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.
摘要：
BACKGROUND: Studies have documented associations among workplace violence (WPV), psychological capital (PsyCap), and professional commitment (PC). But limited research has investigated how PsyCap mediates the relationship between WPV and PC, particularly among nursing interns. OBJECTIVE: This study assessed the current status of WPV, PsyCap, and PC among Chinese nursing students, analyzed thier interrelationships and further determined whether PsyCap mediated the association between WPV and PC. METHODS: A cross-sectional survey of 520 nursing interns used validated instruments: a demographic questionnaire, the WPV Scale, the PC Scale, and the PsyCap Questionnaire (Chinese version of PCQ). Pearson correlation analyzed the relationships among PsyCap, WPV, and PC, while hierarchical regression tested the mediation model. RESULTS: The total scores for PC and PsyCap among nursing students were (77.04 ± 17.04) and (91.90 ± 16.16), respectively. Approximately 31.54% of the participants reported experiencing WPV. PsyCap was inversely associated with WPV (r = -0.619, p = 0.024) and positively associated with PC (r = 0.620, p < 0.001), in contrast WPV showed a negative correlation with PC (r = -0.807, p = 0.005). Mediation analysis revealed that PsyCap mediated the WPV-PC relationship, accounting for 47.5% of the total effect. CONCLUSION: Nursing students exhibited moderate levels of PsyCap and PC, with the prevalence of WPV being slightly lower than reported in comparable studies. And PsyCap fully mediated the relationship between WPV and PC. These findings revealed that nursing administrators and educators should enhance and develop nursing students' PsyCap to lower the adverse effects of WPV and promote higher levels of PC.
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.
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.
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.
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：
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.
通讯机构：
[Xiao, FB ] U;[Du, WF ] H;Univ South China, Sch Publ Hlth, Hengyang Med Sch, Hunan Key Lab Typ Environm Pollut & Hlth Hazards, Hengyang 421001, Peoples R China.;Hunan Inst Technol, Sch Chem & Environm Engn, Hengyang 421002, Peoples R China.
关键词：
Glutathione;Structural color hydrogel;Competitive coordination reaction;Colorimetric detection;Smartphone-assisted detection
摘要：
AnAg(+)-functionalized structural color hydrogel (Ag(+)-SCH) sensor is constructed for colorimetric detection of glutathione (GSH). The hydrogel is prepared by using the coordination of Ag(+) and 1-vinylimidazole (1-VI) as cross-linking network. GSH acts as a competitive ligand to break the coordination between Ag(+) and 1-VI, leading to the expansion and structural color change of the hydrogel. Quantification was achieved by measuring particle spacing changes, yielding a dynamic range of 0.1-200μM with a limit of detection (LOD) of 0.04μM. Alternatively, smartphone-based hue analysis enables sensitive GSH detection with a LOD of 0.79μM. The sensor has proven to show high selectivity, excellent reusability, and long-term stability. In human serum tests, the Ag(+)-SCH performed comparably to commercial kits, while offering significantly lower cost. This portable, low-cost platform meets practical needs for GSH monitoring in diverse settings.
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.
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.
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.
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：
[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.
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：
While numerous genetic risk loci are linked to kidney disease, a unifying therapeutic target for diverse renal pathologies remains elusive. Here, through large-cohort polymorphic locus screening, we identify the SLC39A8 A391T variant (rs13107325) as a shared modifier of multiple kidney diseases. Functional characterization using Slc39a8 A391T knock-in mice and kidney-specific Slc39a8 knockout mice reveals that loss of SLC39A8 function reduces renal zinc accumulation, thereby mitigating susceptibility to kidney injury and disease progression. Mechanistically, we demonstrate that perturbed zinc homeostasis drives renal damage, and limiting zinc levels-whether via impaired SLC39A8 activity or direct chelation-activates the zinc-AKT-FOXO1-G6PC axis to confer protection. Critically, zinc chelation with EDTA recapitulates this benefit, significantly preventing and ameliorating experimental acute and chronic kidney disease. These findings establish renal zinc homeostasis as a key therapeutic node, with SLC39A8 and zinc-modulating strategies representing promising avenues for treating a broad range of kidney diseases.
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.
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.
摘要：
Lactic acid has aroused increasing attention due to its close association with serious diseases. A real-time, dynamic, and intelligent detection method is vital for sensitive detection of lactic acid. Here, a machine learning (ML)-assisted perspiration-driven self-powered sensor (PDS sensor) is fabricated using Ni-ZIF-8@lactate oxidase and pyruvate oxidase (Ni-ZIF-8@LOx&POx)/laser-induced graphene (LIG), bilirubin oxidase (BOD)/LIG, and a microchannel for highly sensitive and real-time monitoring of lactic acid in sweat. Driven by the oxidation reaction of lactic acid, PDS sensors exhibit excellent sensitivity, a wide detection range, good reproducibility, and excellent selectivity for lactic acid detection in sweat. When subjects with different body mass index (BMI) undergo aerobic or anaerobic exercise or maintain a sedentary state, PDS sensors can monitor lactic acid in sweat wirelessly and in real-time. Moreover, a ML algorithm was employed to assist PDS sensors to detect lactic acid in the subjects' sweat with a high prediction accuracy of 96.0%.
