Innate Immunity最新文献

{"title":"TRPM2 deficiency contributes to M2b macrophage polarization via the PI3K/AKT/CREB pathway in murine sepsis.","authors":"Yanping Shen, Rana Dhar, Jujun Liu, Shenghui Hong, Huifang Tang, Xiaowei Qian","doi":"10.1177/17534259251343377","DOIUrl":"10.1177/17534259251343377","url":null,"abstract":"<p><p>BackgroundPrevious studies suggest that transient receptor potential melastatin 2 (TRPM2) plays a protective role in sepsis by enhancing bacterial clearance. This effect is mediated through the modulation of macrophage phenotypic changes, which strengthen the immune response against infection. However, the specific role and underlying mechanism of TRPM2 in macrophage polarization during sepsis remain unclear.MethodCecal ligation and puncture (CLP) was used to establish a mouse sepsis model, and bone marrow-derived macrophages (BMDMs) and peritoneal macrophages were prepared from C57BL/6 wild-type and TRPM2 knockout (<i>trpm</i>2^-/-) mice. IPI549 was utilized as a specific inhibitor of PI3K. Macrophage polarization, bactericidal ability, and the PI3K/protein kinase B (AKT)/cyclic adenosine monophosphate response element-binding protein signaling pathway were assessed. In addition, survival rate, bacterial burden, lung wet/dry weight ratio, lung and liver injury scores, and cytokine levels were measured in CLP-induced septic mice.ResultsIn lipopolysaccharide (LPS)-stimulated BMDMs, <i>trpm</i>2 deficiency increased the expression of characteristic markers associated with the M2b phenotype, reduced the bactericidal ability, and activated the PI3K/AKT/CREB signaling pathway. Consequently, both <i>trpm</i>2^-/- BMDMs and <i>trpm2</i>^-/- mice exhibited impaired bactericidal clearance during CLP-induced sepsis. Furthermore, IPI549 attenuated TRPM2 deletion-induced M2b polarization and restored the bactericidal function of BMDMs. Notably, IPI549 preconditioning reversed the increased susceptibility of the <i>trpm</i>2^-/- mice to sepsis. The 7-day mortality rate was 92% in <i>trpm</i>2^-/- mice, compared to 42% in IPI549-pretreated <i>trpm</i>2^-/- mice. Moreover, IPI549-treated mice exhibited improved lung wet/dry ratios, reduced lung and liver injury scores, reversed M2b polarization and decreased bacterial load.ConclusionThe PI3K/AKT/CREB pathway mediates the effect of TRPM2 by inhibiting M2b macrophage polarization and promoting bacterial clearance during sepsis.</p>","PeriodicalId":13676,"journal":{"name":"Innate Immunity","volume":"31 ","pages":"17534259251343377"},"PeriodicalIF":2.8,"publicationDate":"2025-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12102566/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144127398","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Resveratrol reduces radiation-induced liver damage and fibrosis, and may be related to inhibiting cellular aging and reducing inflammation.","authors":"Songhui Zhai, He Xu, Jianxin Xue, Lu Gan, Fang Gao, Lijuan Hu","doi":"10.1177/17534259251352623","DOIUrl":"10.1177/17534259251352623","url":null,"abstract":"<p><p>ObjectiveTo research whether radiation-induced liver damage and fibrosis could be mitigated by resveratrol (RSV) and to elucidate its underlying mechanism.MethodsA radiation-induced liver damage (RILD) model of murine was constructed. RSV was used as an intervention agent. The effects of RSV on inflammatory reaction, apoptosis, senescence, fibrosis, survival, and liver functions were detected by β-Gal, Sirius red, Masson's trichrome, and Tunnel staining using an automated biochemistry analyzer. The protein expression levels of P16 and P21 were detected by Western blot.ResultsRSV alleviated inflammatory injury of RILD mice. RSV decreased the serum pro-inflammatory cytokines of RILD mice. RSV alleviated radiation-induced hepatocellular senescence. The protein expression levels of P16 and P21 in RILD mice were decreased with RSV administration. RSV decreased the number of apoptotic cells in the early stage of RILD. RSV alleviated liver fibrosis and liver function in RILD mice.ConclusionsRSV reduces RILD and fibrosis, and may be related to inhibiting cellular aging and reducing inflammation.