Precision nutrition最新文献

{"title":"Efficacy, biosafety, and metabolic impacts of feeding mice egg yolks enriched with three bioactive nutrients in different combinations","authors":"Keith J. Ou, A. Magnuson, X. Lei","doi":"10.1097/PN9.0000000000000039","DOIUrl":"https://doi.org/10.1097/PN9.0000000000000039","url":null,"abstract":"Background: Docosahexaenoic acid (DHA), 25-hydroxyvitamin D3 (25-OH D3), and astaxanthin (AST) are three bioactive and health-promoting nutrients. We previously enriched eggs with DHA alone and in combination with 25-OH D3 and (or) AST as a novel food source of these nutrients by the public. This study was to determine dietary efficacy, biosafety, and metabolic impacts and mechanisms of feeding these egg yolks with four different enrichments of the three nutrients in mice. Methods: Eighty mice (23- to 40-week-old, n = 8, four males and females each) were divided into two experiments and were fed a sucrose-yeast basal diet with control egg yolk (BD) or one of the four types of enriched yolks (BD + DHA, BD + DHA + 25-OH D3, BD + DHA + AST, and BD + DHA + 25-OH D3 + AST) at recommended (1X, Experiment I) and high dose (5X, Experiment II) for 6 weeks. Concentrations of fatty acids, 25-OH D3, AST, and lipids and expression of genes and proteins related to lipid and vitamin D metabolism in the plasma, liver, and (or) heart were determined. Data within each experiment were analyzed by one-way ANOVA. Results: Compared with BD, the four diets with enriched yolks at the 1X level elevated (P < 0.001, up to 61%) hepatic DHA concentrations. Feeding the enriched yolks at either dose did not affect body weights or plasma glucose and triacylglycerol concentrations. In Experiment I, total cholesterol concentrations were 40% higher (P < 0.05) in the liver of BD + DHA than BD and were 1.5-fold higher (P < 0.05) in the heart of BD + DHA + 25-OH D3 + AST than BD + DHA + 25-OH D3. Compared with BD + DHA, BD + DHA + 25-OH D3 upregulated (P < 0.05) hepatic Dgat1 gene expression by 1.4-fold and hepatic DGAT1 protein expression by 1.7-fold. Conclusions: Feeding mice egg yolks enriched with DHA alone or with other nutrients at two doses (1X and 5X) improved hepatic DHA status and exerted moderate impacts on tissue lipid profiles and the related gene expressions. These eggs may be safe for future human trials.","PeriodicalId":74488,"journal":{"name":"Precision nutrition","volume":"2 1","pages":"e00039"},"PeriodicalIF":0.0,"publicationDate":"2023-05-24","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"46850517","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"β-hydroxybutyrate inhibits cellular proliferation, EMT, stemness, migration, and invasion in glioma cells","authors":"Junrong Yang, Ning Zhang, Zhengping Wang, Qingpeng Wang, Jun Han, Muhammad Akram Khan, Aayesha Riaz, Chongfei Chang","doi":"10.1097/PN9.0000000000000038","DOIUrl":"https://doi.org/10.1097/PN9.0000000000000038","url":null,"abstract":"Glioma is the most common and account for 81% of intracranial malignancies. Ketogenic dietary intervention in patients with glioma has been more and more popular. However, the current research mechanism on β-hydroxybutyrate (BHB) and glioma is not clear, and we have explored the mechanism of BHB inhibiting glioma. Western blot, polymerase chain reaction (PCR), and immunofluorescence were used to study the relationship between BHB and proliferation, stemness, epithelial mesenchymal transformation, migration, and invasion of glioma U251 cells. In the present study, our results showed that BHB treatment downregulated the expressions of epithelial-to-mesenchymal transition (EMT)-related proteins including N-cadherin and vimentin, while upregulated the expression of E-cadherin in U251 glioma cells, when compared with control group. Meanwhile, the expressions of matrix metallopeptidase (MMP)2, MMP9, and vascular endothelial growth factor A (VEGFA) proteins were decreased in BHB-treated group. The expression levels of TGF-β, p-phosphatidylinositol-3-kinase (PI3K), p-protein kinase B (Akt), p-glycogen synthase kinase 3β (GSK-3β), Wnt5a, β-catenin, and Snail were decreased in the BHB-treated group, as our results showed. Additionally, BHB treatment downregulated the expressions of p-Janus kinase 2 (JAK2) and p-signal transducer and activator of transcription 3 (STAT3) proteins, which are related to migration of glioma cells, respectively. In addition, BHB inhibited glioma stemness genes such as CD133, ALDH1, SOX2, and Olig2. Altogether, present study concluded that BHB inhibited proliferation, EMT, and migration of glioma cells by inhibiting transforming growth factor (TGF)-β/PI3K/Akt/GSK-3β, Wnt5a/β-catenin/Snail, and interleukin (IL)-6/JAK2/STAT3 signaling pathways, therefore, with a diet containing BHB will benefit the glioma patients.","PeriodicalId":74488,"journal":{"name":"Precision nutrition","volume":"2 1","pages":"e00038"},"PeriodicalIF":0.0,"publicationDate":"2023-05-17","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"45229993","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Prenatal Nutrition and Developmental Origins of Health and Disease.","authors":"Xiaobin Wang","doi":"10.1097/PN9.0000000000000040","DOIUrl":"10.1097/PN9.0000000000000040","url":null,"abstract":"","PeriodicalId":74488,"journal":{"name":"Precision nutrition","volume":"2 2","pages":"e00040"},"PeriodicalIF":0.0,"publicationDate":"2023-05-17","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://ftp.ncbi.nlm.nih.gov/pub/pmc/oa_pdf/bd/e1/pn9-2-e00040.PMC10599801.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"54232738","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":"Independent and joint association of cord plasma pantothenate and cysteine levels with autism spectrum disorders and other neurodevelopmental disabilities in children born term and preterm.","authors":"Ramkripa Raghavan,&nbsp;Guoying Wang,&nbsp;Xiumei Hong,&nbsp;Colleen Pearson,&nbsp;Hehuang Xie,&nbsp;William G Adams,&nbsp;Marilyn Augustyn,&nbsp;Xiaobin Wang","doi":"10.1097/PN9.0000000000000036","DOIUrl":"10.1097/PN9.0000000000000036","url":null,"abstract":"<p><strong>Background: </strong>Pantothenate (vitamin B5) is a precursor for coenzyme A (CoA) synthesis, which serves as a cofactor for hundreds of metabolic reactions. Cysteine is an amino acid in the CoA synthesis pathway. To date, research on the combined role of early life pantothenate and cysteine levels in childhood neurodevelopmental disabilities is scarce.</p><p><strong>Objective: </strong>To study the association between cord pantothenate and cysteine levels and risk of autism spectrum disorder (ASD), attention deficit hyperactivity disorder (ADHD) and other developmental disabilities (DD) in children born term and preterm.</p><p><strong>Methods: </strong>The study sample (<i>n</i> = 996, 177 born preterm) derived from the Boston Birth Cohort included 416 neurotypical children, 87 ASD, 269 ADHD, and 224 other DD children, who were mutually exclusive. Participants were enrolled at birth and were followed up prospectively (from October 1, 1998, to June 30, 2018) at the Boston Medical Center. Cord blood sample was collected at birth. Plasma pantothenate and cysteine levels were measured using liquid chromatography-tandem mass spectrometry.</p><p><strong>Results: </strong>Higher cord pantothenate (≥50th percentile <i>vs.</i> <50th percentile) was associated with a greater risk of ASD (adjusted odds ratio [aOR]: 1.94, 95% confidence interval [CI]: 1.06, 3.55) and ADHD (aOR: 1.66, 95% CI: 1.14, 2.40), after adjusting for potential confounders. However, cord cysteine alone was not associated with risk of ASD, ADHD, or other DD. When considering the joint association, greater ASD risk was noted when both cord pantothenate and cysteine levels were elevated (≥50th percentile) (aOR: 3.11, 95% CI: 1.24, 7.79), when compared to children with low cord pantothenate (<50th percentile) and high cysteine. Even though preterm and higher pantothenate independently increased the ASD risk, the greatest risk was found in preterm children who also had elevated pantothenate (≥50th percentile), which was true for all three outcomes: ASD (aOR: 5.36, 95% CI: 2.09, 13.75), ADHD (aOR: 3.31, 95% CI: 1.78, 6.16), and other DD (aOR: 3.39, 95% CI: 1.85, 6.24).