摘要：
A multifunctional electrochemiluminescence (ECL) coreaction accelerator, AuAgPt nanoframes (NFs), is described for use in an ECL aptasensor for highly sensitive aflatoxin B1 (AFB1) detection. As a signal quencher, the broad UV-vis absorption spectrum of AuAgPt nanosheets (NSs) overlaps the ECL emission spectrum of g-C(3)N(4)@Au, triggering an ECL resonance energy transfer (ECL-RET). By the adjustment of the dosage of hydrogen peroxide (H(2)O(2)), the AuAgPt NSs are transformed into AuAgPt NFs because H(2)O(2) etches Ag in AuAgPt NSs into Ag(+), which disrupts the RET process. The as-formed AuAgPt NFs act as a coreaction accelerator to enhance the ECL response of the g-C(3)N(4)@Au/K(2)S(2)O(8) system. Without AFB1, the Ag-dependent DNAzyme is inactive, and a strong ECL signal is observed. After AFB1 is added, the AFB1 aptamer targets AFB1 and the DNAzyme active site is exposed. As-generated Ag(+) further activates DNAzyme to cut the substrate strand (S-DNA), which causes AuAgPt NFs to detach from the electrode surface and the ECL signal to significantly decrease. Under optimal conditions, the proposed ECL aptasensor exhibits high sensitivity with a limit of detection (LOD) of 0.11 fg/mL in the range of 1 fg/mL to 1 μg/mL for AFB1 detection.
摘要：
Microcystin-LR (MC-LR) is a toxin that causes hepatic steatosis. Our previous study found that exposure to 60 μg/L MC-LR for 9 months resulted in liver lipid accumulation, but the underlying mechanisms remain elusive. Herein, for the first time, fatty acid-targeted metabolome and RNA-seq were combined to probe the effect and mechanism of chronic (12-month) MC-LR treatment on mice lipid metabolism at environmental-related levels (1, 60, and 120 μg/L). It was found that MC-LR dose-dependently raised serum and liver lipid levels. The total cholesterol (TC) levels in the liver were significantly increased following treatment with 1 μg/L MC-LR (equivalent to 0.004 μ/L in human). Treatment with 60 and 120 μg/L MC-LR significantly elevated TC and triglyceride (TG) levels in both serum and liver. Serum fatty acid-targeted metabolome analysis demonstrated that exposure to 1, 60, and 120 μg/L MC-LR caused significant alterations in the fatty acid profile. Chronic 1, 60, and 120 μg/L MC-LR treatment significantly increased serum polyunsaturated fatty acids (PUFAs), including conjugated linoleic acid and eicosapentaenoic acid, which positively correlated with serum or liver TG levels. Chronic exposure to 120 μg/L MC-LR led to a significant decrease in the accumulation of saturated fatty acids, including citramalic acid, pentadecanoic acid, and docosanoic acid, which were negatively correlated with serum or liver lipid levels. These findings suggested that 1 μg/L MC-LR exposure caused mild lipid metabolism disruption, while 60 and 120 μg/L MC-LR treatment resulted in pronounced hepatic steatosis in mice. Transcriptome analysis revealed that chronic environmental MC-LR treatment regulated the expression of genes involved in the phosphatidylinositol 3-kinase (PI3K) complex and fatty acid metabolism. Western blotting and RT-qPCR confirmed that chronic environmental MC-LR exposure activated the PI3K/AKT/mTOR signaling pathway, the downstream of fads3 gene that participates in fatty acid desaturation was upregulated, fatty acid degradation-related genes, including acsl1, acsl4, and ehhadh were inhibited, and lipid transport-related genes, including slc27a4 and apol7a, were promoted. Thus, chronic environmental MC-LR exposure boosts hepatic steatosis. Our work indicated that the limit concentration of 1 μg/L MC-LR in human drinking water for safety needs to be discussed. The study provides the first evidence of the fatty acid profile and gene changes and gains new insights into the mechanisms of chronic environmental MC-LR treatment-induced hepatic steatosis.
摘要：
The combined effect of environmental exposure and dietary behavior plays a vital role in the occurrence of diseases. Bisphenol S (BPS) and bisphenol F (BPF) are the most commonly used substitutes for bisphenol A (BPA). Previous studies have shown that the combined exposure to BPA and fructose caused significant disturbances in glycolipid metabolism in adipose tissue, however, the interference caused by the combined exposure to BPS and fructose or BPF and fructose on adipose tissue is still unclear. In the present study, we performed a integrated analysis of targeted energy metabolomics and widely targeted quantitative lipidomics on the adipose tissue of Sprague Dawley rats after combined exposure to 2 levels of BPS or BPF (lower dose: 0.25, and higher dose: 25 μg/kg every other day) and 5% fructose for 6 months. Based on the results, lower dose BPS combined with fructose increased succinate significantly, while higher dose BPS or lower dose BPF combined with fructose decreased succinate significantly. Additionally, lower dose BPS combined with fructose might lead to polyunsaturated lipid depletion, while higher dose BPS combined with fructose exposure might lead to choline and carnitine depletion; lower dose BPF combined with fructose might inhibit lipolysis, while higher dose BPF combined with fructose might cause accumulation of free fatty acids. These results indicated the response patterns of adipose tissue to different dose of BPS or BPF combined with fructose were significantly different, and the adipocyte succinate signaling pathway might be the important target for metabolic remodeling in adipose tissue.
关键词：
Drug reposition;Enrichment score;Immunoregulation;LINCS;Lenalidomide;Radioprotection
摘要：
Ionizing radiation induces DNA damage and impairs genomic integrity, leading to cell death and tissue injuries or carcinogenesis. Medical radiation protectors are essential and necessary. However, there are limited radioprotectors in clinics, which can't meet the growing demand for countering radiation emergencies. Traditional drug discovery approach has been proven expensive and risky. Computational drug repositioning provides an attractive strategy for radioprotector discovery. Here we constructed a systematic workflow to identify repositioning radioprotectors by comparison of biosimilarity between γ-ray and known medicines characterized by gene expression signatures from GEO and LINCS. Using enrichment scoring, medicines with negative scores were considered as candidates of revising or mitigating radiation injuries. Seven approved medicines were identified, and their targets enriched in steroid and estrogen metabolic, chemical carcinogenesis associated pathways. Lenalidomide, an approved medicine for multiple myeloma and anemia, was further verified as a promising potential radioprotector. It increases survival of mice after lethal doses of irradiation by alleviating bone marrow and intestinal injury in vivo, and inhibits apoptosis of cultured irradiated AHH- 1 and IEC- 6 cells in vitro. This study introduces rational drug repositioning to radiation medicine and provides viable candidates for radioprotective therapeutic regimens.
