Obesity Medicine最新文献

{"title":"Real-world comparative outcomes of glucagon like peptide-1 receptor agonists and bariatric surgery in inflammatory bowel disease: A multi-center cohort study","authors":"Joshua Chen,&nbsp;Riya Patel,&nbsp;Husam Mikati,&nbsp;Sasha Mangray,&nbsp;Jennifer Salluzzo,&nbsp;Stephen J. Bickston,&nbsp;Raseen Tariq","doi":"10.1016/j.obmed.2026.100727","DOIUrl":"10.1016/j.obmed.2026.100727","url":null,"abstract":"<div><h3>Aims</h3><div>Obesity is common in patients with inflammatory bowel disease (IBD) and may influence disease course. This study aimed to compare Glucagon-like peptide-1 receptor agonists (GLP-1RA) and metabolic bariatric surgery (MBS) outcomes in IBD patients.</div></div><div><h3>Methods</h3><div>Retrospective cohort study utilizing the TriNetX database comparing IBD-specific and weight loss outcomes, with sub analysis by IBD type, for patients with obesity treated with GLP-1RA versus MBS. Primary outcomes were intravenous (IV) steroid use, oral steroid use, IBD related surgery, and hospitalization/emergency department(ED) visits. Secondary outcomes included body mass index (BMI) weight loss, Hemoglobin A1c(A1c) 1month–3 years after the index event, 1:1 propensity score matching (PSM) was performed.</div></div><div><h3>Results</h3><div>We identified 455 patients in the MBS cohort (mean age 45.9 ± 11.9 years, 84.4% female, 76.3% white) and 4546 patients in the GLP-1RA cohort (mean age 54.4 ± 12.8 years, 70.5% female, 77.2% white). After PSM, MBS was associated with a significantly lower risk of IV steroid use (OR: 0.664; 95% CI: 0.477–0.925; <em>p</em> = 0.0152) and oral steroid use (OR: 0.605; 95% CI: 0.456–0.803; <em>p</em> = 0.0005) compared to GLP-1RA. MBS group demonstrated lower mean BMI, weight, and A1c all had p &lt; 0.0001.</div></div><div><h3>Conclusions</h3><div>MBS was associated with decreased IV steroid use, oral steroid use and improved metabolic outcomes compared to GLP-1RA in IBD patients.</div></div>","PeriodicalId":37876,"journal":{"name":"Obesity Medicine","volume":"62 ","pages":"Article 100727"},"PeriodicalIF":0.0,"publicationDate":"2026-07-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148477044","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":"Ceramide accumulation and microbiota-derived sphingolipids: A novel axis in obesity-linked diabetic inflammation","authors":"Saksham Saxena,&nbsp;Irshad Ahmed,&nbsp;Rajeev Kumar Jha,&nbsp;Sushree Swagatika,&nbsp;Naveen Kumar,&nbsp;Mansi Saxena,&nbsp;Susmita Chakrabarty,&nbsp;Ranjay Kumar Choudhary,&nbsp;Aniruddha Bhattacharjee","doi":"10.1016/j.obmed.2026.100723","DOIUrl":"10.1016/j.obmed.2026.100723","url":null,"abstract":"<div><div>Obesity and type 2 diabetes are associated with chronic low-grade inflammation and metabolic abnormalities, in which ceramide accumulation is identified as a core pathogenic factor. Ceramides are bioactive sphingolipids synthesized through both de novo and salvage pathways that repress insulin signaling, induce programmed cell death, and initiate inflammatory cascades. It was reviewed that the gut microbiota is another sphingolipid source, particularly via Bacteroides-derived metabolites, which can modulate host lipid metabolism and immune function. Obesity-associated dysbiosis disrupts sphingolipid production by the gut microbiota, leading to changes in systemic lipids and heightened inflammatory responses induced by ceramides. This ceramide–microbiome-sphingolipid axis contributes to insulin resistance, adipose tissue macrophage activation, and hepatic metabolic stress, linking the ecology of the gut microbiota to diabetic inflammation. In this review, we aim to summarize recent advances in ceramide metabolism, microbial sphingolipid production and their intersection in obesity-associated diabetes. We also addressed the potential of therapeutic interventions (ie, dietary modulation, probiotics, and pharmacological inhibitors) targeting lipid homeostasis to alleviate immunometabolic dysfunction. Deciphering this new axis provides translational chances for biomarker discovery and precision therapies of metabolic disorders.