BiogerontologyPub Date : 2025-05-03DOI: 10.1007/s10522-025-10241-y
Denisa F V Pirscoveanu, Denissa Greta Olaru, Dirk M Hermann, Thorsten R Doeppner, Flavia Semida Ghinea, Aurel Popa-Wagner
{"title":"Correction: Immune genes involved in synaptic plasticity during early postnatal brain development contribute to post-stroke damage in the aging male rat brain.","authors":"Denisa F V Pirscoveanu, Denissa Greta Olaru, Dirk M Hermann, Thorsten R Doeppner, Flavia Semida Ghinea, Aurel Popa-Wagner","doi":"10.1007/s10522-025-10241-y","DOIUrl":"https://doi.org/10.1007/s10522-025-10241-y","url":null,"abstract":"","PeriodicalId":8909,"journal":{"name":"Biogerontology","volume":"26 3","pages":"98"},"PeriodicalIF":4.4,"publicationDate":"2025-05-03","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12049334/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143961182","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
BiogerontologyPub Date : 2025-05-03DOI: 10.1007/s10522-025-10242-x
Ali Hemadeh, Carlota Lema-Arranz, Stefano Bonassi, Leonardo Buscarini, Francesco Infarinato, Paola Romano, Alessia Finti, Franco Marinozzi, Fabiano Bini, Natalia Fernández-Bertólez, João Paulo Teixeira, Laura Lorenzo-López, Vanessa Valdiglesias, Blanca Laffon
{"title":"Lifestyle, environment and other major determinants of frailty in older adults: a population-based study from the UK Biobank.","authors":"Ali Hemadeh, Carlota Lema-Arranz, Stefano Bonassi, Leonardo Buscarini, Francesco Infarinato, Paola Romano, Alessia Finti, Franco Marinozzi, Fabiano Bini, Natalia Fernández-Bertólez, João Paulo Teixeira, Laura Lorenzo-López, Vanessa Valdiglesias, Blanca Laffon","doi":"10.1007/s10522-025-10242-x","DOIUrl":"https://doi.org/10.1007/s10522-025-10242-x","url":null,"abstract":"<p><p>Frailty is a geriatric multidimensional syndrome characterized by a loss of physiologic reserves and disproportionate vulnerability to external stressors and associated with increased risk of multiple negative health outcomes. Since frailty can be prevented, controlled, and even reverted in its early stages, identifying the main factors involved in its development is crucial to implement preventive and/or restorative interventions. The aim of this study was to assess the impact of a broad range of parameters, including host factors, lifestyle, diet, and environmental and occupational conditions, on the development of frailty in later life. A cross-sectional study was conducted on 221,896 individuals aged 60 and over classified as non-frail (119,332, 53.8%), pre-frail (93,180, 42.0%), and frail (9384, 4.2%) according to the frailty phenotype. Using principal component analysis and machine learning to streamline the data, significant associations were found between frailty risk and air quality, diet, smoking, working conditions, and heavy alcohol consumption. Early-life factors, including breastfed as a baby and maternal smoking around birth, also emerged as predictors of frailty, which was further characterized by clinical indicators like polypharmacy, levels of C-reactive protein and other biomarkers of inflammageing. This study provided robust and original evidence on the association between a large battery of potential risk factors, from early to later stages of life, and the occurrence of frailty in older age. These results will contribute to the development of effective prevention strategies and facilitate the early detection of individuals at high risk of developing frailty.</p>","PeriodicalId":8909,"journal":{"name":"Biogerontology","volume":"26 3","pages":"100"},"PeriodicalIF":4.4,"publicationDate":"2025-05-03","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12049404/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143973391","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
BiogerontologyPub Date : 2025-04-25DOI: 10.1007/s10522-025-10236-9
Shuai Huang, Hang Shi, Zhidan Shi, Jiawei Wu, Ling He