作者机构：
[Tang, Jingjing; Tang, Wei; Li, Yanlin; Li, Zhenkui] Univ South China, Inst Pathogen Biol, Sch Basic Med Sci, Hengyang Med Sch, Hengyang 421001, Hunan, Peoples R China.;[Tang, Jingjing; Tang, Wei; Li, Yanlin; Li, Zhenkui] Univ South China, Sch Basic Med Sci, Hengyang Med Sch, Key Lab Special Pathogen Prevent & Control Hunan P, Hengyang 421001, Hunan, Peoples R China.;[Liu, Cong] Univ South China, Sch Publ Hlth, Hengyang Med Sch, Dept Hlth Inspect & Quarantine, Hengyang 421001, Hunan, Peoples R China.
通讯机构：
[Li, ZK ] U;Univ South China, Inst Pathogen Biol, Sch Basic Med Sci, Hengyang Med Sch, Hengyang 421001, Hunan, Peoples R China.;Univ South China, Sch Basic Med Sci, Hengyang Med Sch, Key Lab Special Pathogen Prevent & Control Hunan P, Hengyang 421001, Hunan, Peoples R China.
摘要：
Malaria, a severe parasitic disease caused by Plasmodium infections, remains a major global health challenge. Efforts to eradicate malaria are complicated by the parasite’s intricate life cycle, which alternates between vertebrate hosts and mosquito vectors. Host-derived factors and parasite-sourced components exert crucial roles in regulating this biological process. This review explores the critical role of host-derived factors in shaping Plasmodium sexual differentiation and transmission. We examine how vertebrate and mosquito host-specific factors either promote or restrict parasite development, influencing the transition from vertebrates to mosquitoes. Understanding these host-mediated mechanisms is crucial for developing novel transmission-blocking strategies to reduce malaria prevalence. By highlighting key interactions between hosts and parasites, this review provides insights into potential interventions that could disrupt Plasmodium transmission and contribute to malaria control efforts.
Malaria, a severe parasitic disease caused by Plasmodium infections, remains a major global health challenge. Efforts to eradicate malaria are complicated by the parasite’s intricate life cycle, which alternates between vertebrate hosts and mosquito vectors. Host-derived factors and parasite-sourced components exert crucial roles in regulating this biological process. This review explores the critical role of host-derived factors in shaping Plasmodium sexual differentiation and transmission. We examine how vertebrate and mosquito host-specific factors either promote or restrict parasite development, influencing the transition from vertebrates to mosquitoes. Understanding these host-mediated mechanisms is crucial for developing novel transmission-blocking strategies to reduce malaria prevalence. By highlighting key interactions between hosts and parasites, this review provides insights into potential interventions that could disrupt Plasmodium transmission and contribute to malaria control efforts.
期刊：
International Journal of Molecular Sciences,2025年26(14) ISSN：1661-6596
通讯作者：
Zhou, Ping-Kun;Gu, YQ
作者机构：
[Wang, Yilong; Zhu, Jiaojiao; Zhou, Lin; Yan, Ziyan; Gu, Yongqing; Liu, Yuhao; Zhou, Ping-Kun] Beijing Inst Radiat Med, Beijing 100850, Peoples R China.;[Chen, Huixi; Gu, Yongqing] Univ South China, Hengyang Med Coll, Hengyang 421001, Peoples R China.;[Hou, Yifan; Gu, Yongqing] Hebei Univ, Coll Life Sci, Baoding 071001, Peoples R China.;[Zhang, Xinyu; Gu, Yongqing] Univ South China, Sch Publ Hlth, Hengyang 421001, Peoples R China.;[Chen, Zhongmin] PLA Rocket Force Characterist Med Ctr, Beijing 100850, Peoples R China.
通讯机构：
[Zhou, PK; Gu, YQ ] B;Beijing Inst Radiat Med, Beijing 100850, Peoples R China.;Univ South China, Hengyang Med Coll, Hengyang 421001, Peoples R China.;Hebei Univ, Coll Life Sci, Baoding 071001, Peoples R China.;Univ South China, Sch Publ Hlth, Hengyang 421001, Peoples R China.
关键词：
DNA methylation;MassArray;RRBS;episignatures;lung cancer;radon
摘要：
Radon (Rn) exposure has a strong association with lung cancer risk and is influenced by epigenetic modifications. To investigate the characterization of DNA methylation (DNAm) episignatures for radon-induced lung cancer, we detected the specific changes in DNAm in blood and lung tissues using reduced representation bisulfite sequencing (RRBS). We identified the differentially methylated regions (DMRs) induced by radon exposure. The bioinformatics analysis of the DMR-mapped genes revealed that pathways in cancer were affected by radon exposure. Among them, the DNAm episignatures of MAPK10, PLCG1, PLCβ3 and PIK3R2 were repeated between lung tissue and blood, and validated by the MassArray. In addition, radon exposure promoted lung cancer development in the genetic engineering mouse model (GEMM), accompanied by decreased MAPK10 and increased PLCG1, PLCβ3, and PIK3R2 with mRNA and protein levels. Conclusively, radon exposure significantly changes the genomic DNAm patterns in lung tissue and blood. The DNAm episignatures of MAPK10, PLCG1, PLCβ3 and PIK3R2 have a significant influence on radon-induced lung cancer. This brings a new perspective to understanding the pathways involved in radon-induced lung cancer and offers potential targets for developing blood-based biomarkers and epigenetic therapeutics.
