Toxicology最新文献

{"title":"Corrigendum to “Chronic oral depleted uranium leads to reproductive damage in male rats through the ROS-hnRNP A2/B1-COX-2 signaling pathway” [Toxicology 449 (2021) 152666]","authors":"Binghui Lu , Yonghong Ran , Shuang Wang, Juan Li, Yazhen Zhao, Xinze Ran, Rong Li, Yuhui Hao","doi":"10.1016/j.tox.2025.154133","DOIUrl":"10.1016/j.tox.2025.154133","url":null,"abstract":"","PeriodicalId":23159,"journal":{"name":"Toxicology","volume":"515 ","pages":"Article 154133"},"PeriodicalIF":4.8,"publicationDate":"2025-04-10","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143937188","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Particulate matter 2.5 stimulates pyroptosis and necroptosis via the p38 MAPK/Akt/NF-κB signaling pathway in human corneal epithelial cells","authors":"Da Hye Kim ,&nbsp;Hyesook Lee ,&nbsp;Min Yeong Kim ,&nbsp;Hyun Hwangbo ,&nbsp;Seon Yeong Ji ,&nbsp;EunJin Bang ,&nbsp;Su Hyun Hong ,&nbsp;Gi Young Kim ,&nbsp;Sun-Hee Leem ,&nbsp;Dongryeol Ryu ,&nbsp;JaeHun Cheong ,&nbsp;Yung Hyun Choi","doi":"10.1016/j.tox.2025.154138","DOIUrl":"10.1016/j.tox.2025.154138","url":null,"abstract":"<div><div>Particulate matter 2.5 (PM_2.5) exposure poses significant health risks, particularly to the eyes. This study aimed to investigate the cytotoxic effects of PM_2.5 on human corneal epithelial cells (HCECs) and to elucidate the mechanisms involved in pyroptosis and necroptosis. HCECs were exposed to PM_2.5, and cytotoxicity, reactive oxygen species (ROS) levels, and the expression of pyroptosis- and necroptosis-related proteins were assessed. The roles of nuclear factor-kappa B (NF-κB) and nucleotide-binding domain, leucine-rich-containing family, pyrin domain-containing-3 (NLRP3) inflammasome signaling pathways were also investigated. Exposure to PM_2.5 caused a dose-dependent decrease in cell viability, accompanied by significant NLRP3 inflammasome activation, leading to pyroptosis and the release of pro-inflammatory cytokines. Enhanced ROS generation and mitochondrial dysfunction have also been observed, along with indicators of necroptosis, such as increased levels of mixed-lineage kinase domain-like proteins. Importantly, activation of the NF-κB signaling pathway was crucial for these responses. The suppression of p38 mitogen-activated protein kinase (MAPK) and activation of protein kinase B (Akt) using pharmacological modulators SB203580 and SC79, respectively, significantly reduced PM_2.5-mediated cellular damage. These findings indicate that p38 MAPK inhibition and Akt activation are key regulatory mechanisms that help attenuate the deleterious effects of PM_2.5 on HCECs. In conclusion, our findings offer new insights into the mechanisms by which PM_2.5 induces pyroptosis and necroptosis in HCECs, especially by activating the NLRP3 inflammasome and NF-κB signaling pathways. The critical regulatory roles of p38 MAPK and Akt underscore their potential as therapeutic targets to alleviate PM-induced ocular damage.</div></div>","PeriodicalId":23159,"journal":{"name":"Toxicology","volume":"515 ","pages":"Article 154138"},"PeriodicalIF":4.8,"publicationDate":"2025-04-06","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143800343","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Atrazine exposure induces TDP-43 protein translocation: A potential mechanism for prefrontal cortical neurodegeneration induced by environmental pollutants","authors":"Yuan Ma ,&nbsp;Kaidong Wang ,&nbsp;Yuxuan Jiao ,&nbsp;Yujing Li ,&nbsp;Rong Hu ,&nbsp;Yang Li ,&nbsp;Ge Shi ,&nbsp;Min Huang","doi":"10.1016/j.tox.2025.154128","DOIUrl":"10.1016/j.tox.2025.154128","url":null,"abstract":"<div><div>Atrazine (ATR) is a widely utilized herbicide that has been demonstrated to exert a multitude of deleterious effects on the environment, particularly with regard to water and soil contamination. Moreover, its disruption of endocrine function and