</div></div>","PeriodicalId":37876,"journal":{"name":"Obesity Medicine","volume":"62 ","pages":"Article 100723"},"PeriodicalIF":0.0,"publicationDate":"2026-07-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148477045","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":"Intergenerational obesity prevention through nanogenomic targeting of gestational diabetes-induced epigenetic programming","authors":"Somanaboina Padmakar","doi":"10.1016/j.obmed.2026.100726","DOIUrl":"10.1016/j.obmed.2026.100726","url":null,"abstract":"<div><div>Gestational diabetes mellitus (GDM) represents one of the most consequential metabolic complications of pregnancy, affecting an estimated 14–17% of all pregnancies globally and establishing an intergenerational metabolic legacy that perpetuates cycles of obesity, type 2 diabetes, and cardiometabolic disease in offspring. Beyond its acute clinical ramifications, the diabetogenic intrauterine microenvironment exerts profound and durable epigenetic reprogramming on the fetal genome by dysregulating DNA methylation at imprinted loci, altering histone modification landscapes, and aberrantly expressing non-coding RNAs. Consequently, exposed offspring may develop long-term metabolic vulnerability long before the onset of overt disease. These mechanistic insights have catalyzed the emergence of the field of nanogenomics, which combines nanotechnology and genomic medicine to develop precision therapeutic platforms capable of intervening at the molecular level of epigenetic dysregulation during and after GDM-complicated pregnancy. This study comprehensively reviews the molecular architecture of GDM-associated epigenetic programming, with particular emphasis on the <em>IGF2</em>/<em>H19</em> imprinting axis, adipokine gene methylation, mitochondrial biogenesis regulators (<em>PPARGC1A</em>), and the emerging roles of miR-210, miR-21, and long non-coding RNAs in determining fetal metabolic fate. We further delineate how diverse nanocarrier platforms, including lipid nanoparticles (LNPs), poly (lactic-co-glycolic acid) (PLGA) polymeric nanoparticles, dendrimers, exosome-mimetic vesicles, and CRISPR-loaded nanoformulations, can be engineered for the precision delivery of epigenome-modulating payloads (siRNA, miRNA mimics, antisense oligonucleotides, DNMT inhibitors, and Cas9 mRNA) to placental and fetal tissues. A critical evaluation of preclinical evidence reveals that nanogenomic interventions can substantially reverse GDM-induced epigenetic aberrations, ameliorate fetal metabolic programming, and potentially disrupt the intergenerational transmission of obesity.</div></div>","PeriodicalId":37876,"journal":{"name":"Obesity Medicine","volume":"62 ","pages":"Article 100726"},"PeriodicalIF":0.0,"publicationDate":"2026-07-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148477047","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":"Selective vascular insulin resistance as a potential integrative mechanism linking obesity, type 1 and type 2 diabetes to vascular complications","authors":"Uri Gabbay,&nbsp;Doron Carmi","doi":"10.1016/j.obmed.2026.100722","DOIUrl":"10.1016/j.obmed.2026.100722","url":null,"abstract":"<div><div>Type 1 and Type 2 diabetes, despite fundamentally different etiologies, lead to remarkably similar microvascular and macrovascular complications. This shared phenotype is not fully explained by hyperglycemia alone or by differences in insulin exposure. We propose that, at the vascular level, a common state of selective vascular insulin resistance characterized by impaired PI3K/Akt-mediated vasoprotective signaling with relative preservation of MAPK-mediated pro-inflammatory and vasoconstrictive signaling may contribute to these shared vascular outcomes. This Perspective advances a hypothesis-generating conceptual framework intended to integrate existing mechanistic and clinical observations rather than establish a definitive causal model.