Evolution of Microstructure and Mechanical Property during Long-Term Aging in Udimet 720Li

Thermal stabilities of microstructure and mechanical property have been investigated on super- alloy U72OLi, which is of great interest of application for jet engine and land-based turbine disc. The results showed that, the primary and secondary γ’?particles maintain good thermal stability at 650 and 7000C with aging time up to 3000 h, while the tertiary γ’?is apparently dependent on aging temperature and time. The tertiary γ’?particles undergo a procedure of coarsening, dissolution and eventually complete disappearance with the increasing of aging time and temper- ature. They exhibit unusual high sensibility upon aging temperature, which is attributed to the lattice misfit between the γ’?precipitates and the matrix in the alloy. The grain boundary phase M23C6 remains stable without forming of sigma phase even with aging time up to 3000 h at 700℃. Microhardness decreases apparently with increasing aging time and aging temperature. Theoretical analysis based on dislocation mechanism indicates that the change of microhardness should be attributed to the evolution of the tertiary γ’?during aging.

Microstructure and diffraction pattern changes resulted from long-term aging of martensite CuZnAlMnNi shape memory alloy

Microstructures of a CuZnAlMnNi shape memory alloy in the as-quenched andlong-term aged conditions were investigated by transmission electron microscopy. Aged for one yearin martensite phase, an equilibrium α-phase with fcc structure was observed in the M18R martensitematrix, accompanied by the appearance of a novel diffraction pattern. By analysis, it was suggestedthat the novel pattern results from the α-phase and the martensite matrix remaining in seven fineplates which produce intense secondary diffraction effect when the diffraction beams enter from onephase into another.

Effects of electric field treatment on microstructures of GH4199 superalloy after long-term aging

The effects of electric field intensity and treatment temperature on the microstructures of GH4199 superalloy after long-term aging were investigated. The results show that the number and size of carbides and TCP(σphase andμphase) phase in the alloy increase with increasing electric field intensity at the same heat treatment temperature and holding time. While the number and size of carbides and TCP phase are weekly influenced by treatment temperature with lower electric field intensity of 2 kV/cm. When the treat temperature is up to 1 093 K, annealing twins appear in the alloy, and the number of twins increases with increasing holding time. Since the electric field can provide the enough energy for the movement of vacancies and atom, it is considered that the nucleus of the twins formed with formation stack faults due to the mismatch of local atom in crystal caused by the vacancies, and the twins will grow with the increase of holding time. Meanwhile, such promoting effects on atom movement of the electric field increase with the increase of the electric field intensity, meantime the carbides and TCP phase grow fast with the increase of electric field intensity.

Characterization and numerical simulation of nucleation-growth-coarsening kinetics of precipitates in G115 martensitic heat resistance steel during long-term aging

The service performance of heat resistance steels is largely determined by the precipitation kinetics.The nucleation-growth-coarsening behaviors of precipitates in G115 martensitic heat resistance steel during long-term aging at 650℃ have been systemically investigated.The microstructural characteristics,precipitate morphology and alloying element distribution were studied by scanning electron microscopy,transmission electron microscopy and scanning transmission electron microscopy.The lognormal distribution fitting combined with the multiple regression analysis was adopted to evaluate the precipitate size distributions.Laves phase has longer incubation time,and its coarsening rate is almost one order of magnitude higher in comparison with that of M_(23)C_(6) carbide.Furthermore,the nucleation rate,number density,average radius,and volume fraction of two precipitates are simulated based on the classical nucleation theory and the modified Langer-Schwartz model.The precipitation behavior of Laves phase can be well explained with the Fe-W system as the interfacial energy takes 0.10 J/m^(2).In contrast,the simulation results of M_(23)C_(6) carbide in the Fe-Cr-C system are significantly overestimated,which results from the inhibitory effect of boron on coarsening.

Strengthening Active Aging through Older People’s Association and Economic Activity of the Older People in Nepal

Aging is a natural lifelong process ending in death. Many older people are living in poverty. Older people are generally considered dependent on others as they grow older. The purpose of this article is to explore the entrepreneurship activities of Nepalese older adults. Data for this study were collected from the project Help Age International (HAI) implemented in Nepal. Qualitative data observations and interviews were used to collect data. The findings of this study show the formation of the Older People’s Association (OPA) has supported many older people to participate outside the home in various social activities. Moreover, regular deposits through OPAs offer little help. OPAs support older people in their need of financial support to implement minor entrepreneurship. Older people who received support were pleased and were actively involved in their activities and also regularly deposited money in them. Subsequently, older people’s participation in social activities has increased and also helped to lower elderly abuse, loneliness, and depression. Local governments should promote such activities which will help with healthy aging.

