Journal of Lipid and Atherosclerosis最新文献

{"title":"Triglyceride-Related Parameters and Symptomatic Atherosclerotic Lesions in Patients With Ischemic Stroke.","authors":"Ki-Woong Nam, Hyung-Min Kwon, Yong-Seok Lee","doi":"10.12997/jla.2024.13.2.155","DOIUrl":"10.12997/jla.2024.13.2.155","url":null,"abstract":"<p><strong>Objective: </strong>Recently, evidence has suggested that the pathophysiology and risk factors of intracranial atherosclerosis (ICAS) differs from those of extracranial atherosclerosis (ECAS). In addition, novel parameters reflecting metabolic conditions, such as insulin resistance or atherogenic dyslipidemia, based on triglycerides (TG) and other biomarkers, have emerged. In this study, we evaluated the association between TG-related parameters and symptomatic cerebral atherosclerosis in patients with acute ischemic stroke resulting from large artery atherosclerosis (LAA).</p><p><strong>Methods: </strong>We assessed consecutive acute LAA-stroke patients between January 2010 and December 2020. Based on the radiological findings, we classified the relevant symptomatic arteries that caused the index stroke into LAA-ICAS and LAA-ECAS. As TG-related parameters, the atherogenic index of plasma (AIP) and TG-glucose (TyG) index were calculated according to the following formulas: AIP = log₁₀ (TG Level/High-density Lipoprotein Cholesterol Level), TyG Index = Ln (TG Level × Glucose Level/2).</p><p><strong>Results: </strong>A total of 519 patients with LAA-stroke were evaluated. In multivariable logistic regression analysis to identify predictors of LAA-ICAS, AIP was significantly associated with LAA-ICAS (adjusted odds ratio [aOR], 3.60; 95% confidence interval [CI], 1.60-8.06). TyG index also showed a statistically significant relationship with LAA-ICAS (aOR, 1.60; 95% CI, 1.11-2.32). However, TG per se did not show a statistical association with LAA-ECAS.</p><p><strong>Conclusion: </strong>TG-related parameters were more closely associated with stroke by ICAS than by ECAS. The metabolic conditions reflected by the AIP or TyG index, rather than hypertriglyceridemia itself, may play a greater role in determining the relevant vessel causally involved in a stroke.</p>","PeriodicalId":16284,"journal":{"name":"Journal of Lipid and Atherosclerosis","volume":"13 2","pages":"155-165"},"PeriodicalIF":0.0,"publicationDate":"2024-05-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11140243/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141198585","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Letter by Hinpetch Daungsupawong Regarding Article, The Role of COVID-19 Vaccination for Patients With Atherosclerotic Cardiovascular Disease in the Upcoming Endemic Era.","authors":"Hinpetch Daungsupawong, Viroj Wiwanitkit","doi":"10.12997/jla.2024.13.2.212","DOIUrl":"10.12997/jla.2024.13.2.212","url":null,"abstract":"","PeriodicalId":16284,"journal":{"name":"Journal of Lipid and Atherosclerosis","volume":"13 2","pages":"212"},"PeriodicalIF":0.0,"publicationDate":"2024-05-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11140246/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141200257","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Association of Higher Hemoglobin Level With Significant Carotid Artery Plaque in the General Population.","authors":"Seong Soon Kwon, Seug Yun Yoon, Kyoung-Ha Kim, Byoung-Won Park, Min-Ho Lee, Hyoungnae Kim, Duk Won Bang","doi":"10.12997/jla.2024.13.2.184","DOIUrl":"10.12997/jla.2024.13.2.184","url":null,"abstract":"<p><strong>Objective: </strong>Serum hemoglobin (Hb) level affects the viscosity of blood. Several studies have reported that Hb level is associated with adverse cardiovascular outcome. However, there is a paucity of evidence on the association between serum Hb level and the risk of subclinical atherosclerosis. Thus, the objective of this study was to investigate the relationship between Hb level and risk of carotid plaque in a health checkup cohort.