GeroScience最新文献

{"title":"Standardizing Preoperative Care for Elective Spine Surgery: The University of Oklahoma Elective Spine Surgery Protocol.","authors":"Lonnie Smith,David Barkyoumb,William C Kaiser,Fauziyya Muhammad,Tara Sukut,Ishan Purani,Chao Li, DO,Karl Balsara,Hakeem J Shakir,M Burhan Janjua,John F Burke,Andrew Jea,Zachary A Smith","doi":"10.1007/s11357-025-01908-y","DOIUrl":"https://doi.org/10.1007/s11357-025-01908-y","url":null,"abstract":"As rates of spinal surgery in the United States continue to rise, the field has undergone a paradigm shift towards standardized, evidence-based care aimed at optimizing surgical outcomes. Indeed, numerous Enhanced Recovery After Surgery (ERAS) protocols have emerged and demonstrated significant success in improving outcomes in spinal surgery. In this article, we present a preoperative optimization protocol for elective spinal surgery from our own institution, which is in a state with notoriously high rates of comorbidities relative to the rest of the nation. This standardized protocol addresses six critical aspects of patient care: preoperative evaluation, bone health, diabetes, nutritional status, social risk factors, and medical comorbidities. By targeting these pillars of preoperative evaluation and management in an evidence-based, standardized manner, our protocol aims to enhance patient safety, minimize complications, and optimize the overall quality of care for our elective spinal surgery patients. In doing so, this protocol meets the growing demand for improved patient care in the expanding field of spinal surgery and lays the foundation for future advancements in elective spine protocols, thus contributing to the ongoing pursuit of optimized surgical outcomes and overall quality of care in the field.","PeriodicalId":12730,"journal":{"name":"GeroScience","volume":"193 1","pages":""},"PeriodicalIF":5.6,"publicationDate":"2025-09-26","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145153457","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":"Aging-related decline in the liver and brain is accelerated by refined diet consumption.","authors":"Franziska Kromm,Haktan Övül Bozkir,Annette Brandt,Timur Yergaliyev,Amélia Camarinha-Silva,Ina Bergheim","doi":"10.1007/s11357-025-01897-y","DOIUrl":"https://doi.org/10.1007/s11357-025-01897-y","url":null,"abstract":"Studies suggest that diets rich in highly/ultra-processed foods may contribute to the development of diseases. In rodents, the intake of refined (purified) diets has also been associated with the development of various metabolic diseases. Here, performing two experiments, we assess the impact of a refined diet with and without fiber enrichment on aging related health decline in mice. Experiment 1: Male C57BL/6J mice were fed standard chow or refined diet until the age of 86 weeks. Experiment 2: Male C57BL/6J mice fed a refined diet until showing signs of aging related intestinal barrier dysfunction were fed a fiber enriched refined diet (7.5% oat β-glucan or 7.5% cellulose) for 18 weeks. Cognition was assessed at the beginning and end of the dietary fiber intervention, while glucose tolerance was determined at the end of each experiment. Markers of senescence, liver damage, neuroinflammation, intestinal barrier function, and microbiota composition were assessed. Refined diet-fed mice showed higher markers of senescence in plasma and aging-associated liver decline, impaired glucose metabolism and cognitive decline compared to standard diet-fed mice. These changes were associated with differences in intestinal microbiota composition and higher portal bacterial endotoxin levels. Enriching the refined diet with the fibers decelerated the aging-associated cognitive impairments while not affecting aging-related liver decline, insulin resistance or markers of intestinal barrier function. In conclusion, these data suggest that while decelerating aging-related cognitive decline, fiber fortification of a refined diet may not attenuate the diet-induced acceleration of aging related decline in other organs in mice.","PeriodicalId":12730,"journal":{"name":"GeroScience","volume":"41 1","pages":""},"PeriodicalIF":5.6,"publicationDate":"2025-09-26","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145140394","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":"Functional assessments of short-term spatial memory in the Dog Aging Project identify strong associations with age that are not moderated by body mass.","authors":"Stephanie H Hargrave, Amber J Keyser, Emma Kristal, Gene E Alexander, Theadora A Block, Emily