最新刊期

    Zhao Yan, Han Mei-Qiong, Pu Jia-Yuan, Bai Ming

    DOI:10.11855/j.issn.0577-7402.1560.2026.0506
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    摘要:Obstructive sleep apnea (OSA) is a common sleep-related breathing disorder characterized by recurrent upper airway collapse and intermittent hypoxia. With advances in the understanding of OSA pathophysiology, pharmacological therapy has emerged as a potential adjunct to continuous positive airway pressure (CPAP). Current evidence suggests that pharmacological interventions primarily exert their effects by improving metabolic status, enhancing upper airway stability, and modulating ventilatory drive, thereby reducing respiratory events and hypoxic burden to some extent. However, some combination therapies have not demonstrated clear synergistic effects, and robust evidence regarding long-term efficacy and safety remains limited. In addition, considerable heterogeneity exists among studies, most of which are constrained by small sample sizes and short follow-up durations. This review focuses on three key pathophysiological domains—metabolic regulation, upper airway neuromuscular control, and ventilatory stability—and summarizes the mechanisms of action and clinical research progress of related pharmacological agents, with representative drugs highlighted. The aim is to provide a reference for identifying appropriate patient populations and optimizing pharmacological strategies within the comprehensive management of OSA.  
    关键词:obstructive sleep apnea;pharmacotherapy;therapeutic advances   
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    更新时间:2026-05-07

    Li Ding, Chen Jia-Ning, Liu Xue-Chen, Lin-Ying, Gao Qi-Chang, Xu Jing, Zhang Xi

    DOI:10.11855/j.issn.0577-7402.2253.2026.0507
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    摘要:ObjectiveTo identify risk factors for sleep disorders in high-altitude migrants and to develop and validate an individualized nomogram prediction model based on readily obtainable variables.MethodsFrom July to August 2025, a questionnaire survey was conducted among eligible high-altitude migrants residing at various elevations in the Xizang Autonomous Region using a cluster random sampling method. Data regarding demographics, lifestyle habits, high-altitude residence history, past medical history, sleep quality, and fatigue levels were collected from a total of 1,405 participants. The surveyed cohort was randomly allocated into a training set (n = 984) and a validation set (n = 421) at a 7:3 ratio. Independent risk factors were identified using univariate analysis, least absolute shrinkage and selection operator (LASSO) regression, and multivariate logistic regression, which were subsequently utilized to construct a predictive nomogram. The model's discrimination, calibration, and clinical utility were internally validated employing receiver operating characteristic (ROC) curves, calibration plots, the Hosmer-Lemeshow test, and decision curve analysis (DCA).ResultsAfter preliminary screening of potential variables via univariate analysis and LASSO regression, subsequent multivariate logistic regression analysis identified seven independent risk factors for high-altitude sleep disorders: education level, altitude of residence, duration of high-altitude residence, durations of hyperlipidemia, hyperuricemia, and lumbar disc herniation, and the total score of the Multidimensional Fatigue Inventory-20 (MFI-20). A predictive nomogram model was established based on these risk factors and subsequently validated. The areas under the receiver operating characteristic curve (AUC) for the nomogram in the training and validation sets were 0.857 and 0.818, respectively. Calibration curves exhibited good consistency between the predicted and observed probabilities, and the Hosmer-Lemeshow test yielded P-values of 0.433 and 0.087 in the training and validation sets, respectively, indicating a satisfactory goodness-of-fit. Furthermore, decision curve analysis (DCA) demonstrated that the model could provide significant clinical net benefit when the threshold probabilities ranged from 0.1 to 0.9 in the training set and from 0.15 to 1.0 in the validation set.ConclusionsEducation level, altitude of residence, duration of high-altitude residence, durations of hyperlipidemia, hyperuricemia, and lumbar disc herniation, along with the MFI-20 total score, are risk factors for sleep disorders among high-altitude migrants. The nomogram model developed in this study, based on readily obtainable questionnaire data, demonstrates robust predictive performance for evaluating the overall risk of sleep disorders in this population.  
    关键词:high-altitude;sleep disorders;nomogram;Logistic regression   
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    更新时间:2026-05-07

    Liang Shu-Ling, Tong Lin, Xia Xue-Yan, Huang Xian-Tu, Zhang Biao

    DOI:10.11855/j.issn.0577-7402.2333.2026.0507
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    摘要:Sepsis-associated encephalopathy (SAE) is a diffuse cerebral dysfunction induced by sepsis, without direct infection of the central nervous system (CNS), structural abnormality, or other types of encephalopathy. Its main clinical manifestations include altered consciousness, cognitive impairment, somnolence and coma. The pathogenic mechanisms of SAE involve neuroinflammation, oxidative stress, blood brain barrier (BBB) disruption, complement system activation, and neurotransmitter imbalance. Regulatory T cells (Tregs) act as key regulators of systemic immune homeostasis. They do not rely solely on immunosuppressive functions; instead, they participate in the pathological regulation of SAE by targeting key pathological processes, including neuroinflammation, oxidative stress, BBB integrity, complement system activity, and neurotransmitter balance. They play a pivotal role in the development of SAE. This review systematically summarizes the mechanisms and therapeutic strategies of Tregs in the pathophysiological processes of SAE, aiming to deepen the understanding of SAE modulation by Tregs and provide a theoretical basis as well as novel research directions for the immunotargeted therapy of SAE.  
    关键词:regulatory T cells;sepsis-associated encephalopathy;sepsis   
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    更新时间:2026-05-07

    Wang Qing-Qing, Ding Jie, Li Hai-Wen, Liu Huai-E, Geng Peng, Li Sheng-Hao, Yang Yong-Rui

