International immunopharmacology最新文献

{"title":"Aloperine exerts anti-tumor effect and activates the tumor cell-intrinsic STING pathway in gallbladder cancer","authors":"Yushun Chang ,&nbsp;Jie Lin ,&nbsp;Bo Yang ,&nbsp;Yuxuan Shen ,&nbsp;Weijun Zhao ,&nbsp;Hao Shen ,&nbsp;Quan Yang ,&nbsp;Haowen Lu ,&nbsp;Xiujun Cai ,&nbsp;Yifan Wang ,&nbsp;Wen Hua","doi":"10.1016/j.intimp.2025.115590","DOIUrl":"10.1016/j.intimp.2025.115590","url":null,"abstract":"<div><h3>Background</h3><div>Aloperine (ALO), a quinolizidine-type alkaloid isolated from a natural Chinese herb, exhibits anticancer activity in several malignancies, but its efficacy and mechanisms in gallbladder cancer (GBC) remain undefined.</div></div><div><h3>Methods</h3><div>Human GBC cell lines (GBCs) were treated with ALO and assessed for viability, colony formation, 5-Ethynyl-2′-deoxyuridine (EdU) incorporation and apoptosis. Autophagic flux and related signaling were evaluated by western blotting and immunofluorescence. In vivo antitumor activity was determined in a nude mouse xenograft model.</div></div><div><h3>Results</h3><div>ALO markedly inhibited the proliferation ability of GBCs and disrupted autophagosome–lysosome fusion, leading to reactive oxygen species (ROS) accumulation and apoptosis. Furthermore, ALO induced DNA damage and nuclear release of double-stranded DNA (dsDNA) to cytoplasm, leading to cyclic-GMP-AMP synthase (cGAS)–stimulator of interferon genes (STING)-mediated interferon (IFN) pathway activation and enhancing natural killer cells (NK cells) activation in vitro. In vivo, ALO reduced subcutaneous GBCs xenograft volume and weight and, along with increased cleaved caspase-3 and BAX expression in tumor tissues, confirming tumor cell apoptosis.</div></div><div><h3>Conclusions</h3><div>These findings indicate that ALO may serve as a novel therapeutic candidate for gallbladder cancer by inhibiting autophagic flux to induce ROS-mediated apoptosis while activating the cGAS–STING–IFN pathway to enhance antitumor immunity.</div></div>","PeriodicalId":13859,"journal":{"name":"International immunopharmacology","volume":"166 ","pages":"Article 115590"},"PeriodicalIF":4.7,"publicationDate":"2025-09-23","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145120016","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Six1 promotes alveolar epithelium senescence in pulmonary fibrosis through regulating Tp53","authors":"Yan Fan,&nbsp;Zhen Tian,&nbsp;Hongyan Zheng,&nbsp;Rongman Xu,&nbsp;Boyu Li,&nbsp;Shanshan Wang,&nbsp;Zhenli Huang,&nbsp;Meijia Wang,&nbsp;Dan Ding,&nbsp;Jianping Zhao,&nbsp;Jungang Xie","doi":"10.1016/j.intimp.2025.115554","DOIUrl":"10.1016/j.intimp.2025.115554","url":null,"abstract":"<div><div>Idiopathic pulmonary fibrosis (IPF) is a deadly respiratory condition distinguished by gradual fibrotic restructuring and diminishing pulmonary capacity, with cellular senescence serving as a critical factor in its pathogenesis. This study investigated the function of Sine oculis homeobox homologue 1 (Six1), a transcription factor, in pulmonary fibrosis (PF) and assessed its therapeutic potential as a target. The expression of Six1 was reduced in type II alveolar epithelial cells (AECII) in both patients with IPF and mouse models of PF induced by bleomycin (BLM). Conditional overexpression of Six1 in AECII exacerbated fibrosis severity, as confirmed by histological analysis and impaired lung function. RNA sequencing indicated the involvement of Six1 in pathways related to immune response, inflammation, and cellular senescence. Mechanistic studies revealed that Six1 promotes cellular senescence in AECII by directly upregulating Tp53 transcription, a process mitigated by treatment with PFN-α, a Tp53 inhibitor. Inhibition of Six1 using the specific repressor NCGC00378430 (NCG) attenuated fibrotic changes and improved pulmonary function in both Six1-overexpressing and wild-type mice. These findings suggest that Six1 is a contributor to the progression of IPF by regulating AECII senescence, emphasizing the therapeutic potential of targeting Six1 to alleviate PF. This study underscores the necessity of exploring Six1 inhibitors further as promising candidates for treating IPF.