Aging Process Research Articles

Plane Problem of Impact on Composite Two-Layer Material Reinforced by Crystalline Fibers

A generalized approach was developed for solving contact problems in a dynamic elastic-plastic formulation. For the design of composite and reinforced materials, a technique for solving dynamic contact problems in more adequate an elastic-plastic mathematical formulation is used. To consider the physical nonlinearity of the deformation process, the method of successive approximations is used, which makes it possible to reduce the nonlinear problem to a solution of the sequences of linear problems. The problem of a plane strain state of a beam made from the composite reinforced two-layer material is being solved. The reinforced or armed composite material consists of three materials: metal of top thin layer, the main material of glass and the reinforcing crystalline seven fibers of basalt. Glass is a non-crystalline, often transparent amorphous solid, that has widespread practical and technological use in the modern industry. Glass has high strength and is not affected by the processes of aging of the material, corrosion, and creep. In addition, this material is cheap and widely available. The reinforced composite beam is rigidly linked to an absolutely solid base and on which an absolutely solid impactor acts from above in the centre on a different size of the area of initial contact.

Effects of Biological and Enzymatic Ageing on the Surface Properties of Mg-modified Biochar

The excellent surface properties of Mg-modified biochar have highlighted a broad application prospect for soil heavy metal mitigation. However, the soil biotic aging process can have an impact on the physical and chemical properties of biochar as well as the heavy metal removal performance. Therefore, MgCl2-modified biochar was subjected to a six-month microbial and enzymatically aged test to explore the effects of different biotic aging processes on the physical and chemical properties. The Pb2+ adsorption performance of Mg-modified biochar that experienced different aging processes was compared using isothermal adsorption experiments. The results showed that after microbial aging, the Mg-modified biochar pyrolyzed at 700 ℃ displayed a low persistent free radical signal, with the biofilm secreted by microorganisms wrapped on the surface of the biochar, leading to the increase in the oxygen-containing functional groups on the biochar surface and the increase in the maximum adsorption capacity of Pb2+ from 55.31 mg·g-1 to 86.27 mg·g-1. In contrast, a higher free radical signal of 500 ℃ pyrolyzed biochar suggested that the free radical inhibited the growth and reproduction of microorganisms on the biochar surface, resulting in an insignificant enhancement in maximum adsorption capacity to Pb2+ compared to that with unmodified biochar. The pores of the Mg-modified biochar were severely damaged during the enzymatically aged process, resulting in a decrease in the adsorption capacity of Pb2+ to 22.18 mg·g-1, which was significantly lower than that of the unmodified biochar. Therefore, the adsorption capacity of microbially aged Mg-modified biochar is superior to that of enzymatically aged Mg-modified biochar, mainly because the oxygen-containing functional groups exhibited on the surface of the biochar covered by microorganisms come from the extracellular secretions of microorganisms, which promote the removal of Pb2+.

SGLT2 inhibitor downregulates ANGPTL4 to mitigate pathological aging of cardiomyocytes induced by type 2 diabetes

