BMC Immunology最新文献

{"title":"Treponema pallidum induces pathological injury of the rabbit testis and sperm through NLRP3 inflammasome activation-mediated pyroptosis.","authors":"Tong Zheng, Meiping Ye, Yilan Yang, Linxin Yao, Danyang Zou, Chunjie Liao, Xin Feng, Tingli Tian, Zhuojun Tang, Pingyu Zhou","doi":"10.1186/s12865-026-00835-7","DOIUrl":"https://doi.org/10.1186/s12865-026-00835-7","url":null,"abstract":"<p><strong>Background: </strong>Treponema pallidum (T. pallidum) can invade various organs and tissues. However, there have been few studies on the pathological injury of T. pallidum to the testis and sperm. The NOD-like receptor protein 3 (NLRP3) inflammasome, upon activation, leads to pyroptosis-a programmed, pro-inflammatory cell death process, and promotes inflammatory responses. Previous investigations have found that the NLRP3 inflammasome is elevated in the testis tissues of rabbits infected with T. pallidum. This study aimed to investigate whether T. pallidum induced pathological injury of the rabbit testis and sperm through NLRP3 inflammasome-mediated pyroptosis.</p><p><strong>Methods: </strong>While rabbits in the T. pallidum group received an intratesticular injection of 1 mL of a bacterial suspension containing 10⁷/mL treponemes, those in the sham group were administered an equal volume of normal saline to serve as the injection procedure control. 14 days later, testis tissues were harvested for IHC and H&E staining, and analysis of qPCR. In vitro, GC-2spd cells were stimulated by T. pallidum (MOI = 20). After administering MCC950, the expression levels of the inflammasome NLRP3 and downstream pyroptosis-related molecules were subsequently detected.</p><p><strong>Results: </strong>T. pallidum caused obvious pathological damage to the rabbit testis and sperm reduction. Meanwhile, the gene expression levels of NLRP3, ASC, GSDMD, Caspase-1, IL-Iβ, and IL-18 in the T. pallidum group were higher than those of the sham group. Additionally, T. pallidum induced cell injury and pyroptosis in GC-2spd cells, which was improved by the NLRP3 inflammasome inhibitor MCC950.</p><p><strong>Conclusions: </strong>Our findings validated that T. pallidum induced pathological damage to the testis and sperm reduction via NLRP3 inflammasome activation and pyroptosis. By specifically inhibiting the NLRP3 inflammasome, MCC950 has the potential to ameliorate sperm cell damage under in vitro conditions via the blockade of pyroptotic cell death.</p>","PeriodicalId":9040,"journal":{"name":"BMC Immunology","volume":" ","pages":""},"PeriodicalIF":2.7,"publicationDate":"2026-05-09","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147855861","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Extracellular vesicles from miR-146a-overexpressing mesenchymal stem cells reduce ligature-induced periodontitis by modulating inflammatory cytokines.","authors":"Wen Chu, Yinuo Zhang, Shiying Shen, Zhilu Wang, Yanxu Guo, Yanfang Yu, Dahai Huang, Nara Davtyan","doi":"10.1186/s12865-026-00839-3","DOIUrl":"https://doi.org/10.1186/s12865-026-00839-3","url":null,"abstract":"<p><strong>Background: </strong>Periodontitis is a long-lasting inflammatory disorder of structures attached, which is significantly influenced by insufficient or dysregulated immune responses. Mesenchymal stem cells (MSCs) and their extracellular vesicles (EVs) are a promising therapeutic modality. This study explores the therapeutic efficacy of EVs derived from miR-146a-overexpressing bone marrow-derived mesenchymal stem cells (BMSCs) in a ligature-induced periodontitis model.