Molecular Medicine最新文献

{"title":"Immunogenicity and memory B-cell potency induced by an inactivated COVID-19 vaccine in pregnant women.","authors":"Gui-Ping Wen, Yi-Zhen Wang, Min-Ming Wang, Wen-Rong Wang, Si-Ling Wang, Zheng Wang, Zi-Min Tang, Zhen-Yu Luo, Zi-Hao Chen, Jia-Yan Chen, Mei-Jiao Cai, Yun-Sheng Ge, Zi-Zheng Zheng, Yu-Lin Zhou","doi":"10.1186/s10020-025-01357-5","DOIUrl":"10.1186/s10020-025-01357-5","url":null,"abstract":"<p><p>During pregnancy, profound immunological, hormonal, and metabolic adaptations occur to support fetal development. The impact of pregnancy on vaccine-induced immunity remains incompletely characterized, as previous studies have primarily focused on serological antibody levels but not immune memory. Immune memory is critical for vaccine effectiveness, but effect of pregnancy on immune memory remain unknown. In addition, the memory B cell response profile induced by inactivated coronavirus disease 2019 (COVID-19) vaccines in pregnant women remains unclear. This study comprehensively investigated the serological responses and memory B cell response induced by an inactivated COVID-19 vaccine in pregnant women. The results demonstrated that while pregnant women and non-pregnant women of childbearing age showed comparable serological antibody levels, vaccine-induced monoclonal antibodies (mAbs) from pregnant women exhibited significantly lower binding potency to severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) spike protein and its segments and weaker neutralizing potency and breadth than those from non-pregnant women. Vaccine-induced mAbs from pregnant women were derived predominantly from IGHV3-30, whereas those from non-pregnant women were derived diverse germline genes. Most of mAbs from pregnant women targeted the receptor-binding domain (RBD) (40.9%) and S2 domain (31.8%), whereas most of mAbs from non-pregnant women targeted the RBD (51.3%) and N-terminal domain (30.8%). These findings suggested that pregnancy may impair the potency of vaccine-induced memory B cells. These insights may be valuable for the development of vaccination strategies for pregnant women.</p>","PeriodicalId":18813,"journal":{"name":"Molecular Medicine","volume":"31 1","pages":"297"},"PeriodicalIF":6.4,"publicationDate":"2025-09-26","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12465604/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145176864","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Stochastic epigenetic mutation profiles as biomarkers of clinical activity in juvenile idiopathic arthritis: a multi-omic machine learning approach for gene prioritization.","authors":"Giacomo Cavalca, Matteo Vergani, Davide Cangelosi, Alessandro Consolaro, Marco Gattorno, Angelo Ravelli, Jane Munro, Boris Novakovic, Anna Duncan, Paolo Uva, Giovanni Fiorito","doi":"10.1186/s10020-025-01348-6","DOIUrl":"10.1186/s10020-025-01348-6","url":null,"abstract":"<p><strong>Background: </strong>Juvenile idiopathic arthritis (JIA) is a rare autoimmune disease arising from a complex interplay between genetic and environmental factors. Epigenetic modifications such as DNA methylation (DNAm) have been described as potential mediators in gene-environment interactions, contributing to immune system dysregulation. Emerging evidence suggests that DNAm profiles also predict therapeutic responses in autoimmune diseases. This study aims to identify epigenetic biomarkers and epigenetic-driven gene expression changes associated with JIA clinical activity.</p><p><strong>Methods: </strong>We reanalyzed a publicly available dataset of 44 JIA patients, with whole-genome DNAm and gene expression from CD4 + T cells measured at two points: at anti-TNF therapy withdrawal (T₀) and eight months later (T_end). At T_end, 30 patients maintained inactive disease (ID) while 14 did not (NO ID). We investigated differences between ID and NO ID patients in the epigenetic mutation load and various epigenetic clocks through linear regression models, and prioritized genomic regions with significantly higher number of epimutations in NO ID patients through machine learning.