Homocysteinemia and Depression in Community-Dwelling Older Adults: The Cohort Longitudinal Study “InveCeAb” (Brain Aging in Abbiategrasso)

Depression is a major health problem, especially for elderly people. According to the “homocysteine hypothesis of depression”, high homocysteine levels may cause depression of mood via cerebrovascular diseases. Whilst biologically plausible, such hypothesis needs yet confirmation. We aimed at: 1) studying the relationships between homocysteinemia (HCY) and depression in a community-dwelling cohort of people aged 70 to 75 years at baseline;2) investigating plasma levels of HCY and 3) comparing these levels between males and females, in the same population. We exploited the data from four waves (2010, 2012, 2014 and 2018) of the longitudinal study “InveCeAb”, with specific regard towards mood assessment, by Geriatric Depression Scale (GDS) scoring, and diagnosis of clinically relevant or subthreshold depression. HCY plasma levels were measured in the waves 2012, 2014 and 2018. Sample attrition was due mainly to death or overall worsening. No statistically significant differences were found in plasma homocysteine levels in each wave, according to depressive symptoms. No correlations were found between plasma HCY levels in each wave with their corresponding GDS scores, even after adjustment for folate and cobalamin blood concentrations. Dichotomized levels of HCY (≤15 vs >15 μM/l) were not associated with dichotomized GDS scores (≤4 vs higher), clinically relevant and subthreshold depression diagnosis and any antidepressive use, in any wave. First (2012) HCY levels increased with participants’ increasing age, cross-sectionally. Listwise HCY concentrations decreased along the 3 waves. HCY levels were always higher in males than in females. Our results may challenge the “homocysteine hypothesis” of depression, whilst supporting the role of high homocysteinemia as a marker of overall bad health.

Regulation of aging by NELF-A and RNA polymerase Ⅱ elongation

Epigenetic regulation of aging:Aging is defined as the gradual decline of physiological function and cellular integrity,causing o rganismal vulnerability to age-onset diseases and morbidity.Studies in different animal models have led to the identification of twelve aging hallmarks that shared several features:its age-associated manifestation.

Astrocyte syncytium:from neonatal genesis to aging degeneration

Modern neuroscience began from all reaching and fierce conflict between“neuronismo and reticulismo”——between neuronal and reticular theories of the organization of the nervous system;the conflict culminated in December of 1906 in Stockholm where Santiago Ramon y Cajal(the proponent of the neuronal doctrine)and Camillo Golgi(who advocated the syncytial reticular organization of neural networks)delivered their Noble prize lectures(Verkhratsky,2009).

Preventing brain aging by the artificial enforcement of the unfolded protein response:future directions

As the life expectancy of the world’s population increases,age-related diseases are emerging as one of the greatest problems facing modern society.The onset of dementia and neurodegenerative diseases is strictly dependent on aging as a major risk factor and has a profound impact on various aspects of the lives of individuals and their families.

Effects of Maillard reaction and its product AGEs on aging and age-related diseases

Maillard reaction(MR)is a non-enzymatic browning reaction commonly seen in food processing,which occurs between reducing sugars and compounds with amino groups.Despite certain advantages based on Maillard reaction products(MRPs)found in some food for health and storage application have appeared,however,the MR occurring in human physiological environment can produce advanced glycation end products(AGEs)by non-enzymatic modification of macromolecules such as proteins,lipids and nucleic acid,which could change the structure and functional activity of the molecules themselves.In this review,we take AGEs as our main object,on the one hand,discuss physiologic aging,that is,age-dependent covalent cross-linking and modification of proteins such as collagen that occur in eyes and skin containing connective tissue.On the other hand,pathological aging associated with autoimmune and inflammatory diseases,neurodegenerative diseases,diabetes and diabetic nephropathy,cardiovascular diseases and bone degenerative diseases have been mainly proposed.Based on the series of adverse effects of accelerated aging and disease pathologies caused by MRPs,the possible harm caused by some MR can be slowed down or inhibited by artificial drug intervention,dietary pattern and lifestyle control.It also stimulates people's curiosity to continue to explore the potential link between the MR and human aging and health,which should be paid more attention to for the development of life sciences.