implications for antibiotic resistance underscore the urgent need to prioritize alternative solutions for both ecosystems and human health. Therefore, the objective of this study was to investigate a range of neurotoxic effects associated with atrazine-induced damage in the prefrontal lobe of mice. The results of this study indicate that treatment with ATR in C57BL/6 J mice resulted in cognitive-related behavioral deficits, including anxiety and depression, as well as motor impairments. In vivo analyses demonstrated that ATR exposure resulted in a reduction in neuronal synapse density at the microstructural level, while also compromising prefrontal morphological integrity, nociceptor count, and overall neuronal health within the brain. These findings collectively suggest that synaptic deficits are implicated in ATR-induced behavioral abnormalities observed in these mice. Furthermore, our findings revealed that ATR exposure resulted in elevated TDP-43 expression levels that were ectopically localized within the cytoplasm. This alteration led to impaired functionality of mRNP granules and contributed to the development of abnormal synaptic defects. Conversely, TDP-43 has the potential to localize ectopically to mitochondria, where it activates the mitochondrial unfolded protein response (UPRmt), which ultimately results in mitochondrial dysfunction. These findings collectively indicate a strong correlation between TDP-43 dysregulation and the progression of neurodegenerative diseases. Further investigation into the potential neurotoxicity of atrazine may foster heightened awareness, leading to more stringent regulatory measures, research into safer alternatives, and the adoption of sustainable practices, which are essential for safeguarding environmental integrity alongside human health.</div></div>","PeriodicalId":23159,"journal":{"name":"Toxicology","volume":"515 ","pages":"Article 154128"},"PeriodicalIF":4.8,"publicationDate":"2025-04-05","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143804248","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Multi-omics analysis reveals BPF exposure causes hepatic glucose and lipid metabolism disorder in rats by disrupting energy homeostasis","authors":"Zhi Li ,&nbsp;Yuanyuan Wu ,&nbsp;Mingqing Qian ,&nbsp;Bingya Zhang ,&nbsp;Xinxin Deng ,&nbsp;Penghui Mao ,&nbsp;Zhonghua Fan ,&nbsp;Xu Fang ,&nbsp;Lin Cheng ,&nbsp;Xuan Liu ,&nbsp;Li Wang ,&nbsp;Hui Liu","doi":"10.1016/j.tox.2025.154130","DOIUrl":"10.1016/j.tox.2025.154130","url":null,"abstract":"<div><div>Bisphenol F (BPF) is one of the main substitutes for Bisphenol A (BPA) and is widely used in the manufacture of household products. In addition, BPF threatens human health through environmental pollution and the food chain. However, the hepatotoxicity of BPF and its effects on glucose and lipid metabolism remain unclear. This study used male SD rats as an animal model to investigate the hepatotoxicity of BPF and its effects on glucose and lipid metabolism. The results of the HE staining, serum and liver biochemical indicators show that BPF can damage the basic structure of the liver, cause liver dysfunction and lead to disorders of liver glucose metabolism and lipid metabolism. Furthermore, we conducted metabolomics and proteomics analyses on the livers of the BPF exposed group at 100 mg/kg/d in comparison with the control group. The results indicated that BPF exposure had a significant effect on liver metabolism. Combined with biological analysis and the validation of changes in genes and proteins related to glucose and lipid metabolism in the liver, it was elucidated that BPF can promote fatty acid oxidation and inhibit fatty acid synthesis through the AMPK and PPAR signaling pathways, leading to a reduction in fatty acids. Furthermore, it has been demonstrated that BPF can promote glycogen synthesis and gluconeogenesis via the AKT pathway, which can result in disorders of glucose metabolism.