Cardiovascular Research最新文献

{"title":"CKD disrupts cardiac energy metabolism and aggravates cardiac inflammation, oxidative stress, and dysfunction post-infarction.","authors":"Corinna Schulte, Julia Wollenhaupt, Sina Hourtz, Eva Harlacher, Julia Moellmann, Carolina Victoria Cruz Junho, Michael Kohlhaas, Vera Jankowski, Han Jin, Martin Reugels, Sidrah Maryam, Franca Hausmann, Dickson W L Wong, Emiel P C van der Vorst, Martin Berger, Sonja Vondenhoff, Berkan Kurt, Bart Ghesquière, Constanze Mueller, Ulrike Schulze-Späte, Philippe Schmitt-Kopplin, Erik A L Biessen, Leticia Prates-Roma, Moritz Biener, Evangelos Giannitsis, Hugo A Katus, Stefan Schunk, Danilo Fliser, Katharina Marx-Schütt, Michael Lehrke, Rafael Kramann, Florian Kahles, Peter Boor, Claudia Goettsch, Sikander Hayat, Joachim Jankowski, Christoph Maack, Yvonne Döring, Nikolaus Marx, Heidi Noels","doi":"10.1093/cvr/cvag152","DOIUrl":"10.1093/cvr/cvag152","url":null,"abstract":"<p><strong>Aims: </strong>Patients with chronic kidney disease (CKD) display a reduced survival following myocardial infarction (MI). As the underlying mechanisms remain unclear, we examined the impact of CKD on cardiac remodeling and function post-MI using a mouse model of adenine-induced CKD.</p><p><strong>Methods and results: </strong>After MI, CKD mice showed a stronger cardiac dysfunction compared to non-CKD controls. While immunohistochemical and immunofluorescence analyses did not reveal changes in cardiomyocyte apoptosis, infarction size, or myofibroblast content, CKD mice exhibited an increased number of circulating myeloid cells post-infarction and more neutrophil infiltration in the heart. Combining RNAseq, untargeted kinome profiling, western blotting, and mass spectrometry revealed that post-MI, CKD enhanced cardiac oxidative stress and the acute stress complex S100A8/A9 in circulation and the heart, and enforced cardiac MAP-kinase p38 activation and NR4A1 phosphorylation as pathways underlying cardiomyocyte dysfunction. S100A8/A9 also exerted an acute detrimental impact on calcium flux and sarcomere shortening in cardiomyocytes ex vivo. Increased myeloid cell-derived S100A8/A9 expression was confirmed in the infarcted human heart by single-nucleus RNAseq, and CKD patients had higher post-infarction S100A8/A9 levels compared to patients without kidney dysfunction. Furthermore, integrating metabolomics, RNAseq, and mitochondrial analysis uncovered a disturbed cardiac metabolism with impaired glycolysis, a reduced glycerol-3-phosphate-shuttle, and a reduced Coenzyme A-bioavailability in CKD vs. non-CKD mice post-MI. These alterations were associated with poorer cardiac performance post-MI, without intrinsic defects in mitochondrial function observed.</p><p><strong>Conclusion: </strong>Our study reveals innate immune activation, inflammation, oxidative stress, and metabolic alterations indicative of reduced glycolytic entry and CoA bioavailability along with aggravated cardiac dysfunction post-MI in CKD compared to non-CKD conditions, independent of infarct size, and with poorer cardiac performance in CKD associated with the cardiac metabolic alterations. Combined, this could contribute to the worsened outcome of CKD patients post-MI and reveals cardiac metabolism in CKD as an interesting translational research target.</p>","PeriodicalId":9638,"journal":{"name":"Cardiovascular Research","volume":" ","pages":"1834-1850"},"PeriodicalIF":12.5,"publicationDate":"2026-09-24","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13604849/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148577036","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}

