American journal of physiology. Heart and circulatory physiology最新文献

{"title":"Insights into the effect of pre- and postnatal nicotine exposure on cardiovascular development and function.","authors":"Benjamin Rodriguez, Ashton Oliver, Han Le, Chanel Harris, Andrea G Marshall, Pamela Martin, Amadou Gaye, Lori Banks, Antentor Hinton","doi":"10.1152/ajpheart.00768.2024","DOIUrl":"10.1152/ajpheart.00768.2024","url":null,"abstract":"","PeriodicalId":7692,"journal":{"name":"American journal of physiology. Heart and circulatory physiology","volume":" ","pages":"H1051-H1053"},"PeriodicalIF":4.1,"publicationDate":"2025-05-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143456529","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":"X's, Y's, and vascular ties: exploring the role of sex chromosomes in arterial stiffness and vascular aging.","authors":"Zachary S Clayton, Kerrie L Moreau","doi":"10.1152/ajpheart.00130.2025","DOIUrl":"10.1152/ajpheart.00130.2025","url":null,"abstract":"","PeriodicalId":7692,"journal":{"name":"American journal of physiology. Heart and circulatory physiology","volume":"328 5","pages":"H1083-H1085"},"PeriodicalIF":4.1,"publicationDate":"2025-05-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12117583/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144061944","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Parental obesity predisposes male and female offspring to exacerbated cardiac dysfunction and increased mortality after myocardial infarction.","authors":"Jussara M do Carmo, Ana C M Omoto, John E Hall, Xuemei Dai, Emily C Ladnier, Marilia C Mouro, Odecio E S Tosta, Zhen Wang, Xuan Li, Alexandre A da Silva","doi":"10.1152/ajpheart.00827.2024","DOIUrl":"10.1152/ajpheart.00827.2024","url":null,"abstract":"<p><p>Acute myocardial infarction (MI) is a leading cause of death worldwide, accounting for >1 million deaths/year in the United States alone. Although parental obesity is a risk factor for offspring cardiovascular diseases, the impact of parental obesity on offspring outcomes after MI is unknown. This study examined if non-obese male and female offspring from obese Sprague-Dawley rat parents fed a high-fat diet (HFD-Offs, <i>n</i> = 11-19/sex) are at greater risk of death and worse cardiac dysfunction after MI, compared with offspring from lean parents fed a normal diet (ND-Offs, <i>n</i> = 12-15/sex). All offspring were fed ND from weaning and subjected to left descending coronary artery ligation at 12 wk of age to induce MI. Survival rate 24 h post-MI was examined, and cardiac function was measured by echocardiography and intraventricular catheterization with a Millar catheter on <i>day 7</i> post-MI. Compared with ND-Offs, male and female HFD-Offs exhibited increased ventricular fibrillation and reduced survival post-MI (male: 37% vs. 80% and female: 55% vs. 83% for HFD-Offs and ND-Offs, respectively). In surviving rats, systolic dysfunction was more pronounced in male and female HFD-Offs compared with ND-Offs at <i>day 7</i> post-MI, despite similar infarct size in all groups. We also found reductions in baseline O₂ consumption rate and pyruvate-supported mitochondrial respiration, as well as increased mitochondria-derived superoxide production in cardiac fibers from HFD-Offs. Thus, parental obesity is associated with an increased 24-h mortality rate in their offspring after induction of MI and worse systolic function even when the offspring are fed a healthy diet after weaning and remain lean.<b>NEW & NOTEWORTHY</b> A major new finding of this study is that parental obesity markedly reduces survival rate and exacerbates cardiac dysfunction after myocardial infarction in their offspring, and this effect is independent of offspring sex.