</div></div>","PeriodicalId":13859,"journal":{"name":"International immunopharmacology","volume":"166 ","pages":"Article 115554"},"PeriodicalIF":4.7,"publicationDate":"2025-09-23","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145109758","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Exploring the potential toxic mechanisms of bisphenol F exposure in acute myeloid leukemia: Insights from network toxicology, molecular docking and experimental validation","authors":"Yali Tao ,&nbsp;Biao Ran ,&nbsp;Jinjin Wang ,&nbsp;Qian Hu ,&nbsp;Yi Wen ,&nbsp;Qiang Qiu ,&nbsp;Ting Niu","doi":"10.1016/j.intimp.2025.115579","DOIUrl":"10.1016/j.intimp.2025.115579","url":null,"abstract":"<div><div>Bisphenol F (BPF), a major alternative to bisphenol A (BPA), is now widely used worldwide, posing significant risks to human health and the environment. Acute myeloid leukemia (AML) is a highly aggressive hematologic malignancy with a poor prognosis. This investigation aims to systematically evaluate the potential hematotoxic of BPF in AML through an integrated computational biology approach combining network toxicology, molecular docking simulations and experimental validation. The study is designed to identify critical molecular targets and elucidate the mechanistic basis of BPF-mediated toxicity in AML. Using network toxicology and molecular docking techniques, we identified potential BPF targets through the SwissTargetPrediction, PharmMapper, and SEA databases. A total of 162 targets associated with BPF and AML were identified, with 25 key targets—including EGFR, ALB, BCL2, HSP90AA1, and ESR1—screened using STRING and Cytoscape tools. GO and KEGG enrichment analysis showed that “Pathways in cancer”, “PI3K-Akt signaling pathway”, “reactive oxygen species”, “EGFR tyrosine kinase inhibitor resistance” and “Th17 cell differentiation” were mainly involved in potential toxicity of BPF in AML. Molecular docking with the CB-Dock online tool confirmed the stable interaction between BPF and key targets. Experimental validation supported these predictions: BPF exposure induced proliferation promotion in AML cell lines (HL-60/KG-1/MV4–11), along with rapid activation of EGFR/PI3K/AKT phosphorylation and BCL2 upregulation. In conclusion, this study provides a foundation for understanding the molecular mechanisms of potential toxicity of BPF in AML, provides valuable insights for risk assessment and public health policy, and emphasizes the need for stricter regulation and intervention of BPF exposure.</div></div>","PeriodicalId":13859,"journal":{"name":"International immunopharmacology","volume":"166 ","pages":"Article 115579"},"PeriodicalIF":4.7,"publicationDate":"2025-09-23","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145119928","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Corrigendum to \"Alteration of immunomodulatory properties of locally applied gingival-derived mesenchymal stem cells by the oral inflammatory environment via Caspase-3/8 in periodontitis\" [Int. Immunopharmacol. 161 (2025) 114978].","authors":"Zhong Li, Ze Zhao, Bin Gu, Fei Duan, Qi Chen, Pengli Li, Yanyi Wang, Tong Zhang, Ning Wen","doi":"10.1016/j.intimp.2025.115292","DOIUrl":"10.1016/j.intimp.2025.115292","url":null,"abstract":"","PeriodicalId":13859,"journal":{"name":"International immunopharmacology","volume":" ","pages":"115292"},"PeriodicalIF":4.7,"publicationDate":"2025-09-23","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144794361","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Retraction notice to \"Ameliorative effects of vanillin against pentylenetetrazole-induced epilepsy and associated memory loss in mice: The role of Nrf2/HO-1/NQO1 and HMGB1/RAGE/TLR4/NFκB pathways\" [Int. Immunopharmacol. 