</div></div>","PeriodicalId":23159,"journal":{"name":"Toxicology","volume":"515 ","pages":"Article 154130"},"PeriodicalIF":4.8,"publicationDate":"2025-04-04","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143796326","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Cadmium treatment induces oxidative damage and apoptosis in vitro skeletal muscle cells","authors":"Li Wenhong ,&nbsp;Jie Yang ,&nbsp;Yuan Zhao ,&nbsp;Nan Zhang ,&nbsp;Bo Zhao ,&nbsp;Li Rongxian ,&nbsp;Gu Shiyan ,&nbsp;He Zuoshun","doi":"10.1016/j.tox.2025.154139","DOIUrl":"10.1016/j.tox.2025.154139","url":null,"abstract":"<div><div>Cadmium is a prevalent environmental contaminant, and current research indicates that exposure to cadmium is a significant risk factor contributing to the increased incidence of sarcopenia. However, the precise mechanisms by which cadmium exposure leads to skeletal muscle damage remain to be fully elucidated. Utilizing an in vitro culture model of mouse C2C12 myoblasts, this study exposed cells to 0, 2, 4, and 8 μmol/L cadmium chloride for 24 hours to evaluate the cellular damage and explore the potential mechanisms. Our present data of this study demonstrate that cadmium treatment results in a reduction of C2C12 cell viability, an increased release of lactate dehydrogenase, and an imbalance in the oxidative-antioxidant system characterized by an excessive accumulation of reactive oxygen species, elevated malondialdehyde production, and decreased superoxide dismutase activity. Additionally, there is an upregulation of nuclear factor-erythroid 2-related factor 2, heme oxygenase-1, NAD(P)H quinone oxidoreductase 1, and glutamate-cysteine ligase catalytic subunit protein expression, along with a downregulation of superoxide dismutase 1 protein expression. Furthermore, cadmium exposure mediates an increase in cysteinyl aspartate specific proteinase-dependent apoptosis via the mitochondrial pathway, as indicated by an increased apoptosis rate, elevated Bcl-2 associated X protein and cysteinyl aspartate specific proteinase 3 protein expression, and a decreased expression of B-cell lymphoma-2 protein. Our findings elucidate the mechanisms of cadmium-induced cytotoxic damage in skeletal muscle cells from the perspectives of oxidative injury and apoptosis, thereby providing a theoretical basis for the prevention and treatment of cadmium toxicity.</div></div>","PeriodicalId":23159,"journal":{"name":"Toxicology","volume":"515 ","pages":"Article 154139"},"PeriodicalIF":4.8,"publicationDate":"2025-04-04","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143791425","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"MLKL triggers NLRP3 activation in sodium arsenite-induced myocardial necroinflammation","authors":"Yixin Cui ,&nbsp;Meng Zhang ,&nbsp;Yi Xiao ,&nbsp;Jinren Liu ,&nbsp;Yonghui Chen ,&nbsp;Xingran Ruan ,&nbsp;Xu Zhao ,&nbsp;Yinan Liu ,&nbsp;Yawen Shi ,&nbsp;Jing Tian ,&nbsp;Lian Li ,&nbsp;Xinhe Zhang ,&nbsp;Mingzhao Jia ,&nbsp;Yi Wang ,&nbsp;Xuewei Yang ,&nbsp;Zhaoxing Lin ,&nbsp;Jinghong Chen","doi":"10.1016/j.tox.2025.154132","DOIUrl":"10.1016/j.tox.2025.154132","url":null,"abstract":"<div><div>Prolonged exposure to arsenic elevates the risk of developing a range of cardiovascular disorders. However, the mechanisms underlying myocardial damage from arsenic exposure remain elusive. Our earlier research suggest that drinking arsenic-contaminated water can lead to substantial inflammatory and necrotic injury in the myocardium of rats. This study was to ascertain whether mixed lineage kinase domain-like protein (MLKL) triggers Nod-like receptor protein-3 (NLRP3) activation during arsenic-induced myocardial necroinflammation in H9C2 cardiomyocytes and <em>Mlkl</em> knockout C57BL/6 mice. We demonstrated that arsenic exposure induces necroptosis by activating the receptor-interacting serine/threonine-protein kinase-3 (RIPK3)/MLKL pathway <em>in vivo</em> and <em>in vitro</em>. Consistent with our hypotheses, we found that necroptosis inhibitors (RIPK1 inhibitor necrostatin-1 [Nec-1], RIPK3 inhibitor [GSK-872], MLKL inhibitor [NSA]) and <em>Mlkl</em> genetic knockout can partially protect against arsenic-induced inflammatory damage. Additionally, these strategies can downregulate the expression of key proteins associated with the activation of the NLRP3 inflammasome, including NLRP3, Caspase-1, and interleukin-1β (IL-1β). Taken together, our findings demonstrate that MLKL triggers NLRP3 inflammasome activation and plays an essential role in arsenic-induced myocardial necroinflammation.</div></div>","PeriodicalId":23159,"journal":{"name":"Toxicology","volume":"515 ","pages":"Article 154132"},"PeriodicalIF":4.8,"publicationDate":"2025-04-04","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143796312","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Corrigendum to “Hippocampal MEF2C phosphorylation mediates synaptic plasticity in lead-induced learning and memory impairments” [Toxicology 512 (2025) 154082]","authors":"Shuo Yang ,&nbsp;Yanhui Zhu ,&nbsp;Jinmei Xiao ,&nbsp;Lingyu Yan ,&nbsp;Xuebing Zhuang ,&nbsp;Qi Li ,&nbsp;Yue Li ,&nbsp;Jie Xie ,&nbsp;Guihua Du ,&nbsp;Fankun Zhou ,&nbsp;Guangqin Fan ,&nbsp;Chang Feng","doi":"10.1016/j.tox.2025.154135","DOIUrl":"10.1016/j.tox.2025.154135","url":null,"abstract":"","PeriodicalId":23159,"journal":{"name":"Toxicology","volume":"514 ","pages":"Article 154135"},"PeriodicalIF":4.8,"publicationDate":"2025-04-04","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143788420","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Organochlorine pesticides: occurrence, spatial distribution of residues, toxicity, and toxic mechanisms","authors":"Ziying Zhang ,&nbsp;Yunfei Pan ,&nbsp;Yumei Fang ,&nbsp;Shuangshuang Mao,&nbsp;Zihong Zhou,&nbsp;Can Zhang,&nbsp;Qin Song,&nbsp;Jun Yang,&nbsp;Rong Chen","doi":"10.1016/j.tox.2025.154134","DOIUrl":"10.1016/j.tox.2025.154134","url":null,"abstract":"<div><div>Organochlorine pesticides (OCPs) are a class of synthetic, broad-spectrum insecticides that have been widely used for plant pest control over the last century. OCPs are persistent organic pollutants (POPs) with mutagenic, teratogenic, and carcinogenic properties. Although most OCPs are banned to use now, they are ubiquitous in the environment and food, and identified in the serum and urine of humans. Exposure to OCPs could affect the human nervous system, auditory system, and endocrine system, leading to neurodegenerative diseases, hearing loss, cancer, and other diseases. Further, the toxic mechanisms of OCPs are explored from oxidative stress, DNA damage, and inflammatory response. Overall, this review offers a comprehensive insight into the occurrence, spatial distribution of residues, toxicity, and toxic mechanisms of OCPs.</div></div>","PeriodicalId":23159,"journal":{"name":"Toxicology","volume":"515 ","pages":"Article 154134"},"PeriodicalIF":4.8,"publicationDate":"2025-04-03","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143788857","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Regulation of in vitro human hematopoietic differentiation by dioxin-like compounds","authors":"D M Isha Olive Khan ,&nbsp;Robert B. Crawford ,&nbsp;Norbert E. Kaminski","doi":"10.1016/j.tox.2025.154136","DOIUrl":"10.1016/j.tox.2025.154136","url":null,"abstract":"<div><div>Certain dioxin-like compounds (DLCs) pose health concerns. However, their impact on human hematopoiesis has not been explored. Role of 2,3,4,7,8-pentachlorodibenzofuran (PeCDF), 3,4,4′,5-tetrachlorobiphenyl (PCB81), and 3,3′,4,4′,5-pentachlorobiphenyl (PCB126) in lineage specification from human cord-blood derived CD34⁺ hematopoietic stem and progenitor cells (HSPCs) was investigated. We compared these DLCs in relation to 2,3,7,8-tetrachlorodibenzo-<em>p</em>-dioxin (TCDD). Over