Archives of Toxicology最新文献

{"title":"A quantitative framework for animal-to-human extrapolation of inhaled aerosols using species-specific respiratory dosimetry.","authors":"Ji-Hun Jang, Seung-Hyun Jeong","doi":"10.1007/s00204-026-04550-5","DOIUrl":"https://doi.org/10.1007/s00204-026-04550-5","url":null,"abstract":"<p><p>Quantitative extrapolation of inhalation toxicity data from experimental animals to humans remains challenging because identical external aerosol exposures do not necessarily produce equivalent internal respiratory doses across species. This study aimed to establish a quantitative computational framework for animal-to-human extrapolation by integrating species-specific respiratory dosimetry using the Multiple-Path Particle Dosimetry (MPPD) model. Species-specific respiratory dosimetry models were developed for mice, rats, and adult humans using MPPD v3.04 under identical aerosol exposure conditions. Regional respiratory deposition was compared across species, while the effects of aerosol particle size (mass median aerodynamic diameter, MMAD) and human breathing scenarios were systematically evaluated. Regional deposition outputs were further integrated to derive quantitative dosimetry indices, human equivalent concentrations (HECs), and species correction factors (SCFs) for animal-to-human extrapolation. Marked interspecies differences were observed in regional respiratory deposition despite identical aerosol exposure conditions. Rodents exhibited predominant deposition within the extrathoracic region, whereas humans demonstrated substantially greater pulmonary deposition. Species-specific deposition differences became more pronounced with increasing MMAD, and pulmonary delivery in humans was strongly influenced by breathing scenario. Quantitative dosimetry analysis demonstrated that pulmonary deposition in humans was approximately three-fold greater than in rodents under the reference exposure condition, resulting in substantially different regional respiratory deposition metric despite equivalent external exposures. The proposed HEC and SCF metrics enabled quantitative comparison and translation of animal and human exposure conditions using MPPD-derived regional deposition metrics rather than external aerosol concentration alone. This study presents a species-specific respiratory dosimetry framework for quantitative animal-to-human extrapolation of inhaled aerosols. By integrating regional respiratory deposition with HEC and SCF analyses, the proposed framework provides a mechanistically informed strategy for inhalation dosimetry, human equivalent exposure estimation, and future integration with physiologically based pharmacokinetic modeling and inhalation risk assessment.</p>","PeriodicalId":8329,"journal":{"name":"Archives of Toxicology","volume":" ","pages":""},"PeriodicalIF":10.9,"publicationDate":"2026-09-17","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148988005","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Artificial intelligence in toxicology: current advances, challenges and future directions.","authors":"Kamil Kuca, Siddhi Otari, Namrata Singh, Monita Gide, Rakesh Somani, Jiri Krenek, Dominik Palla, Eugenie Nepovimova","doi":"10.1007/s00204-026-04551-4","DOIUrl":"10.1007/s00204-026-04551-4","url":null,"abstract":"<p><p>Toxicology has traditionally relied on in vivo animal studies and in vitro assays to assess the safety of drugs, chemicals and environmental contaminants. These approaches are constrained by cost, duration, ethical concerns and difficulties in cross-species extrapolation. Artificial intelligence (AI) offers an alternative paradigm in which safety-relevant signals are extracted from large, heterogeneous datasets. This review traces the development of AI in toxicology from rule-based expert systems to contemporary deep learning, large language model and multimodal architectures. It critically evaluates the evidence base for AI-based toxicity prediction, assesses current challenges and considers the trajectory toward next-generation risk assessment. A structured literature search was conducted in PubMed/MEDLINE, Web of Science and Scopus (2000-2026), supplemented by guidance documents from OECD, FDA, EMA, EFSA and EPA. Studies were selected based on methodological quality, availability of external validation data and regulatory relevance. Graph