    DOI:10.11855/j.issn.0577-7402.2075.2026.0429
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    摘要:ObjectiveTo explore the impact of hypochloremia on the short-term poor prognosis of patients with grade 2/3 cirrhotic ascites.MethodsA total of 119 patients hospitalized for grade 2/3 cirrhotic ascites from October 1, 2022 to September 30, 2023 were consecutively enrolled in this retrospective cohort study. The optimal cut-off value of serum Cl⁻ was calculated using X-tile software. The three independent study endpoints were poor clinical outcomes at one year after admission, namely mortality, advanced decompensation and readmission due to ascites. The predictive value of serum Cl⁻ was evaluated through Cox regression, Kaplan-Meier curves, and time-dependent ROC curves, and subgroup analyses were also performed based with or without hepatic malignancy.ResultsThe optimal cut-off value of serum Cl⁻ for predicting the 1-year risk of poor outcomes in patients with grade 2/3 cirrhotic ascites was 104.9 mmol/L. Multivariate Cox regression analysis showed that serum Cl⁻<104.9 mmol/L was an independent risk factor for 1-year mortality (HR=0.230, 95%CI 0.13-0.67), advanced decompensation (HR=0.31, 95%CI 0.16-0.59), and readmission due to ascites (HR=0.47, 95%CI 0.24-0.94) in patients with grade 2/3 cirrhotic ascites (P<0.05). Kaplan-Meier curves showed that the cumulative risk of the above poor outcomes was significantly higher in patients with serum Cl⁻<104.9 mmol/L than in those with serum Cl⁻ ≥104.9 mmol/L (Log-rank P<0.05). Time-dependent ROC curves and Delong tests showed that the predictive efficacy of serum Cl⁻ level was comparable to that of traditional Child-Pugh and MELD scores (P>0.05). Serum Cl⁻<104.9 mmol/L had a good predictive value for mortality in both subgroups with or without liver malignancy, but the prediction of advanced decompensation only existed in the subgroup without hepatic malignancy, and the prediction of readmission due to ascites was not significant in either subgroup.ConclusionLower serum Cl⁻ (<104.9 mmol/L) is an independent risk factor for short-term poor prognosis in patients with grade 2/3 ascites due to liver cirrhosis, and treatment of hypochloremia is probably an important strategy to improve the prognosis of such patients.  
    关键词:hypochloremia;cirrhosis;ascites;poor prognosis   
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    更新时间:2026-05-05

    Wang Min-Min, Liu Zhi-You, Cheng Meng-Yao, Zhang Li-Xia, Zhang Zheng

    DOI:10.11855/j.issn.0577-7402.2116.2026.0424
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    摘要:ObjectiveTo investigate the predictive value of the triglyceride-glucose-body mass index (TyG-BMI) combined with glycated hemoglobin (HbA1c) for in-stent restenosis (ISR) in patients with coronary artery disease undergoing percutaneous coronary intervention (PCI).MethodsThis retrospective study collected and analyzed the clinical data of 1908 patients diagnosed with coronary heart disease who underwent successful drug-eluting stent (DES) implantation at the Department of Cardiology, the First Hospital of Lanzhou University, between January 1, 2022, and December 31, 2024, and received follow-up coronary angiography (CAG) 9~12 months later. Based on follow-up CAG findings, 390 patients who developed ISR were assigned to the ISR group, and 1518 patients without ISR were assigned to the NISR group. Propensity score matching (PSM) was performed at a 1:2 ratio, resulting in a matched cohort of 848 patients, including 310 in the ISR group and 538 in the NISR group. Univariate and multivariate logistic regression analyses were performed to identify risk factors for ISR, and an interaction term (TyG-BMI×HbA1c) was additionally included in the multivariate model to assess the potential interaction between TyG-BMI and HbA1c. Multivariable-adjusted restricted cubic spline (RCS) models were used to evaluate the dose–response relationships of TyG-BMI and HbA1c with ISR risk, and threshold effect analysis was performed to identify potential inflection points. Receiver operating characteristic (ROC) curves were generated, and the area under the curve (AUC) was calculated to assess the predictive value of TyG-BMI and HbA1c for ISR. Differences in AUC between individual and combined indicators were compared using DeLong's test.ResultsAfter PSM, TyG-BMI and HbA1c levels were significantly higher in the ISR group than in the NISR group (P<0.001). Univariate logistic regression analysis indicated that both TyG-BMI and HbA1c were associated with ISR (P<0.001), and multivariate logistic regression analysis further showed that TyG-BMI (OR=1.03, 95%CI 1.02~1.04) and HbA1c (OR=1.75, 95%CI 1.49~2.07) were independent risk factors for ISR (P<0.001). ROC curve analysis with DeLong's test demonstrated that among the individual indicators, TyG-BMI showed the best predictive performance for ISR (AUC=0.770, 95%CI 0.736~0.804), outperforming TyG (AUC=0.725) and HbA1c (AUC=0.742). Furthermore, the combination of TyG-BMI and HbA1c provided significantly higher predictive efficacy than any single indicator (AUC=0.810, 95%CI 0.779~0.841, P<0.001). Multivariable-adjusted restricted cubic spline analysis indicated a positive linear association between TyG-BMI and ISR risk (Pnon-linear=0.431), whereas HbA1c exhibited a significant nonlinear association with ISR risk (Pnon-linear<0.001).ConclusionsTyG-BMI and HbA1c are independent risk factors and significant predictors for ISR post-PCI in coronary heart disease patients, with their combination providing superior predictive performance.  
    关键词:triglyceride glucose-body mass index;glycated hemoglobin;in-stent restenosis;insulin resistance   
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    更新时间:2026-04-29