</p><p><strong>Results: </strong>We found a higher mutation load in NO ID than ID patients, both at T₀ and at T_end, with the differences at T_end reaching statistical significance (p = 0.02). In contrast, we found no evidence of association between epigenetic clocks and JIA clinical activity. Using a multi-omic approach, we identified a List of candidate epigenetically-driven differentially expressed genes, 80 up-regulated and 77 down-regulated, in NO ID patients. Finally, comparing our candidate gene list with the Connectivity Map database, we identified new candidate potential therapeutic targets. Key findings were validated in independent datasets: DNAm profiles from CD4 + T cells (56 JIA patients, 57 controls) and transcriptomic data from PBMCs of JIA patients with active or inactive disease, confirming dysregulation of pathways such as TNF-α signaling via NF-kB and TGF-β signaling among others.</p><p><strong>Conclusions: </strong>We described a significant association of epigenetic mutations with JIA clinical activity, indicating that epigenetic changes might precede clinical symptoms and may serve as biomarkers for early disease monitoring. Further, our results shed light on biomolecular mechanisms of JIA, supporting the development of more effective treatments.</p>","PeriodicalId":18813,"journal":{"name":"Molecular Medicine","volume":"31 1","pages":"289"},"PeriodicalIF":6.4,"publicationDate":"2025-09-25","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12465343/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145150123","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Correction: Miglustat ameliorates isoproterenol-induced cardiac fibrosis via targeting UGCG.","authors":"Jing Liu, Wenqi Li, Ran Jiao, Zhigang Liu, Tiantian Zhang, Dan Chai, Lingxin Meng, Zhongyi Yang, Yuming Liu, Hongliang Wu, Xiaoting Gu, Xiaohe Li, Cheng Yang","doi":"10.1186/s10020-025-01360-w","DOIUrl":"10.1186/s10020-025-01360-w","url":null,"abstract":"","PeriodicalId":18813,"journal":{"name":"Molecular Medicine","volume":"31 1","pages":"288"},"PeriodicalIF":6.4,"publicationDate":"2025-09-23","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12455839/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145131378","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Correction: Peripheral tissue BDNF expression is affected by promoter IV defect and enriched environments in mice: negative hippocampus-intestine and positive thymus-serum-muscle correlations.","authors":"Janet Wang, William Schupp, Kazuko Sakata","doi":"10.1186/s10020-025-01317-z","DOIUrl":"10.1186/s10020-025-01317-z","url":null,"abstract":"","PeriodicalId":18813,"journal":{"name":"Molecular Medicine","volume":"31 1","pages":"287"},"PeriodicalIF":6.4,"publicationDate":"2025-09-08","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12418611/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145023780","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Correction: Mucosal implications of oral Jak3-targeted drugs in COVID patients.","authors":"Narendra Kumar, Daniel Segovia, Priyam Kumar, Hima Bindu Atti, Soaham Kumar, Jayshree Mishra","doi":"10.1186/s10020-025-01359-3","DOIUrl":"10.1186/s10020-025-01359-3","url":null,"abstract":"","PeriodicalId":18813,"journal":{"name":"Molecular Medicine","volume":"31 1","pages":"286"},"PeriodicalIF":6.4,"publicationDate":"2025-09-06","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12413737/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145008309","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"RHBDF2 governs microglial neuroinflammation during cerebral ischemia-reperfusion injury and is positively regulated by the m6A reader YTHDF1.","authors":"Lisi Xu, Ruonan Zhang, Xiaolin Zhang, Bing Liu, Xiuli Shang, Daifa Huang","doi":"10.1186/s10020-025-01326-y","DOIUrl":"10.1186/s10020-025-01326-y","url":null,"abstract":"<p><strong>Background: </strong>Neuroinflammation mediated by microglia activation is the key pathological mechanisms for cerebral ischemia-reperfusion injury (CIRI). This study investigated the role and underlying molecular mechanism of Rhomboid 5 homolog 2 (RHBDF2) in neuroinflammation during CIRI.