Cardiovascular Research最新文献

{"title":"A new PCSK-9 monoclonal antibody for lowering LDL-cholesterol and lipoprotein(a) in Chinese patients with familial hypercholesterolaemia.","authors":"Seyed Saeed Tamehri Zadeh,Dick C Chan,Gerald F Watts","doi":"10.1093/cvr/cvaf160","DOIUrl":"https://doi.org/10.1093/cvr/cvaf160","url":null,"abstract":"","PeriodicalId":9638,"journal":{"name":"Cardiovascular Research","volume":"35 1","pages":""},"PeriodicalIF":10.8,"publicationDate":"2025-09-10","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145031716","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Toll-like receptor 4 induces trained innate immune tolerance in the heart in a model of stress-induced cardiomyopathy.","authors":"Kenji Rowel Q Lim,Junedh Amrute,Attila Kovacs,Abhinav Diwan,David L Williams,Douglas L Mann","doi":"10.1093/cvr/cvaf158","DOIUrl":"https://doi.org/10.1093/cvr/cvaf158","url":null,"abstract":"AIMSAlthough the ability of the heart to adapt to environmental stress has been studied extensively, the molecular and cellular mechanisms responsible for cardioprotection are not yet fully understood. In this study, we sought to elucidate these mechanisms for cytoprotection using a model of stress-induced cardiomyopathy.METHODS AND RESULTSWe administered Toll-like receptor (TLR) agonists or diluent to wild-type mice and assessed for cardioprotection against injury from a high intraperitoneal dose of isoproterenol (ISO) administered 7 days later. Cardioprotective effects were analyzed through serum cardiac troponin I levels, immune profiling via flow cytometry, echocardiography, and multiomic single-nuclei RNA/ATAC sequencing. Pretreatment with the TLR4 agonist lipopolysaccharide (LPS), but not TLR1/2 or TLR3 agonists, conferred cardioprotection, as demonstrated by reduced cardiac troponin I leakage, decreased inflammation, preserved cardiac structure and function, and improved survival. Remarkably, LPS-induced tolerance was reversed by β-glucan treatment. Multiomic analysis showed that LPS-tolerized hearts had greater chromatin accessibility and upregulated gene expression versus hearts treated with LPS and β-glucan (reverse-tolerized). LPS tolerance was associated with upregulation of interferon response pathways across various cell types, including cardiac myocytes and stromal cells. Blocking both type 1 and 2 interferon signaling eliminated LPS-induced tolerance against ISO, while pretreatment with recombinant type 1 and 2 interferons conferred cardiac protection. Multiomic sequencing further revealed enhanced cytoprotective signaling in interferon-treated hearts. Analysis of cell-cell communication networks indicated increased autocrine signaling by cardiac myocytes, as well as greater paracrine signaling between stromal cells and myeloid cells, in LPS-tolerized versus reverse-tolerized hearts.CONCLUSIONSLPS pretreatment confers cardiac protection against ISO-induced injury through TLR4-mediated type 1 and 2 interferon signaling, consistent with trained innate immune tolerance. The observation that LPS-induced protection in cardiac myocytes involves both cell-autonomous and non-cell-autonomous mechanisms underscores the complexity of innate immune tolerance in the heart, warranting further investigation into this cardioprotective phenotype.","PeriodicalId":9638,"journal":{"name":"Cardiovascular Research","volume":"35 1","pages":""},"PeriodicalIF":10.8,"publicationDate":"2025-09-09","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145025443","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Microplastics and nanoplastics: tiny threats for cardiovascular diseases?","authors":"Raffaele Marfella,Francesco Prattichizzo,Giuseppe Paolisso","doi":"10.1093/cvr/cvaf143","DOIUrl":"https://doi.org/10.1093/cvr/cvaf143","url":null,"abstract":"","PeriodicalId":9638,"journal":{"name":"Cardiovascular Research","volume":"83 1","pages":""},"PeriodicalIF":10.8,"publicationDate":"2025-09-08","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145008790","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Recaticimab