Current Research in Toxicology最新文献

{"title":"A novel non-invasive imaging technique for mapping microplastic accumulation and distribution in different organ systems of Indian major carp Labeo rohita (Ham. 1822)","authors":"Sneha Siwach ,&nbsp;Aviral Singh ,&nbsp;Soumyadeep Paul ,&nbsp;Vanika Gupta ,&nbsp;Ishaan Gupta ,&nbsp;Ram Krishan Negi","doi":"10.1016/j.crtox.2026.100294","DOIUrl":"10.1016/j.crtox.2026.100294","url":null,"abstract":"<div><div>Microplastic (MP) pollution poses an increasing threat to the aquatic ecosystems, yet most existing detection methods remain largely destructive and spatially limited. Here, we present a novel, non-invasive imaging framework integrated with micro-computed tomography (µ-CT) and fluorescence microscopy to investigate ingestion, accumulation and internal distribution of fluorescently labelled polystyrene microplastics (PS-MP) in the commercially important fish species <em>Labeo rohita</em>. Fluorescence microscopy confirmed presence of MPs in the gastrointestinal (GI) tract, gills, muscle tissues and excreta of exposed fish, whereas, micro-computed tomography (µ-CT) facilitated non-destructive, three-dimensional whole-body imaging, allowing precise localization and visualization of internalized particles within intact organisms. A clear, progressive and exposure-dependent increase in microplastic presence was observed over the 28-day experimental period, supported by non-parametric trend and effect-size analyses, with consistently higher relative burdens under waterborne exposure compared to the dietary exposure, as revealed by complementary µ-CT and fluorescence imaging. Detection of microplastics in muscle tissue indicates systemic translocation beyond primary uptake organs, whereas their presence in excreta confirms active elimination processes. Strong spatial concordance between µ-CT and fluorescence microscopy validates the robustness of the dual-imaging approach. Collectively, this study advances microplastic ecotoxicology by establishing a scalable, high-resolution, non-invasive imaging framework for mapping and tracking microplastic fate in freshwater systems as well as organ-specific microplastic distribution and burden in freshwater fish under environmentally realistic exposure conditions.</div></div>","PeriodicalId":11236,"journal":{"name":"Current Research in Toxicology","volume":"10 ","pages":"Article 100294"},"PeriodicalIF":2.9,"publicationDate":"2026-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147702655","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Research on the safety risk of oral nicotine products and its prospects","authors":"YanLing Yang,&nbsp;Huan Liang,&nbsp;Yi Liu,&nbsp;Qi Zhang","doi":"10.1016/j.crtox.2026.100305","DOIUrl":"10.1016/j.crtox.2026.100305","url":null,"abstract":"<div><div>Oral nicotine products are a category of novel tobacco products that deliver nicotine through oral consumption. With increasing tobacco control measures worldwide and growing public health awareness, its safety risk has gained attention. However, the regulatory authorities still lack long-term data for oral nicotine products and limited data on additives, so the continued in-depth research is required in the future. By integrating data from chemical analyses, animal/cell studies, and human cohorts, this review first introduces the main commercially available oral nicotine products and their classifications, analyzes the potentially harmful substances and their concentrations, and then systematically elucidates the health effects of oral nicotine products (including on oral and cardiovascular systems) and their underlying mechanisms. Finally, based on relevant research, it proposes future directions for safety risk studies on oral nicotine products. In summary, this review offers consumers a clearer understanding of the safety risks of oral nicotine products, provides evidence to support their rational use, and delivers insights for companies and regulators to develop effective policies and reduce health risks.