Experimental biology and medicine (Maywood, N.J.)最新文献

{"title":"MiR-200c-3p increased HDMEC proliferation through the notch signaling pathway.","authors":"Xianyu Hu,&nbsp;Suwen Bai,&nbsp;Lingyi Li,&nbsp;Pengfei Tian,&nbsp;Sun Wang,&nbsp;Ning Zhang,&nbsp;Bing Shen,&nbsp;Juan Du,&nbsp;Shengxiu Liu","doi":"10.1177/1535370220981859","DOIUrl":"https://doi.org/10.1177/1535370220981859","url":null,"abstract":"<p><p>Excessive proliferation of vascular endothelial cells can cause hemangioma. Although typically benign, hemangiomas can become life-threatening. The microRNA miR-200c-3p is abnormally expressed in some types of tumors, but its expression, biological role, and mechanism of action in infantile hemangioma remain to be fully elucidated. The expression levels of miR-200c-3p in hemangioma tissue were compared with those in adjacent healthy tissue by using bioinformatics analyses and TargetScan. Western blot, enzyme-linked immunosorbent assay, and Cell Counting Kit 8 analyses were used to determine the biological function and site of action of miR-200c-3p in human dermal microvascular endothelial cells (HDMECs). MiR-200c-3p was one of the top 10 differentially expressed genes between healthy tissue, and hemangiomas tissues, having markedly decreased expression in hemangioma tissue. Reduction of miR-200c-3p expression in HDMECs through the transfection of a miR-200c-3p inhibitor significantly increased HDMEC proliferation. The addition of the Notch signaling pathway inhibitor DAPT to HDMECs transfected with the miR-200c-3p inhibitor eliminated the inhibitor-induced enhancement of proliferation in HDMECs. These findings indicate that miR-200c-3p targets the Notch signaling pathway to promote the proliferation of vascular endothelial cells, suggesting that miR-200c-3p plays an important role in the pathogenesis of hemangioma.</p>","PeriodicalId":520623,"journal":{"name":"Experimental biology and medicine (Maywood, N.J.)","volume":" ","pages":"897-905"},"PeriodicalIF":3.2,"publicationDate":"2021-04-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1177/1535370220981859","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"38840677","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"SIRT3 deficiency increases mitochondrial oxidative stress and promotes migration of retinal pigment epithelial cells.","authors":"Jing-Xian Wang,&nbsp;Yuan Yang,&nbsp;Wen-Ying Li","doi":"10.1177/1535370220976073","DOIUrl":"https://doi.org/10.1177/1535370220976073","url":null,"abstract":"<p><p>Retinal pigment epithelial cells are closely associated with the pathogenesis of diabetic retinopathy. The mechanism by which diabetes impacts retinal pigment epithelial cell function is of significant interest. Sirtuins are an important class of proteins that primarily possess nicotinamide adenine dinucleotide-dependent deacetylases activity and involved in various cellular physiological and pathological processes. Here, we aimed to examine the role of sirtuins in the induction of diabetes-associated retinal pigment epithelial cell dysfunction. High glucose and platelet-derived growth factor (PDGF) treatment induced epithelial-mesenchymal transition and the migration of retinal pigment epithelial cells, and decreased sirtuin-3 expression. Sirtuin-3 knockdown using siRNA increased epithelial-mesenchymal transition and migration of retinal pigment epithelial cells. In contrast, sirtuin-3 overexpression attenuated the effects caused by high glucose and PDGF on epithelial-mesenchymal transition and migration of retinal pigment epithelial cells, suggesting that sirtuin-3 deficiency contributed to retinal pigment epithelial cell dysfunction induced by high glucose and PDGF. Mechanistically, sirtuin-3 deficiency induced retinal pigment epithelial cell dysfunction by the overproduction of mitochondrial reactive oxygen species. These results suggest that sirtuin-3 deficiency mediates the migration of retinal pigment epithelial cells, at least partially by increasing mitochondrial oxidative stress, and shed light on the importance of sirtuin-3 and mitochondrial reactive oxygen species as potential targets in diabetic retinopathy therapy.