Translational Research最新文献

{"title":"Mechanism of adipose-derived stem cell-derived extracellular vesicles affecting macrophage efferocytosis by mediating ADAM17/MerTK in the apoptosis of tubular epithelial cells after sepsis-associated acute kidney injury","authors":"Zhixiang Bian,&nbsp;Xiangxiang Wang,&nbsp;Xiaoxuan Su,&nbsp;Ming Yang,&nbsp;Rui Zhu,&nbsp;Shunjie Chen","doi":"10.1016/j.trsl.2025.05.002","DOIUrl":"10.1016/j.trsl.2025.05.002","url":null,"abstract":"<div><h3>Objective</h3><div>This study explored the molecular mechanism of adipose-derived stem cell-derived extracellular vesicles (ADSC-EVs) improving post-sepsis-associated acute kidney injury (S-AKI) tubular epithelial cell (TEC) apoptosis by modulating ADAM17/MerTK-mediated macrophage efferocytosis.</div></div><div><h3>Methods</h3><div>The S-AKI mouse model was established by caecal ligation and puncture and intravenously injected with ADSC-EVs. Mouse kidney macrophages were cultured with LPS, cultured with EVs while transfecting with oe-ADAM17 or si-MerTK, then incubated with Jurkat cells. Mouse serum urea and creatinine, and KIM-1, efferocytosis- and apoptosis-related protein, inflammatory factor, cytokine, and soluble MerTK (sMerTK) levels were determined using colorimetric assay, immunohistochemistry, Western blot, and ELISA. Renal tubular injury, TEC apoptosis, macrophage efferocytosis, and M1/M2 polarization levels were assessed via HE staining, TUNEL staining, immunofluorescence, and flow cytometry, respectively. <em>In vivo</em> validation experiments were conducted.</div></div><div><h3>Results</h3><div>S-AKI mice displayed elevated levels of serum urea, creatinine, KIM-1, pro-inflammatory factors, pro-apoptotic proteins and ADAM17 protein, decreased anti-apoptotic protein and MerTK protein levels, and diminished M2 polarization. ADSC-EVs down-regulated ADAM17 and sMerTK, and increased cell membrane MerTK, macrophage recognition of apoptotic cells and efferocytosis, and M2 polarization in renal tissues of S-AKI mice and LPS-induced mouse renal macrophages, indicating that ADSC-EVs regulated ADAM17/MerTK-mediated macrophage efferocytosis and promoted M2 polarization. MerTK silencing partially reversed ADSC-EVs-regulated LPS-induced mouse renal macrophage efferocytosis and M2 polarization. <em>In vivo</em>, ADAM17 upregulation partly averted ADSC-EVs-regulated post-S-AKI TEC apoptosis in mouse renal tissues.</div></div><div><h3>Conclusion</h3><div>ADSC-EVs down-regulated sMerTK level and up-regulated macrophage membrane MerTK protein level by modulating ADAM17 to promote macrophage efferocytosis and ameliorate post-S-AKI TEC apoptosis and inflammation.</div></div>","PeriodicalId":23226,"journal":{"name":"Translational Research","volume":"281 ","pages":"Pages 14-30"},"PeriodicalIF":6.4,"publicationDate":"2025-05-20","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144129922","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Modeling diabetic epitheliopathy using 3D-Organotypic corneal epithelium","authors":"Grazia Maugeri ,&nbsp;Agata Grazia D’Amico ,&nbsp;Salvatore Saccone ,&nbsp;Francesca Bruno ,&nbsp;Elisabetta Pricoco ,&nbsp;Davide Scollo ,&nbsp;Teresio Avitabile ,&nbsp;Antonio Longo ,&nbsp;Velia D’Agata","doi":"10.1016/j.trsl.2025.05.003","DOIUrl":"10.1016/j.trsl.2025.05.003","url":null,"abstract":"<div><div>Diabetic keratopathy (DK) is a degenerative corneal disease occurring in more than 50 % of diabetic patients. DK is correlated with the hyperglycemic state causing morphological and functional changes in corneal layers. Currently, most studies on the cornea are performed on two-dimensional (2D) cultures <em>in vitro</em> or animal models. Although 2D culture models can provide large amounts of data at low cost, they poorly represent the complex pathophysiology of the human cornea and hardly predict <em>in vivo</em> responses