HL, LPL, and LCAT, significantly increase HDL-C and apoA1, and significantly reduce the levels of inflammatory factors IL-6 and TNF-α. Therefore, consuming sprouted brown rice can reduce the risk of hyperlipidemia, inflammation, and tumor occurrence by promoting fat breakdown, and can also increase the abundance of metabolic-promoting microorganisms (especially Euryarchaeota and Lactobacillus) in the intestine, improving the entire metabolic ecological network of rats. Show less