</p><p><strong>Results: </strong>BMSCs were transfected to overexpress miR-146a, and their EVs were isolated. Periodontitis was induced in 30 female C57Bl/6 mice and divided into three groups: a control group receiving PBS, a miR-control EV-treated group, and a miR-146a-EV-treated group. EVs were administered subgingivally, and clinical parameters were evaluated. Levels of proinflammatory cytokines interleukin (IL)-1β, IL-8, tumor necrosis factor (TNF)-α, and IL-6, as well as anti-inflammatory cytokines IL-10, IL-4, and transforming growth factor (TGF)-β, were quantified using enzyme-linked immunosorbent assay (ELISA) and quantitative real-time polymerase chain reaction (PCR). Phosphorylated p38, JNK, ERK1/2, and NF-κB p65 were also quantified by ELISA, and TRAF6 and IRAK1 mRNA and protein levels were assessed to evaluate inflammatory signaling pathways. In the gingival tissue and systemic circulation, the proinflammatory cytokines IL-1β, IL-8, TNF-α, and IL-6 were significantly downregulated, while the levels of the anti-inflammatory mediators IL-10, IL-4, and TGF-β were significantly increased in the miR-146a-EV group when compared with the control group. miR-146a-EV treatment significantly reduced MAPK and NF-κB activation while downregulating TRAF6 and IRAK1 expression in gingival tissues.</p><p><strong>Conclusion: </strong>miR-146a-transduced MSC-derived EVs ameliorated ligature-induced periodontitis by modulating local and systemic cytokine expression. These results indicate that miR-146a-EVs can be a novel, cell-free therapy for the treatment of periodontitis.</p>","PeriodicalId":9040,"journal":{"name":"BMC Immunology","volume":" ","pages":""},"PeriodicalIF":2.7,"publicationDate":"2026-05-09","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147863587","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"SIRT1-mediated deacetylation of DRP1 suppresses excessive mitophagy and ameliorates pediatric functional dyspepsia.","authors":"Shuan Yin, Dongdong Dai, Gaoyan Wang, Shaomei Zhou","doi":"10.1186/s12865-026-00842-8","DOIUrl":"https://doi.org/10.1186/s12865-026-00842-8","url":null,"abstract":"<p><p>Functional dyspepsia (FD) is a prevalent gastrointestinal disorder in children, but its underlying molecular mechanisms remain poorly understood. Mitochondrial dysfunction and excessive mitophagy have been implicated in FD, but the underlying mechanisms remain poorly understood. This study aimed to investigate the role of SIRT1 in mitochondrial quality control and its potential therapeutic value in pediatric FD. Serum samples from pediatric FD patients and healthy controls were analyzed for SIRT1 expression and inflammatory cytokines. Human gastric smooth muscle cells (HGSMCs) were treated with carbonyl cyanide m-chlorophenyl hydrazone (CCCP) to induce mitochondrial stress. Mitochondrial function, mitophagy, oxidative stress, and protein interactions were assessed using qPCR, Western blot, co-immunopcipitation, and functional assays including ATP levels, mitochondrial membrane potential, ROS, MDA, SOD, and GSH-Px. The results showed that SIRT1 was significantly downregulated in both pediatric FD patient sera and CCCP-stimulated HGSMCs, accompanied by elevated pro-inflammatory cytokines including IL-6, TNF-α, and IL-1β. Overexpression of SIRT1 improved cell viability, ATP production, mitochondrial membrane potential, and suppressed excessive mitophagy and oxidative stress. Conversely, DRP1 knockdown phenocopied the protective effects of SIRT1, reducing mitophagy and oxidative stress in CCCP-stimulated cells. SIRT1 directly interacted with DRP1 and promoted its deacetylation at lysine 283, leading to accelerated DRP1 degradation. Rescue experiments confirmed that DRP1 overexpression reversed the protective effects of SIRT1 on mitochondrial function and redox homeostasis. In conclusion, SIRT1 exerts protective effects in pediatric FD by deacetylating DRP1 at K283, thereby inhibiting excessive mitophagy and ameliorating mitochondrial dysfunction and oxidative stress. These findings identify the SIRT1-DRP1 axis as a potential therapeutic target for pediatric FD.</p>","PeriodicalId":9040,"journal":{"name":"BMC Immunology","volume":" ","pages":""},"PeriodicalIF":2.7,"publicationDate":"2026-05-08","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147855882","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Elevated serum TNF-α in patients with immune-mediated necrotizing myopathy correlates with muscle damage.","authors":"Xingyu Han, Huizhen Ge, Qing Zhang, Mengge Yang, Bitao Bu","doi":"10.1186/s12865-026-00834-8","DOIUrl":"https://doi.org/10.1186/s12865-026-00834-8","url":null,"abstract":"<p><strong>Objective: </strong>This study aimed to investigate serum levels of tumor necrosis factor-alpha (TNF-α) in patients with immune-mediated necrotizing myopathy (IMNM) and to explore its correlation with disease activity.