Frontiers in aging最新文献

{"title":"Editorial: Understanding the impact of loneliness and social isolation on the health of older adults with cancer.","authors":"Keith M Bellizzi, Rebecca M Saracino","doi":"10.3389/fragi.2026.1930051","DOIUrl":"https://doi.org/10.3389/fragi.2026.1930051","url":null,"abstract":"","PeriodicalId":73061,"journal":{"name":"Frontiers in aging","volume":"7 ","pages":"1930051"},"PeriodicalIF":4.9,"publicationDate":"2026-07-22","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13454724/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148708798","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":"Association between frailty and incidence of AMD among middle-aged and older people: evidence from the UK Biobank.","authors":"Hao Mou, Chang-Jun Zhang","doi":"10.3389/fragi.2026.1838979","DOIUrl":"10.3389/fragi.2026.1838979","url":null,"abstract":"<p><strong>Background: </strong>To explore the association between age-related macular degeneration (AMD) and frailty and the link between frailty and neurological aging diseases in AMD patients.</p><p><strong>Methods: </strong>This study included 354,334 individuals aged ≥40 years without AMD at baseline from the UK Biobank. Frailty was assessed using the Fried phenotype. Cox proportional hazard models were used to analyze the association between frailty and AMD incidence. Logistic regression models were used to examine the link between frailty and nervous system-related diseases among AMD patients.</p><p><strong>Results: </strong>Frailty was associated with AMD incidence (hazard ratio [HR] 1.36 [95% confidence interval [95% CI] 1.29-1.44] for prefrailty; HR 2.12 [95% CI 1.86-2.42] for frailty). All five frailty components were associated with AMD: weight loss (HR 1.11 [95% CI 1.03-1.20]), exhaustion (HR 1.13 [95% CI 1.03-1.23]), low physical activity (HR 1.12 [95% CI 1.01-1.23]), low grip strength (HR 1.23 [95% CI 1.14-1.32]), and slow walking pace (HR 1.23 [95% CI 1.12-1.35]). Additionally, among AMD patients, frailty was linked to neurodegenerative diseases (odds ratio [OR] 3.09 [95% CI 1.58-6.07]), neurovascular diseases (OR 3.77 [95% CI 2.16-6.60]), and mental diseases (OR 2.09 [95% CI 1.12-3.93]).</p><p><strong>Conclusion: </strong>Frailty is a significant risk factor for AMD incidence, with all five components showing a positive association with AMD. Furthermore, frailty is linked to neural system-related diseases in AMD patients. Early detection and intervention for frailty may help prevent or delay AMD onset.</p>","PeriodicalId":73061,"journal":{"name":"Frontiers in aging","volume":"7 ","pages":"1838979"},"PeriodicalIF":4.9,"publicationDate":"2026-07-22","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13438126/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148681269","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":"Accelerated biological aging: the role of chronic inflammation, weathering and novel therapeutic strategies.","authors":"Frances M Marin-Maldonado, Mitzy J Santiago-Rosario, Wilfred Fonseca-Ferrer, Cornelis P Vlaar, Magaly Martinez-Ferrer, Jose Colon-Saez, Jorge Duconge-Soler","doi":"10.3389/fragi.2026.1863781","DOIUrl":"10.3389/fragi.2026.1863781","url":null,"abstract":"<p><p>Biological aging is a gradual, multisystem process characterized by progressive functional decline, diminished physiological resilience, and increased susceptibility to chronic diseases. Growing evidence suggests that persistent exposure to adverse social environments, chronic psychological stress, and socioeconomic disadvantage can accelerate biological aging by altering age-related biomarkers and stress-response pathways. The weathering hypothesis provides a framework to explain how the cumulative burden of psychosocial adversity becomes biologically embedded, resulting in physiological wear and tear that hastens age-related deterioration over time. A central mechanism underlying this process is chronic low-grade inflammation, which contributes to the pathogenesis of numerous age-related conditions, including cancer and neurodegenerative diseases (NDDs). These disorders are highly prevalent among Caribbean Hispanics, a population disproportionately affected by social disadvantages and rapid population aging. Recent advances in the biology of inflammation and cellular senescence have generated interest in therapeutic strategies aimed at modulating fundamental mechanisms of aging. Emerging approaches, including senolytics, anti-inflammatory agents, and non-coding RNA-based interventions, offer promising opportunities for precision medicine; however, RNA-based therapies remain largely experimental, and their clinical translation to address stress-related aging and health disparities has yet to be established. In this review, we examine the interplay between weathering and inflammation in shaping biological aging and discuss the potential of innovative precision medicine approaches to mitigate age-related decline and reduce health disparities in vulnerable populations.