Frontiers in toxicology最新文献

{"title":"Dimethyl sulfoxide perturbs sleep-related behavioral organization in multiple species and confounds interpretation of sleep phenotypes.","authors":"Nanami Udo, Manabu Sekiguchi, Etsuko Sawatari, Taichi Q Itoh","doi":"10.3389/ftox.2026.1907359","DOIUrl":"10.3389/ftox.2026.1907359","url":null,"abstract":"<p><strong>Introduction: </strong>Dimethyl sulfoxide (DMSO) is a very commonly used solvent in biological research and generally considered an inert experimental vehicle. However, DMSO can alter physiological functions, raising concerns regarding its effects on behavioral phenotypes. Such concerns may be particularly important in sleep research because sleep-related behaviors are highly sensitive to physiological perturbations.</p><p><strong>Methods: </strong>In this study, we systematically examined the effects of DMSO on sleep-related behaviors in <i>Drosophila melanogaster</i> and <i>Hydra vulgaris</i>.</p><p><strong>Results: </strong>In <i>Drosophila</i>, DMSO dose-dependently altered nighttime sleep, increased locomotor activity, prolonged sleep latency, reduced average sleep-bout length, and increased sleep-bout number. In <i>Hydra</i>, 2% DMSO increased total sleep-like behavior together with an increased number of sleep bouts while reducing waking locomotor activity and sleep latency. Although the direction of total sleep changes differed between these species, both organisms exhibited disrupted sleep-related behavioral organization following DMSO exposure. Furthermore, high concentrations of DMSO induced severe physiological impairment, including a shortened lifespan in <i>Drosophila</i> and morphological deterioration and death in <i>Hydra</i>.</p><p><strong>Discussion: </strong>These findings demonstrate that DMSO is not merely a passive solvent in sleep research, but a biologically active perturbant, which is capable of confounding sleep-related behavioral phenotypes in both <i>Drosophila</i> and <i>Hydra</i>. Our study highlights the importance of carefully evaluating solvent effects in behavioral and pharmacological studies of sleep.</p>","PeriodicalId":73111,"journal":{"name":"Frontiers in toxicology","volume":"8 ","pages":"1907359"},"PeriodicalIF":5.1,"publicationDate":"2026-08-21","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13541398/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148889619","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Editorial: Environmental toxicity in metabolism.","authors":"Tracey Woodlief","doi":"10.3389/ftox.2026.1925459","DOIUrl":"10.3389/ftox.2026.1925459","url":null,"abstract":"","PeriodicalId":73111,"journal":{"name":"Frontiers in toxicology","volume":"8 ","pages":"1925459"},"PeriodicalIF":5.1,"publicationDate":"2026-08-21","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13541389/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148889615","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Case Report: Serial blood benzene and urinary phenol monitoring during extracorporeal treatment after severe acute oral ingestion of a benzene-containing solvent.","authors":"Junting Liu, Quan Gan, Geng Zhang","doi":"10.3389/ftox.2026.1875489","DOIUrl":"10.3389/ftox.2026.1875489","url":null,"abstract":"<p><strong>Background: </strong>Acute oral benzene poisoning is uncommon, and evidence to guide extracorporeal treatment and bedside toxicokinetic interpretation in this setting is limited. Most published experience concerns inhalational exposure or chronic hematotoxicity, leaving clinicians with little practical guidance for managing large intentional ingestions.</p><p><strong>Case report: </strong>An 18-year-old man presented approximately 12 h after ingesting about 200 mL of a commercial benzene standard solution in ethyl acetate as intentional self-poisoning. On admission he had tachycardia, persistent gastrointestinal symptoms, and laboratory confirmation of exposure, with benzene detected in gastric fluid (2,966 μg/L), blood (457 μg/L), and urine (224 μg/L). Before gastric lavage, toxicological confirmation was obtained in all three matrices. After decontamination and supportive care, sequential hemoperfusion and continuous veno-venous hemodiafiltration (CVVHDF) were initiated. Serial toxicological monitoring showed rapid decline of the parent compound-blood benzene decreased to 228 μg/L at 20 h, 78 μg/L at 28 h, and became undetectable by 32 h-whereas urinary phenol rose later, peaking at 3231.5 mg/L at 32 h before declining over subsequent days. The clinical course included rhabdomyolysis, transient liver injury, erosive gastritis, and transient nonspecific white-matter abnormalities on brain magnetic resonance imaging (MRI). The patient recovered without persistent neurologic deficit and returned to usual activities.