Journal of Biochemical and Molecular Toxicology最新文献

{"title":"Correction to [A tsRNA Suppresses Lung Adenocarcinoma Progression Through Targeting Glucose-6-Phosphate Dehydrogenase]","authors":"","doi":"10.1002/jbt.71122","DOIUrl":"10.1002/jbt.71122","url":null,"abstract":"<p>2. Department of Hematology and Oncology, Hai'an People's Hospital of Jiangsu Province, Hai'an, Nantong, Jiangsu Province, China.</p>","PeriodicalId":15151,"journal":{"name":"Journal of Biochemical and Molecular Toxicology","volume":"40 10","pages":""},"PeriodicalIF":3.6,"publicationDate":"2026-10-09","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1002/jbt.71122","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149136880","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":"Edaravone Mitigates Di(2-ethylhexyl) Phthalate-Induced Nephrotoxicity Through Attenuation of Oxidative Stress and Endoplasmic Reticulum Stress","authors":"Mohammed Nazish Quasmi,&nbsp;Jiten Singh,&nbsp;Rachna Yadav,&nbsp;Dinesh Kumar,&nbsp;Talat Azam,&nbsp;Mary K. Ekka,&nbsp;Dinesh Dhingra,&nbsp;Ashok Jangra","doi":"10.1002/jbt.71125","DOIUrl":"10.1002/jbt.71125","url":null,"abstract":"<p>Di(2-ethylhexyl) phthalate (DEHP) is a plasticizer used in various plastic items and is hazardous for the environment with significant nephrotoxic potential. Edaravone is a potent anti-oxidant that strongly scavenges the free radicals and protects the cells against oxidative stress. The objective of the present study was to examine the ameliorative potential of edaravone against DEHP-induced nephrotoxicity via targeting oxidative stress and ER stress-related proteins. Twenty-four male albino Wistar rats were randomly divided into four groups. The control group received corn oil orally for 28 days. The DEHP group received DEHP (500 mg/kg, p.o.) for 28 days. Additionally, two treatment groups received 500 mg/kg DEHP for 28 days and edaravone (5 and 10 mg/kg) for the last 14 days (Days 15 to 28). On the 29th day, animals were euthanized, and blood and kidney samples were collected. The renal function test, oxido-nitrosative stress parameters, and histopathology analysis were performed along with the western blotting test. Findings revealed that DEHP significantly increased levels of BUN, creatinine, and urea along with a substantial reduction in GSH levels and an increase in MDA and nitrite levels. The DEHP group also showed upregulated protein levels of GRP78, CHOP, and caspase-12. These alterations were accompanied by histological damage. Edaravone treatment alleviated DEHP-induced renal injury by modulation of oxidative stress and ER stress-related markers. These findings give us a mechanistic insight on how edaravone can regulate ER stress-related proteins in DEHP-induced nephrotoxicity and provide its ameliorative effect.</p>","PeriodicalId":15151,"journal":{"name":"Journal of Biochemical and Molecular Toxicology","volume":"40 10","pages":""},"PeriodicalIF":3.6,"publicationDate":"2026-10-09","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1002/jbt.71125","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149136860","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":"Renal Tubular Epithelial Cells Senescence Induced by 1-Aminopyrene Activates Fibroblast via BRD4 Driven Senescence-Associated Secretory Phenotype Signaling","authors":"Atul Katarkar,&nbsp;Ankita Bagde,&nbsp;Diwakar Maurya,&nbsp;Bhavana Chahare,&nbsp;Namita Mane,&nbsp;Saravanadevi Sivanesan,&nbsp;K. Krishnamurthi","doi":"10.1002/jbt.71124","DOIUrl":"10.1002/jbt.71124","url":null,"abstract":"<p>Epidemiological evidence links environmental pollution to chronic kidney disease (CKD). However, the molecular mechanisms by which diesel-derived pollutants trigger and sustain renal fibrosis are still unclear. In this study, we show that 1-aminopyrene (1-AP), a metabolite of diesel exhaust, leads to genomic instability and renal tubular epithelial cell (RTEC) senescence. Exposure of RTECs to sub-cytotoxic concentrations of 1-AP caused persistent DNA damage, as shown by comet assay