With an increased utilization of carbon fiber reinforced polymers(CFRPs)in high temperature environments,investigating their effects on materials becomes exceedingly important.This study presents a comparative investi...With an increased utilization of carbon fiber reinforced polymers(CFRPs)in high temperature environments,investigating their effects on materials becomes exceedingly important.This study presents a comparative investigation of thermo-oxidative aging effects on the flexural performance of two carbon fiber reinforced composite laminates(CFRCLs):a quasi-isotropic plain-woven CFRCL and a quasi-isotropic unidirectional layup CFRCL(designated as PW-CFRCL and UD-CFRCL,respectively).The CFRCLs were subjected to thermo-oxidative aging for specific durations,and their flexural strength was evaluated through three-point bending tests.The flexural strength of the laminates decreased with the prolonged aging duration.Despite having lower fiber content,PW-CFRCLs showed higher flexural strength than UD-CFRCLs.After eight days of aging,the flexural strength of PW-CFRCLs decreased by merely 4%-5%,while that of UD-CFRCLs decreased by 11%-14%.After 32 days of aging,the thinner PW-CFRCL with the lowest fiber content exhibited the highest flexural strength(595.52 MPa),followed by the thinner UD-CFRCL(549.83 MPa),then the thicker PW-CFRCL(445.29 MPa)and finally,the thicker UD-CFRCL(393.90 MPa).The decline in flexural properties of the laminates was primarily attributed to matrix cracking and interface debonding resulting from matrix oxidation.To validate the universality of this result,the finite element method was employed,showing a good correlation with the experimental findings.展开更多
The changes of crosslinking network of perfluorinated elastomer(FFKM)cured by TAIC and DBPH under thermo-oxidative aging conditions were investigated.Two competitive processes including post-curing and network destruc...The changes of crosslinking network of perfluorinated elastomer(FFKM)cured by TAIC and DBPH under thermo-oxidative aging conditions were investigated.Two competitive processes including post-curing and network destruction occur simultaneously,which directly affect the storage modulus and crosslinking density.With the increase of aging temperature,the network destruction becomes dominant.FTIR and XPS characterizations further reveal that the network destruction happens preferentially on the crosslink points of TAIC structure,and the post-curing is mainly caused by the decomposition of residual curing agent DBPH.Unlike the easier breaking of TAIC structure in the crosslinking network,both the backbone and the pendent groups of FFKM itself are much more stable.To further figure out the destruction mechanism,TGAFTIR-GC-MS test was also conducted and a schematic degradation process of TAIC structure was proposed.It is found that the destruction of TAIC crosslinking points happens first on the unstable exocyclic C―N bonds and the intermediate ring radicals could eventually decompose into volatile hydrogen isocyanate(HCNO)under extreme condition.展开更多
The aging of natural rubber(NR)at high temperatures will seriously affect its service lifetime in many key applications.In the present work,the changes in microstructure and mechanical properties of semi-efficient vul...The aging of natural rubber(NR)at high temperatures will seriously affect its service lifetime in many key applications.In the present work,the changes in microstructure and mechanical properties of semi-efficient vulcanized NR/carbon black(CB)vulcanizates during thermooxidative aging at high temperatures(150-200℃)and a moderate temperature(95℃)were compared.At high temperatures,a two-stage aging behavior,which was characteristic of a first rapid decline and then a continuous rise in the crosslinking density(ve),was identified and was found to be closely related to the depletion behavior of antioxidants.The surface cracking behavior observed in the second stage of high-temperature aging was discussed in terms of the grafting reaction of macromolecular radicals on CB particles and thermal expansion.In contrast,the aging of NR at moderate temperatures was much mild,which featured a continuous increase in ve and an oxidation mechanism dominated by peroxy radicals attacking double bonds.In general,the mechanical properties of NR vulcanizates during high-temperature aging depended on the competition effects of structural evolution in the crosslinked network and oxidation-induced chain scission.展开更多
This study investigated the characteristics of wood fiber/polycaprolactone composite after an artificial accelerated thermo-oxidative aging treatment.The effect of time,temperature and humidity during the treatment on...This study investigated the characteristics of wood fiber/polycaprolactone composite after an artificial accelerated thermo-oxidative aging treatment.The effect of time,temperature and humidity during the treatment on their mechanical,chemical and morphology properties were evaluated.The composite was prepared from melted wood fibers and modified polycaprolactone by a molding process.A temperature and humidity controllable test chamber was used for the thermo-oxidative aging of the composite.The thermo-oxidative aging caused surface of the composite to be much more rougher and even a few cracks and holes appeared on it.According to the spectra of Fourier Transform Infrared(FTIR)and Gel Permeation Chromatography(GPC),C=O in the molecular chain of polycaprolactone was hydrolyzed and C–O was broken after the aging treatment,which resulted in a reduction in average molecular weight of the composite.Moreover,results showed that the mechanical strength decreased a lot with the increase in time,temperature and humidity,and the effect of temperature and humidity was more significant compared with that of time.Controlling the temperature and humidity during thermo-oxidative aging treatment could accelerate the aging of composite,which provided a quick and effective method for evaluating the aging resistance of the composite.展开更多