</p><p><strong>Conclusion: </strong>In severe acute oral ingestion of a benzene-containing solvent, paired monitoring of the parent compound and a major metabolite provided clinically useful information to contextualize extracorporeal treatment when formal decision thresholds were unavailable. This case cannot establish treatment efficacy, but it illustrates a pragmatic monitoring framework that may assist clinicians interpreting late toxicokinetic trends in rare but high-risk solvent ingestions.</p>","PeriodicalId":73111,"journal":{"name":"Frontiers in toxicology","volume":"8 ","pages":"1875489"},"PeriodicalIF":5.1,"publicationDate":"2026-08-20","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13537749/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148882784","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"A new high-accuracy QSAR model based on ultra-curated data for predicting thyroid receptor-related endocrine activity.","authors":"Emel Ay-Albrecht, Zlatomir Todorov, Franklin J Bauer, Marie Darracq-Ghitalla-Ciock, Carole Charmeau-Genevois, Satinder S Sarang, Paul C Thomas","doi":"10.3389/ftox.2026.1852502","DOIUrl":"10.3389/ftox.2026.1852502","url":null,"abstract":"<p><strong>Introduction: </strong>Endocrine active substances interfere with hormone signalling and represent a major regulatory concern. The thyroid system is particularly vulnerable, with disruption linked to neurodevelopmental, metabolic, and cardiovascular effects. Current in vitro assays may improve mechanistic understanding but are resource-intensive while screening databases (e.g., Tox21 assays) is insufficient for large-scale chemical coverage or for assessing new materials. In silico tools such as QSAR models offer scalable alternatives, yet existing thyroid receptor (TR) models suffer from poor data curation, class imbalance, and limited regulatory acceptance.</p><p><strong>Methods: </strong>This study aimed to develop a high-accuracy QSAR model, aligned with the OECD QSAR Assessment Framework, to accurately predict TR-related endocrine activity, thereby supporting the reduction of animal testing and regulatory decision-making. In this work, data from Tox21 TR luciferase agonist and antagonist assays were combined with curated BindingDB data, followed by expert review of activity-cytotoxicity relationships and strict filtering of low-affinity interactions (termed here as \"ultra-curation\"). Agonists and antagonists were grouped together as \"actives\". The final dataset comprised 291 active and 6,049 inactive compounds. Each substance was associated with a standardised SMILES, to locate duplicates (subsequently removed), and the dataset split into training, internal validation, and external validation sets with chemical diversity balancing. A Support Vector Machine (SVM) classifier using circular fingerprints (FCFP6) was optimised via grid search. Model performance was evaluated with cross-validation and external validation, complemented by an applicability domain (AD) framework based on analogues.</p><p><strong>Results: </strong>The SVM achieved strong performance in training (balanced accuracy = 96.03%; AUC-ROC = 99.91%; AUC-PR = 99.21%) and robust performance on the external validation set (balanced accuracy = 92.46%; sensitivity = 87.65%; specificity = 99.42%). Incorporation of the AD framework improved minority class (active) detection, raising balanced accuracy to 96.15%, sensitivity to 92.30%, and specificity to 100%, while excluding ~14% of compounds with uncertain predictions.</p><p><strong>Discussion: </strong>The QSAR model developed here demonstrates good predictive accuracy for thyroid receptor-related endocrine activity and addresses key regulatory concerns through rigorous data ultra-curation and applicability domain assessment. This high-accuracy QSAR provides a promising in silico tool to support integrated approaches to testing and assessment (IATA) and regulatory evaluation of endocrine disruption potential.