</div><div>Prior work has defined selective insulin resistance at the cellular level; here, we propose extending this concept to a disease-level framework that may explain the parallel development of complications in both forms of diabetes. In Type 2 diabetes, metabolic insulin resistance drives this imbalance in the setting of compensatory hyperinsulinemia, whereas in Type 1 diabetes, nonphysiologic peripheral insulin delivery combined with metabolic stress may promote a comparable signaling disturbance. This review synthesizes mechanistic and clinical observations into a unified, testable hypothesis and outlines potential avenues for validation. Rather than replacing established glucotoxic mechanisms, this model suggests that impaired insulin signaling may modify tissue susceptibility to metabolic injury and offers a framework for evaluating therapies aimed at restoring physiologic vascular insulin action.</div></div>","PeriodicalId":37876,"journal":{"name":"Obesity Medicine","volume":"62 ","pages":"Article 100722"},"PeriodicalIF":0.0,"publicationDate":"2026-07-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148477049","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":"Obesity and cardiovascular disease: Mechanistic insights and multimodal management strategies","authors":"Polu Picheswara Rao","doi":"10.1016/j.obmed.2026.100729","DOIUrl":"10.1016/j.obmed.2026.100729","url":null,"abstract":"<div><h3>Purpose of the review</h3><div>This review synthesizes current mechanistic insights linking obesity to cardiovascular disease and evaluates evidence-based multimodal management strategies. We examine the complex pathophysiological pathways including adipose tissue dysfunction, chronic inflammation, insulin resistance, and ectopic fat accumulation that drive cardiovascular risk in obesity, while critically appraising therapeutic interventions across lifestyle, pharmacological, surgical, and emerging precision medicine approaches.</div></div><div><h3>Recent findings</h3><div>Novel glucagon-like peptide-1 receptor agonists, particularly semaglutide and tirzepatide, demonstrate unprecedented efficacy with 15-20% weight reduction and 20% reduction in major adverse cardiovascular events. Bariatric surgery continues to provide superior outcomes, reducing cardiovascular mortality by 40-50% in severely person/people with obesity patients. Emerging evidence highlights the cardiovascular benefits of sodium-glucose cotransporter-2 inhibitors beyond glycemic control. Device-based neuromodulation therapies, including vagal nerve stimulation, offer promising less-invasive alternatives. Precision medicine approaches utilizing genetic profiling and biomarker analysis are enabling personalized treatment selection, while digital health technologies with artificial intelligence integration facilitate continuous monitoring and real-time intervention optimization.</div></div><div><h3>Summary</h3><div>Obesity-related cardiovascular disease requires comprehensive, individualized management integrating lifestyle modification, evidence-based pharmacotherapy, and when appropriate, surgical intervention. The emergence of cardioprotective obesity management medications (OMMs) and advances in precision medicine are transforming therapeutic paradigms. Future success depends on multidisciplinary approaches incorporating novel therapeutic targets, digital health solutions, and personalized strategies based on genetic and metabolic profiling to optimize cardiovascular outcomes in this high-risk population.</div></div>","PeriodicalId":37876,"journal":{"name":"Obesity Medicine","volume":"62 ","pages":"Article 100729"},"PeriodicalIF":0.0,"publicationDate":"2026-07-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148477051","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":"Precision glycemic management in non-insulin-treated type 2 diabetes using continuous glucose monitoring","authors":"R. Selva Balaji,&nbsp;V. Vinith,&nbsp;R. Kannan,&nbsp;Murugan Ramadurai,&nbsp;Pachaiyappan Murugan","doi":"10.1016/j.obmed.2026.100724","DOIUrl":"10.1016/j.obmed.2026.100724","url":null,"abstract":"<div><div>Continuous glucose monitoring (CGM) is increasingly applied in adults with non–insulin-treated type 2 diabetes mellitus (T2DM), yet its clinical effectiveness in this population remains underexplored. This systematic review evaluated 32 randomized controlled trials involving 2783 adults comparing CGM with self-monitoring of blood glucose (SMBG). CGM use was associated with a notable increase in Time-in-Range (70–180 mg/dL) of +6.36%, equivalent to approximately 1.5 additional hours per day within target glucose. Glycemic variability improved, with reductions in coefficient of variation and standard deviation, while HbA1c decreased by 0.31–0.70% without elevating hypoglycemia risk. Time-Below-Range (&lt;70 mg/dL) declined by −0.66%, and extreme glucose excursions (TAR&gt;250 mg/dL; TBR&lt;54 mg/dL) were minimal, highlighting the safety profile of CGM. These findings demonstrate that CGM enhances glycemic optimization and stability, supporting its integration as a precision monitoring and behavioral intervention tool for non–insulin-treated T2DM.