Journal of biomedical nanotechnology最新文献_第4页

Mechanism of miR-190b with Albumin Nanoparticles as Carrier Mediating Islet β Cells in Gestational Diabetes Mellitus 以白蛋白纳米颗粒为载体的 miR-190b 在妊娠糖尿病中介导胰岛 β 细胞的机制

IF 2.9 4区医学

Journal of biomedical nanotechnology Pub Date : 2024-04-01 DOI: 10.1166/jbn.2024.3807

Xing Wang, Yu Lu, Suyu Wang, Xueqin Wang, Shufang Yang, Chengyuan Zhao

{"title":"Mechanism of miR-190b with Albumin Nanoparticles as Carrier Mediating Islet β Cells in Gestational Diabetes Mellitus","authors":"Xing Wang, Yu Lu, Suyu Wang, Xueqin Wang, Shufang Yang, Chengyuan Zhao","doi":"10.1166/jbn.2024.3807","DOIUrl":"https://doi.org/10.1166/jbn.2024.3807","url":null,"abstract":"A variety of diseases are often observed during pregnancy and miR-190b involves in gestational diabetes mellitus (GDM). This study assesses miR-190b’s role in GDM. Electron microscopy analyzed the size of nanoparticles. miR-190b expression in tissues was detected and its effects\u0000 on islet cells were detected by MTT method, BrdU staining method and ELISA method. Insulin secretion was further detected by molecular biology techniques. Electron microscopy showed similar average particle size of each formulation. miR-190b was overexpressed in the placental tissues of GDM\u0000 and its overexpression promoted cell proliferation and insulin secretion, whereas downregulation of miR-190b exerted opposite effects. In addition, miR-190b negatively modulated NKX6-1 level and their relationship was confirmed by bioinformatics techniques and a luciferase reporter gene. NKX6-1\u0000 overexpression reversed miR-190b mimics’ effect, and miR-190b knockdown promoted insulin secretion by upregulating NKX6-1. The inhibitory effect of miR-190b overexpression on islet β cells using nano-albumin particles as a carrier was partially reversed by NKX6-1 overexpression.\u0000 Silencing of miR-190b by nano-albumin particles as a carrier promoted β-cell function, which may be one of the mechanisms by which miR-190b affects GDM.","PeriodicalId":15260,"journal":{"name":"Journal of biomedical nanotechnology","volume":null,"pages":null},"PeriodicalIF":2.9,"publicationDate":"2024-04-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"140354231","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}

引用次数: 0

Potential Role of Odanacatib in the Treatment of Postmenopausal Intervertebral Disc Degeneration 奥达卡替布在治疗绝经后椎间盘退变中的潜在作用

IF 2.9 4区医学

Journal of biomedical nanotechnology Pub Date : 2024-04-01 DOI: 10.1166/jbn.2024.3820

Peng Liu, Songqi Liu, Tiantian Gao, Zhengping Zhang, Junsong Yang, Jijun Liu, Dichen Li

{"title":"Potential Role of Odanacatib in the Treatment of Postmenopausal Intervertebral Disc Degeneration","authors":"Peng Liu, Songqi Liu, Tiantian Gao, Zhengping Zhang, Junsong Yang, Jijun Liu, Dichen Li","doi":"10.1166/jbn.2024.3820","DOIUrl":"https://doi.org/10.1166/jbn.2024.3820","url":null,"abstract":"Odanacatib (ODN), a cathepsin K (CatK) inhibitor, is widely used for the treatment of postmenopausal osteoporosis. However, whether ODN is efficient in delaying intervertebral disc degeneration (IVDD) remaining unknown. We aimed to explore the effect of ODN in the postmenopausal IVDD\u0000 using an ovariectomized (OVX) mouse model. We collected the disc tissues from female spinal fracture patients and analyzed the CatK expression in different estrogen levels. Besides, we injected ranged concentration of OND subcutaneously in the OVX mice and tested the disc height index (DHI),\u0000 aggrecan positive area, collagen I, collagen II, inflammatory factors, and apoptosis-related gene expression comparing to control. The intervertebral disc degraded and the CatK gene expression decreased in the disc lacking of estrogen. OVX method increased the collagen I, MMP-3, MMP-13, caspase-3,\u0000 and caspase-8 expression, but reduced DHI, and the content of aggrecan and collagen II, indicating an IVDD tendency. However, the ODN treatment could suppress MMP-3, MMP-13, caspase-3, and caspase-8 and protect the stability of extracellular matrix (ECM). ODN is a potential drug to delay the\u0000 IVDD by suppressing apoptosis and ECM degradation.","PeriodicalId":15260,"journal":{"name":"Journal of biomedical nanotechnology","volume":null,"pages":null},"PeriodicalIF":2.9,"publicationDate":"2024-04-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"140356087","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}

