Journal of Biochemical and Molecular Toxicology最新文献

{"title":"Studying the Toxicity of Trolox on Hepatocytes and Drug-Induced Liver Injury","authors":"Nidal A. Qinna,&nbsp;Ola N. Estatieh,&nbsp;Bayan Y. Ghanem,&nbsp;Eyad M. Mallah,&nbsp;Qasem Abdallah,&nbsp;Mohammad Ahmad","doi":"10.1002/jbt.70359","DOIUrl":"https://doi.org/10.1002/jbt.70359","url":null,"abstract":"<div>\u0000 \u0000 <p>The Vitamin E analogue Trolox (Tx) is a well-known reference compound utilized in various In Vitro antioxidant assays. In Vivo experimentation of the scavenging and protective potential of Tx is increasing, however, its impact on healthy and stressed models has not been thoroughly examined. The current study evaluates Tx under both In Vitro and In Vivo settings, employing the classical acetaminophen (APAP)-induced hepatotoxicity model to assess its ability to manage and prevent liver injury. Primary mouse hepatocytes and C57/B6 mice were treated with Tx either alone or before exposure to APAP. Cell modality and viability were evaluated In Vitro, along with In Vivo hepatic functions and histological changes. The mRNA levels of stress response and cell-death associated genes were analyzed in liver homogenates, along with the levels of NRF2 proteins, a crucial intracellular antioxidant regulator. The conducted experiments revealed that Tx (1 mM) reduced cell viability, triggered apoptosis, and led to DNA leakage in cells, while exacerbating injury when administered as a pretreatment before APAP exposure in mice. This damage was correlated with dose-dependent hemorrhagic necrosis observed in liver tissue sections and a dose-dependent increase in serum LDH. Tx affected the mRNA expression of CYP metabolism enzymes, as well as <i>Sult1a1</i> expression and genes related to NRF2/ARE pathway. Furthermore, NRF2 activity was diminished following pretreatment with Tx doses. Despite its recognized antioxidant properties, Tx induced liver injury in a concentration-dependent manner in both normal and stressed liver models. Consequently, the use of Tx may pose injury that is evident and requires further investigation across various pathological models.</p></div>","PeriodicalId":15151,"journal":{"name":"Journal of Biochemical and Molecular Toxicology","volume":"39 6","pages":""},"PeriodicalIF":3.2,"publicationDate":"2025-06-16","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144292485","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":"Cancer-Associated Fibroblast-Derived RIPK4 Confers Cisplatin Resistance in Gastric Cancer by Activating the PI3K/AKT Pathway","authors":"Rui Chen,&nbsp;Junfang Dai,&nbsp;Bo Wang,&nbsp;Guofei Peng,&nbsp;Yao Xun,&nbsp;Yan Li","doi":"10.1002/jbt.70320","DOIUrl":"https://doi.org/10.1002/jbt.70320","url":null,"abstract":"<div>\u0000 \u0000 \u0000 <section>\u0000 <p>Cancer-associated fibroblasts (CAFs) play a central role in cancer progression and are involved in modulating cancer cell proliferation, invasion, metastasis, drug resistance and so on. Receptor Interacting Serine/Threonine Kinase 4 (RIPK4) was demonstrated to promote gastric cancer (GC) metastasis and tumorigenesis. Here, this study aimed to explore whether GC-derived CAFs affected cisplatin (DDP) resistance in GC cells via RIPK4. DDP-resistant GC cells were first established. Levels of RIPK4 mRNA and proteins were detected using qRT-PCR and western blotting. The IC50 values of DDP, cell proliferation, invasion, and migration were analyzed using MTT, 5-ethynyl-2′-deoxyuridine, transwell, and wound healing assays, respectively. PI3K/AKT pathway-related proteins were measured by western blotting. Animal experiments were performed for in vivo analysis. Here, we found that CAFs enhanced DDP resistance in DDP-resistant cells by promoting cell proliferation, invasion and migration. CAFs led to an increased RIPK4 expression in DDP-resistant cells. The silencing of RIPK4 suppressed DDP resistance in DDP-resistant cells. Moreover, RIPK4 silencing in CAFs could also reduce DDP resistance in GC. Mechanistically, CAFs could activate the PI3K/AKT pathway by RIPK4. In vivo assay also showed that RIPK4 silencing in CAFs attenuated CAF-induced DDP resistance. In conclusion, RIPK4-decreased CAFs suppressed DDP resistance in GC by blocking the activation of the PI3K/AKT pathway, recommending a novel method for overcoming DDP resistance in gastric cancer.