</p>","PeriodicalId":7692,"journal":{"name":"American journal of physiology. Heart and circulatory physiology","volume":" ","pages":"H1039-H1050"},"PeriodicalIF":4.1,"publicationDate":"2025-05-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12128619/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143668897","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Inherited Burdens: the Cardiac Cost of Parental Obesity in Offspring Following Myocardial Infarction.","authors":"Madison D Cooper, Yonggang Ma","doi":"10.1152/ajpheart.00291.2025","DOIUrl":"https://doi.org/10.1152/ajpheart.00291.2025","url":null,"abstract":"","PeriodicalId":7692,"journal":{"name":"American journal of physiology. Heart and circulatory physiology","volume":" ","pages":""},"PeriodicalIF":4.1,"publicationDate":"2025-04-30","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143957600","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":"Splenic Modulation of the Early Inflammatory Response to Regional and Global Ischemia/Reperfusion Injury in Swine.","authors":"Tyler J Rolland, Emily R Hudson, Luke A Graser, Sumbule Zahra, Daniel Cucinotta, Brian R Weil","doi":"10.1152/ajpheart.00714.2024","DOIUrl":"https://doi.org/10.1152/ajpheart.00714.2024","url":null,"abstract":"<p><p><b>Background:</b> The spleen has been identified as a source of pro-inflammatory leukocytes mobilized after local ischemic injury in rodents. However, the role of the spleen in the inflammatory response to regional or global ischemia/reperfusion injury (IRI) in larger mammals is unknown. We investigated the spleen's contribution to early IRI-associated inflammation in porcine models of acute reperfused myocardial infarction (AMI) and sudden cardiac arrest (SCA). <b>Methods:</b> Swine were randomized to splenectomy (SPLX; n=15) or sham surgery (SHAM; n=15) 1-week before a 75-minute coronary occlusion (AMI; n=6/group) or 8-minutes of ventricular fibrillation and CPR (SCA; n=9/group). Hemodynamic assessment and echocardiography were performed before and after IRI, with serial blood sampling to assess leukocyte mobilization and cytokine release. Heart and brain samples were collected for post-mortem evaluation of injury and leukocyte infiltration. <b>Results:</b> Early post-IRI leukocyte mobilization, cytokine levels, and leukocyte infiltration were similar between groups in each protocol. After SCA, SHAM animals showed a significant 41±5% increase in hematocrit and 30±4% rise in arterial O2-content during CPR that was absent after SPLX. These differences persisted for up to 90-minutes and were associated with prolonged time to return of spontaneous circulation (ROSC) and increased vasopressor support in the SPLX group. <b>Conclusions:</b> Contrary to findings in rodents, the spleen is not required for the early inflammatory response to regional or global IRI in swine. However, splenic erythrocyte mobilization during SCA leads to an increase in arterial O2-content that is associated with earlier ROSC and reduced reliance on vasopressors during CPR and the post-resuscitation period.</p>","PeriodicalId":7692,"journal":{"name":"American journal of physiology. Heart and circulatory physiology","volume":" ","pages":""},"PeriodicalIF":4.1,"publicationDate":"2025-04-18","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143955951","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":"High-fat feeding has sex-dependent effects on the structure and biomechanical properties of cerebral parenchymal arterioles and cognitive function.","authors":"Jessica T Yen, Theresa A Lansdell, Erinn Laimon-Thomson, Martina Yen, William F Jackson, Anne M Dorrance","doi":"10.1152/ajpheart.00295.2024","DOIUrl":"https://doi.org/10.1152/ajpheart.00295.2024","url":null,"abstract":"<p><p>One-third of dementia cases could be prevented by correcting modifiable risk factors, including obesity caused by consuming a high-fat (HF) diet consumption. Dementia is associated with white matter injury, which is associated with impaired cerebral parenchymal arteriole (PA) function. Yet the impact of HF feeding on PAs remains understudied. We tested the hypothesis that HF feeding would result in structural and biomechanical remodeling of the PAs from male and female rats. We also proposed that HF feeding would impair endothelium-dependent dilation and that these changes would be associated with cognitive decline and neuroinflammation. Three-week-old male and female Sprague Dawley rats were fed a control or HF diet for 20-24 weeks. HF feeding increased body weight and blood pressure in both sexes but caused hyperglycemia only in females. Pial artery blood flow was unchanged by HF feeding in both sexes. The PAs from HF-fed