    Liu Jia-Yu, Jian Ning-Zhang

    DOI:10.11855/j.issn.0577-7402.2567.2026.0418
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    摘要:Brain-computer interface and neuromodulation technologies are promoting the intervention for neuropsychiatric disorders to evolve from fixed-parameter stimulation towards personalization, closed-loop operation, and intelligence. Focusing on representative scenarios such as Parkinson's disease, treatment-resistant depression, Alzheimer's disease, drug-resistant focal epilepsy, and post-stroke hemiplegia rehabilitation, this article integrates and reviews the application status of deep brain stimulation, responsive neurostimulation, non-invasive brain stimulation, and brain-computer interface-assisted rehabilitation, incorporating recent clinical research and technological advances. Overall, the evidence for neuromodulation in Parkinson's disease and some epilepsies is relatively robust, providing a practical foundation for further advancement towards closed-loop and intelligent systems. Applications related to depression, Alzheimer's disease, and stroke rehabilitation remain primarily exploratory and translational, with their efficacy stability, indication boundaries, and long-term benefits requiring further validation. Artificial intelligence shows potential in signal decoding, parameter optimization, and follow-up management, but most research remains in early stages, with a distance from standardized clinical application. This article aims to assess the practical foundation, key issues, and feasible directions for the integrated development of brain-computer interfaces and neuromodulation from a clinical practice perspective, providing references for the standardized application of related technologies and subsequent research.  
    关键词:neuromodulation;brain-computer interface;closed-loop stimulation;artificial intelligence;neuropsychiatric disorders   
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    更新时间:2026-04-28

    Liu Lu, Xiao Kun, Zhang Chun-Yang, Ding Yi-Wei, Zhang Shuo, Tan Zhou-Li, Chen Xu-Xin, Han Zhi-Hai

    DOI:10.11855/j.issn.0577-7402.0054.2026.0427
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    摘要:ObjectiveTo fabricate ultrasmall soluble ruthenium nanoparticles (sRuNP) with favorable water solubility and biocompatibility, and to evaluate their protective effects against H2O2-induced oxidative stress injury in lung epithelial cells as well as the underlying mechanism.MethodsSoluble ultrasmall Ru nanoparticles were synthesized via thermal decomposition combined with ligand exchange. Transmission electron microscopy (TEM), particle size analysis, and X-ray photoelectron spectroscopy (XPS) were used to characterize their morphology, particle size, elemental composition, valence states, and surface chemical properties, as well as their dispersion stability in normal saline and complete RPMI-1640 medium in vitro. The CCK-8 assay was performed to determine the viability of A549 lung epithelial cells treated with different concentrations of sRuNP. A549 cells were divided into three groups: control group, H2O2 group, and H2O2+sRuNP (10 μg/ml) group. Cell death was assessed by Calcein-AM/PI double staining. Commercial kits were used to measure malondialdehyde (MDA) content and superoxide dismutase (SOD) activity. The expression levels of acetylated SOD2 (ac-SOD2) and total SOD2 were detected by Western blotting.ResultsThe prepared sRuNP had a uniform particle size of (2.00±0.18) nm. XPS spectra showed characteristic peaks of Ru, C, and O. Ru existed mainly in metallic (Ru0) and oxidized (Ru4+) states, while the C 1s and O 1s spectra confirmed surface modification with organic ligands. No obvious precipitation was observed for sRuNP at 0, 4, 40, and 400 μg/ml in saline at 25 ℃ for 24 h, or at 0, 1, and 10 μg/ml in complete RPMI-1640 medium at 37 ℃ for 24 h. After 24 h of treatment, 1 μg/ml and 10 μg/ml sRuNP showed no significant difference in A549 cell viability compared with the control group (P>0.05). Compared with control group, H2O2 group exhibited increased cell death, elevated MDA content, reduced SOD activity, and a higher ac-SOD2/SOD2 ratio (P<0.05). In contrast, compared with H2O2 group, H2O2+sRuNP group showed decreased cell death, lower MDA levels, higher SOD activity, and a lower ac-SOD2/SOD2 ratio (P<0.05).ConclusionssRuNP at 10 μg/ml exhibit good stability and biosafety in vitro. They exert significant antioxidant effects on lung epithelial cells, and inhibition of SOD2 acetylation as a potential molecular mechanism.  
    关键词:ultrasmall ruthenium nanoparticles;oxidative stress;acute lung injury;lung epithelial cells;acetylated superoxide dismutase 2   
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    更新时间:2026-04-28

    Dong Xiao-Yan, Abulizi Ayinuer, Mahati Shaya, Aimudula Ainiwaer

    DOI:10.11855/j.issn.0577-7402.0578.2026.0422
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    摘要:ObjectiveTo explore the expression of IGF2BP2 (insulin growth factor 2 mRNA binding protein 2) in cervical cancer (CC) and its Impact on the Malignant phenotype of Cervical Cancer Cells.MethodsTo compare the expression of IGF2BP2 in cervical cancer and normal tissues, as well as its correlation with patient staging and survival used by the Cancer Genome Atlas (TCGA) database, the Genotype-Tissue Expression (GTEx) database, and the Gene Expression Omnibus (GEO) database.The expression of IGF2BP2 was confirmed by tissue microarray immunohistochemistry, qRT-PCR and Western blot.Infect cervical cancer cells SiHa and Caski with lentiviruses to construct IGF2BP2 downregulation groups (IGF2BP2 knockdown), IGF2BP2 upregulation groups (IGF2BP2 overexpression), and control groups (downregulation control, upregulation control). Observe the effects of IGF2BP2 expression changes on the proliferation, apoptosis, migration, invasion, and epithelial-mesenchymal transition (EMT)-related protein expression of cervical cancer cells.ResultsThe expression level of IGF2BP2 in cervical cancer tissues and cells was significantly higher than that in normal tissues (P<0.05). In cervical cancer, the expression level of IGF2BP2 was not significantly correlated with the clinical stage or overall survival time of patients (P>0.05), but was correlated with median survival time (P<0.05). Compared with the downregulated control group, the downregulated IGF2BP2 group showed significantly inhibited proliferation and colony formation ability of cervical cancer cells, increased apoptosis rate, decreased migration and invasion abilities, downregulated expression of N-cadherin and Vimentin, and upregulated expression of E-cadherin, with all differences being statistically significant (P<0.05). Compared with the upregulated control group, the upregulated IGF2BP2 group exhibited increased proliferation and colony formation ability of cervical cancer cells, decreased apoptosis rate, enhanced migration and invasion abilities, upregulated expression of N-cadherin and Vimentin, and downregulated expression of E-cadherin (P<0.05).ConclusionIGF2BP2 is upregulated in cervical cancer and enhances the malignant phenotype of cervical cancer cells.  
    关键词:cervical cancer;IGF2BP2;proliferation;migration;invasion   
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    更新时间:2026-04-24