</div></div>","PeriodicalId":37876,"journal":{"name":"Obesity Medicine","volume":"62 ","pages":"Article 100724"},"PeriodicalIF":0.0,"publicationDate":"2026-07-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148477046","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":"Waist circumference associates with ultrasound-defined steatosis grade in NAFLD patients characterized by uniformly suboptimal diet","authors":"Caner Özyildirim,&nbsp;Mustafa Aydemir,&nbsp;Nurcan Yabanci Ayhan","doi":"10.1016/j.obmed.2026.100728","DOIUrl":"10.1016/j.obmed.2026.100728","url":null,"abstract":"<div><h3>Background</h3><div>Non-alcoholic fatty liver disease (NAFLD) clinical phenotypes involve complex interactions between adiposity and diet. A particularly underexplored question is whether dietary quality differs across steatosis severity grades in clinically complex, high-risk cohorts with prevalent T2DM. We hypothesized that specific dietary patterns would be associated with disease severity, independent of anthropometric indices.</div></div><div><h3>Methods</h3><div>In this cross-sectional study, 160 adults with confirmed NAFLD were evaluated using structured questionnaires, anthropometric measurements, and a 108-item food frequency questionnaire. Steatosis severity (Grades 1–3) was determined by ultrasonography. Healthy Eating Index-2015 (HEI-2015), Dietary Inflammatory Index (DII), Potential Renal Acid Load (PRAL), and Plant-Based Diet Index (PDI) were computed. Hierarchical binary logistic regression was performed using complete-case analysis (n = 122), adjusting for sex, type 2 diabetes, and total energy intake.</div></div><div><h3>Results</h3><div>Body weight, BMI, and waist circumference increased significantly across steatosis grades (p &lt; 0.001). No significant differences were observed in HEI-2015, DII, PRAL, or PDI across groups (p &gt; 0.05), and none showed independent associations with steatosis grade in adjusted models. Dietary quality was uniformly suboptimal across all severity grades. Waist circumference was consistently associated with higher ultrasound-assigned steatosis grades across all models in this selected cohort (OR: 1.10, 95% CI: 1.05–1.16, p &lt; 0.001), accounting for 27% of the variance explained by the base logistic model.</div></div><div><h3>Conclusion</h3><div>A key finding is that dietary quality was uniformly suboptimal across all steatosis severity grades, including the mildest stage, supporting consideration of nutritional assessment and intervention from early disease stages regardless of disease severity. In this highly selected clinical cohort with a high burden of metabolic comorbidities, waist circumference demonstrated a consistent independent association with ultrasound-defined steatosis grade. These findings should not be generalized beyond this specific metabolic phenotype.</div></div>","PeriodicalId":37876,"journal":{"name":"Obesity Medicine","volume":"62 ","pages":"Article 100728"},"PeriodicalIF":0.0,"publicationDate":"2026-07-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148477050","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":"Redox modulation in diabesity-related cancer: The role of plant-derived nanoparticles in antioxidant and metabolic reprogramming","authors":"Daniel Ejim Uti,&nbsp;Esther Ugo Alum","doi":"10.1016/j.obmed.2026.100725","DOIUrl":"10.1016/j.obmed.2026.100725","url":null,"abstract":"<div><div>Diabesity, defined by the coexistence and pathophysiological interaction of obesity and type 2 diabetes mellitus (T2DM), promotes a systemic metabolic-inflammatory state characterized by hyperinsulinemia, chronic low-grade inflammation, dyslipidemia, and sustained oxidative stress. These conditions promote oncogenesis