females exhibited inward remodeling; PAs from males were not remodeled but were less distensible. Endothelial function and myogenic tone generation in the PAs were not impacted by HF feeding in either sex. The changes observed in the males were associated with impaired spatial memory and reduced cerebral myelin basic protein expression. HF feeding increased the number of microglia in both sexes, but soma size was only increased in the males. These data suggest that HF feeding impairs cognitive function in males, which is associated with increased stiffness in PAs and increased microglial hypertrophy, while HF-fed females remain cognitively normal despite exhibiting significant PA remodeling.</p>","PeriodicalId":7692,"journal":{"name":"American journal of physiology. Heart and circulatory physiology","volume":" ","pages":""},"PeriodicalIF":4.1,"publicationDate":"2025-04-11","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143968052","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":"Carotid artery stiffness mechanisms, heart failure events, and atrial fibrillation in MESA: the Multi-Ethnic Study of Atherosclerosis.","authors":"Ryan Pewowaruk, Claudia E Korcarz, David A Bluemke, Mohamed H Hamdan, Susan R Heckbert, Joao A C Lima, Yacob Tedla, Adam D Gepner","doi":"10.1152/ajpheart.00047.2025","DOIUrl":"10.1152/ajpheart.00047.2025","url":null,"abstract":"<p><p>Arterial stiffness can be separated into two main mechanisms: <i>1</i>) load-dependent stiffening from higher blood pressure and <i>2</i>) structural stiffening due to remodeling of the vessel wall. The relationship of stiffness mechanisms with heart failure (HF) and atrial fibrillation (AF) is unknown. MESA (multi-ethnic study of atherosclerosis) participants with baseline carotid ultrasound images were included in this study (HF <i>n</i> = 6,278; AF <i>n</i> = 5,292). Carotid pulse wave velocity (cPWV) was calculated from B-mode carotid ultrasound to represent total stiffness. Structural stiffness was calculated by adjusting cPWV to a 120/80 mmHg blood pressure with participant-specific models. Load-dependent stiffness was the difference between total and structural stiffness. Associations with incident heart failure events and atrial fibrillation diagnosis were assessed with adjusted Cox hazard models. Four hundred-seven HF events and 1,157 AF diagnoses occurred during a median 17.7 and 16.8 years of follow-up. The associations of carotid artery stiffness mechanisms with HF events were: total cPWV adjusted HR per 1 SD 1.09 [0.98-1.22], <i>P</i> = 0.11; structural cPWV adjusted HR 1.06 [0.94-1.18], <i>P</i> = 0.33; and load-dependent PWV adjusted HR 1.23 [1.05-1.44] per 1 m/s, <i>P</i> = 0.009. The associations of carotid artery stiffness mechanisms with AF diagnoses were: total cPWV adjusted HR 1.11 (1.04-1.20), <i>P</i> = 0.004; structural cPWV adjusted HR 1.10 [1.02-1.16], <i>P</i> = 0.017; load-dependent cPWV adjusted HR 1.12 [1.02-1.23], <i>P</i> = 0.020. Both structural and load-dependent cPWV were associated with the development of AF, and load-dependent cPWV was associated with HF events. These findings indicate that load-dependent cPWV may be a potential treatment target to reduce the incidence of both HF and AF.<b>NEW & NOTEWORTHY</b> We evaluated associations between novel components of arterial stiffness: <i>1</i>) load-dependent stiffening from higher blood pressure and <i>2</i>) structural stiffening due to remodeling of the vessel wall and their associations with incident heart failure (<i>n</i> = 6,278) and atrial fibrillation (<i>n</i> = 5,292) over ∼17 years of follow-up. We found that both baseline structural and load-dependent stiffness were associated with the development of atrial fibrillation and load-dependent stiffness was associated with heart failure events.