Microstructure evolution of a new directionally solidified Ni-based superalloy after long-term aging at 950 ℃ upto 1 000 h

The microstructure evolution of a new directionally solidified（DS） Ni-based superalloy used for gas turbine blades after long-term aging at 950 ℃ was investigated.The results show that the γ ＇ phase becomes more regular in dendritic arm and interdendritic area,while both the mass fraction and the size of γ ＇ phase increase gradually with increasing aging time.During long-term aging,the MC carbide dissolves on the edge to provide the carbon for the formation of M23C6 carbide by the precipitation of Cr at the grain boundary.The rose-shaped γ ＇/γ eutectic partly dissolves into γ matrix and the aging promotes it transform into raft-shape γ ＇.The microstructure is generally stable and no needle-like topologically close-packed phase（TCP） can be found after aging for 1 000 h.

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

Thermal stabilities of microstructure and mechanical property have been investigated on superalloy U720Li, which is of great interest of application for jet engine and land-based turbine disc. The results showed that, the primary and secondary gamma' particles maintain good thermal stability at 650 and 700 degreesC with aging time up to 3000 h, while the tertiary gamma' is apparently dependent on aging temperature and time. The tertiary gamma' particles undergo a procedure of coarsening, dissolution and eventually complete disappearance with the increasing of aging time and temperature. They exhibit unusual high sensibility upon aging temperature, which is attributed to the lattice misfit between the gamma' 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 degreesC. 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 gamma' 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.

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).

Dendritic spine degeneration:a primary mechanism in the aging process

Recent reports suggest that aging is not solely a physiological process in living beings;instead, it should be considered a pathological process or disease(Amorim et al., 2022). Consequently, this process involves a wide range of factors, spanning from genetic to environmental factors, and even includes the gut microbiome(GM)(Mayer et al., 2022). All these processes coincide at some point in the inflammatory process, oxidative stress, and apoptosis, at different degrees in various organs and systems that constitute a living organism(Mayer et al., 2022;AguilarHernández et al., 2023).

Decline and fall of aging astrocytes:the human perspective

“Last scene of all that ends this strange,eventful history,is second childishness and mere oblivion.I am sans teeth,sans eyes,sans taste,sans everything.”William Shakespeare‘As You Like It'Act 2,Sc.7,l.139Aging of the human brain is characterized by a progressive decline of its functional capacity;this decline however varies widely,and cognitive longevity differs substantially between individuals.

Imperative for long-term management and surveillance in Kawasaki disease

Kawasaki disease(KD)is a significant pediatric vasculitis known for its potential to cause severe coronary artery complications.Despite the effectiveness of initial treatments,such as intravenous immunoglobulin,KD patients can experience long-term cardiovascular issues,as evidenced by a recent case report of an adult who suffered a ST-segment elevation myocardial infarction due to previous KD in the World Journal of Clinical Cases.This editorial emphasizes the critical need for long-term management and regular surveillance to prevent such complications.By drawing on recent research and case studies,we advocate for a structured approach to follow-up care that includes routine cardiac evaluations and preventive measures.

Neuronal regulated cell death in aging-related neurodegenerative diseases:key pathways and therapeutic potentials

Regulated cell death(such as apoptosis,necroptosis,pyroptosis,autophagy,cuproptosis,ferroptosis,disulfidptosis)involves complex signaling pathways and molecular effectors,and has been proven to be an important regulatory mechanism for regulating neuronal aging and death.However,excessive activation of regulated cell death may lead to the progression of aging-related diseases.This review summarizes recent advances in the understanding of seven forms of regulated cell death in age-related diseases.Notably,the newly identified ferroptosis and cuproptosis have been implicated in the risk of cognitive impairment and neurodegenerative diseases.These forms of cell death exacerbate disease progression by promoting inflammation,oxidative stress,and pathological protein aggregation.The review also provides an overview of key signaling pathways and crosstalk mechanisms among these regulated cell death forms,with a focus on ferroptosis,cuproptosis,and disulfidptosis.For instance,FDX1 directly induces cuproptosis by regulating copper ion valency and dihydrolipoamide S-acetyltransferase aggregation,while copper mediates glutathione peroxidase 4 degradation,enhancing ferroptosis sensitivity.Additionally,inhibiting the Xc-transport system to prevent ferroptosis can increase disulfide formation and shift the NADP^(+)/NADPH ratio,transitioning ferroptosis to disulfidptosis.These insights help to uncover the potential connections among these novel regulated cell death forms and differentiate them from traditional regulated cell death mechanisms.In conclusion,identifying key targets and their crosstalk points among various regulated cell death pathways may aid in developing specific biomarkers to reverse the aging clock and treat age-related neurodegenerative conditions.

Decoding molecular mechanisms:brain aging and Alzheimer's disease

The complex morphological,anatomical,physiological,and chemical mechanisms within the aging brain have been the hot topic of research for centuries.The aging process alters the brain structure that affects functions and cognitions,but the worsening of such processes contributes to the pathogenesis of neurodegenerative disorders,such as Alzheimer's disease.Beyond these observable,mild morphological shifts,significant functional modifications in neurotransmission and neuronal activity critically influence the aging brain.Understanding these changes is important for maintaining cognitive health,especially given the increasing prevalence of age-related conditions that affect cognition.This review aims to explore the age-induced changes in brain plasticity and molecular processes,differentiating normal aging from the pathogenesis of Alzheimer's disease,thereby providing insights into predicting the risk of dementia,particularly Alzheimer's disease.