and γ-H2AX foci. Sustained DNA damage activated the p21-mediated cellular senescence, followed by induction of SASP factors (IL-6, IL-1β, CXCL1, MCP-1, and TGF-β1). Conditioned media from senescent RTECs promoted activation and extracellular matrix gene expression in renal fibroblasts, establishing epithelial–mesenchymal crosstalk as a key driver of fibrogenic signaling. Although 1-AP activated aryl hydrocarbon receptor (AhR) but AhR inhibition failed to suppress SASP expression and fibroblast activation. On epigenetic level, 1-AP exposure on RTECs causes chromatin remodeling characterized by increased H3K9 acetylation and loss of H3K9me3 and H3K27me3, facilitating recruitment of the epigenetic reader BRD4 to SASP gene loci. Pharmacological inhibition of BRD4 suppressed SASP transcription, blocked paracrine activation of fibroblast and promotes apoptosis of RTECs. Hence, BRD4 may be a potential therapeutic target for treating pollution-related CKD.</p>","PeriodicalId":15151,"journal":{"name":"Journal of Biochemical and Molecular Toxicology","volume":"40 10","pages":""},"PeriodicalIF":3.6,"publicationDate":"2026-10-07","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13644541/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149127614","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":"Blood Lead and Cumulative Lead Burden: Matching Exposure Biomarkers to the Time Scale of Chronic Toxicity","authors":"Prasenjit Mitra","doi":"10.1002/jbt.71132","DOIUrl":"10.1002/jbt.71132","url":null,"abstract":"","PeriodicalId":15151,"journal":{"name":"Journal of Biochemical and Molecular Toxicology","volume":"40 10","pages":""},"PeriodicalIF":3.6,"publicationDate":"2026-10-06","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149110146","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":"Quercetin in Myocardial Ischemia–Reperfusion Injury: Mechanistic Evidence, Cardioprotective Effects, and Translational Challenges","authors":"Rony Abdi Syahputra,&nbsp;Princella Halim,&nbsp;Sasniwiati Sari Hasibuan,&nbsp;Adhayani Lubis","doi":"10.1002/jbt.71130","DOIUrl":"10.1002/jbt.71130","url":null,"abstract":"<p>Myocardial ischemia–reperfusion (I/R) injury remains a major limitation in cardiovascular therapy, where restoration of blood flow paradoxically initiates oxidative stress, inflammation, mitochondrial dysfunction, and cardiomyocyte death. Although multiple pharmacological strategies have been investigated, clinical translation remains limited by inconsistent efficacy and incomplete pathway coverage. Quercetin, a naturally occurring flavonoid with pleiotropic biological activity, has attracted increasing interest as a potential modulator of I/R-associated injury. This systematic review evaluated current evidence regarding the cardioprotective effects and mechanistic actions of quercetin in myocardial I/R injury. A structured literature search identified 25 eligible studies comprising predominantly preclinical in vivo animal investigations, together with limited ex vivo, in vitro, and clinical evidence. Across studies, quercetin consistently reduced infarct size, attenuated myocardial injury biomarkers, and improved cardiac functional parameters. Mechanistically, these effects were associated with suppression of oxidative stress and inflammatory signaling, particularly through modulation of ROS generation, NF-κB activation, PI3K/Akt signaling, mitochondrial dysfunction, and apoptosis-related pathways. Several studies also demonstrated preservation of endogenous antioxidant systems and mitochondrial integrity. However, substantial heterogeneity in experimental design, limited mitochondrial-specific analyses, and the scarcity of comparative clinical studies remain major barriers to translation. Collectively, current evidence supports quercetin as a multi-pathway cardioprotective candidate in myocardial I/R injury, although further standardized and clinically oriented investigations are required to clarify its therapeutic relevance.