{"title":"Postmortem DNA methylation profiling uncovers signatures associated with left ventricle size.","authors":"Steffan Noe Niikanoff Christiansen, Kristine Boisen Olsen, Sara Tangmose Larsen, Pernille Heimdal Holm, Marie Kroman Palsøe, Marie-Louise Kampmann, Stine Bøttcher Jacobsen, Mikkel Meyer Andersen, Jytte Banner, Niels Morling, Jacob Tfelt-Hansen, Jeppe Dyrberg Andersen","doi":"10.1093/cvr/cvag202","DOIUrl":"https://doi.org/10.1093/cvr/cvag202","url":null,"abstract":"","PeriodicalId":9638,"journal":{"name":"Cardiovascular Research","volume":" ","pages":""},"PeriodicalIF":12.5,"publicationDate":"2026-09-24","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149030033","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":"Unlocking cardiac repair: YAP-mediated control of IFN-γ/STAT1 in myocarditis.","authors":"Christina Gkantsinikoudi, Federica M Marelli-Berg","doi":"10.1093/cvr/cvag177","DOIUrl":"10.1093/cvr/cvag177","url":null,"abstract":"","PeriodicalId":9638,"journal":{"name":"Cardiovascular Research","volume":" ","pages":"1725-1727"},"PeriodicalIF":12.5,"publicationDate":"2026-09-24","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13604830/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148788410","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}

{"title":"From one plaque to many: the coming tsunami of pan-vascular disease: bringing pan-vascular disease to the centre of cardiovascular prevention.","authors":"Vladyslav Kyslyi, Tomasz J Guzik","doi":"10.1093/cvr/cvag176","DOIUrl":"https://doi.org/10.1093/cvr/cvag176","url":null,"abstract":"","PeriodicalId":9638,"journal":{"name":"Cardiovascular Research","volume":"122 13","pages":"1728-1731"},"PeriodicalIF":12.5,"publicationDate":"2026-09-24","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149036605","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":"Healthy bone marrow transplantation into hypertriglyceridemic rats improves cardiac reparative fibrosis post-myocardial infarction","authors":"Lisaidy Ramos-Regalado, Sebastià Alcover, Teresa Padró, Malcolm Walker, Guillermo Gómez de Segura-Melcón, Gemma Sancho-Pardo, Lina Badimon, Gemma Arderiu, Josep Balart, Gemma Vilahur","doi":"10.1093/cvr/cvag204","DOIUrl":"https://doi.org/10.1093/cvr/cvag204","url":null,"abstract":"Aims Acute myocardial infarction (AMI) triggers an immune response characterized by a dynamic interplay between the bone marrow (BM) and the ischemic heart. However, the effect of metabolic alterations such as hypertriglyceridemia (HTG) on this inter-organ communication remains unknown. In the present study we have investigated, in a rat model of crossed-BM transplant, the impact of HTG on the BM-heart axis response to AMI under constant metabolic stress. Methods and results: Wistar rats (n = 56) were assigned to two groups: one fed a high-sucrose diet to induce HTG and the other fed a regular chow [normolipemic (NL)-animals]. After three weeks, all combinations of crossed-BM transplants were performed (NL-BM/NL-recipient, NL-BM/HTG-recipient, HTG-BM/NL-recipient and HTG-BM/HTG-recipient) following total body irradiation (9.5 Gy). All animals, except for NL-BM/NL-recipient group, continued on a high-sucrose diet for three weeks. Then, AMI was induced by transient coronary artery ligation and five days later, animals were sacrificed. We determined infarct size, and performed echocardiography, 1H-NMR spectroscopy and multiple molecular and histological analyses. NL-BM/HTG-recipients exhibited smaller infarcts vs the other groups and showed a resolving inflammatory response, lower lipotoxicity, higher ω3 content, increased AMPK activation and S1P-related enzymes, and reparative fibrosis in the healing scar. Although no differences were detected in LVEF post-AMI among all groups, NL-BM/HTG-recipients exhibited improved systolic and diastolic parameters. Circulating triglyceride levels were significantly reduced in NL-BM/HTG-recipients three weeks post-BM transplant, whereas, conversely, they were found to be enhanced in HTG-BM/NL-recipients developing a HTG state. Furthermore, recipients of a HTG-BM showed worsened lipid profile, liver steatosis and inflammation, higher weight gain, leptin levels and lower lipoprotein lipase, AMPK and acetyl-CoA carboxylase activity in the visceral adipose tissue vs NL-BM-recipient animals. Conclusions Transplantation of healthy BM into HTG animals enhances the capacity to counteract myocardial injury post-AMI