</p>","PeriodicalId":7692,"journal":{"name":"American journal of physiology. Heart and circulatory physiology","volume":" ","pages":"H1019-H1025"},"PeriodicalIF":4.1,"publicationDate":"2025-04-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143668895","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":"Oxidative stress and pediatric diabetic cardiovascular complications: emerging research and clinical applications.","authors":"Saman Saedi, Yi Tan, Sara E Watson, Joshua D Sparks, Kupper A Wintergerst, Lu Cai","doi":"10.1152/ajpheart.00673.2024","DOIUrl":"10.1152/ajpheart.00673.2024","url":null,"abstract":"<p><p>The prevalence and incidence of diabetes in pediatrics have dramatically increased over the last three decades. Comparatively, pediatric diabetes has faster pancreatic β-cells decline and early progression to complications compared with adult diabetes. Therefore, diabetic complications are a major concern in children and adolescents with diabetes. Diabetes has detrimental effects on the macro- and microvascular systems, resulting in cardiovascular diseases, leading causes of morbidity and mortality in youth with diabetes. Oxidative stress plays a critical role in developing cardiovascular complications in the context of pediatric diabetes. In pediatric patients with diabetes, several factors can contribute to the development of excess reactive oxygen species and oxidative stress, including nutritional deficiencies, puberty, environmental exposures, and metabolic disorders such as obesity and high blood pressure. The present study aims to raise awareness of diabetic cardiovascular complications in children and adolescents with diabetes and the role of oxidative stress and their molecular mechanisms in the pathogenesis of cardiovascular complications. In addition, some novel therapeutic strategies for the treatment and prevention of diabetic cardiovascular complications in the pediatric populations are highlighted. In summary, children and adolescents with diabetes no matter type 1 diabetes (T1D) or type 1 diabetes (T2D), have many features similar to those in adults with same kinds of diabetes, but also have many their own features distinct from adults. By developing targeted therapies and preventive measures, healthcare providers can better address the rising incidence of diabetes-related complications in children and adolescents.</p>","PeriodicalId":7692,"journal":{"name":"American journal of physiology. Heart and circulatory physiology","volume":" ","pages":"H945-H962"},"PeriodicalIF":4.1,"publicationDate":"2025-04-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12038818/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143522456","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Warm-ischemia and cold storage induced modulation of ferroptosis observed in human hearts donated after circulatory death and brain death.","authors":"Shiyi Li, Katherine V Nordick, Abdussalam E Elsenousi, Rishav Bhattacharya, Randall P Kirby, Adel M Hassan, Camila Hochman-Mendez, Todd K Rosengart, Kenneth K Liao, Nandan K Mondal","doi":"10.1152/ajpheart.00806.2024","DOIUrl":"10.1152/ajpheart.00806.2024","url":null,"abstract":"<p><p>We investigated ferroptosis, a type of programmed cell death mechanism, in human hearts donated after brain death (DBD) and those donated after circulatory death (DCD), focusing on warm ischemia time (WIT) and cold storage. A total of 24 hearts were procured, with six from the DBD group and 18 from the DCD group. The DCD group was divided into three subgroups, each containing six hearts, based on different WITs of 20, 40, and 60 min. All procured hearts were placed in cold storage for up to 6 h. Left ventricular biopsies were performed at 0, 2, 4, and 6 h. We measured ferroptosis regulators [glutathione peroxidase 4 (GPX4), acyl-CoA synthetase long chain family member 4 (ACSL4), and transferrin receptor], iron content (Fe²⁺ and Fe³⁺), and lipid peroxidation (malondialdehyde, MDA) in the cardiac tissue. Modulation of ferroptosis was observed in both DBD and DCD hearts. Warm ischemia injury increased myocardial vulnerability to ferroptotic cell death. For DBD hearts, up to 6 h of cold storage increases cardiac levels of MDA, iron content, and ACSL4, thereby increasing vulnerability to ferroptotic cell death. In contrast, for DCD hearts with a WIT of 40 min or more, warm ischemia injury was identified as the primary factor contributing to increased myocardial susceptibility to ferroptotic cell death. Ferroptosis may serve as a promising target to optimize cold preservation for DBD hearts. For DCD hearts, strategies to inhibit ferroptosis should focus on the early warm ischemia phase to assess donor heart quality and suitability for transplantation.