</p>","PeriodicalId":13676,"journal":{"name":"Innate Immunity","volume":"31 ","pages":"17534259251352623"},"PeriodicalIF":2.8,"publicationDate":"2025-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12205186/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144505635","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"The imbalance of circulating PD-L1-expressing non-classical/ classical monocytes is involved in immunocompromised host related pulmonary opportunistic infection.","authors":"Danhong Zhou, Yujia Jin, Yifan Jin, Yu Shen, Qiuxia Qu, Cheng Chen","doi":"10.1177/17534259251316152","DOIUrl":"10.1177/17534259251316152","url":null,"abstract":"<p><p>The application of biological therapy and glucocorticoids in Auto-immune diseases (AID) patients will cause immunocompromised host (ICH) prone to infection. And monocytes play a key role in both innate and adaptive immune responses. We aimed to investigate the changes of circulating monocyte subsets in AID or AID-ICH patients with pulmonary infection. The subgroups and PD-L1 expression of monocytes were measured by flow cytometry in healthy individuals (HC), new-onset AID patients (AID cohort) and AID-ICH patients with pulmonary opportunistic infection (AID-ICH cohort). Flow cytometry analysis was used to determine the distribution of monocyte subsets, including classical monocytes (CL, CD14⁺⁺CD16^-), intermediate monocytes (ITM, CD14⁺⁺CD16⁺) and non-classical monocytes (NC, CD14^+/-CD16⁺⁺), as well as the dynamic change of PD-L1 ⁺cluster among monocyte subsets. Among total monocyte, AID-ICH displayed decreased CL subset along with increased NC subset compared to HCs and AID. Regarding PD-L1 ⁺monocytes, although CL subset constituted the majority of that in HCs, AIDs and AID-ICHs, imbalance of NC/CL within PD-L1 ⁺monocytes was only noticed in AID-ICHs (<i>P</i> < 0.05). Furthermore, when AID subjects were developed into immunocompromised status (ICH), PD-L1 ⁺cluster in CL was minorly decreased (<i>P</i> > 0.05). Clinically, the lower ratio of PD-L1 ⁺cluster among CL subset (<i>P</i> < 0.05) and the less differentiated CL in PD-L1 ⁺monocytes (<i>P</i> < 0.05) was more likely to leaded to disease progression. The imbalance of circulating NC/CL subset was remarkable in immunocompromised host with pulmonary opportunistic infection, especially involvement of PD-L1⁺ cluster, which served as a potential biomarker in clinical practice.</p>","PeriodicalId":13676,"journal":{"name":"Innate Immunity","volume":"31 ","pages":"17534259251316152"},"PeriodicalIF":2.8,"publicationDate":"2025-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11774481/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143023329","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Emerging roles of SLAMF7 in immune cells and related diseases.","authors":"Zheng Zhang, Ying Zhang, Zeyu Chen, Lin Xia","doi":"10.1177/17534259251326700","DOIUrl":"10.1177/17534259251326700","url":null,"abstract":"<p><p>Immune cells are heterogeneous and perform different functions in different microenvironment, thus playing different roles in different stages of diseases. Studies have shown that immune cells are involved in the pathogenesis of many diseases, and there is a causal association of immune cells with disease states. Signaling Lymphocyte Activation Molecule family (SLAMF) members are a newly appreciated group of specific receptors that are mainly expressed in immune cells and whose role is to regulate the function of immune cells. SLAMF7, also known as CD319, has been widely reported in multiple myeloma, and in recent years, more and more studies have shown that SLAMF7 is widely involved in the function of immune cells and the progression of breast cancer, acquired immune deficiency syndrome, systemic lupus erythematosus and other immune cells-related diseases. However, the mechanisms underlying the regulatory role of SLAMF7 on immune cells, and the impact on the progression of immune cells-related diseases remain poorly elucidated. In this review, we summarize current knowledge about the role of SLAMF7 in immune cells and related diseases such as cancer, infectious disease, autoimmune disease and atherosclerosis, and the therapeutic strategy targeting SLAMF7 is also described. By better understanding the role and regulation of SLAMF7, we hope to provide new insights and directions for improving the diagnosis and treatment of inflammation.