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2025-4 Contents
2025, 38(4): 1-2.
Editorial
Identification of High-Risk Populations: The Cornerstone of Effective and Cost-Efficient Cancer Screening
Wei Cao, Fei Wang, Ni Li
2025, 38(4): 401-402. doi: 10.3967/bes2025.044
Original Article
Role of Gold Nanorods Functionalized by Nucleic Acid Nanostructures Carrying Doxorubicin in Synergistic Anti-Cancer Therapy
Hao Wu, Huangshui Ma, Xinghan Wu, Qiang Sun, Lin Feng, Ruifang Jiang, Yanhong Li, Quan Shi
2025, 38(4): 403-415. doi: 10.3967/bes2024.152
  Objective   Cancer remains a significant global health challenge, necessitating the development of effective treatment approaches. Developing synergistic therapy can provide a highly promising strategy for anti-cancer treatment through combining the benefits of various mechanisms.  Methods   In this study, we developed a synergistic strategy for chemo-photothermal therapy by constructing nanocomposites using gold nanorods (GNRs) and tetrahedral framework nucleic acids (tFNA) loaded with the anti-tumor drug doxorubicin (DOX).  Results   Our in vitro studies have systematically clarified the anti-cancer behaviors of tFNA-DOX@GNR nanocomposites, characterized by their enhanced cellular uptake and proficient lysosomal escape capabilities. It was found that the key role of tFNA-DOX@GNR nanocomposites in tumor ablation is primarily due to their capacity to induce cytotoxicity in tumor cells via a photothermal effect, which generates instantaneous high temperatures. This mechanism introduces various responses in tumor cells, facilitated by the thermal effect and the integrated chemotherapeutic action of DOX. These reactions include the induction of endoplasmic reticulum stress, characterized by elevated reactive oxygen species levels, the promotion of apoptotic cell death, and the suppression of tumor cell proliferation.  Conclusion   This work exhibits the potential of synergistic therapy utilizing nanocomposites for cancer treatment and offers a promising avenue for future therapeutic strategies.
Construction of a Prognostic Model for Lysosome-dependent Cell Death in Gastric Cancer Based on Single-cell RNA-seq and Bulk RNA-seq Data
Peng Ni, Kaixin Guo, Tianyi Liang, Xinshuang Fan, Yanqiao Hua, Yangye Gao, Shuaiyin Chen, Guangcai Duan, Rongguang Zhang
2025, 38(4): 416-432. doi: 10.3967/bes2024.159
  Objective  To identify prognostic genes associated with lysosome-dependent cell death (LDCD) in patients with gastric cancer (GC).  Methods  Differentially expressed genes (DEGs) were identified using The Cancer Genome Atlas - Stomach Adenocarcinoma. Weighted gene co-expression network analysis was performed to identify the key module genes associated with LDCD score. Candidate genes were identified by DEGs and key module genes. Univariate Cox regression analysis, and least absolute shrinkage and selection operator regression and multivariate Cox regression analyses were performed for the selection of prognostic genes, and risk module was established. Subsequently, key cells were identified in the single-cell dataset (GSE183904), and prognostic gene expression was analyzed. Cell proliferation and migration were assessed using the Cell Counting Kit-8 assay and the wound healing assay.  Results  A total of 4,465 DEGs, 95 candidate genes, and 4 prognostic genes, including C19orf59, BATF2, TNFAIP2, and TNFSF18, were identified in the analysis. Receiver operating characteristic curves indicated the excellent predictive power of the risk model. Three key cell types (B cells, chief cells, and endothelial/pericyte cells) were identified in the GSE183904 dataset. C19orf59 and TNFAIP2 exhibited predominant expression in macrophage species, whereas TNFAIP2 evolved over time in endothelial/pericyte cells and chief cells. Functional experiments confirmed that interfering with C19orf59 inhibited proliferation and migration in GC cells.  Conclusion  C19orf59, BATF2, TNFAIP2, and TNFSF18 are prognostic genes associated with LDCD in GC. Furthermore, the risk model established in this study showed robust predictive power.
Threshold-Effect Associations of Serum 25-hydroxyvitamin D on Bone Turnover Markers and GC rs2282679 Variants in Chinese Women of Childbearing Age
Xiaoyun Shan, Yuting Li, Xiayu Zhao, Yichun Hu, Siran Li, Huidi Zhang, Yang Cao, Rui Wang, Lichen Yang
2025, 38(4): 433-446. doi: 10.3967/bes2024.151
  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.  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.  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.  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.