neural networks, multi-task deep learning and related AI approaches have shown competitive performance in selected benchmark studies of drug-induced liver injury (DILI), hERG cardiotoxicity and Ames mutagenicity, although performance varies substantially across datasets and validation settings. Explainable AI frameworks such as SHAP are aligning model outputs with adverse outcome pathways (AOPs). Federated learning enables privacy-preserving multi-institutional collaboration, as demonstrated by the MELLODDY consortium. Critical gaps remain: external validation is inconsistently reported, endpoint-specific models struggle to generalise and hallucination in large language models poses unresolved regulatory risks. AI is becoming an increasingly important component of toxicological science, although its readiness for routine application varies substantially across methods and endpoints. Realising this potential requires adherence to the TREAT validation principles and sustained regulatory engagement. AI models augment, but cannot yet replace, experimental toxicology.</p>","PeriodicalId":8329,"journal":{"name":"Archives of Toxicology","volume":" ","pages":""},"PeriodicalIF":10.9,"publicationDate":"2026-09-17","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148988011","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Doxorubicin-induced hepatotoxicity: a multifaceted pathogenesis from mitochondrial collapse to immune remodeling and epigenetic memory.","authors":"Bohuai Tang, Zengbin Wang","doi":"10.1007/s00204-026-04534-5","DOIUrl":"https://doi.org/10.1007/s00204-026-04534-5","url":null,"abstract":"<p><p>Doxorubicin's clinical utility is constrained by cumulative toxicities, including a significantly underestimated hepatotoxicity. As the primary metabolic hub, the liver accumulates doxorubicin via active transport, leading to mitochondrial crisis through quinone redox cycling and concurrent blockade of mitophagic flux. This drives hepatocytes toward synchronized regulated cell death, prominently featuring ferroptosis and pyroptosis. The injury is amplified by hepatic immune remodeling, characterized by Kupffer cell depletion and the formation of neutrophil extracellular traps. Furthermore, a proposed epigenetic component, driven by DNA hypomethylation and histone acetylation imbalances, may contribute to persistent hepatic dysfunction. By integrating these multidimensional mechanisms, this review evaluates forward-looking strategies, highlighting the potential of natural products, intelligent nanodelivery systems, and repurposed drugs to achieve hepatoprotection while critically addressing the inherent challenge of avoiding tumor protection.</p>","PeriodicalId":8329,"journal":{"name":"Archives of Toxicology","volume":" ","pages":""},"PeriodicalIF":10.9,"publicationDate":"2026-09-17","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148988053","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Phase I metabolism of the methadone analog methiodone (IC-26) in pooled human liver microsomes and its detection in seven authentic human cases.","authors":"Johannes Kutzler, Antonia Postupka, Volker Auwärter","doi":"10.1007/s00204-026-04546-1","DOIUrl":"https://doi.org/10.1007/s00204-026-04546-1","url":null,"abstract":"<p><p>The recent detection of methiodone (IC-26; 4-(Ethanesulfonyl)-N, N-dimethyl-4,4-diphenylbutan-2-amine) in Europe, a new synthetic opioid associated with a growing number of fatal intoxications, highlights the need for reliable toxicological markers to support its detection in routine screening. As a structural analog of methadone, methiodone exemplifies the structural diversity of new emerging synthetic opioids. In this study, the metabolism of methiodone was investigated using an integrated approach combining in silico prediction (GLORYx, EAWAG-PPS, BioTransformer 3.0), in vitro incubation with pooled human liver microsomes (pHLM), and liquid chromatography-quadrupole time-of-flight tandem mass spectrometry (LC-QTOF/MS) analysis of authentic biological samples from one non-fatal intoxication and six post-mortem cases. Two major phase I metabolites were identified, N-desmethyl methiodone (M1) and N, N-didesmethyl methiodone (M2), and both were consistently detected across all fatal cases by LC-QTOF/MS. Seven additional minor metabolites, likely formed via hydroxylation or combined