<b>NEW & NOTEWORTHY</b> The first human heart research explored the effects of ischemia on the myocardial ferroptotic cell death mechanism. Prolonged cold storage increases the susceptibility of DBD hearts to ferroptotic cell death. In contrast, warm ischemic injury appears to be the main factor leading to the vulnerability of DCD heart ferroptosis. Targeting ferroptosis could be beneficial in optimizing cold preservation for DBD hearts. However, for DCD hearts, interventions should focus on the early phase of warm ischemia.</p>","PeriodicalId":7692,"journal":{"name":"American journal of physiology. Heart and circulatory physiology","volume":" ","pages":"H923-H936"},"PeriodicalIF":4.1,"publicationDate":"2025-04-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143584163","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":"Exploring the mechanisms of sex-specific proarrhythmia in long QT syndrome through computational modeling.","authors":"Isabella Doherty, Roshni Shetty, Haibo Ni, Stefano Morotti, Eleonora Grandi","doi":"10.1152/ajpheart.00792.2024","DOIUrl":"10.1152/ajpheart.00792.2024","url":null,"abstract":"<p><p>Females exhibit longer QT intervals and a higher risk of long QT syndrome (LQTS) associated arrhythmogenesis compared with males. Although several studies suggest these sex disparities result from the effect of sex hormones on cardiac ion channels, the underlying mechanisms remain incompletely understood. This research investigates the arrhythmogenic effects, sex-specific risk, and mechanisms associated with LQTS linked to either to loss-of-function of the rapidly activating delayed rectifier K⁺ current (<i>I</i>_Kr), or gain-of-function of the L-type Ca²⁺ current (<i>I</i>_CaL). We primarily used the Tomek-Rodriguez (ToR-ORd) model of human ventricular cardiomyocytes and incorporated sex-specific parameterizations based on previous studies. The O'Hara-Rudy and Grandi-Bers models were used to demonstrate model-independence of the findings. We used a populations-of-models approach to assess early afterdepolarization (EAD) susceptibility in control and LQTS male and female groups. All female models had consistently longer action potentials and were more prone to EADs than male models. In the ToR-ORd model, <i>I</i>_Kr loss-of-function led to EADs in 65.8% of females versus 22.8% of males. <i>I</i>_CaL gain-of-function led to EADs in 66.2% of females but only 3.6% of males. Using logistic regression analysis, we identified key ionic predictors of EAD susceptibility, with maximal conductance of the L-type Ca²⁺ current (<i>G</i>_CaL) and maximal transport rate of the Na⁺/Ca²⁺ exchanger (<i>G</i>_NCX) consistently emerging as positively and maximal conductance of the rapidly activating delayed rectifier K⁺ current (<i>G</i>_Kr) as negatively associated to EADs across both sexes and LQTS types. Notably, higher <i>G</i>_NCX but lower <i>G</i>_Kr in female versus male cardiomyocytes could explain heightened female EAD risk. Our studies explore the ionic traits that favor (or confer resilience against) EADs with potential implications for personalized treatments. <b>NEW & NOTEWORTHY</b> We explored sex disparities in long QT syndrome (LQTS) using sex-specific human ventricular cardiomyocyte models. We showed that females exhibit greater susceptibility to early afterdepolarizations (EADs) than males, and identified key ionic predictors of EAD risk, including increases in the voltage-gated L-type Ca²⁺ current and electrogenic Na⁺/Ca²⁺ exchanger, and downregulation of the rapidly activating delayed rectifier K⁺ current. These findings offer new insights into sex-specific mechanisms underlying arrhythmogenesis in LQTS, with potential implications for personalized treatments.</p>","PeriodicalId":7692,"journal":{"name":"American journal of physiology. Heart and circulatory physiology","volume":" ","pages":"H963-H972"},"PeriodicalIF":4.1,"publicationDate":"2025-04-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12034239/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143623108","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}