that can be achieved with animal model studies. However, the use of the latter presents ethical problems. Therefore, it is necessary to identify new strategies and models that can integrate the information validly and effectively, to reduce the number of animals used. Here, we used human corneal epithelial cells (hCECs) derived from donor cornea differentiated into three-dimensional (3D)-organotypic air-liquid interface (ALI), which resemble the features of the corneal epithelium. The 3D-organotypic ALI corneal epithelium was subjected to high-glucose conditions to generate a model of diabetic epitheliopathy. Our model showed well-established molecular and cellular characteristics of this pathology, such as epithelial defects and inflammation, with increased expression of IL-1β, TNF-<span><math><mi>α</mi></math></span>, p-NF-kB, COX-2, MMP-2 and MMP-9. The data provided highlight the utility of 3D-organotypic corneal epithelium in modeling diabetic epitheliopathy, offering new avenues in drug screening, as well as in precision and personalized medicine.</div></div>","PeriodicalId":23226,"journal":{"name":"Translational Research","volume":"280 ","pages":"Pages 55-63"},"PeriodicalIF":6.4,"publicationDate":"2025-05-17","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144103120","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Abundance of dopamine and its receptors in the brain and adipose tissue following diet-induced obesity or caloric restriction","authors":"Fleur W Hukema ,&nbsp;Susanne Hetty ,&nbsp;Christakis Kagios ,&nbsp;Sofia Zelleroth ,&nbsp;Giovanni Fanni ,&nbsp;Maria J Pereira ,&nbsp;Maria K Svensson ,&nbsp;Magnus Sundbom ,&nbsp;Anna Nilsson ,&nbsp;Per E Andrén ,&nbsp;Erika Roman ,&nbsp;Jan W Eriksson","doi":"10.1016/j.trsl.2025.05.001","DOIUrl":"10.1016/j.trsl.2025.05.001","url":null,"abstract":"<div><div>While obesity and type 2 diabetes (T2D) are associated with altered dopaminergic activity in the central nervous system and in adipose tissue (AT), the directions and underlying mechanisms remain inconclusive. Therefore, we characterized changes in the abundance of dopamine, its metabolites, and receptors DRD1 and DRD2 in the brain and AT upon dietary intervention or obesity. Male Wistar rats were fed either a standard pellet diet, a cafeteria diet inducing obesity and insulin resistance, or a calorie-restricted diet for 12 weeks. Abundance of dopamine and its receptors DRD1 and DRD2 were examined in brain regions relevant for feeding behavior and energy homeostasis. Furthermore, DRD1 and DRD2 protein levels were analyzed in rat inguinal and epidydimal AT and in human subcutaneous and omental AT from individuals with or without obesity. Rats with diet-induced obesity displayed higher dopamine levels, as well as DRD1 or DRD2 receptor levels in the caudate putamen and the nucleus accumbens core. Surprisingly, caloric restriction induced similar changes in DRD1 and DRD2, but not in dopamine levels, in the brain. Both diets reduced DRD1 abundance in inguinal and epidydimal AT, but upregulated DRD2 levels in inguinal AT. Furthermore, in human obesity, DRD1 protein levels were elevated only in omental AT, while DRD2 was upregulated in both omental and subcutaneous AT. These findings highlight dopaminergic responses to changes in energy balance, occurring both in the brain and AT. We propose that dopaminergic pathways are involved in tissue crosstalk during the development of obesity and T2D.