GeroScience最新文献

{"title":"Expression of progerin enhances disease-related endpoints in a tau seeding reporter cell system.","authors":"Zhuang Zhuang Han,Sang-Gyun Kang,Erik Gomez-Cardona,Serene Wohlgemuth,Klinton Shmeit,Luis Arce,Jiri G Safar,Olivier Julien,David Westaway","doi":"10.1007/s11357-025-01737-z","DOIUrl":"https://doi.org/10.1007/s11357-025-01737-z","url":null,"abstract":"Sporadic Alzheimer's disease and some forms of frontotemporal lobar degeneration (FTLD-tau) are neurological disorders of later life where cognitive deficits follow from the progressive accumulation of microtubule-associated tau protein. Disease-related tau accumulation is marked by altered subcellular distribution and rearrangement of this natively unstructured protein into alternative conformational forms, including highly organized fibrillar assemblies. With a partial analogy to effects seen in prion diseases, pathological tau conformers have a templating activity called seeding that may be measured in cellular and cell-free systems. Moreover, cellular systems and disease models can recapitulate \"strain effects\" wherein the same tau amino acid sequence can adopt markedly different conformations. Here we analyzed FTLD-tau conformers in cellular reporter systems expressing a pro-aging mutant form of the lamin A protein termed \"progerin.\" Measured versus the baseline performance of a reporter system based on HEK293 cells, the addition of tau burden or progerin expression produced only mild changes in proteomic analyses or morphology, whereas application of both stressors produced a notable shift in ER stress and homeostasis, including increased levels of DNAJC10 and DNAJA2. The phenotypic effects scored here appear unrelated to the generation of new tau strains or to the type of strain input, insofar as progerin-expressing cells were more responsive to tau seeding by diverse brain samples containing different populations of tau conformers. Thus, premature aging and disease-associated tau conformers can exhibit an additive relationship in a model system.","PeriodicalId":12730,"journal":{"name":"GeroScience","volume":"84 1","pages":""},"PeriodicalIF":5.6,"publicationDate":"2025-07-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144630040","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":"Testing retrogenesis and physiological explanations for tract-wise white matter aging: links to developmental order, fiber calibre, and vascularization.","authors":"Tyler D Robinson, Jordan A Chad, Yutong L Sun, Paul T H Chang, J Jean Chen","doi":"10.1007/s11357-025-01773-9","DOIUrl":"https://doi.org/10.1007/s11357-025-01773-9","url":null,"abstract":"<p><p>To understand observed spatial distributions of white-matter (WM) aging, developmentally driven theories termed \"retrogenesis\" have gained traction, positing that WM tract development order predicts order of declines, with later developing regions expected to deteriorate first, i.e., \"last-in-first-out.\" Alternatively, regions that develop most rapidly may decline most rapidly in aging, i.e., \"gains-predict-loss.\" The validity of such theories remains uncertain, partly due to lack of clarity in defining developmental order. Recent findings suggest that WM aging is also associated with physiological parameters such as perfusion and fiber size. Here, we address the extent to which degrees of WM aging are determined by development trajectory (i.e., retrogenesis) and/or physiological states. We obtained microstructural and perfusion data from the Human Connectome Project in Aging (HCP-A), complemented by a meta-analysis involving maps of fiber calibre and macrovascular volume. Our results suggest (1) myelination development order explains more associations with WM health than prenatal emergence order; (2) earlier-myelinating tracts exhibit higher microstructural integrity and less susceptibility to microstructural deterioration in aging but lower perfusion and longer arterial-transit times (ATT), suggestive of collateral blood supply; (3) earlier-emerging tracts show longest ATT and greatest ATT increase across aging; (4) tracts with larger axons and higher macrovascular density in young adulthood show longer ATT and less susceptibility to microstructure/perfusion degeneration irrespective of developmental order; and (5) negligible support for \"gains-predict-loss.\" These findings were sex-dependent in a tract-specific manner. Future work will investigate the role of macrovascular collateral flow and tract-wise influences of metabolic demand.