</p><p><strong>Methods: </strong>The in vivo middle cerebral artery occlusion and reperfusion (MCAO/R) mouse model and in vitro HMC3 microglia subjected to oxygen glucose deprivation and reperfusion (OGD/R) were established to mimic CIRI. Real-time PCR, western blot, immunohistochemistry, immunofluorescence, flow cytometry, and co-immunoprecipitation assays were used to confirm RHBDF2 expression and explore the molecular mechanism of microglia-specific RHBDF2 knockdown in CIRI. Methylated RNA immunoprecipitation was used to detect the m6A methylation level of RHBDF2 mRNA both in vivo and in vitro. RNA sequencing analysis was performed in OGD/R-treated HMC3 cells with or without RHBDF2 knockdown.</p><p><strong>Results: </strong>Our finding showed that RHBDF2 expression increased in both in vivo and in vitro CIRI models. Microglial-specific RHBDF2 knockdown reduced brain injury in MCAO/R mice, as evidenced by the reduction in the cerebral infarct volume and amelioration of the neurological deficits. Furthermore, we demonstrated that RHBDF2 knockdown alleviated neuroinflammation by inhibiting microglial M1 polarization and promoting microglial M2 polarization in MCAO/R mouse ischemic penumbra. Mechanistically, RHBDF2 interacted with STING and promoted the activation of the STING-TBK1-IRF3/p65 signaling pathway. Rescue experiments confirmed that RHBDF2 knockdown suppressed inflammation via the inhibition of STING-TBK1 signaling pathway. In addition, the m6A methylation level of RHBDF2 mRNA was significantly increased in the MCAO/R mouse brain tissues and OGD/R-treated HMC3 cells. YTHDF1 recognized the m6A sites of RHBDF2 and promote its expression in an m6A manner. Through RNA-seq, the possible downstream effectors of RHBDF2 in CIRI was predicted.</p><p><strong>Conclusions: </strong>Microglial-specific RHBDF2 knockdown inhibits neuroinflammation in CIRI via STING-TBK1 signaling pathway, and is positively regulated by the m6A reader YTHDF1. This suggests RHBDF2 as a potential therapeutic target in ischemic stroke.</p>","PeriodicalId":18813,"journal":{"name":"Molecular Medicine","volume":"31 1","pages":"284"},"PeriodicalIF":6.4,"publicationDate":"2025-09-02","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12403488/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144961763","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Human papillomavirus-related syntaxin 11 reprograms tumor-associated macrophages to induce breast cancer cell apoptosis via PI3K/AKT signaling.","authors":"Chuan Hu, Tingting Hu, Jian Wen, Zengrong Jia","doi":"10.1186/s10020-025-01325-z","DOIUrl":"10.1186/s10020-025-01325-z","url":null,"abstract":"<p><strong>Background: </strong>Human papillomavirus (HPV) is closely associated with tumor progression and the tumor microenvironment (TME), but its role in breast cancer (BC), which can be affected by HPV, has not been reported.</p><p><strong>Methods: </strong>Ten independent BC cohorts were included to generate two HPV-related gene-based signatures. The CIBERSORT and ESTIMATE algorithms were used to quantify the immune cell fraction and TME scores, and the correlations between HPV-related gene-based signatures and scores were analyzed. The expression patterns and clinical significance of STX11 were determined through bioinformatics analysis, and its effects on modulating tumor-associated macrophages (TAMs) were confirmed by real-time qPCR and Western blotting. The anticancer role of STX11 in macrophages and its underlying mechanisms were analyzed in vitro and in vivo.