129 (2024) 111657].","authors":"Mervt M Almostafa, Maged E Mohamed, Nancy S Younis","doi":"10.1016/j.intimp.2025.115575","DOIUrl":"10.1016/j.intimp.2025.115575","url":null,"abstract":"","PeriodicalId":13859,"journal":{"name":"International immunopharmacology","volume":" ","pages":"115575"},"PeriodicalIF":4.7,"publicationDate":"2025-09-23","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145137460","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Immunomodulatory and neuroprotective effects of miR-146a-enriched MSC-derived extracellular vesicles in experimental autoimmune encephalomyelitis","authors":"Fatemeh Shahryari ,&nbsp;Morteza Jafarinia ,&nbsp;Mojtaba Jafarinia ,&nbsp;Maryam Azimzadeh","doi":"10.1016/j.intimp.2025.115584","DOIUrl":"10.1016/j.intimp.2025.115584","url":null,"abstract":"<div><h3>Background</h3><div>Mesenchymal stem cell-derived extracellular vesicles (MSC-EVs) have emerged as promising cell-free therapeutics due to their immunomodulatory and reparative properties, especially through microRNAs (miRNAs). This study investigates the therapeutic potential of EVs enriched with miR-146a-EVs, a key regulator of inflammatory signaling, in experimental autoimmune encephalomyelitis (EAE), a murine model of MS.</div></div><div><h3>Methods</h3><div>Human adipose-derived MSCs (hADSCs) were transfected with miR-146a mimics or miR-control, and their EVs were isolated. After EAE induction in C57BL/6 mice, they were treated intravenously with miR-146a-enriched EVs, control EVs, or PBS. Clinical scores were monitored for 30 days. Cytokine levels (tumor necrosis factor (TNF)-α, interferon-gamma (IFN-γ), interleukin (IL)-17, IL-4, IL-10, transforming growth factor beta (TGF-β)) were measured in splenocytes and spinal cord tissue using enzyme-linked immunosorbent assay (ELISA) and quantitative polymerase chain reaction (qPCR), respectively. Histopathology (Hematoxylin and Eosin (H&amp;E), Luxol Fast Blue (LFB)) and immunohistochemistry (Myelin Basic Protein (MBP)) assessed inflammation and demyelination.</div></div><div><h3>Results</h3><div>miR-146a-enriched EVs significantly attenuated EAE severity, reducing pro-inflammatory cytokines (TNF-α, IFN-γ, IL-17) and elevating anti-inflammatory cytokines (IL-10, TGF-β) in both splenocyte cultures and spinal cord tissue. The miR-146a-EV-treated group also showed a significant downregulation in Interleukin-1 Receptor-Associated Kinase 1 (IRAK1) and Tumor Necrosis Factor Receptor-Associated Factor 6 (TRAF6) mRNA levels. Histopathological analysis revealed diminished neuroinflammation and demyelination, alongside enhanced myelin preservation in miR-146a-enriched EVs-treated mice.</div></div><div><h3>Conclusion</h3><div>These findings demonstrate that miR-146a-enriched EVs effectively modulate immune responses, suppress neuroinflammation, and promote neuroprotection in EAE, highlighting their potential as a novel therapeutic strategy for MS. By targeting both inflammatory and degenerative pathways, miR-146a-enriched EVs represent a multifaceted approach to address the unmet needs in MS treatment.</div></div>","PeriodicalId":13859,"journal":{"name":"International immunopharmacology","volume":"166 ","pages":"Article 115584"},"PeriodicalIF":4.7,"publicationDate":"2025-09-23","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145119929","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"VDR activation ameliorates intermittent hypoxia-related cognitive impairment by upregulating TREM2 transcription","authors":"Jiahuan Xu ,&nbsp;Hongyu Jin ,&nbsp;Hui Shen ,&nbsp;Hong Huang ,&nbsp;Lujia Zhang ,&nbsp;Yutong Wu ,&nbsp;Ying Zou ,&nbsp;Wei Wang ,&nbsp;Wenyang Li","doi":"10.1016/j.intimp.2025.115543","DOIUrl":"10.1016/j.intimp.2025.115543","url":null,"abstract":"<div><div>Neuroinflammation induced by intermittent hypoxia (IH) plays an essential role in the