    Tao Yong, Tu Shu

    DOI:10.11855/j.issn.0577-7402.0404.2026.0421
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    摘要:Inflammatory vitreoretinal disease (IVRD) comprises a heterogeneous group of blinding disorders characterized by immune-inflammatory injury in the posterior segment, including infectious and noninfectious uveitis as well as selected retina/choroid disorders in which inflammation is a major driver of tissue damage. Recent advances indicate that IVRD management is shifting from empirical inflammation control toward mechanism-based precision care. On the diagnostic side, polymerase chain reaction, metagenomic next-generation sequencing, cytokine profiling, immunogenetic markers and microRNA-based assays have improved etiologic identification and immune phenotyping. On the therapeutic side, sustained-release corticosteroids, suprachoroidal drug delivery, anti-TNF-α and anti-IL-6 receptor biologics, and JAK inhibitors have expanded options for refractory disease, whereas exosomes, nanocarriers and gene-editing delivery systems are opening new avenues for long-acting and minimally invasive posterior segment therapy. This article aims to provide a comprehensive overview of the latest advances in the diagnosis and treatment of IVRD, focusing on molecular diagnostics, immune marker detection, and emerging therapeutic technologies. It also addresses the main challenges in the current treatment of IVRD, such as the lack of standardized disease classification and the insufficient clinical translation of biomarkers. The article proposes that future precision medicine efforts should prioritize evidence-based approaches, focusing on "precise stratification, targeted drug delivery, and long-term safety evaluation" to improve visual outcomes and reduce the risks of recurrence and blindness.  
    关键词:inflammatory vitreoretinal disease;immune markers;targeted therapy;biological agents   
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    更新时间:2026-04-23

    Luo Kun, Wu Miao, Yuan Yuan-Hong

    DOI:10.11855/j.issn.0577-7402.1839.2026.0413
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    摘要:ObjectiveA neural network model was established by integrating biological indicators such as regulatory T cells (Treg) and helper T cell 17 (Th17) with clinical indicators, providing personalized predictions for elderly patients at high risk of intestinal necrosis due to incarcerated hernia.Methods140 elderly patients with incarcerated inguinal hernia who visited our hospital from January 2023 to January 2025 were selected as the research subjects, with 95 males and 45 females. The age ranged from 65 to 83 years, with an average age of (74.6±8.2) years. According to the presence or absence of intestinal necrosis during operation, the patients were divided into non-intestinal necrosis group (n=88) and intestinal necrosis group (n=52). The clinical data of the two groups were collected and compared. The least absolute shrinkage and selection operator (LASSO) regression method was used to screen the influencing factors of intestinal necrosis in elderly incarcerated hernia. Logistic regression analysis was employed to identify the risk factors for intestinal necrosis in elderly incarcerated hernia. The total sample (n=140) was divided into a training set (n=98) and an internal validation set (n=42) in a 7:3 ratio using the random number generation method of the computer. The back propagation (BP) neural network model was constructed using Python 3.6 on the training set. Using R software (version 3.5.3) in conjunction with the rms package, a calibration curve was drawn to evaluate the consistency between the predicted probabilities of the model and the actual occurrence probabilities. The receiver operating characteristic (ROC) and the area under the curve (AUC) were used to assess the predictive efficacy of the model. The clinical net benefit of the model at different threshold probabilities was evaluated using decision curve analysis (DCA).Results(1) Oral anticoagulant history, abdominal surgery history, incarceration history, incarceration type, incarceration time, D-dimer, neutrophil count (NEUT) and Treg/Th17 were risk factors for intestinal necrosis in elderly patients with incarcerated hernia (P<0.05). (2) Treg/Th17 had the highest contribution to model classification, followed by D-dimer, impaction time, impaction type, NEUT, impaction history, oral anticoagulant history, abdominal surgery history. The predicted probabilities in the training set and the validation set were highly consistent with the actual probabilities (Brier score=0.073, 0.075), suggesting good model calibration. The prediction accuracy of the BP neural network model in the training set was 94.21%, with an AUC of 0.913 (95% CI 0.821-0.965, P<0.001). The prediction accuracy in the validation set was 90.45%, with an AUC of 0.896 (95% CI 0.815-0.957, P<0.001), the accuracy of this model is very good. DCA analysis showed that the model had high clinical value.ConclusionsThe neural network model based on Treg/Th17 fusion has a high predictive value for the risk of intestinal necrosis in elderly patients with incarcerated hernia.  
    关键词:the elderly;incarcerated hernia;intestinal necrosis;Treg/Th17;neural network model   
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    更新时间:2026-04-21

    Ma Hong-Bo, Liu Xu, Zeng Wei, Jiang Qing-Quan, Wang Ya-Ning, He Li-Sha, Zheng Chuan

    DOI:10.11855/j.issn.0577-7402.2340.2026.0416
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    摘要:Acute High Altitude Illness (AAI) is a prevalent disorder among individuals ascending rapidly to high altitudes, resulting from systemic physiological dysregulation in response to the hypoxic environment. In recent years, significant progress has been made in non-pharmacological management of AAI within both Western and Traditional Chinese Medicine (TCM) frameworks. Western medical includes oxygen therapy, graded acclimatization, regulated physical and respiratory training, and environmental adjustments to promote physiological adaptation. TCM modalities, such as acupuncture and traditional exercises (e.g., Qi-yuan Qigong and guided diaphragmatic breathing), have been shown to enhance hypoxia tolerance. Moreover, the development of risk prediction models incorporating multidimensional indicators has become critical for the early identification of high-risk populations and paves the way for precise prevention and treatment. This review synthesizes current research advances in this field, with the objective of informing more practical, evidence-based strategies for high-altitude health management.  
    关键词:acute high altitude illnesses;prophylaxis and therapy;Western medicine;Traditional Chinese Medicine;non-pharmacological   
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    更新时间:2026-04-21