</p>","PeriodicalId":520623,"journal":{"name":"Experimental biology and medicine (Maywood, N.J.)","volume":" ","pages":"877-887"},"PeriodicalIF":3.2,"publicationDate":"2021-04-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1177/1535370220976073","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"38802192","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Retinol-binding protein, retinol, and modified-relative-dose response in Ugandan children aged 12-23 months and their non-pregnant caregivers.","authors":"Ralph D Whitehead,&nbsp;Nicole D Ford,&nbsp;Carine Mapango,&nbsp;Laird J Ruth,&nbsp;Ming Zhang,&nbsp;Rosemary L Schleicher,&nbsp;Sarah Ngalombi,&nbsp;Siti Halati,&nbsp;Martin Ahimbisibwe,&nbsp;Abdelrahman Lubowa,&nbsp;Jesse Sheftel,&nbsp;Sherry A Tanumihardjo,&nbsp;Maria Elena D Jefferds","doi":"10.1177/1535370220985473","DOIUrl":"https://doi.org/10.1177/1535370220985473","url":null,"abstract":"<p><p>Retinol-binding protein (RBP), retinol, and modified-relative-dose response (MRDR) are used to assess vitamin A status. We describe vitamin A status in Ugandan children and women using dried blood spot (DBS) RBP, serum RBP, plasma retinol, and MRDR and compare DBS-RBP, serum RBP, and plasma retinol. Blood was collected from 39 children aged 12-23 months and 28 non-pregnant mothers aged 15-49 years as a subsample from a survey in Amuria district, Uganda, in 2016. DBS RBP was assessed using a commercial enzyme immunoassay kit, serum RBP using an in-house sandwich enzyme-linked immunosorbent assay, and plasma retinol/MRDR test using high-performance liquid chromatography. We examined (a) median concentration or value (Q1, Q3); (b) <i>R</i>² between DBS-RBP, serum RBP, and plasma retinol; and (c) Bland-Altman plots. Median (Q1, Q3) for children and mothers, respectively, were as follows: DBS-RBP 1.15 µmol/L (0.97, 1.42) and 1.73 (1.52, 1.96), serum RBP 0.95 µmol/L (0.78, 1.18) and 1.47 µmol/L (1.30, 1.79), plasma retinol 0.82 µmol/L (0.67, 0.99) and 1.33 µmol/L (1.22, 1.58), and MRDR 0.025 (0.014, 0.042) and 0.014 (0.009, 0.019). DBS RBP-serum RBP <i>R</i>² was 0.09 for both children and mothers. The mean biases were -0.19 µmol/L (95% limits of agreement [LOA] 0.62, -0.99) for children and -0.01 µmol/L (95% LOA -1.11, -1.31) for mothers. DBS RBP-plasma retinol <i>R</i>² was 0.11 for children and 0.13 for mothers. Mean biases were 0.33 µmol/L (95% LOA -0.37, 1.03) for children, and 0.29 µmol/L (95% LOA -0.69, 1.27) for mothers. Serum RBP-plasma retinol <i>R</i>² was 0.75 for children and 0.55 for mothers, with mean biases of 0.13 µmol/L (95% LOA -0.23, 0.49) for children and 0.18 µmol/L (95% LOA -0.61, 0.96) for mothers. Results varied by indicator and matrix. The serum RBP-retinol <i>R</i>² for children was moderate (0.75), but poor for other comparisons. Understanding the relationships among vitamin A indicators across contexts and population groups is needed.</p>","PeriodicalId":520623,"journal":{"name":"Experimental biology and medicine (Maywood, N.J.)","volume":" ","pages":"906-915"},"PeriodicalIF":3.2,"publicationDate":"2021-04-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1177/1535370220985473","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"38836651","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Particulate matter inhalation and the exacerbation of cardiopulmonary toxicity due to metabolic disease.","authors":"Lisa Kobos,&nbsp;Jonathan Shannahan","doi":"10.1177/1535370220983275","DOIUrl":"https://doi.org/10.1177/1535370220983275","url":null,"abstract":"<p><p>Particulate matter is a significant public health issue in the United States and globally. Inhalation of particulate matter is associated with a number of systemic and organ-specific adverse health outcomes, with the pulmonary and cardiovascular systems being particularly vulnerable. Certain subpopulations are well-recognized as being more susceptible to inhalation exposures, such as the elderly and those with pre-existing respiratory disease. Metabolic syndrome is becoming increasingly prevalent in our society and has known adverse effects on the heart, lungs, and vascular systems. The limited evaluations of individuals with metabolic syndromehave demonstrated that theymay compose a sensitive subpopulation to particulate exposures. However, the toxicological mechanisms responsible for this increased vulnerability are not fully understood. This review evaluates the