</p>","PeriodicalId":73111,"journal":{"name":"Frontiers in toxicology","volume":"8 ","pages":"1852502"},"PeriodicalIF":5.1,"publicationDate":"2026-08-20","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13540040/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148889602","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Editorial: Insights in nanotoxicology.","authors":"Luisa Campagnolo, Bengt Fadeel","doi":"10.3389/ftox.2026.1960533","DOIUrl":"10.3389/ftox.2026.1960533","url":null,"abstract":"","PeriodicalId":73111,"journal":{"name":"Frontiers in toxicology","volume":"8 ","pages":"1960533"},"PeriodicalIF":5.1,"publicationDate":"2026-08-18","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13529291/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148868126","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Neurodevelopmental outcomes relevant to autism in juvenile mice exposed to PCB 11 in the maternal diet throughout gestation and lactation.","authors":"Rebecca J Wilson, Harmanpreet K Panesar, Ilknur Dursun, Rosalia Mendieta, Peter M Andrew, Xueshu Li, Hans-Joachim Lehmler, Pamela J Lein","doi":"10.3389/ftox.2026.1816944","DOIUrl":"10.3389/ftox.2026.1816944","url":null,"abstract":"<p><p>Polychlorinated biphenyls (PCBs) pose a significant risk to the developing human brain, and recent epidemiological data suggest PCBs increase the risk and/or severity of neurodevelopmental disorders (NDD), including autism spectrum disorder (autism). Experimental animal studies confirm that PCBs disrupt neurodevelopment, resulting in behavioral deficits. Historically, research on the developmental neurotoxicity of PCBs has focused on the higher-chlorinated PCBs found in legacy commercial mixtures; however, lower-chlorinated PCBs (LC-PCBs), including congeners not present in commercial mixtures, predominate in contemporary human exposures. Previous <i>in vitro</i> studies demonstrated that one such LC-PCB, PCB 11, altered dendritic arborization, a cellular phenotype common to multiple NDD. Whether PCB 11 modulates dendritic morphogenesis <i>in vivo</i> is not known. In this study, we investigated how gestational and lactational exposure to PCB 11 in the maternal diet affected critical neurodevelopmental processes in juvenile male and female mice. C57BL/6J mouse dams were exposed to vehicle or PCB 11 at 0.1 or 1.0 mg/kg/day in their diet for 2 weeks prior to mating and throughout gestation and lactation. Brain tissue was collected from offspring at postnatal day (P)4 and P21 to assess dendritic arborization, apoptosis, glial reactivity, and neurogenesis in the hippocampus and neocortex. PCB 11 dose-dependently reduced the dendritic arborization of pyramidal neurons in the neocortex by 13%-25% but had no significant effect on the dendritic morphogenesis of pyramidal neurons in the hippocampus. Apoptosis was not altered by PCB 11 in either brain region of either sex at either age. While PCB 11 had no effect on neurogenesis at P4, it dose-dependently decreased neurogenesis by 15%-70% in the dentate gyrus at P21. GFAP immunoreactivity and the morphological complexity of astrocytes were increased by 40%-60% and 20%-60%, respectively, in the CA1 hippocampus of female mice exposed to 0.1 mg/kg/day PCB 11; in contrast, PCB 11 had no effect on IBA1 immunoreactivity. These findings demonstrate that developmental exposure to PCB 11 promoted NDD-relevant cellular phenotypes in a dose, sex, and region-dependent manner, providing experimental evidence in support of epidemiological data identifying PCBs as potential NDD risk modifiers. Ongoing studies are investigating behavioral responses in weanling mice developmentally exposed to PCB 11.