    Qiao Qian, Chen Zhao-Feng, Liu Min

    DOI:10.11855/j.issn.0577-7402.1869.2026.0416
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    摘要:ObjectiveTo examine the independent and joint associations of physical activity (PA) and minimally processed food (MPF) intake with mortality risk among patients with metabolic dysfunction-associated steatotic liver disease (MASLD)..MethodsData were obtained from the National Health and Nutrition Examination Survey (NHANES) 2007-2018. A total of 1825 participants with MASLD were included. PA was quantified as metabolic equivalent minutes per week (MET-min/week) using the Global Physical Activity Questionnaire (GPAQ). MPF intake was estimated from 24-hour dietary recall data according to the NOVA food processing classification system. Cox proportional hazards models were used to evaluate the associations of PA and MPF intake with all-cause, cardiovascular, and non-cardiovascular mortality. Joint association analyses and restricted cubic spline (RCS) models were further performed to assess dose-response relationships. Sensitivity analyses were conducted using alternative MASLD definitions [fatty liver index (FLI) >30, United States fatty liver index (US-FLI) >60, and US-FLI >30] and by excluding participants who died within the first 24 months of follow-up.ResultsAmong 1,825 patients with MASLD followed for a median of 87 months, 149 deaths were recorded, including 45 cardiovascular deaths and 104 non-cardiovascular deaths. In the fully adjusted model, high PA (≥1500 MET-min/week) was associated with a borderline increased risk of all-cause mortality (HR=1.14, 95%CI 1.00-1.29), whereas higher MPF intake was associated with lower risks of all-cause mortality (HR=0.73, 95%CI 0.65-0.81), cardiovascular mortality (HR=0.73, 95%CI 0.65-0.82), and non-cardiovascular mortality (HR=0.73, 95%CI 0.65-0.82). Joint analysis showed that the combination of high MPF intake and low PA was associated with the lowest mortality risk (all-cause mortality: HR=0.75, 95%CI 0.63-0.88; cardiovascular mortality: HR=0.76, 95%CI 0.64-0.90; non-cardiovascular mortality: HR=0.76, 95%CI 0.64-0.91). Restricted cubic spline analysis revealed significant nonlinear associations between PA and the risks of all-cause, cardiovascular, and non-cardiovascular mortality (all P_non-linearity<0.001). Although MPF intake showed an overall inverse association with mortality risk that appeared approximately linear, tests for nonlinearity indicated that the association was not strictly linear (all P_non-linearity<0.05). Sensitivity analyses confirmed the robustness of these findings.ConclusionIn patients with MASLD, high PA did not show a consistently protective association with mortality, whereas higher MPF intake was generally associated with lower mortality risk. Joint analysis suggested that dietary optimization may provide additional benefits beyond simply increasing PA. The combination of moderate PA and higher MPF intake may represent a more favorable lifestyle pattern for individuals with MASLD and may have implications for individualized management and public health strategies.  
    关键词:metabolic dysfunction-associated steatotic liver disease;physical activity;unprocessed food;mortality;NHANES   
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    更新时间:2026-04-21

    Tian Na, Su Nan, Yu Ying

    DOI:10.11855/j.issn.0577-7402.2598.2026.0420
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    摘要:The lung is vital human respiratory organ that are susceptible to damage caused by infections, physical or chemical stimuli, and other factors. Effective repair following lung injury is crucial for maintaining pulmonary function homeostasis. The process of lung injury repair is regulated by various factors, with pulmonary macrophages playing a pivotal role in this process. Pulmonary macrophages promote the repair process after lung injury through phagocytosis, phenotypic polarization, secretion of cytokines, and interaction with alveolar epithelial cells and vascular endothelial cells. Therefore, targeted intervention in the differentiation of pulmonary macrophages may represent an effective approach to mitigating lung injury and promoting tissue repair. This article reviews the research progress on the molecular mechanisms which pulmonary macrophages contribute to lung injury repair, aiming to provide new perspectives for understanding the pathophysiological processes of pulmonary diseases, and a theoretical reference for new therapeutic strategies targeting pulmonary macrophages.  
    关键词:acute lung injury;lung injury repair;pulmonary macrophages;alveolar macrophages   
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    更新时间:2026-04-21

    Li Huan, Yan Hong-Lin, Long Hui, Chen Xi, Wu Yu, Huang Xue-Fang

    DOI:10.11855/j.issn.0577-7402.2012.2026.0416
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    摘要:ObjectiveTo investigate the clinical manifestations, endoscopic features, pathological characteristics, therapeutic strategies, and prognostic outcomes of isolated Langerhans cell histiocytosis (LCH) involving the stomach in adult patients.MethodsThe clinical data of one adult patient with isolated gastric LCH were analyzed retrospectively. Relevant literatures from PubMed, China National Knowledge Infrastructure (CNKI), and Wanfang Data were retrieved to summarize the disease's clinical features, endoscopic findings, pathological characteristics, treatment, and prognosis.ResultsA 61-year-old female was admitted with "intermittent epigastric pain for 1 month, worsening over 15 days". Gastroscopy revealed a congestive and erosive lesion on the greater curvature of the gastric antrum. Pathological examination showed abnormally proliferated Langerhans cells distributed in nests and sheets in the gastric mucosal lamina propria; these medium-sized cells had slightly eosinophilic cytoplasm, oval nuclei with indistinct nucleoli and visible nuclear grooves, accompanied by background inflammatory cells (eosinophils, lymphocytes, plasma cells). Immunohistochemistry demonstrated positivity for CD1α, S-100, Langerin, CyclinD1, and CD68; scattered cells were positive for p53; the Ki-67 proliferation index was 20%. Gastroscopy reexamination after 2 months revealed that the original erosion lesion on the greater curvature of the gastric antrum was basically healed, while scattered erosion lesions were observed on the greater curvature of the antral-body junction. A literature search identified 28 reported cases of adult isolated gastric LCH, mostly in males (mean age: 45 years). Endoscopically, elevated lesions or polyps were the main manifestations. Pathology combined with immunohistochemistry was the diagnostic gold standard, with consistent positivity for CD1α, S-100, Langerin, and CyclinD1.ConclusionsIsolated gastric LCH is rare, often lacks specific clinical symptoms, and presents with diverse endoscopic features, yet has a favorable prognosis. Endoscopists and pathologists should base diagnoses on pathological and immunohistochemical findings to avoid missed or misdiagnoses.  
    关键词:isolated Langerhans cell histiocytosis of the stomach;endoscopic findings;pathological characteristics   
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    Zhang Bao-Hua, Liu Yuan, Zhao Ming-Xing, Li Chun-Lin, Zhang Shan