E Bray, Laura E L C Douglas, Brenda S Kennedy, Daniel E L Promislow, David A Raichlen, Dog Aging Project Consortium, Evan L MacLean","doi":"10.1007/s11357-025-01867-4","DOIUrl":"10.1007/s11357-025-01867-4","url":null,"abstract":"<p><p>Companion dogs have emerged as a valuable model in the study of cognitive aging, but assessments of cognitive function in large, diverse, and geographically distributed samples of dogs are challenging to obtain. We developed two novel functional assessments of short-term spatial memory that were administered by community science participants in a sample of 6,753 dogs through the Dog Aging Project. We compared data generated by community scientists to those gathered by research professionals, estimated relationships between age and task performance, and tested the hypothesis that associations between age and cognitive performance vary by dog body mass, as a proxy for expected lifespan. Community scientists generated similar data to research professionals and both cognitive tasks were sensitive to age-related deficits, beginning in midlife. Relationships between age and cognitive function were highly similar across small and large dogs and, for both tasks, comparison of models with and without an interaction between age and body mass yielded decisive evidence for the model without the interaction. Large dogs exhibit accelerated aging across many traits, and so the lack of evidence for accelerated cognitive aging raises the possibility that their large size confers a neuroprotective advantage. We consider possible mechanisms underlying this effect and address how experimental studies of dog cognition using community science methods can support future research on mechanisms of brain and cognitive aging.</p>","PeriodicalId":12730,"journal":{"name":"GeroScience","volume":" ","pages":""},"PeriodicalIF":5.4,"publicationDate":"2025-09-25","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145137286","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":"Glucagon receptor signaling is indispensable for the healthspan effects of caloric restriction in aging male mice.","authors":"Kassandra R Bruner, Isabella R Byington, Tyler J Marx, Anastasiia Vasileva, Temara Fletcher, Susma Ghimire, India J Zappia, Yashika Shaju, Janan Zeng, Hallie R Wachsmuth, Thadeus W Carlyon, David G Besselsen, Daniel J Drucker, Frank A Duca, Jennifer H Stern","doi":"10.1007/s11357-025-01899-w","DOIUrl":"10.1007/s11357-025-01899-w","url":null,"abstract":"<p><p>Obesity and type 2 diabetes mellitus accelerate aging, shortening the duration of healthspan. Conversely, chronic calorie restriction (CR) extends healthspan. Research aimed at understanding the mechanism by which CR slows aging has focused heavily on insulin and downstream signaling cascades. Glucagon, a hormone that counter-regulates insulin, is commonly affected by these same interventions. To investigate the role of glucagon in aging, we used dietary manipulation, global and liver-specific glucagon receptor knockout, and pharmacological glucagon receptor activation. We found that globally eliminating glucagon receptor signaling (Gcgr KO) decreases median lifespan by 35% in lean mice. Extending these findings to metabolic health, we found that glucagon receptor signaling is indispensable to the metabolic response to chronic CR in young and aged mice. While CR decreased liver fat, serum triglyceride, and serum cholesterol in WT mice, these metabolic benefits were absent in Gcgr KO mice. In line with these observations, we found that critical nutrient-sensing pathways known to improve aging are dysregulated in mice lacking glucagon receptor signaling at the liver (Gcgr^hep-/-). Liver-specific deletion of the glucagon receptor decreases hepatic AMP kinase activation in aging mice, regardless of diet. Further, CR decreases hepatic mTOR activity in WT mice but not in Gcgr^hep-/- mice. Together, these findings propose that glucagon signaling plays a critical role in both normal aging and the lifespan and healthspan extension driven by caloric restriction.