BackgroundSenescence is recognized as a principal risk factor for cardiovascular diseases, with a significant association between the senescence of cardiomyocytes and inferior cardiac function. Furthermore, type 2 diabetes exacerbates this aging process. Sodium-glucose co-transporter 2 inhibitor (SGLT2i) has well-established cardiovascular benefits and, in recent years, has been posited to possess anti-aging properties. However, there are no reported data on their improvement of cardiomyocytes function through the alleviation of aging. Consequently, our study aims to investigate the mechanism by which SGLT2i exerts anti-aging and protective effects at the cardiac level through its action on the FOXO1-ANGPTL4 pathway.MethodsTo elucidate the underlying functions and mechanisms, we established both in vivo and in vitro disease models, utilizing mice with diabetic cardiomyopathy (DCM) induced by type 2 diabetes mellitus (T2DM) through high-fat diet combined with streptozotocin (STZ) administration, and AC16 human cardiomyocyte cell subjected to stimulation with high glucose (HG) and palmitic acid (PA). These models were employed to assess the changes in the senescence phenotype of cardiomyocytes and cardiac function following treatment with SGLT2i. Concurrently, we identified ANGPTL4, a key factor contributing to senescence in DCM, using RNA sequencing (RNA-seq) technology and bioinformatics methods. We further clarified ANGPTL4 role in promoting pathological aging of cardiomyocytes induced by hyperglycemia and hyperlipidemia through knockdown and overexpression of the factor, as well as analyzed the impact of SGLT2i intervention on ANGPTL4 expression. Additionally, we utilized chromatin immunoprecipitation followed by quantitative real-time PCR (ChIP-qPCR) to confirm that FOXO1 is essential for the transcriptional activation of ANGPTL4.ResultsThe therapeutic intervention with SGLT2i alleviated the senescence phenotype in cardiomyocytes of the DCM mouse model constructed by high-fat feeding combined with STZ, as well as in the AC16 model stimulated by HG and PA, while also improving cardiac function in DCM mice. We observed that the knockdown of ANGPTL4, a key senescence-promoting factor in DCM identified through RNA-seq technology and bioinformatics, mitigated the senescence of cardiomyocytes, whereas overexpression of ANGPTL4 exacerbated it. Moreover, SGLT2i improved the senescence phenotype by suppressing the overexpression of ANGPTL4. In fact, we discovered that SGLT2i exert their effects by regulating the upstream transcription factor FOXO1 of ANGPTL4. Under conditions of hyperglycemia and hyperlipidemia, compared to the control group without FOXO1, the overexpression of FOXO1 in conjunction with SGLT2i intervention significantly reduced both ANGPTL4 mRNA and protein levels. This suggests that the FOXO1-ANGPTL4 axis may be a potential target for the cardioprotective effects of SGLT2i.ConclusionsCollectively, our study demonstrates that SGLT2i ameliorate the pathological aging of cardiomyocytes induced by a high glucose and high fat metabolic milieu by regulating the interaction between FOXO1 and ANGPTL4, thereby suppressing the transcriptional synthesis of the latter, and consequently restoring cardiac function.Graphical abstract

Electric-field-induced aging dynamics of triple-cation lead iodide perovskite at nanoscale

Herein, we report the nanoscale cations dynamics in Cs0.1MA0.15FA0.75PbI3 films during the electric-field-induced aging process using infrared scattering scanning near-field microscopy (IR s-SNOM) combined with a series of complementary analytical techniques such as PL-microscopy, SEM/EDX and ToF-SIMS. The revealed major field-induced aging pathways are related to the anodic oxidation of I− and the cathodic reduction of MA+ and FA+, which finally result in the depletion of organic species in the device channel and the formation of metallic lead. FA+ cations show significantly higher stability with respect to electrochemical reduction as compared to MA+ cations. Formamidinium cations are preserved on the surface of the near-cathode film area even after 40 days of the 1 V/μm field exposure, while MA+ cations demonstrate complete decomposition after 24 days. The obtained results demonstrate that IR s-SNOM represents a powerful technique for studying the spatially resolved field-induced degradation dynamics of hybrid perovskite absorbers and the identification of more promising materials resistant to the electric field.

Older is order: entropy reduction in cortical spontaneous activity marks healthy aging

BackgroundEntropy trajectories remain unclear for the aging process of human brain system due to the lacking of longitudinal neuroimaging resource.ResultsWe used open data from an accelerated longitudinal cohort (PREVENT-AD) that included 24 healthy aging participants followed by 4 years with 5 visits per participant to establish cortical entropy aging curves and distinguish with the effects of age and cohort. This reveals that global cortical entropy decreased with aging, while a significant cohort effect was detectable that people who were born earlier showed higher cortical entropy. Such entropy reductions were also evident for large-scale cortical networks, although with different rates of reduction for different networks. Specifically, the primary and intermediate networks reduce their entropy faster than the higher-order association networks.ConclusionsOur study confirmed that cortical entropy decreases continually in the aging process, both globally and regionally, and we conclude two specific characteristics of the entropy of the human cortex with aging: the shift of the complexity hierarchy and the diversity of complexity strengthen.

