Vascular pharmacology最新文献

{"title":"Indobufen versus aspirin in patients with indication for antiplatelet therapy: A systematic review and meta-analysis","authors":"Deivyd Vieira Silva Cavalcante ,&nbsp;Mrinal Murali Krishna ,&nbsp;Meghna Joseph ,&nbsp;Ana Clara Felix de Farias Santos ,&nbsp;Beatriz Ximenes Mendes ,&nbsp;Nicole Asbeg ,&nbsp;Wilton Francisco Gomes","doi":"10.1016/j.vph.2025.107465","DOIUrl":"10.1016/j.vph.2025.107465","url":null,"abstract":"<div><h3>Introduction</h3><div>Aspirin is commonly recommended for individuals who have experienced stroke or myocardial infarction (MI). Indobufen, a cyclooxygenase-1 inhibitor, has been studied as a potential alternative. We conducted a meta-analysis and trial sequential analysis (TSA) to compare indobufen with aspirin in patients requiring antiplatelet therapy.</div></div><div><h3>Methods</h3><div>We searched PubMed, Scopus, and Cochrane Central for studies that compared indobufen and aspirin antiplatelet therapies. We focused on efficacy outcomes, such as composite vascular events, MI, and ischemic stroke, and safety outcomes, such as major bleeding and any bleeding. Heterogeneity was assessed using I2 statistics, and our analysis followed the PRISMA guidelines.</div></div><div><h3>Results</h3><div>The review included 5 studies with 11,943 patients (indobufen <em>n</em> = 5952, 49.84 %), three involving post-MI and two involving post-stroke patients. No significant differences were found between the groups in composite vascular events at 90 days (RR 0.84; 95 % CI 0.46–1.53; <em>p</em> = 0.560; I2 = 53 %) and 1-year (RR 1.13; 95 % CI 0.99–1.29; <em>p</em> = 0.08; I2 = 0 %). MI (RR 0.73; 95 % CI 0.43–1.22; <em>p</em> = 0.22; I2 = 0 %), ischemic stroke (RR 1.16; 95 % CI 0.99–1.37; <em>p</em> = 0.06; I2 = 0 %), and cardiovascular death (RR 1.35; 95 % CI 0.80–2.26; <em>p</em> = 0.257; I2 = 0 %) at 1-year also showed no significant differences. Major bleeding at 1 year (RR 0.73; 95 % CI 0.41–1.31; <em>p</em> = 0.297; I2 = 64 %) was comparable, but any bleeding at 1 year showed a significant difference (RR 0.65; 95 % CI 0.43–0.98; <em>p</em> = 0.03; I2 = 87 %) favoring indobufen. Subgroup analysis of RCTs showed marginally significant increased risk regarding ischemic stroke with indobufen (RR 1.18; 95 % CI 1.00–1.39; <em>p</em> = 0.05).</div></div><div><h3>Conclusion</h3><div>The efficacy and safety of antiplatelet therapy with indobufen were comparable to those of aspirin alone. Therefore, indobufen can be considered as a suitable alternative for patients who are intolerant or hypersensitive to aspirin. Nevertheless, additional trials involving larger populations are required to establish their clinical applicability.</div></div>","PeriodicalId":23949,"journal":{"name":"Vascular pharmacology","volume":"158 ","pages":"Article 107465"},"PeriodicalIF":3.5,"publicationDate":"2025-01-23","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143042498","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"The lncRNA DSCR9 is modulated in pulmonary arterial hypertension endothelial cell models and is associated with alterations in the nitric oxide pathway","authors":"N. Bernardi ,&nbsp;B.F. Neep ,&nbsp;S. Garibaldi ,&nbsp;E. Bianconi ,&nbsp;J. Aman ,&nbsp;A. Llucià-Valldeperas ,&nbsp;D. Sirello ,&nbsp;G. Zoppoli ,&nbsp;F.S. de Man ,&nbsp;P. Ameri","doi":"10.1016/j.vph.2025.107464","DOIUrl":"10.1016/j.vph.2025.107464","url":null,"abstract":"<div><div>Long non-coding RNA (lncRNA) may be involved in dysfunction of pulmonary artery endothelial cells (PAEC) and, thus, in pulmonary arterial hypertension (PAH) pathobiology.