</p>","PeriodicalId":12730,"journal":{"name":"GeroScience","volume":" ","pages":""},"PeriodicalIF":5.3,"publicationDate":"2025-07-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144636795","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":"Outdoor light at night and neuropsychiatric symptoms in dementia.","authors":"Manuela Tondelli,Tommaso Filippini,Giulia Vinceti,Najara Iacovino,Teresa Urbano,Sofia Costanzini,Francesca Despini,Claudia De Luca,Simona Tondelli,Marco Vinceti,Annalisa Chiari,Giovanna Zamboni","doi":"10.1007/s11357-025-01745-z","DOIUrl":"https://doi.org/10.1007/s11357-025-01745-z","url":null,"abstract":"There is growing interest about the relation between exposure to artificial light at night (LAN) and mental health. This study aims, for the first time, to explore the association between LAN exposure and neuropsychiatric symptoms in individuals with dementia, investigating its role as a potential environmental risk factor. We collected data about 150 patients with dementia in Modena, Italy. We assessed LAN exposure using satellite imagery, while neuropsychiatric symptoms were evaluated through the Neuropsychiatric Inventory (NPI), a caregiver-administered questionnaire measuring the presence and severity of psychiatric symptoms. We used logistic regression models to examine associations between LAN exposure and neuropsychiatric features. Higher LAN exposure was associated with increased risk of psychiatric symptoms, particularly in the domains of psychosis and sleep disturbances. Specifically, individuals exposed to LAN levels above the median (LAN median = 26.32 nW/cm2/sr) demonstrated an elevated risk of delusions, hallucinations, and sleep disturbances (OR = 2.09, 95% CI 0.03-4.25), compared to those in the \"below the median\" category. Associations with other symptom domains, such as apathy and affective disturbances, showed weaker associations. Our findings indicate that artificial nighttime light exposure may negatively impact the mental well-being of individuals with dementia, potentially exacerbating psychotic symptoms and sleep disturbances. However, caution is warranted when interpreting these results due to the limited sample size and the possibility of unexamined residual confounding.","PeriodicalId":12730,"journal":{"name":"GeroScience","volume":"12 1","pages":""},"PeriodicalIF":5.6,"publicationDate":"2025-07-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144630041","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":"Quality of life in end of life.","authors":"Lavinia Valeriani, Barbara Carrano, Fabrizio Vecchio","doi":"10.1007/s11357-025-01781-9","DOIUrl":"https://doi.org/10.1007/s11357-025-01781-9","url":null,"abstract":"<p><p>Assessing quality of life (QOL) in end-of-life patients is vital for understanding the complex impacts of terminal illnesses on individual well-being. This study aims to compare two widely used QOL assessment tools: the Karnofsky Performance Status Scale (KPSS) and the Short-Form-36 (SF-36) Health Survey among patients with late-stage diseases. KPSS, a clinician-rated scale measuring functional capacity, provides an objective perspective on a patient's clinical status. Conversely, the SF-36 offers a patient-reported overview across eight dimensions, including physical and mental health. The study enrolled 68 patients with an average Karnofsky score of about 37. Results demonstrate a significant interaction between Karnofsky scores and SF-36 dimensions, indicating that patients with higher Karnofsky scores reported better physical, social, and emotional functioning. Strong positive correlations were found between high Karnofsky scores and specific SF-36 components, including Physical Functioning, Role Physical, and Social Functioning, suggesting that these aspects critically influence overall QOL. Notably, no correlation was identified between age and KPSS, highlighting that disease severity rather than age impacts QOL. Findings underscore the complementary roles of KPSS and SF-36 in assessing QOL in terminally ill patients; while some measures in SF-36 aligned closely with KPSS, others offered essential insights into patient experiences. This comprehensive approach emphasizes the need for robust QOL evaluations in palliative care, facilitating more patient-centered care aligned with individuals' values and needs.