</p><p><strong>Conclusions: </strong>In this prospective birth cohort, we showed that higher cord pantothenate individually and in combination with higher cysteine or preterm birth were associated with increased risk of ASD and ADHD. More study is needed to explore this biologically plausible pathway.</p>","PeriodicalId":74488,"journal":{"name":"Precision nutrition","volume":"2 2","pages":"e00036"},"PeriodicalIF":0.0,"publicationDate":"2023-05-11","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://ftp.ncbi.nlm.nih.gov/pub/pmc/oa_pdf/40/3c/pn9-2-e00036.PMC10513014.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"41174244","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":"Defining longitudinal trajectory of body mass index percentile and predicting childhood obesity: methodologies and findings in the Boston Birth Cohort.","authors":"Wanyu Huang,&nbsp;Anat Yaskolka Meir,&nbsp;Bolanle Olapeju,&nbsp;Guoying Wang,&nbsp;Xiumei Hong,&nbsp;Maya Venkataramani,&nbsp;Tina L Cheng,&nbsp;Tak Igusa,&nbsp;Liming Liang,&nbsp;Xiaobin Wang","doi":"10.1097/PN9.0000000000000037","DOIUrl":"10.1097/PN9.0000000000000037","url":null,"abstract":"<p><strong>Background: </strong>Overweight or obesity (OWO) in school-age childhood tends to persist into adulthood. This study aims to address a critical need for early identification of children at high risk of developing OWO by defining and analyzing longitudinal trajectories of body mass index percentile (BMIPCT) during early developmental windows.</p><p><strong>Methods: </strong>We included 3029 children from the Boston Birth Cohort (BBC) with repeated BMI measurements from birth to age 18 years. We applied locally weighted scatterplot smoothing with a time-limit scheme and predefined rules for imputation of missing data. We then used time-series <i>K</i>-means cluster analysis and latent class growth analysis to define longitudinal trajectories of BMIPCT from infancy up to age 18 years. Then, we investigated early life determinants of the BMI trajectories. Finally, we compared whether using early BMIPCT trajectories performs better than BMIPCT at a given age for predicting future risk of OWO.</p><p><strong>Results: </strong>After imputation, the percentage of missing data ratio decreased from 36.0% to 10.1%. We identified four BMIPCT longitudinal trajectories: early onset OWO; late onset OWO; normal stable; and low stable. Maternal OWO, smoking, and preterm birth were identified as important determinants of the two OWO trajectories. Our predictive models showed that BMIPCT trajectories in early childhood (birth to age 1 or 2 years) were more predictive of childhood OWO (age 5-10 years) than a single BMIPCT at age 1 or 2 years.</p><p><strong>Conclusions: </strong>Using longitudinal BMIPCT data from birth to age 18 years, this study identified distinct BMIPCT trajectories, examined early life determinants of these trajectories, and demonstrated their advantages in predicting childhood risk of OWO over BMIPCT at a single time point.</p>","PeriodicalId":74488,"journal":{"name":"Precision nutrition","volume":"2 2","pages":"e00037"},"PeriodicalIF":0.0,"publicationDate":"2023-04-21","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://ftp.ncbi.nlm.nih.gov/pub/pmc/oa_pdf/22/e2/pn9-2-e00037.PMC10513013.