Toxicology Mechanisms and Methods最新文献

{"title":"Food safety analysis: network toxicology, molecular docking, machine learning and single-cell analysis to interpret sodium benzoate-induced renal injury from multiple perspectives.","authors":"Jingwei Li, Hailong Yang, Jingjia Yang, Jintao Liang, Yalun Liang, Yimao Wu, Runfeng Zhang","doi":"10.1080/15376516.2025.2553859","DOIUrl":"https://doi.org/10.1080/15376516.2025.2553859","url":null,"abstract":"<p><strong>Background: </strong>Sodium benzoate, a common food additive, has raised safety concerns despite its general recognition as safe. This study aimed to investigate the mechanisms of sodium benzoate-induced nephrotoxicity.</p><p><strong>Method: </strong>A network toxicology approach was used to identify key targets and core pathways involved in sodium benzoate nephrotoxicity. Molecular docking validated the binding affinity between these targets and sodium benzoate. Machine learning and single-cell analysis further explored the underlying mechanisms using dataset validation.</p><p><strong>Result: </strong>Protein-protein interaction (PPI) network analysis revealed five key targets with the lowest binding energies (Matrix metalloproteinase 2 (MMP2), Estrogen Receptor 1 (ESR1), Poly (ADP-ribose) polymerase 1 (PARP1), Prostaglandin-endoperoxide synthase 2 (PTGS2), Mitogen-activated protein kinase 14 (MAPK14)) as central to sodium benzoate-induced renal injury. Enrichment analysis indicated 'diabetic nephropathy' (DN) as the primary pathway. Machine learning and single-cell analysis confirmed PTGS2 as the dominant factor exerting nephrotoxicity among the key genes.</p><p><strong>Conclusion: </strong>This multi-method study uncovered potential mechanisms of sodium benzoate-induced renal injury, providing a basis for improving food safety evaluations.</p>","PeriodicalId":23177,"journal":{"name":"Toxicology Mechanisms and Methods","volume":" ","pages":"1-15"},"PeriodicalIF":2.7,"publicationDate":"2025-09-09","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145024245","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"<i>In vivo</i>, <i>in vitro</i>, and <i>in silico</i> toxicology studies of nanoplastics and their modeling.","authors":"Batuhan Inanlar, Filiz Altay","doi":"10.1080/15376516.2025.2546518","DOIUrl":"10.1080/15376516.2025.2546518","url":null,"abstract":"<p><p>Nanoplastics (NPs) are nanoscale plastic particles that pose possible risks to health and the environment. Therefore, the study of their toxicity is critical for regulating their use, traceability, and impact assessment. Despite their prevalence in the life cycle, research on NP toxicity remains limited due to their diverse sources, routes of exposure, and increasing presence in nature. Moreover, regulatory frameworks lack adequate characteristic values to detect NPs in food and the environment, and there are currently no defined thresholds for harmful particles. This review examines key parameters in toxicity studies of NPs, focusing on <i>in vivo</i>, <i>in vitro</i>, <i>in silico</i>, and modeling approaches, as well as uptake pathways. NP analysis involves three basic steps: pretreatment, identification, and quantification. In these steps, parameters such as size, shape, zeta potential, surface charge, and density play important roles. Combining these approaches offers complementary insights, improving the understanding of NP toxicity. These findings underscore the need for comprehensive toxicity studies to inform regulations and reduce the risks associated with NPs in various contexts.</p>","PeriodicalId":23177,"journal":{"name":"Toxicology Mechanisms and Methods","volume":" ","pages":"1-19"},"PeriodicalIF":2.7,"publicationDate":"2025-09-09","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144817468","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Evaluation of novel surfactants for the decontamination of chemical warfare agents.","authors":"Marek Matula, Jaroslav Pejchal, Jan Marek, Viktoria Ernestová, Natalie Zivná, Aneta Voparilova Markova, Helena Rehulkova, Alzbeta Dlabkova","doi":"10.1080/15376516.2025.2554912","DOIUrl":"https://doi.org/10.1080/15376516.2025.2554912","url":null,"abstract":"<p><p>The decontamination of chemical warfare agents or compounds involved in