Investigation of Mechanical Properties and Color Changes of 3D-Printed Parts with Different Infill Ratios and Colors After Aging

Since their inception, plastics have become indispensable materials. However, plastics used for extended periods in industrial applications are prone to aging, which negatively impacts their material behavior and performance. To ensure the long-term usability of these materials, they must be tested in real-time, in-service environments to assess degradation. In practice, however, accelerated aging techniques are commonly employed to avoid time loss. Over time, various indicators of degradation in plastics emerge, such as changes in molecular weight, cracking, and mechanical properties like strain at break and impact strength. Among these, color deterioration or change is a critical factor that helps evaluate the service life of these materials. Considering the increasing use of plastics in 3D printing today, and the growing focus on strength over aesthetics in these applications, it is particularly useful to evaluate aging in plastics based on the relationship between color and strength. The wide application of 3D printing in various industries necessitates understanding material properties under aging conditions. This study examines the effects of aging on the mechanical behavior of polylactic acid (PLA) with three different colors (yellow, orange, and red) and three different infill ratios (20%, 60%, and 100%). The samples underwent an accelerated aging process of 432 h, which included 8 h of UV radiation, 15 min of water spraying, followed by 3 h and 45 min with the UV lamps turned off. Tensile tests, bending tests, hardness measurements, and color evaluations were conducted on the samples, linking the color changes after aging with the materials’ mechanical properties. The results show that after aging, yellow samples with a 100% infill ratio exhibited a 6.9% increase in tensile strength (44.50 MPa to 47.58 MPa). Orange samples with a 100% infill ratio were less affected by aging, while red samples experienced a decrease in tensile strength across all infill ratios. Regarding bending force, increases were observed in the orange, yellow, and red samples by 10.37%, 25.05%, and 8.87%, respectively. This study underscores the importance of color selection when designing 3D-printed materials for long-term applications.

Aging Lung: Molecular Drivers and Impact on Respiratory Diseases—A Narrative Clinical Review

The aging process significantly impacts lung physiology and is a major risk factor for chronic respiratory diseases, including chronic obstructive pulmonary disease (COPD), idiopathic pulmonary fibrosis (IPF), asthma, and non-IPF interstitial lung fibrosis. This narrative clinical review explores the molecular and biochemical hallmarks of aging, such as oxidative stress, telomere attrition, genomic instability, epigenetic modifications, proteostasis loss, and impaired macroautophagy, and their roles in lung senescence. Central to this process are senescent cells, which, through the senescence-associated secretory phenotype (SASP), contribute to chronic inflammation and tissue dysfunction. The review highlights parallels between lung aging and pathophysiological changes in respiratory diseases, emphasizing the role of cellular senescence in disease onset and progression. Despite promising research into modulating aging pathways with interventions like caloric restriction, mTOR inhibitors, and SIRT1 activators, clinical evidence for efficacy in reversing or preventing age-related lung diseases remains limited. Understanding the interplay between aging-related mechanisms and environmental factors, such as smoking and pollution, is critical for developing targeted therapies. This review underscores the need for future studies focusing on therapeutic strategies to mitigate aging’s detrimental effects on lung health and improve outcomes for patients with chronic respiratory conditions.