{"title":"Vorinostat, a potential hormetin, extends lifespan and enhances stress resistance via the SKN-1 pathway in Caenorhabditis elegans.","authors":"Shuai Huang, Hang Shi, Zhidan Shi, Jiawei Wu, Ling He","doi":"10.1007/s10522-025-10236-9","DOIUrl":"https://doi.org/10.1007/s10522-025-10236-9","url":null,"abstract":"<p><p>Vorinostat, a pan histone deacetylases (HDACs) inhibitor clinically approved for cutaneous T-cell lymphoma, exerts therapeutic effects by inducing tumor cell death and cycle arrest. Intriguingly, a previously unrecognized hormetic role of low-dose vorinostat in Caenorhabditis elegans. Subtoxic concentrations of vorinostat (1 μM) significantly extended lifespan, enhanced healthspan, and improved resistance to oxidative and heat stress, while ameliorating Aβ-induced paralysis. qPCR analysis demonstrated dose-dependent bidirectional regulation of stress-resistance genes (sod-3, hsp-16.2, skn-1, gst-4, act-1), with low doses of vorinostat upregulating these genes whereas higher doses (10 μM) exerted suppressive or neutral effects. Mechanistically, vorinostat-induced hormesis required functional SKN-1 signaling, as evidenced by its capacity to activate skn-1 and downstream targets (hsp-16.2, gst-4, act-1). Crucially, RNAi-mediated skn-1 knockdown completely abolished the pro-longevity and stress-resistant phenotypes. These findings establish vorinostat as a novel hormetin that enhances organismal resilience through SKN-1 pathway activation, providing new insights into HDAC inhibitor biology and aging intervention strategies.</p>","PeriodicalId":8909,"journal":{"name":"Biogerontology","volume":"26 3","pages":"97"},"PeriodicalIF":4.4,"publicationDate":"2025-04-25","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143965667","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
BiogerontologyPub Date : 2025-04-21DOI: 10.1007/s10522-025-10238-7
Eun-Joo Lee, SunYoung Park, Kyu-Shik Jeong
{"title":"Sirt2 deficiency aggravates intramuscular adipose tissue infiltration and impairs myogenesis with aging in male mice.","authors":"Eun-Joo Lee, SunYoung Park, Kyu-Shik Jeong","doi":"10.1007/s10522-025-10238-7","DOIUrl":"https://doi.org/10.1007/s10522-025-10238-7","url":null,"abstract":"<p><p>Sarcopenia, closely associated with other diseases such as diabetes, metabolic syndrome, and osteoporosis, significantly impacts aging populations. It is characterized by muscle atrophy, increased intramuscular adipose tissue, impaired myogenesis, chronic low-grade inflammation, and reduced muscle function. The mechanisms behind aging muscle remain incompletely understood. This study aims to elucidate the role of Sirt2 in the aging process of skeletal muscles and enhance our understanding of the underlying mechanisms. Sirt2 expression was reduced in aging muscle of male mice by 40%, compared to young muscle. Aged male Sirt2 knockout mice exhibit increased intramuscular adipose tissue infiltration by 8.5-fold changes. Furthermore, the deletion of Sirt2 exacerbated myogenesis impairment in aged muscle by decreasing the expression of Pax7 (50%) and NogoA (80%), compared to age- and sex- matched counterparts, emphasizing the role of Sirt2 in pathology of aging muscle. Additionally, long-term Sirt2 deletion affected other Sirtuin subfamily members, with decreased expressions of Sirt1 (65%), Sirt4 (94%), and Sirt5 (71%), and increased expressions of Sirt6 (4.6-fold) and Sirt7 (2.8-fold) in old male Sirt2 knockout mice, while there was no difference of these gene expression in young male mice. This study underscores the critical need for a deeper investigation into Sirt2, promising new insights that could lead to targeted therapies for sarcopenia, ultimately improving the quality of life in the elderly.</p>","PeriodicalId":8909,"journal":{"name":"Biogerontology","volume":"26 3","pages":"93"},"PeriodicalIF":4.4,"publicationDate":"2025-04-21","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143956760","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