The mechanical, morphological and thermo-oxidative aging properties of the glass fiber reinforced polypropylene (RGF-PP) were studied based on four different maleic anhydride grafted polypropylene (PP-g-MAH) compatibi...The mechanical, morphological and thermo-oxidative aging properties of the glass fiber reinforced polypropylene (RGF-PP) were studied based on four different maleic anhydride grafted polypropylene (PP-g-MAH) compatibilizers with different content of residual maleic anhydride (MAH). It was shown that PP-g-MAH compatibilizer could significantly improve the mechanical properties of RGF-PP, while from thermal and morphological analysis results, the content of residual MAH had negative influence on long term thermo- oxidative aging properties of RGF-PP with adding PP-g-MAH compatibilizer;the lower the residual content of MAH is, the better the thermo stability of the PP-g-MAH is, and also the better the thermo-oxidative aging properties was obtained.展开更多
Isotactic poly（butene-1） （iPB） with spherical morphology was synthesized successfully with bulk precipitation polymerization without post-treatment of the products. The bulk precipitation polymerization process ma...Isotactic poly（butene-1） （iPB） with spherical morphology was synthesized successfully with bulk precipitation polymerization without post-treatment of the products. The bulk precipitation polymerization process made it possible for iPB to be used as general plastic due to the acceptable decreased cost compared with the solution polymerization process. The influence of catalyst residues on the aging and thermal stability of iPB synthesized by bulk precipitation polymerization method was investigated by gel permeation chromatography, mechanical performance testing, thermogravimetric analysis and infrared spectroscopic analysis. Commercial iPB and the lab-made iPB with varied catalyst residue contents were studied. The results demonstrated that the catalyst residues played an important role in the aging process of the iPB. A possible mechanism of aging promotion by catalyst residues was proposed.展开更多
SKI family transcriptional corepressor 1(SKOR1also known as LbxCor1, Fussel15, or CORL1), is a member of the SKI family of proteins and is transcribed from a protein-coding gene located on chromosome 15 in humans, tha...SKI family transcriptional corepressor 1(SKOR1also known as LbxCor1, Fussel15, or CORL1), is a member of the SKI family of proteins and is transcribed from a protein-coding gene located on chromosome 15 in humans, that has a molecular weight of approximately 100 kDa. Skor1 is highly expressed in neurons in the central nervous system of both humans and rodents.展开更多
In modern ZnO varistors,traditional aging mechanisms based on increased power consumption are no longer relevant due to reduced power consumption during DC aging.Prolonged exposure to both AC and DC voltages results i...In modern ZnO varistors,traditional aging mechanisms based on increased power consumption are no longer relevant due to reduced power consumption during DC aging.Prolonged exposure to both AC and DC voltages results in increased leakage current,decreased breakdown voltage,and lower nonlinearity,ultimately compromising their protective performance.To investigate the evolution in electrical properties during DC aging,this work developed a finite element model based on Voronoi networks and conducted accelerated aging tests on commercial varistors.Throughout the aging process,current-voltage characteristics and Schottky barrier parameters were measured and analyzed.The results indicate that when subjected to constant voltage,current flows through regions with larger grain sizes,forming discharge channels.As aging progresses,the current focus increases on these channels,leading to a decline in the varistor’s overall performance.Furthermore,analysis of the Schottky barrier parameters shows that the changes in electrical performance during aging are non-monotonic.These findings offer theoretical support for understanding the aging mechanisms and condition assessment of modern stable ZnO varistors.展开更多
Aging is a physiological and complex process produced by accumulative age-dependent cellular damage,which significantly impacts brain regions like the hippocampus,an essential region involved in memory and learning.A ...Aging is a physiological and complex process produced by accumulative age-dependent cellular damage,which significantly impacts brain regions like the hippocampus,an essential region involved in memory and learning.A crucial factor contributing to this decline is the dysfunction of mitochondria,particularly those located at synapses.Synaptic mitochondria are specialized organelles that produce the energy required for synaptic transmission but are also important for calcium homeostasis at these sites.In contrast,non-synaptic mitochondria primarily involve cellular metabolism and long-term energy supply.Both pools of mitochondria differ in their form,proteome,functionality,and cellular role.The proper functioning of synaptic mitochondria depends on processes such as mitochondrial dynamics,transport,and quality control.However,synaptic mitochondria are particularly vulnerable to age-associated damage,characterized by oxidative