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"41174243","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":"A triple enrichment of three bioactive nutrients in eggs of laying hens elicited moderate interactions on related gene expression","authors":"Keith J. Ou, A. Magnuson, Ziqiao Sun, Sahil Kalia, T. Sun, Xingen Lei","doi":"10.1097/PN9.0000000000000034","DOIUrl":"https://doi.org/10.1097/PN9.0000000000000034","url":null,"abstract":"Background: Dietary intakes of docosahexaenoic acid (DHA), 25-hydroxyvitamin D3 (25-OH D3), and astaxanthin (AST) are associated with reduced risks of chronic diseases. Because the commonly consumed foods by the public do not provide adequate intakes of these three bioactive nutrients, chicken eggs have emerged as an economical and convenient carrier for such dietary supplementation. The objective of this study was to enrich poultry eggs with DHA, 25-OH D3, and AST and to explore the potential interactions from the enrichments. Methods: Fifty laying hens were individually housed and fed a corn-soybean meal basal diet (BD), BD + DHA, BD + DHA + 25-OH D3, BD + DHA + AST, or BD + DHA + 25-OH D3 + AST for 6 weeks (n = 10). Animal health and production status, fatty acid profiles, 25-OH D3 and AST levels, and gene expressions in eggs, plasma, and tissues were measured. Data were analyzed by one-way analysis of variance (ANOVA). Results: BD + DHA resulted in 16 mg DHA/g yolk, whereas the enrichment was decreased by the addition of AST (13%) but not 25-OH D3. DHA was also deposited into the liver and adipose tissue. Egg yolk and hepatic arachidonic acid (ARA) concentrations were lowered (34%) in BD + DHA in response to the DHA supplementation. Enrichments of 25-OH D3 and AST reached 160 ng/g yolk and 5.5 µg/g yolk, respectively. BD + DHA upregulated hepatic expressions of ELOVL5 and SRB1, but the addition of 25-OH D3 diminished the ELOVL5 upregulation and downregulated FABP2 and the addition of AST lowered CPT1A expressions. Conclusions: This study demonstrated a successful triple enrichment of DHA, 25-OH D3, and AST in the egg yolks to nutritionally relevant levels for human consumption. The additional 25-OH D3 and (or) AST supplementations prompted novel effects on the yolk DHA enrichment and lipid-related gene expressions in the liver and intestine. Our findings provided the scientific evidence and feasibility for the animal and food industry to produce a new-type of health-promoting eggs.","PeriodicalId":74488,"journal":{"name":"Precision nutrition","volume":"2 1","pages":"e00034"},"PeriodicalIF":0.0,"publicationDate":"2023-04-06","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"45482357","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Erratum: Hunger-free hospital initiative: fighting \"the skeleton in the hospital closet\": Erratum.","authors":"","doi":"10.1097/PN9.0000000000000025","DOIUrl":"https://doi.org/10.1097/PN9.0000000000000025","url":null,"abstract":"<p><p>[This corrects the article DOI: 10.1097/PN9.0000000000000018.].</p>","PeriodicalId":74488,"journal":{"name":"Precision nutrition","volume":"2 1","pages":"e00025"},"PeriodicalIF":0.0,"publicationDate":"2023-03-16","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://ftp.ncbi.nlm.nih.gov/pub/pmc/oa_pdf/f1/78/pn9-2-e00025.PMC10513019.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"41171307","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":"Gut microbiota and cancer-associated malnutrition","authors":"Qinyue Wang, Dan Li, Jingtao Sun, Jiai Yan, Yingyu Wang, Ju Yang, Feng Zhang","doi":"10.1097/PN9.0000000000000033","DOIUrl":"https://doi.org/10.1097/PN9.0000000000000033","url":null,"abstract":"Cancer-associated malnutrition (CAM) is a great threat to the survive and life quality of patients with cancer. Several mechanisms have been elucidated in the occurrence and development of CAM. In recent decades, roles of the disordered gut microbiota in the malignant tumor and the malnutrition drew more and more attention. However, study on the correlation between gut microbiota with CAM still remains in its infancy. This review demonstrates the trigger for the CAM resulting from the dysbiosis of the gut microbiota induced by the nutrition deficiency or excess and the alleviation of CAM by the modulation of the gut microbiota. The underlying mechanisms of the gut microbiota in the aggravation or amelioration of CAM are also discussed. Further study is still warranted in the roles of the gut microbiota in the influence of CAM.","PeriodicalId":74488,"journal":{"name":"Precision nutrition","volume":"2 