a 28-day period, HSPCs were cultured <em>in vitro</em> in the presence of TCDD and DLCs at concentrations ranging from 0.1 to 50 nM. Cells were collected every 7 days for analysis. TCDD, PeCDF, PCB-126, and PCB-81 reduced percentage of CD10⁺ lymphoid progenitors and CD10 protein expression in a concentration-dependent manner. PeCDF was more potent than TCDD, and PCB81 had higher potency than PCB126. TCDD and PeCDF also induced reduction in CD34 expressing cells and CD1c⁺ dendritic cells, and an increase in promyelocytes at multiple time-points. These changes were mediated through the aryl hydrocarbon receptor (AHR). With increasing concentrations of TCDD and PeCDF, there was a trend towards decreases in CD41⁺ megakaryocyte progenitors and increases in CD14⁺ monocytes. This study demonstrated that these DLCs altered human HSPC differentiation process towards specific myeloid hematopoietic lineages at the expense of lymphoid progenitors, similar to TCDD, which may lead to reduced immune competence. Lineages that were most sensitive to developmental modulation by DLCs were identified. Interestingly, the relative potency of these DLCs in eliciting these effects in humans was different from the compounds’ relative toxicological profiles as reported in murine studies, with important implications for human risk assessment for these compounds.</div></div>","PeriodicalId":23159,"journal":{"name":"Toxicology","volume":"514 ","pages":"Article 154136"},"PeriodicalIF":4.8,"publicationDate":"2025-04-03","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143783044","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Copper oxide nanoparticles induce pulmonary inflammation via triggering cellular cuproptosis","authors":"Xiaojing Zhang,&nbsp;Zhongqi Peng,&nbsp;Qian Wang,&nbsp;Wei Zhang,&nbsp;Qian Bu,&nbsp;Donglei Sun","doi":"10.1016/j.tox.2025.154131","DOIUrl":"10.1016/j.tox.2025.154131","url":null,"abstract":"<div><div>Copper oxide nanoparticles (CuO NPs) are increasingly used in various industrial fields, and the toxicity of CuO NPs raises concerns. However, the CuO NPs-induced pulmonary inflammation and the underlying mechanism have not been fully illustrated. Cellular cuproptosis provides a new perspective to elucidate the toxicity of CuO NPs. Here, we exposed C57BL/6 mice and murine alveolar macrophage cells (MH-S) to CuO NPs, respectively. A suspension of 2 mg/mL CuO NPs was directly once administered by intratracheal instillation, and mice were sacrificed on day 7. The histopathology results showed that CuO NPs induced pulmonary inflammation in C57BL/6 mice. CuO NPs increased Cu^2 + levels by 203.0 % in mouse lung tissues. Also, CuO NPs increased the cuproptosis-related indicators of ferredoxin (FDX1), dihydrolipoamide succinyltransferase (DLST), dihydrolipoamide acetyltransferase (DLAT) and Cu transporter 1 (CTR1) in both mouse lung tissues and MH-S cells. Transcript sequencing and non-targeted metabolomics indicated that CuO NPs induced cellular cuproptosis and inflammatory responses both <em>in vivo</em> and <em>in vitro</em>. Interleukin-17a (IL-17A) was remarkably increased in the process of CuO NPs-induced cellular cuproptosis. Additionally, interference of FDX1 reduced cellular cuproptosis and decreased the release of IL-17A. In summary, CuO NPs increased the accumulation of intracellular Cu²⁺ and the expressions of cuproptosis-related proteins, induced FDX1-mediated cuproptosis, and led to pulmonary inflammation in mice. This study highlights the respiratory toxicity of CuO NPs and reveals a unique cuproptosis-driven mechanism underlying the CuO NPs-induced pulmonary inflammation.</div></div>","PeriodicalId":23159,"journal":{"name":"Toxicology","volume":"514 ","pages":"Article 154131"},"PeriodicalIF":4.8,"publicationDate":"2025-04-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143769219","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}