Exploring the Efficacy of BMSC Transplantation via Various Pathways for Treating Cholestatic Liver Fibrosis in Mice
Junjie Ren, Zixu Li, Xinrui Shi, Tingting Lyu, Xiaonan Li, Min Ge, Qizhi Shuai, Tingjuan Huang
2025, 38(4): 447-458. doi: 10.3967/bes2024.180
  Objective  To compare the therapeutic efficacy of portal and tail vein transplantation of bone marrow-derived mesenchymal stem cells (BMSCs) against cholestatic liver fibrosis in mice.   Methods  BMSCs were isolated and co-cultured with starvation-activated hepatic stellate cells (HSCs). HSC activation markers were identified using immunofluorescence and qRT-PCR. BMSCs were injected into the liver tissues of bile duct ligation (BDL) mice via the tail and portal veins. Histomorphology, liver function, inflammatory cytokines, and the expression of key proteins were all determined in the liver tissues.  Results  BMSCs inhibited HSC activation by reducing α-SMA and collagen I expression. Compared to tail vein injection, DIL-labeled BMSCs injected through the portal vein maintained a high homing rate in the liver. Moreover, BMSCs transplanted through the portal vein resulted in greater improvement in liver color, hardness, and gallbladder size than did those transplanted through the tail vein. Furthermore, BMSCs injected by portal vein, but not tail vein, markedly ameliorated liver function, reduced the secretion of inflammatory cytokines, including TNF-α, IL-6, and IL-1β, and decreased α-SMA + hepatic stellate cell (HSC) activation and collagen fiber formation.  Conclusion  The therapeutic effect of BMSCs on cholestatic liver fibrosis in mice via portal vein transplantation was superior to that of tail vein transplantation. This comparative study provides reference information for further BMSC studies focused on clinical cholestatic liver diseases.
Homocysteine Levels and Determinants among Chinese Women at Mid-pregnancy, Late Pregnancy, and Postpartum
Zhenyu Guo, Hongtian Li, Yirui Ma, Ying Meng, Yubo Zhou, Jianmeng Liu
2025, 38(4): 459-468. doi: 10.3967/bes2024.155
  Objective   Data on homocysteine (Hcy) status and its determinants are limited among women during pregnancy and postpartum. This cross-sectional study aimed to investigate Hcy levels during pregnancy and postpartum, and to explore the determinants like geographic factor.  Methods   This study was conducted in women at mid-pregnancy, late-pregnancy and postpartum from southern, central and northern China. Approximately 132 women were included in each stratum by the three phases and regions. Plasma Hcy concentrations were assessed using high-performance liquid chromatography (HPLC), with hyperhomocysteinemia defined as > 10.0 µmol/L. Quantile regression was to estimate medians and interquartile ranges (IQRs), and logistic regression to examine the determinants of hyperhomocysteinemia.  Results   For 1,190 women included, the median (IQR) Hcy concentration was 5.66 (4.62, 7.37) μmol/L. The adjusted median in mid-pregnancy, late-pregnancy and postpartum women was 4.75 (4.13, 5.54), 5.72 (4.81, 6.85) and 7.09 (5.65, 8.75) μmol/L, respectively, showing an increasing trend (P < 0.001). This increasing trend persisted across the three regions. Higher Hcy concentrations were observed in women residing in northern region and those with younger age or lower economic status. A total of 106 (8.9%) women had hyperhomocysteinemia, with a higher prevalence in those residing in northern region (16.0%), or in postpartum women (16.5%).  Conclusion   Hcy levels, varying with geographic region, maternal age and economic status, are increased from mid-pregnancy to late-pregnancy and postpartum, indicating a need to monitor Hcy levels in pregnant and postpartum women to control potential risks related to elevated Hcy levels.
Antibiotic-Depleted Lung Microbiota Modulates Surfactant Proteins Expression and Reduces Experimental Silicosis
Qiang Zhou, Meiyu Chang, Ning Li, Yi Guan, Sanqiao Yao
2025, 38(4): 469-483. doi: 10.3967/bes2025.012
  Objective   Recent studies have overturned the traditional concept of the lung as a “sterile organ” revealing that pulmonary microbiota dysbiosis and abnormal surfactant proteins (SPs) expression are involved in the progression of silicosis. This study aimed to investigate the relationship between abnormal SPs expression and dysbiosis of lung microbiota in silica-induced lung fibrosis, providing insights into mechanisms of silicosis.  Methods   Lung pathology, SPs expression, and microbiota composition were evaluated in silica-exposed mice. A mouse model of antibiotic-induced microbiota depletion was established, and alveolar structure and SPs expression were assessed. The roles of the lung microbiota and SPs in silicosis progression were further evaluated in mice with antibiotic-induced microbiota depletion, both with and without silica exposure.  Results   Silica exposure induced lung inflammation and fibrosis, along with increased expression of SP-A expression. Antibiotics (Abx)-induced microbiota depletion elevated SP-A and SP-D expression. Furthermore, silica exposure altered lung microbiota composition, enriching potentially pathogenic taxa. However, antibiotic-induced microbiota depletion prior to silica exposure reduced silica-mediated lung fibrosis and inflammation.  Conclusion   Lung microbiota is associated with silica-induced lung injury. Overproduction of SP-A and SP-D, induced by Abx-induced microbiota depletion, may enhance the resistance of mouse lung tissue to silica-induced injury.