Chaperone-mediated autophagy as a modulator of aging and longevity

Chaperone-mediated autophagy (CMA) is the lysosomal degradation of individually selected proteins, independent of vesicle fusion. CMA is a central part of the proteostasis network in vertebrate cells. However, CMA is also a negative regulator of anabolism, and it degrades enzymes required for glycolysis, de novo lipogenesis, and translation at the cytoplasmic ribosome. Recently, CMA has gained attention as a possible modulator of rodent aging. Two mechanistic models have been proposed to explain the relationship between CMA and aging in mice. Both of these models are backed by experimental data, and they are not mutually exclusionary. Model 1, the “Longevity Model,” states that lifespan-extending interventions that decrease signaling through the INS/IGF1 signaling axis also increase CMA, which degrades (and thereby reduces the abundance of) several proteins that negatively regulate vertebrate lifespan, such as MYC, NLRP3, ACLY, and ACSS2. Therefore, enhanced CMA, in early and midlife, is hypothesized to slow the aging process. Model 2, the “Aging Model,” states that changes in lysosomal membrane dynamics with age lead to age-related losses in the essential CMA component LAMP2A, which in turn reduces CMA, contributes to age-related proteostasis collapse, and leads to overaccumulation of proteins that contribute to age-related diseases, such as Alzheimer’s disease, Parkinson’s disease, cancer, atherosclerosis, and sterile inflammation. The objective of this review paper is to comprehensively describe the data in support of both of these explanatory models, and to discuss the strengths and limitations of each.

Role of chemokines in aging and age-related diseases

Chemokines (chemotactic cytokines) play essential roles in developmental process, immune cell trafficking, inflammation, immunity, angiogenesis, cellular homeostasis, aging, and tumorigenesis. Chemokines also modulate response to immunotherapy, and consequently influence the therapeutic outcome. The mechanisms underlying these processes are accomplished by interaction of chemokines with their cognate cell surface G protein-coupled receptors (GPCRs) and subsequent cellular signaling pathways. Chemokines play crucial role in influencing aging process and age-related diseases across various tissues and organs, primarialy through inflammatory responses (inflammaging), recruitment of macrophages, and orchestrated trafficking of other immune cells. Chemokines are categorized in four distinct groups based on the position and number of the N-terminal cysteine residues; namely, the CC, CXC, CX3C, and (X)C. They mediate inflammatory responses, and thereby considerably impact aging process across multiple organ-systems. Therefore, understanding the underlying mechanisms mediated by chemokines may be of crucial importance in delaying and/or modulating the aging process and preventing age-related diseases. In this review, we highlight recent progress accomplished in understanding the role of chemokines and their cellular signaling pathways involved in aging and age-relaed diseases of various organs. Moreover, we explore potential therapeutic strategies involving chemokines and chemokine receptor antagonists aimed at reducing aging and mitigating age-related diseases. One of the modern methods in this direction involves use of chemokine receptor antagonists and anti-chemokines, which suppress the pro-inflammatory response, thereby helping in resolution of inflammation. Considering the wide-spectrum of functional involvements of chemokines in aging and associated diseases, several clinical trials are being conducted to develop therapeutic approaches using chemokine receptor antagonists to improve life span and promote healthy aging.

Mutual Storytelling, Cultural Humility, and Broaching: Bridging the Gap When Working with Culturally Diverse Older Adults

ABSTRACT As the number of older adults significantly increases in the next three decades, more research on best practices for this population is necessary. Older adults experience numerous mental and physical health difficulties, many of which are encapsulated with the aging process. Nonetheless, older adults encounter many challenges when seeking mental health treatment. An intervention integrating mutual storytelling, cultural humility, and broaching is proposed to aid counselors in their multicultural competence while working with older adults. The authors present a case illustration to demonstrate the implementation of a culturally informed intervention and discuss the implications for counseling practice and research.