引用次数: 0

Linc00958 Promotes Lung Cancer Proliferation and Migration Through Regulating microRNA-490-3p Linc00958 通过调控 microRNA-490-3p 促进肺癌增殖和迁移

IF 2.9 4区医学

Journal of biomedical nanotechnology Pub Date : 2024-04-01 DOI: 10.1166/jbn.2024.3817

Kunjie Wang, Lin An, Aimin Zang, Yumiao Li, Yue Huo

{"title":"Linc00958 Promotes Lung Cancer Proliferation and Migration Through Regulating microRNA-490-3p","authors":"Kunjie Wang, Lin An, Aimin Zang, Yumiao Li, Yue Huo","doi":"10.1166/jbn.2024.3817","DOIUrl":"https://doi.org/10.1166/jbn.2024.3817","url":null,"abstract":"This study aimed to investigate the role of long intergenic non-protein coding RNA 00958 (Linc00958) in lung cancer (LCa) progression and its underlying mechanism. The study assessed Linc00958 expression in LCa tissues and adjacent tissues using qRT-PCR, and its impact on patient prognosis\u0000 was analyzed through Kaplan-Meier survival analysis. Additionally, Linc00958 expression in LCa and normal lung cell lines was examined in vitro. Functional assays, including CCK-8, EdU, and transwell assays, were conducted to evaluate the effects of Linc00958 knockdown on LCa cells.\u0000 To uncover the molecular mechanism, a dual-luciferase reporter assay was used to confirm the binding relationship between Linc00958 and microRNA-490-3p, a downstream gene. Co-transfection experiments were performed to elucidate microRNA-490-3p’s role in Linc00958’s impact on LCa\u0000 cell functions. The results showed that Linc00958 was overexpressed in LCa tissues and cells, and high Linc00958 expression correlated with reduced patient survival. in vitro experiments revealed that Linc00958 promoted tumor proliferation and migration in LCa cells. Both computational\u0000 predictions and dual-luciferase reporter assays demonstrated binding sites between microRNA-490-3p and Linc00958. Co-transfection experiments confirmed that Linc00958 facilitated LCa cell proliferation and migration through modulating microRNA-490-3p expression. In summary, Linc00958 promotes\u0000 LCa cell proliferation and migration by regulating microRNA-490-3p.","PeriodicalId":15260,"journal":{"name":"Journal of biomedical nanotechnology","volume":null,"pages":null},"PeriodicalIF":2.9,"publicationDate":"2024-04-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"140357028","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}

引用次数: 0

Effect of Curcumin-Loaded Zein/Polysaccharides Nanoparticles on Fatigue Stress Injury 姜黄素包裹的玉米蛋白/多糖纳米颗粒对疲劳应激损伤的影响

IF 2.9 4区医学

Journal of biomedical nanotechnology Pub Date : 2024-04-01 DOI: 10.1166/jbn.2024.3812

Qin Liu

引用次数: 0

Activation of Nuclear Factor Erythroid 2-Related Factor 2 Antagonizes the Reactive Oxygen Species Modulator 1-Induced Oxidative Stress in Nucleus Pulposus Cells 激活红细胞核因子 2 相关因子 2 可拮抗活性氧调节因子 1 诱导的核浆细胞氧化应激

IF 2.9 4区医学

Journal of biomedical nanotechnology Pub Date : 2024-04-01 DOI: 10.1166/jbn.2024.3819