currently available literature regarding how the response of an individual's pulmonary and cardiovascular systems is influenced by metabolic syndrome and metabolic syndrome-associated conditions such as hypertension, dyslipidemia, and diabetes. Further, we will discuss potential therapeutic agents and targets for the alleviation and treatment of particulate-matter induced metabolic illness. The information reviewed here may contribute to the understanding of metabolic illness as a risk factor for particulate matter exposure and further the development of therapeutic approaches to treat vulnerable subpopulations, such as those with metabolic diseases.</p>","PeriodicalId":520623,"journal":{"name":"Experimental biology and medicine (Maywood, N.J.)","volume":" ","pages":"822-834"},"PeriodicalIF":3.2,"publicationDate":"2021-04-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1177/1535370220983275","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"38841080","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Antibody-based delivery of interleukin-9 to neovascular structures: Therapeutic evaluation in cancer and arthritis.","authors":"Baptiste Gouyou,&nbsp;Tiziano Ongaro,&nbsp;Samuele Cazzamalli,&nbsp;Roberto De Luca,&nbsp;Anne Kerschenmeyer,&nbsp;Philippe Valet,&nbsp;Alessandra Villa,&nbsp;Dario Neri,&nbsp;Mattia Matasci","doi":"10.1177/1535370220981578","DOIUrl":"https://doi.org/10.1177/1535370220981578","url":null,"abstract":"<p><p>Interleukin-9 is a cytokine with multiple functions, including the ability to activate group 2 innate lymphoid cells, which has been postulated to be therapeutically active in mouse models of arthritis. Similarly, interleukin-9 has been suggested to play an important role in tumor immunity. Here, we describe the cloning, expression, and characterization of three fusion proteins based on murine interleukin-9 and the F8 antibody, specific to the alternatively spliced EDA domain of fibronectin. EDA is strongly expressed in cancer and in various arthritic conditions, while being undetectable in the majority of healthy organs. Interleukin-9-based fusion proteins with an irrelevant antibody specific to hen egg lysozyme served as negative control in our study. The fusion proteins were characterized by quantitative biodistribution analysis in tumor-bearing mice using radioiodinated protein preparations. The highest tumor uptake and best tumor:organ ratios were observed for a format, in which the interleukin-9 moiety was flanked by two units of the F8 antibody in single-chain Fv format. Biological activity of interleukin-9 was retained when the payload was fused to antibodies. However, the targeted delivery of interleukin-9 to the disease site resulted in a modest anti-tumor activity in three different murine models of cancer (K1735M2, CT26, and F9), while no therapeutic benefit was observed in a collagen induced model of arthritis. Collectively, these results confirm the possibility to deliver interleukin-9 to the site of disease but cast doubts about the alleged therapeutic activity of this cytokine in cancer and arthritis, which has been postulated in previous publications.</p>","PeriodicalId":520623,"journal":{"name":"Experimental biology and medicine (Maywood, N.J.)","volume":" ","pages":"940-951"},"PeriodicalIF":3.2,"publicationDate":"2021-04-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1177/1535370220981578","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"38843161","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Analyses of short-chain fatty acids and exhaled breath volatiles in dietary intervention trials for metabolic diseases.","authors":"Jisun Hj Lee,&nbsp;Jiangjiang Zhu","doi":"10.1177/1535370220979952","DOIUrl":"https://doi.org/10.1177/1535370220979952","url":null,"abstract":"<p><p>As an alternative to pharmacological treatment to diseases, lifestyle interventions, such as dietary changes and physical activities, can help maintain healthy metabolic conditions. Recently, the emerging analyses of volatile organic compounds (VOCs) from breath and short-chain fatty acids (SCFAs) from plasma/feces have been considered as useful tools for the diagnosis and mechanistic understanding of metabolic diseases. Furthermore, diet-induced changes of SCFAs in individuals with diagnosed metabolic abnormalities have been correlated with the composition changes of the gut microbiome. More interestingly, the analysis of exhaled breath (breathomics) has gained attention as a useful technique to measure the human VOC profile altered as a result of dietary interventions. In this mini-review, we examined recent clinical trials that performed promising dietary interventions, SCFAs analysis in plasma/feces, and VOC profile analysis in exhaling breath to understand the relationship between dietary intervention and metabolic health.