</div></div>","PeriodicalId":11236,"journal":{"name":"Current Research in Toxicology","volume":"11 ","pages":"Article 100305"},"PeriodicalIF":4.7,"publicationDate":"2026-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13279749/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148293534","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":"Subchronic low dose dioxin exposure disrupts hepatic and metabolic homeostasis in a sex- and diet-dependent manner","authors":"Oluwanifemi E. Bolatimi,&nbsp;Yuan Hua,&nbsp;Gavin J. Phillips,&nbsp;Abigail Ekuban,&nbsp;Paxton Brizendine-Ames,&nbsp;Walter H. Watson,&nbsp;Mayukh Banerjee,&nbsp;Frederick A. Ekuban,&nbsp;Banrida Wahlang","doi":"10.1016/j.crtox.2026.100311","DOIUrl":"10.1016/j.crtox.2026.100311","url":null,"abstract":"<div><div>Persistent organic pollutants (POPs) such as “dioxins” have been associated with liver disease development. Population studies have highlighted sex-specific susceptibility to POP-induced liver damage, yet toxicological models looking at sex-specific toxic responses and the combined effects of dioxin mixtures remain insufficiently characterized. This study addresses a critical knowledge gap by investigating sex-dependent effects from exposure to a mixture of dioxin and dioxin-like compounds in the context of sex differences and dietary patterns. Male and female C57BL/6 J mice were fed either a low- (LFD) or high-fat diet (HFD) and administered a weekly dose of 2,3,7,8-tetrachlorodibenzo-<em>p</em>-dioxin (TCDD-10 ng/kg), 3,4,7,8-pentachlorodibenzofuran (PeCDF-80 ng/kg) and polychlorinated biphenyl 126 (PCB126-140 ng/kg) or vehicle control. After 12 weeks, the study was terminated and samples collected for downstream analyses. LFD-fed females exposed to the dioxin mixture displayed reduced liver weight but elevated hepatic triglycerides alongside elevated circulating alanine aminotransferase levels and upregulation of the hepatic fatty acid transport gene <em>Cd36</em>. This observation was absent in diet-matched males. Instead, exposed LFD-fed males showed suppressed de novo lipogenic gene expression coupled with impaired glucose tolerance. Aryl hydrocarbon receptor (AHR) activation (↑<em>Cyp1a1</em>, <em>Cyp1a2</em>) was observed with exposure regardless of sex or diet, although HFD diminished AHR signaling, especially in males. Exposure also resulted in constitutive androstane receptor (CAR) activation (↑<em>Cyp2b10</em>, <em>Cyp2c29</em>), specifically in LFD-fed males. Notably, the dioxin mixture did not exacerbate HFD effects. Sex-specific toxicant responses were observed including dioxin-mediated steatotic liver phenotype in females and glucose perturbation in males, highlighting the negative impact of these chemicals on liver and metabolic outcomes even at low doses.</div></div>","PeriodicalId":11236,"journal":{"name":"Current Research in Toxicology","volume":"11 ","pages":"Article 100311"},"PeriodicalIF":4.7,"publicationDate":"2026-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13316181/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148359790","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: Pluripotent stem cells in discovery and mechanistic toxicology","authors":"David G Belair","doi":"10.1016/j.crtox.2026.100293","DOIUrl":"10.1016/j.crtox.2026.100293","url":null,"abstract":"","PeriodicalId":11236,"journal":{"name":"Current Research in Toxicology","volume":"10 ","pages":"Article 100293"},"PeriodicalIF":4.7,"publicationDate":"2026-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148322937","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Determination of the half-life of di(2-ethylhexyl) phthalate (DEHP) in a preterm neonate using blood transfusion as the source of intravenous exposure","authors":"Michael Furlong ,&nbsp;Venkata Gupta ,&nbsp;Stephanie Galanti ,&nbsp;Srinivasan Narasimhan ,&nbsp;Divya Pulivarthi ,&nbsp;Syam S. Andra ,&nbsp;Annemarie Stroustrup","doi":"10.1016/j.crtox.2026.100287","DOIUrl":"10.1016/j.crtox.2026.100287","url":null,"abstract":"<div><div>In the neonatal intensive care unit (NICU), infants face treatments that convey high-dose exposure to phthalates, a family of ubiquitous endocrine-disrupting organic chemicals. Past research shows that NICU-based phthalate exposure, particularly exposure to di (2-ethylhexyl) phthalate (DEHP), is