</p>","PeriodicalId":15151,"journal":{"name":"Journal of Biochemical and Molecular Toxicology","volume":"40 10","pages":""},"PeriodicalIF":3.6,"publicationDate":"2026-10-06","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13641088/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149110159","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":"Quercetin Attenuates Cisplatin-Induced Nephrotoxicity While Enhancing Antitumor Efficacy in Gastric Cancer via Cell Type-Specific Modulation of the ERK1/2 Pathway","authors":"Gen Xia,&nbsp;Shuning Gu,&nbsp;Xiaojie Li,&nbsp;Kun Li,&nbsp;Shizheng Li","doi":"10.1002/jbt.71121","DOIUrl":"10.1002/jbt.71121","url":null,"abstract":"<p>Cisplatin (DDP) is a cornerstone chemotherapeutic agent for gastric cancer, yet its clinical application is often limited by severe adverse effects, particularly dose-dependent nephrotoxicity. Quercetin (Que) is a dietary flavonoid widely present in everyday foods such as onions, apples, tea, and broccoli. It has been reported to possess both renoprotective and antitumor properties. This study evaluated the therapeutic potential of combining DDP with Que in gastric cancer treatment. In vitro, CCK-8 assays, flow cytometry, and scratch wound tests were employed to assess the impact of Que on DDP-induced nephrotoxicity and chemosensitivity, while potential mechanisms were investigated through western blot analysis. In vivo, the combined regimen was tested in tumor-bearing nude mice by monitoring tumor growth and renal function. Our results showed that Que alleviated DDP-induced suppression of proliferation and apoptosis in HK-2 cells, indicating protection against nephrotoxicity. In comparison, in AGS gastric cancer cells, Que potentiated DDP-induced inhibition of proliferation and migration, and improved apoptosis. Mechanistically, Que inhibited ERK1/2 activation in both cell types. In HK-2 cells, ERK1/2 inhibition increased c-Myc expression and decreased cleaved caspase-3 levels, whereas in AGS cells, ERK1/2 inhibition reduced c-Myc and MMP-2 levels while elevating cleaved caspase-3 expression. These effects were reversed upon TBHQ treatment. In vivo, Que enhanced the antitumor efficacy of DDP while attenuating its nephrotoxicity. Collectively, these results indicate that Que achieves the abovementioned dual effect via cell type-specific modulation of the ERK1/2 pathway, supporting its potential as an adjuvant for gastric cancer chemotherapy.</p>","PeriodicalId":15151,"journal":{"name":"Journal of Biochemical and Molecular Toxicology","volume":"40 10","pages":""},"PeriodicalIF":3.6,"publicationDate":"2026-10-05","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13637060/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149110117","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":"Luteolin Alleviates Axitinib-Induced Cardiomyocyte Apoptosis in Mice","authors":"Si-Wen Ji,&nbsp;Xu Li,&nbsp;Dong Tang,&nbsp;Lin Bai,&nbsp;Chun-Lei Yu,&nbsp;Na Niu","doi":"10.1002/jbt.71120","DOIUrl":"10.1002/jbt.71120","url":null,"abstract":"<div>\u0000 \u0000 \u0000 <section>\u0000 <p>Axitinib, a tyrosine kinase inhibitor (TKI), is associated with a risk of cardiotoxicity in clinical practice. However, its underlying toxicological mechanisms remain unclear, and effective cardioprotective strategies are lacking. This study aims to investigate the mechanisms of axitinib-induced cardiac injury and evaluate the protective effects of luteolin. In this study, C57BL/6 mice were randomly divided into four groups: Control, Axitinib, Axitinib + Luteolin, and Luteolin alone. Ventricular systolic function (EF/FS/LVEDD/LVESD) was evaluated by echocardiography. Serum cardiac troponin T (cTnT) levels were measured to assess cardiotoxicity. Histopathological changes were observed via HE and Masson's trichrome staining. Myocardial apoptosis was quantified using TUNEL staining, and apoptosis-related proteins (Bax/Bcl2) were analyzed by Western blot. Reactive oxygen species (ROS) accumulation was evaluated using DHE staining. The results showed that compared with the control group, axitinib did not