期刊：
Science of The Total Environment,2025年958:178088 ISSN：0048-9697
通讯作者：
Fei Yang<&wdkj&>Hongli Tan
作者机构：
[Li, Jing] School of Public Health, Health Science Center, Xi'an Jiaotong University, Xi'an 710061, China;[Li, Jing] Key Laboratory of Environment and Genes Related to Diseases (Xi'an Jiaotong University), Ministry of Education, Xi'an 710061, China;[Yang, Liu] School of Geography, Earth & Environmental Sciences, University of Birmingham, Birmingham B15 2TT, UK;[Ding, Yuying] Guangdong Engineering Research Center of Chinese Medicine & Disease Susceptibility, School of Traditional Chinese Medicine, Jinan University, Guangzhou 510632, China;[Ding, Yuying] School of Chinese Materia Medica, Yunnan University of Chinese Medicine, Kunming 650500, China
通讯机构：
[Fei Yang] H;[Hongli Tan] G;Hunan Province Key Laboratory of Typical Environmental Pollution and Health Hazards, School of Public Health, Hengyang Medical School, University of South China, Hengyang 421001, China<&wdkj&>Guangdong Engineering Research Center of Chinese Medicine & Disease Susceptibility, School of Traditional Chinese Medicine, Jinan University, Guangzhou 510632, China
关键词：
Health risk;Indoor dust;Organophosphate esters;Spatial variations;Temporal trends
摘要：
This study investigated the presence of 20 organophosphate esters (OPEs) in indoor dust samples collected from the Chinese cities of Lanzhou, Xining, and Lhasa. The results demonstrate the ubiquitous presence of most OPEs in these three cities, with the highest concentrations of ΣOPEs found in Xining. We also summarized the occurrence of OPEs in indoor environments from 38 studies with 1875 samples collected across various regions of mainland China from 2012 to 2023. The weighted-median concentration of ΣOPEs in indoor dust exhibited region-specific variations, range from 381.9 to 6622.5 ng/g. Chloroalkyl-OPEs (Cl-OPEs) (e.g., tris(2-chloroethyl) phosphate (TCEP), tri(1-chloro-2-propyl) phosphate (TCIPP), and tri (1,3-dichloro-2-propyl) phosphate (TDCIPP)) predominated in all seven regions (range: 38.9 %–71.4 %). TCIPP was predominant in the Central China, North China, Northeast China, Northwest China, Southwest China, and Southwest China regions, while TCEP dominated in the Eastern China region. A significant downward trend in OPE concentrations in indoor environments was observed during the investigated period. Dust ingestion was identified as the predominant pathway of human exposure to OPEs indoors. The hazard quotients for Cl-OPEs were below the non-carcinogenic threshold, suggesting significant health risks are unlikely. This study underscores the widespread occurrence of OPEs in indoor dust across mainland China, emphasizing the necessity for ongoing monitoring and regulation of these chemicals.
This study investigated the presence of 20 organophosphate esters (OPEs) in indoor dust samples collected from the Chinese cities of Lanzhou, Xining, and Lhasa. The results demonstrate the ubiquitous presence of most OPEs in these three cities, with the highest concentrations of ΣOPEs found in Xining. We also summarized the occurrence of OPEs in indoor environments from 38 studies with 1875 samples collected across various regions of mainland China from 2012 to 2023. The weighted-median concentration of ΣOPEs in indoor dust exhibited region-specific variations, range from 381.9 to 6622.5 ng/g. Chloroalkyl-OPEs (Cl-OPEs) (e.g., tris(2-chloroethyl) phosphate (TCEP), tri(1-chloro-2-propyl) phosphate (TCIPP), and tri (1,3-dichloro-2-propyl) phosphate (TDCIPP)) predominated in all seven regions (range: 38.9 %–71.4 %). TCIPP was predominant in the Central China, North China, Northeast China, Northwest China, Southwest China, and Southwest China regions, while TCEP dominated in the Eastern China region. A significant downward trend in OPE concentrations in indoor environments was observed during the investigated period. Dust ingestion was identified as the predominant pathway of human exposure to OPEs indoors. The hazard quotients for Cl-OPEs were below the non-carcinogenic threshold, suggesting significant health risks are unlikely. This study underscores the widespread occurrence of OPEs in indoor dust across mainland China, emphasizing the necessity for ongoing monitoring and regulation of these chemicals.
作者机构：
[Yao, Xiang-Rong; He, Jun-Yan] Univ South China, Affiliated Hosp 1, Hengyang Med Sch, Dept Oncol, Hengyang, Peoples R China.;[Yao, Xiang-Rong; Xiao, Fang-Zhu] Univ South China, Sch Publ Hlth, Hengyang, Peoples R China.;[Xiao, Wen-Tao] Nantong Univ, Affiliated Hosp, Med Sch, Dept Radiat Oncol, Nantong, Peoples R China.;[Huang, Cui-Qin] Univ South China, Hengyang Med Sch, Affiliated Hosp 1, Dept Pathol, Hengyang, Peoples R China.
通讯机构：
[He, JY ; Huang, CQ ] U;Univ South China, Affiliated Hosp 1, Hengyang Med Sch, Dept Oncol, Hengyang, Peoples R China.;Univ South China, Hengyang Med Sch, Affiliated Hosp 1, Dept Pathol, Hengyang, Peoples R China.
摘要：
Head and neck squamous cell carcinoma (HNSC) is a prevalent and aggressive malignancy with poor prognosis, underscoring the need for novel biomarkers and therapeutic strategies. This study investigates the role of C16orf74 as a potential diagnostic and prognostic biomarker in HNSC. Bioinformatics analyses revealed that C16orf74 is significantly overexpressed in HNSC and is associated with advanced disease stages, therapy resistance, and shorter overall and progression-free survival. A prognostic nomogram integrating C16orf74 expression with clinicopathological features demonstrated robust predictive performance. Functional enrichment and immune infiltration analyses suggest that high C16orf74 expression might contribute to an immunosuppressive tumor microenvironment by reducing key immune cell populations, such as B cells, T cells, and natural killer cells, which are critical for anti-tumor immunity. Moreover, C16orf74 expression was inversely associated with immune checkpoint expression and immunotherapy response, highlighting its potential as a predictive biomarker for immune checkpoint blockade (ICB) efficacy. Drug sensitivity analyses identified potential therapeutic agents, including arsenic trioxide, carmustine, vincristine, quercetin, and carboplatin for patients with high C16orf74 expression. These findings highlight the potential of C16orf74 as a biomarker and therapeutic target to improve HNSC management.