in adult heterozygous familial hypercholesterolemia (REMAIN-3): A multicentre, randomised, double-blind, placebo-controlled phase 3 study","authors":"Liwen Li, Yujie Zhou, Chanjuan Deng, Jianlong Sheng, Daoquan Peng, Zhiyu Ling, Luya Wang, Cuilian Dai, Kai Huang, Qiufang Lian, Zaixin Yu, Haibo Yang, Yuying Hu, YuGang Dong, Nan Wang, Zhen Wang, Wei Zhang, Xuebin Han, Zhuhua Yao, Qiyun Liu, Yingzi Liang, Biao Xu, Ying Wang, Tingyan Zhong, Jiyan Chen","doi":"10.1093/cvr/cvaf155","DOIUrl":"https://doi.org/10.1093/cvr/cvaf155","url":null,"abstract":"Aims Heterozygous familial hypercholesterolemia (HeFH) is a genetic disorder, characterised by high plasma concentrations of low-density lipoprotein cholesterol (LDL-C) from birth. This study aimed to assess the efficacy and safety of recaticimab, a new humanised anti-PCSK9 antibody capable of reducing LDL-C levels in patients with poorly controlled HeFH. Methods and Results REMAIN-3 was a multicentre, randomised, double-blind, placebo-controlled phase 3 study done at 25 sites in China. Patients with a genetic or clinical diagnosis of HeFH, who were on stable lipid-lowering therapy for ≥28 days, had fasting LDL-C ≥2.6 mmol/L (or ≥1.8 mmol/L for those with a history of atherosclerotic cardiovascular disease), and had fasting triglyceride ≤5.6 mmol/L, were randomly allocated in a 2:1 ratio to receive subcutaneous recaticimab at 150 mg or matching placebo every 4 weeks for 12 weeks. The primary endpoint was the percentage change in LDL-C from baseline to week 12. Overall, 143 patients underwent randomisation and received recaticimab (n = 95) or placebo (n = 48). At week 12, the mean percentage change in LDL-C from baseline was -54.4% (95% CI, -57.9% to -50.8%) in the recaticimab group and -4.5% (95% CI, -9.4% to 0.3%) in the placebo group, with a treatment difference of -49.8% (95% CI, -55.8% to -43.9%; p < 0.0001). Recaticimab was superior to placebo in improving other lipid variables, including non-high-density lipoprotein cholesterol, apolipoprotein B, and lipoprotein a. Treatment-related adverse events (TRAEs) were comparable between groups (27.4% with recaticimab vs. 25.0% with placebo). The most common TRAEs occurring more frequently with recaticimab than placebo were injection site reaction (8.4% vs. 0%) and increased blood creatine phosphokinase (5.3% vs. 2.1%). Conclusions Recaticimab significantly lowered the LDL-C level compared with placebo, with an acceptable safety profile, providing a new effective treatment option for patients with inadequately controlled HeFH. ClinicalTrials.gov Identifier NCT04844125","PeriodicalId":9638,"journal":{"name":"Cardiovascular Research","volume":"15 1","pages":""},"PeriodicalIF":10.8,"publicationDate":"2025-09-05","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145003104","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Modulating myocardial metabolism in preclinical hypertrophic cardiomyopathy (HCM) pathogenic variant carriers: a window of opportunity or wishful thinking?","authors":"Betty Raman,Emil Brociek","doi":"10.1093/cvr/cvaf157","DOIUrl":"https://doi.org/10.1093/cvr/cvaf157","url":null,"abstract":"","PeriodicalId":9638,"journal":{"name":"Cardiovascular Research","volume":"33 1","pages":""},"PeriodicalIF":10.8,"publicationDate":"2025-09-05","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145002804","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"In PLN-R14del mice, SR structure restoration, rather than calcium cycling, is the dominant effector of PLN-ASO treatment.","authors":"Liu Sun,Tim R Eijgenraam,Carl Amilon,David Janzén,Kenny M Hansson,Dieter A Kubli,Daniela Später,Adam E Mullick,Peter van der Meer,Vivian Oliveira Nunes Teixeira,Herman H W Silljé","doi":"10.1093/cvr/cvaf156","DOIUrl":"https://doi.org/10.1093/cvr/cvaf156","url":null,"abstract":"AIMSPhospholamban (PLN) acts as an inhibitory regulator of calcium uptake in the sarco-/endoplasmic reticulum (SR) of cardiomyocytes. The pathogenic variant, PLN-R14del, leads to dilated and/or arrhythmogenic cardiomyopathy. Previous studies demonstrated that PLN-targeting antisense oligonucleotides (ASOs) can mitigate disease progression in mice. However, it remains unclear whether the protective effects of PLN-ASO therapy are due to improved calcium homeostasis or via reduction of abnormal PLN-SR clusters, a hallmark of this disease.METHODS AND RESULTS: Homozygous PLN-R14del (R14Δ/Δ) mice were randomized to injections with various doses of PLN-ASO (3, 7, 15 or 25 mg/kg) or a scrambled control. Consistent with previous findings, R14Δ/Δ mice exhibited severe cardiac dysfunction, myocardial fibrosis, and aberrant SR clusters by 7 weeks of age. ASO-treated R14Δ/Δ mice displayed a dose-dependent preservation of cardiac function with diminished remodeling and extended lifespan. Correspondingly, abnormal PLN-SR clustering was diminished by ASO therapy in a dose-dependent manner, and SR structure returned to a normal state. Calcium dynamics were investigated separately on isolated cardiomyocytes from treated mice. In wild-type (WT) mice, ASO (25 mg/kg) mediated PLN depletion significantly enhanced calcium and contractile dynamics, confirming effective target engagement. In R14Δ/Δ cardiomyocytes, however, ASO treatment showed limited effects on calcium dynamics. Calcium transient decay and sarcomeric shortening were already enhanced in R14Δ/Δ cardiomyocytes compared to WT, suggesting a partial loss of the PLN-R14del calcium inhibitory function. This preexisting acceleration of calcium dynamics likely accounts for the limited impact of ASO therapy on calcium regulation in R14Δ/Δ mice.CONCLUSIONSPLN-ASO treatment demonstrated a dose-dependent restoration of SR organization and a concomitant increase in lifespan in PLN-R14del mice. The enhanced SR calcium uptake in PLN-R14del mice suggests a partial loss of inhibitory function, limiting ASO therapy's effects on calcium dynamics. This implies that PLN-ASO therapy acts predominantly via restoration of SR structure in PLN-R14del cardiomyopathy.","PeriodicalId":9638,"journal":{"name":"Cardiovascular Research","volume":"52 1","pages":""},"PeriodicalIF":10.8,"publicationDate":"2025-09-04","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144962675","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"In vitro and in vivo disease models of cardiac amyloidosis: progress, pitfalls and potential","authors":"Jiabin Qin, Zeping Qiu, Yingze Fan, Qipeng Xiong, Zhiyong Lei, Jin Wei, Pim van der Harst, Monique C Minnema, Joost P G Sluijter, Alain van Mil, Marish I F J Oerlemans","doi":"10.1093/cvr/cvaf152","DOIUrl":"https://doi.org/10.1093/cvr/cvaf152","url":null,"abstract":"Amyloid light chain (AL) and transthyretin amyloidosis (ATTR)-induced cardiomyopathy are life-threatening protein misfolding disorders characterized by amyloid fibril deposition in the heart, which significantly impairs cardiac function. The lack of representative disease models has impeded progress in understanding the underlying mechanisms and hindered the discovery and development of specific biomarkers and effective therapies. To address this, researchers have developed various cell and animal models to recapitulate these diseases. In AL amyloidosis, cell and mouse models have highlighted the toxic effects of both soluble light chains (LCs) and LC-derived amyloid fibrils, such as lysosomal dysfunction, ER stress, and oxidative stress. Transgenic mouse models, particularly those without mouse heavy chain and with amyloid seeds addition, have successfully replicated systemic AL amyloidosis, with clear effects on the heart. For ATTR amyloidosis, acid-induced transthyretin (TTR) fibrils induce cellular dysfunction, such as increased intracellular ROS level, disorganized sarcomere and prolonged calcium handling in 2D cell models. Transgenic mouse models expressing human WT or variant TTR have offered insights into development of amyloid cardiomyopathy, but