chemical industry incidents poses a significant challenge to environmental protection and human health. These compounds are highly toxic and could be relatively resistant to conventional decontamination methods. In recent years, surfactants have emerged as a promising option, as they can enhance the solubility of organophosphorus compounds in aqueous solutions while promoting their degradation or adsorption onto surfaces. In this study, 35 compounds (surfactants based on quartenary ammonium salts) were tested using the model pesticide fenitrothion, with the compounds from the 43 C series (quaternary ammonium salts with two hydroxyl functional groups) showing the highest decontamination potential. The 43 C series compounds were further tested <i>in vitro</i> for the degradation of nerve agents sarin, soman, and VX, as well as the blistering agent sulfur mustard. The compounds labeled 43C14 and 43C16 (benzoxonia with the 14- and 16-carbon chains) exhibited the best potential. Due to the possible use in protective applications for military personnel, an <i>in vivo</i> acute skin irritation test on 43C14 and 43C16 was also conducted in rats. No skin pathology was observed after a 4-h application and during the subsequent 72-h observation period, suggesting its potential for practical use.</p>","PeriodicalId":23177,"journal":{"name":"Toxicology Mechanisms and Methods","volume":" ","pages":"1-14"},"PeriodicalIF":2.7,"publicationDate":"2025-09-08","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145016116","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Unveiling the molecular toxicity of Isoniazid and Rifampicin in tuberculosis therapy: emerging insights and therapeutic strategies.","authors":"Priyadharshini Shivaji, Sabina Evan Prince","doi":"10.1080/15376516.2025.2554918","DOIUrl":"https://doi.org/10.1080/15376516.2025.2554918","url":null,"abstract":"<p><p>Tuberculosis, caused by <i>Mycobacterium tuberculosis</i>, persists as a significant worldwide health issue, resulting in millions of infections and fatalities each year. Treatment predominantly depends on first-line antibiotics, including Isoniazid (INH) and Rifampicin (RIF). Nevertheless, extended use of these medications is linked to considerable adverse effects, leading to various organ toxicities, especially hepatotoxicity and nephrotoxicity. INH causes liver and kidney damage by pathways that include oxidative stress, mitochondrial malfunction, and inflammation. RIF induces organ damage by blocking drug-metabolizing enzymes, facilitating lipid peroxidation, and triggering apoptosis and cholestasis. Although both medications are crucial in TB treatment, their synergistic effect on organ damage remains little comprehended. RIF is recognized for exacerbating INH-induced hepatic damage by increasing CYP2E1 metabolism, indicating intricate interactions. This study analyses the molecular toxicity processes generated by INH and RIF, summarizes current clinical and experimental data, and investigates the preventive potential of natural substances, such as antioxidants and phytochemicals. It also explores alternative treatment techniques, nanobiotechnology designed to mitigate drug-induced organ toxicity by giving protective agents at the same time and targeting specific mechanisms. This review presents an innovative viewpoint on the management of INH and RIF toxicity and underscores potential avenues for further research.</p>","PeriodicalId":23177,"journal":{"name":"Toxicology Mechanisms and Methods","volume":" ","pages":"1-32"},"PeriodicalIF":2.7,"publicationDate":"2025-09-08","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145016125","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Betanin and vanillic acid reduce bleomycin-induced mitochondrial dysfunction in rat lung isolated mitochondria; a hormetic mode of action for vanillic acid.","authors":"Ahmad Salimi, Behrooz Elyasi, Mohammad Shabani, Hanieh Delavari, Hassan Ghobadi","doi":"10.1080/15376516.2025.2556846","DOIUrl":"https://doi.org/10.1080/15376516.2025.2556846","url":null,"abstract":"<p><p>Mechanistic studies have been suggested that toxic effects of bleomycin are generally attributed to formation of free radicals, mitochondria damages, oxidative stress and inflammation. For this