by altering tissue microenvironments and activating intracellular signalling cascades that drive malignant transformation, disease progression, and therapeutic resistance. A major target is redox dysregulation: abundant reactive oxygen species (ROS) arising from mitochondrial overload, the NADPH-oxidases, endoplasmic reticulum stress, glycation chemistry; ROS and advanced glycation end products which interact with macromolecules, and also serve as secondary messengers, which activate some of these signalling pathways; (PI3K/Akt/mTOR, NF-kappaB, Janus kinase (JAK)/signal transducer and activator of transcription (STAT), and hypoxia-inducible factor-1 alpha (HIF-1α). Tumour cells adapt their antioxidant defenses including glutathione synthesis and other components, forming a metabolic feedback loop relevant in diabesity. Plant-derived nanoparticles (PDNPs), produced via green synthesis, act as multifunctional redox modulators, improving the stability and bioavailability of the plant bioactives. They scavenge reactive oxygen species (ROS), modulate Nrf2/ARE pathways, and suppress inflammatory responses, thereby influencing glycolytic and lipid metabolism in tumour and stromal cells. This review highlights the mechanisms linking diabesity and cancer, emphasizing the role of PDNPs in normalizing redox balance and metabolic reprogramming.</div></div>","PeriodicalId":37876,"journal":{"name":"Obesity Medicine","volume":"62 ","pages":"Article 100725"},"PeriodicalIF":0.0,"publicationDate":"2026-07-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148477048","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":"The role of gut microbiome-produced trimethylamine in targeting insulin resistance","authors":"Tianru Jin","doi":"10.1016/j.obmed.2026.100695","DOIUrl":"10.1016/j.obmed.2026.100695","url":null,"abstract":"","PeriodicalId":37876,"journal":{"name":"Obesity Medicine","volume":"61 ","pages":"Article 100695"},"PeriodicalIF":0.0,"publicationDate":"2026-05-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147995483","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":"Pathophysiological impacts of lifestyle transitions on obesity: A molecular overview of metabolic dynamics","authors":"Vetriselvan Subramaniyan ,&nbsp;Rajan Logesh ,&nbsp;Srikanth Jeyabalan ,&nbsp;V. Chitra ,&nbsp;Madhu Gupta ,&nbsp;Yuan Seng Wu ,&nbsp;Sivaraman Dhanasekaran ,&nbsp;Chetan Ashok ,&nbsp;Saminathan Kayarohanam ,&nbsp;Thakur Gurjeet Singh","doi":"10.1016/j.obmed.2026.100705","DOIUrl":"10.1016/j.obmed.2026.100705","url":null,"abstract":"<div><div>The rise in obesity worldwide is closely linked to lifestyle variables, specifically bad eating habits, sedentary lifestyles, and long-term psychological stress, all of which contribute to metabolic dysregulation at the molecular and cellular levels. By concentrating on important molecular mechanisms, such as disturbed metabolic pathways, hormonal imbalances, impaired energy homeostasis, dysregulated nutrient-sensing systems, adipocyte dysfunction, and chronic low-grade inflammation, this review critically investigates the pathophysiological effects of lifestyle-induced changes. We draw attention to the ways in which these interrelated mechanisms exacerbate obesity and its related comorbidities by causing excessive adiposity, insulin resistance, metabolic inflexibility, and systemic inflammation. Particular attention is paid to the molecular underpinnings of metabolic disruptions brought on by stress and how they contribute to the development of visceral fat and inflammatory signals. We also go over new ways to intervention that focus on these molecular anomalies, such as precision dietary changes, novel gene-based techniques, and pharmaceutical therapy. When taken as a whole, this study offers a thorough molecular framework that connects lifestyle modifications to the pathophysiology of obesity, enhancing our understanding of mechanisms and directing the development of new treatments.</div></div>","PeriodicalId":37876,"journal":{"name":"Obesity Medicine","volume":"61 ","pages":"Article 100705"},"PeriodicalIF":0.0,"publicationDate":"2026-05-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147803375","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}