</div><div>We screened the RNA expression profile of commercial human PAEC (hPAEC) exposed to increased hydrostatic pressure, and found that the lncRNA Down syndrome critical region 9 (DSCR9) was the most regulated transcript (log2FC 1.89 vs control). We confirmed by RT-qPCR that DSCR9 levels were higher in PAEC isolated from patients with idiopathic PAH (iPAH-PAEC), as well as in induced pluripotent stem cell-derived endothelial cells (iPSC-EC) from a patient with <em>BMPR2</em>-mutated PAH, than in relevant controls. Moreover, a re-analysis of the publicly available <span><span>GSE117261</span><svg><path></path></svg></span> microarray dataset revealed that DSCR9 was upregulated in the lung tissue of PAH patients. In silico simulation indicated that DSCR9 would be mainly located in the nucleus and could interact with calcium/calmodulin-dependent protein kinase II beta (<em>CAMK2B</em>) and nitric oxide synthase 3 (<em>NOS3</em>, encoding eNOS). <em>CAMK2B</em> levels resulted 3.4-fold higher (<em>p</em> &lt; 0.05) in iPAH-PAEC transfected with a DSCR9-GFP carrying plasmid than with a GFP-only-carrying one. A trend for higher <em>NOS3</em> expression was also noted. GFP immunostaining was predominantly nuclear and cytoplasmic upon DSCR9-GFP or GFP-only transfection, respectively. <em>CAMK2B</em> and <em>NOS3</em> mRNA were also higher in iPAH-PAEC than control-PAEC in basal conditions. Instead, variations in total and phosphorylated CAMK2B, eNOS, and NO synthesis were inconsistent. We conclude that DSCR9 is upregulated in PAH-related endothelial cell models and influences <em>CAMK2B</em> and <em>NOS3</em> expression. Future studies are necessary to determine whether DSCR9 affects NO availability, including in PAH.</div></div>","PeriodicalId":23949,"journal":{"name":"Vascular pharmacology","volume":"158 ","pages":"Article 107464"},"PeriodicalIF":3.5,"publicationDate":"2025-01-21","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143029653","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Stay connected: The myoendothelial junction proteins in vascular function and dysfunction","authors":"Giulia Querio ,&nbsp;Federica Geddo ,&nbsp;Susanna Antoniotti ,&nbsp;Saveria Femminò ,&nbsp;Maria Pia Gallo ,&nbsp;Claudia Penna ,&nbsp;Pasquale Pagliaro","doi":"10.1016/j.vph.2025.107463","DOIUrl":"10.1016/j.vph.2025.107463","url":null,"abstract":"<div><div>The appropriate regulation of peripheral vascular tone is crucial for maintaining tissue perfusion. Myoendothelial junctions (MEJs), specialized connections between endothelial cells and vascular smooth muscle cells, are primarily located in peripheral resistance vessels. Therefore, these junctions, with their key membrane proteins, play a pivotal role in the physiological control of relaxation-contraction coupling in resistance arterioles, mainly mediated through endothelium-derived hyperpolarization (EDH). This review aims to illustrate the mechanisms involved in the initiation and propagation of EDH, emphasizing the role of membrane proteins involved in its generation (TRPV4, Piezo1, ASIC1a) and propagation (connexins, Notch). Finally, we discuss relevant studies on pathological events linked to EDH dysfunction and discuss novel approaches, including the effects of natural and dietary bioactive molecules, in modulating EDH-mediated vascular tone.</div></div>","PeriodicalId":23949,"journal":{"name":"Vascular pharmacology","volume":"158 ","pages":"Article 107463"},"PeriodicalIF":3.5,"publicationDate":"2025-01-14","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143012926","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Elucidating emerging signaling pathways driving endothelial dysfunction in cardiovascular aging","authors":"Anna De Bartolo ,&nbsp;Tommaso Angelone ,&nbsp;Carmine Rocca","doi":"10.1016/j.vph.2025.107462","DOIUrl":"10.1016/j.vph.2025.107462","url":null,"abstract":"<div><div>The risk for developing cardiovascular diseases dramatically increases in older individuals, and aging vasculature plays a crucial role in determining their morbidity and mortality. Aging disrupts endothelial balance between vasodilators and vasoconstrictors, impairing function and promoting pathological vascular remodeling. In this Review, we discuss the impact of key and emerging molecular pathways that transduce aberrant inflammatory signals (i.e.