</p><p><strong>Results: </strong>Two novel HPV-related gene-based signatures were established that can effectively predict the overall survival and disease-free survival of patients with BC. HPV-related gene-based signatures were significantly associated with the immune score and 19 types of immune cells in BC tissues. STX11 was downregulated in BC and was associated with favorable clinical prognosis, and it was expressed mainly in M1 TAMs. Mechanistically, STX11 promoted the M1 polarization of macrophages, and macrophages overexpressing STX11 can inhibit BC proliferation and migration by regulating the PI3K-AKT pathway. In orthotopic BC models, macrophages overexpressing STX11 significantly suppressed tumor growth.</p><p><strong>Conclusions: </strong>HPV-related risk signatures were constructed, which showed prognostic predictive ability for patients with BC. STX11 is associated with a favorable prognosis in patients with BC and facilitates M1 polarization, and macrophages overexpressing STX11 can inhibit BC malignancy by regulating the PI3K-AKT pathway, suggesting its role as a potential immunotherapeutic candidate.</p>","PeriodicalId":18813,"journal":{"name":"Molecular Medicine","volume":"31 1","pages":"285"},"PeriodicalIF":6.4,"publicationDate":"2025-09-02","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12403928/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144961716","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Bidirectional shifts in Pm20d1 expression impact thermogenesis and metabolism.","authors":"Marcela R Simoes, Ana L Gallo-Ferraz, Bruna Bombassaro, Fernando Valdivieso-Rivera, Guilherme A S Nogueira, Milena Monfort-Pires, Marcos Vinicius da Cruz, Ariane M Zanesco, Nayra Fernanda-Oliveira, Leonardo Reis Silveira, Roger F Castilho, Carlos H Sponton, Licio A Velloso","doi":"10.1186/s10020-025-01345-9","DOIUrl":"10.1186/s10020-025-01345-9","url":null,"abstract":"<p><strong>Background: </strong>Peptidase M20 domain containing 1 (PM20D1) is a secreted N-fatty acyl amino synthase and hydrolase that controls tissue and blood levels of N-fatty acyl amino acids. In brown adipocytes, N-fatty acyl amino acids bind to mitochondria and act as uncouplers of mitochondria, independent of UCP1. Interventions aimed at increasing or inhibiting PM20D1 expression considerably impact energy balance and metabolism; however, little is known about naturally occurring variants of the PM20D1/Pm20d1 gene and their impact on phenotype.</p><p><strong>Methods: </strong>In vivo, gene expression of Pm20d1 in BALB/c, C57BL/6, and Ucp1 KO in brown adipose tissue and other metabolic tissues was measured. In vitro, transcriptional activity of Pm20d1 and brown adipocytes' oxygen consumption in primary culture were assessed. Human PM20D1 circulating levels were quantified. In silico analysis of the Pm20d1 gene sequencing and human polymorphisms associated with PM20D1 was performed.</p><p><strong>Results: </strong>Here, we identified a gain-of-function variant in the Pm20d1 promoter region present in BALB/c mice and absent in C57BL/6 mice. The presence of this variant is accompanied by increased expression of Pm20d1 in brown and white adipose tissues, muscle, liver, and hypothalamus; moreover, it leads to increased cold tolerance and UCP1-independent brown adipose tissue mitochondrial respiration. Inhibition of Pm20d1 in brown adipose tissue results in defective cold tolerance in BALB/c, whereas the brown adipose tissue overexpression of Pm20d1 results in increased cold tolerance in C57BL/6 mice. In humans, variants of the PM20D1 gene are associated with changes in body mass index, whereas at least one variant in the promoter region is associated with increased body mass index and metabolic syndrome.</p><p><strong>Conclusion: </strong>Thus, PM20D1 plays a bidirectional role in regulating thermogenesis and body mass, and, at least in part, variants in the promoter region can partially explain the differences in PM20D1 expression and its impact on the metabolic phenotype.