1","pages":"e00033"},"PeriodicalIF":0.0,"publicationDate":"2023-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"45099156","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Nonalcoholic fatty liver disease: pathogenesis and intervention","authors":"Lei Hao, Z. Chai","doi":"10.1097/PN9.0000000000000029","DOIUrl":"https://doi.org/10.1097/PN9.0000000000000029","url":null,"abstract":"Nonalcoholic fatty liver disease (NAFLD) is the most frequent liver disease in Western nations. NAFLD is characterized by intrahepatic fat accumulation (first “hit”) and can progress to nonalcoholic steatohepatitis by the second “hit,” such as free fatty acid lipotoxicity, and oxidative stress. It is believed that multifactorial complex interactions between diet, lifestyle, gut microbiota, and genetic background determine the development of NAFLD. Currently, the management of NAFLD is based on lifestyle modification, such as diet and physical activity, and pharmacological intervention. As the understanding of NAFLD pathophysiology furthers, some interesting novel approaches to treating NAFLD are emerging, such as antioxidants and probiotics. This review is focused on the pathogenesis of NAFLD and potential therapeutic approaches to treat the disease.","PeriodicalId":74488,"journal":{"name":"Precision nutrition","volume":"2 1","pages":"e00029"},"PeriodicalIF":0.0,"publicationDate":"2023-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"47829271","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Evidence-based guideline on immunonutrition in patients with cancer","authors":"J. Cui, Yudi Liu, Fan Li, W. Zhuo, Lan Huang, Chuan Xu, Wei Li, Jianyong Qin, Xuejun Sun, H. Tian, Tingting Liang, Ping-An Chen, Bo Chen, Qiuyan Liu, J. Ying, Ningning Li, An-ping Zhang, Yang Yu, Zhi-Feng Zhou, Xiu-Dong Wu, Xiao‐Kai Guo, Lingdi Zhao, Junya Zhai, Zhao-yang Yang, J. Yang, Xia Li, Yong Li, Guo-en Liu, Guo-rui Sun, Zhenguo Han, Xiaojun Yang, Wei Cui, F. Chen, Yuehua Wu, Liang Liu, Gui-Rong Li, Jing Dai, Zheng Zhao, B. Zhao, Xiaoyan Kuang, Xinfeng Zhou, Y. Tan, Han-ping Shi","doi":"10.1097/PN9.0000000000000031","DOIUrl":"https://doi.org/10.1097/PN9.0000000000000031","url":null,"abstract":"Background: Malnutrition in patients with malignant tumors caused by the tumor or related treatment is a significant problem in clinical practice. “Cancer immunonutrition” therapy improves patients’ nutritional condition and immune function. It uses specific nutrients to improve the nutritional status of patients with cancer and regulates the body’s immune and inflammatory responses. To date, cancer immunonutrition has been used in surgery, chemoradiotherapy, hematopoietic stem cell transplantation (HSCT), treatment of tumor complications, and other fields. Therefore, we aimed to develop rigorous and detailed evidence-based practice guidelines for cancer immunonutrition therapy. Methods: The guideline strictly followed the latest guidelines from the Institution of Medicine and was constructed according to the World Health Organization handbook for guideline development. It was written according to the Reporting Items for practice Guidelines in Healthcare criteria. The quality of evidence and strength of the recommendations were assessed using the Grading of Recommendations Assessment, Development, and Evaluation method. Results: Twenty-three recommendations were formulated regarding surgery, chemoradiotherapy, HSCT, treatment of tumor complications, and other fields. Conclusions: We developed clinical practice guidelines for cancer immunonutrition therapy based on the latest evidence-based practice to provide more comprehensive and detailed advice to healthcare providers. This guideline broadens the application scope of immunonutrition therapy for cancer and promotes its standardized application in clinical practice.","PeriodicalId":74488,"journal":{"name":"Precision nutrition","volume":"2 1","pages":"e00031"},"PeriodicalIF":0.0,"publicationDate":"2023-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"48367168","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}