</p>","PeriodicalId":520623,"journal":{"name":"Experimental biology and medicine (Maywood, N.J.)","volume":" ","pages":"778-789"},"PeriodicalIF":3.2,"publicationDate":"2021-04-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1177/1535370220979952","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"38380074","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"YAP activation in melanoma contributes to anoikis resistance and metastasis.","authors":"Bei Zhao,&nbsp;Jun Xie,&nbsp;Xiyuan Zhou,&nbsp;Lixia Zhang,&nbsp;Xiankui Cheng,&nbsp;Chenglin Liang","doi":"10.1177/1535370220977101","DOIUrl":"https://doi.org/10.1177/1535370220977101","url":null,"abstract":"<p><p>Melanoma is inherently heterogeneous, providing resistance to apoptosis. Anoikis resistance is a hallmark feature of metastatic melanoma to escape apoptosis when cells lose contact with adjacent cells or extracellular matrix. The yes-associated protein transcription co-activator is the effector of Hippo pathway. Herein, we investigated the function of yes-associated protein in anoikis resistance of melanoma cells. When melanoma cells were grown under anchorage-independent condition, anoikis-resistant cells displayed higher levels of yes-associated protein activation than the cells that were attached to the basement membrane, as evidenced by downregulated phosphorylated yes-associated protein at Ser127 and higher expression of downstream genes <i>BCL2</i> and <i>MCL-1</i>. Yes-associated protein overexpression directly enhanced the anoikis resistance and metastatic potential of melanoma cells. Conversely, yes-associated protein inhibitor CA3 exhibited Dose-dependent induction of anoikis in resistant melanoma cells and exerted great inhibition on cell migration. Knockdown of yes-associated protein expression by shRNA also rendered melanoma cells susceptible to anoikis and interrupted cell invasiveness. Yes-associated protein inhibition in anoikis-resistant cells also reduced the number of metastatic nodules in the lung sections of SCID mice. Clinically, higher yes-associated protein level in the lung metastasis tissues correlated with higher BCL2 and MCL1 expressions compared with the non-metastasis tissues. Overall, our finding suggests that the aberrant activation of yes-associated protein exerts important role on anoikis resistance and metastatic capability of melanoma cells.</p>","PeriodicalId":520623,"journal":{"name":"Experimental biology and medicine (Maywood, N.J.)","volume":" ","pages":"888-896"},"PeriodicalIF":3.2,"publicationDate":"2021-04-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1177/1535370220977101","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"38700781","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Emerging roles for lymphatics in acute kidney injury: Beneficial or maleficent?","authors":"Heidi A Creed,&nbsp;Joseph M Rutkowski","doi":"10.1177/1535370220983235","DOIUrl":"https://doi.org/10.1177/1535370220983235","url":null,"abstract":"<p><p>Acute kidney injury, a sudden decline in renal filtration, is a surprisingly common pathology resulting from ischemic events, local or systemic infection, or drug-induced toxicity in the kidney. Unchecked, acute kidney injury can progress to renal failure and even recovered acute kidney injury patients are at an increased risk for developing future chronic kidney disease. The initial extent of inflammation, the specific immune response, and how well inflammation resolves are likely determinants in acute kidney injury-to-chronic kidney disease progression. Lymphatic vessels and their roles in fluid, solute, antigen, and immune cell transport make them likely to have a role in the acute kidney injury response. Lymphatics have proven to be an attractive