    DOI:10.11855/j.issn.0577-7402.2636.2026.0416
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    摘要:ObjectiveTo clarify the relationship between Life's Essential 8 (LE8) scores and cognitive impairment in elderly patients with H-type hypertension and to explore the potential effect modification of high-sensitivity C-reactive protein (hs-CRP).MethodsMedical records of 512 elderly patients with H-type hypertension admitted to the Second Medical Center of Chinese PLA General Hospital in Beijing from June 2020 to June 2025 were collected. Patients were divided into a cognitive impairment group (n=225) and a control group (n=287) based on cognitive status. Baseline characteristics were compared between the two groups. Multivariate logistic regression was used to identify independent risk factors for cognitive impairment. Patients were stratified by hs-CRP levels, and weighted stepwise logistic regression was applied to analyze the association between LE8 scores and cognitive impairment within each stratum.ResultsRisk factors for cognitive impairment in elderly patients with H-type hypertension included age (OR=1.087, 95%CI 1.006-1.172), hyperlipidemia (OR=1.745, 95%CI 0.846-4.852), LE8 score (OR=0.879, 95%CI 0.642-1.176), and hs-CRP (OR=1.215, 95%CI 1.052-1.403, P<0.05). After stratifying patients into low and high hs-CRP groups and adjusting for confounders, each 10-point increase in LE8 score was associated with a significant reduction in cognitive impairment risk in both groups (low hs-CRP group: OR=0.66, 95%CI 0.59-0.75; high hs-CRP group: OR=0.85, 95%CI 0.66-0.94, P<0.05). The protective effect was 19% greater in the low hs-CRP group compared to the high hs-CRP group.ConclusionLE8 scores have a positive protective effect on cognitive function, particularly in patients with lower hs-CRP levels, where the protective role is more pronounced.  
    关键词:hypertension;homocysteine;cognitive impairment;life's essential 8 score;high-sensitivity C-reactive protein   
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    更新时间:2026-04-20

    Wang Yu-Bo, Wang Hai-Xia, Du Shu-Zhen, Zhao Jing, Zhang Zheng

    DOI:10.11855/j.issn.0577-7402.2064.2026.0416
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    摘要:Anthracycline-related cardiotoxicity is a major complication that limits cancer therapy. Its pathogenesis involves multiple mechanisms, including oxidative stress, mitochondrial dysfunction, topoisomerase IIβ-mediated DNA damage, ferroptosis, inflammatory responses, and myocardial fibrosis. This review summarizes recent advances in sodium-glucose cotransporter 2 inhibitors (SGLT2i) for the prevention and management of anthracycline-related cardiotoxicity. Based on the major pathophysiological mechanisms of anthracycline-related cardiotoxicity, the potential cardioprotective actions of SGLT2i are discussed, including reprogramming of myocardial energy metabolism, preservation of mitochondrial structural and functional homeostasis, attenuation of oxidative stress, regulation of apoptosis and autophagy, inhibition of ferroptosis, suppression of inflammatory responses, and alleviation of fibrotic remodeling. Current basic, translational, and preliminary clinical evidence is also summarized and critically appraised. Finally, future research priorities are proposed in view of the current limitations, particularly insufficient clinical evidence and uncertainty regarding the target population and timing of intervention, so as to provide a reference for the prevention and management of anthracycline-related cardiotoxicity and for optimizing cardiovascular care in patients with cancer.  
    关键词:sodium-glucose cotransporter 2 inhibitors;anthracyclines;cardiotoxicity;cardiac protection;cardio-oncology   
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    更新时间:2026-04-20

    Zhu Fei, Feng Jing, Qin Nan, Liu Xinyu, Lian Ke, Du Genlai, Dong Jinyao, Zhang Yanyan, Li Qingliang, Zhang Xunwei, Shi Ruyi