</p><p><strong>Methods: </strong>This retrospective study analyzed a total of 3,805 individuals without history of cardiovascular disease (CVD) who underwent carotid ultrasonography (USG) between January 2016 and June 2018. Participants were divided into 4 groups based on Hb quartiles in each of male and female. Carotid plaque score was calculated based on USG reports. Multivariable logistic regression analysis was performed for each index of quartile groups regarding the risk of carotid plaque.</p><p><strong>Results: </strong>Of 3,805 individuals (mean age, 52.62±10.25 years; 2,674 [70.28%] males), mean Hb level was 15.11±0.75 g/dL in male and 13.35±0.74 g/dL in female. When the Q1 group was compared to the Q4, increasing quartile of Hb was associated with the presence of significant carotid plaque (plaque score ≥3) in male (adjusted odds ratio [OR], 1.538; 95% confidence interval [CI], 1.182-2.001; <i>p</i>=0.001) and female (adjusted OR, 1.749; 95% CI, 1.058-2.676; <i>p</i>=0.01).</p><p><strong>Conclusion: </strong>A high Hb level is associated with an increased risk of carotid plaques in individuals without history of CVD. This finding may support the need for early screening of CVD in individuals with high Hb levels.</p>","PeriodicalId":16284,"journal":{"name":"Journal of Lipid and Atherosclerosis","volume":"13 2","pages":"184-193"},"PeriodicalIF":0.0,"publicationDate":"2024-05-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11140247/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141200200","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"BDNF Signaling in Vascular Dementia and Its Effects on Cerebrovascular Dysfunction, Synaptic Plasticity, and Cholinergic System Abnormality.","authors":"Juhyun Song","doi":"10.12997/jla.2024.13.2.122","DOIUrl":"10.12997/jla.2024.13.2.122","url":null,"abstract":"<p><p>Vascular dementia (VaD) is the second most common type of dementia and is characterized by memory impairment, blood-brain barrier disruption, neuronal cell loss, glia activation, impaired synaptic plasticity, and cholinergic system abnormalities. To effectively prevent and treat VaD a good understanding of the mechanisms underlying its neuropathology is needed. Brain-derived neurotrophic factor (BDNF) is an important neurotrophic factor with multiple functions in the systemic circulation and the central nervous system and is known to regulate neuronal cell survival, synaptic formation, glia activation, and cognitive decline. Recent studies indicate that when compared with normal subjects, patients with VaD have low serum BDNF levels and that BDNF deficiency in the serum and cerebrospinal fluid is an important indicator of VaD. Here, we review current knowledge on the role of BDNF signaling in the pathology of VaD, such as cerebrovascular dysfunction, synaptic dysfunction, and cholinergic system impairment.</p>","PeriodicalId":16284,"journal":{"name":"Journal of Lipid and Atherosclerosis","volume":"13 2","pages":"122-138"},"PeriodicalIF":0.0,"publicationDate":"2024-05-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11140249/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141200253","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"The Effect of Omega-3 Supplementation on Heart Failure Outcome: A Meta-Analysis of Randomized Clinical Trial.","authors":"Bambang Dwiputra, Ade Meidian Ambari, Dwita Rian Desandri, Budhi Setianto Purwowiyoto, Basuni Radi, Bashar Adi Wahyu Pandhita, Serlie Fatrin, Anwar Santoso","doi":"10.12997/jla.2024.13.2.89","DOIUrl":"10.12997/jla.2024.13.2.89","url":null,"abstract":"<p><p>The effect of omega-3 supplementation on cardiovascular (CV) disease has been widely studied in several large clinical trials. However, the evidence of the effect of omega-3 supplementation in patients with heart failure (HF) remains controversial. This meta-analysis investigated the effects of omega-3 supplementation on patients with HF. We conducted a literature search on MEDLINE, Embase, and Cochrane databases for clinical trials and preprints of relevant articles. Following a literature search and critical appraisal, 5 studies were included in the meta-analysis. The pooling of the result of the studies shows that there were no significant association between omega-3 supplementation and CV mortality (odds ratio [OR], 0.94; 95% confidence interval [CI], 0.84-1.05, <i>p</i>=0.16) nor hospitalization due to HF (OR, 0.94; 95% CI, 0.88-1.02; <i>p</i>=0.13). Our systematic review and meta-analysis showed that omega-3 supplementation has no beneficial effect in patients with HF.