</p>","PeriodicalId":13676,"journal":{"name":"Innate Immunity","volume":"31 ","pages":"17534259251326700"},"PeriodicalIF":2.8,"publicationDate":"2025-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11912174/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143648513","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Association of killer immunoglobulin-like receptor genotypes and haplotypes with acute lymphoblastic leukemia risk.","authors":"Jameel Al-Tamimi, Suliman Alomar, Ali Aljuaimlani, Lamjed Mansour","doi":"10.1177/17534259251314774","DOIUrl":"10.1177/17534259251314774","url":null,"abstract":"<p><strong>Background: </strong>Killer immunoglobulin-like receptors (KIRs) are key molecules used by natural killer (NK) cells to interact with target cells. These receptors exhibit extensive genotypic polymorphism which has been associated with varying outcomes in immune responses against diseases. This study aimed to investigate the relationships between <i>KIR</i> genotypes and haplotypes with acute lymphoblastic leukemia (ALL) in Saudi patients.</p><p><strong>Methods: </strong>A total of 259 Saudi subjects including 145 cases of acute lymphoblastic leukemia (ALL) and 114 healthy controls living in Riyadh were genotyped for 16 <i>KIR</i> genes and the two <i>HLA-C1</i> and <i>-C2</i> allotypes using PCR-SSP genotyping method.</p><p><strong>Results: </strong>A significant high frequency of the two inhibitory <i>KIR</i> genes; <i>2DL1</i> (OR = 2.4; <i>p</i> < 0.0001) and <i>3DL1</i>(OR = 10.87; <i>p</i> = 0.0068) in ALL compared to healthy group was observed. In contrast, the activating <i>2DS4</i> gene was significantly higher in healthy controls (OR = 0.15, <i>p</i> < 0.0001) compared to ALL patients. Haplotype analysis shows that BX haplogroup was strongly associated with the occurrence of ALL (OR = 4.39; <i>p</i> < 0.0001). Further combinatory analysis of <i>KIR</i> genes with their <i>HLA-C1</i> and <i>-C2</i> ligands demonstrated strong statistically protective effect of the <i>2DS1-C2</i> combination from ALL (OR = 0.06; <i>p</i> = 0.0003).</p><p><strong>Conclusion: </strong>This study presents strong evidence supporting the connection between certain <i>KIR</i> genotypes, haplotypes, and <i>KIR-HLA</i> combinations with acute ALL in the Saudi population. The heightened occurrence of inhibitory <i>KIR</i> genes (<i>2DL1</i> and <i>3DL1</i>) and the BX haplotype in ALL patients indicates a possible involvement of these genetic variability with the dysfunctional of NK cells in the context of ALL disease.</p>","PeriodicalId":13676,"journal":{"name":"Innate Immunity","volume":"31 ","pages":"17534259251314774"},"PeriodicalIF":2.8,"publicationDate":"2025-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11774482/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143004944","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Pre-stimulation of precision-cut bovine udder slices with zymosan before LPS exposure indicates aspects of trained immunity especially in the absence of FCS.","authors":"Viviane Filor, Joanna Myslinska, Amitis Saliani, Jesmond Dalli, Peter Olinga, Wolfgang Bäumer, Dirk Werling","doi":"10.1177/17534259251360484","DOIUrl":"https://doi.org/10.1177/17534259251360484","url":null,"abstract":"<p><p>Mastitis in cattle poses a significant health challenge and results in substantial economic losses for the dairy industry. This study aimed to extend the existing precision-cut bovine udder slices (PCBUS) model as an <i>in vitro</i> model to explore the potential of inducing trained immunity in the udder with the goal to use the resulting knowledge for potential new treatment strategies. Interestingly, incubation of PCBUS with 10% fetal calf serum (FCS), but no 2% or FCS-free, negatively affected the production of some of the chemokines/cytokines analysed. When trained immunity was induced by zymosan, followed by stimulation with <i>E. coli</i>-derived