purpose, we explored the direct exposure of bleomycin and protective effects of the betanin and vanillic acid separately against its possible toxicity in rat lung isolated mitochondria. Various mitochondrial toxicity parameters were evaluated including; succinate dehydrogenases (SDH) activity, reactive oxygen species (ROS) formation, mitochondrial swelling, mitochondrial membrane potential (MMP) collapse, malondialdehyde (MDA) and glutathione disulfide (GSSG) levels. It was found that the direct exposure of isolated mitochondria with bleomycin (500 μM) resulted in a significant decrease of SDH activity (<i>p</i> < 0.001), a significant increase of ROS formation (<i>p</i> < 0.001), MDA content (<i>p</i> < 0.01), mitochondrial swelling (<i>p</i> < 0.001) and collapse of MMP (<i>p</i> < 0.05). Except MMP collapse and GSSG level, betanin treatment had strong protection attenuating the SDH activity (<i>p</i> < 0.001), ROS formation (<i>p</i> < 0.001), mitochondrial swelling (<i>p</i> < 0.001) and MDA production (<i>p</i> < 0.05) in presence of toxic concentration of bleomycin. Additionally, vanillic acid treatment had the same protective effect, but at higher concentrations. However, according to our observations, it seems vanillic acid can be toxic in rat lung isolated mitochondria at concentrations of 100 μM and higher. It was concluded that betanin and vanillic acid could be considered as potential mitochondrial-targeted agents in the reduction of bleomycin-induced toxicity <i>via</i> inhibition of mitochondrial swelling, ROS formation and improvement SDH activity in rat lung isolated mitochondria.</p>","PeriodicalId":23177,"journal":{"name":"Toxicology Mechanisms and Methods","volume":" ","pages":"1-14"},"PeriodicalIF":2.7,"publicationDate":"2025-09-08","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145016135","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Investigating the mechanism of phthalates in breast cancer using molecular docking and network toxicology.","authors":"Jinrui Zhang, Wenjie Zhang, Lei Zhang, Jia He, Yudan Dong, Jintao Yuan","doi":"10.1080/15376516.2025.2553099","DOIUrl":"10.1080/15376516.2025.2553099","url":null,"abstract":"<p><p>Phthalate esters (PAEs) are ubiquitous environmental contaminants, with certain congeners potentially exhibiting breast cancer-promoting effects. However, their toxicological mechanisms remain poorly characterized. This study systematically investigates PAEs' direct interactions with breast cancer pathways using an integrated computational approach combining molecular docking-based inverse virtual screening with network toxicology. We computational screened 12 representative PAEs against 275 breast cancer-related proteins. Through rigorous network analysis using Cytoscape software with CytoNCA plugin, we identified six pivotal molecular targets: E1A binding protein p300 (EP300), somatic cytochrome c (CYCS), mechanistic target of rapamycin kinase (MTOR), prostaglandin-endoperoxide synthase 2 (PTGS2), peroxisome proliferator-activated receptor gamma (PPARγ), and progesterone receptor (PGR). KEGG pathway enrichment analysis revealed significant associations with two major oncogenic pathways: the cancer pathway and Kaposi's sarcoma-associated herpesvirus (KSHV) infection signaling pathway. Differential gene expression analysis and survival prognosis validation further substantiated these core targets' clinical relevance. Notably, this work identified six pivotal molecular targets (EP300, CYCS, MTOR, PTGS2, PPARγ, and PGR) and for the first time, linked PAEs to the KSHV infection pathway. Our findings establish a novel network toxicology framework for elucidating shared molecular mechanisms underlying PAEs-induced breast carcinogenesis, providing mechanistic insights to support environmental monitoring and preventive strategies against PAEs-associated breast cancer risks.