{"title":"Longevity mechanisms in cardiac aging: exploring calcium dysregulation and senescence.","authors":"Neetu Agrawal, Muhammad Afzal, Waleed Hassan Almalki, Suhas Ballal, Girish Chandra Sharma, T Krithiga, Rajashree Panigrahi, Suman Saini, Haider Ali, Kavita Goyal, Mohit Rana, Abida Khan","doi":"10.1007/s10522-025-10229-8","DOIUrl":"https://doi.org/10.1007/s10522-025-10229-8","url":null,"abstract":"<p><p>Cardiac aging is a multistep process that results in a loss of various structural and functional heart abilities, increasing the risk of heart disease. Since its remarkable discovery in the early 1800s, when limestone is heated, calcium's importance has been defined in numerous ways. It can help stiffen shells and bones, function as a reducing agent in chemical reactions, and play a central role in cellular signalling. The movement of calcium ions in and out of cells and between those is referred to as calcium signalling. It influences the binding of the ligand, enzyme activity, electrochemical gradients, and other cellular processes. Calcium signalling is critical for both contraction and relaxation under the sliding filament model of heart muscle. However, with age, the heart undergoes changes that lead to increases in cardiac dysfunction, such as myocardial fibrosis, decreased cardiomyocyte function, and noxious disturbances in calcium homeostasis. Additionally, when cardiac tissues age, cellular senescence, a state of irreversible cell cycle arrest, accumulates and begins to exacerbate tissue inflammation and fibrosis. This review explores the most recent discoveries regarding the role of senescent cell accumulation and calcium signalling perturbances in cardiac aging. Additionally, new treatment strategies are used to reduce aged-related heart dysfunction by targeting senescent cells and modulating calcium homeostasis.</p>","PeriodicalId":8909,"journal":{"name":"Biogerontology","volume":"26 3","pages":"94"},"PeriodicalIF":4.4,"publicationDate":"2025-04-21","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143965423","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
BiogerontologyPub Date : 2025-04-21DOI: 10.1007/s10522-025-10237-8
Joice da Silva Castro, Carolynne Martins Teixeira, Daniela Mayumi Usuda Prado Rocha, Andréia Queiroz Ribeiro, Ana Claudia Pelissari Kravchychyn, Helen Hermana Miranda Hermsdorff
{"title":"Dietary inflammatory index (DII) and telomere length: a systematic review.","authors":"Joice da Silva Castro, Carolynne Martins Teixeira, Daniela Mayumi Usuda Prado Rocha, Andréia Queiroz Ribeiro, Ana Claudia Pelissari Kravchychyn, Helen Hermana Miranda Hermsdorff","doi":"10.1007/s10522-025-10237-8","DOIUrl":"https://doi.org/10.1007/s10522-025-10237-8","url":null,"abstract":"<p><p>Dietary intake influences inflammation and may impact telomere length (TL), a biomarker of biological aging. However, the relationship between the inflammatory potential of the diet and TL remains unclear. This review systematically assessed whether higher Dietary Inflammatory Index (DII) scores, indicative of pro-inflammatory diets, are associated with shorter TL. Searches in PubMed, Embase, Scopus, Web of Science, and Cochrane up to October 2024 identified nine eligible studies, involving 123,923 participants (53% women), aged 9-80 years. Seven studies were cross-sectional, and two were longitudinal, with follow-ups of 5-10 years. Most studies (n = 4) examined adult and older adult populations of both sexes. DII values ranged from -6.48 (anti-inflammatory) to 3.98 (pro-inflammatory). None included all DII parameters, and three adjusted for energy intake. Four studies linked higher DII to shorter TL, focusing on European adults with and without cardiovascular risk, healthy American adults, and Chinese older adults with mild cognitive impairment. This systematic review presents limited data to provide a definitive conclusion on the association between higher DII and shorter TL. Additional studies that address the limitations identified in this review are needed.</p>","PeriodicalId":8909,"journal":{"name":"Biogerontology","volume":"26 3","pages":"95"},"PeriodicalIF":4.4,"publicationDate":"2025-04-21","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143962699","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
BiogerontologyPub Date : 2025-04-21DOI: 10.1007/s10522-025-10240-z
Ekaterina Rudnitsky, Alex Braiman, Marina Wolfson, Khachik K Muradian, Vera Gorbunova, Gadi Turgeman, Vadim E Fraifeld