</p>","PeriodicalId":16284,"journal":{"name":"Journal of Lipid and Atherosclerosis","volume":"13 2","pages":"89-96"},"PeriodicalIF":0.0,"publicationDate":"2024-05-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11140252/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141200261","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Applicability of Artificial Intelligence in the Field of Clinical Lipidology: A Narrative Review.","authors":"Walter Masson, Pablo Corral, Juan P Nogueira, Augusto Lavalle-Cobo","doi":"10.12997/jla.2024.13.2.111","DOIUrl":"10.12997/jla.2024.13.2.111","url":null,"abstract":"<p><p>The development of advanced technologies in artificial intelligence (AI) has expanded its applications across various fields. Machine learning (ML), a subcategory of AI, enables computers to recognize patterns within extensive datasets. Furthermore, deep learning, a specialized form of ML, processes inputs through neural network architectures inspired by biological processes. The field of clinical lipidology has experienced significant growth over the past few years, and recently, it has begun to intersect with AI. Consequently, the purpose of this narrative review is to examine the applications of AI in clinical lipidology. This review evaluates various publications concerning the diagnosis of familial hypercholesterolemia, estimation of low-density lipoprotein cholesterol (LDL-C) levels, prediction of lipid goal attainment, challenges associated with statin use, and the influence of cardiometabolic and dietary factors on the discordance between apolipoprotein B and LDL-C. Given the concerns surrounding AI techniques, such as ethical dilemmas, opacity, limited reproducibility, and methodological constraints, it is prudent to establish a framework that enables the medical community to accurately interpret and utilize these emerging technological tools.</p>","PeriodicalId":16284,"journal":{"name":"Journal of Lipid and Atherosclerosis","volume":"13 2","pages":"111-121"},"PeriodicalIF":0.0,"publicationDate":"2024-05-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11140245/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141200198","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Differences in Risk Factors for Coronary Atherosclerosis According to Sex.","authors":"Hack-Lyoung Kim","doi":"10.12997/jla.2024.13.2.97","DOIUrl":"10.12997/jla.2024.13.2.97","url":null,"abstract":"<p><p>Interest in sex differences related to coronary artery disease (CAD) has steadily increased, and the risk factors for CAD show distinct sex differences. For women, cardiovascular risk increases significantly after menopause due to a decrease in estrogen levels. In older individuals, increased arterial stiffness results in a higher pulse pressure, leading to a more common occurrence of isolated systolic hypertension; these changes are more noticeable in women. While the incidence of diabetes is similar in both sexes, women with diabetes face a 50% higher relative risk of fatal coronary heart disease compared to men. Smoking significantly increases the risk of ischemic heart disease in women, particularly those who are younger. The decrease in estrogen in women leads to a redistribution of fat, resulting in increased abdominal obesity and, consequently, an elevated cardiovascular risk. Pregnancy and reproductive factors also have a significant impact on CAD risks in women. Additionally, disparities exist in medical practice. Women are less likely to be prescribed cardioprotective drugs, referred for interventional or surgical treatments, or included in clinical research than men. By increasing awareness of these sex differences and addressing the disparities, we can progress toward more personalized treatment strategies, ultimately improving patient outcomes.