Weibin Li, Yasen Cao

{"title":"Activation of Nuclear Factor Erythroid 2-Related Factor 2 Antagonizes the Reactive Oxygen Species Modulator 1-Induced Oxidative Stress in Nucleus Pulposus Cells","authors":"Weibin Li, Yasen Cao","doi":"10.1166/jbn.2024.3819","DOIUrl":"https://doi.org/10.1166/jbn.2024.3819","url":null,"abstract":"This study investigates the role of Reactive Oxygen Species Modulator 1 (ROMO1) in oxidative stress within nucleus pulposus (NP) cells and its potential regulation by Nuclear factor erythroid 2-related factor 2 (Nrf2). Intervertebral disc samples from patients were collected, and ROMO1,\u0000 Nrf2, collagen I/II levels were analyzed to establish their potential connection. Human NP cells were cultured and exposed to H2O2 to induce oxidative stress. To elucidate ROMO1’s impact on NP cell metabolism, NP cells were transfected with ROMO1. Concurrently,\u0000 Nrf2 activators and inhibitors were used to modulate Nrf2 expression during culturing. Oxidative stress was assessed through CAT and SOD1 gene expression analysis and measurement of cellular reactive oxygen species (ROS) production. NP cell status was determined by evaluating cell viability\u0000 and collagen I/II expression. Results indicated elevated ROMO1 expression in severe intervertebral disc degeneration (IDD) and after H2O2 treatment. ROMO1 overexpression increased ROS production, suppressed CAT, SOD, and collagen II expression, while elevating collagen I and negatively affecting\u0000 cell viability. However, Nrf2 activation effectively suppressed ROMO1 expression and protected NP cells from oxidative stress induced by H2O2 or ROMO1. In conclusion, ROMO1 exacerbates oxidative stress and contributes to NP cell degeneration, a process mitigated by Nrf2\u0000 activation.","PeriodicalId":15260,"journal":{"name":"Journal of biomedical nanotechnology","volume":null,"pages":null},"PeriodicalIF":2.9,"publicationDate":"2024-04-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"140352914","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}

引用次数: 0

LncRNA BACE1-AS Accelerates the Progression of Gastric Cancer Through Regulating as a ceRNA of miR-422a to Positively Control BRD4 Expression LncRNA BACE1-AS 作为 miR-422a 的 ceRNA 积极控制 BRD4 的表达，从而加速胃癌的进展

IF 2.9 4区医学

Journal of biomedical nanotechnology Pub Date : 2024-04-01 DOI: 10.1166/jbn.2024.3816

Wei Cao, Yang Yang, Xiaosong Wei, Weichang Chen

{"title":"LncRNA BACE1-AS Accelerates the Progression of Gastric Cancer Through Regulating as a ceRNA of miR-422a to Positively Control BRD4 Expression","authors":"Wei Cao, Yang Yang, Xiaosong Wei, Weichang Chen","doi":"10.1166/jbn.2024.3816","DOIUrl":"https://doi.org/10.1166/jbn.2024.3816","url":null,"abstract":"Gastric cancer (GC) is a leading global cause of cancer-related mortality, necessitating urgent research on its pathogenesis, prevention, and treatment. In this study, we investigated the expressions of LncRNA BACE1-AS, mRNA BRD4, and miR-422a in GES-1 and GC cells under various treatments\u0000 using RT-PCR. Western Blots confirmed protein expressions in HGC-27 and SNU-1 cells. EDU and MTT assays assessed cell proliferation, while Transwell tests determined invasion capacity, and flow cytometry analyzed apoptosis. BACE1-AS and BRD4 were significantly elevated in cancerous tissues\u0000 compared to paired non-cancerous tissues. BACE1-AS knockdown inhibited invasion and proliferation, promoting apoptosis. miR-422a mimics suppressed proliferation and invasion while enhancing apoptosis, and miR-422a mimics with BRD4 overexpression had the opposite effect. Moreover, BAX protein\u0000 increased in the si-BACE1-AS group but decreased in the si-BACE1-AS+miR-422a inhibitor group. Si-BACE1-AS and miR-422a mimics reduced the expression of C-Myc, CyclinD1, Survivin, CDK4, and Bcl-2, while the si-BACE1-AS+miR-422a inhibitor and miR-422a mimics+BRD4-OV groups showed the opposite\u0000 trend. Our findings suggest that LncRNA BACE1-AS positively regulates gastric cancer progression by modulating BRD4 as a competitive endogenous RNA for miR-422a. This LncRNA BACE1-AS/BRD4/miR-422a signaling axis presents potential targets for developing therapeutic strategies against gastric\u0000 cancer.","PeriodicalId":15260,"journal":{"name":"Journal of biomedical nanotechnology","volume":null,"pages":null},"PeriodicalIF":2.9,"publicationDate":"2024-04-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"140356871","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}