{"title":"Mesenchymal stem cells and their derivatives as potential longevity-promoting tools.","authors":"Ekaterina Rudnitsky, Alex Braiman, Marina Wolfson, Khachik K Muradian, Vera Gorbunova, Gadi Turgeman, Vadim E Fraifeld","doi":"10.1007/s10522-025-10240-z","DOIUrl":"https://doi.org/10.1007/s10522-025-10240-z","url":null,"abstract":"<p><p>Mesenchymal stem cells (MSCs) and blood plasma/MSC-derived extracellular vesicles (EVs) offer promising tools to promote longevity and treat age-related diseases. MSCs have low immunogenicity and tumorigenicity, and their efficacy is relatively independent of the donor age in humans (but not in rodents). Systemic administration of MSCs and stem cell/blood-derived EVs modified the omic profiles of various organs of aged rodents towards the young ones. The application of EVs appears to be even more beneficial than MSCs. Remarkably, over 70% of microRNAs, which are over-presented in ESC-derived EVs, were found to target longevity-associated genes. Along with MSCs, other types of stem cells were reported to display health- and lifespan-extending effects. Pluripotent Muse cells, a specific subpopulation of MSCs, which possess a number of unique features, could be particularly relevant for promoting healthspan. The rejuvenation potential of MSCs, EVs, and Muse cells warrants further investigation in both animal models and clinical trials, using aging clocks for biological age determination as one of the endpoints.</p>","PeriodicalId":8909,"journal":{"name":"Biogerontology","volume":"26 3","pages":"96"},"PeriodicalIF":4.4,"publicationDate":"2025-04-21","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12011939/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143975965","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
{"title":"Environmental enrichment: a neurostimulatory approach to aging and ischemic stroke recovery and rehabilitation.","authors":"Sijina Kinattingara Parambath, Navami Krishna, Rajanikant Golgodu Krishnamurthy","doi":"10.1007/s10522-025-10232-z","DOIUrl":"https://doi.org/10.1007/s10522-025-10232-z","url":null,"abstract":"<p><p>Environmental enrichment (EE) represents a robust experimental framework exploring the intricate interplay between genes and the environment in shaping brain development and function. EE is recognized as a non-invasive intervention, easily translatable to elderly human cohorts, and extrapolated from research on animal aging models. Age is the most important risk factor for ischemic stroke. Research indicates that EE, characterized by increased sensory, cognitive, and social stimulation, leads to structural changes in the brain, such as enhanced dendritic complexity and synaptic density, particularly in the hippocampus and cortex. Tailored EE interventions for elderly stroke survivors include cognitively stimulating activities and participation in social groups. These interventions enhance cognitive function and support recovery by promoting neural repair. Additionally, EE helps to mitigate sensory deficits commonly observed in older adults, ultimately improving mental performance and quality of life. EE has shown promise in preventing relapse, enhancing attention, reducing anxiety, forestalling age-related DNA methylation alterations, and amplifying neurogenesis through heightened neural progenitor cell (NPC) populations. Aligning preclinical studies with clinical trials can enhance neurorehabilitation conditions for stroke patients, thereby optimizing the environments in which they recover. This can be achieved through the concerted efforts of multidisciplinary teams working collaboratively. This review explores how EE specifically impacts the aging brain and ischemic stroke, a major age-related neurological disorder with global health implications. The potential of enviro-mimetics and relevant clinical studies on EE's effects on ischemic stroke survivors are discussed. This review enhances our understanding of the effects of EE on aging and ischemic stroke, motivating further research aimed at refining strategies for stroke management and recovery.</p>","PeriodicalId":8909,"journal":{"name":"Biogerontology","volume":"26 3","pages":"92"},"PeriodicalIF":4.4,"publicationDate":"2025-04-16","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143957726","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