<em>,</em> chronic low-grade inflammation-inflammaging), oxidative stress, and mitochondrial dysfunction in aging vascular compartment. We focus on the interplay between these events, which contribute to generating a vicious cycle driving the progressive alterations in vascular structure and function during cardiovascular aging. We also discuss the primary role of senescent endothelial cells and vascular smooth muscle cells, and the potential link between vascular and myeloid cells, in impairing plaque stability and promoting the progression of atherosclerosis. The aim of this summary is to provide potential novel insights into targeting these processes for therapeutic benefit.</div></div>","PeriodicalId":23949,"journal":{"name":"Vascular pharmacology","volume":"158 ","pages":"Article 107462"},"PeriodicalIF":3.5,"publicationDate":"2025-01-11","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142979273","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Interplay between CD28 and PD-1 in T cell immunotherapy","authors":"Zuhayr Jafri ,&nbsp;Jingwen Zhang ,&nbsp;Connor H. O'Meara ,&nbsp;Anthony M. Joshua ,&nbsp;Christopher R. Parish ,&nbsp;Levon M. Khachigian","doi":"10.1016/j.vph.2024.107461","DOIUrl":"10.1016/j.vph.2024.107461","url":null,"abstract":"<div><div>Immune checkpoint therapy targeting the PD-1/PD-L1 axis has revolutionised the treatment of solid tumors. However, T cell exhaustion underpins resistance to current anti-PD-1 therapies, resulting in lower response rates in cancer patients. CD28 is a T cell costimulatory receptor that can influence the PD-1 signalling pathway (and <em>vice versa</em>). CD28 signalling has the potential to counter T cell exhaustion by serving as a potential complementary response to traditional anti-PD-1 therapies. Here we discuss the interplay between PD-1 and CD28 in T cell immunotherapy and additionally how CD28 transcriptionally modulates T cell exhaustion. We also consider clinical attempts at targeting CD28; the challenges faced by past attempts and recent promising developments.</div></div>","PeriodicalId":23949,"journal":{"name":"Vascular pharmacology","volume":"158 ","pages":"Article 107461"},"PeriodicalIF":3.5,"publicationDate":"2024-12-27","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142903745","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Sexual dimorphism in aortic aneurysm: A review of the contributions of sex hormones and sex chromosomes","authors":"Hao-Nan Chen ,&nbsp;Yan-Ni Hu ,&nbsp;Li-Ling Ran ,&nbsp;Mi Wang ,&nbsp;Zheng Zhang","doi":"10.1016/j.vph.2024.107460","DOIUrl":"10.1016/j.vph.2024.107460","url":null,"abstract":"<div><div>Aortic aneurysm is a common cardiovascular disease. Over time, the disease damages the structural and functional integrity of the aorta, causing it to abnormally expand and potentially rupture, which can be fatal. Sex differences are evident in the disease, with men experiencing an earlier onset and higher incidence. However, women may face a worse prognosis and a higher risk of rupture. While there are some studies on the cellular and molecular mechanisms of aneurysm formation, it remains unclear how sex factors contribute to sexual dimorphism. Therefore, this review aims to summarize the role of sex in the occurrence of aortic aneurysms, offering valuable insights for disease prevention and the development of appropriate treatment options.</div></div>","PeriodicalId":23949,"journal":{"name":"Vascular pharmacology","volume":"158 ","pages":"Article 107460"},"PeriodicalIF":3.5,"publicationDate":"2024-12-21","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142882878","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Endostatin in disease modulation: From cancer to beyond","authors":"J. Anakha,&nbsp;Yenisetti Rajendra Prasad,&nbsp;Abhay H. Pande","doi":"10.1016/j.vph.2024.107459","DOIUrl":"10.1016/j.vph.2024.107459","url":null,"abstract":"<div><div>Angiogenesis plays a pivotal role in various pathological conditions, making it a key target in therapeutic development. Anti-angiogenic