challenges persist in fully replicating the human phenotype. This review offers a comprehensive overview of the significant advancements, challenges and future perspectives in the development of various cell and animal models for studying AL and ATTR amyloidosis-induced cardiomyopathy, thereby providing valuable insights into disease pathophysiology, early accurate biomarkers identification and development of novel therapies.","PeriodicalId":9638,"journal":{"name":"Cardiovascular Research","volume":"69 1","pages":""},"PeriodicalIF":10.8,"publicationDate":"2025-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144928253","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Vascular regenerative deficiencies in people with elevated lipoprotein(a): the Lp(a)-VRCE CardioLink-16 translational study","authors":"Michael Moroney, Jack H Casey, Hwee Teoh, Aishwarya Krishnaraj, Yi Pan, Adrian Quan, Shubh K Patel, Fallon Dennis, Arianna Z He, Brady Park, Raj Verma, Elizabeth Misner, Ryuta Seguchi, Syed M Ali Hassan, Cole J Dennis, Gus Meglis, Ambarish Pandey, Javed Butler, Cyril David Mazer, Robert A Byrne, Marlys L Koschinsky, David A Hess, Subodh Verma","doi":"10.1093/cvr/cvaf142","DOIUrl":"https://doi.org/10.1093/cvr/cvaf142","url":null,"abstract":"Aims Lipoprotein(a) [Lp(a)] is a causal risk factor for atherosclerotic cardiovascular disease (ASCVD); however, the relationship between Lp(a) and the capacity for vascular repair remains unclear. Depletion of vascular regenerative (VR) progenitor cells has been shown to be a novel indicator of compromised vascular repair in people living with cardiometabolic disorders. The purpose of this study was to determine if elevated levels of Lp(a) modify VR cell content properties. Methods and results The cross-sectional, multi-site Lipoprotein(a) and Vascular Regenerative Cell Content CardioLink-16 [Lp(a)-VRCE] study enrolled 40 individuals—20 with Lp(a) ≥100 nmol/L and 20 with Lp(a) <100 nmol/L. Isolated peripheral blood mononuclear cells were analysed by multi-parameter flow cytometry. VR progenitor cells were identified based on high aldehyde dehydrogenase (ALDH) activity, in combination with primitive vs. mature lineage-specific cell surface markers. The Lp(a) ≥100 nmol/L group exhibited baseline characteristic differences compared with the Lp(a) <100 nmol/L group such as lower estimated glomerular filtration rate (86.9 vs. 100.1 mL/min/1.73 m2), lower total cholesterol (4.0 vs. 4.8 mmol/L), greater statin use (90 vs. 60%), and a higher prevalence of ASCVD (60 vs. 25%). The Lp(a) ≥100 nmol/L group had lower frequencies of pro-angiogenic ALDHhiSSClowCD133+ (P = 0.0008) and ALDHhiSSClowCD34+CD133+ (P = 0.005) progenitor cells with pro-angiogenic secretory function. Compared with those in the Lp(a) <100 nmol/L group, individuals in the Lp(a) ≥100 nmol/L group demonstrated a higher frequency of M1-polarized pro-inflammatory monocytes (ALDHhiSSCmidCD86+CD163−; P = 0.007) and a lower frequency of ALDHhiSSChiCD49d+ granulocyte precursor cells (P = 0.04) that are involved in vessel repair. Conclusion In this translational study, people with an Lp(a) ≥100 nmol/L had fewer VR cells and more pro-inflammatory polarized monocyte precursor cells than those with Lp(a) levels <100 nmol/L. These findings suggest that vessel repair activities may be compromised in individuals with elevated Lp(a) levels. Registration Lp(a)-VRCE ClinicalTrials.gov: NCT06626659","PeriodicalId":9638,"journal":{"name":"Cardiovascular Research","volume":"66 1","pages":""},"PeriodicalIF":10.8,"publicationDate":"2025-08-30","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144930640","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Effects of iron deficiency anemia on maternal hemodynamics and cardiac function in pregnant spontaneously hypertensive rats","authors":"Jad-Julian R Rachid, Jennie Vu, Si Ning Liu, Sareh Panahi, Navdeep S Badhan, Claudia D Holody, Rohini Roy Roshmi, Alyssa R Wiedemeyer, Ronan M N Noble, Stephane L