</p>","PeriodicalId":16284,"journal":{"name":"Journal of Lipid and Atherosclerosis","volume":"13 2","pages":"97-110"},"PeriodicalIF":0.0,"publicationDate":"2024-05-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11140242/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141200254","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Mitochondrial Genome Editing: Exploring the Possible Relationship of the Atherosclerosis-Associated Mutation m.15059G>A With Defective Mitophagy.","authors":"Vasily N Sukhorukov, Victoria A Khotina, Vladislav A Kalmykov, Alexander D Zhuravlev, Vasily V Sinyov, Daniil Y Popov, Andrey Y Vinokurov, Igor A Sobenin, Alexander N Orekhov","doi":"10.12997/jla.2024.13.2.166","DOIUrl":"10.12997/jla.2024.13.2.166","url":null,"abstract":"<p><strong>Objective: </strong>The aim of this study was to evaluate the effect of the m.15059G>A mitochondrial nonsense mutation on cellular functions related to atherosclerosis, such as lipidosis, pro-inflammatory response, and mitophagy. Heteroplasmic mutations have been proposed as a potential cause of mitochondrial dysfunction, potentially disrupting the innate immune response and contributing to the chronic inflammation associated with atherosclerosis.</p><p><strong>Methods: </strong>The human monocytic cell line THP-1 and cytoplasmic hybrid cell line TC-HSMAM1 were used. An original approach based on the CRISPR/Cas9 system was developed and used to eliminate mitochondrial DNA (mtDNA) copies carrying the m.15059G>A mutation in the <i>MT-CYB</i> gene. The expression levels of genes encoding enzymes related to cholesterol metabolism were analyzed using quantitative polymerase chain reaction. Pro-inflammatory cytokine secretion was assessed using enzyme-linked immunosorbent assays. Mitophagy in cells was detected using confocal microscopy.</p><p><strong>Results: </strong>In contrast to intact TC-HSMAM1 cybrids, Cas9-TC-HSMAM1 cells exhibited a decrease in fatty acid synthase (<i>FASN</i>) gene expression following incubation with atherogenic low-density lipoprotein. TC-HSMAM1 cybrids were found to have defective mitophagy and an inability to downregulate the production of pro-inflammatory cytokines (to establish immune tolerance) upon repeated lipopolysaccharide stimulation. Removal of mtDNA harboring the m.15059G>A mutation resulted in the re-establishment of immune tolerance and the activation of mitophagy in the cells under investigation.</p><p><strong>Conclusion: </strong>The m.15059G>A mutation was found to be associated with defective mitophagy, immune tolerance, and impaired metabolism of intracellular lipids due to upregulation of <i>FASN</i> in monocytes and macrophages.</p>","PeriodicalId":16284,"journal":{"name":"Journal of Lipid and Atherosclerosis","volume":"13 2","pages":"166-183"},"PeriodicalIF":0.0,"publicationDate":"2024-05-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11140244/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141200258","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"The Relationship of Fetuin-A with Coronary Calcification, Carotid Atherosclerosis, and Mortality Risk in Non-Dialysis Chronic Kidney Disease.","authors":"Osama Nady Mohamed, Mahmoud Ragab Mohamed Mohamed, Israa Gamal Hassan, Atef Farouk Alakkad, Ashraf Othman, Amr Setouhi, Ahmed S Issa","doi":"10.12997/jla.2024.13.2.194","DOIUrl":"10.12997/jla.2024.13.2.194","url":null,"abstract":"<p><strong>Objective: </strong>This study investigated the relationship of fetuin-A with coronary calcification, carotid atherosclerosis, and mortality risk in non-dialysis chronic kidney disease (CKD).