lipopolysaccharide (LPS), production of interleukin (IL)-1β, IL-6, tumor necrosis factor α and interferon (IFNγ) was downregulated while production of IL-17A and pro-resolving lipid mediators (leukotrienes and prostaglandins) was upregulated. While the current experimental setup did not definitively confirm the induction of trained immunity for all parameters analysed in PCBUS, it validated the utility of PCBUS as a robust <i>in vitro</i> model for studying bovine udder inflammation. This model offers a promising platform for developing innovative mastitis treatments, particularly given the growing concern over antimicrobial resistance, as well as offering alternatives to the use of live animals in experimental studies in line with the 3Rs principles. It also provides a valuable tool for advancing our understanding of immune responses in the bovine udder. By adapting the precision-cut tissue slice technique to bovine udders, this model enables extensive research into new therapeutic approaches and supports basic research efforts to characterise complex pathophysiological processes associated with mastitis. Furthermore, our data highlight the potential limitations of FCS in <i>in vitro</i> studies. Our data should not only stimulate the discussion about FCS in homologues or heterologues species, but should also be kept in mind regarding the need for foetal calves to generate FCS in line with the 3Rs guideline.</p>","PeriodicalId":13676,"journal":{"name":"Innate Immunity","volume":"31 ","pages":"17534259251360484"},"PeriodicalIF":2.8,"publicationDate":"2025-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12374038/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144953035","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Effect of <i>Cardamine violifolia</i> on muscle protein degradation and anti-oxidative capacity in weaned piglets after Lipopolysaccharide challenge.","authors":"Nianbang Wu, Shunkang Li, Yanling Kuang, Wensheng He, Huiling Zhu, Qingyu Gao, Liping Liu, Shuiyuan Cheng, Yulan Liu, Xin Cong, Dan Wang","doi":"10.1177/17534259251322589","DOIUrl":"10.1177/17534259251322589","url":null,"abstract":"<p><p>This study aimed to investigate the impact of <i>Cardamine violifolia</i> on muscle protein degradation, the inflammatory response and antioxidant function in weaned piglets following LPS challenge. Twenty-four weaned piglets were used in a 2 × 2 factorial experiment with dietary treatment (sodium selenite or <i>Cardamine violifolia</i>) and LPS challenge. After 28 days of feeding, pigs were injected intraperitoneally with 100 μg/kg LPS or saline. Dietary supplementation with <i>Cardamine violifolia</i> mitigated the reduction in insulin and growth hormone levels induced by LPS. It also curbed the LPS-induced elevation of plasma glucagon, urea nitrogen, and creatinine concentrations. <i>Cardamine violifolia</i> reduced muscle damage caused by LPS, as evidenced by increased protein content and protein/DNA ratio and decreased TNF-α and IL-1β mRNA expression. Furthermore, <i>Cardamine violifolia</i> modulated the expression of FOXO1, FOXO4, and MuRF1 in muscle, indicative of the protective effect against muscle protein degradation. Enhanced muscle antioxidant function was observed in the form of increased T-AOC, reduced MDA concentration, and decreased mRNA expression of GPX3, DIO3, TXNRD1, SELENOS, SELENOI, SELENOO, and SEPHS2 in LPS-treated piglets. The findings suggest that <i>Cardamine violifolia</i> supplementation can effectively alleviate muscle protein degradation induced by LPS and enhance the antioxidant capacity in piglets.