associated with increased risk of abnormal multisystem outcomes among preterm infants. Blood product transfusion is a recognized significant source of DEHP exposure in hospitalized patients. In this pilot study we collected serial urine samples from one preterm subject following a clinically indicated blood transfusion as a sentinel DEHP exposure. Each specimen was analyzed for DEHP metabolites via liquid chromatography coupled with triple quadrupole tandem mass spectrometry. The calculated half-lives of DEHP metabolites in this subject were generally shorter than reported for adults. Our pilot data demonstrate the need for future studies to estimate population-level half-lives of DEHP metabolites in preterm infants to allow for more accurate NICU-based DEHP source identification than possible with estimates of DEHP metabolism in adults. Source identification is critical to mitigate exposure in the highly vulnerable NICU population.</div></div>","PeriodicalId":11236,"journal":{"name":"Current Research in Toxicology","volume":"10 ","pages":"Article 100287"},"PeriodicalIF":2.9,"publicationDate":"2026-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147384961","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Food preservative tBHQ modulates Th17/Treg balance through AHR/NRF2 xenosensors and increases the sensitivity of T cells to activation stimuli","authors":"Zoltán Palczert,&nbsp;Krisztina Németh,&nbsp;Nóra Fekete,&nbsp;Éva Pállinger,&nbsp;Márta Békés-Kanalas,&nbsp;Péter Petschner,&nbsp;Edit I. Buzás,&nbsp;Miklós Csala,&nbsp;Viola Tamási","doi":"10.1016/j.crtox.2026.100314","DOIUrl":"10.1016/j.crtox.2026.100314","url":null,"abstract":"<div><div>In this study, we investigated the effect of the food preservative tert-butylhydroquinone (tBHQ) on the activation of murine CD4⁺ T cells. We assessed the role of the nuclear factor erythroid 2–related factor 2 (NRF2) and the aryl hydrocarbon receptor (AHR) and conducted protein interaction studies to identify potential molecular targets of tBHQ.</div><div>BALB/c mice received tBHQ orally (1.5% [<em>w</em>/w]), after which splenic T cells (Th1, Th2, Th17, T_reg) were analyzed for number and activation sensitivity.</div><div>While the number of effector T cells remained unchanged, their response to stimulation was accelerated in tBHQ treated animals. In contrast, T_reg cells increased in number after treatment with this food additive but displayed reduction in count upon activation.</div><div><em>In vitro</em> experiments showed that tBHQ modulates the differentiation of Th17 and T_reg cells. Pretreating these cells with NRF2 inhibitor trigonelline and/or AHR inhibitor TMF (6, 2, 4′-trimetoxi-flavone) altered the effect of tBHQ on these cells.</div><div>We found 14 candidate targets of this chemical (AHR, KEAP1, NQO1, RORC, TBX21, IL6, GATA3, BCL2, FOXP3, IFNG, JAK2, ALB, TGFBR1, and HSP90AA1). Network analysis revealed coordinated regulation of pathways associated with inflammation, T cell differentiation, and xenobiotic response.</div><div>In conclusion, our studies highlight the importance of the T cell response after tBHQ exposure and suggest multiple proteins and pathways that are relevant to the immunotoxicity of this compound.</div></div>","PeriodicalId":11236,"journal":{"name":"Current Research in Toxicology","volume":"11 ","pages":"Article 100314"},"PeriodicalIF":4.7,"publicationDate":"2026-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13392857/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148577457","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":"SSO targets CD36 to regulate lipid metabolism disorders and improve SiO2 induced fibrosis","authors":"Xinyao Wang,&nbsp;Yingshu Zhang,&nbsp;Yi Hu,&nbsp;Xiaodi Liu,&nbsp;Bo Zhang,&nbsp;Hongli Wang,&nbsp;Heliang Liu,&nbsp;Hailan He","doi":"10.1016/j.crtox.2026.100315","DOIUrl":"10.1016/j.crtox.2026.100315","url":null,"abstract":"<div><div>Silicosis is an occupational disease caused by inhalaling free silicon dioxide (SiO₂). Lipid metabolism plays an important role in silicosis. CD36 is a key factor involved in lipid transport, but its mechanism of action in silicosis remains unclear. This study aims