摘要：
The proliferation of cyanobacteria due to eutrophication has become a critical environmental issue, adversely affecting aquatic ecosystems and water quality. This study explores the potential of silicon carriers to promote diatom growth as a strategy to outcompete harmful cyanobacteria, utilizing both continuous flow reactors and in-situ enclosures in a eutrophic lake. The carriers effectively supplemented metasilicates, increasing diatom biomass by 6.3 times while suppressing cyanobacterial densities by 50 %. Diatoms completely covering the carriers absorbed phosphorus from the water for their proliferation, thereby securing a competitive advantage over cyanobacteria in phosphorus utilization. This led to an 84 % reduction in total phosphorus (TP) concentrations, higher dissolved oxygen levels, and increased water transparency. The resource-based competition model demonstrated the competitive dynamics between diatoms and cyanobacteria mediated by carrier systems, while establishing the critical silicon-to-phosphorus ratio threshold (≥ max[566, 251 + 6.88/TP]) required for diatom dominance under a dilution rate of 0.1 per day. These findings highlight the potential of silicon carriers as an innovative approach for controlling cyanobacterial blooms while simultaneously improving water quality through silicon supplementation and enhancing the competitiveness of diatoms.
The proliferation of cyanobacteria due to eutrophication has become a critical environmental issue, adversely affecting aquatic ecosystems and water quality. This study explores the potential of silicon carriers to promote diatom growth as a strategy to outcompete harmful cyanobacteria, utilizing both continuous flow reactors and in-situ enclosures in a eutrophic lake. The carriers effectively supplemented metasilicates, increasing diatom biomass by 6.3 times while suppressing cyanobacterial densities by 50 %. Diatoms completely covering the carriers absorbed phosphorus from the water for their proliferation, thereby securing a competitive advantage over cyanobacteria in phosphorus utilization. This led to an 84 % reduction in total phosphorus (TP) concentrations, higher dissolved oxygen levels, and increased water transparency. The resource-based competition model demonstrated the competitive dynamics between diatoms and cyanobacteria mediated by carrier systems, while establishing the critical silicon-to-phosphorus ratio threshold (≥ max[566, 251 + 6.88/TP]) required for diatom dominance under a dilution rate of 0.1 per day. These findings highlight the potential of silicon carriers as an innovative approach for controlling cyanobacterial blooms while simultaneously improving water quality through silicon supplementation and enhancing the competitiveness of diatoms.
摘要：
Air pollution has emerged as an essential risk factor for overweight and obesity. However, the combined effects of multiple air pollutants on overweight/obesity development in children and adolescents are not fully understood. In this study, a total of 189,448 children and adolescents in China were included. Logistics, weighted quantile sum, quantile g-computation, and bayesian kernel machine regression models were used to systematically assess the association between long-term outdoor air pollution exposure and overweight/obesity, and identified the major contributors. Our results revealed a significantly positive association of PM 2.5 , PM 10 , CO, and NO 2 concentrations with overweight/obesity risk. Multi-pollutant models consistently demonstrated a positive association between the air pollutant mixture and the risk of overweight/obesity (OR: 1.825; 95 % CI: 1.036, 2.614). PM 2.5 and PM 10 were identified as the most significant contributors. Furthermore, we found significantly positive overall effects and interactions of these pollutants on an additive risk of overweight/obesity. The effects of air pollutants on overweight/obesity were pronounced in boys, rural residents, smokers, and primary school students. Our findings demonstrated that long-term exposure to air pollutants, particularly PM 2.5 and PM 10 was positively linked with an increased risk of overweight/obesity in children and adolescents. The cross-sectional design and potential confounders limited the ability to establish causality. Prospective cohort studies and specific mechanism investigations are needed to provide more precise and robust evaluations in the future. Coordinated policies to reduce air pollutants and mitigate their combined effects are essential for addressing this public health issue.
Air pollution has emerged as an essential risk factor for overweight and obesity. However, the combined effects of multiple air pollutants on overweight/obesity development in children and adolescents are not fully understood. In this study, a total of 189,448 children and adolescents in China were included. Logistics, weighted quantile sum, quantile g-computation, and bayesian kernel machine regression models were used to systematically assess the association between long-term outdoor air pollution exposure and overweight/obesity, and identified the major contributors. Our results revealed a significantly positive association of PM 2.5 , PM 10 , CO, and NO 2 concentrations with overweight/obesity risk. Multi-pollutant models consistently demonstrated a positive association between the air pollutant mixture and the risk of overweight/obesity (OR: 1.825; 95 % CI: 1.036, 2.614). PM 2.5 and PM 10 were identified as the most significant contributors. Furthermore, we found significantly positive overall effects and interactions of these pollutants on an additive risk of overweight/obesity. The effects of air pollutants on overweight/obesity were pronounced in boys, rural residents, smokers, and primary school students. Our findings demonstrated that long-term exposure to air pollutants, particularly PM 2.5 and PM 10 was positively linked with an increased risk of overweight/obesity in children and adolescents. The cross-sectional design and potential confounders limited the ability to establish causality. Prospective cohort studies and specific mechanism investigations are needed to provide more precise and robust evaluations in the future. Coordinated policies to reduce air pollutants and mitigate their combined effects are essential for addressing this public health issue.