and restores metabolic disturbances improving overall recovery.","PeriodicalId":9638,"journal":{"name":"Cardiovascular Research","volume":"47 1","pages":""},"PeriodicalIF":10.8,"publicationDate":"2026-09-23","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149020367","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":"Endothelial TLR4 coordinates angiogenesis and inflammation through a CXCR2–neutrophil–oxidative axis","authors":"Iuliia Molokotina, Josh Ford, Olha Kyrychek, Irina Zhevlakova, Moses Lee, Eugene A Podrez, Anish Korrapati, Olga A Cherepanova, Tatiana V Byzova","doi":"10.1093/cvr/cvag211","DOIUrl":"https://doi.org/10.1093/cvr/cvag211","url":null,"abstract":"Aims To determine the endothelial-intrinsic role of TLR4 in inflammatory vascular remodeling and cytokine signaling, and to define how exogenous microbial and oxidation-derived endogenous signals are integrated by endothelial TLR4 to regulate vascular function. Methods and results Single-cell transcriptomic analyses of human tissues identified endothelial cells as a coherent, lineage-consistent TLR4-expressing population across tissues and disease states, distinguishing TLR4 from other endothelial Toll-like receptors. Using tamoxifen-inducible endothelial-specific TLR4 knockout mice (Cdh5-CreERT2; Tlr4flox/flox) we show that lack of TLR4 markedly impaired early venular remodeling, junctional loosening, vascular leakage, and neutrophil recruitment during skin wound healing, and suppressed tumor angiogenesis and growth in a syngeneic cancer model. Mechanistically, endothelial TLR4 activation induced a focused chemokine program dominated by CXCL1/2/5–CXCR2 signaling, promoting neutrophil recruitment and lipid-oxidation responses. Loss of endothelial TLR4 reduced myeloperoxidase (MPO)-positive inflammatory-cell accumulation and carboxyethylpyrrole lipid-peroxidation adduct deposition, supporting a feed-forward inflammatory loop in which neutrophil-derived oxidized lipids act as endogenous TLR4 ligands. Pharmacologic CXCR2 inhibition or combined ROS/MPO suppression phenocopied endothelial TLR4 deletion. Conclusions Endothelial-intrinsic TLR4 functions as a vascular inflammatory integrator that links microbial pattern recognition with endogenous oxidation-derived danger signaling to coordinate chemokine production, neutrophil recruitment, MPO-linked lipid-oxidation amplification, and angiogenesis. These findings identify endothelial TLR4 as a distinct and targetable vascular inflammatory node, functionally separable from hematopoietic TLR4, with implications for sterile inflammatory cardiovascular disease.","PeriodicalId":9638,"journal":{"name":"Cardiovascular Research","volume":"56 1","pages":""},"PeriodicalIF":10.8,"publicationDate":"2026-09-22","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149027542","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":"Vitamin D in coronary heart disease: a Mendelian randomization meta-analysis of data stratified by 25(OH)D levels.","authors":"Maria Fusaro, Pasquale Perrone Filardi, Gianfranco Sinagra, Maria Luisa Brandi, Maurizio Gallieni, Jean-Yves Reginster, Eugene McCloskey, Etienne Cavalier, Mario Plebani, Martina Zaninotto, Nicola Napoli, Sandro Giannini, Paolo Simioni, Francesco Bertoldo, Thomas Nickolas, Colin Gerard Egan, Luca De Nicola, Mario Cozzolino, Antonio Bellasi, Maura Ravera, José Manuel Valdivielso, Juan Miguel Díaz-Tocados, Alexandros Kasiakogias, Raffaele De Caterina, Giovanni Tripepi","doi":"10.1093/cvr/cvag213","DOIUrl":"https://doi.org/10.1093/cvr/cvag213","url":null,"abstract":"","PeriodicalId":9638,"journal":{"name":"Cardiovascular Research","volume":" ","pages":""},"PeriodicalIF":12.5,"publicationDate":"2026-09-22","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149015624","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":"Spatial heterogeneity of APD under long QT conditions: characterisation and relationship to sinus activation sequence.","authors":"R J Gilchrist, D T Humphreys, S Heitmann, A P Hill, F L Burton, J D McClure, J I Vandenberg, G