Advancing elderly care through big data analytics and machine learning for daily activity characterization

<p>Confronted with the ongoing demographic shift characterized by an aging population, society grapples with emerging challenges that extend beyond the provision of targeted health services for the elderly. The focus has broadened to encompass the promotion of well-being and vitality throughout the aging process. Addressing these multifaceted issues demands a comprehensive approach that integrates biomedical components with physical, psychological, and social interventions. In the context of my project, a unique strategy is employed, placing significant emphasis on leveraging big data analytics and machine learning. The primary objective is to systematically observe and characterize the physiological conditions of the elderly, facilitating healthcare professionals in monitoring behaviors and promoting active aging. This undertaking involves meticulous data collection and analysis, employing machine learning algorithms (support vector machine (SVM), gradient boosting) within a framework that harnesses extensive data analytics. Ultimately, this approach enables the identification and characterization of daily routines and physiological states of individuals, contributing to a holistic understanding of aging.</p>

Effect of EVA on the rheological properties of SBR-modified asphalt binder and its behavioral evolution during the thermo-oxidative aging process

Effect of EVA on the rheological properties of SBR-modified asphalt binder and its behavioral evolution during the thermo-oxidative aging process

Dynamic strain ageing of L12-strengthened Ni-Co base high-entropy alloy and unraveling its deformation mechanisms in strain ageing process

Dynamic strain ageing (DSA) of L12-strengthened Ni-Co base high-entropy alloy (HEA) was examined at temperatures varying from 20 to 600 °C with strain rates between 10–2 to 10–4 s-1. In normal DSA regimes, elevating temperature or lowering strain rate advances the DSA behavior, resulting in the lowered critical strain and raised amplitude of serrations. Based on strain-rate jump tests, the negative strain-rate sensitivity induced by DSA was observed at the elevated temperature regime, and high apparent activation volumes ranging from 97∼ 737b3 correspond to the strong obstacles effect from the precipitates and the additional pinning strengthening of solute atoms. Transmission electron microscopy evidence suggests that stacking faults prevailed at all testing temperatures, while the serration changes are the outcomes of their dynamic interactions with precipitates and condensed Cr, Co-rich solute cloud. Subsequently, in normal DSA regimes, activation energies required for the onset of type A, a mixture of type A and type A + C, and a mixture of type A + B and type C serrations are 30.6, 65.8, and 101.1 kJ/mol determined by strain ageing model at strain rates of 10–2, 10–3, and 10–4 s-1, respectively. Lastly, a two-time parameter-based Cottrell-Bilby strain aging kinetic model that considers the solute-dislocation interaction in a pipe diffusion manner is applied to evaluate the DSA strengthening concerning strain, strain rate, and temperature.

Coupling of mitochondrial state with active zone plasticity in early brain aging

Neurodegenerative diseases typically emerge after an extended prodromal period, underscoring the critical importance of initiating interventions during the early stages of brain aging to enhance later resilience. Changes in presynaptic active zone proteins ("PreScale") are considered a dynamic, resilience-enhancing form of plasticity in the process of early, still reversible aging of the Drosophila brain. Aging, however, triggers significant changes not only of synapses but also mitochondria. While the two organelles are spaced in close proximity, likely reflecting a direct functional coupling in regard to ATP and Ca2+ homeostasis, the exact modes of coupling in the aging process remain to understood.We here show that genetic manipulations of mitochondrial functional status, which alters brain oxidative phosphorylation, ATP levels, or the production of reactive oxygen species (ROS), can bidirectionally regulate PreScale during early Drosophila brain aging. Conversely, genetic mimicry of PreScale resulted in decreased oxidative phosphorylation and ATP production, potentially due to reduced mitochondrial calcium (Ca2+) import.Our findings indicate the existence of a positive feedback loop where mitochondrial functional state and PreScale are reciprocally coupled to optimize protection during the early stages of brain aging.