stress,impaired energy production,and calcium dysregulation.These changes compromise synaptic transmission,reducing synaptic activity and cognitive decline during aging.In the context of neurodegenerative diseases such as Alzheimer’s,Parkinson’s,and Huntington’s,the decline of synaptic mitochondrial function is even more pronounced.These diseases are marked by pathological protein accumulation,disrupted mitochondrial dynamics,and heightened oxidative stress,accelerating synaptic dysfunction and neuronal loss.Due to their specialized role and location,synaptic mitochondria are among the first organelles to exhibit dysfunction,underscoring their critical role in disease progression.This review delves into the main differences at structural and functional levels between synaptic and non-synaptic mitochondria,emphasizing the vulnerability of synaptic mitochondria to the aging process and neurodegeneration.These approaches highlight the potential of targeting synaptic mitochondria to mitigate age-associated cognitive impairment and synaptic degeneration.This review emphasizes the distinct vulnerabilities of hippocampal synaptic mitochondria,highlighting their essential role in sustaining brain function throughout life and their promise as therapeutic targets for safeguarding the cognitive capacities of people of advanced age.展开更多
As the aging population continues to grow,age-related health issues are becoming increasingly prominent,attracting widespread attention and concern from society.While research on the mechanisms of aging is relatively ...As the aging population continues to grow,age-related health issues are becoming increasingly prominent,attracting widespread attention and concern from society.While research on the mechanisms of aging is relatively extensive,studies on the association between aging and related diseases remain limited.G.lucidum,a traditional medicinal fungus,has garnered significant attention due to its diverse bioactive properties.Recent studies have revealed that G.lucidum and its active components exhibit significant potential in anti-aging and regulating dysregulation of glucose and lipid metabolism.However,a comprehensive and detailed review of recent research findings has yet to be thoroughly explored.This paper summarizes and elucidates the latest advances in the pathological mechanisms of aging-related glucose and lipid metabolism disorders by retrieving data from databases such as X-mol and PubMed,provides a detailed account of the regulatory effects of G.lucidum’s primary active components on aging and lipid metabolism,and explores their potential mechanisms.Additionally,it discusses the application prospects of G.lucidum in the fields of anti-aging and metabolic regulation,aiming to provide a reference for research on aging-mediated lipid metabolism disorders and to lay a theoretical foundation for the further development and application of G.lucidum.展开更多
Mitochondrial dysfunction and oxidative stress are widely regarded as primary drivers of aging and are associated with several neurodegenerative diseases.The degeneration of motor neurons during aging is a critical pa...Mitochondrial dysfunction and oxidative stress are widely regarded as primary drivers of aging and are associated with several neurodegenerative diseases.The degeneration of motor neurons during aging is a critical pathological factor contributing to the progression of sarcopenia.However,the morphological and functional changes in mitochondria and their interplay in the degeneration of the neuromuscular junction during aging remain poorly understood.A defined systematic search of the Pub Med,Web of Science and Embase databases(last accessed on October 30,2024)was conducted with search terms including'mitochondria','aging'and'NMJ'.Clinical and preclinical studies of mitochondrial dysfunction and neuromuscular junction degeneration during aging.Twentyseven studies were included in this systematic review.This systematic review provides a summary of morphological,functional and biological changes in neuromuscular junction,mitochondrial morphology,biosynthesis,respiratory chain function,and mitophagy during aging.We focus on the interactions and mechanisms underlying the relationship between mitochondria and neuromuscular junctions during aging.Aging is characterized by significant reductions in mitochondrial fusion/fission cycles,biosynthesis,and mitochondrial quality control,which may lead to neuromuscular junction dysfunction,denervation and poor physical performance.Motor nerve terminals that exhibit redox sensitivity are among the first to exhibit abnormalities,ultimately leading to an early decline in muscle strength through impaired neuromuscular junction transmission function.Parg coactivator 1 alpha is a crucial molecule that regulates mitochondrial biogenesis and modulates various pathways,including the mitochondrial respiratory chain,energy deficiency,oxidative stress,and inflammation.Mitochondrial dysfunction is correlated with neuromuscular junction denervation and acetylcholine receptor fragmentation,resulting in muscle atrophy and a decrease in strength during aging.Physical therapy,pharmacotherapy,and gene therapy can alleviate the structural degeneration and functional deterioration of neuromuscular junction by restoring mitochondrial function.Therefore,mitochondria are considered potential targets for preserving neuromuscular junction morphology and function during aging to treat sarcopenia.展开更多