摘要：
African swine fever virus (ASFV) predominantly infects Argasidae and suids, resulting in high morbidity and mortality in pigs. Despite the crucial role that viral sequences resembling those of the host play in the virus's survival, there are limited comprehensive studies on the genomic similarities between ASFV and its hosts. Consequently, this study employs homology analysis to construct a similarity network between ASFV and its hosts (Argasidae and suids), investigating the distribution, function, evolution, and origins of these similar sequences in ASFV. Our findings indicate that the host-similar fragments are mainly distributed between positions 70000 and 180000 of the ASFV genome, primarily within non-coding regions. Notably, these non-coding fragments are often associated with promoter functions. Furthermore, the analysis of suid proteins that share similarities with ASFV proteins reveals that they predominantly exhibit RNA polymerase activity and are involved in metabolic processes. Evolutionary analysis indicates that pan-similar sequences of ASFV exist in an open state, highlighting the diversity of these analogous sequences. Additionally, a positive correlation was identified between the occurrence of recombination breakpoints and similar sequences, indicating that homologous recombination may serve as a crucial mechanism driving the formation of these analogous sequences.
作者机构：
[Zi-An Wang] The School of Medicine & Holistic Integrative Medicine, Nanjing University of Chinese Medicine, Nanjing, China;[Fangfang Huang; Yashi Feng] The Guangxi Key Laboratory of Environmental Exposomics and Entire Lifecycle Heath, School of Public Health, Guilin Medical University, Guilin, China;[Yunchang Cao] The Department of Molecular Biology, School of Intelligent Medicine and Biotechnology, Guilin Medical University, Guilin, China;[Wuxiang Wang] The School of Public Health, University of South China, Hengyang, China;The State Key Laboratory of Organic Geochemistry, Guangzhou Institute of Geochemistry, Chinese Academy of Sciences, Guangzhou, China
通讯机构：
[Shaolong Feng] T;The Guangxi Key Laboratory of Environmental Exposomics and Entire Lifecycle Heath, School of Public Health, Guilin Medical University, Guilin, China<&wdkj&>The School of Public Health, University of South China, Hengyang, China<&wdkj&>The State Key Laboratory of Organic Geochemistry, Guangzhou Institute of Geochemistry, Chinese Academy of Sciences, Guangzhou, China
摘要：
Titanium dioxide nanoparticles (TiO(2)-NPs) have been ever increasingly exposed to people through all possible routes, while studies focusing on their potential cardiovascular risks are relatively lacking, especially the underlying biological mechanisms that are not yet elucidated. In this study, the ferroptotic effect of TiO(2)-NPs (30 nm) at environmentally relevant concentrations (0, 3, 12, and 48 μg/mL) on human umbilical vein endothelial cells (HUVECs) and the potential molecular mechanism were studied with the corresponding biochemical and molecular biology assays. The results showed that TiO(2)-NPs at the tested concentrations could reduce HUVEC viability, but ferrostatin-1 might rescue this reduction in cell viability. Also, TiO(2)-NPs exposure increased Fe(2+), reactive oxygen species, and malondialdehyde, but decreased glutathione, mitochondrial membrane potential, and activities of anti-oxidative enzymes (catalase, superoxide dismutase, and glutathione peroxidase) in HUVECs through an integrated signaling pathway. Meanwhile, enhanced p38 protein phosphorylation and keap1 protein and decreased Nrf2 protein phosphorylation with reductions in mRNA expressions of downstream anti-oxidative enzyme genes (catalase, superoxide dismutase, glutathione peroxidase, and phospholipid hydroperoxidase) were identified in the TiO(2)-NPs-exposed HUVECs. These indicated that TiO(2)-NPs exposure induced ferroptosis in HUVECs via the p38/keap1 inhibiting Nrf2 pathway. EC ferroptosis will be a promising biomarker for assessing the cardiovascular health risks of environmental contaminants.
作者机构：
[Li, Jingxian; Lyu, Yifan; Shen, Yan; Li, Yujin; Wang, Futing; Cai, Ren; Tan, Weihong] Hunan Univ, Mol Sci & Biomed Lab, State Key Lab Chemo Biosensing & Chemometr, Coll Mat Sci & Engn,Coll Chem & Chem Engn,Coll Bio, Changsha 410082, Peoples R China.;[Li, Yujin] Xinyang Normal Univ, Coll Chem & Chem Engn, Xinyang 464000, Peoples R China.;[Yang, Dan] RMIT Univ, Sch Engn, Melbourne, Vic 3000, Australia.;[Yang, Hongfen] Univ South China, Sch Publ Hlth, Hengyang Med Sch, Hunan Key Lab Typ Environm Pollut & Hlth Hazards, Hengyang 421001, Peoples R China.;[Tan, Weihong] Chinese Acad Sci, Univ Chinese Acad Sci, Zhejiang Canc Hosp, Hangzhou Inst Med HIM,Canc Hosp, Hangzhou 310022, Zhejiang, Peoples R China.
通讯机构：
[Yang, HF ] U;[Cai, R ] H;Hunan Univ, Mol Sci & Biomed Lab, State Key Lab Chemo Biosensing & Chemometr, Coll Mat Sci & Engn,Coll Chem & Chem Engn,Coll Bio, Changsha 410082, Peoples R China.;Univ South China, Sch Publ Hlth, Hengyang Med Sch, Hunan Key Lab Typ Environm Pollut & Hlth Hazards, Hengyang 421001, Peoples R China.
摘要：
A highly sensitive self-powered biosensor is designed based on gold-platinum nanorods (AuPt NRs) and the cascade reaction of catalytic hairpin assembly (CHA) and hybrid chain reaction (HCR) toward the miRNA-141 assay. As a cosignal accelerator, AuPt NRs enhance electrical conductivity between glucose oxidase (GOD) and a carbon paper (CP) electrode, thereby assisting in output signal enhancement. The cascade reaction of CHA-HCR is employed to efficiently amplify the detection signal and improve the sensitivity of the self-powered biosensor. Consequently, the self-powered biosensor provides highly sensitive detection of miRNA-141 with a wide linear response in the range of 0.1-10(4) fM and exhibits a low limit of detection (LOD) of 0.034 fM (S/N = 3). In addition, the self-powered biosensor exhibits high applicability in a real sample for the miRNA-141 assay.