</p>","PeriodicalId":12730,"journal":{"name":"GeroScience","volume":" ","pages":""},"PeriodicalIF":5.3,"publicationDate":"2025-07-12","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144617238","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":"Association of accelerometer-measured physical activity and sedentary behavior with unplanned hospitalization in older adults: a 6-year longitudinal study.","authors":"Joan Ars,Giorgi Beridze,Pau Farrés-Godayol,Laura M Pérez,Marco Inzitari,Amaia Calderón-Larrañaga,Anna-Karin Welmer","doi":"10.1007/s11357-025-01756-w","DOIUrl":"https://doi.org/10.1007/s11357-025-01756-w","url":null,"abstract":"Regular physical activity (PA) and reduced sedentary behavior (SB) are well-established factors in promoting health and lowering the risk of chronic diseases. However, their relationship with unplanned hospitalizations remains unclear. Our aim was to investigate the associations between PA and SB parameters and the risk of unplanned hospital admissions, and the length of hospital stays in older adults. We analyzed data from 657 older adults aged ≥ 66 years from the Swedish SNAC-K study (2016-2018). The ActivPAL3 accelerometer was used to assess PA and SB. Multi-adjusted Cox and Laplace regressions were applied to examine PA and SB in relation to 6-year unplanned hospitalizations. Negative Binomial Regression models were employed to examine their associations with the length of hospital stays. For each 1000 steps/day, 100 low-intensity PA (LPA) walking events, and 15 min/day of time spent in moderate-to-vigorous PA (MVPA), the risk of unplanned admissions decreased (hazard ratio [HR] 0.95, 95% confidence interval [CI] 0.91-0.99, HR 0.77, 95%CI 0.61-0.96, and HR 0.91, 95%CI 0.83-1.00, respectively). Higher step counts and MVPA were also associated with shorter hospital stays (IRR per 1,000 steps: 0.91, 95% CI: 0.86-0.96; IRR per 15 min MVPA: 0.85, 95% CI: 0.75-0.96). No significant associations were found for SB or walking events with hospital stay in fully adjusted models. Our results suggest that higher step counts and greater participation in MVPA are associated with a reduced risk of hospital admissions and shorter hospital stays in older adults. Additionally, a greater number of LPA walking events was linked to lower risk of hospital admissions. These results support the promotion of regular walking and frequent PA as strategies to reduce healthcare burden in aging populations.","PeriodicalId":12730,"journal":{"name":"GeroScience","volume":"280 1","pages":""},"PeriodicalIF":5.6,"publicationDate":"2025-07-12","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144612887","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":"Epigenetic information loss is a common feature of multiple diseases and aging.","authors":"Naor Sagy, Chieh Chang, Maayan Gal, Daniel Z Bar","doi":"10.1007/s11357-025-01767-7","DOIUrl":"https://doi.org/10.1007/s11357-025-01767-7","url":null,"abstract":"<p><p>Aging is a major risk factor for a plethora of diseases. The information theory of aging posits that epigenetic information loss is a principal driver of the aging process. Despite this, the connection between epigenetic information loss and disease has not been thoroughly investigated. Here, we analyzed tissue-unique methylation patterns in healthy and diseased human organs, revealing that for several diseases these patterns degrade, regressing to a mean form. We interpret this as epigenetic information loss, where tissue-unique patterns erode. Information loss is not limited to diseases. Age-related erosion of unique methylation patterns was observed in some tissues and cells, while other tissues and cells diverged away from the mean. Our findings demonstrate that analyzing methylation patterns in tissue-unique sites can effectively distinguish between patients and healthy controls at least in some diseases, and underscore the role of epigenetic information loss as a common feature in various pathological conditions.</p>","PeriodicalId":12730,"journal":{"name":"GeroScience","volume":" ","pages":""},"PeriodicalIF":5.3,"publicationDate":"2025-07-11","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144608225","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":"Nervonic acid and 15-epi-PGA1 mediate systemic mitochondrial dysfunction in AD dementia.","authors":"Stephanie Robyn Heimler,K Allison Amick,Jaclyn Bergstrom,Marcos Moliné,Gargi Mahapatra,Suzanne Craft,Anthony J A Molina","doi":"10.1007/s11357-025-01776-6","DOIUrl":"https://doi.org/10.1007/s11357-025-01776-6","url":null,"abstract":"Systemic mitochondrial dysfunction is apparent in the pathophysiology of Alzheimer's disease (AD). However, the factors driving bioenergetic decline remain unclear. This study utilized serum samples from