cognitive impairment associated with obstructive sleep apnea (OSA). It has been reported that the activation of Vitamin D receptor (VDR) can alleviate the neuroinflammation and neuronal injury in some neurodegenerative diseases However, it remains unknown whether VDR can play a similar role in OSA-related cognitive impairment and how it works. This study found that activating VDR by calcitriol enhanced the expression of triggering receptor on myeloid cells 2 (TREM2), promoted microglia M2 polarization, further mitigated neuroinflammation and neuronal damage induced by IH in mice and in BV2 cells. These improvements were attenuated in BV2 cells exposed to IH with calcitriol when TREM2 was knockdown. To determine how VDR regulated the expression of TREM2, potential binding sites between VDR and TREM2 promoter were identified in HEK293T cells. These results indicated that the activation of VDR could ameliorate IH-induced cognitive impairment by binding to TREM2 promoter region and promoting the transcription of TREM2. This study provides a potential therapeutic target for cognitive impairment in patients with OSA.</div></div>","PeriodicalId":13859,"journal":{"name":"International immunopharmacology","volume":"166 ","pages":"Article 115543"},"PeriodicalIF":4.7,"publicationDate":"2025-09-23","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145119925","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Bruceine D promotes TNBC regression by inhibiting M2-like tumor-associated macrophage polarization induced Wnt3a/β-catenin pathway","authors":"Yiwen Ma ,&nbsp;Di Cao ,&nbsp;Xue Han ,&nbsp;Zhiqiang Hu ,&nbsp;Xiaoyun Ding ,&nbsp;Jing Wang","doi":"10.1016/j.intimp.2025.115596","DOIUrl":"10.1016/j.intimp.2025.115596","url":null,"abstract":"<div><div>Triple-negative breast cancer (TNBC) is distinguished by its marked invasiveness and high recurrence rate, making it the subtype of breast cancer with the most dismal prognosis. Effective treatment modalities for TNBC remains elusive. Tumor-associated macrophages (TAMs) are essential stromal components within the tumor microenvironment, significantly contributing to TNBC progression. Herein, we demonstrated that Bruceine D (BD), a natural quassinoid isolated from Chinese herb <em>Brucea javanica</em> (L.) Merr., diminished the secretion of Wnt3a and downregulated the expression of β-catenin, thereby not only inhibiting the polarization of M2-like macrophages and enhancing the ratio of M1/M2 macrophage but also suppressing M2-like macrophage-promoted proliferation and metastasis of tumor cells. Importantly, BD impeded the polarization of infiltrating M2-like TAMs and inhibited the Wnt3a/β-catenin signaling in tumors, consequently suppressing tumor growth and the formation of metastatic lesions in the lungs and livers of TNBC-bearing mice. This study highlights the promising therapeutic potential of BD in remodeling TAMs as a strategy to address TNBC.</div></div>","PeriodicalId":13859,"journal":{"name":"International immunopharmacology","volume":"166 ","pages":"Article 115596"},"PeriodicalIF":4.7,"publicationDate":"2025-09-23","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145119927","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Expression of membrane-bound Interleukin-15 sustains the growth and survival of CAR-NK cells","authors":"Dongdong Feng ,&nbsp;Lu Sun ,&nbsp;Dongxue Hu ,&nbsp;Jiamin Wu ,&nbsp;Fangfang Xu ,&nbsp;Xiangzhu Kong ,&nbsp;Ruikang Yang ,&nbsp;Guangyi Jiang ,&nbsp;Liehao Jiang ,&nbsp;Shu Wang ,&nbsp;Weijia Fang ,&nbsp;Jianqing Zhu ,&nbsp;Zhicheng Du ,&nbsp;Zhuo Tan","doi":"10.1016/j.intimp.2025.115577","DOIUrl":"10.1016/j.intimp.2025.115577","url":null,"abstract":"<div><div>Natural killer (NK) cells display a short lifespan <em>in vivo</em> without cytokine support. In the present study, we investigated whether the expression of a membrane-bound interleukin-15 (IL-15) on chimeric antigen receptor (CAR)-NK