</p>\u0000 </section>\u0000 </div>","PeriodicalId":15151,"journal":{"name":"Journal of Biochemical and Molecular Toxicology","volume":"39 6","pages":""},"PeriodicalIF":3.2,"publicationDate":"2025-06-16","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144292487","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":"EIF3B Promotes KRAS Gene Mutation-Driven Colon Adenocarcinoma Progression Through the TBK1 and PI3K/AKT Signaling Pathways","authors":"Chongren Ren,&nbsp;Yaxin Qin,&nbsp;Dujuan Cao,&nbsp;Xiaojing Ren,&nbsp;Haoliang Zhao,&nbsp;Jianli Han,&nbsp;Gang Du","doi":"10.1002/jbt.70353","DOIUrl":"https://doi.org/10.1002/jbt.70353","url":null,"abstract":"<div>\u0000 \u0000 <p>Therapeutic targets involved in multiple signaling pathways offer promising treatment options for cancers driven by KRAS gene mutations (KRAS^mut). EIF3B has emerged as a potential therapeutic target for colorectal cancer (CRC). To elucidate the role of EIF3B and its interactions with potential targets in CRC, we utilized bioinformatics techniques alongside clinicopathological analyses. RNA sequencing identified signaling pathways associated with EIF3B. The expression levels of relevant genes and their associated pathways were measured using RT-qPCR and western blot analyses. RNA immunoprecipitation (RIP) confirmed the interactions between EIF3B and these specific genes. Analysis of data from The Cancer Genome Atlas (TCGA), combined with clinicopathological studies, revealed significantly elevated levels of EIF3B and TBK1 mRNA and proteins in KRAS^mut colorectal adenocarcinoma (COAD) compared to normal tissues. Silencing EIF3B inhibited the proliferation and progression of KRAS^mut COAD and disrupted the TBK1, PI3K/AKT, and JAK2/STAT3 pathways. EIF3B also regulated the translation of TBK1 and PIK3CA. Targeting EIF3B presents a novel approach to modulating various cellular signaling pathways, offering a promising therapeutic strategy for patients with KRAS^mut COAD.</p></div>","PeriodicalId":15151,"journal":{"name":"Journal of Biochemical and Molecular Toxicology","volume":"39 6","pages":""},"PeriodicalIF":3.2,"publicationDate":"2025-06-12","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144264622","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":"Hsa_circ_0049271 Facilitates Esophageal Squamous Cell Carcinoma Progression and Cisplatin Resistance by Enhancing Cellular Senescence via miR-455-5p/ETS1","authors":"Erwen Bao,&nbsp;Shuai Li,&nbsp;Peipei Shen,&nbsp;Danqi Qian,&nbsp;Yu Xu,&nbsp;Jialiang Zhou","doi":"10.1002/jbt.70328","DOIUrl":"https://doi.org/10.1002/jbt.70328","url":null,"abstract":"<div>\u0000 \u0000 <p>Cisplatin resistance is a major therapeutic challenge in esophageal squamous cell carcinoma (ESCC). circRNAs play an important role in cisplatin resistance. The aim of this paper was to investigate the role and mechanism of hsa_circ_0049271 in ESCC progression and drug resistance. GEO database was retrieved to collect circRNAs, miRNAs, and mRNAs associated with cisplatin resistance in ESCC. Reverse transcription-quantitative PCR (RT-qPCR) was used to detect hsa_circ_0049271 expression levels in ESCC cell lines. CCK-8 assay, flow cytometric assay, and cell migration/invasion assays were used to examine the function of hsa_circ_0049271 in ESCC cells. RT-qPCR and coculture assays were used to detect the