</p>","PeriodicalId":73111,"journal":{"name":"Frontiers in toxicology","volume":"8 ","pages":"1816944"},"PeriodicalIF":5.1,"publicationDate":"2026-08-12","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13506163/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148820521","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Per- and polyfluoroalkyl substances mixture exposure is associated with colorectal cancer TNM stage.","authors":"Ning Kang, Yang Zhao, Zhi Huang, Rongbin Li, Xiaoqian Ma, Shigang Ding, Fei Li, Shengju Yin, Weiwei Fu","doi":"10.3389/ftox.2026.1904192","DOIUrl":"10.3389/ftox.2026.1904192","url":null,"abstract":"<p><p>Environmental pollutants have been implicated in colorectal cancer risk, but the association between plasma per- and polyfluoroalkyl substance (PFAS) concentrations and TNM stage remains unclear. We recruited 110 patients with colorectal cancer in Beijing, China, between March and June 2024. Plasma concentrations of 32 PFAS were measured, and 23 PFAS with detection rates greater than 70% were included in the analysis. Random forest analysis was used to identify the highest-ranking PFAS for TNM-stage classification, followed by multivariable ordinal logistic regression and restricted cubic spline models to evaluate single-PFAS associations and concentration-response patterns. Bayesian kernel machine regression was further applied to assess the joint associations of the selected PFAS mixture, and stratified analyses were conducted by sex and age. PFOA and n-PFOS showed the highest median concentrations, at 2.899 ng/mL and 2.444 ng/mL, respectively. Random forest analysis identified PFPeS, PFTrDA, PFTeDA, HFPO-DA and 8:2 Cl-PFESA as five highest-ranking PFAS for TNM-stage classification. In single-pollutant models, HFPO-DA was positively associated with more advanced TNM stage (odds ratio 2.76, 95% confidence interval 1.39-5.46; P = 0.004), with a linear concentration-response association suggested by restricted cubic spline analysis (overall P = 0.012). Mixture analysis further indicated that higher combined PFAS concentrations were associated with more advanced TNM stage, with a more pronounced positive mixture-response pattern among female patients. These findings suggest that higher plasma PFAS concentrations, particularly HFPO-DA, may be associated with more advanced TNM stage in colorectal cancer and warrant confirmation in larger prospective studies.</p>","PeriodicalId":73111,"journal":{"name":"Frontiers in toxicology","volume":"8 ","pages":"1904192"},"PeriodicalIF":5.1,"publicationDate":"2026-08-11","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13504314/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148820527","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Duloxetine ameliorates acute pancreatitis-associated inflammation and modulates pain related neuroinflammatory pathways via modulation of SP-related neurokinin signaling and PAR2/TRPV1 pathways.","authors":"Khaled H Almutary, Ahmed R Elsheakh, Manar A Nader, Marwa S Zaghloul","doi":"10.3389/ftox.2026.1891784","DOIUrl":"https://doi.org/10.3389/ftox.2026.1891784","url":null,"abstract":"<p><strong>Background: </strong>Acute pancreatitis (AP) is an inflammatory pancreatic disorder, often illustrated by neuropathic, inflammatory, and/or visceral pain. Pain is a medical indicator of pancreatic inflammation and growing evidence evokes that it exerts a significant role in AP progression via the widespread neuronal network surrounding the pancreas.</p><p><strong>Objectives: </strong>evaluate the possible defensive action of duloxetine (DUX), a serotonin/norepinephrine reuptake inhibitor (SNRI), in L-arginine (L-Arg)- provoked AP and multiple organ injury (MOI), and to explore the potential mechanism of action of DUX-mediated modulation of neuroinflammatory pain in AP.</p><p><strong>Methods: </strong>AP was induced in rats by intraperitoneal injection of L-Arg (100 mg/100 g) and two different doses of DUX (10 and 30 mg/kg) was examined.</p><p><strong>Results: </strong>DUX improved the histopathological architecture of the pancreas, liver, lung, and kidney. Additionally, it restored the normal levels of serum pancreatic enzymes, liver enzymes, and kidney biomarkers that were significantly elevated following L-Arg administration. In addition, DUX improved tissue antioxidant state. Moreover, DUX decreased the levels of transient receptor potential cation channel subfamily V member 1 (TRPV1), proteinase-activated receptor-2 (PAR2), substance P (SP), neurokinin, trypsin, leukotriene B4 (LTB4), signal transducer and activator of transcription 3 (STAT3) and significantly reduced TNF-α expression in the pancreatic tissues.