Influence of Variable Intensity Ultraviolet on the Performance of SBS Modified Asphalt

Previous scholars studied UV aged asphalt performance under constant UV intensity. This study proposed a method of UV aged asphalt based on the time-varying UV intensity, which is more capable of realistically simulating the UV aging of asphalt under natural conditions. The softening point, viscosity, and DSR tests were used to analyze changes in conventional and rheological properties of UV aged asphalt and compared them with RTFO (Rolling Thin-Film Oven) aged asphalt. Fourier transform infrared (FTIR) spectroscopy and scanning electron microscope (SEM) tests were analyzed for the microscopic characteristics. The aging index was also used to evaluate the percentage of asphalt aging attributable to each UV aging cycle. The results show that the softening point is more susceptible to UV radiation, with UV-6 cycles exceeding the softening point increment of RTFO. On the contrary, the viscosity is more susceptible to thermo-oxidative aging, and the viscosity increment of RTFO is 39.3% higher than that of UV-12 cycles. Based on DSR's test results, the rutting factor magnitude of RTFO was between 9-12 UV aging cycles The phase angle results indicate that thermo-oxidative aging is more likely to convert asphalt to elastomer than RTFO asphalt. UV aging process of asphalt produced sulfinyl and, carbonyl and other polar functional groups, asphalt intermolecular forced to enhance the production of a harder oxidation layer, the asphalt surface began to appear cracks. As aging time increases, the cracks become longer and deeper. Practical image recognition technology can identify the areas of the cracks. The crack area follows a linear pattern during cycles 3 to 9, while the growth rate slows down during cycles 9 to 12.

Analysis of factors related to the incidence of hypertension in the elderly

Introduction: Hypertension or high blood pressure is one of the main health problems in the elderly population in various parts of the world. The elderly are more susceptible to hypertension due to the ageing process that affects the elasticity of blood vessels, as well as increased peripheral resistance. In addition, various risk factors, such as an unhealthy lifestyle, poor diet, and certain medical conditions, can worsen the condition of hypertension in the elderly. Objective: This study aims to analyze factors related to the incidence of hypertension in the elderly. Methods: This research uses a cross-sectional design, an analytical study that studies the causes of incidents or incidents. Data collection uses a questionnaire. The sample in this study was 64 elderly hypertensive patients in the working—data analysis using the chi-square test. Result: The results of this study indicate that there is a relationship between physical activity (p=0.000), obesity (p=0.000), diet (p= 0.029), smoking habits (p=0.000) and work (p=0.020) with the incidence of hypertension in the elderly in working. Conclusion: The incidence of hypertension in the elderly with the variables studied shows that there is a relationship, and the most related variable is obesity. So, it is hoped that the elderly, especially those who are obese, should be given intervention to maintain their diet so that complications do not occur and can reduce the risk of hypertension.

Endothelial Cell Aging and Autophagy Dysregulation.

Entropy is a natural process that affects all living cells, including senescence, an irreversible physiological process that impairs cell homeostasis. Age is a significant factor in disease development, and the pathogenesis of endothelial cell aging is multifactorial. Autophagy dysfunction accelerates endothelial cell aging and cell death, while autophagy preserves endothelial cell youthfulness through intracellular homeostasis and gene expression regulation. Sirt, mTORC1, and AMPK are youthfulness genes that induce autophagy by inhibiting mTOR and upregulating FIP200/Atg13/ULK1. Aged endothelial cells have decreased levels of Lamin B1, γH2AX, Ki67, BrdU, PCNA, and SA β-Gal. Maintaining healthy young endothelial cells can prevent most cardiovascular diseases. Autophagy targeting is a potential future therapeutic strategy to modify endothelial cell age and potentially slow or reverse the aging process. This article provides state-of-the-art research on the role of autophagy in endothelial cell aging. Hypothesizing that autophagy dysregulation is associated with early endothelial cell dysfunction and further clinical sequelae, including atherosclerosis formation, leading to various cardiovascular diseases.