effect of circRNA_103615 on cellular senescence under cisplatin treatment. Hsa_circ_0049271, miR-455-5p, and <i>ETS1</i> were dysregulated in ESCC tissues. ESCC cell lines had increased levels of hsa_circ_0049271 and <i>ETS1</i> mRNA compared with normal cells and normal tissues, as well as decreased levels of miR-455-5p. Functionally, small interfering RNA silencing of hsa_circ_0049271 by small interfering RNA resulted in suppression of cell growth, migration, and invasion in both non-senescent and senescent cells. MiR-455-5p was significantly increased, but <i>ETS1</i> expression was significantly decreased after hsa_circ_0049271 knockdown. Hsa_circ_0049271 promoted the secretion of senescence-associated secretory phenotypes, including <i>IL1B</i>, <i>IL6</i>, <i>CXCL5</i>, and <i>MMP3</i>. Hsa_circ_0049271 may enhance DDP treatment-induced cellular senescence to promote ESCC progression and chemoresistance through the miR-455-5p/<i>ETS1</i> axis.</p></div>","PeriodicalId":15151,"journal":{"name":"Journal of Biochemical and Molecular Toxicology","volume":"39 6","pages":""},"PeriodicalIF":3.2,"publicationDate":"2025-06-12","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144264664","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":"Cerebral Hemorrhage-Related Inflammatory Response Mediated by NINJ1 and the Protective Effects of Atorvastatin","authors":"Guanghui Yang,&nbsp;Nan Li,&nbsp;Zeming Li,&nbsp;Ruiqi Wang,&nbsp;Kaikai Sun,&nbsp;Pengshuai Zhang,&nbsp;Zhibing Ma,&nbsp;Zhiwen Kang,&nbsp;Yang Wang,&nbsp;Zhenfeng Han,&nbsp;Zhuohui Ning","doi":"10.1002/jbt.70349","DOIUrl":"https://doi.org/10.1002/jbt.70349","url":null,"abstract":"<div>\u0000 \u0000 <p>We investigated the relationship between NINJ1 and the inflammatory response in cerebral hemorrhage, as well as the relationship with the protective effects of atorvastatin. A cerebral hemorrhage model was constructed using injection of Type IV collagenase, and open field tests, Y-maze, and mNSS were used to evaluate the behavioral and neurological functions of mice. Enzyme-linked immunosorbent assays were used to detect the expression of tissue inflammatory factors. H&amp;E and Nissl staining were used to detect tissue pathological changes. Western blotting was used to detect the relative expression levels of proteins. NINJ1 transgenic mice showed a more severe inflammatory response and neurological damage compared to wild-type mice, but intervention with NINJ1 monoclonal antibody Ab and atorvastatin could reduce the activation of NLRP3 mediated by NINJ1, decrease tissue inflammation, and, at the cellular level, atorvastatin could inhibit BV2 inflammation. IP experiment results showed that atorvastatin could interact with NINJ1 and inhibit its mediation of NLRP3 activation. Our research results show that NINJ1 in cerebral hemorrhage can promote the activation of NLRP3, further promoting neuroinflammation. Atorvastatin can interact with NINJ1, inhibiting its mediation of NLRP3 activation. NINJ1 is a new target for the treatment of cerebral hemorrhage, and we have revealed a new pharmacological mechanism and target for atorvastatin.</p></div>","PeriodicalId":15151,"journal":{"name":"Journal of Biochemical and Molecular Toxicology","volume":"39 6","pages":""},"PeriodicalIF":3.2,"publicationDate":"2025-06-12","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144264621","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":"Evaluation of the Efficacy and Safety of DC-CIK Bioimmunotherapy in the Treatment of Advanced Non-Small Cell Lung Cancer","authors":"Qiugan Qi,&nbsp;Na Ji,&nbsp;Hongwei Duan,&nbsp;Gaoyuan Yang,&nbsp;Qiang Shi,&nbsp;Yanchao Qi","doi":"10.1002/jbt.70338","DOIUrl":"https://doi.org/10.1002/jbt.70338","url":null,"abstract":"<div>\u0000 \u0000 <p>Non-small cell lung cancer (NSCLC) is a malignant tumor with a high incidence rate