Regeneration mechanisms and therapeutic strategies for neuromuscular junctions in aging and diseases

The neuromuscular junction(NMJ)is an essential synaptic structure composed of motor neurons,skeletal muscles,and glial cells that orchestrate the critical process of muscle contraction(Li et al.,2018).The typical NMJ structure is classically described as having a“pretzel-like”shape in mice(Figure 1),whereas human NMJs have a smaller,fragmented structure throughout adulthood.Degenerated NMJs exhibit smaller or fragmented endplates,partial denervation,reduced numbers of synaptic vesicles,abnormal presynaptic mitochondria,and dysfunctional perisynaptic Schwann cells(Alhindi et al.,2022).

Clinical manifestations,diagnosis and long-term prognosis of adult autoimmune enteropathy:Experience from Peking Union Medical College Hospital

BACKGROUND Autoimmune enteropathy(AIE)is a rare disease whose diagnosis and long-term prognosis remain challenging,especially for adult AIE patients.AIM To improve overall understanding of this disease’s diagnosis and prognosis.METHODS We retrospectively analyzed the clinical,endoscopic and histopathological characteristics and prognoses of 16 adult AIE patients in our tertiary medical center between 2011 and 2023,whose diagnosis was based on the 2007 diagnostic criteria.RESULTS Diarrhea in AIE patients was characterized by secretory diarrhea.The common endoscopic manifestations were edema,villous blunting and mucosal hyperemia in the duodenum and ileum.Villous blunting(100%),deep crypt lymphocytic infiltration(67%),apoptotic bodies(50%),and mild intraepithelial lymphocytosis(69%)were observed in the duodenal biopsies.Moreover,there were other remarkable abnormalities,including reduced or absent goblet cells(duodenum 94%,ileum 62%),reduced or absent Paneth cells(duodenum 94%,ileum 69%)and neutrophil infiltration(duodenum 100%,ileum 69%).Our patients also fulfilled the 2018 diagnostic criteria but did not match the 2022 diagnostic criteria due to undetectable anti-enterocyte antibodies.All patients received glucocorticoid therapy as the initial medication,of which 14/16 patients achieved a clinical response in 5(IQR:3-20)days.Immunosuppressants were administered to 9 patients with indications of steroid dependence(6/9),steroid refractory status(2/9),or intensified maintenance medication(1/9).During the median of 20.5 months of followup,2 patients died from multiple organ failure,and 1 was diagnosed with non-Hodgkin’s lymphoma.The cumulative relapse-free survival rates were 62.5%,55.6%and 37.0%at 6 months,12 months and 48 months,respectively.CONCLUSION Certain histopathological findings,including a decrease or disappearance of goblet and Paneth cells in intestinal biopsies,might be potential diagnostic criteria for adult AIE.The long-term prognosis is still unsatisfactory despite corticosteroid and immunosuppressant medications,which highlights the need for early diagnosis and novel medications.

How do neurons age?A focused review on the aging of the microtubular cytoskeleton

Aging is the leading risk factor for Alzheimer’s disease and other neurodegenerative diseases. We now understand that a breakdown in the neuronal cytoskeleton, mainly underpinned by protein modifications leading to the destabilization of microtubules, is central to the pathogenesis of Alzheimer’s disease. This is accompanied by morphological defects across the somatodendritic compartment, axon, and synapse. However, knowledge of what occurs to the microtubule cytoskeleton and morphology of the neuron during physiological aging is comparatively poor. Several recent studies have suggested that there is an age-related increase in the phosphorylation of the key microtubule stabilizing protein tau, a modification, which is known to destabilize the cytoskeleton in Alzheimer’s disease. This indicates that the cytoskeleton and potentially other neuronal structures reliant on the cytoskeleton become functionally compromised during normal physiological aging. The current literature shows age-related reductions in synaptic spine density and shifts in synaptic spine conformation which might explain age-related synaptic functional deficits. However, knowledge of what occurs to the microtubular and actin cytoskeleton, with increasing age is extremely limited. When considering the somatodendritic compartment, a regression in dendrites and loss of dendritic length and volume is reported whilst a reduction in soma volume/size is often seen. However, research into cytoskeletal change is limited to a handful of studies demonstrating reductions in and mislocalizations of microtubule-associated proteins with just one study directly exploring the integrity of the microtubules. In the axon, an increase in axonal diameter and age-related appearance of swellings is reported but like the dendrites, just one study investigates the microtubules directly with others reporting loss or mislocalization of microtubule-associated proteins. Though these are the general trends reported, there are clear disparities between model organisms and brain regions that are worthy of further investigation. Additionally, longitudinal studies of neuronal/cytoskeletal aging should also investigate whether these age-related changes contribute not just to vulnerability to disease but also to the decline in nervous system function and behavioral output that all organisms experience. This will highlight the utility, if any, of cytoskeletal fortification for the promotion of healthy neuronal aging and potential protection against age-related neurodegenerative disease. This review seeks to summarize what is currently known about the physiological aging of the neuron and microtubular cytoskeleton in the hope of uncovering mechanisms underpinning age-related risk to disease.