L Smith, R C Myles","doi":"10.1093/cvr/cvag209","DOIUrl":"https://doi.org/10.1093/cvr/cvag209","url":null,"abstract":"<p><strong>Aims: </strong>Enhanced spatial variation in ventricular action potential duration (APD) is known to contribute to arrhythmia development under long QT conditions, although the causes of APD variation are unclear. Specifically, between-individual variation in the locations of pro-arrhythmic long APD islands and associated repolarisation gradients is difficult to explain in the context of established regional variation in electrophysiology. This study aimed to explore the mechanisms underlying the spatial heterogeneity of ventricular APD under baseline and long QT conditions.</p><p><strong>Methods and results: </strong>New Zealand White rabbit hearts (n = 26) were Langendorff-perfused with oxygenated Tyrode's solution and loaded with blebbistatin and FluoVolt. Optical mapping of transmembrane voltage from the anterior epicardial surface of the right (RV) and left ventricles (LV) during sinus rhythm revealed a strong inverse relationship between activation time and APD90 in all hearts (linear regression slope: -0.85 ± 0.17, r2: 0.60 ± 0.12, p < 0.0001), despite considerable between-heart variation in the activation sequence. Lengthening of the pacing cycle length (350 to 1000 ms) and dofetilide-induced IKr blockade each induced greater AP prolongation in ventricular sites with earlier sinus activation, contributing to increased spatial heterogeneity of APD90. Optical measurement of APD90 from cardiomyocytes isolated after optical mapping of the intact heart indicated that myocytes from ventricular sites with earlier sinus activation had longer intrinsic APD90. Isolated RV myocytes also exhibited shorter average APD90 than LV myocytes. Measurement of the mRNA levels of 22 genes encoding cardiac ion channel, transporter and regulatory proteins demonstrated that ventricular sites with distinct sinus activation times exhibit different gene expression profiles. With increasing sinus activation time, the mRNA levels of Scn5a and most repolarisation genes decreased while that of Kcnip2 increased.</p><p><strong>Conclusion: </strong>Ventricular sites with distinct sinus activation times exhibit different electrophysiological properties which contribute to enhanced spatial heterogeneity of APD under long QT conditions.</p>","PeriodicalId":9638,"journal":{"name":"Cardiovascular Research","volume":" ","pages":""},"PeriodicalIF":12.5,"publicationDate":"2026-09-21","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149012130","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":"Beyond glucose: metabolic substrate provision enhances cardiac energetics, function and stability ex vivo: a simple recipe for healthier hearts?","authors":"Zoe Hoare, Yu Jin Chung, Edward C T Waters, Abbie Hayes, Katie Tompkins, Christopher O'Shea, Davor Pavlovic, Richard Southworth, Thomas R Eykyn, Michael J Shattock","doi":"10.1093/cvr/cvag212","DOIUrl":"https://doi.org/10.1093/cvr/cvag212","url":null,"abstract":"<p><strong>Aims: </strong>In 1932, Hans Krebs and Kurt Henseleit introduced a bicarbonate-based solution for liver perfusion containing only 5.55 mM glucose. This bicarbonate-based Krebs-Henseleit buffer (KHB) has been frequently modified over many years but typically includes only glucose as a substrate, often to hyperglycaemic levels. However, despite its popularity, hearts perfused under these conditions are close to the limits of substrate and oxygen availability and unable to sustainably respond to increased demand. The aim of the present study was to compare the function, stability and energetics of hearts perfused with standard glucose-containing KHB with those perfused with a Full Metabolic Buffer (FMB) containing a physiologically appropriate range of substrates, including (in mM): fatty acids (0.4), lactate (1), pyruvate (0.1), glucose (5), glutamate (0.5), β-hydroxybutyrate (4), and insulin (5 mIU/L).