Deletion of Stimulator of Interferons Genes Aggravated Cardiac Dysfunction in Physiological Aged Mice

BackgroundStimulator of interferons genes (STING) is crucial for innate immune response. It has been demonstrated that cGAS-STING pathway was the driver of aging-related inflammation. However, whether STING is involved in cardiac dysfunction during the physiological aging process remains unclear. MethodsGene expression profiles were obtained from the Gene Expression Omnibus database, followed by weighted gene co-expression network analysis, gene ontology analysis and protein network interaction analysis to identify key pathway and genes associated with aging. The effects of STING on cardiac function, glucose homeostasis, inflammation, and autophagy in physiological aging were investigated with STING knockout mice. ResultsBioinformatics analysis revealed STING emerged as a hub gene of interest. Subsequent experiments demonstrated the activation of STING pathway in the heart of aged mice. Knockout of STING alleviated the inflammation in aged mice. However, Knockout of STING impaired glucose tolerance, inhibited autophagy, enhanced oxidative stress and aggravated cardiac dysfunction in aged mice. ConclusionAlthough reducing inflammation, long-term STING inhibition by genetic ablation exacerbated cardiac dysfunction in aged mice. Given the multifaceted nature of aging and the diverse cellular functions of STING beyond immune regulation, the negative effects of targeting STING as a strategy to mitigate aging phenotype should be fully considered.

Healthful plant-based diets are negatively associated with the rate of biological aging: A national study based on US adults

Plant-based diets are recognized for their health benefits. However, evidence on the association between plant-based diet quality and aging in the US population is limited. This study aimed to investigate the association between different plant-based diet indices, phenotypic age acceleration (PhenoAgeAccel), and biological age acceleration (BioAgeAccel). We hypothesized that healthful plant-based diets would negatively affect PhenoAgeAccel and BioAgeAccel in US adults. The cross-sectional analysis included 22,363 participants, and information was obtained from the National Health and Nutrition Examination Survey database. The quality of plant-based diet was assessed using three indices: overall plant-based diet index (PDI), healthful PDI (hPDI), and unhealthful PDI (uPDI). Phenotypic age (PA) and biological age (BA) was calculated based on a linear combination of chronological age and 12 multi-system clinical chemistry biomarkers in accordance with the previously established method. PhenoAgeAccel and BioAgeAccel are the residuals of the PA and BA. Weighted linear regression analyses were performed to evaluate the relationships between PDI, hPDI and uPDI, and PhenoAgeAccel and BioAgeAccel. After adjusting for all covariates, we observed that a 10-unit higher PDI score was associated with 0.80 years lower PhenoAgeAccel (β: −0.80, 95% confidence interval [CI]: -0.94,-0.67), and 1.91 years lower BioAgeAccel (β: −1.91, 95% CI: -2.42,-1.40). A 10-unit higher hPDI score was associated with 0.83 years lower PhenoAgeAccel (β: −0.83, 95% CI: -0.96,-0.70), and 1.76 years lower BioAgeAccel (β: −1.76, 95% CI: -2.18,-1.34). Conversely, a 10-unit higher uPDI score was associated with 0.77 years higher PhenoAgeAccel (β: 0.77, 95% CI: 0.66,0.89) and 1.21 years higher BioAgeAccel (β: 1.21, 95% CI: 0.80,1.62). These findings suggest that US adults may be able to slow the aging process by increasing adherence to a healthy plant-based diet.

Aging and periodontium: Slowing aging process by improving periodontal health

Introduction: Aging is characterized by a progressive decline or loss of physiological functions, leading to increased susceptibility to disease or death. The periodontium, a complex structure surrounding and supporting the teeth, is composed of the gingiva, periodontal ligament, cementum, and alveolar bone. Supportive and protective roles of the periodontium are very critical to sustain life, but the periodontium undergoes morphological and physiological changes with age. Purpose: The aim of this review is to summarize the current findings of delaye aging process by improving periodontal health. Conclusion: Daily oral hygiene maintenance with toothbrushing, flossing, mouthrinsing and appropriate use of anti-oxidants, such as vitamin C, as well as regular visit to dentist or periodontist is mandatory to maintain healthy periodontal tissue which support general health, also slowing down aging process