Single-cell transcriptomic atlas of goat ovarian aging

Background The ovaries are one of the first organs that undergo degenerative changes earlier in the aging process,and ovarian aging is shown by a decrease in the number and quality of oocytes.However,little is known about the molecular mechanisms of female age-related fertility decline in different types of ovarian cells during aging,especially in goats.Therefore,the aim of this study was to reveal the mechanisms driving ovarian aging in goats at single-cell resolution.Results For the first time,we surveyed the single-cell transcriptomic landscape of over 27,000 ovarian cells from newborn,young and aging goats,and identified nine ovarian cell types with distinct gene-expression signatures.Functional enrichment analysis showed that ovarian cell types were involved in their own unique biological processes,such as Wnt beta-catenin signalling was enriched in germ cells,whereas ovarian steroidogenesis was enriched in granulosa cells(GCs).Further analysis showed that ovarian aging was linked to GCs-specific changes in the antioxidant system,oxidative phosphorylation,and apoptosis.Subsequently,we identified a series of dynamic genes,such as AMH,CRABP2,THBS1 and TIMP1,which determined the fate of GCs.Additionally,FOXO1,SOX4,and HIF1A were identified as significant regulons that instructed the differentiation of GCs in a distinct manner during ovarian aging.Conclusions This study revealed a comprehensive aging-associated transcriptomic atlas characterizing the cell typespecific mechanisms during ovarian aging at the single-cell level and offers new diagnostic biomarkers and potential therapeutic targets for age-related goat ovarian diseases.

Mechanistic insights into fasting-induced autophagy in the aging heart

Autophagy is a prosurvival mechanism for the clearance of accumulated abnormal proteins,damaged organelles,and excessive lipids within mammalian cells.A growing body of data indicates that autophagy is reduced in aging cells.This reduction leads to various diseases,such as myocardial hypertrophy,infarction,and atherosclerosis.Recent studies in animal models of an aging heart showed that fasting-induced autophagy improved cardiac function and longevity.This improvement is related to autophagic clearance of damaged cellular components via either bulk or selective autophagy(such as mitophagy).In this editorial,we summarize the mechanisms of autophagy in normal and aging hearts.In addition,the protective effect of fasting-induced autophagy in cardiac aging has been highlighted.

Developing an atmospheric aging evaluation model of acrylic coatings:A semi-supervised machine learning algorithm

To study the atmospheric aging of acrylic coatings,a two-year aging exposure experiment was conducted in 13 representative climatic environments in China.An atmospheric aging evaluation model of acrylic coatings was developed based on aging data including11 environmental factors from 567 cities.A hybrid method of random forest and Spearman correlation analysis was used to reduce the redundancy and multicollinearity of the data set by dimensionality reduction.A semi-supervised collaborative trained regression model was developed with the environmental factors as input and the low-frequency impedance modulus values of the electrochemical impedance spectra of acrylic coatings in 3.5wt%NaCl solution as output.The model improves accuracy compared to supervised learning algorithms model(support vector machines model).The model provides a new method for the rapid evaluation of the aging performance of acrylic coatings,and may also serve as a reference to evaluate the aging performance of other organic coatings.