N-demethylation and hydroxylation, were tentatively identified exclusively in authentic biological samples by LC-MS/MS. In the non-fatal case, M1 was the sole detectable analyte in serum, suggesting its particular value as a long-term exposure marker. The detection of trace M1 in microsome-free control incubations indicates a minor non-enzymatic degradation pathway, with implications for the cautious interpretation of low-level M1 findings, e.g. in hair analysis. Blood methiodone concentrations in fatal cases ranged from 25 to 930 ng/mL, and in urine from 220 to 37,700 ng/mL. The integration of methiodone, M1, and M2 into routine opioid screening methods is strongly recommended to ensure reliable detection across all stages of drug elimination.</p>","PeriodicalId":8329,"journal":{"name":"Archives of Toxicology","volume":" ","pages":""},"PeriodicalIF":10.9,"publicationDate":"2026-09-16","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148975671","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Genotoxicity of anthraquinone dyes and dye intermediates: a comprehensive review.","authors":"Anna Itkonen, Harri Kovakoski, Mikko Herrala, Jaana Rysä","doi":"10.1007/s00204-026-04514-9","DOIUrl":"https://doi.org/10.1007/s00204-026-04514-9","url":null,"abstract":"<p><p>Anthraquinone dyes and dye intermediates are widely used across industrial, pharmaceutical, and biological applications. Despite evidence that both synthetic and naturally occurring anthraquinones may exhibit genotoxic effects, a complete assessment of their genotoxic potential is currently lacking. This review provides a comprehensive evaluation of genotoxicity data for anthraquinone dyes and dye intermediates derived from bacterial assays, mammalian in vitro systems, and in vivo models. Data from studies assessing gene mutation, chromosomal damage, DNA damage, and DNA repair were integrated. Genotoxic activity was common but substance-specific and frequently confined to particular endpoints or strains rather than consistent across the test battery. Of the 63 anthraquinones evaluated, ten including 1-amino-2-methyl-anthraquinone, 2-aminoanthraquinone, aloe emodin, chrysazin, emodin, Disperse Blue 3, Disperse Blue 7, Disperse Red 11, rubiadin and Acid Blue 62 showed consistent evidence of genotoxic activity, whereas carminic acid can be considered non-genotoxic on the available evidence. For many compounds the evidence remained insufficient to draw definitive conclusions, highlighting the need for further studies conducted in accordance with Organisation for Economic Co-operation and Development guidelines.</p>","PeriodicalId":8329,"journal":{"name":"Archives of Toxicology","volume":" ","pages":""},"PeriodicalIF":10.9,"publicationDate":"2026-09-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148975650","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Derivation of guidance values under the EU Drinking Water Directive : the case study of trifluoroacetic acid.","authors":"Robin Sur, Richard Bartlett, Bastian Becker, Anja Hueser, Felix M Kluxen, Volker Laabs, Jyotigna Mehta, Stephanie Melching-Kollmuss, Ursula G Sauer, Emily Scorgie, Derek F Wallace","doi":"10.1007/s00204-026-04530-9","DOIUrl":"https://doi.org/10.1007/s00204-026-04530-9","url":null,"abstract":"<p><p>Trifluoroacetic acid (TFA) is a metabolite of e.g., pesticides, refrigerants and propellants, and it is considered a 'non-relevant metabolite' of pesticides under the EU Drinking Water Directive (DWD) as current exposures have not been found to provide a consumer health risk. Since an EU-harmonised concept for the derivation of drinking water guidance values is unavailable, various guidance values have been proposed or implemented on the Member State level for TFA in drinking water. This causes uncertainty with respect to the adequacy of such values. To address this uncertainty, the scientific rationale underlying the different guidance values is reviewed here. It is further shown that TFA should not be included in the DWD definitions for per- and polyfluoroalkyl substances; this is relevant for one of the suggested guidance values. Finally, a science-based approach for deriving guidance values for substances in drinking water is proposed. Application of this approach to TFA as an example yields a health-based guidance value of 294 µg/L TFA in drinking water. To foster harmonisation and acceptance across agencies, this guidance value should be complemented with appropriate risk management measures (such as introduction of an upper limit for hygienic reasons); however, such further considerations are outside the scope of the present article. All stakeholders are encouraged to align on an EU-harmonised approach to derive scientifically justified and robust guidance values for substances in drinking water to adequately protect consumers.