older adults with normal cognition, mild cognitive impairment, and dementia to identify circulating molecules that can drive mitochondrial dysfunction in the context of AD. We used mass spectrometry to measure the abundance of lipid metabolites and applied tiered selection criteria to identify candidate \"mito-inhibitory\" molecules. These criteria were based on correlations with (1) in vitro bioenergetic effects of whole serum samples on naïve cells, (2) the bioenergetic capacity of blood cells from the serum donor, and (3) cognition, as measured by the modified mini-mental state exam. Mito-inhibitory lipid candidates were validated by examining their bioenergetic effects on neurons, myoblasts, and fibroblasts in vitro. Our results indicate that nervonic acid and 15-epi Prostaglandin A1 (15-epi-PGA1) are elevated in participants with dementia compared to those with normal cognition. Importantly, both metabolites inhibited mitochondrial function across multiple cell types in vitro. High resolution respirometric analyses reveal that inhibitory effects from lipid treatment occur via broad inhibition of the electron transfer system (ETS) with no change in overall mitochondrial content. This study provides insights into the mechanisms underlying systemic bioenergetic decline associated with AD dementia. The identification of circulating factors that drive mitochondrial bioenergetic decline may inform the development of mitochondrial therapeutics for AD.","PeriodicalId":12730,"journal":{"name":"GeroScience","volume":"4 1","pages":""},"PeriodicalIF":5.6,"publicationDate":"2025-07-11","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144603987","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":"Age-dependent impairment of cardiac function and physical performance in male mice with diet-induced obesity.","authors":"Patricia Baumgarten,Justus Kamp,Niklas Hegemann,Stefanie Deubel,Nikolaus Berndt,Jana Grune,Wolfgang M Kuebler,Christopher L Axelrod,John P Kirwan,Annika Höhn,Sophie Heider,Christiane Ott,Tilman Grune","doi":"10.1007/s11357-025-01775-7","DOIUrl":"https://doi.org/10.1007/s11357-025-01775-7","url":null,"abstract":"Aging in the context of obesity exacerbates the risk of morbidity and mortality related to cardiovascular disease. However, the maladaptive responses in the heart that arise from prolonged obesity and the specific influence of biological age remain somewhat elusive. This study investigated the effects of diet-induced obesity (DIO) and aging on physical performance and cardiovascular function in mice. 22- and 76-week-old male C57BL/6J mice were randomized to 8 weeks of chow or high-fat diet. Body weight was assessed weekly. Body composition was measured at the beginning and the end of the diet treatment. Muscular and cardiac function were evaluated at the end intervention. Aged mice with DIO exhibited faster and greater body weight gain and fat mass accumulation, reduced running distance, and lower aerobic capacity. Aged HFD mice also exhibited increased cardiac lipid accumulation and cardiomyocyte hypertrophy, with no major morphological changes observed in skeletal muscle. Proteomic analysis revealed differential expression of heart proteins associated with metabolic function in young mice, which was not observed in aged mice with DIO. Subsequently, aged mice with DIO developed overt heart failure with reduced ejection fraction, while cardiac function was unaffected by DIO in young mice. In conclusion, young mice with DIO were protected against diet-induced cardiac dysfunction, whereas DIO in aged mice led to heart failure and impaired physical performance. The protective effects observed in younger mice appear to be explained by proteomic-level remodeling of the heart oriented to sustain cardiac function.","PeriodicalId":12730,"journal":{"name":"GeroScience","volume":"22 1","pages":""},"PeriodicalIF":5.6,"publicationDate":"2025-07-10","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144594223","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":"Kynurenine pathway dysregulation via loss of QPRT drives declines in activity and altered metabolism in mice.","authors":"Reyhan Westbrook,Vinal Menon,Joy Cagmat,Timothy Garrett,Robert Schwarcz,Jeremy Walston,Peter M Abadir,Tae Chung","doi":"10.1007/s11357-025-01735-1","DOIUrl":"https://doi.org/10.1007/s11357-025-01735-1","url":null,"abstract":"Chronic inflammatory pathway activation increases with age and is epidemiologically linked to multiple aging-related pathophysiological processes, phenotypes such as physical