and mortality rate. This study aims to explore the efficacy and safety of dendritic cell cytokine-induced killer cell (DC-CIK) bioimmunotherapy in advanced NSCLC. Sixty-four NSCLC patients treated in our hospital from June 2019 to February 2021 were chosen as the DC-CIK group, all of whom received DC-CIK bioimmunotherapy based on synchronous radiotherapy and chemotherapy. Following the 1:1 matching principle, another 64 NSCLC patients treated with synchronous chemotherapy admitted at the same time were picked as the control group. The clinical efficacy, adverse effects, survival period, the content of immune-related indexes (NK, CD3⁺, CD4⁺, CD4⁺/CD8⁺), and peripheral blood tumor markers [embryonic antigen (CEA), cancer antigen (CA) 125, cytokeratin 19 serum fragment 211 (CYFRA211), squamous cell carcinoma-associated antigen (SCCAg)] were compared before and after treatment. The overall remission rate was 85.94% in the DC-CIK group, which was much higher than 65.63% of the control group after treatment (<i>p</i> &lt; 0.05). The treatment obviously decreased the content of CD3⁺ and CD4⁺ and largely elevated CD4⁺/CD8⁺ in two groups. The DC-CIK group had a significantly elevated level of NK, which was largely decreased in the control group (<i>p</i> &lt; 0.05). The DC-CIK group had a markedly higher content of NK, CD3⁺, CD4⁺, and CD4⁺/CD8⁺ than the control (<i>p</i> &lt; 0.01). After treatment, the content of CEA, CA125, CYFRA211, and SCC-Ag was significantly decreased in two groups than before (<i>p</i> &lt; 0.05), which was lower in the DC-CIK group than the control (<i>p</i> &lt; 0.05). The DC-CIK group had a much lower incidence of fever, granulocytopenia, and gastrointestinal reactions than the control (<i>p</i> &lt; 0.01). The DC-CIK group and the control group had a median survival of 17 months and 13 months respectively. Kaplan-Meier survival curve and log-rank test further proved that DC-CIK bioimmunotherapy prolonged the survival period of patients (<i>p</i> &lt; 0.05). In conclusion, DC-CIK bioimmunotherapy was clinically effective in the treatment of advanced NSCLC, which improved patients' immune function, elevated the survival time of patients within 2 years with a certain degree of safety.</p></div>","PeriodicalId":15151,"journal":{"name":"Journal of Biochemical and Molecular Toxicology","volume":"39 6","pages":""},"PeriodicalIF":3.2,"publicationDate":"2025-06-12","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144264671","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":"S1PR2 Mediates Smooth Muscle Cell Proliferation and Endothelial Cell Permeability via Akt/mTOR and RhoA/ROCK1 in Atherosclerosis","authors":"Jie Ouyang,&nbsp;Haijiao Long,&nbsp;Shuhua Chen,&nbsp;Hong Xiang,&nbsp;Zhihao Shu,&nbsp;Xuewen Wang,&nbsp;Jing Zhang,&nbsp;Huiqin Liu,&nbsp;Baiyi Tang,&nbsp;Jie Xiao,&nbsp;Quanjun Liu,&nbsp;Zishun Zhan,&nbsp;Ruifang Chen,&nbsp;Hongwei Lu","doi":"10.1002/jbt.70351","DOIUrl":"https://doi.org/10.1002/jbt.70351","url":null,"abstract":"<div>\u0000 \u0000 <p>Atherosclerosis is a complex disease involving a series of interrelated events, among which endothelial cell dysfunction and vascular smooth muscle cell proliferation play pivotal roles in the early formation of atherosclerotic plaques. Sphingosine 1-phosphate, a product of sphingomyelin metabolism, serves as a signaling molecule implicated in the pathogenesis of atherosclerosis and other conditions by binding to sphingosine 1-phosphate receptors (S1PRs). However, the precise mechanism by which S1PRs influence atherosclerosis remains incompletely understood. Here, we identified a dual role for S1PR2 in vascular cells treated with oxidized-low-density lipoprotein. In smooth muscle cells, decreased S1PR2 upregulated PCNA expression by activating Akt/mTOR, leading to abnormal cell proliferation. Conversely, in endothelial