Bourque","doi":"10.1093/cvr/cvaf149","DOIUrl":"https://doi.org/10.1093/cvr/cvaf149","url":null,"abstract":"Aim Hypertensive disorders of pregnancy (HDP) are characterized by adverse or inadequate maternal cardiovascular adaptations and are associated with poor perinatal outcomes. Iron deficiency (ID) is a common pregnancy complication that elicits numerous cardiovascular adaptations. Though generally considered deleterious in pregnancy, whether ID mitigates or exacerbates maternal cardiovascular dysfunction in HDP has not been investigated. Methods and Results Pregnant spontaneously hypertensive rats (SHR) and normotensive Wistar Kyoto (WKY) rats were fed either an iron-replete or an iron-restricted diet prior to and throughout pregnancy. Pregnant dams underwent tail-cuff plethysmography and echocardiography throughout pregnancy, as well as pressure-volume loop assessments and in-vivo blood pressure (BP) measurements on GD21 (term=GD22). Data were analyzed by 2-Way ANOVA with Holm-Šídák's post-hoc test. Dietary iron restriction caused progressive BP lowering throughout gestation that was most apparent in SHR dams. By GD21, all ID dams had moderate anemia, whereas ID fetuses of both strains exhibited signs of severe anemia, asymmetric growth restriction, and placentomegaly. Maternal ID was associated with left ventricular remodeling in both strains, albeit circulating NT-proBNP levels—a marker of pathological stretch—were reduced in ID-SHR dams. Maternal ID hearts exhibited enhanced ventricular performance reflected by increased stroke volume and cardiac output relative to their iron-replete counterparts. ID also improved cardiac efficiency and ventriculo-arterial coupling, and these latter effects were most pronounced in SHR dams. Conclusions ID in pregnancy was associated with greater BP lowering and improved cardiac performance in SHR dams compared to normotensive WKY dams, albeit ID fetuses from both strains exhibited growth restriction and placentomegaly. These findings highlight a complex interaction between ID anemia in pre-existing hypertension in pregnancy, and if translated to humans, could have important implications for the identification and management of both prevalent health conditions.","PeriodicalId":9638,"journal":{"name":"Cardiovascular Research","volume":"20 1","pages":""},"PeriodicalIF":10.8,"publicationDate":"2025-08-29","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144915743","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Trajectories of cardiovascular ageing-from molecular mechanisms to clinical implementation.","authors":"Stefano Ministrini, Florian A Wenzl, Thomas F Lüscher, Giovanni G Camici","doi":"10.1093/cvr/cvae178","DOIUrl":"10.1093/cvr/cvae178","url":null,"abstract":"<p><p>Due to its peculiar structure and function, the cardiovascular system is particularly vulnerable to the detrimental effects of ageing. Current knowledge about the molecular mechanisms of ageing revealed the processes actively promoting ageing, e.g. progressive telomere shortening, and the mechanisms opposing it, e.g. endogenous production of antioxidant substances. This knowledge can be used to measure biological age at cellular and molecular levels and to interfere with it by pharmacological or non-pharmacological interventions. Biological ageing is determined by the simultaneous occurrence of independent hallmarks, which encompass a wide range of biological processes, from genomic changes to systemic inflammation and dysbiosis. This narrative review will summarize the role of ageing hallmarks in the cardiovascular system, how they can be measured, and what are the possible interventions to counteract their effects.</p>","PeriodicalId":9638,"journal":{"name":"Cardiovascular Research","volume":" ","pages":"1509-1523"},"PeriodicalIF":13.3,"publicationDate":"2025-08-28","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12391673/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142035340","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}