therapies are gaining traction for their potential in treating a range of angiogenesis-dependent diseases. Among these, endogenous angiogenesis inhibitors, particularly endostatin, have garnered significant attention for their therapeutic potential. While extensively studied for its anti-angiogenic effects in cancer, endostatin also exhibits anti-atherosclerotic and anti-fibrotic properties, broadening its therapeutic scope. Despite the successful clinical use of recombinant human endostatin in China for nearly two decades, its broader therapeutic potential remains underexplored. Thus, this review delves into the multifaceted applications of endostatin, examining its role in ocular diseases, inflammation, reproductive disorders, and tumor angiogenesis. Furthermore, it provides a comprehensive overview of its emerging roles beyond angiogenesis, particularly in the context of atherosclerosis and fibroproliferative conditions.</div></div>","PeriodicalId":23949,"journal":{"name":"Vascular pharmacology","volume":"158 ","pages":"Article 107459"},"PeriodicalIF":3.5,"publicationDate":"2024-12-19","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142873024","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Targeting the Ca2+ signaling toolkit as an alternative strategy to mitigate SARS-CoV-2-induced cardiovascular adverse events","authors":"Simona Scorza ,&nbsp;Valentina Brunetti ,&nbsp;Giorgia Scarpellino ,&nbsp;Maira Certini ,&nbsp;Andrea Gerbino ,&nbsp;Francesco Moccia","doi":"10.1016/j.vph.2024.107458","DOIUrl":"10.1016/j.vph.2024.107458","url":null,"abstract":"<div><div>Ca²⁺ signaling events are essential for maintaining cardiovascular health, regulating critical functions in both endothelial and cardiac cells. SARS-CoV-2 infection impinges this delicate balance, leading to severe cardiovascular complications. SARS-CoV-2 binds to the ACE2 receptor on endothelial and cardiomyocyte surfaces, triggering abnormal increases in intracellular Ca²⁺ levels that promote endothelial dysfunction, inflammation, and hypercoagulation. In endothelial cells, this dysregulation activates a pro-inflammatory state and compromises vascular integrity. In cardiomyocytes, SARS-CoV-2-induced Ca²⁺ imbalances contribute to arrhythmias and heart failure by promoting abnormal Ca²⁺ cycling and energy metabolism disruptions. Additionally, the cytokine storm associated with COVID-19 amplifies these effects by further altering Ca²⁺ handling, enhancing inflammatory responses, and promoting thrombosis. Targeting Ca²⁺ channels, particularly endolysosomal two-pore channels, represents a promising therapeutic approach to counteract SARS-CoV-2’s effects on Ca²⁺ dynamics. Several FDA-approved drugs that modulate Ca²⁺ signaling could be repurposed to prevent viral entry and mitigate cardiovascular damage. Understanding these Ca²⁺-related mechanisms offers valuable insights for developing treatments to reduce cardiovascular risk in COVID-19 and potentially future viral infections impacting the cardiovascular system.</div></div>","PeriodicalId":23949,"journal":{"name":"Vascular pharmacology","volume":"158 ","pages":"Article 107458"},"PeriodicalIF":3.5,"publicationDate":"2024-12-17","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142865441","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"The role of Epsins in atherosclerosis: From molecular mechanisms to therapeutic applications","authors":"Siarhei A. Dabravolski ,&nbsp;Alexey V. Churov ,&nbsp;Alessio L. Ravani ,&nbsp;Amina E. Karimova ,&nbsp;Igor G. Luchinkin ,&nbsp;Vasily N. Sukhorukov ,&nbsp;Alexander N. Orekhov","doi":"10.1016/j.vph.2024.107457","DOIUrl":"10.1016/j.vph.2024.107457","url":null,"abstract":"<div><div>Atherosclerosis is a multifaceted disease characterised by chronic inflammation and vascular remodelling, leading to plaque formation and cardiovascular complications. Recent evidence highlights the critical role of epsins, a family of endocytic proteins, in the pathogenesis of atherosclerosis. This manuscript