to explore the mechanism by which the CD36 inhibitor sulfo-n-succinimide oleate (SSO) targets CD36 to regulate lipid metabolism disorders in silicosis and improve fibrosis. The results showed that SiO₂ stimulation led to an increase in CD36 expression, a decrease in LXR and ABCA1 expression, and an increase in lipid dropper formation in rat alveolar macrophages NR8383. The SSO intervention can reverse these changes, resulting in the decrease in CD36 expression, the increase in LXR and ABCA1 expression, the reduction in IL-1β, IL-6 levels and TGF-β1 secretion. Subsequently, after stimulating primary fibroblasts with the supernatants of macrophages in each group, it was found that SSO stimulation reduced the increase of α-SMA and collagen-I induced by SiO₂ and improved the level of fibrosis. In addition, in vivo animal experiments have found that SSO intervention alleviated the levels of inflammation, lipid metabolism and fibrosis induced by SiO₂ in silicosis mice, and improved the lung function of silicosis mice. These results indicate that SSO regulates SiO₂-induced lipid metabolism disorders by targeting CD36, thereby improving SiO₂-induced fibrosis. Therefore, SSO targeting CD36 may be a new strategy for treating silica-induced silicosis injury.</div></div>","PeriodicalId":11236,"journal":{"name":"Current Research in Toxicology","volume":"11 ","pages":"Article 100315"},"PeriodicalIF":4.7,"publicationDate":"2026-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148642216","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":"Direct exposure to vinclozolin induces sex-dependent mitochondrial dysfunction in mouse liver","authors":"Hwayeon Lim ,&nbsp;Jisun Choi ,&nbsp;Joo Young Huh ,&nbsp;Hoonsung Cho ,&nbsp;Sooim Shin","doi":"10.1016/j.crtox.2026.100302","DOIUrl":"10.1016/j.crtox.2026.100302","url":null,"abstract":"<div><div>Vinclozolin is a dicarboximide anti-androgenic fungicide that has endocrine-disrupting impact on mammals. Endocrine disruptors are reported to impair mitochondrial function and reduce adenosine triphosphate (ATP) production. Moreover, increasing evidence has linked exposure to endocrine disruptors with metabolic diseases. However, the toxicity of direct exposure to vinclozolin on mitochondrial function remains insufficiently explored. In this study, mitochondria were isolated from mouse liver—one of the primary organs involved in the uptake and processing of toxicants—and directly exposed to vinclozolin. Several markers, including citrate synthase, mitochondrial complex IV (CIV) activity, ATP production, reactive oxygen species/reactive nitrogen species (ROS/RNS) levels, cytochrome <em>c</em> release, glutathione (GSH) levels, and superoxide dismutase (SOD) activity were measured. The results indicated that vinclozolin decreased citrate synthase activity in both sexes and significantly reduced CIV activity only in males. ATP levels showed a decreasing tendency, while ROS/RNS levels showed an increasing tendency particularly in males, without statistical significance. Notably, SOD activity exhibited a sex-dependent increase specifically in females, whereas vinclozolin exposure did not significantly alter GSH levels in either sex. Despite this, basal GSH levels remained significantly higher in females than in males. In both sexes, an increase in cytochrome <em>c</em> release was observed. Collectively, direct mitochondrial exposure to vinclozolin induced dysfunction by impairing energy production, a process mediated by sex-specific antioxidant responses.</div></div>","PeriodicalId":11236,"journal":{"name":"Current Research in Toxicology","volume":"10 ","pages":"Article 100302"},"PeriodicalIF":2.9,"publicationDate":"2026-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148167723","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"CC16 alleviates PM2.5-induced airway inflammation in asthmatic mice by targeting the E-cadherin-mediated ferroptosis regulatory axis","authors":"Aili Wang,&nbsp;Shuo Yang,&nbsp;Fang Xu,&nbsp;Jianling Liu,&nbsp;Jinle Lin,&nbsp;Jian Wu","doi":"10.1016/j.crtox.2026.100310","DOIUrl":"10.1016/j.crtox.2026.100310","url":null,"abstract":"<div><div>Airway epithelial ferroptosis