cells could help to overcome the hurdle. The CAR-NK cells were generated through electroporation of a <em>piggyBac</em> transposase plasmid and a bicistronic vector containing a 2nd generation natural killer group 2 member D (NKG2D) CAR gene and a cDNA fragment encoding human IL-15 linked to the CD8 hinge and transmembrane domain (membrane-bound interleukin-15, mbIL15), followed by repeated stimulation with K562 artificial antigen-presenting cells. This protocol resulted in a robust expansion of the CAR-NK cells up to 590,000-fold and CAR expression over 90 %. mbIL15 substantially enhanced the <em>in vitro</em> survival of the CAR-NK cells when being cultured without IL-2 support or in the presence of low concentrations of IL-2. Importantly, mbIL15 enhanced the <em>in vivo</em> survival of the CAR-NK cells in normal mice. In mice with tumors, the <em>in vivo</em> expansion of mbIL15/NKG2D CAR-NK cells was observable. These CAR-NK cells were effective in lysing target human cancer cells <em>in vitro</em> and in reducing tumor burden in a mouse xenograft model generated with human cancer cells expressing the NKG2D ligands. Our work provides empirical evidence that the co-expression of mbIL15 is a potential approach to improve the therapeutic potential of CAR-NK cells.</div></div>","PeriodicalId":13859,"journal":{"name":"International immunopharmacology","volume":"166 ","pages":"Article 115577"},"PeriodicalIF":4.7,"publicationDate":"2025-09-22","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145109757","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"A rapid ex vivo co-culture of memory-like NK and activated T cells enhances anti-tumor response in gastric cancer.","authors":"Wenxiu Chen,&nbsp;Manman Tian,&nbsp;Jie Shen,&nbsp;Qin Liu,&nbsp;Rutian Li,&nbsp;Baorui Liu,&nbsp;Jie Shao","doi":"10.1016/j.intimp.2025.115569","DOIUrl":"10.1016/j.intimp.2025.115569","url":null,"abstract":"<div><h3>Background</h3><div>Adoptive transfer of NK or T cells alone requires a long preparation time. We developed a rapid co-culture system, including cytokine-induced memory-like NK (CIML NK) cells and activated T cells (Ac-T), as well as tumor-penetrating peptide iRGD.</div></div><div><h3>Methods</h3><div>PBMCs were pretreated with IL-12/15/18 for 16 h, then washed to induce a memory NK phenotype. K562-CD48-41BBL-mbIL-21 cells were generated by lentiviral transduction and used as feeder cells to expand and activate NK cells from PBMCs for 7 days. On day 7, an anti-CD3 monoclonal antibody (OKT3) and an anti-CD28 monoclonal antibody (CD28.2) were added and washed overnight for 24 h. The in vitro (cytotoxicity, cytokines) and in vivo (tumor inhibition, survival) functions of iRGD-modified CIML NK&amp;Ac-T cells (CIML NK&amp;Ac-T-iRGD) were compared to CIML NK&amp;T-iRGD without addition of CD3/CD28.</div></div><div><h3>Results</h3><div>We established a one-week rapid co-culture system comprising NK and T cells. This system markedly increased cytokine secretion and demonstrated potent in vitro cytotoxicity against gastric cancer cell lines, significantly inhibited tumor growth, and prolonged survival in a gastric cancer xenograft model. Notably, iRGD-modified CIML NK&amp;Ac-T cells showed superior efficacy compared with CIML NK&amp;T cells.</div></div><div><h3>Conclusion</h3><div>Our data suggest that the rapid co-culture system of iRGD-modified CIML NK&amp;Ac-T cells used for adoptive cell transfer demonstrates potent anti-tumor effects in gastric cancer. This approach is time-efficient and cost-saving, with potential for broader clinical application compared with conventional NK cell therapies.</div></div>","PeriodicalId":13859,"journal":{"name":"International immunopharmacology","volume":"166 ","pages":"Article 115569"},"PeriodicalIF":4.7,"publicationDate":"2025-09-22","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145109753","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}