</p>","PeriodicalId":73061,"journal":{"name":"Frontiers in aging","volume":"7 ","pages":"1863781"},"PeriodicalIF":4.9,"publicationDate":"2026-07-21","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13433523/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148674680","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":"The negligible biological impact of reproductive history on aging: a high-resolution variance analysis.","authors":"Marco Roccetti","doi":"10.3389/fragi.2026.1888676","DOIUrl":"10.3389/fragi.2026.1888676","url":null,"abstract":"<p><p>Modern epigenetics increasingly employs biological clocks to quantify the impact of women's reproductive history on aging, with a very recent study claiming that childbearing significantly decelerates biological senescence in women. This article critically re-examines these claims, challenging the growing trend of biological determinism imposed on reproductive choices. By performing a secondary upper-bound analysis on demographic and epigenetic data, we quantify the predictive power of reproductive history relative to the dominant influence of genetic and stochastic factors. Our analysis reveals that a reported 1-year acceleration in biological aging for women without children, while statistically significant in massive cohorts, possesses negligible explanatory power. When evaluated against the standard deviation of high-longevity populations, this 1-year shift corresponds to ∼1.2% of variance scale in female lifespan, leaving 98.8% governed by stochastic noise. With a standardized effect size near zero (<i>d</i> = 0.11) and a survival distribution overlap of 95.6% between groups, the epigenetic signals attributed to childbearing are shown to be practically irrelevant for individual life expectancy. These findings demonstrate how microscopic p-values in large-scale datasets can alter scientific reality thus generating unjustified societal anxiety. This work calls for a return to scientific realism in biometrics, distinguishing between molecular <i>non-sequiturs</i> and tangible health outcomes to prevent the pathologization of reproductive trajectories and defend the fundamental stochastic freedom of human life (i.e., the inherent randomness and unpredictability of human lifespan).</p>","PeriodicalId":73061,"journal":{"name":"Frontiers in aging","volume":"7 ","pages":"1888676"},"PeriodicalIF":4.9,"publicationDate":"2026-07-20","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13429766/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148671491","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":"Breaking barriers in pulmonary health of patients with metabolic diseases: senolytics and beyond.","authors":"Michaela Rennerova, Marie Zaloudikova, Martin Haluzik, Sona Stemberkova Hubackova","doi":"10.3389/fragi.2026.1812724","DOIUrl":"10.3389/fragi.2026.1812724","url":null,"abstract":"<p><p>Aging is the primary risk factor for most chronic diseases and is accompanied by the progressive accumulation of senescent cells within tissues. While cellular senescence initially serves as a protective mechanism that limits the proliferation of damaged cells, its persistent presence contributes to tissue dysfunction through the secretion of a broad spectrum of inflammatory and profibrotic mediators. The resulting chronic low-grade inflammation, oxidative stress, immune dysregulation, and impaired regenerative capacity are increasingly recognized as hallmarks of age-related pathology. Chronic pulmonary diseases, including chronic obstructive pulmonary disease and idiopathic pulmonary fibrosis, increase markedly with age and are increasingly regarded as manifestations of accelerated lung aging. Their development and progression are further exacerbated by obesity and type 2 diabetes mellitus, two highly prevalent metabolic disorders characterized by chronic metabolic stress, mitochondrial dysfunction, systemic inflammation, and enhanced accumulation of senescent cells. Emerging evidence suggests that cellular senescence represents a common biological denominator linking metabolic and pulmonary disease. Through persistent inflammatory and