    DOI:10.11855/j.issn.0577-7402.0024.2026.0402
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    摘要:ObjectiveBased on cell experiments, animal experiments and network pharmacology, the function and molecular mechanism of Astragalus extract against hepatocellular carcinoma (HCC) were explored.MethodsMHCC-97H and HCC-LM3 cells were used as the research objects. MTT assay was used to detect the cell viability after treatment with different drug concentrations (0, 0.25, 0.5, 0.75, 1.0 mg/ml) of Astragalus extract for 48 h, and the half inhibitory concentration (IC50) was calculated. The proliferation ability of single cells was detected by colony formation assay. Scratch test and Transwell test were used to detect cell migration and invasion ability. Apoptosis was detected by flow cytometry. The hepatocellular carcinoma model of nude mice was constructed by subcutaneous injection of MHCC-97H and HCC-LM3 cells. The nude mice were randomly divided into control group and experimental group (n=4). The control group was given 200 μL pure water, and the experimental group was given 200 μL concentration of 100 mg/kg Astragalus extract. The volume and weight of the tumor were measured to explore the effect of Astragalus extract on the tumor in vivo. The active components and targets of Astragali Radix were obtained through the Traditional Chinese Medicine Systems Pharmacology (TCMSP) database. GeneCards, DisGeNET, TTD and OMIM databases were used to summarize HCC disease targets. The Astragali Radix-HCC intersection genes were imported into the DAVID database for gene ontology (GO) and Kyoto Encyclopedia of Genes and Genomes (KEGG) analysis. String online platform was used for protein interaction analysis, and ChimeraX 1.8 software was used for molecular docking. The expression of related proteins after 0.5 mg/ml Astragalus extract treatment for 48 h was detected by immunofluorescence.ResultsMTT assay showed that The IC50 values of the two HCC cells were 0.462 mg/ml and 0.496 mg/ml, respectively, after 48 h of treatment with Astragalus extract, and both were close to 0.5 mg/ml. Therefore, the 0 mg/ml Astragalus extract treatment group was the control group, and the 0.5 mg/ml Astragalus extract treatment group was the experimental group, The proliferation of HCC cells was significantly inhibited. Compared with the control group, the number of clones, migration and invasion ability of the experimental group were significantly decreased (P<0.01), and the apoptosis rate was significantly increased (P<0.01). In vivo experiments showed that there was no significant difference in the average body weight of nude mice between different treatment groups after intragastric administration of Astragalus extract, and there was no significant difference in tumor weight and volume in vivo (P>0.05). In terms of network pharmacology, there were 52 intersection targets between Astragali Radix and HCC. The results of GO analysis showed that the anti-HCC of Astragali Radix is related to the negative regulation of apoptosis, phosphorylation and other biological processes. It is also related to cell components such as cytoplasm and protein-containing complexes, as well as molecular functions such as protein binding and enzyme binding. KEGG results showed that the key targets of Astragali Radix against HCC mainly involved pathway in cancer, PI3K/AKT signaling pathway and so on. The network diagram of disease-drug-pathway-target showed that the main active components of Astragali Radix against HCC were quercetin, (3R)-3-(2-hydroxy-3,4-dimethoxyphenyl)chroman-7-ol, kaempferol, isorhamnetin and so on. Protein-Protein Interaction networks analysis showed that the core targets of Astragali Radix anti-HCC were TP53, EGFR, AKT1, MYC, SRC, etc. The results of molecular docking showed that the docking binding energies of quercetin, (3R)-3-(2-hydroxy-3,4-dimethoxyphenyl)chroman-7-ol , kaempferol and isorhamnetin with TP53, EGFR and MYC were all≤-7 kcal/mol, indicating that they had strong binding activity. The results of cellular immunofluorescence showed that compared with the control group, the expression level of P53 protein was significantly up-regulated (P<0.01) and the expression level of AKT1 protein was significantly down-regulated (P<0.05) after treatment with 0.5 mg/ml Astragalus extract for 48 h.ConclusionAstragali Radix can significantly inhibit the proliferation, migration and invasion of HCC cells, and induce apoptosis. The results of network pharmacology suggest that Astragali Radix plays an inhibitory role in HCC through multiple components, multiple pathways and multiple targets. Its anti-tumor mechanism may be closely related to the PI3K/AKT signaling pathway.  
    关键词:Astragali Radix;hepatocellular carcinoma;network pharmacology;molecular docking;mechanism of action   
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    更新时间:2026-04-15

    Liu Zhengdao, WANG Hong, Wang Zhi, LI Baoan, ZHANG Lei, QI Zhenyang

    DOI:10.11855/j.issn.0577-7402.0126.2026.0402
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    摘要:ObjectiveTo explore the correlation between the distribution of pathogenic bacteria causing urinary tract infections after radical prostatectomy for prostate cancer (PCa), and the occurrence of stress urinary incontinence (SUI) as well as changes in inflammatory factors.MethodsA total of 213 patients with prostate cancer who underwent robot-assisted radical prostatectomy in Nanyang First People's Hospital Affiliated to Henan University from January 2021 to January 2024 were retrospectively selected as the research objects. The patients were divided into the infection group (n=66) and the non-infection group (n=147) according to whether they had a urinary tract infection after surgery. The patients were divided into the SUI group (n=61) and the normal urination group (n=152) according to whether SUI occurred three months after surgery. The pathogenic bacteria detected in patients with postoperative urinary tract infections were cultured, isolated, and identified, and the composition of the infection group and the non-infection group, the SUI group, and the normal urination group was compared. The levels of interleukin (IL)-1, IL-6, prostaglandin E2 (PGE2), tumor necrosis factor-α (TNF-α), prostate volume, preoperative urethral length of the uninfected+normal urination group (n=136), uninfected+SUI group (n=11), infected+normal urination group (n=16), and infected+SUI group (n=50) were compared. Multivariate linear regression analysis was used to analyze the correlation between IL-1, IL-6, PGE2, TNF-α and bladder function. Multivariate Logistic regression analysis was used to analyze the risk factors affecting postoperative SUI. The restricted cubic spline model was used to analyze the dose-response relationship between IL-1, IL-6, PGE2, TNF-α and the risk of urinary tract infection occurrence. The Hayes Process program was used to analyze the mediating effect of IL-1, IL-6, PGE2, and TNF-α on the relationship between postoperative combined urinary tract infection and bladder function.ResultsAmong the 66 patients who developed urinary tract infections after surgery, a total of 85 pathogenic bacteria were detected. The main pathogens were Escherichia coli and Staphylococcus aureus. The age of the infection group, the proportion of patients with a history of preoperative stress urinary incontinence and those who had a urinary catheter inserted through the urethra and had postoperative urinary retention, the duration of postoperative urinary catheter placement, the length of hospital stay, IL-1, IL-6, PGE2, TNF-α, and the residual urine volume in the bladder were significantly higher than those in the non-infection group (P<0.05). The proportion of patients who had preventive use of antibacterial drugs before surgery and the bladder pressure were significantly lower than those in the non-infection group (P<0.05). The SUI group had significantly higher ages, BMIs, prostate volumes, preoperative urethral lengths, operation durations, the proportions of those with abdominal surgery history and preoperative SUI history, as well as those with urinary tract infections compared to the normal voiding group (P<0.05). IL-1, IL-6, PGE2, and TNF-α were negatively correlated with bladder pressure (P<0.05) and positively correlated with residual urine volume in the bladder (P<0.05). Age ≥58 years old, BMI ≥24.69 kg/m2, prostate volume ≥50.06 cm3, preoperative urethral length <14.08 mm, abdominal surgery history, preoperative SUI history, urinary tract infection, IL-1 ≥2.05 pg/ml, IL-6 ≥16.43 pg/ml, PGE2 ≥116.91 pg/ml, and TNF-α ≥1.03 ng/ml were independent risk factors for postoperative SUI in patients (P<0.05). The levels of IL-1, IL-6, PGE2, and TNF-α in patients of the "uninfected+SUI" group and the "infected+normal urination" group were significantly higher than those in the "uninfected+normal urination" group (P<0.05); the level of IL-1 in the "infected+normal urination" group was significantly higher than that in the "uninfected+SUI" group (P<0.05); the levels of IL-1, IL-6, PGE2, and TNF-α in the "infected+SUI" group were significantly higher than those in the other three groups (P<0.05). There was a non-linear dose-response relationship between IL-1, IL-6, PGE2, TNF-α and the risk of urinary tract infection. When IL-1 >2.09 pg/ml, IL-6 >16.51 pg/ml, PGE2 >117.02 pg/ml, and TNF-α >0.97 ng/ml, the risk of urinary tract infection increased with the increase of their levels (non-linear P<0.05, total P<0.05). IL-1, IL-6, PGE2, and TNF-α had significant mediating regulatory effects between postoperative combined urinary tract infection and bladder pressure and bladder residual urine volume (P<0.001).ConclusionThe main pathogenic bacteria causing urinary tract infections after radical prostatectomy are Escherichia coli and Staphylococcus aureus. Postoperative urinary tract infections and stress urinary incontinence are both independently associated with enhanced systemic inflammatory response, and their coexistence shows a synergistic effect. IL-1, IL-6, PGE2, and TNF-α have significant mediating regulatory roles between postoperative urinary tract infections and bladder function.  
    关键词:prostate cancer;urinary tract infection;bacterial distribution;stress urinary incontinence;inflammatory factor   
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    更新时间:2026-04-15