期刊：
JOURNAL OF TOXICOLOGY AND ENVIRONMENTAL HEALTH-PART A-CURRENT ISSUES,2025年88(10):385-394 ISSN：1528-7394
通讯作者：
Yang, Yue;Yang, F;Yang, Y
作者机构：
[Zhang, Yin; Yang, F; Dai, Manni; Yang, Yue; Yang, Fei; Guan, Ying] Univ South China, Sch Publ Hlth, Hengyang Med Sch, Hunan Prov Key Lab Typ Environm Pollut & Hlth Haza, Hengyang 421001, Peoples R China.;[Yang, Yue] Univ South China, Affiliated Hosp 1, Hengyang Med Sch, Hengyang, Hunan, Peoples R China.;[Yang, Yue] Cent Hosp Shaoyang, Dept Publ Hlth, Shaoyang, Peoples R China.;[Yang, F; Yang, Fei] Hunan Prov Maternal & Child Hlth Care Hosp, Changsha, Hunan, Peoples R China.
通讯机构：
[Yang, F ; Yang, Y] U;[Yang, Y ] C;Univ South China, Sch Publ Hlth, Hengyang Med Sch, Hunan Prov Key Lab Typ Environm Pollut & Hlth Haza, Hengyang 421001, Peoples R China.;Cent Hosp Shaoyang, Dept Publ Hlth, Shaoyang, Peoples R China.;Hunan Prov Maternal & Child Hlth Care Hosp, Changsha, Hunan, Peoples R China.
摘要：
Microcystin-LR (MC-LR) a cyclic toxin produced by cyanobacterial species is known to exert detrimental effects on various organs, including lung. Several investigators demonstrated that MC-LR exerts pulmonary toxicity, but the underlying mechanisms remain unclear. This study aimed to investigate whether exposure to MC-LR-induced lung inflammation and examine the underlying mechanisms. Thirty specific pathogen-free (SPF) male mice were allocated into control and MC-LR treatment groups. Mice were intraperitoneally injected with physiological saline or MC-LR (20 mu g/kg) daily for a total of 21 days. Our findings indicated that exposure to MC-LR-produced histopathological changes in lung tissue, including thickening of alveolar walls and inflammatory infiltration. MC-LR was found to upregulate mRNA expression levels of pro-inflammatory cytokines TNF alpha, IL-6, IL-1 beta, and IL-18. Further, MC-LR significantly elevated the expression levels of proteins associated with the NF-kappa B/NLRP3 pathway p-NF-kappa B, NLRP3, Caspase-1, ASC. The activation of NF-kappa B/NLRP3 pathway further promoted the release of inflammatory cytokine IL-1 beta and cleavage of pyroptosis-associated GSDMD protein. These findings indicate that MC-LR may induce lung inflammation by promoting cell pyroptosis via the activation of the NF-kappa B/NLRP3 pathway.
摘要：
BACKGROUND: Maternal oxidative stress during pregnancy plays a role as a hazardous factor of offspring neurodevelopment in animal models. However, epidemiological evidence remains limited. In this prospective cohort, we aimed to investigate the associations between maternal oxidative stress biomarkers (OSBs) across pregnancy and neurodevelopmental outcomes in different stages across early childhood. METHODS: This was a prospective cohort study conducted in 1791 mother-child pairs from Wuhan, China. Three OSBs, including DNA oxidative damage marker (8-hydroxy-2'-deoxyguanosine, 8-OHdG), RNA oxidative damage marker (8-hydroxyguanosine, 8-OHG) and lipid oxidative damage marker (4-hydroxy nonenal mercapturic acid, HNE-MA), were measured in repeatedly collected urine samples in three trimesters across pregnancy. We followed children at age 2, age 3, and age 6 years. At age 2 years, the Bayley Scales of Infant Development of China Revision (BSID-CR) was employed to assess children's mental and psychomotor development. Brain-derived neurotrophic factor (BDNF) levels were measured in children's plasma at age 3 years. The Wechsler Preschool and Primary Scale-Fourth Edition (WPPSI-IV) was used to assess children's intelligence quotients at ages 6 years. Generalized estimating equation models were applied to estimate the associations between OSBs and neurodevelopmental outcomes. RESULTS: Higher maternal HNE-MA levels in late pregnancy were associated with lower mental development index at age 2 years (β = - 0.95, 95% confidence interval (CI): - 1.78, - 0.11). Elevated early pregnancy HNE-MA levels were associated with decreased BDNF levels at age 3 years (β = - 0.07, 95% CI: - 0.13, - 0.01). Each one-unit increase in natural log-transformed concentrations of 8-OHdG and 8-OHG in mid pregnancy was associated with a decrease in full-scale intelligence quotient at age 6 years by 1.55 points (95% CI: - 2.84, - 0.26) and 1.89 points (95% CI: - 3.30, - 0.49), respectively. CONCLUSIONS: This study suggested that higher levels of OSBs in each trimester of pregnancy might be a risk factor of consistently suboptimal neurodevelopment across early childhood. This finding provides new epidemiological data on the linkages of oxidative stress across pregnancy to child neurodevelopment and gives clues to the possible sensitive windows.
摘要：
Although the adverse effects induced by acute high-dose radiation from nuclear accidents have been intensively explored, the biological effects of low-dose radiation remain unclear. This study aimed to identify the role of low-dose radiation in three-dimensional (3D) lung organoids using transcriptomic and metabolomic analyses. An irradiation dose of 0 01 Gy was utilized to simulate environmental radiation exposure. Lung organoids were included in the study. Through metabolomic analysis, compared to the control, 290, 284, and 492 metabolites were significantly up-regulated, while 150, 605, and 310 metabolites were significantly down-regulated in the 0.01 Gy, 0.05 Gy, and 2 Gy groups, respectively. However, only the metabolites in the glycerophospholipid metabolism pathway increased significantly in the group treated with 0. 01 Gy radiation, with the lipid substances Carnitine C18:0(Car (18: 0)), palmitoylcarnitine, and PE (18: 3 (9 Z, 12 Z, 15 Z)/P- 16: 0) showing the most significant increase. Significantly, compared to the control, lipid metabolism can be affected by 0.01 Gy radiation. Furthermore, these altered lipid metabolites, such as triglycerides and sterols, were enriched in pathways related to cell signaling and affected cell proliferation, differentiation, and death after bioinformatics analysis. Through transcriptomic analysis, compared with the 0 Gy group, the expression of 19 genes in the 0.01 Gy group was up-regulated, while the expression of 6 genes was down-regulated. The 0.01 Gy irradiation affects the cardiac muscle contraction pathway and glycerolipid metabolism pathway. Moreover, using lung epithelial cells, we further identified that compared with the control group, there was no significant change in cystine uptake capacity, lipid peroxide levels, or mitochondrial membrane potential under irradiation conditions of 0.01 Gy and 0.05 Gy. In summary, our combined transcriptomic and metabolomic analysis of lung organoids provides an effective approach to understanding the biological effects of low-dose radiation exposure.