explores the multifarious functions of epsins in atherosclerosis, focusing on their involvement in angiogenesis, lymphangiogenesis, and the modulation of key signalling pathways. We discuss how epsins facilitate EndoMT through their interaction with the TGFβ signalling pathway, which contributes to vascular smooth muscle cell-like phenotypes and plaque instability. Additionally, we examine the therapeutic potential of targeting epsins, elucidating their interactions with crucial partners such as LDLR, LRP-1, and TLR 2/4, among others, in mediating lipid metabolism and inflammation. Furthermore, we highlight the promising prospects of epsin-targeting peptides and small interfering RNAs as therapeutic agents for atherosclerosis treatment. Despite these advancements, the research faces limitations, including a reliance on specific mouse models and a need for comprehensive studies on the long-term effects of epsin modulation. Therefore, future investigations should focus on elucidating the detailed mechanisms of epsin function and their implications in cardiovascular health, fostering collaborations to translate basic research into innovative therapeutic strategies. This work underscores the necessity for further exploration of epsins to unlock their full therapeutic potential in combating atherosclerosis and related cardiovascular diseases.</div></div>","PeriodicalId":23949,"journal":{"name":"Vascular pharmacology","volume":"158 ","pages":"Article 107457"},"PeriodicalIF":3.5,"publicationDate":"2024-12-11","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142822174","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Unravelling molecular mechanisms in atherosclerosis using cellular models and omics technologies","authors":"Dimitris Kardassis ,&nbsp;Cécile Vindis ,&nbsp;Camelia Sorina Stancu ,&nbsp;Laura Toma ,&nbsp;Anca Violeta Gafencu ,&nbsp;Adriana Georgescu ,&nbsp;Nicoleta Alexandru-Moise ,&nbsp;Filippo Molica ,&nbsp;Brenda R. Kwak ,&nbsp;Alexandrina Burlacu ,&nbsp;Ignacio Fernando Hall ,&nbsp;Elena Butoi ,&nbsp;Paolo Magni ,&nbsp;Junxi Wu ,&nbsp;Susana Novella ,&nbsp;Luke F. Gamon ,&nbsp;Michael J. Davies ,&nbsp;Andrea Caporali ,&nbsp;Fernando de la Cuesta ,&nbsp;Tijana Mitić","doi":"10.1016/j.vph.2024.107452","DOIUrl":"10.1016/j.vph.2024.107452","url":null,"abstract":"<div><div>Despite the discovery and prevalent clinical use of potent lipid-lowering therapies, including statins and PCSK9 inhibitors, cardiovascular diseases (CVD) caused by atherosclerosis remain a large unmet clinical need, accounting for frequent deaths worldwide. The pathogenesis of atherosclerosis is a complex process underlying the presence of modifiable and non-modifiable risk factors affecting several cell types including endothelial cells (ECs), monocytes/macrophages, smooth muscle cells (SMCs) and T cells. Heterogeneous composition of the plaque and its morphology could lead to rupture or erosion causing thrombosis, even a sudden death. To decipher this complexity, various cell model systems have been developed. With recent advances in systems biology approaches and single or multi-omics methods researchers can elucidate specific cell types, molecules and signalling pathways contributing to certain stages of disease progression. Compared with animals, <em>in vitro</em> models are economical, easily adjusted for high-throughput work, offering mechanistic insights. Hereby, we review the latest work performed employing the cellular models of atherosclerosis to generate a variety of omics data. We summarize their outputs and the impact they had in the field. Challenges in the translatability of the omics data obtained from the cell models will be discussed along with future perspectives.</div></div>","PeriodicalId":23949,"journal":{"name":"Vascular pharmacology","volume":"158 ","pages":"Article 107452"},"PeriodicalIF":3.5,"publicationDate":"2024-12-10","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142818826","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}