</p>","PeriodicalId":23177,"journal":{"name":"Toxicology Mechanisms and Methods","volume":" ","pages":"1-19"},"PeriodicalIF":2.7,"publicationDate":"2025-09-08","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144970507","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Assessment of docosahexaenoic acid's preventive efficacy against unconjugated bilirubin neurotoxicity through MRP1 protein expression.","authors":"Denghui Wang, Xianyang Liang, Jingliang Du, Zhen Wang, Qianhao Wang, Ruile Shen","doi":"10.1080/15376516.2025.2553853","DOIUrl":"https://doi.org/10.1080/15376516.2025.2553853","url":null,"abstract":"<p><strong>Objective: </strong>Jaundice in neonates promotes unconjugated hyperbilirubinemia (UCB), which causes neurological disorders, and its management remains a challenge. This study evaluated the protective effect of docosahexaenoic acid (DHA) against UCB-induced neurotoxicity.</p><p><strong>Method: </strong>Astrocyte cell lines were prepared and separated into four different groups: SAL group; DHA group treated with 50 µM DHA; UCB group treated with 50 µM UCB; and UCB + DHA group treated with 50 µM UCB along with 50 µM DHA. The effect of DHA was assessed on cell viability percentage and apoptosis rate. Levels of Ca²⁺, glutamate, and ATP were assessed in the DHA-treated cell line, and Western blot assay was performed to estimate the expression of MRP1 protein.</p><p><strong>Results: </strong>Data show that treatment with DHA significantly reduces (<i>p</i> < 0.001) apoptosis rate and increases cell viability compared to the UCB group. The UCB + DHA group showed a decrease in glutamate and Ca²⁺, and ATP levels were significantly higher than in the UCB-treated neuronal cell line. Expression of MRP1 protein was significantly (<i>p</i> < 0.05) enhanced in the UCB + DHA group compared to the UCB and SAL groups.</p><p><strong>Conclusion: </strong>In conclusion, data show treatment with DHA protects against neurotoxicity in UCB-induced cellular injury, as it ameliorates alterations in glutamate levels, intracellular Ca²⁺, and ATP by enhancing MRP1 protein expression.</p>","PeriodicalId":23177,"journal":{"name":"Toxicology Mechanisms and Methods","volume":" ","pages":"1-8"},"PeriodicalIF":2.7,"publicationDate":"2025-09-04","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144993329","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"<i>In silico and in vivo</i> toxicity assessment of cysteamine-modified nanoparticles: implications for pharmacotherapy application.","authors":"Babatunde Alabi, Sodiq Kolawole Lawal, Samuel Oluwaseun Olojede, Amina Suleiman, Olamide Adesanya, Diana Odey Ochuole, Fisayo Nathaniel Ogunleye, Benneth Ben-Azu","doi":"10.1080/15376516.2025.2538128","DOIUrl":"https://doi.org/10.1080/15376516.2025.2538128","url":null,"abstract":"<p><strong>Background: </strong>Given the increasing therapeutic potential of cysteamine (CYST) at appropriate doses and expert concerns regarding the toxicity of nanoparticles, this study aimed to assess the toxicity profile of both CYST and silver nanoparticles conjugated with cysteamine (CYST-AgNPs).</p><p><strong>Methods: </strong>For the acute study, a 300 mg/kg starting dose of CYST (i.p administration) produced a toxic response in some mice (<i>n</i> = 3/group), and a 300 mg/kg beginning dose of CYST-AgNPs produced delayed mild toxicity. Lower doses of CYST and CYST-AgNPs (50, 100, and 200 mg/kg; <i>n</i> = 3/group) were administered (i.p) for further acute toxicological evaluation. The sub-acute toxicity test was conducted for 21 days, and female mice (<i>n</i> = 5/group) were divided into control, CYST (25 and 50 mg/kg), and CYST-AgNPs (25 and 50 mg/kg). AgNPs and CYST-AgNPs were characterized with FTIR spectroscopy, UV spectrophotometer, HR-TEM, and SEM-EDX. Blood samples were collected <i>via</i> cardiac puncture and processed according to the standard hematological analysis protocols.</p><p><strong>Results: </strong>The UV-vis absorbance wavelength range of 400-800 nm was observed. HR-TEM showed mostly spherical nanoparticles ranging from 30 to 90 nm. FTIR showed a functional group of O-H, C = C stretching vibration for AgNPs and O-H, S-H, N-H, C = C stretching vibration for CYST-AgNPs. EDX spectroscopy showed silver, carbon, oxygen, sodium, and chloride elements for AgNPs and CYST-AgNPs. The CYST decreased the WBC, RBC, and platelet counts significantly (<i>p</i> < 0.05), while CYST-AgNPs (25 and 50 mg/kg) reduced only the RBC counts (<i>p</i> < 0.05).</p><p><strong>Conclusion: </strong>This investigation presents the <i>in vivo</i> safety analysis and pharmacological potential of cysteamine-modified silver nanoparticles (CYST-AgNPs), suggesting enhanced therapeutic activity.