引用次数: 0

Novel Synthesis of Fluorescein Isothiocyanate-Based Fluorescent Nanoprobes in Imaging Lung Inflammation 基于异硫氰酸荧光素的荧光纳米探针在肺部炎症成像中的新型合成方法

IF 2.9 4区医学

Journal of biomedical nanotechnology Pub Date : 2024-04-01 DOI: 10.1166/jbn.2024.3795

Li Dai, Wenjun Wang, Jie Yan, Yong Liu

引用次数: 0

Down-Regulation Assession of Methyl CpG Binding Protein 2 in Diabetic Nephropathy 糖尿病肾病中甲基 CpG 结合蛋白 2 的降调分析

IF 2.9 4区医学

Journal of biomedical nanotechnology Pub Date : 2024-04-01 DOI: 10.1166/jbn.2024.3811

Yanyan Li, Zugui Huang, Chaoqun You, Qiao Chen, Dezhi Kong, Qifeng Wei, Bin Deng, Ting Chen, Zhanlin Liao, Liangzhi Huang

{"title":"Down-Regulation Assession of Methyl CpG Binding Protein 2 in Diabetic Nephropathy","authors":"Yanyan Li, Zugui Huang, Chaoqun You, Qiao Chen, Dezhi Kong, Qifeng Wei, Bin Deng, Ting Chen, Zhanlin Liao, Liangzhi Huang","doi":"10.1166/jbn.2024.3811","DOIUrl":"https://doi.org/10.1166/jbn.2024.3811","url":null,"abstract":"Diabetes nephropathy (DN) is the most significant microvascular complication of diabetes worldwide due to hyperglycemiainduced podocyte injury and apoptosis. The role of methyl CpG binding protein 2 (MECP2) has been observed, but its specific involvement in DN remains unclear. In this\u0000 study, an in vitro DN model was established using human glomerular podocytes exposed to high glucose (HG, 30 mM). MECP2 expression was assessed using qRT-PCR and Western Blot. Proliferation and migration were evaluated through CCK-8 and transwell assays in both the HG group and the HG + MECP2\u0000 knockdown group. Apoptosis was assessed by flow cytometry and Western Blot. RNA-Sequencing identified differentially expressed genes (DEGs) between HG and HG+MECP2 knockdown groups, with subsequent enrichment analysis using KEGG and GSEA databases. Our results revealed elevated MECP2 expression\u0000 in HG-treated podocytes compared to the control group. Podocytes with MECP2 knockdown displayed increased proliferation and migration compared to the HG group. MECP2 knockdown significantly inhibited HG-induced apoptosis in podocytes, with lower expression of pro-apoptotic protein (cleaved-caspase3,\u0000 Bax, BAD, Desmin) and higher expression of anti-apoptotic protein Bcl-2 in the HG+MECP2 shRNA group. RNA sequencing identified 123 upregulated and 129 downregulated DEGs. Enrichment analysis highlighted apoptosis-related pathways like PPAR, TNF, p53, RELAXIN, WNT, and RAP1 signaling. Podocytes\u0000 with MECP2 knockdown showed reduced apoptosis upon HG treatment. In summary, downregulation of MECP2 in podocytes effectively mitigated apoptosis caused by high glucose, suggesting a potential strategy to improve diabetes nephropathy outcomes.","PeriodicalId":15260,"journal":{"name":"Journal of biomedical nanotechnology","volume":null,"pages":null},"PeriodicalIF":2.9,"publicationDate":"2024-04-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"140772717","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}

引用次数: 0

Polydopamine Nanoparticles Activate Apelin/Apelin Receptor Signaling and Smad3 to Inhibit Tumor Cells in Lung Cancer 多多巴胺纳米粒子激活杏仁蛋白/杏仁蛋白受体信号和 Smad3，抑制肺癌中的肿瘤细胞

IF 2.9 4区医学

Journal of biomedical nanotechnology Pub Date : 2024-04-01 DOI: 10.1166/jbn.2024.3806