Although the adverse effects induced by acute high-dose radiation from nuclear accidents have been intensively explored, the biological effects of low-dose radiation remain unclear. This study aimed to identify the role of low-dose radiation in three-dimensional (3D) lung organoids using transcriptomic and metabolomic analyses. An irradiation dose of 0 01 Gy was utilized to simulate environmental radiation exposure. Lung organoids were included in the study. Through metabolomic analysis, compared to the control, 290, 284, and 492 metabolites were significantly up-regulated, while 150, 605, and 310 metabolites were significantly down-regulated in the 0.01 Gy, 0.05 Gy, and 2 Gy groups, respectively. However, only the metabolites in the glycerophospholipid metabolism pathway increased significantly in the group treated with 0. 01 Gy radiation, with the lipid substances Carnitine C18:0(Car (18: 0)), palmitoylcarnitine, and PE (18: 3 (9 Z, 12 Z, 15 Z)/P- 16: 0) showing the most significant increase. Significantly, compared to the control, lipid metabolism can be affected by 0.01 Gy radiation. Furthermore, these altered lipid metabolites, such as triglycerides and sterols, were enriched in pathways related to cell signaling and affected cell proliferation, differentiation, and death after bioinformatics analysis. Through transcriptomic analysis, compared with the 0 Gy group, the expression of 19 genes in the 0.01 Gy group was up-regulated, while the expression of 6 genes was down-regulated. The 0.01 Gy irradiation affects the cardiac muscle contraction pathway and glycerolipid metabolism pathway. Moreover, using lung epithelial cells, we further identified that compared with the control group, there was no significant change in cystine uptake capacity, lipid peroxide levels, or mitochondrial membrane potential under irradiation conditions of 0.01 Gy and 0.05 Gy. In summary, our combined transcriptomic and metabolomic analysis of lung organoids provides an effective approach to understanding the biological effects of low-dose radiation exposure.
摘要：
Uranium is the core material for the development of the nuclear industry, but its irreversible radiation damage poses a significant threat to human health. In this context, an innovative dual-mode colorimetric and electrochemical sensor was developed for the detection of uranyl ions (UO(2)(2+)), utilizing a covalent organic framework@gold nanoclusters (AuNCs@COF) composite. The synthesis of AuNCs@COF was simple, and the incorporation of AuNCs imparted the composite with exceptional peroxidase-like catalytic activity and enhanced electrochemical properties. By regulating the adsorption and desorption of aptamers on the AuNCs@COF surface, both peroxidase-like activity and conductivity were modulated, enabling the detection of UO(2)(2+) utilizing colorimetric and electrochemical dual signals. Under optimal conditions, the sensor revealed a broad linear detection range and a low detection limit, with ranges of 1.36 × 10(-10)-1.36 × 10(-5)mol/L for colorimetric detection and 5.0 × 10(-10)-2.5 × 10(-5)mol/L for electrochemical detection, achieving detection limitsfor these two methodsof 107 pmol/L and 347 pmol/L, respectively. Unlike other single-mode sensorsfor UO(2)(2+) detection, this dual-mode sensor demonstrated superior sensitivity, specificity, and repeatability. Furthermore, the results of spiked recovery experiments in real water samples highlight the promising potential of this dual-mode sensor for environmental water monitoring applications.
期刊：
JOURNAL OF OBSTETRICS AND GYNAECOLOGY RESEARCH,2025年51(1):e16120- ISSN：1341-8076
通讯作者：
Wu, CQ
作者机构：
[Wu, CQ; Xie, Yinghao; Wu, Chengqiu; Zhu, Qiong] Univ South China, Sch Publ Hlth, Hengyang, Peoples R China.;[Liu, Jun] Hengyang Cent Dis Control & Prevent, Hengyang, Peoples R China.
通讯机构：
[Wu, CQ ] U;Univ South China, Sch Publ Hlth, Hengyang, Peoples R China.
关键词：
CD1a;ovarian cancer;prognosis;recurrence;recurrent ovarian cancer
摘要：
OBJECTIVE: Explored the correlation between CD1a expression in recurrence and prognosis of ovarian cancer (OV). METHODS: The CD1a expression profile in OV, recurrent OV, and normal tissues, as well as corresponding clinical data, were obtained from The Cancer Genome Atlas (TCGA), International Cancer Genome Consortium (ICGC), Gene Expression Omnibus (GEO), and Genotype Tissue Expression (GTEx) databases. Meanwhile, immunohistochemical detection of CD1a expression in normal and OV tissues. Kaplan-Meier curves were plotted to estimate the hazard ratio (HR) of survival in OV. In addition, the correlation between CD1a and immune cells in OV, as well as the CD1a expression profile and corresponding survival time in pan-cancer were obtained from TCGA database. RESULTS: CD1a was overexpressed in OV and was significantly under-expressed in recurrent OV (TCGA-OV, p < 0.0001 and ICGC-OV, p < 0.0001). CD1a immunohistochemistry is significantly overexpressed in OV compared to normal tissue (p < 0.05). Recurrent OV (ICGC, p < 0.001; GSE17260, p < 0.001; GSE32062, p < 0.05). The prognosis in OV was significantly better when CD1a is overexpressed compared to under-expressed (HR [low], 1.426: 95% confidence interval [CI], 0.912-2.128; p = 0.050). Meanwhile, the overexpression of CD1a has a better prognosis than low expression in OV and recurrent OV (p = 0.004, HR [low] = 2.462, 95%CI [1.346-4.504] and p = 0.011, HR [low] = 2.199, 95%CI [1.202-4.024]). In addition, CD1a expression was closely correlated with immune cells, the CD8+ T cells, macrophages, and NK cells, while uncharacterized cells were significantly different (p = 2.65e-6, p = 7.52e-13, p = 8.28e-12, and p = 5.89e-8, respectively). Moreover, CD1a expression affected the prognosis in various other cancers. CONCLUSIONS: CD1a expression affected the recurrence and prognosis of OV and is closely related to various immune cell levels.