</div></div>","PeriodicalId":23226,"journal":{"name":"Translational Research","volume":"280 ","pages":"Pages 41-54"},"PeriodicalIF":6.4,"publicationDate":"2025-05-08","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143948444","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Information for Readers","authors":"","doi":"10.1016/S1931-5244(25)00045-3","DOIUrl":"10.1016/S1931-5244(25)00045-3","url":null,"abstract":"","PeriodicalId":23226,"journal":{"name":"Translational Research","volume":"279 ","pages":"Page IBC"},"PeriodicalIF":6.4,"publicationDate":"2025-05-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143886500","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Editorial Advisory Board","authors":"","doi":"10.1016/S1931-5244(25)00043-X","DOIUrl":"10.1016/S1931-5244(25)00043-X","url":null,"abstract":"","PeriodicalId":23226,"journal":{"name":"Translational Research","volume":"279 ","pages":"Page ii"},"PeriodicalIF":6.4,"publicationDate":"2025-05-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143886498","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Author Guidelines","authors":"","doi":"10.1016/S1931-5244(25)00044-1","DOIUrl":"10.1016/S1931-5244(25)00044-1","url":null,"abstract":"","PeriodicalId":23226,"journal":{"name":"Translational Research","volume":"279 ","pages":"Pages iii-iv"},"PeriodicalIF":6.4,"publicationDate":"2025-05-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143886499","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Cardioprotective effects of PARP Inhibitors: A meta-analysis of animal studies","authors":"Seong Kyung Kim ,&nbsp;Jae Hyun Kim ,&nbsp;Inyeong Moon ,&nbsp;Jiwon Min ,&nbsp;Jieun Park ,&nbsp;Myeong Gyu Kim","doi":"10.1016/j.trsl.2025.04.004","DOIUrl":"10.1016/j.trsl.2025.04.004","url":null,"abstract":"<div><div>Poly(adenosine diphosphate [ADP] ribose) polymerase (PARP) inhibitors are expected to provide benefits to the cardiovascular system. However, the cardioprotective effect of PARP inhibitors has not been systematically reviewed or quantitatively analyzed. This study aimed to assess the cardioprotective effects of PARP inhibitors through a meta-analysis of animal studies. Three databases PubMed, Web of Sciences, and Embase were searched until September 1, 2023. The risk of bias was assessed using SYRCLE’s Risk of Bias. A total of 74 animal studies that investigated the cardiac function of PARP inhibitors compared to placebo or vehicle, were included. Outcome measures were hemodynamic indexes, cardiac contractility, and biomarkers of myocardial injury. Pooled effect size was estimated using a random-effects model with RevMan 5.4. PARP inhibitors were associated with enhanced hemodynamic indexes, including cardiac output (standardized mean difference, 0.86 [95 % CI, 0.54 to 1.17]; <em>p</em> &lt; 0.00001) and stroke volume (0.42 [0.07 to 0.76]; <em>p</em> = 0.02). PARP inhibitors were associated with increased cardiac contractility, including ejection fraction (0.71 [0.42 to 1.01]; <em>p</em> &lt; 0.00001) and fractional shortening (0.96 [0.62 to 1.31]; <em>p</em> &lt; 0.00001). PARP inhibitors were associated with decreased troponin І (-1.42 [-2.16 to -0.68]; <em>p</em> = 0.0002), plasma B-type natriuretic peptide (-0.95 [-1.56 to -0.33]; <em>p</em> = 0.003), creatine kinase (-1.81 [-2.63 to -0.99]; <em>p</em> &lt; 0.0001), and infarct size (-1.58 [-2.01 to -1.14]; <em>p</em> &lt; 0.00001). PARP inhibitors improve cardiac functions and attenuate myocardial injury in animals, which indicate the cardioprotective effects. Further human studies are necessary.</div></div>","PeriodicalId":23226,"journal":{"name":"Translational Research","volume":"280 ","pages":"Pages 29-40"},"PeriodicalIF":6.4,"publicationDate":"2025-04-30","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143921176","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"tiRNA-HAR contributes to ischemic myocardial injury via facilitating HuR-mediated stability of p53","authors":"Changhao Wang ,&nbsp;Yuelin Gao ,&nbsp;Kuiwu Liu ,&nbsp;Yaozhi Zhang ,&nbsp;Zhiyong Sun ,&nbsp;Min Huang ,&nbsp;Zhezhe Qu ,&nbsp;Shuting Yu ,&nbsp;Jiaqi Han ,&nbsp;Zhongting Mei ,&nbsp;Shunkang Dou ,&nbsp;Jianhao Jiang ,&nbsp;Ying Li ,&nbsp;Na Li ,&nbsp;Chuanhao Huang ,&nbsp;Yuechao Dong ,&nbsp;Baofeng Yang ,&nbsp;Weijie Du","doi":"10.1016/j.trsl.2025.04.002","DOIUrl":"10.1016/j.trsl.2025.04.002","url":null,"abstract":"<div><div>Cardiomyocyte death due to heart occlusion of coronary artery is the main driver to myocardial infarction (MI) and subsequent heart failure progression. tsRNA, a small RNA fragment from tRNA, has been shown to be implicated in many physiological and pathological processes by exerting different biological functions, but the roles of tsRNA in ischemic cardiac injury remain to be determined. The present study identified a hypoxia responsive-tiRNA (tiRNA-HAR) was markedly upregulated in ischemic mouse myocardium and hypoxic cardiomyocytes, respectively. Enforced expression of tiRNA-HAR by transfecting its mimic caused and aggravated, while knockdown of tiRNA-HAR mitigated cardiomyocyte apoptosis upon hypoxia. Cardiac specific knockdown of tiRNA-HAR mediated by AAV9 (adeno-associated virus 9) harboring an antisense oligonucleotide reduced cardiomyocytes apoptosis and improved cardiac function after MI. Mechanistically, tiRNA-HAR directly bound to HuR and enhanced the binding capacity of HuR and p53, thereby increasing the stability of p53. Silencing of HuR partially reversed the aggravative effects of tiRNA-HAR overexpression on cardiomyocyte apoptosis in the context of hypoxia. Collectively, our study reveals that tiRNA-HAR play a critical role in regulating cardiomyocytes apoptosis and cardiac injury via targeting HuR/p53 signaling axis after MI, and tiRNA-HAR might be a novel therapeutic target for treatment of ischemic heart disease.</div></div>","PeriodicalId":23226,"journal":{"name":"Translational Research","volume":"280 ","pages":"Pages 17-28"},"PeriodicalIF":6.4,"publicationDate":"2025-04-17","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143906469","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Loss of peptidylarginine deiminase 4 mitigates maladaptive cardiac remodeling after myocardial infarction through inhibition of inflammatory and profibrotic pathways","authors":"Michelle Holthaus ,&nbsp;Xiaolin Xiong ,&nbsp;Kaveh Eghbalzadeh ,&nbsp;Clara Großmann ,&nbsp;Simon Geißen ,&nbsp;Fabian Piontek ,&nbsp;Martin Mollenhauer ,&nbsp;Ali T. Abdallah ,&nbsp;Thomas Kamphausen ,&nbsp;Markus Rothschild ,&nbsp;Thorsten Wahlers ,&nbsp;Adnana Paunel-Görgülü","doi":"10.1016/j.trsl.2025.04.003","DOIUrl":"10.1016/j.trsl.2025.04.003","url":null,"abstract":"<div><div>Inflammation and progressive fibrosis represent predictive risk factors for heart failure (HF) development following myocardial infarction (MI). Peptidylargininine deiminase 4 (PAD4) catalyzes the citrullination of arginine residues in polypeptides and has recently been identified as a contributor to HF pathogenesis. This study aimed to evaluate the role of PAD4 in monocytes / macrophages (Mo/Mφ) and cardiac fibroblasts (CFs) for cardiac repair following MI and HF progression. Cardiac <em>Padi4</em> expression significantly increased in mice subjected to MI by permanent coronary artery ligation as well as in humans who died from MI. Transcriptome analysis revealed marked downregulation of inflammation-related genes in infarcted hearts and cardiac Mo/Mφ from global PAD4 knockout (PAD4^−/−) mice on day 7 post-MI accompanied by increased frequency of reparative CD206⁺ macrophages. Mechanistically, pharmacological and genetic PAD4 inhibition abrogated nuclear NF-κB translocation and inflammatory gene expression in bone marrow-derived macrophages (BMDM). Simultaneously, reduced inflammation and diminished cardiac levels of transforming growth factor-β (TGF-β) along with impaired IL-6 / TGF-β signaling in PAD4^−/− CFs were associated with decreased expression of fibrotic genes, reduced collagen deposition, improved cardiac function, and enhanced 28-day survival in PAD4^−/− mice. Strikingly, whereas pharmacological PAD inhibition in the acute phase after MI exacerbated cardiac damage, treatment starting on day 7 ameliorated cardiac remodeling and improved long-term survival in mice. Collectively, we here identified PAD4 as a critical regulator of inflammatory genes in Mo/Mφ and of profibrotic pathways in CFs. Thus, therapeutic approaches directed against PAD4 are promising interventions to alleviate adverse cardiac remodeling and subsequent HF development.