</p><p><strong>Conclusion: </strong>DUX displayed analgesic, anti-inflammatory, and antioxidant effects. Therefore, DUX is a promising therapeutic candidate for the management of AP-related neuroinflammatory pain. The proposed analgesic and anti-inflammatory mechanisms of DUX may be linked to the modulation of SP related NK signaling and PAR2/TRPV1 pathways pointing to a possible role for these pathways in the observed beneficial action of DUX.</p>","PeriodicalId":73111,"journal":{"name":"Frontiers in toxicology","volume":"8 ","pages":"1891784"},"PeriodicalIF":5.1,"publicationDate":"2026-08-07","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13493082/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148802547","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Case Report: acute and long-term effects of a massive beta-mercaptoethanol inhalation.","authors":"Marion Bernard, Philippe Van Brussel, Cécile Lardinois, Virginie Doyen, François M Carlier, Thomas Planté-Bordeneuve","doi":"10.3389/ftox.2026.1916362","DOIUrl":"https://doi.org/10.3389/ftox.2026.1916362","url":null,"abstract":"<p><strong>Introduction: </strong>β-mercaptoethanol is widely used in biochemistry and industrial applications. Animal toxicity has been demonstrated but very limited data exists regarding its human effects.</p><p><strong>Case description: </strong>A 40-year-old male patient was exposed to β-mercaptoethanol vapours after an accidental occupational spillage. He developed dizziness, blurred vision, a headache and epistaxis within minutes alongside dyspnoea and cough in the following hours. Lung function tests displayed bronchial hyperreactivity and increased resistances, consistent with a reactive airways dysfunction syndrome. Neuropsychological testing showed memory difficulties affecting both working and long-term verbal memory, together with attentional and executive weaknesses. Twenty months after the incident, the patient still experienced memory impairment and dyspnoea while bronchial hyperreactivity remained present.</p><p><strong>Conclusion: </strong>Respiratory exposure to large quantities of β-mercaptoethanol vapours can cause reactive airways dysfunction syndrome and is associated with long-term neurological and respiratory symptoms.</p>","PeriodicalId":73111,"journal":{"name":"Frontiers in toxicology","volume":"8 ","pages":"1916362"},"PeriodicalIF":5.1,"publicationDate":"2026-08-06","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13489590/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148802598","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Impact of intranasal cigarette smoke exposure on murine peripheral immune responses and lung pathology.","authors":"Laura G Bartlett, Yasmin Azizbayli, Amanda L Tatler, Adam J Watkins, Lucy C Fairclough","doi":"10.3389/ftox.2026.1884554","DOIUrl":"10.3389/ftox.2026.1884554","url":null,"abstract":"<p><p>Chronic obstructive pulmonary disease (COPD) is driven primarily by cigarette smoke exposure, yet modelling its immunopathogenesis in mice is complicated by systemic stress and welfare concerns associated with conventional exposure models. Here, we employ a refined intranasal cigarette smoke extract (CSE) model to examine pulmonary pathology and peripheral immune responses in male and female C57BL/6J mice. Repeated intranasal CSE exposure over 12 weeks was well tolerated and induced dose-dependent pulmonary neutrophilia, airway remodelling, and collagen deposition, with more pronounced pathology observed in female mice at higher exposure levels. In contrast, longitudinal multiparametric flow cytometric analysis revealed no consistent dose-dependent alterations in peripheral immune cell composition or activation, as confirmed by both conventional gating and unbiased clustering approaches. These findings demonstrate that COPD-like lung pathology can arise in the absence of overt systemic immune disruption and highlight the importance of lung inflammatory processes in disease development. This refined intranasal model provides a welfare-conscious platform for studying pulmonary immunopathology in COPD.</p>","PeriodicalId":73111,"journal":{"name":"Frontiers in toxicology","volume":"8 ","pages":"1884554"},"PeriodicalIF":5.1,"publicationDate":"2026-08-03","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13477786/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148766036","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}