cells, elevated S1PR2 expression reduced VE-cadherin expression by activating the RhoA/ROCK1 pathway, increasing endothelial permeability. In an apolipoprotein E-deficient mouse model, S1PR2 agonist treatment reduced the abnormal proliferation of aortic smooth muscle cells, while S1PR2 antagonist treatment alleviated barrier function damage in aortic endothelial cells. However, both S1PR2 agonist and antagonist treatments showed limited efficacy on aortic plaques due to their opposing effects on endothelial cells and smooth muscle cells. Thus, therapies targeting specific cell types hold significant promise, and S1PR2 may be a potential target for the prevention and treatment of atherosclerosis.</p></div>","PeriodicalId":15151,"journal":{"name":"Journal of Biochemical and Molecular Toxicology","volume":"39 6","pages":""},"PeriodicalIF":3.2,"publicationDate":"2025-06-11","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144256169","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":"Correction to “Citronellal Alleviates Doxorubicin-Induced Cardiotoxicity by Suppressing Oxidative Stress and Apoptosis via Na + /H+ Exchanger-1 Inhibition”","authors":"","doi":"10.1002/jbt.70337","DOIUrl":"https://doi.org/10.1002/jbt.70337","url":null,"abstract":"<p>X. Liu, Y. Qiu, N. Huang, et al., “Citronellal Alleviates Doxorubicin-Induced Cardiotoxicity by Suppressing Oxidative Stress and Apoptosis via Na + /H+ Exchanger-1 Inhibition,” <i>Journal of Biochemical and Molecular Toxicology</i> 35, no. 2 (2021): e22971.</p><p>In Figure 3A, the panel of Figure 3A(e) is duplicated to the Figure 3A(a) by the Computer operation error.</p><p>Replaced Figure 3.</p><p>We apologize for this error.</p>","PeriodicalId":15151,"journal":{"name":"Journal of Biochemical and Molecular Toxicology","volume":"39 6","pages":""},"PeriodicalIF":3.2,"publicationDate":"2025-06-11","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1002/jbt.70337","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144256170","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Correction to “Tumor-Derived Exosomal circ_0020095 Promotes Colon Cancer Cell Proliferation and Metastasis by Inhibiting M1 Macrophage Polarization”","authors":"","doi":"10.1002/jbt.70325","DOIUrl":"https://doi.org/10.1002/jbt.70325","url":null,"abstract":"<p>1. The correct ethical review committee should be Shandong Provincial Third Hospital, which should be correctly stated before the reference in the article. The statement has been stated here below for your review.</p><p><b>Ethics approval and consent to participate</b></p><p>The present study was approved by the ethical review committee of <b>Shandong Provincial Third Hospital.</b> Written informed consent was obtained from all enrolled patients.</p><p>2. There was a spelling mistake <i>exosomes</i> corrected in Figure 3C. Here is the corrected version below</p><p>We apologize for the errors.</p><p><b>Signature:</b> </p>","PeriodicalId":15151,"journal":{"name":"Journal of Biochemical and Molecular Toxicology","volume":"39 6","pages":""},"PeriodicalIF":3.2,"publicationDate":"2025-06-11","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1002/jbt.70325","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144256171","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Comments on Gui Et Al. (2021) “Rosmarinic Acid Relieves Cisplatin-Induced Ovary Toxicity in Female Mice Via Suppression of Oxidative Stress and Inflammation”","authors":"Mehran Hosseini","doi":"10.1002/jbt.70355","DOIUrl":"https://doi.org/10.1002/jbt.70355","url":null,"abstract":"","PeriodicalId":15151,"journal":{"name":"Journal of Biochemical and Molecular Toxicology","volume":"39 6","pages":""},"PeriodicalIF":3.2,"publicationDate":"2025-06-10","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144244986","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}