</p><p><strong>Methods: </strong>The study included 135 adult patients with CKD at stages 3-5, who were divided into coronary artery calcification (CAC) and non-CAC groups. We excluded current smokers and individuals with diabetes mellitus, inflammatory conditions, liver diseases, acute kidney failure, chronic hemodialysis, and cancer. We conducted kidney function tests, complete blood counts, and measured serum levels of fetuin-A, tumor necrosis factor-alpha (TNF-α), high-sensitivity C-reactive protein (hs-CRP), interleukin-6 (IL-6), total cholesterol (TC), total triglycerides (TG), high-density lipoprotein cholesterol, and low-density lipoprotein cholesterol. Cardiac spiral computed tomography was used to calculate the CAC score, employing the Agatston method. Carotid ultrasonography was performed to assess carotid intima-media thickness (CIMT) and to detect the presence of plaques.</p><p><strong>Results: </strong>CAC patients had considerably higher levels of TNF-α (<i>p</i><0.001), IL-6 (<i>p</i><0.001), hs-CRP (<i>p</i>=0.006), TC, TG, parathyroid hormone (PTH) (<i>p</i><0.001) and phosphorus (<i>p</i><0.001) than non-CAC patients. They also had significantly lower levels of fetuin-A (<i>p</i><0.001). Fetuin-A was considerably lower in CKD subgroups as CKD progressed. Fetuin-A (<i>p</i>=0.046), age (<i>p</i>=0.009), TNF-α (<i>p</i>=0.027), IL-6 (<i>p</i>=0.005), TG (<i>p</i>=0.002), PTH (<i>p</i>=0.002), and phosphorus (<i>p</i>=0.004) were significant predictors of CAC. CAC and fetuin-A were strong predictors of all-cause mortality and cardiovascular (CV) mortality. Fetuin-A was a significant predictor of CIMT (<i>p</i>=0.045).</p><p><strong>Conclusion: </strong>Fetuin-A reliably predicted CAC and CIMT. Fetuin-A and CAC emerged as significant risk factors for all-cause and CV mortality in non-dialysis CKD.</p>","PeriodicalId":16284,"journal":{"name":"Journal of Lipid and Atherosclerosis","volume":"13 2","pages":"194-211"},"PeriodicalIF":0.0,"publicationDate":"2024-05-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11140250/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141200262","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Dyslipidemia Treatment and Cerebrovascular Disease: Evidence Regarding the Mechanism of Stroke.","authors":"Sang Hee Ha, Bum Joon Kim","doi":"10.12997/jla.2024.13.2.139","DOIUrl":"10.12997/jla.2024.13.2.139","url":null,"abstract":"<p><p>Dyslipidemia stands as a significant risk factor for stroke, on par with the impact of hypertension, diabetes, and smoking. While the role of dyslipidemia is firmly established in the context of coronary artery disease, its influence on strokes remains somewhat enigmatic. This complexity likely arises from the diverse mechanisms underpinning strokes, which encompass a heterogeneous spectrum (hemorrhagic and ischemic; large artery atherosclerosis, small vessel occlusion, cardioembolism, and etc.). The extent to which lipid-lowering treatments affect stroke outcomes may vary depending on the specific stroke subtype. For instance, in cases of large artery atherosclerosis (LAA), the optimal target level of low-density lipoprotein cholesterol (LDL-C) is relatively clear. However, when dealing with other stroke subtypes like small vessel occlusion or cardioembolism, the appropriate LDL-C target remains uncertain. Furthermore, reperfusion therapy has emerged as the foremost treatment for acute ischemic stroke. Nevertheless, the precise relationship between LDL-C levels and outcomes in patients undergoing reperfusion therapy remains shrouded in uncertainty. Consequently, we have undertaken an in-depth exploration of the existing evidence supporting the utilization of lipid-lowering medications such as statins, ezetimibe, and proprotein convertase subtilisin/kexin type 9 (PCSK9) inhibitors. Our objective is to elucidate their role in secondary stroke prevention and the management of dyslipidemia across the various stroke subtypes.</p>","PeriodicalId":16284,"journal":{"name":"Journal of Lipid and Atherosclerosis","volume":"13 2","pages":"139-154"},"PeriodicalIF":0.0,"publicationDate":"2024-05-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11140251/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141200256","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}