Hydrogen Sulfide Alleviates Lipid Peroxidation-Mediated Carbonyl Stress in Uranium-Intoxicated Kidney Cells via Nrf2/ARE Signaling
Jialin Liu, Min Wang, Rui Zhang, Jifang Zheng, Xixiu Jiang, Qiaoni Hu
2025, 38(4): 484-500. doi: 10.3967/bes2025.021
  Objective  To explore the protective effects and underlying mechanisms of H2S against lipid peroxidation-mediated carbonyl stress in the uranium-treated NRK-52E cells.  Methods  Cell viability was evaluated using CCK-8 assay. Apoptosis was measured using flow cytometry. Reagent kits were used to detect carbonyl stress markers malondialdehyde, 4-hydroxynonenal, thiobarbituric acid reactive substances, and protein carbonylation. Aldehyde-protein adduct formation and alcohol dehydrogenase, aldehyde dehydrogenase 2, aldo-keto reductase, nuclear factor E2-related factor 2 (Nrf2), and cystathionine β-synthase (CBS) expression were determined using western blotting or real-time PCR. Sulforaphane (SFP) was used to activate Nrf2. RNA interference was used to inhibit CBS expression.  Results  GYY4137 (an H2S donor) pretreatment significantly reversed the uranium-induced increase in carbonyl stress markers and aldehyde-protein adducts. GYY4137 effectively restored the uranium-decreased Nrf2 expression, nuclear translocation, and ratio of nuclear to cytoplasmic Nrf2, accompanied by a reversal of the uranium-decreased expression of CBS and aldehyde-metabolizing enzymes. The application of CBS siRNA efficiently abrogated the SFP-enhanced effects on the expression of CBS, Nrf2 activation, nuclear translocation, and ratio of nuclear to cytoplasmic Nrf2 and concomitantly reversed the SFP-enhanced effects of the uranium-induced mRNA expression of aldehyde-metabolizing enzymes. Simultaneously, CBS siRNA reversed the SFP-mediated alleviation of the uranium-induced increase in reactive aldehyde levels, apoptosis rates, and uranium-induced cell viability.  Conclusion  H2S induces Nrf2 activation and nuclear translocation, which modulates the expression of aldehyde-metabolizing enzymes and the CBS/H2S axis. Simultaneously, the Nrf2-controlled CBS/H2S axis may at least partially promote Nrf2 activation and nuclear translocation. These events form a cycle-regulating mode through which H2S attenuates the carbonyl stress-mediated NRK-52E cytotoxicity triggered by uranium.
Letter
Development and Validation of Machine Learning Models for Lung Cancer Risk Prediction in High-Risk Population: A Retrospective Cohort Study
Yu Su, Haoran Zhan, Shangyao Li, Yitong Lu, Ruhuan Ma, Hai Fang, Tingting Xu, Yu Tian
2025, 38(4): 501-505. doi: 10.3967/bes2025.038
Risk Factors and Predictive Model for Acute Mountain Sickness among Han Chinese Travelers to Xizang Autonomous Region
Qianhui Gong, Qiong Li, Zhichao Xu, Xiaowei Chen, Xiaobing Shen
2025, 38(4): 506-510. doi: 10.3967/bes2025.030
Kitchen Ventilation Attenuate the Association of Solid Fuel Use with Sarcopenia: A Cross-Sectional and Prospective Study
Yinghao Yuchi, Wei Liao, Jia Qiu, Ruiying Li, Ning Kang, Xiaotian Liu, Wenqian Huo, Zhenxing Mao, Jian Hou, Lei Zhang, Chongjian Wang
2025, 38(4): 511-515. doi: 10.3967/bes2025.031
Experimental Study on Distribution and Deposition Characteristics of Phi-X174 and MS2 Bacteriophages in an Air Chamber
Baoying Zhang, Cuicui Ma, Yanyan Wang, Jin Shen
2025, 38(4): 516-518. doi: 10.3967/bes2025.032
Role of the Gut–Brain Axis in Chronotype-Driven Alzheimer’s Disease: A Mendelian Randomization Study
Jingting Kong, Mengxue Wang, Xuezi Zhang, Zan Wang, Qingguo Ren
2025, 38(4): 519-524. doi: 10.3967/bes2025.033