BiogerontologyPub Date : 2025-04-10DOI: 10.1007/s10522-025-10233-y
Wei-Hsuan Su, Jessica J Smith, Evien Cheng, Megan S Nishitani, Catherine Y Choi, Kelsey R Lee, Alexia Pardos Salzano, Samuel E Schriner
{"title":"Spermidine toxicity in Saccharomyces cerevisiae due to mitochondrial complex III deficiency.","authors":"Wei-Hsuan Su, Jessica J Smith, Evien Cheng, Megan S Nishitani, Catherine Y Choi, Kelsey R Lee, Alexia Pardos Salzano, Samuel E Schriner","doi":"10.1007/s10522-025-10233-y","DOIUrl":"https://doi.org/10.1007/s10522-025-10233-y","url":null,"abstract":"<p><p>Spermidine is a naturally occurring polyamine present in all cells and is necessary for viability in eukaryotic cells. The cellular levels of spermidine decline as an organism ages, and its supplementation has been found to extend lifespan in yeast, worms, flies, mice, and human cultured cells. The lifespan extending effect of spermidine is thought to be due to its ability to induce autophagy, a turnover of cellular components. Mitochondrial dysfunction is believed to be a major driver of the aging process. We asked whether spermidine could rescue mitochondrial dysfunction using the yeast Saccharomyces cerevisiae lacking mtDNA (ρ<sup>0</sup> cells) as a model. Not only was spermidine unable to rescue survival in ρ<sup>0</sup> cells, but it appeared to exhibit toxicity resulting in a shortened lifespan. This toxicity appears to not be due to the loss of mitochondrial respiration, elevated oxidative stress, or depleted ATP. Spermidine toxicity could be recapitulated by the genetic or pharmacological inactivation of mitochondrial complex III. It can also be prevented by the impairment of autophagy, through the inactivation of ATG8, or by impairment of mitochondrial complex II through the inactivation of SDH2. Spermidine toxicity in ρ<sup>0</sup> cells was present in yeast strains BY4741 and W303, but not D273-10B, demonstrating genetic variance in the phenotype. Thus, caution may be suggested regarding the use of spermidine to alleviate aging in humans. Depending on the genotype of the individual, spermidine could potentially harm the very individuals it is intended to help.</p>","PeriodicalId":8909,"journal":{"name":"Biogerontology","volume":"26 2","pages":"91"},"PeriodicalIF":4.4,"publicationDate":"2025-04-10","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11985560/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143973655","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
BiogerontologyPub Date : 2025-04-10DOI: 10.1007/s10522-025-10230-1
Edward J Calabrese, Peter Pressman, A Wallace Hayes, Evgenios Agathokleous, Gaurav Dhawan, Rachna Kapoor, Japjee Parmar, Ibrahim Mssillou, Vittorio Calabrese
{"title":"Fisetin: hormesis accounts for many of its chemoprotective effects.","authors":"Edward J Calabrese, Peter Pressman, A Wallace Hayes, Evgenios Agathokleous, Gaurav Dhawan, Rachna Kapoor, Japjee Parmar, Ibrahim Mssillou, Vittorio Calabrese","doi":"10.1007/s10522-025-10230-1","DOIUrl":"https://doi.org/10.1007/s10522-025-10230-1","url":null,"abstract":"<p><p>The present paper provides the first integrated assessment of the capacity of the flavonol, fisetin, to induce hormetic dose responses. Fisetin was shown to induce hormetic dose responses in cellular and in vivo animal model systems affecting a broad range of endpoints of potential therapeutic and public health significance across the entire lifespan. Fisetin was effective in slowing aging processes, acting as a senolytic agent in multiple organ systems, in an hormetic fashion. In addition, fisetin was broadly neuroprotective, including during fetal development, and preventing the toxicity of methylmercury. Since these findings indicate that fisetin may have the potential to induce multi-system chemoprotective effects, it indicates the need to better clarify the absorption and bioavailability of fisetin and ways to enhance its efficiency.</p>","PeriodicalId":8909,"journal":{"name":"Biogerontology","volume":"26 2","pages":"90"},"PeriodicalIF":4.4,"publicationDate":"2025-04-10","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143967274","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}