is critically involved in PM2.5-driven asthmatic airway damage, and our previous studies have demonstrated the protective role of club cell protein 16 (CC16) against fine particulate matter (PM2.5)-induced airway inflammation by inhibiting airway epithelial ferroptosis using C57BL/6 J mouse and TC-1 cell model. Nevertheless, it remains unclarified whether CC16 exerts its anti-ferroptotic effects through interacting with E-cadherin, which represents a core research gap absent in our previous studies. Herein, we established PM2.5-intervened asthmatic mice and TC-1 cell models to explore the undiscovered molecular mechanism. Quantitative proteomics combined with bioinformatics screening identified E-cadherin as a pivotal downstream target of CC16. PM2.5 exposure markedly inhibited E-cadherin expression and aggravated epithelial ferroptosis, while CC16 intervention efficiently restored E-cadherin levels, elevated NRF2/GPX4/SLC7A11 expression, suppressed ACSL4, and reduced lipid peroxidation. This study first verified the direct binding interaction between CC16 and E-cadherin via molecular docking, Co-IP and pull-down assays. Furthermore, CDH1 knockdown completely abolished CC16-mediated inhibition of ferroptosis and epithelial injury. Collectively, this work establishes a novel CC16/E-cadherin/ferroptosis signaling axis, demonstrating that E-cadherin is an indispensable mediator for CC16 to relieve PM2.5-triggered airway damage. These findings substantially complement and advance the mechanistic system of CC16-related airway protection, providing novel targets for environmental asthma therapy.</div></div>","PeriodicalId":11236,"journal":{"name":"Current Research in Toxicology","volume":"11 ","pages":"Article 100310"},"PeriodicalIF":4.7,"publicationDate":"2026-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13320470/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148367506","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":"Zearalenone exposure may increase the risk of non-alcoholic fatty liver disease by activating CYP1B1-SCD1","authors":"Haonan Ruan ,&nbsp;Jing Zhang ,&nbsp;Yunyun Wang ,&nbsp;Dan Zhang ,&nbsp;Jiaoyang Luo ,&nbsp;Meihua Yang","doi":"10.1016/j.crtox.2025.100277","DOIUrl":"10.1016/j.crtox.2025.100277","url":null,"abstract":"<div><div>Zearalenone (ZEN) is an oestrogen-like mycotoxin that widely contaminates food and feed worldwide. Current research suggests that ZEN causes liver injury by disrupting hepatic lipid metabolism. Furthermore, prolonged disturbances in hepatic lipid metabolism are believed to play a role in the progression of non-alcoholic fatty liver disease (NAFLD). However, the exact association between ZEN exposure and the development of NAFLD is unclear. In this study, we established a rat model of ZEN-induced hepatic lipid accumulation (2.5, 5, 10 mg/kg/d b.w.,14 d, i.g.) to investigate the key targets of ZEN-induced hepatic lipid accumulation and to explore the potential link between ZEN exposure and NAFLD. Histological staining of rat liver showed that ZEN caused significant pathological changes and lipid accumulation; biochemical analysis showed that ZEN significantly and dose-dependently increased serum levels of aspartate aminotransferase (AST) and alanine aminotransferase (ALT) and disrupted the serum lipid profile in rats; proteomic analysis showed that ZEN significantly altered protein expression levels in rat liver, especially SOAT1, SOAT2, CYP1B1 and SCD1 (p &lt; 0.05). Through bioinformatics analyses, we combined ZEN exposure with a database of NAFLD clinical samples to reveal that ZEN exposure may increase the risk of NAFLD through activation of the CYP1B1-SCD1 pathway, and further animal experiments confirmed this. This study identifies the key target of ZEN-induced lipid accumulation and provides a basis for further research on the intrinsic link between ZEN exposure and NAFLD.</div></div>","PeriodicalId":11236,"journal":{"name":"Current Research in Toxicology","volume":"10 ","pages":"Article 100277"},"PeriodicalIF":2.9,"publicationDate":"2026-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145788188","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}