</p>","PeriodicalId":12730,"journal":{"name":"GeroScience","volume":" ","pages":""},"PeriodicalIF":5.4,"publicationDate":"2025-09-25","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145137274","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":"Real-world walking patterns are associated with regional brain atrophy and white matter lesions in middle-aged and older people: a Watch Walk-UK Biobank study.","authors":"Takahiro Tajimi,Lloyd L Y Chan,Yoshiro Okubo,Stephen R Lord","doi":"10.1007/s11357-025-01878-1","DOIUrl":"https://doi.org/10.1007/s11357-025-01878-1","url":null,"abstract":"Clinic-based gait performance is associated with cognitive function and brain structure. This study investigated associations between multiple remotely collected digital gait biomarkers and brain structural changes in a large population-based cohort. Cross-sectional analysis of 6412 participants from the UK Biobank, with both valid wrist-worn accelerometer and brain MRI data. Digital gait parameters, including step count, usual and maximal gait speed, cadence, and stride regularity, were derived from accelerometry data using the validated Watch Walk algorithm. Brain volumes (total brain volume, white matter lesion volume, and frontal lobe, hippocampal, insular, and amygdala gray matter volumes) were measured using MRI. Multiple linear regression models were used to assess associations between gait parameters and brain volumes, adjusting for potential confounders, including demographic, lifestyle, and health-related factors. Restricted cubic splines explored the shape of associations. Faster maximal and usual gait speed and higher stride regularity were associated with lower white matter lesion volume and larger frontal lobe, hippocampal, insular, and amygdala gray matter volumes. Restricted cubic spline analyses revealed that the relationships between maximal gait speed and stride regularity, on one hand, and white matter lesion volume, frontal lobe, hippocampal, insular, and amygdala gray matter volumes, on the other hand, were predominantly linear. Gait speed and stride regularity, objectively measured using wrist-worn accelerometers in real-world settings, are significantly associated with brain structural integrity. These findings highlight the potential of digital gait biomarkers as scalable and cost-effective tools for monitoring brain health and identifying individuals at risk for cognitive decline.","PeriodicalId":12730,"journal":{"name":"GeroScience","volume":"38 1","pages":""},"PeriodicalIF":5.6,"publicationDate":"2025-09-24","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145127255","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":"Air pollution and impulsive choice in aging: evidence from delay discounting.","authors":"Maya R Kilcullen,Jamie-Nicole Luistro,Melanie Kos,Jeremy Mennis,David V Smith,Ingrid R Olson","doi":"10.1007/s11357-025-01906-0","DOIUrl":"https://doi.org/10.1007/s11357-025-01906-0","url":null,"abstract":"Heightened air pollution exposure is associated with an increased risk for developing neurodegenerative disorders such as Alzheimer's disease and Parkinson's disease, yet it is unclear how pollution impacts the aging brain more broadly. Rodent research has shown that higher air pollution exposure is associated with increased impulsive behavior, operationalized as a preference for immediate reward in delay discounting tasks. We examined this relationship in middle-aged and older humans by analyzing associations between residential pollution exposure and time-based reward preferences. One hundred three (103) adults aged 40-80 completed a delay discounting task. We estimated long-term residential exposure to fine particulate matter (PM2.5), a prominent air pollutant, using participant address information and satellite pollution data. We found that higher residential PM2.5 exposure was significantly associated with a higher preference for more immediate rewards, even after controlling for demographic factors including income and education. A preference for immediate rewards has been independently associated with a higher risk of addictive behaviors, including substance abuse and gambling disorders, indicating that PM2.5 exposure may increase the emergence of these conditions. We discuss these results in detail along with potential underlying biological mechanisms, implications on human behavior, and future research directions.","PeriodicalId":12730,"journal":{"name":"GeroScience","volume":"10 1","pages":""},"PeriodicalIF":5.6,"publicationDate":"2025-09-24","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145127256","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":"Impaired early type I interferon responses to influenza virus infection in aged mice are associated with subsequent increased pulmonary inflammation.","authors":"Wenxin Wu,Jeremy S Alexander,J Leland Booth,Chaoqun Huang,Lin Liu,Craig A Miller,Douglas A Drevets,Jordan P Metcalf","doi":"10.1007/s11357-025-01892-3","DOIUrl":"https://doi.org/10.1007/s11357-025-01892-3","url":null,"abstract":"Seasonal influenza is responsible for