作者机构：
[Liu, Jinquan; Xiao, Xilin; Wu, Qian; Xiao, XL; Liu, Zhen] Univ South China, Sch Publ Hlth, Hengyang Sch Med, Hengyang, Hunan, Peoples R China.;[Liu, Xing] Univ South China, Sch Nucl Sci & Technol, Hengyang, Hunan, Peoples R China.;[Xiao, Xilin; Xiao, XL] Hunan Univ, State Key Lab Chemo Biosensing & Chemometr, Changsha, Hunan, Peoples R China.
通讯机构：
[Xiao, XL ] U;Univ South China, Sch Publ Hlth, Hengyang Sch Med, Hengyang, Hunan, Peoples R China.;Hunan Univ, State Key Lab Chemo Biosensing & Chemometr, Changsha, Hunan, Peoples R China.
摘要：
Food is essential for the proper functioning of the human body, and small molecule contaminants, such as antibiotics, have become a growing concern due to their harmful effects on both biological systems and the environment. These contaminants can enter the food supply through the use of antibiotics in animals, potentially causing significant health and ecological damage. As a result, detecting these pollutants, especially at trace levels, has become increasingly important. Aptamer sensors have gained popularity for this purpose because of their high stability, specificity, ease of modification, and low cost. To improve the sensitivity of these sensors, various signal enhancement strategies are used. These strategies aim to better detect small molecule contaminants, with many relying on nanomaterials and nucleic acid amplification techniques to amplify signals. Nanomaterials, which come in different forms such as zero-dimensional, one-dimensional, two-dimensional, and three-dimensional, play a crucial role in improving the performance of these sensors. This article provides an overview of these signal enhancement approaches, discussing the challenges and potential future directions for the development of aptamers in food contamination detection.
关键词：
25-hydroxyvitamin D;Gene polymorphism;Osteocalcin;Procollagen type 1 N-terminal propeptide;β-CrossLaps of type 1 collagen containing cross-linked C-telopeptide
摘要：
Objective This study aimed to investigate possible serum 25-hydroxyvitamin D [25(OH)D] cutoffs for the associations between 25(OH)D and Bone turnover markers (BTMs), and how GC gene variation influences such cutoffs in Chinese women of childbearing age.
This study aimed to investigate possible serum 25-hydroxyvitamin D [25(OH)D] cutoffs for the associations between 25(OH)D and Bone turnover markers (BTMs), and how GC gene variation influences such cutoffs in Chinese women of childbearing age.
Methods In total, 1,505 non-pregnant or non-lactating women (18–45 years) were recruited from the 2015 Chinese Adult Chronic Disease and Nutrition Surveillance. Serum 25(OH)D, osteocalcin (OC), procollagen type 1 N-terminal propeptide (P1NP), β-CrossLaps of type 1 collagen containing cross-linked C-telopeptide (β-CTX), and single nucleotide polymorphisms were determined. Locally weighted regression and smoothing scatterplot and segmented regression were performed to estimate the 25(OH)D thresholds.
In total, 1,505 non-pregnant or non-lactating women (18–45 years) were recruited from the 2015 Chinese Adult Chronic Disease and Nutrition Surveillance. Serum 25(OH)D, osteocalcin (OC), procollagen type 1 N-terminal propeptide (P1NP), β-CrossLaps of type 1 collagen containing cross-linked C-telopeptide (β-CTX), and single nucleotide polymorphisms were determined. Locally weighted regression and smoothing scatterplot and segmented regression were performed to estimate the 25(OH)D thresholds.
Results The median serum 25(OH)D was 16.63 (11.96–22.55) ng/mL and the prevalence of low serum 25(OH)D (< 12 ng/mL) was 25.2%. Women with the lowest 25(OH)D had the highest β-CTX. After adjustment for the confounders, 25(OH)D cutoffs for OC [14.04 (12.84–15.23) ng/mL], β-CTX [13.94 (12.49–15.39) ng/mL], and P1NP [13.87 (12.37–15.37) ng/mL] in the whole population, cutoffs for OC [12.30 (10.68–13.91) ng/mL], β-CTX [12.23 (10.22–14.23) ng/mL], and P1NP [11.85 (10.40–13.31) ng/mL] in women with the GC rs2282679 G allele, and cutoffs for OC [12.75 (11.81–13.68) ng/mL], β-CTX [13.05 (11.78–14.32) ng/mL], and P1NP [12.81 (11.57–14.06) ng/mL] in women with the GC rs2282679 T allele, were observed. Below these cutoffs, BTMs were negatively associated with 25(OH)D, while above these cutoffs, BTMs plateaued.
The median serum 25(OH)D was 16.63 (11.96–22.55) ng/mL and the prevalence of low serum 25(OH)D (< 12 ng/mL) was 25.2%. Women with the lowest 25(OH)D had the highest β-CTX. After adjustment for the confounders, 25(OH)D cutoffs for OC [14.04 (12.84–15.23) ng/mL], β-CTX [13.94 (12.49–15.39) ng/mL], and P1NP [13.87 (12.37–15.37) ng/mL] in the whole population, cutoffs for OC [12.30 (10.68–13.91) ng/mL], β-CTX [12.23 (10.22–14.23) ng/mL], and P1NP [11.85 (10.40–13.31) ng/mL] in women with the GC rs2282679 G allele, and cutoffs for OC [12.75 (11.81–13.68) ng/mL], β-CTX [13.05 (11.78–14.32) ng/mL], and P1NP [12.81 (11.57–14.06) ng/mL] in women with the GC rs2282679 T allele, were observed. Below these cutoffs, BTMs were negatively associated with 25(OH)D, while above these cutoffs, BTMs plateaued.
Conclusion In Chinese women of childbearing age, there were thresholds effect of serum 25(OH)D concentrations on BTMs. The results indicated that serum 25(OH)D concentrations < 13.87 ng/mL in this population had adverse influences on maintaining bone remodeling. BTMs were suppressed at a relatively lower serum 25(OH)D in women with the GC rs2282679 G allele compared with those with the T allele.
In Chinese women of childbearing age, there were thresholds effect of serum 25(OH)D concentrations on BTMs. The results indicated that serum 25(OH)D concentrations < 13.87 ng/mL in this population had adverse influences on maintaining bone remodeling. BTMs were suppressed at a relatively lower serum 25(OH)D in women with the GC rs2282679 G allele compared with those with the T allele.