</p><p><strong>Methods and results: </strong>Isolated rat hearts were perfused with either KHB or FMB, followed by isoprenaline (1 μM for 20 mins) to induce stress. Cardiac function was measured via an intraventricular balloon, while energetics and metabolism were assessed with 31P and 1H NMR spectroscopy while action potential/calcium transients were assessed with cardiac optical mapping. An adapted FMB was also developed for culturing isolated cardiomyocytes, and glycolytic flux in these cells was measured with 2H NMR spectroscopy. In hearts perfused with FMB, basal left ventricular developed pressure was higher (160 ± 7 mmHg vs. 126 ± 6 mmHg in KHB), PCr/ATP ratio was elevated (1.67 ± 0.1 vs. 1.28 ± 0.05), Gibbs free energy of ATP hydrolysis was increased -2.9 ± 0.3 kJ/mol more negative, and mitochondrial membrane potential was more polarized by -19 ± 7 mV. Under stress, Langendorff-perfused FMB hearts maintained contractile function with fewer arrhythmias and maintained higher PCr/ATP ratio. The metabolic profile was significantly different between hearts perfused with either buffer, with higher levels of key mitochondrial metabolites such as succinate and fumarate in FMB hearts. FMB supressed pacing induced calcium transient duration alternans compared to KHB perfused hearts.</p><p><strong>Conclusion: </strong>Compared to KHB, FMB provides substantial advantages for cardiac energetics, metabolism, and function, and is therefore a more appropriate buffer to use in cardiovascular metabolism studies.</p>","PeriodicalId":9638,"journal":{"name":"Cardiovascular Research","volume":" ","pages":""},"PeriodicalIF":12.5,"publicationDate":"2026-09-21","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149012084","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":"A human engineered mini-heart platform for mimicking ventricular pump function.","authors":"Marcelo C Ribeiro, Mariel Cano-Jorge, Simone Ten Den, Danique Snippert, Marcel Karperien, Tom Kamperman, Guillaume Lajoinie, Michel Versluis, Robert Passier","doi":"10.1093/cvr/cvag210","DOIUrl":"https://doi.org/10.1093/cvr/cvag210","url":null,"abstract":"<p><strong>Aim: </strong>Engineered cardiac tissue models for in vitro physiological studies often fail to replicate the pump function of the heart. Despite promising advancements, the use of engineered cardiac chambers is often hindered by complex fabrication processes and invasive characterization techniques. Here, we engineered a chamber-like human cardiac model with pumping function, referred to as a 'mini-heart', by employing a novel sacrificial molding approach within a customized bioreactor.</p><p><strong>Methods and results: </strong>Human pluripotent stem cell-derived cardiomyocytes and human cardiac fibroblasts were embedded in a fibrin mix and casted around two gelatin bodies within a customized bioreactor. After fibrin polymerization, thermal degradation of gelatin was induced to obtain a single-inlet cardiac chamber coupled to a glass capillary inlet.The mini-heart's pumping capability was confirmed through optical recording of fluid displacement at the engineered tissue inlet, enabling the non-invasive acquisition of hemodynamic parameters such as stroke volume, stroke work, ejection fraction, and developed pressure. Morphological analysis of the engineered tissues revealed organized sarcomeres and extracellular matrix self-determination, highlighting the advantage of our degradable mold technology. Additionally, we have measured calcium transients during both spontaneous and electrically-paced beating, and observed a positive inotropic response to the β-adrenergic agonist drug isoproterenol.</p><p><strong>Conclusions: </strong>We present a biomimetic, chamber-like human cardiac model with intrinsic pumping function that enables non-invasive functional assessment of cardiac hemodynamics in vitro.</p>","PeriodicalId":9638,"journal":{"name":"Cardiovascular Research","volume":" ","pages":""},"PeriodicalIF":12.5,"publicationDate":"2026-09-21","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149012067","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}