significantly alter echocardiographic parameters but significantly elevated serum cTnT levels, indicating subclinical cardiotoxicity. Furthermore, axitinib induced notable histopathological changes, promoted aberrant ROS accumulation, upregulated the Bax/Bcl2 ratio, and triggered cardiomyocyte apoptosis. Co-administration of luteolin significantly reduced ROS levels, restored the Bax/Bcl2 balance, and effectively alleviated axitinib-induced cardiotoxicity and apoptosis. In conclusion, axitinib induces subclinical cardiac injury by promoting ROS generation and disrupting the Bax/Bcl2 balance, thereby activating cardiomyocyte apoptosis. Luteolin exerts significant cardioprotective effects by suppressing ROS accumulation and rectifying apoptotic pathway dysregulation, providing a promising novel strategy for the prevention and treatment of targeted therapy-induced cardiotoxicity.</p>\u0000 </section>\u0000 </div>","PeriodicalId":15151,"journal":{"name":"Journal of Biochemical and Molecular Toxicology","volume":"40 10","pages":""},"PeriodicalIF":3.6,"publicationDate":"2026-10-05","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13635869/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149110153","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":"Mechanism of ORC1 Regulating Cancer Stemness and Cisplatin Resistance in Non-Small Cell Lung Cancer","authors":"Jianhui Sheng,&nbsp;Yingjian Song","doi":"10.1002/jbt.71078","DOIUrl":"10.1002/jbt.71078","url":null,"abstract":"<p>This study aimed to investigate the role and molecular mechanisms of origin recognition complex 1 (ORC1) in Cisplatin resistance and tumor stemness in non-small cell lung cancer (NSCLC), and to evaluate its potential as a target for reversing chemotherapy resistance. ORC1 expression and its clinical significance in NSCLC were analyzed using TCGA and GTEx databases. ORC1-knockdown NSCLC cell lines and Cisplatin-resistant A549 DDP cells were established. Colony formation, Transwell, tumor sphere formation, and flow cytometry assays were performed to assess proliferation, invasion, stemness, and drug resistance phenotypes. A subcutaneous xenograft model in nude mice was used to evaluate the in vivo antitumor efficacy of lentivirus-mediated ORC1 knockdown combined with Cisplatin. Protein expression levels of stemness markers (LGR5, NANOG, CD44), the resistance-associated protein P-gp, and EMT-related proteins were detected by Western blotting. ORC1 was significantly overexpressed in NSCLC tissues and resistant cells, and its expression positively correlated with poor prognosis and tumor stemness markers. ORC1 knockdown markedly inhibited proliferation, invasion, EMT, and sphere-forming capacity, and downregulated stemness-associated proteins. In A549 DDP cells, ORC1 knockdown reduced the Cisplatin IC₅₀, restored chemosensitivity, downregulated MDR1/P-gp, and enhanced Cisplatin-induced apoptosis. In vivo, ORC1 knockdown combined with Cisplatin significantly suppressed resistant tumor growth, reduced the proportion of CD133⁺CD44⁺ cancer stem cells, and promoted apoptosis. ORC1 mediated Cisplatin resistance in NSCLC by regulating tumor stemness and EMT. Targeted silencing of ORC1 effectively reversed resistance both in vitro and in vivo, representing a potential molecular target for overcoming Cisplatin resistance in NSCLC.</p>","PeriodicalId":15151,"journal":{"name":"Journal of Biochemical and Molecular Toxicology","volume":"40 10","pages":""},"PeriodicalIF":3.6,"publicationDate":"2026-09-25","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1002/jbt.71078","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149038684","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":"E3 Ubiquitin Ligase NEDD4-Mediated CTSB Ubiquitination Prevents Microglial Ferroptosis After Subarachnoid Hemorrhage","authors":"Xiuyou Yan,&nbsp;Lu Feng,&nbsp;Xuanhao Zhu,&nbsp;Panxing Wu,&nbsp;Wei Chen,&nbsp;Hao Yan,&nbsp;Chao Ding","doi":"10.1002/jbt.71084","DOIUrl":"10.1002/jbt.71084","url":null,"abstract":"<div>\u0000 \u0000 \u0000 <section>\u0000 <p>To investigate the role of cathepsin B (CTSB) in microglial ferroptosis after subarachnoid hemorrhage (SAH) and its upstream regulatory mechanisms. A SAH mouse model was established, and BV2 microglial cell line was utilized. Gene expression was detected by qRT-PCR and western blot. Co-immunoprecipitation was performed to verify the interaction between NEDD4 and CTSB. CCK-8 and PI staining were used to evaluate cell viability and death. Immunofluorescence was employed to observe protein localization and oxidative stress marker levels. TUNEL staining was conducted to detect neuronal apoptosis. CTSB was specifically upregulated in microglia after SAH. CTSB knockdown significantly enhanced cell viability, reduced cell death, and reversed the abnormal changes in ferroptosis-related proteins and oxidative stress markers induced by hemin/RSL3. Mechanistically, NEDD4 was identified as an E3 ubiquitin ligase for CTSB, capable of directly binding and ubiquitinating CTSB protein for degradation. NEDD4 overexpression effectively reduced CTSB protein levels in SAH mouse brains while simultaneously alleviating brain edema, neuronal apoptosis, and neurological deficits, significantly inhibiting ferroptosis after SAH. NEDD4 attenuates secondary brain injury after SAH by ubiquitinating and degrading CTSB, thereby inhibiting microglial ferroptosis.</p>\u0000 </section>\u0000 </div>","PeriodicalId":15151,"journal":{"name":"Journal of Biochemical and Molecular Toxicology","volume":"40 10","pages":""},"PeriodicalIF":3.6,"publicationDate":"2026-09-24","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1002/jbt.71084","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149038742","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":"Microplastics as Emerging Neurotoxins: Brain Accumulation, Neuroinflammation, and Neurodegeneration Risk","authors":"Alfi Sophian,&nbsp; Asmariani,&nbsp;Erika Ismayani","doi":"10.1002/jbt.71070","DOIUrl":"10.1002/jbt.71070","url":null,"abstract":"<p>Microplastics (MPs) and nanoplastics (NPs) have emerged as ubiquitous environmental contaminants with profound implications for human neurological health. Recent landmark findings confirm the bioaccumulation of MPs/NPs in human brain tissue—with concentrations reaching 4917 μg/g in 2024 autopsy samples and up to 10-fold higher levels in individuals with dementia—underscoring the urgent need for mechanistic understanding. This review synthesizes current evidence on the routes by which MPs/NPs traverse the blood-brain barrier (BBB) and the olfactory pathway, their cellular effects within the central nervous system (CNS), and the molecular cascades that link plastic particle exposure to neuroinflammation and neurodegeneration. Key mechanisms include: disruption of tight junction proteins and BBB integrity; activation of microglia and the NLRP3 inflammasome; induction of oxidative stress via reactive oxygen species (ROS); mitochondrial dysfunction through impairment of the electron transport chain; synaptic toxicity and neurotransmitter dysregulation; and direct promotion of pathological protein aggregation—including amyloid-beta (Aβ), tau hyperphosphorylation, and α-synuclein fibrillation—implicated in Alzheimer's disease (AD) and Parkinson's disease (PD). Indirect neurotoxicity via the gut-brain axis is also addressed. Finally, critical research gaps and future directions are proposed, including standardized exposure models, longitudinal human cohort studies, and evaluation of therapeutic targets. This review positions MPs/NPs as a novel environmental risk factor for neurodegenerative diseases warranting priority attention in neuroscience and public health research.</p>","PeriodicalId":15151,"journal":{"name":"Journal of Biochemical and Molecular Toxicology","volume":"40 10","pages":""},"PeriodicalIF":3.6,"publicationDate":"2026-09-24","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1002/jbt.71070","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149038690","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}