</p>","PeriodicalId":8329,"journal":{"name":"Archives of Toxicology","volume":" ","pages":""},"PeriodicalIF":10.9,"publicationDate":"2026-09-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148975581","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Characterization and quantitation of urinary metabolites of 2-monochloropropane-1,3-diol (2-MCPD) in Wistar rats.","authors":"Thorsten Henning, Cornelius Goerdeler, Ahmed H El-Khatib, Klas Meyer, Gustav Bruer, Bernhard H Monien","doi":"10.1007/s00204-026-04542-5","DOIUrl":"https://doi.org/10.1007/s00204-026-04542-5","url":null,"abstract":"<p><p>Fatty acid esters of 2-monochlorpropane-1,2-diol (2-MCPD) are process contaminants formed during the heat treatment of foodstuffs containing fat and salt. The limited information on 2-MCPD metabolism hinders investigating the mechanisms of toxic effects observed in skeletal and heart muscle as well as kidneys of rats treated with 2-MCPD dissolved in water by gavage over 28 days. The aim of the present work was to expand the scheme of 2-MCPD metabolism in rats. After oral administration of [¹³C₃]2-MCPD (30 mg/kg bodyweight; bw) or 2-MCPD (3 or 30 mg/kg bw) by gavage, urine samples were collected between 0 and 8 h, 8-24 h and 24-48 h. Novel metabolites were identified by ¹³C nuclear magnetic resonance (NMR) spectroscopy and high-resolution mass spectrometry (HRMS), and the most abundant metabolites were quantified by isotope-dilution GC-MS and UPLC-MS/MS. The main compounds were 2-MCPD itself and the oxidation product 2-chlorohydracrylic acid (2-ClHA). Eight metabolites were detected for the first time. Products of conjugation reactions were 2-MCPD sulfate and 2-MCPD glucuronide. Six metabolites formed after degradation of glutathione conjugates were thiodiglycolic acid (TDGA), thionyldiglycolic acid (TNDGA), 3-(S-carboxymethyl)mercaptolactic acid (CMMLA), S-(carboxymethyl)-CysGly (CMCG), N-acetyl-S-(1-carboxy-2-hydroxyethyl)-Cys (CHEMA), and 2-[(2-carboxy-2-oxoethyl)sulfanyl]hydracrylic acid (2-COSHA). The mean excretion ratios of four main compounds quantified in male (m) and female (f) urine collected over 48 h following the low dose administration of 3 mg/kg bw were: 2-MCPD itself (m: 12.5%, f: 11.6%), 2-ClHA (m: 30.4%, f: 26.0%), TDGA (m: 8.5%, f: 8.1%) and 2-MCPD sulfate (m: 0.19%, f: 0.23%). In summary, the metabolites covered at least 51.6% (m) or 45.9% (f) of the dose, which allowed proposing a comprehensive scheme of metabolic pathways. Given that 2-MCPD and each of its metabolites may exert a toxic effect, two pairs of metabolites stand out due to their reactivity with glutathione: 2-chloroacetaldehyde/2-chloroacetic acid as well as 2-chlorolactaldehyde/2-ClHA.</p>","PeriodicalId":8329,"journal":{"name":"Archives of Toxicology","volume":" ","pages":""},"PeriodicalIF":10.9,"publicationDate":"2026-09-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148975632","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"From in vitro hazard to inhalation risk: exposure context matters for flavoured-air inhaler toxicity.","authors":"Zhichao Zhao, Xin Zhang, Ting Shen","doi":"10.1007/s00204-026-04547-0","DOIUrl":"https://doi.org/10.1007/s00204-026-04547-0","url":null,"abstract":"","PeriodicalId":8329,"journal":{"name":"Archives of Toxicology","volume":" ","pages":""},"PeriodicalIF":10.9,"publicationDate":"2026-09-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148975601","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Combined immune modulation reveals carbamazepine-associated CD8⁺ T cell-dependent skin inflammation in HLA-A*31:01 knock-in mice.","authors":"Shigeki Aoki, Maho Ichikawa, Yuichi Masuda, Kaetsu Komiya, Satoru Nakada, Takaya Yokoyama, Naomoto Harada, Takeshi Susukida, Akira Kazaoka, Kousei Ito","doi":"10.1007/s00204-026-04536-3","DOIUrl":"https://doi.org/10.1007/s00204-026-04536-3","url":null,"abstract":"<p><p>Human leukocyte antigen (HLA) alleles are among the strongest genetic risk factors for idiosyncratic drug toxicity. HLA-A*31:01 is a risk factor for carbamazepine (CBZ)-induced delayed drug hypersensitivity, yet allele carriage alone is insufficient for disease development. CD8⁺ T cells are implicated in these reactions; however, their activation mechanism remains unclear. Using HLA-A*31:01 knock-in (A31-KI) mice, we investigated whether CBZ exposure elicited CD8⁺ T-cell responses in vivo. The mice received CBZ for 7 days by oral administration (300 mg/kg/day) and auricular application (25 mg/kg/day). CBZ alone did not induce clear CD8⁺ T-cell activation. Under CD4⁺ T-cell depletion, CBZ markedly increased programmed cell death protein 1 (PD-1) expression in CD44^highCD62L^low CD8⁺ T cells, suggesting PD-1-mediated restraint of CBZ-responsive activation. Subsequent PD-1 blockade enhanced CD8⁺ T-cell activation in auricular lymph nodes and induced skin inflammation with elevated serum thymus and activation-regulated chemokine; both were attenuated by CD8⁺ T-cell depletion. To clarify how CBZ activated CD8⁺ T cells, we performed ex vivo analyses using splenocytes. CBZ (50 µM) induced proliferation of CD44^highCD8⁺ T cells, whereas this response was absent in purified CD8⁺ T-cell cultures and reduced by HLA class I and costimulatory blockade, supporting an antigen-presenting cell-dependent mechanism. Collectively, CBZ can activate CD8⁺ T cells; however, this response is restrained and remains latent. When immune control is disrupted, particularly in an HLA-A*31:01-bearing host, the response can progress to a CD8⁺ T cell-dependent inflammatory phenotype. Thus, A31-KI mice provide an in vivo platform for understanding CBZ-associated idiosyncratic toxicity and pathogenesis.</p>","PeriodicalId":8329,"journal":{"name":"Archives of Toxicology","volume":" ","pages":""},"PeriodicalIF":10.9,"publicationDate":"2026-09-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148975606","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"In vitro approaches for modelling gut-liver crosstalk in drug-induced liver injury.","authors":"Ynske Janssen, Jian Jiang, Doris Vandeputte, Mathieu Vinken","doi":"10.1007/s00204-026-04537-2","DOIUrl":"https://doi.org/10.1007/s00204-026-04537-2","url":null,"abstract":"<p><p>Drug-induced liver injury (DILI) remains a major challenge in drug development and clinical practice due to its limited predictability in current preclinical models. Increasing evidence indicates that the gut-liver axis, through bidirectional interactions between the gut and the liver, plays an important role in modulating drug metabolism and hepatotoxicity. Nevertheless, the exact role of our gut, its microbiota and microbiota-derived metabolites in the manifestation of DILI remains poorly understood, highlighting the need for more human-relevant in vitro models taking along gut-liver interactions. To address this need, this review paper aimed to map the current landscape of in vitro gut-liver models and evaluate their potential applicability for future DILI research. A literature screening using the PubMed database identified 95 articles published on this subject between 2000 and 2026. The in vitro models were categorized into 5 groups, including monocultures, Transwell^® systems, hydrogel-based systems, organ-on-a-chip platforms and microfluidic bioreactors. Each category features distinct advantages and disadvantages with respect to physiological relevance, complexity, integration of gut microbiota interactions and industrial applicability. Despite these differences, several key gaps remain across all in vitro gut-liver models, including the limited incorporation of a gut microbiota component, insufficient modelling of interindividual variability and the lack of physiologically relevant flow conditions. Future optimization efforts of these models, combined with integration with in silico tools, may improve the prediction of human DILI, ultimately resulting in reduced late-stage drug attrition, less reliance on animal studies and the development of safer pharmaceutical drugs.</p>","PeriodicalId":8329,"journal":{"name":"Archives of Toxicology","volume":" ","pages":""},"PeriodicalIF":10.9,"publicationDate":"2026-09-12","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148954659","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}