</p><p><strong>Methods: </strong>Serum TNF-α levels were measured using an enzyme-linked immunosorbent assay (ELISA). TNF-α mRNA expression in muscle tissues from IMNM patients was detected by reverse transcription quantitative real-time PCR (RT-qPCR). In vitro experiments were performed on human muscle cells stimulated with TNF-α to assess cell viability and the expression of downstream molecules.</p><p><strong>Results: </strong>Serum TNF-α levels were significantly elevated in IMNM patients compared to healthy controls (p = 0.0002). In IMNM patients, TNF-α levels showed a significant positive correlation with serum creatine kinase (CK; p = 0.0004) and lactate dehydrogenase (LDH; p = 0.0137). TNF-α mRNA was also overexpressed in muscle biopsies from patients with IMNM. In vitro, TNF-α stimulation significantly reduced muscle cell viability and upregulated the mRNA expression of downstream inflammatory mediators, including IP-10, MCP-1, IL-6, and phosphorylated p65.</p><p><strong>Conclusion: </strong>Elevated serum TNF-α in IMNM patients is associated with muscle damage and may contribute to disease pathogenesis by amplifying the inflammatory response. These findings suggest that TNF-α could serve as a potential biomarker for assessing disease severity in IMNM.</p>","PeriodicalId":9040,"journal":{"name":"BMC Immunology","volume":" ","pages":""},"PeriodicalIF":2.7,"publicationDate":"2026-05-07","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147833362","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"The diagnostic and prognostic value of miR-200b on severe pneumonia.","authors":"Shuying Zheng, Xiaopei Zhou, Changhao Cheng","doi":"10.1186/s12865-026-00836-6","DOIUrl":"https://doi.org/10.1186/s12865-026-00836-6","url":null,"abstract":"<p><strong>Background: </strong>Severe pneumonia (SP) is a critical infectious disease characterized by excessive inflammatory responses, and the molecular mechanisms underlying its progression remain incompletely understood.</p><p><strong>Objective: </strong>To investigate the expression pattern, diagnostic value, and potential functional regulatory mechanisms of miR-200b in SP.</p><p><strong>Methods: </strong>RT-qPCR was used to detect miR-200b expression levels; ROC curve analysis was used to evaluate its diagnostic performance; prognostic indicators of miR-200b were compared between high- and low-expression groups, and Cox regression was employed to identify independent prognostic factors. In vitro validation of the pro-inflammatory effects of miR-200b. Target genes were identified through Venn diagram-based prediction and dual luciferase reporter assays. Functional recovery experiments were conducted to elucidate regulatory pathways.</p><p><strong>Result: </strong>miR-200b expression was significantly higher in SP patients than in CP/HC groups, with an ROC curve AUC of 0.848 distinguishing SP from CP/HC, demonstrating good diagnostic performance. Elevated miR-200b expression significantly correlated with poorer prognostic indicators and served as an independent risk factor for adverse SP outcomes. In vitro experiments demonstrated that miR-200b expression was upregulated in a concentration- and time-dependent manner following LPS stimulation, promoting IL-6 and TNF-α secretion. RHOA was identified as a direct target gene of miR-200b, and miR-200b exerts pro-inflammatory effects by inhibiting RHOA and activating the NF-κB pathway.</p><p><strong>Conclusion: </strong>miR-200b serves as a potential diagnostic and prognostic biomarker for SP. By targeting RHOA to activate the NF-κB pathway, it promotes inflammatory damage in SP, thus providing a novel therapeutic target for clinical intervention.