作者机构：
[Li, Gang; Han, Yang; Bai, Chenjun; Zhao, Hongling; Guan, Hua; Gao, Shanshan; Jia, Jin; Luo, Jinhua; Zhou, Ping-Kun; Liu, Xiaochang; Xie, Dafei; Guo, Hejiang; Xuan, Lihui; Gu, Yongqing; Tan, Jinpeng; Huang, Xin; Hu, Weixiang; Guan, H; Liu, Yuhao] Beijing Inst Radiat Med, Dept Radiat Biol, Beijing Key Lab Radiobiol, Beijing, Peoples R China.;[Huang, Ruixue; Luo, Jinhua; Xuan, Lihui] Cent South Univ, Xiangya Sch Publ Hlth, Dept Occupat & Environm Hlth, Changsha, Hunan, Peoples R China.;[Li, Zhongjun; Ran, Qian] Army Mil Med Univ, Affiliated Hosp 2, Lab Med Ctr, Dept Blood Transfus,Lab Radiat Biol, Chongqing, Peoples R China.;[Li, Gang; Jia, Jin; Zhou, Ping-Kun; Tan, Jinpeng] Univ South China, Hengyang Med Coll, Sch Publ Hlth, Hengyang, Hunan, Peoples R China.;[Ma, Teng] Capital Med Univ, Beijing Chest Hosp, Beijing TB & Thorac Tumor Res Inst, Canc Res Ctr, Beijing, Peoples R China.
通讯机构：
[Guan, H; Zhou, PK ] B;[Huang, RX ] C;Beijing Inst Radiat Med, Dept Radiat Biol, Beijing Key Lab Radiobiol, Beijing, Peoples R China.;Cent South Univ, Xiangya Sch Publ Hlth, Dept Occupat & Environm Hlth, Changsha, Hunan, Peoples R China.;Univ South China, Hengyang Med Coll, Sch Publ Hlth, Hengyang, Hunan, Peoples R China.
摘要：
Chemo-/radioresistance of malignant tumors hampers cancer control and increases patient mortality. Efficient repair of damaged DNA is critical for the maintenance of genomic integrity and fidelity of genetic information. In reverse, increased DNA repair capability in cancer cells contributes to chemo-/radioresistance of malignant tumors. DNA double-strand break (DSB) is the most serious DNA damage and is also the principal molecular basis of radiotherapy. Upon DNA damage, the Ku80 is recruited and forms a critical DNA-PK complex at the DSB sites with Ku70 and the catalytic subunit (DNA-PKcs) to initiate DNA repair. How DNA-PK is assembled and activated is not fully understood. Based on the identification of radiation-reduced Ku80 K568 crotonylation through quantitative global lysine crotonylome analysis, we reveal that Ku80 K568 is crotonylated by p300-CBP-associated factor (PCAF). Upon DNA damage, the K568cr is decrotonylated by HDAC8 (Histone deacetylase 8). Decrotonylation of K568cr empties this site for the subsequent SUMOylation of Ku80 by CBX4. The conversion of Ku80 from K568 crotonylation to SUMOylation facilitates the assembly of DNA-PK complex and autophosphorylation of DNA-PKcs S2056, consequently activating the DSB repair. Moreover, mutation disrupting the post-translational modification (PTM) of Ku80 K568 site sensitizes cancer cells to radiotherapy in tumor-bearing nude mice models. This study elucidates the conversion model between two different forms of PTMs in the regulation of DNA-PK complex assembly and DSB repair, highlighting this model's potential in controlling chemo-/radioresistance of malignant tumors, as well as expands the atlas of therapeutic targets.
期刊：
JOURNAL OF TOXICOLOGY AND ENVIRONMENTAL HEALTH-PART A-CURRENT ISSUES,2025年88(8):339-348 ISSN：1528-7394
通讯作者：
Liu, Jun;Zhan, CH
作者机构：
[Liu, Jun; Zhan, Chunhua; Yang, Yue; Yang, Fei; Wang, Yaqi] Univ South China, Sch Basic Med Sci, Sch Publ Hlth, Hunan Key Lab Typ Environm Pollut & Hlth Hazards,H, Hengyang 421001, Hunan, Peoples R China.;[Zeng, Wen; Zhan, Chunhua] Cent Hosp Shaoyang, Dept Publ Hlth, Shaoyang, Peoples R China.;[Yuan, Mei] Univ South China, Affiliated Hosp 2, Hengyang Med Sch, Dept Neurol, Hengyang, Hunan, Peoples R China.;[Zhan, Chunhua] Univ South China, Key Lab Rare Pediat Dis, Minist Educ, Hengyang 421001, Hunan, Peoples R China.
通讯机构：
[Liu, J; Zhan, CH ] U;Univ South China, Sch Basic Med Sci, Sch Publ Hlth, Hunan Key Lab Typ Environm Pollut & Hlth Hazards,H, Hengyang 421001, Hunan, Peoples R China.;Univ South China, Key Lab Rare Pediat Dis, Minist Educ, Hengyang 421001, Hunan, Peoples R China.
关键词：
MC-LR;Apoptosis;TNF-R1;RIPK1;HEK293
摘要：
In recent years, the outbreak of cyanobacterial blooms has become increasingly frequent. Microcystin-LR (MC-LR), a metabolite of cyanobacteria, poses a significant threat to the ecosystem and human health. Several studies have demonstrated that MC-LR might induce renal cell apoptosis, as a consequence of tissue damage. However, the molecular mechanisms underlying MC-LR-initiated renal injury remain to be determined. This investigation aimed to determine the role of apoptosis in MC-LR-induced kidney damage and its potential underlying mechanisms using the human embryonic kidney (HEK293) cell line. The results of TUNEL and immunofluorescence assays indicated that MC-LR induced increased apoptosis in HEK293 cells. Compared to control, the mRNA expression levels of RIPK1, caspase-8, and TNF-α were elevated following incubation with MC-LR, while the mRNA expression level of Bcl-2/Bax was decreased. The protein levels of RIPK1, TNF-R1, and caspase-8 were elevated in the MC-LR-treated HEK293 cells. Data demonstrated that MC-LR induced renal cell apoptosis through activation of the TNF-R1/RIPK1 pathway, providing new insights into understanding the toxic mechanisms attributed to MC-LR.