</p>","PeriodicalId":13676,"journal":{"name":"Innate Immunity","volume":"31 ","pages":"17534259251322589"},"PeriodicalIF":2.8,"publicationDate":"2025-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11837137/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143448993","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Biological significance of extracellular vesicles in innate immune system.","authors":"Budjav Jadamba, Jihye Park, Heedoo Lee","doi":"10.1177/17534259251355029","DOIUrl":"10.1177/17534259251355029","url":null,"abstract":"<p><p>Extracellular vesicles (EVs), which are nanosized membranous structures released by diverse cell types, serve as crucial mediators of intercellular communication. Recent evidence has highlighted the dynamic transfer of various biological components, including proteins, lipids, mRNAs, non-coding RNAs, miRNAs, and DNA, via EVs. Immuno-stimulated cells actively release EVs that play a pivotal role in regulating the innate immune system. This study comprehensively reviews the current scientific findings, shedding light on the intricate biological roles of EVs in regulating innate immune cells and the overall immune system. This discussion encompasses diverse pathophysiological conditions and provides valuable insights into the multifaceted contributions of EVs to innate immune responses.</p>","PeriodicalId":13676,"journal":{"name":"Innate Immunity","volume":"31 ","pages":"17534259251355029"},"PeriodicalIF":2.8,"publicationDate":"2025-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12214353/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144527820","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Novel Concepts in Innate Immunity NCII 2025 - selected abstracts.","authors":"","doi":"10.1177/17534259251374373","DOIUrl":"10.1177/17534259251374373","url":null,"abstract":"","PeriodicalId":13676,"journal":{"name":"Innate Immunity","volume":"31 ","pages":"17534259251374373"},"PeriodicalIF":2.8,"publicationDate":"2025-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12457746/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145225348","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Working in negative space: Type I interferon mediated immuno-modulation through transcriptional suppression in disease and homeostasis.","authors":"Ella L Brunsting, Darren J Perkins","doi":"10.1177/17534259251367263","DOIUrl":"10.1177/17534259251367263","url":null,"abstract":"<p><p>The type I interferon family of cytokines are rapidly produced following innate pattern recognition receptor engagement and establish a critical early state of host defense. Type I interferons act in antiviral immunity as transcriptional activators and the binding of any type I interferon to the common IFNAR receptor triggers the transcription of <u>I</u>nterferon <u>S</u>timulated <u>G</u>enes (ISGs). A defined set of ISGs have been described through exhaustive studies and the protein products of these ISGs function to increase cell intrinsic resistance to viral growth and to promote viral clearance. Simultaneously, interferons also drive a much less well studied program of transcriptional suppression, inhibiting the expression of an unknown number of genes, with poorly understood consequences for disease. The limited number of genes currently known to be transcriptionally suppressed by IFN are enriched for those with immune-mediating activities such as inflammatory cytokines (e.g., IL-1β), cytokine receptors (e.g., IFNγR) and chemokines. Interferon dependent transcriptional suppression of immune response genes is therefore thought to underlie the immune suppression associated with interferon production during many bacterial infections (e.g., mycobacterium tuberculosis and listeria monocytogenes) and may also explain the palliative effects of interferons in some autoimmune diseases. Despite the health relevance of IFN driven transcriptional suppression, no consensus molecular model exists to explain its selectivity or regulation. In this review we highlight the current literature detailing the known targets of IFN transcriptional suppression within the various disease models in which it has been observed. We also review the relevant molecular mechanisms which have been proposed to explain transcriptional suppression by interferons and discuss the remaining open questions in this field with an ambition to stimulate future work in this area.</p>","PeriodicalId":13676,"journal":{"name":"Innate Immunity","volume":"31 ","pages":"17534259251367263"},"PeriodicalIF":2.8,"publicationDate":"2025-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12365442/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144873064","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}