</p>","PeriodicalId":9040,"journal":{"name":"BMC Immunology","volume":" ","pages":""},"PeriodicalIF":2.7,"publicationDate":"2026-05-06","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147833407","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Prognostic significance of inflammatory cytokine polymorphisms in AML: a study of IFNG, TNFA, and IL1B polymorphisms.","authors":"Tsatsralgerel Munkh-Erdene, Takayuki Saitoh, Miri Kitamura, Asumi Kojima, Takafumi Okawa, Tsukasa Oda, Eiji Miyauchi, Nobuo Sasaki, Ikuko Matsumura, Akira Matsumoto, Hisashi Takei, Nobuhiko Kobayashi, Yuri Miyazawa, Yoshiyuki Ogawa, Hiroshi Handa, Nanami Gotoh","doi":"10.1186/s12865-026-00837-5","DOIUrl":"https://doi.org/10.1186/s12865-026-00837-5","url":null,"abstract":"<p><strong>Background: </strong>Inflammatory cytokines influence the pathogenesis and progression of acute myeloid leukaemia (AML), not only by shaping the leukemic microenvironment, but also by supporting leukaemia stem cell survival and resistance to therapy. We, therefore, investigated the associations between the cytokine polymorphisms IFNG+874 A/T, TNFA-857 C/T, and IL1B -31 C/T and AML outcomes, as well as their influence on clinical features.</p><p><strong>Results: </strong>Ninety-three patients with AML and 117 healthy controls were analysed. The T allele of TNFA - 857 C/T (i.e., the high-expression allele) was observed at a significantly higher frequency in the patients with AML vs. the controls (AML vs. control = 24.7% vs. 16.2%, p = 0.04). Patients with the high-expression TT genotype had shorter overall survival (TT vs. CC = 46.0 vs. 224.1 months, p < 0.001). Patients with the high-expression non-CC genotype relapsed more frequently than those with the low-expression CC genotype (relapse vs. non-relapse = 55.8% vs. 26.9%, p = 0.01). No significant associations were observed for the IFNG + 874 A/T and IL1B -31 C/T polymorphism.</p><p><strong>Conclusion: </strong>TNFA - 857 C/T polymorphisms can influence patient susceptibility to AML, as well as its prognosis. This suggests a link between chronic inflammation and leukemogenesis, as well as the potential value of TNFA genotyping in risk assessments.</p>","PeriodicalId":9040,"journal":{"name":"BMC Immunology","volume":" ","pages":""},"PeriodicalIF":2.7,"publicationDate":"2026-05-02","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147811103","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Peripheral immune signatures associated with invasive behavior in pituitary neuroendocrine tumor: a blood-based analysis.","authors":"Hongyu Liu, Liangliang Wu, Chuanbiao Chen, Jialin Liu, Fangye Li, Ling Chen","doi":"10.1186/s12865-026-00840-w","DOIUrl":"https://doi.org/10.1186/s12865-026-00840-w","url":null,"abstract":"<p><strong>Background: </strong>Pituitary neuroendocrine tumors (PitNETs) derived from adenohypophyseal cells are the third most frequent primary intracranial tumor. PitNETs that invades surrounding anatomical structures such as the cavernous sinus are defined as invasive PitNETs. Patients with invasive PitNETs often have co-morbidities and high recurrence rates. This study aimed to identify the cytokines associated with the invasive behavior of PitNETs and characterize the cytokine network and circulating immune cells in the peripheral immune microenvironment of invasive PitNETs.</p><p><strong>Methods: </strong>Peripheral blood samples were collected from 87 patients with PitNET before transsphenoidal surgery for the resection of PitNET. Knosp grade 3 A to 4 tumors on magnetic resonance imaging (MRI) were defined as invasive PitNETs. After strict screening according to the exclusion criteria, 40 patients with invasive PitNET and 41 with noninvasive PitNET were enrolled in this study. Blood samples from 20 patients with invasive PitNET and 21 patients with non-invasive PitNET were randomly selected for multiplex plasma cytokine analysis. In addition, 20 peripheral blood samples were collected from healthy volunteers as controls. Blood samples from the remaining 20 patients with invasive PitNET and 20 patients with non-invasive PitNET were used for peripheral blood cell subpopulation analysis.