Unraveling brain aging through the lens of oral microbiota

The oral cavity is a complex physiological community encompassing a wide range of microorganisms.Dysbiosis of oral microbiota can lead to various oral infectious diseases,such as periodontitis and tooth decay,and even affect systemic health,including brain aging and neurodegenerative diseases.Recent studies have highlighted how oral microbes might be involved in brain aging and neurodegeneration,indicating potential avenues for intervention strategies.In this review,we summarize clinical evidence demonstrating a link between oral microbes/oral infectious diseases and brain aging/neurodegenerative diseases,and dissect potential mechanisms by which oral microbes contribute to brain aging and neurodegeneration.We also highlight advances in therapeutic development grounded in the realm of oral microbes,with the goal of advancing brain health and promoting healthy aging.

Microstructure evolution and stress rupture properties of K4750 alloys with various B contents during long-term aging

The relationship among B content,microstructure evolution and stress rupture properties of K4750 alloy during long-term aging were investigated.After aging at 800℃for 1000 h,the decomposition degree of MC carbides of K4750 alloys with 0 B,0.007 wt.%B and 0.010 wt.%B were basically identical,which indicated that B has no inhibition on MC carbide decomposition during long-term aging.The MC carbide decomposition was accompanied by the formation of M_(23)C_(6) carbides and a small number ofηphases,which was controlled by the outward diffusion of C and Ti combined with the inward diffusion of Ni and Cr from theγmatrix.In addition,M_(23)C_(6) carbides in boron-free alloy were in continuous chain and needle-likeηphases were precipitated near them,while M_(23)C_(6) carbides in boron-containing alloys remained in granular distribution and noηphases precipitation around them.Adding B could delay the agglomeration and coarsening of M_(23)C_(6) carbides during long-term aging,which was because the segregation of B at grain boundary retarded the diffusion of alloy elements,thus weakened the local fluctuation of chemical composition near grain boundary.The stress rupture samples of K4750 alloys with various B contents after aging at 800℃for 1000 h were tested at 750℃/380 MPa.The results indicated that the stress rupture properties of bo ron-containing alloys were significantly better than that of boron-free alloy,which could be attributed to the increase of grain boundary cohesion strength and the optimization of M_(23)C_(6) carbide distribution due to the addition of B.

Effect of grain boundary precipitates on the stress rupture properties of K4750 alloy after long-term aging at 750℃for 8000 h

In K4750 alloy,the evolution of grain boundary(GB)precipitates,including the degradation of blocky MC carbide particles and the precipitation of granular/needle-likeηphase particles,were observed after longterm aging(LA)at 750℃for 8000 h.During MC degradation,the Ti and C released from the MC carbide combined with Ni and Cr,respectively,in theγ’matrix to formη-Ni_(3)Ti phase and Cr-rich M_(23)C_(6)carbide.Large amounts of granularηphase precipitated at GBs and the needle-likeηphase grew gradually from GBs toward the grain interior.Because of the growth of theηphase through absorbingγ’phase,γ-depleted zones were formed around theηphase.The evolution of the MC carbide andηphase was primarily responsible for the decrease of the stress rupture life and the increase of elongation.After an LA sample was tested at 750℃and 360 MPa,the residual strain distribution was investigated by electron backscatter diffraction(EBSD).The results showed that the residual strain mainly distributed at GBs,especially in the region of MC degradation and at the edges ofηphases,which was closely related to the appearance of phase interfaces.Microvoids/cracks easily initiated at phase interfaces,then easily extended along theγ-depleted zones,thus the stress rupture life of LA samples was substantially shorter than that of samples subjected to the standard treatment.In particular,because of large amounts of fine degraded MC,granular M_(23)C_(6)and granularηphase particles distributed at GBs after 750℃/8000 h LA and microvoid/crack formation could be hindered by the formation of dimples,which led to an increase of elongation.

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.

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.

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.

Microglial response to aging and neuroinflammation in the development of neurodegenerative diseases

Cellular senescence and chronic inflammation in response to aging are considered to be indicators of brain aging;they have a great impact on the aging process and are the main risk factors for neurodegeneration.Reviewing the microglial response to aging and neuroinflammation in neurodegenerative diseases will help understand the importance of microglia in neurodegenerative diseases.This review describes the origin and function of microglia and focuses on the role of different states of the microglial response to aging and chronic inflammation on the occurrence and development of neurodegenerative diseases,including Alzheimer's disease,Huntington's chorea,and Parkinson's disease.This review also describes the potential benefits of treating neurodegenerative diseases by modulating changes in microglial states.Therefore,inducing a shift from the neurotoxic to neuroprotective microglial state in neurodegenerative diseases induced by aging and chronic inflammation holds promise for the treatment of neurodegenerative diseases in the future.

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.

基于密度泛函理论研究Ag-Co团簇的结构、电子和光学性能

基于密度泛函理论研究了7个原子Ag-Co团簇结构的稳定性、电子和光学性能.研究结果表明,7个原子Ag-Co团簇的最稳定结构都是十面体结构,Co原子数量较少时,Co原子主要占据十面体的轴向位,Ag原子主要占据赤道位,随着Co原子数的增加,Co原子逐渐替换了赤道位上的Ag原子.当Co原子数增加时,Ag-Co团簇的垂直电离势、垂直电子亲能和最高占据轨道与最低未占据轨道之间的能隙整体上都呈现出下降趋势,表明电子稳定性降低;Ag-Co团簇的吸收光谱整体出现了红移,吸收峰的强度逐渐减弱,吸收谱的宽度变窄.