Wuxin Yu, Yuxin Liu, Xiangning Lan, Yanjuan Zhou, Qiang Wang

{"title":"Polydopamine Nanoparticles Activate Apelin/Apelin Receptor Signaling and Smad3 to Inhibit Tumor Cells in Lung Cancer","authors":"Wuxin Yu, Yuxin Liu, Xiangning Lan, Yanjuan Zhou, Qiang Wang","doi":"10.1166/jbn.2024.3806","DOIUrl":"https://doi.org/10.1166/jbn.2024.3806","url":null,"abstract":"Lung cancer incidence is increasing and different concentrations of polydopamine nanoparticles may exert different anticancer effects. Apelin/APJ plays a certain role in lung cancer. This study focuses on the mechanism of polydopamine nanoparticles in Apelin/APJ signaling pathway activation\u0000 Smad3 on tumor cells in lung cancer rats. 40 rats were randomly assigned into blank group, model group, low-dose, medium-dose, and high-dose groups of polydopamine nanoparticles followed by analysis of tumor weight, Apelin, APJ, Smad3 gene expression, tumor cell viability, cell apoptosis,\u0000 Apelin, APJ, and Smad3 level. Polydopamine nanoparticles were successfully prepared. The polydopamine nanoparticle groups significantly inhibited tumor weight, and the medium-dose group decreased the most. And the groups significantly inhibited the gene expression of Apelin and APJ, with more\u0000 inhibition in medium-dose group, P < 0.05. The polydopamine nanoparticle groups significantly up-regulated Smad3, inhibited tumor cell viability, and promoted apoptosis with significant changes in medium-dose group. In addition, the groups inhibited the protein expression of Apelin\u0000 and APJ, and up-regulated Smad3, with more increase of Smad3 in medium-dose group, P < 0.05. Polydopamine nanoparticles may block the combination of Apelin and APJ by inhibiting the activity of Apelin/APJ pathway, which leads to further activation of Smad3, therefore inhibiting proliferation\u0000 and promoting apoptosis of lung cancer cells. This process is related to down-regulation of Apelin expression.","PeriodicalId":15260,"journal":{"name":"Journal of biomedical nanotechnology","volume":null,"pages":null},"PeriodicalIF":2.9,"publicationDate":"2024-04-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"140353180","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}

引用次数: 0

ASAP1 Promotes Cholangiocarcinoma Progression via Wnt/β-Catenin Pathway ASAP1 通过 Wnt/β-Catenin 通路促进胆管癌进展

IF 2.9 4区医学

Journal of biomedical nanotechnology Pub Date : 2024-04-01 DOI: 10.1166/jbn.2024.3814

Jiaqi He, Han Liu, Jianhua Cai, Sheng Shen, Ji-wen Wang, Houbao Liu

{"title":"ASAP1 Promotes Cholangiocarcinoma Progression via Wnt/β-Catenin Pathway","authors":"Jiaqi He, Han Liu, Jianhua Cai, Sheng Shen, Ji-wen Wang, Houbao Liu","doi":"10.1166/jbn.2024.3814","DOIUrl":"https://doi.org/10.1166/jbn.2024.3814","url":null,"abstract":"This study sought to identify the relationship between ADP-ribosylation factor GTpase-activating protein (ASAP1) expression and clinical outcomes in Cholangiocarcinoma (CC) patients. Quantitative real-time PCR (qRT-PCR), Western blotting, and immunohistochemistry were used to analyze\u0000 the expression of ASAP1 in CC tissue samples and cell lines (IHC). The survival rate and clinicopathological characteristics were also examined. Cell counting kit-8 (CCK-8), colony formation, and 5-ethynyl-2′-deoxyuridine (EdU) assays were used to detect cell proliferation. Flow cytometry\u0000 was used to assess the cell cycle. The terminal deoxynucleotidyl transferase (TdT)-mediated dUTP nick-end labeling (TUNEL) test and flow cytometry were used to identify cell apoptosis. Xenograft tumor development in living mice was reported. ASAP1 expression was increased and associated with\u0000 a poor prognosis in CC tissue samples. The expression of ASAP1 was associated with the tumor’s histological grade and size in clinical specimens. In vitro and in vivo, knocking down ASAP1 expression resulted in decreased ASAP1 cell proliferation, inhibited cell cycle progression,\u0000 and increased apoptosis. ASAP1 cholangiocarcinoma controls the Wnt/β-catenin pathway’s activity, encourages cell apoptosis, migration, and invasion in culture, and fosters tumor development in vivo. ASAP1 was crucial to the origin and growth of CC tumors, which could\u0000 be a beneficial treatment target for CC.","PeriodicalId":15260,"journal":{"name":"Journal of biomedical nanotechnology","volume":null,"pages":null},"PeriodicalIF":2.9,"publicationDate":"2024-04-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"140353753","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}

引用次数: 0