target in regulating inflammation and immunomodulation in other pathologies: might these strategies be employed in acute kidney injury? Acute kidney injury studies have identified elevated levels of lymphangiogenic ligands following acute kidney injury, with an expansion of the lymphatics in several models post-injury. Manipulating the lymphatics in acute kidney injury, by augmenting or inhibiting their growth or through targeting lymphatic-immune interactions, has met with a range of positive, negative, and sometimes inconclusive results. This minireview briefly summarizes the findings of lymphatic changes and lymphatic roles in the inflammatory response in the kidney following acute kidney injury to discuss whether renal lymphatics are a beneficial, maleficent, or a passive contributor to acute kidney injury recovery.</p>","PeriodicalId":520623,"journal":{"name":"Experimental biology and medicine (Maywood, N.J.)","volume":" ","pages":"845-850"},"PeriodicalIF":3.2,"publicationDate":"2021-04-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1177/1535370220983235","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"38840594","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Minireview: Insights into anti-interferon-γ autoantibodies.","authors":"Kriangkrai Chawansuntati,&nbsp;Kritsadee Rattanathammethee,&nbsp;Jiraprapa Wipasa","doi":"10.1177/1535370220981579","DOIUrl":"https://doi.org/10.1177/1535370220981579","url":null,"abstract":"<p><p>The association between the presence of anti-interferon-γ autoantibodies and the onset of immunodeficiency with intracellular infections has been clearly established. No standard regimen to control the production of these pathogenic autoantibodies, apart from antimicrobial therapy to eliminate infections, contributes to the medical burden of this syndrome, which sometimes has a fatal outcome. In this review, we summarize the findings on anti-interferon-γ autoantibodies to facilitate further research and to provide guidance for treatment strategies.</p>","PeriodicalId":520623,"journal":{"name":"Experimental biology and medicine (Maywood, N.J.)","volume":" ","pages":"790-795"},"PeriodicalIF":3.2,"publicationDate":"2021-04-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1177/1535370220981579","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"38808061","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Method used to establish a large animal model of drug-induced acute kidney injury.","authors":"Si-Yang Wang,&nbsp;Chao-Yang Zhang,&nbsp;Guang-Yan Cai,&nbsp;Xiang-Mei Chen","doi":"10.1177/1535370220981756","DOIUrl":"https://doi.org/10.1177/1535370220981756","url":null,"abstract":"<p><p>Acute kidney injury is a serious health hazard disease due to its complex etiology and lack of effective treatments, resulting in high medical costs and high mortality. At present, a large number of basic research studies on acute kidney injury have been carried out. However, acute kidney injury models established in rodents sometimes do not simulate the course of human disease well. Research in large animal models of acute kidney injury is relatively rare, and methods to build a mature model of acute kidney injury have failed. Because its kidney anatomy and morphology are very similar to those in humans, the mini pig is an ideal animal in which to model kidney disease. Nephrotoxic drug-induced acute kidney injury has a high incidence. In this study, we established models of acute kidney injury induced by two drugs (gentamicin and cisplatin). Finally, the model of cisplatin-induced acute kidney injury was developed successfully, but we found the model of gentamycin-induced acute kidney injury was not reproducible. Compared to other models, these models better represent acute kidney injury caused by antibiotics and chemotherapeutic drugs and provide a basis for the study of new treatments for acute kidney injury in a large animal model.</p>","PeriodicalId":520623,"journal":{"name":"Experimental biology and medicine (Maywood, N.J.)","volume":" ","pages":"986-995"},"PeriodicalIF":3.2,"publicationDate":"2021-04-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1177/1535370220981756","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"38836650","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}