Microglia in brain aging:An overview of recent basic science and clinical research developments

Aging is characterized by progressive degeneration of tissues and organs,and it is positively associated with an increased mortality rate.The brain,as one of the most significantly affected organs,experiences age-related changes,including abnormal neuronal activity,dysfunctional calcium homeostasis,dysregulated mitochondrial function,and increased levels of reactive oxygen species.These changes collectively contribute to cognitive deterioration.Aging is also a key risk factor for neurodegenerative diseases,such as Alzheimer's disease and Parkinson's disease.For many years,neurodegenerative disease investigations have primarily focused on neurons,with less attention given to microglial cells.However,recently,microglial homeostasis has emerged as an important mediator in neurological disease pathogenesis.Here,we provide an overview of brain aging from the perspective of the microglia.In doing so,we present the current knowledge on the correlation between brain aging and the microglia,summarize recent progress of investigations about the microglia in normal aging,Alzheimer's disease,Parkinson's disease,Huntington's disease,and amyotrophic lateral sclerosis,and then discuss the correlation between the senescent microglia and the brain,which will culminate with a presentation of the molecular complexity involved in the microglia in brain aging with suggestions for healthy aging.

Functional aspects of the brain lymphatic drainage system in aging and neurodegenerative diseases

The phenomenon of an aging population is advancing at a precipitous rate.Alzheimer's disease(AD)and Parkinson's disease(PD)are two of the most common age-associated neurodegenerative diseases,both of which are primarily characterized by the accumulation of toxic proteins and the progressive demise of neuronal structures.Recent discoveries about the brain lymphatic drainage system have precipitated a growing body of investigations substantiating its novel roles,including the clearance of macromolecular waste and the trafficking of immune cells.Notably,aquaporin 4-mediated glymphatic transport,crucial for maintaining neural homeostasis,becomes disrupted during the aging process and is further compromised in the pathogenesis of AD and PD.Functional meningeal lymphatic vessels,which facilitate the drainage of cerebrospinal fluid into the deep cervical lymph nodes,are integral in bridging the central nervous system with peripheral immune responses.Dysfunction in these meningeal lymphatic vessels exacerbates pathological trajectory of the age-related neurodegenerative disease.This review explores modulatory influence of the glymphatic system and meningeal lymphatic vessels on the aging brain and its associated neurodegenerative disorders.It also encapsulates the insights of potential mechanisms and prospects of the targeted non-pharmacological interventions.

Molecule aging induced by electron attacking

Here we propose a new concept of"molecule aging":with some special treatment,a molecule could be"aged"by losing some unknown tiny particles or pieces from atoms in the molecule,Such"aging"or loss of unknown tiny particles does not change apparently its molecular structure or chemical composition,but some physicochemical properties could be changed irreversibly.We further confirm such"molecule aging"via a long-term electron attacking to age water(H_(2)O)molecules.The IR spectra show no structural difference between the fresh water and the aged one,while the NMR spectra show that the electron attacking can decrease the size of water clusters.Such facts indicate that the electron attacking indeed can"affect"the structure of water molecule slightly but without damaging to its basic molecule frame.Further exploration reveals that the hydrogen evolution reaction(HER)activity of the aged water molecule is lower than the fresh water on the same Pt/C electrocatalyst.The density functional theory calculations indicate that the shortened O-H bond in H_(2)O indeed can present lower HER activity,so the observed size decrease of water clusters from NMR probably could be attributed to the shortening of O-H bond in water molecules.Such results indicate significantly that the molecule aging can produce materials with new functions for new possible applications.

A Novel Method for Aging Prediction of Railway Catenary Based on Improved Kalman Filter

The aging prediction of railway catenary is of profound significance for ensuring the regular operation of electrified trains.However,in real-world scenarios,accurate predictions are challenging due to various interferences.This paper addresses this challenge by proposing a novel method for predicting the aging of railway catenary based on an improved Kalman filter(KF).The proposed method focuses on modifying the priori state estimate covariance and measurement error covariance of the KF to enhance accuracy in complex environments.By comparing the optimal displacement value with the theoretically calculated value based on the thermal expansion effect of metals,it becomes possible to ascertain the aging status of the catenary.To improve prediction accuracy,a railway catenary aging prediction model is constructed by integrating the Takagi-Sugeno(T-S)fuzzy neural network(FNN)and KF.In this model,an adaptive training method is introduced,allowing the FNN to use fewer fuzzy rules.The inputs of the model include time,temperature,and historical displacement,while the output is the predicted displacement.Furthermore,the KF is enhanced by modifying its prior state estimate covariance and measurement error covariance.These modifications contribute to more accurate predictions.Lastly,a low-power experimental platform based on FPGA is implemented to verify the effectiveness of the proposed method.The test results demonstrate that the proposed method outperforms the compared method,showcasing its superior performance.