</p>","PeriodicalId":23177,"journal":{"name":"Toxicology Mechanisms and Methods","volume":" ","pages":"1-19"},"PeriodicalIF":2.7,"publicationDate":"2025-09-02","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144970368","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Neurotoxicity mechanisms of pyrethroids studied by network toxicology and molecular docking.","authors":"Yuting Lin, Wenqi Zeng, Yang Zhang, Yanghui Hu, Zhonghan Liang, Zhixing Chen, Zhuoying Lu, Weien Zhang, Zhenjie Wang, Yanling Jiang, Mingyu Chen, Haining Ma, Yikuan Du, Chunling Ma, Chun Yang","doi":"10.1080/15376516.2025.2548842","DOIUrl":"https://doi.org/10.1080/15376516.2025.2548842","url":null,"abstract":"<p><p>Pyrethroids (PYs), a class of insecticides widely used in agricultural and household pest control, have been reported to trigger neurological damage. However, the underlying mechanisms of toxicity remain unclear. In this study, we applied a network toxicology approach to identify the core targets and signaling pathways associated with the pathogenesis of PYs-induced neurotoxicity syndrome. A molecular docking approach was also used to determine the interactions between PYs and key proteins. In this study, 145 potential targets and 10 core targets of PYs-induced neurotoxicity were identified. The core targets included SRC, EGFR, and KDR, and the signaling pathways involved Prolactin signaling pathway, AGE-RAGE signaling pathway in diabetic complications and Lipid and atherosclerosis. Molecular docking binding showed stable binding of PYs to core targets. This study preliminarily reveals the potential toxicity and possible neurotoxicity mechanism of pyrethroids, which provides new ideas for subsequent prevention and treatment of related diseases.</p>","PeriodicalId":23177,"journal":{"name":"Toxicology Mechanisms and Methods","volume":" ","pages":"1-14"},"PeriodicalIF":2.7,"publicationDate":"2025-09-02","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144970504","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Fucoxanthin ameliorates PM_2.5-mediated skin cell inflammation and senescence.","authors":"Pincha Devage Sameera Madushan Fernando, Kyoung Ah Kang, Mei Jing Piao, Herath Mudiyanselage Udari Lakmini Herath, Herath Mudiyanselage Maheshika Madhuwanthi Senavirathna, Eui Tae Kim, Hee-Sun Kim, Sungwook Chae, Musun Park, Jin Won Hyun","doi":"10.1080/15376516.2025.2500545","DOIUrl":"10.1080/15376516.2025.2500545","url":null,"abstract":"<p><p>Fucoxanthin is a naturally derived carotenoid in marine brown algae that has potential curative benefits for treating diseases such as cancer, diabetes, and obesity. Exposure to particulate matter with a diameter of ≤2.5 µm (PM_2.5) is associated with the occurrence of cardiac disorders, cancer, and senescence. The primary objective of this study was to determine the protective effects of fucoxanthin against PM_2.5-induced dysfunction of human HaCaT keratinocytes. Fucoxanthin decreased PM_2.5-induced production of reactive oxygen species and mitigated lipid peroxidation, DNA damage, and depolarization of the mitochondrial membrane potential. Fucoxanthin inhibited PM_2.5-mediated activation of nuclear factor κB and Nod-like receptor family protein 3 inflammasome and the release of proinflammatory cytokines such as interleukin (IL)-1, IL-6, and cyclooxygenase-2. Additionally, fucoxanthin decreased dysfunctional cell proliferation and reversed the cell cycle arrest in the G₀/G₁ phase. Docking and network analyses revealed that fucoxanthin interacted with seven major proteins related to inflammation and senescence. Senescence-associated β-galactosidase and matrix metalloproteinases were downregulated by fucoxanthin following exposure to PM_2.5. Conclusively, fucoxanthin attenuates the cellular oxidative stress caused by PM_2.5 and suppresses inflammatory responses and senescence, thereby implying its potential in alleviating PM_2.5-induced skin damage.</p>","PeriodicalId":23177,"journal":{"name":"Toxicology Mechanisms and Methods","volume":" ","pages":"809-822"},"PeriodicalIF":2.7,"publicationDate":"2025-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144062097","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}