profibrotic signaling, senescent cells establish a self-perpetuating cycle of chronic inflammation, extracellular matrix remodeling, fibrosis, endothelial dysfunction, and impaired tissue repair, thereby driving progressive deterioration of both metabolic and pulmonary function. The recognition of cellular senescence as one of the important drivers of both chronic pulmonary and metabolic diseases has stimulated growing interest in therapeutic strategies aimed at reducing senescent-cell burden or attenuating its detrimental effects. Current approaches include both novel senotherapies specifically targeting cellular senescence, as well as established therapies used in metabolic diseases that have recently been shown to exert senescence-modulating effects. Although clinical evidence remains limited, targeting cellular senescence offers a unique opportunity to address the underlying biology of aging rather than individual disease manifestations. This review highlights the emerging role of cellular senescence as a mechanistic link between chronic pulmonary diseases and metabolic disorders and discusses its potential as a therapeutic target.</p>","PeriodicalId":73061,"journal":{"name":"Frontiers in aging","volume":"7 ","pages":"1812724"},"PeriodicalIF":4.9,"publicationDate":"2026-07-17","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13424404/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148654284","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":"The Janus face of L-arginine supplementation in cardiovascular health and aging exploration of underlying mechanisms.","authors":"Zhihong Yang, Xiu-Fen Ming, Duilio M Potenza","doi":"10.3389/fragi.2026.1880662","DOIUrl":"10.3389/fragi.2026.1880662","url":null,"abstract":"<p><p>Since the discovery of L-arginine-nitric oxide (NO) pathway in control of cardiovascular function in 1980s, endothelial dysfunction characterized by decreased endothelial NO bioavailability is recognized as a critical hallmark of cardiovascular disease (CVD) and aging, L-arginine supplementation has been proposed as a potential therapeutic intervention primarily due to its role as the sole substrate for endothelial NO-synthase (eNOS). Although many experimental and clinical studies show improvement of endothelial functions by L-arginine supplementation, the beneficial effects could not be translated into the improvement of hard endpoint outcome. Even harmful effects such as worsening of endothelial function, cardiac function, and increased mortality in patients with advanced CVD are reported in the randomized clinical trials. Despite of the reported adverse effects in clinical trials, L-arginine intake is considered safe and is still widely used in our society to boost muscle mass in healthy and aged populations. While we believe that chronic L-arginine supplementation shall be carefully implemented in clinical settings or shall be avoided in patients with advanced CVD and aged population, future studies shall focus on investigation of the underlying mechanisms of the adverse effects of L-arginine supplementation. This is important not only for L-arginine supplementation but also for other amino acid supplementation aimed to improve cardiovascular health, particularly in the elderly population.</p>","PeriodicalId":73061,"journal":{"name":"Frontiers in aging","volume":"7 ","pages":"1880662"},"PeriodicalIF":4.9,"publicationDate":"2026-07-16","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13422544/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148632915","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":"Automated generation of personalized trajectories of aging phenotypes with DyViA-GAN.","authors":"Saumyadipta Pyne, Deep Ray, Meghana Ray","doi":"10.3389/fragi.2026.1724246","DOIUrl":"10.3389/fragi.2026.1724246","url":null,"abstract":"<p><p>With a general increase in human lifespan, the need for technological advances to develop strategies for healthy aging has assumed great importance. In the present study, our goal is to predict the progression of selected aging phenotypes in a given healthy individual as they age past 65 years. Therefore, we developed a novel framework called dynamic views of aging with conditional generative adversarial networks (or DyViA-GAN) that can predict the plausible personalized trajectories of a selected aging phenotype conditioned on the available measurements of the phenotype at a few initial time instances and additional covariates. Given the prevalence of osteoporosis in the aging population, we selected the femoral neck bone mineral density (BMD) of a healthy individual as the phenotype of interest and baseline individual body mass index (BMI) as a covariate. We trained DyViA-GAN on a publicly available longitudinal dataset of a large cohort of mostly white women in the United States of age 65 years or above. It generated, for each individual, continuous phenotype trajectories, along with a corresponding region of acceptable predictions, for an age range of 66-89 years, for eight different combinations, both with and without involving the covariate. The prediction results were subjected to rigorous quality control and multiple comparative analyses. Our results clearly demonstrate the potential of generative deep learning frameworks in healthspan research.</p>","PeriodicalId":73061,"journal":{"name":"Frontiers in aging","volume":"7 ","pages":"1724246"},"PeriodicalIF":4.9,"publicationDate":"2026-07-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13416555/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148622911","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":"Transcriptome analysis of ageing in a long-lived seabird reveals sex-specific differences across age classes in immune and DNA repair pathways.","authors":"Beatrice Berardi, Giacomo Dell'Omo, David Costantini","doi":"10.3389/fragi.2026.1880546","DOIUrl":"10.3389/fragi.2026.1880546","url":null,"abstract":"<p><strong>Introduction: </strong>Sex differences in ageing rate and longevity are widespread across animals, but their molecular bases remain poorly understood. Ageing involves multiple hallmarks of functional decline, and experimental studies suggest sex-specific differences in gene expression, particularly in immune, metabolic, and mitochondrial pathways. Yet, transcriptional variation associated with sex and age in natural populations remains largely unexplored.</p><p><strong>Methods: </strong>Here, we present the first RNA-seq study of a free-living bird, the Scopoli's shearwater (<i>Calonectris diomedea</i>), aimed at investigating sex differences in gene expression across age classes, comparing younger and older individuals of both sexes (16 males and 16 females).</p><p><strong>Results: </strong>We identified a sex-linked transcriptional signature involving genes associated with immune function, stress response, energetics, and development. Age-related reductions in energy metabolism were more pronounced in females, whereas the strongest sex-related differences were detected in immune function and genome stability pathways. Across age classes, males showed higher expression of genes involved in DNA repair and genome maintenance, while females displayed a shift from immune-related processes in early adulthood to stress-response pathways in late adulthood.</p><p><strong>Discussion: </strong>Together, these findings reveal pronounced sex-biased transcriptional regulation across age classes, which we hypothesise is driven by the differentiation of sex-specific reproductive strategies during the egg-laying phase. Furthermore, our results indicate sustained investment in somatic maintenance into late adulthood, consistent with patterns typically observed in long-lived species.</p>","PeriodicalId":73061,"journal":{"name":"Frontiers in aging","volume":"7 ","pages":"1880546"},"PeriodicalIF":4.9,"publicationDate":"2026-07-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13415676/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148622945","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":"Endothelial progenitor cells and circulating microRNAs as possible biomarkers for coronary artery disease.","authors":"Jakub Jozue Wojtacha, Jan Budzianowski, Magdalena Wojciech, Edyta Wawrzyniak-Gramacka, Barbara Morawin, Jarosław Hiczkiewicz, Agnieszka Zembron-Lacny","doi":"10.3389/fragi.2026.1850689","DOIUrl":"10.3389/fragi.2026.1850689","url":null,"abstract":"<p><strong>Introduction: </strong>Endothelial cells and their precursors, i.e., endothelial progenitor cells (EPCs), along with other cell types such as smooth muscle cells and immune cells, release or sequester microRNAs (miRNAs) that actively participate in endothelial dysfunction, smooth muscle cell proliferation, vascular inflammation, and progression of atherosclerotic plaques, ultimately contributing to the transition from stable to acute coronary syndromes. The stability of circulating miRNAs has, for many years, attracted interest in their use as biomarkers in the diagnosis and monitoring of coronary artery disease (CAD).