</p><p><strong>Results: </strong>The expression levels of MIF, MIP-1β, RANTES, IL-9, and TNF-β were increased in the peripheral blood of patients with invasive PitNET. Patients with invasive PitNET had higher levels of CD8⁺ T cells, CD8⁺ memory T cells, CD8⁺ Tregs, CD4⁺ T cells, CD4⁺ activated T cells, CD4⁺ memory T cells, Tregs, and macrophages, and lower levels of natural killer (NK) cells in the peripheral blood.</p><p><strong>Conclusion: </strong>MIF, MIP-1β, RANTES, IL-9, and TNF-β may serve as potential biomarkers for the diagnosis of invasive PitNET. The association between circulating immune cells and the cytokine network in the peripheral immune microenvironment is associated with the invasive behavior of PitNET.</p>","PeriodicalId":9040,"journal":{"name":"BMC Immunology","volume":" ","pages":""},"PeriodicalIF":2.7,"publicationDate":"2026-05-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147811100","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Reduced peripheral natural killer cell counts may be a predictive marker for cesarean scar pregnancy.","authors":"Ye Shen, Jinqiu Zhang, Hua Fang, Li Zhang, Qi Jiang, Hua Gong, Qi Chen, Min Zhao","doi":"10.1186/s12865-026-00841-9","DOIUrl":"https://doi.org/10.1186/s12865-026-00841-9","url":null,"abstract":"<p><p>Cesarean scar pregnancy (CSP), a condition characterised by inflammation, occurs in 0.2% of women with a history of cesarean section(s), and is clinically categorised by type 1 and type 2 according to the ultrasound findings. Recent studies reported that systemic inflammation indices derived from routine whole-blood tests may serve as additional clinical predictive markers for early CSP detection, with lymphocyte counts showing a reduction. However, the specific lymphocyte populations contributing to this reduction remain unclear. This study included 72 women diagnosed with CSP and 50 gestation-matched controls. The subsets of peripheral lymphocytes, including CD45 lymphocytes/monocytes, CD3 T cells, CD4 T helper cells, CD8 cytotoxic T cells, CD19 B cells, total NK cells and NKT-like cells, were measured. We found a significant reduction in peripheral total NK cells and CD8 cytotoxic T cells in CSP women compared to controls. However, there were no differences in peripheral immune cell profiles between type 1 and type 2 CSP. Using total NK cell counts with a cut-off value of 210/µl, the area under the curve (AUC) was 0.698, with a sensitivity of 64%. Our findings suggest that the reduction in peripheral total NK cells and CD8 T cytotoxic cells may play a role in the development of CSP. Additionally, peripheral total NK cell counts, derived from routine whole-blood tests, could serve as a predictive marker for early CSP diagnosis.</p>","PeriodicalId":9040,"journal":{"name":"BMC Immunology","volume":" ","pages":""},"PeriodicalIF":2.7,"publicationDate":"2026-04-30","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147811106","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Evaluation of Th1-Th2 balance in patients with recurrent implantation failure; a systematic review and meta-analysis.","authors":"Armin Derakhshanfar, Alireza Ebrahimi Iraei, Hosein Zarei Sharif, Zahra Yahoo, Maryam Hemmatzadeh, Saeed Aslani, Reza Kargar, Hamed Mohammadi","doi":"10.1186/s12865-026-00815-x","DOIUrl":"https://doi.org/10.1186/s12865-026-00815-x","url":null,"abstract":"","PeriodicalId":9040,"journal":{"name":"BMC Immunology","volume":" ","pages":""},"PeriodicalIF":2.7,"publicationDate":"2026-04-28","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147761304","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Efficiency of bone marrow-derived cells in the treatment of experimental autoimmune type 1 diabetes: immunomodulatory and anti-apoptotic properties.","authors":"Mohamed Nassef, Amira Hafez, Soha Gomaa","doi":"10.1186/s12865-026-00823-x","DOIUrl":"10.1186/s12865-026-00823-x","url":null,"abstract":"","PeriodicalId":9040,"journal":{"name":"BMC Immunology","volume":" ","pages":""},"PeriodicalIF":2.7,"publicationDate":"2026-04-25","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13134314/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147761337","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}