significant mortality and morbidity worldwide. Seventy to ninety percent of these deaths occur in those aged 65 or older. To determine the innate immune responses to influenza A virus (IAV) infection, young (12-week) and old (70-week) C57BL/6 J mice were infected intranasally (i.n.) with IAV PR8. Immune responses were determined by qRT-PCR and single-cell RNA sequencing (scRNA-seq). Old mice, as compared to young mice, had significantly higher viral loads and lower type I interferon (IFN) expression in the lung at 3 days post-infection (dpi). In contrast, at this time point aged mice had significantly higher amounts of type III IFN expression, which correlated with the higher viral loads observed. Histopathology revealed that IAV infection in old mice resulted in lower pathological scores early (at 5 dpi) and higher lung pathological scores of diseases later (at 7 dpi) than in young mice. scRNA-seq analysis revealed that, at 7 dpi, older mice exhibited sustained local inflammatory responses, with higher expression levels of Ddx58, Irf7, Il6, and Tnf across various immune cells, including macrophages, monocytes, Natural killer cells, dendritic cells, and granulocytes, compared to young mice. Our murine model of aging and influenza infection demonstrated that aging dysregulated early IFN responses to influenza infection resulting in enhanced viral replication. These altered IFN responses in old mice also result in enhanced lung inflammation late after infection and may increase the incidence of secondary bacterial infections seen in older individuals.","PeriodicalId":12730,"journal":{"name":"GeroScience","volume":"12 1","pages":""},"PeriodicalIF":5.6,"publicationDate":"2025-09-23","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145127258","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":"Delirium in hospitalized COVID-19 patients is associated with dynamic changes in peripheral immune gene expression.","authors":"Sara C LaHue,Naoki Takegami,Rubinee Simmasalam,Abiya Baqai,Elena Munoz,Anya Sikri,Thibault du Buisson de Courson,Nilika S Singhal,Walter Eckalbar,Charles R Langelier,Carolyn M Hendrickson,Carolyn S Calfee,David J Erle,Matthew F Krummel,Prescott G Woodruff,Tomiko Oskotsky,Marina Sirota,Adam Ferguson,Vanja C Douglas,John C Newman,Samuel J Pleasure,Michael R Wilson,Neel S Singhal","doi":"10.1007/s11357-025-01898-x","DOIUrl":"https://doi.org/10.1007/s11357-025-01898-x","url":null,"abstract":"Delirium is a neurologic syndrome characterized by inattention and cognitive impairment frequently encountered in medically ill older adults. As a hallmark of age-related brain vulnerability, delirium offers a clinical model to investigate how peripheral immune responses contribute to acute brain dysfunction. Peripheral inflammation is a key trigger of delirium, but the patient-specific immune responses that drive delirium onset and recovery remain poorly understood. This retrospective cohort study of prospectively collected biospecimens examines RNA sequencing from peripheral blood mononuclear cells of adults hospitalized for COVID-19 to better understand patient-specific factors associated with delirium (n = 64). Longitudinal transcriptomic analyses highlight persistent immune dysregulation in delirium, marked by increasing expression trajectories of genes linked to innate immune pathways, including complement activation, cytokine production, and monocyte/macrophage recruitment. Genes involved adaptive immunity showed a declining trajectory over time in patients with delirium. Although corticosteroid treatment suppressed some aspects of immune hyperactivation, aberrant responses contributing to delirium were exacerbated. Delirium resolution was characterized by normalization of key transcripts such as CCL2 and innate immune markers. Novel associations with delirium included transcripts related to stress granule assembly and the T cell regulators DUSP2 and KLF10. Delirium in COVID-19 is associated with distinct and dynamic peripheral immune trajectories that are modulated by corticosteroids. Further understanding these mechanisms has important implications for preventing delirium in older adults. These findings provide novel mechanistic insights with translational relevance for immunomodulatory strategies targeting maladaptive immune responses to prevent or treat delirium in medically ill populations.","PeriodicalId":12730,"journal":{"name":"GeroScience","volume":"196 1","pages":""},"PeriodicalIF":5.6,"publicationDate":"2025-09-22","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145103455","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":"Social