</p><p><strong>Methods: </strong>The study was designed to assess the association of total circulating miRNAs with endothelial dysfunction and EPC-related parameters. The study was carried out in seventy-two patients with CAD (73.2 ± 5.6 years). They were compared with eighty healthy controls (HC) (70.9 ± 5.4 years).</p><p><strong>Results: </strong>The lipid-lipoprotein profile including triglycerides, total cholesterol, low-density lipoprotein (LDL), high-density lipoprotein (HDL), non-HDL and oxidized LDL as well as endothelium-specific variables such as nitric oxide, 3-nitrotyrosine, early EPCs and total EPCs were reduced in CAD patients (p <0.001). The lower levels of nitric oxide in CAD patients (77.60 ± 49.58 μmol/L) compared to HC (290.64 ± 151.93 μmol/L) confirmed the impairment of endothelial secretory function. Total circulating miRNA levels were three-fold higher in CAD (9.36 ± 1.48 ng/L) than in HC (3.22 ± 0.48 ng/L). For miRNA, the area under the curve (AUC) was 1.0 (sensitivity 100%, specificity 100%) with a cut-off value of 5.37 ng/L, indicating a strong discriminatory potential between CAD patients and healthy controls. However, the diagnostic performance of total circulating miRNAs (AUC = 1.0) was observed in a relatively small, single-centre cohort and should be considered exploratory, requiring confirmation in larger, independent studies.</p><p><strong>Discussion: </strong>Our study provides further evidence of complex interactions between EPCs and total circulating microRNAs in coronary artery disease. The findings suggest that circulating microRNAs, particularly in combination with EPC-related parameters, may represent promising biomarkers for clinical differentiation and characterization of endothelial dysfunction in CAD patients.</p>","PeriodicalId":73061,"journal":{"name":"Frontiers in aging","volume":"7 ","pages":"1850689"},"PeriodicalIF":4.9,"publicationDate":"2026-07-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13415549/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148622947","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":"Reframing brain aging: neuroinflammation as an interconnected network process.","authors":"Ludmila Müller, Svetlana Di Benedetto, Viktor Müller","doi":"10.3389/fragi.2026.1858763","DOIUrl":"10.3389/fragi.2026.1858763","url":null,"abstract":"<p><p>Neuroinflammation has emerged as a central component of brain aging, shaping the balance between neural resilience and vulnerability to cognitive decline. Rather than representing a simple consequence of neuronal damage, neuroinflammatory processes are increasingly recognized as active regulators of synaptic integrity, neuronal survival, and circuit function. Under physiological conditions, neuroimmune signaling may contribute to tissue homeostasis, synaptic maintenance, and adaptive responses to cellular stress; however, persistent or dysregulated inflammatory activity may disrupt these functions, promoting network instability and increasing vulnerability to age-related pathology. These processes arise from complex interactions among neurons, glial cells, vascular elements, and peripheral immune signals that together form dynamic neuroimmune networks. Within the aging brain, microglia and astrocytes play key roles in coordinating immune surveillance, synaptic remodeling, and inflammatory signaling. Age-related alterations in glial function can disrupt homeostatic communication within neuron-glia networks, promoting persistent low-grade inflammation and altered synaptic regulation. Importantly, neuroinflammatory activity in the brain is strongly influenced by systemic factors, including peripheral immune aging, changes in blood-brain barrier integrity, and signals originating from the gut-brain axis. In this mini-review, we discuss brain aging from a network perspective, emphasizing how multiscale interactions between cellular and systemic processes shape neuroinflammatory trajectories across the lifespan. We further highlight emerging approaches-including multi-omics technologies, advanced neuroimaging, and systems-level analyses-that are enabling a more integrated understanding of neuroinflammatory dynamics. Viewing neuroinflammation as a network phenomenon may provide new insights into mechanisms of cognitive aging and identify potential targets for strategies aimed at preserving brain health.</p>","PeriodicalId":73061,"journal":{"name":"Frontiers in aging","volume":"7 ","pages":"1858763"},"PeriodicalIF":4.9,"publicationDate":"2026-07-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13416349/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148622885","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}