    Chinese Medical Doctor Association Emergency Medical Branch, Chinese People's Liberation Army Emergency Medicine Professional Committee, Beijing Emergency Medicine Society, Emergency Surgery Alliance, Emergency Physicians Branch of Hubei Medical Doctor Association

    DOI:10.11855/j.issn.0577-7402.0214.2026.0412
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    摘要:Acute abdomen is one of the most common critical conditions encountered in the emergency department. Owing to its complex etiologies, abrupt onset, rapid progression, and high risk of missed or delayed diagnosis, standardized evaluation and timely management remain major clinical challenges. This expert consensus was jointly developed by the Emergency Physicians Branch of the Chinese Medical Doctor Association, the Emergency Medicine Committee of the Chinese People's Liberation Army, the Beijing Society of Emergency Medicine, the Emergency Surgery Alliance, and the Emergency Physicians Branch of the Hubei Medical Doctor Association. Focusing on key clinical issues in the diagnosis and treatment of acute abdomen in adults, a systematic literature review was conducted based on the "6S" evidence model, with the search period extending from database inception to October 13, 2025. The quality of evidence and strength of recommendations were graded using the Grading of Recommendations Assessment, Development and Evaluation (GRADE) approach. This consensus addresses epidemiological characteristics, early recognition and risk stratification, laboratory and imaging evaluation, initial resuscitation and analgesia, antimicrobial therapy, selection of surgical timing and approach, and management strategies for special populations including older adults, immunocompromised patients, and patients with malignancies. In particular, it emphasizes the pivotal role of multidisciplinary team collaboration in optimizing diagnostic and therapeutic pathways, improving rescue efficiency, and enhancing patient outcomes. This consensus is intended to provide emergency physicians with evidence-based, practical, and standardized guidance for the management of adult acute abdomen.  
    关键词:acute abdomen;adult;diagnosis;treatment;multidisciplinary team;expert consensus   
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    Liu Xu, Dong Xin, Li Hao-Ting, Nie Jin-Feng, Zhang Zi-Ying, Qin Zi-Kun, Huang Yue-Hong, Shi Ting-Yu, Huang Sheng, Song Tian-Li

    DOI:10.11855/j.issn.0577-7402.2657.2026.0413
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    摘要:Selenium, an essential trace element for the human body, is crucial for maintaining redox homeostasis, regulating immune cell function, and combating pathogen infections through its various forms of selenoproteins. The selenoprotein family, which includes glutathione peroxidase, thioredoxin reductase, and endoplasmic reticulum selenoproteins, collaborates to provide antioxidant defense, regulate calcium signaling, and maintain endoplasmic reticulum homeostasis, thereby influencing multiple facets of innate and adaptive immunity. Selenium exerts an immunomodulatory effect on macrophages, dendritic cells, and natural killer cells by promoting an anti-inflammatory phenotype and activating immune cells, while also regulating T cell differentiation and proliferation, as well as B cell-mediated antibody production, thereby contributing to immune tolerance and the maintenance of immune balance. The "intestinal-immune axis" is an important pathway through which selenium regulates the immune system. Clinical studies have demonstrated that selenium supplementation holds potential therapeutic value in the context of autoimmune diseases, HIV infection, COVID-19, and other immune-related disorders by enhancing immune function and mitigating inflammatory damage. However, selenium exhibits notable bidirectional dose effects, with excessive intake potentially resulting in oxidative stress and toxic reactions, thereby necessitating precise dosage regulation. Organic selenium, nano selenium, and functionalized selenium preparations have shown enhanced biological activity and safety, offering valuable insights for future immunotherapy applications. The molecular mechanisms through which selenium modulates the immune system involve key selenium proteins that maintain redox homeostasis, regulate calcium signaling, influence redox-sensitive signaling pathways, and control cell death pathways. This article reviews the research progress on selenium modulates immune system function and its molecular mechanisms, aiming to provide reference for clinical applications and research.  
    关键词:Selenium;selenoproteins;redox homeostasis;immune regulation;innate immunity;adaptive immunity;immune diseases   
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