frailty and mortality risk in middle-aged and older adults: a prospective cohort study.","authors":"Meng Hao,Zixin Hu,Xu Zhang,Xiangnan Li,Shuming Wang,Yi Li,Jingdong Tang,Shuai Jiang,Hui Zhang","doi":"10.1007/s11357-025-01879-0","DOIUrl":"https://doi.org/10.1007/s11357-025-01879-0","url":null,"abstract":"Social frailty is common and associated with several adverse outcomes in older adults. However, its prevalence and effects on mortality in younger populations and the underlying cause of mortality are poorly understood. To examine the association of social frailty with all-cause and cause-specific mortality in adults across a wide age spectrum, we used data from the UK Biobank, a prospective cohort included 421,644 individuals aged 37-73 years enrolled from 2006 to 2010. Social frailty status was assessed based on Bunt's concept (financial difficulty, live alone, less social activity and rarely contacts with friends/family). The prevalence of pre-social frailty and social frailty were 35.74% and 19.87%, respectively, indicating that more than half of the participants were at risk of cumulative depletion of essential social resources. Both pre-social frailty and social frailty were associated with higher risk of all-cause and cause-specific mortality (including malignant neoplasms, heart disease, cerebrovascular diseases, respiratory diseases, diabetes mellitus, and others caused) in adults across a wide age spectrum, independent of sociodemographic factors, lifestyles, chronic diseases, mental health, and physical frailty status. These findings indicate that social frailty, as a robust and multidimensional construct, effectively captures the risk of losing social resources. Thus, assessing and addressing social frailty can reduce mortality risk.","PeriodicalId":12730,"journal":{"name":"GeroScience","volume":"77 1","pages":""},"PeriodicalIF":5.6,"publicationDate":"2025-09-20","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145089848","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 impact of metformin on testicular aging in Syrian hamsters.","authors":"Alina Cavallotti Gomez,Soledad Paola Rossi,Thaisy Munduruca Pires,Ricardo Saúl Calandra,Vanina Gabriela Da Ros,Débora Juana Cohen,Juan Manuel Riaño Gómez,María Silvia Bianchi,María Susana Theas,María Eugenia Matzkin,Mónica Beatriz Frungieri","doi":"10.1007/s11357-025-01871-8","DOIUrl":"https://doi.org/10.1007/s11357-025-01871-8","url":null,"abstract":"Biochemical and molecular mechanisms associated with testicular aging are still poorly understood. Here, using the Syrian hamster as a natural model of aging, we observed a disturbed spermatogenesis with reduction of the testicular weight and the gonadosomatic index, altered histology including tubular wall fibrosis, increased collagen deposition, and diminished steroidogenesis in testes of aged animals. These changes took place in parallel with an increase in the levels of inflammatory and oxidative stress markers and a reduction in the cell proliferative, survival, DNA repair, and autophagic capacities. Metformin, beyond its current clinical applications, has been proposed as an anti-aging drug. In vitro incubations of testicular fragments from old hamsters with metformin revealed beneficial effects of this drug on the testicular inflammatory-oxidative state together with stimulation of autophagy and cell ability to fix DNA damage. However, in vivo daily oral administration of metformin to aged hamsters for 2 months in a dose equivalent to that usually received by patients with type 2 diabetes mellitus, reduced body and testicular weights, gonadosomatic index and blood glucose, concomitantly with increased levels of indicators of testicular inflammation, oxidation and fibrosis, decreased signs of autophagy, steroidogenesis and DNA repair capacity, and impaired spermatogenesis. Overall, while in vitro studies suggested beneficial effects of metformin in the aging testis evidenced through anti-inflammatory, anti-oxidant, and pro-autophagic actions, in vivo experiments in aged hamsters supplemented with metformin exhibited completely opposite effects. Therefore, the future of metformin as a testicular anti-aging agent should be further investigated, thoroughly reconsidered and, should the need arise, disregarded.","PeriodicalId":12730,"journal":{"name":"GeroScience","volume":"38 1","pages":""},"PeriodicalIF":5.6,"publicationDate":"2025-09-20","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145089847","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}