</div></div>","PeriodicalId":23226,"journal":{"name":"Translational Research","volume":"280 ","pages":"Pages 1-16"},"PeriodicalIF":6.4,"publicationDate":"2025-04-17","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143906470","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Kv1.3 expression on CD4 (+) T cells promotes interleukin-17A-associated airway inflammation and airway remodeling in asthma","authors":"Bingqing Sun ,&nbsp;Jiangtao Lin","doi":"10.1016/j.trsl.2025.04.001","DOIUrl":"10.1016/j.trsl.2025.04.001","url":null,"abstract":"<div><h3>Background</h3><div>Different types of T helper cells play an important role in disease severity and treatment response in patients with asthma. The potassium channel Kv1.3 is a type of potentially therapeutic target in T-cell-mediated inflammatory diseases.</div></div><div><h3>Objective</h3><div>This study aimed to explore the potential of Kv1.3 as a therapeutic target for asthma and to assess the efficacy of the Kv1.3 inhibitor PAP-1 in the treatment of asthma.</div></div><div><h3>Methods</h3><div>Kv1.3 expression on CD4⁺T cells was determined using data from public databases. CD4⁺T cells were isolated from peripheral blood samples obtained from healthy individuals and patients with asthma. The mouse models of OVA-induced asthma and Kv1.3 knockout were established. The underlying mechanism was investigated using mouse splenic CD4⁺T cells and BEAS-2B cells. OVA-induced asthmatic mice were treated with the Kv1.3 selective blocker PAP-1.</div></div><div><h3>Results</h3><div>Based on public data, we determined the distribution of Kv1.3 on CD4⁺T cells, its up-regulation in asthma, and its correlation with Th17/Treg balance. Upregulation of Kv1.3 in CD4⁺T cells was associated with enhanced activation of these cells and airway inflammation in patients and mice with asthma, accompanied by increased IL-17A levels in alveolar lavage fluid. Conversely, Kv1.3 deficiency significantly attenuated airway inflammation, lowered IL-17A levels in bronchoalveolar lavage fluid, and inhibited airway epithelial-mesenchymal transition in asthmatic mice. Furthermore, treatment with the Kv1.3 selective blocker PAP-1 attenuated inflammation in lung tissues and prevented airway remodeling in OVA-induced asthmatic mice.</div></div><div><h3>Conclusions</h3><div>Kv1.3 expression on CD4⁺ T cells was correlated with IL-17A-associated airway inflammation and remodeling in asthma, which may be regarded as a potential diagnostic marker and therapeutic target for asthma.</div></div><div><h3>Translational significance</h3><div>Based on our study, Kv1.3 expression on CD4⁺T cells was correlated with IL-17A-associated airway inflammation and remodeling in asthma, which may be regarded as a potential diagnostic marker and therapeutic target for asthma. The treatment with the Kv1.3 selective blocker PAP-1 attenuated inflammation in lung tissues and prevented airway remodeling in OVA-induced asthmatic mice. Our discoveries offer novel perspectives for a better understanding of IL-17A-associated airway remodeling in asthma. The development of drugs targeting Kv1.3 holds application value for IL-17A-associated asthma.</div></div>","PeriodicalId":23226,"journal":{"name":"Translational Research","volume":"279 ","pages":"Pages 40-54"},"PeriodicalIF":6.4,"publicationDate":"2025-04-10","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143860264","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}