frailty and sarcopenia and early healthspan declines in aging organisms. Despite this, molecular mechanisms that directly connect chronic inflammation to these conditions remain poorly characterized. We hypothesize that chronic inflammation contributes to the development of age-related phenotypes by increasing the degradation of dietary tryptophan into multiple metabolites with unique physiological properties, called kynurenines, via the 'kynurenine pathway' (KP). To understand the impact of elevated KP metabolites on mammalian healthspan we utilized the quinolinate phosphoribosyltransferase knock-out (QPRT-/-) mouse which lacks the terminal enzyme of the KP and thus develops increased levels of downstream kynurenines. We tested the effects of this mutation on glucose handling, spontaneous motor activity, body composition and metabolism using indirect calorimetry, in male and female, young, middle aged and older mice. QPRT - / - mice had significantly altered levels of numerous KP metabolites and nicotinamide. Phenotypic characteristics varied in a sex-specific manner with decreased activity, lean mass and VO2, and impaired glucose clearance as early as 12 months seen in female QPRT-/- compared to age and sex-matched mice. Male QPRT-/- mice developed reduced lean mass by middle age and had altered respiration and food intake. This data indicates that KP dysregulation can drive declines in activity and alter metabolism in mammals and is a potential target to intervene on frailty and functional decline.","PeriodicalId":12730,"journal":{"name":"GeroScience","volume":"21 1","pages":""},"PeriodicalIF":5.6,"publicationDate":"2025-07-10","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144594224","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 motor unit and neuromuscular junction dysfunction in aging and sarcopenia: insights from electromyography in systematic review.","authors":"Can Cui,Yong Hu,Ronald Man Yeung Wong,Ning Zhang,Yuzhou Guan,Wing-Hoi Cheung","doi":"10.1007/s11357-025-01760-0","DOIUrl":"https://doi.org/10.1007/s11357-025-01760-0","url":null,"abstract":"The neuromuscular junction (NMJ) is a vital interface between motor neurons and muscle fibers, and alterations in its structure and function can substantially influence the onset and progression of sarcopenia. Electromyography (EMG) is a critical tool to assess motor unit and NMJ function, providing insights into neuromuscular activation patterns and the integrity of motor unit communication. However, its implications for aging and muscle performance during sarcopenia have not been fully discussed. Therefore, we conducted a systematic review using the PubMed, Embase, and Web of Science databases by employing relevant keywords. A total of 53 articles were included. This review explored the various alterations in the NMJ associated with aging, their functional implications, and potential interventions to mitigate these effects, highlighting the structural and functional alterations of the NMJ during aging and sarcopenia. Key findings include early NMJ transmission instability, motor unit loss and compensatory remodeling, and impaired neuromuscular activation preceding overt muscle atrophy and weakness. Notably, biomarkers such as C-terminal agrin fragment and neurofilament light chain, along with EMG-derived parameters (e.g., jitter, jiggle, MUNE), are sensitive indicators of NMJ deterioration. Both physical inactivity and hormonal changes (e.g., menopause) accelerate NMJ decline, while interventions such as resistance and endurance training, nutritional supplementation, and emerging gene therapies demonstrate potential to preserve or restore NMJ structure and function. In conclusion, this systematic review underscores the importance of NMJ dysfunction in aging and sarcopenia, advocating further research into diagnostic biomarkers and therapeutic strategies to enhance NMJ integrity. The interplay between aging, exercise, and NMJ function is complex and requires a nuanced approach to rehabilitation and exercise strategies tailored to the aging population. Future directions should prioritize the development of sensitive biomarkers, mechanistic studies of NMJ degeneration, and rigorous evaluation of multimodal interventions to mitigate neuromuscular decline and promote healthy aging.","PeriodicalId":12730,"journal":{"name":"GeroScience","volume":"11 1","pages":""},"PeriodicalIF":5.6,"publicationDate":"2025-07-08","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144578537","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}