</p>","PeriodicalId":18813,"journal":{"name":"Molecular Medicine","volume":"31 1","pages":"283"},"PeriodicalIF":6.4,"publicationDate":"2025-08-28","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12395774/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144961735","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"CpG-oligodeoxynucleotides challenged macrophages ameliorate acetaminophen induced liver injury by activating TLR9/IRG1/itaconate metabolic pathway.","authors":"Yibai Qu, Zehui Jiang, Zhixia Chen, Sidan Luo, Bingyao Xie, Xubo Wu, Gang Yuan, Kan Wu, Li Chen, Tian Tian, Shan Li, Haihua Luo, Quan Li, Ding Yuan, Yan Zhang, Yanxia Gao, Jun Zhou, Zhengzheng Yan, Yong Jiang","doi":"10.1186/s10020-025-01324-0","DOIUrl":"https://doi.org/10.1186/s10020-025-01324-0","url":null,"abstract":"<p><strong>Background: </strong>Acetaminophen, or N-acetyl-para-aminophenol (APAP), causes severe liver damage and acute liver failure when overdosed. Oligodeoxynucleotides containing CpG motifs (CpG ODN) can regulate the function of macrophages, which play an important role in drug-induced liver injury. It is unclear whether CpG ODN-treated macrophages play an immune regulation role in APAP-induced liver injury. In the present study, we aim to explore the role of CpG ODN-activated macrophages in APAP-induced liver injury and the underlying mechanism in protecting against the cytotoxicity of APAP.</p><p><strong>Methods: </strong>In vivo, C57BL/6 mice were treated with APAP (300 mg/Kg) or/and CpG ODN (ODN 1826, 1.65 mg/Kg) by intraperitoneal injection, then survival rate, histopathological evaluation, and inflammatory factors were observed to ascertain the protective effect of CpG ODN. Then, CpG ODN-treated macrophages were reinfused into the animal model to determine the effector cells. In vitro, RNA sequencing and untargeted metabolomics detection were performed to illustrate the underlying mechanism. Last, Acod1 siRNA interference was used to clarify the role of IRG1 in resistance to APAP cytotoxicity by ROS and apoptosis indicator detections.</p><p><strong>Results: </strong>We found that CpG ODN showed a protective effect against APAP cytotoxicity by stimulating macrophages rather than hepatic parenchymal cells. In particular, reinfusion of CpG ODN-treated macrophages to mice can alleviate APAP-induced liver injury. Transcriptome and metabolome analysis revealed that the expression of aconitate decarboxylase 1 (Acod1; also known as immune responsive gene 1, IRG1) and the metabolite itaconate generated by IRG1 catalysis increased after CpG ODN stimulation. In addition, we found that the mechanism of this protective effect is ascribed to the increased expression of Acod1 and the antioxidative function of itaconate by the activation of the TLR9/NF-κB signaling pathway.</p><p><strong>Conclusion: </strong>CpG ODN alleviated liver injury induced by APAP through the activation of the TLR9/NF-κB signaling pathway in macrophages, upregulating the expression of IRG1 protein, promoting the production of endogenous metabolite itaconate, and inhibiting macrophage apoptosis which was regulated by upregulating the expression of Nrf2 to inhibit ROS production. This study sheds new light on CpG ODN as a therapeutic strategy in resistance to APAP-induced liver injury.</p>","PeriodicalId":18813,"journal":{"name":"Molecular Medicine","volume":"31 1","pages":"282"},"PeriodicalIF":6.4,"publicationDate":"2025-08-25","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12379469/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144961713","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"CAF-derived exosomes drive the FGF4/SHH feedback loop by encapsulating GREM1 in non-small cell lung cancer.","authors":"Xianqiao Wu, Wei Chen, Tianzheng Fang, Ziyuan Chen, Shuai Fang, Chengwei Zhou","doi":"10.1186/s10020-025-01340-0","DOIUrl":"https://doi.org/10.1186/s10020-025-01340-0","url":null,"abstract":"","PeriodicalId":18813,"journal":{"name":"Molecular Medicine","volume":"31 1","pages":"281"},"PeriodicalIF":6.4,"publicationDate":"2025-08-23","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12375272/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144961784","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}