In recent years,rising life expectancy has led to a significant increase in the prevalence of neurodegenerative disorders,including Alzheimer’s disease(AD),Parkinson’s disease,and age-related cognitive decline.Addit...In recent years,rising life expectancy has led to a significant increase in the prevalence of neurodegenerative disorders,including Alzheimer’s disease(AD),Parkinson’s disease,and age-related cognitive decline.Additionally,other neurological conditions such as glioblastoma,the most common and aggressive brain tumor in adults have been more frequently reported in aging populations.The brain itself is highly vulnerable to age-related changes,particularly disruptions in homeostatic regulation,which further contribute to its functional decline and heightened susceptibility to disease.This has led to a surge of interest in understanding the cellular and molecular mechanisms driving these changes.展开更多
Regenerative medicine is a promising therapeutic avenue for previously incurable diseases.As the risk of chronic and degenerative diseases significantly increases with age,the elderly population represents a major coh...Regenerative medicine is a promising therapeutic avenue for previously incurable diseases.As the risk of chronic and degenerative diseases significantly increases with age,the elderly population represents a major cohort for stem cell-based therapies.However,the regenerative potential of stem cells significantly decreases with advanced age and deteriorating health status of the donor.Therefore,the efficacy of autologous stem cell therapy is significantly compromised in older patients.To overcome these limitations,alternative strategies have been used to restore the age-and disease-depleted function of stem cells.These methods aim to restore the therapeutic efficacy of aged stem cells for autologous use.This article explores the effect of donor age and health status on the regenerative potential of stem cells.It further highlights the limitations of stem cell-based therapy for autologous treatment in the elderly.A comprehensive insight into the potential strategies to address the“age”and“disease”compromised regenerative potential of autologous stem cells is also presented.The information provided here serves as a valuable resource for physicians and patients for optimization of stem cellbased autologous therapy for aged patients.展开更多
The effects of artificial aging(T6)on the creep resistance with tensile stresses in the range of 50−80 MPa at 175℃were investigated for an extruded Mg−1.22Al−0.31Ca−0.44Mn(wt.%)alloy.The Guinier-Preston(G.P.)zones pr...The effects of artificial aging(T6)on the creep resistance with tensile stresses in the range of 50−80 MPa at 175℃were investigated for an extruded Mg−1.22Al−0.31Ca−0.44Mn(wt.%)alloy.The Guinier-Preston(G.P.)zones primarily precipitate in the sample aged at 200℃for 1 h(T6-200℃/1h),while the Al_(2)Ca phases mainly precipitate in the sample aged at 275℃for 8 h(T6-275℃/8h).The T6-200℃/1h sample exhibits excellent creep resistance,with a steady-state creep rate one order of magnitude lower than that of the T6-275℃/8h sample.The abnormally high stress exponent(~8.2)observed in the T6-200℃/1h sample is associated with the power-law breakdown mechanism.TEM analysis illuminates that the creep mechanism for the T6-200℃/1h sample is cross-slip between basal and prismatic dislocations,while the T6-275℃/8h sample exhibits a mixed mechanism of dislocation cross-slip and climb.Compared with the Al_(2)Ca phase,the dense G.P.zones effectively impede dislocation climb and glide during the creep process,demonstrating superior creep resistance of the T6-200℃/1h sample.展开更多
Alzheimer’s disease is initially thought to be caused by age-associated accumulation of plaques,in recent years,research has increasingly associated Alzheimer’s disease with lysosomal storage and metabolic disorders...Alzheimer’s disease is initially thought to be caused by age-associated accumulation of plaques,in recent years,research has increasingly associated Alzheimer’s disease with lysosomal storage and metabolic disorders,and the explanation of its pathogenesis has shifted from amyloid and tau accumulation to oxidative stress and impaired lipid and glucose metabolism aggravated by hypoxic conditions.However,the underlying mechanisms linking those cellular processes and conditions to disease progression have yet to be defined.Here,we applied a disease similarity approach to identify unknown molecular targets of Alzheimer’s disease by using transcriptomic data from congenital diseases known to increase Alzheimer’s disease risk,namely Down syndrome,Niemann-Pick type C disease,and mucopolysaccharidoses I.We uncovered common pathways,hub genes,and miRNAs across in vitro and in vivo models of these diseases as potential molecular targets for neuroprotection and amelioration of Alzheimer’s disease pathology,many of which have never been associated with Alzheimer’s disease.We then investigated common molecular alterations in brain samples from a Niemann-Pick type C disease mouse model by juxtaposing them with brain samples of both human and mouse models of Alzheimer’s disease.Detailed phenotypic,molecular,chronological,and biological aging analyses revealed that the Npc1tm(I1061T)Dso mouse model can serve as a potential short-lived in vivo model for brain aging and Alzheimer’s disease research.This research represents the first comprehensive approach to congenital disease association with neurodegeneration and a new perspective on Alzheimer’s disease research while highlighting shortcomings and lack of correlation in diverse in vitro models.Considering the lack of an Alzheimer’s disease mouse model that recapitulates the physiological hallmarks of brain aging,the short-lived Npc1^(tm(I1061T)Dso) mouse model can further accelerate the research in these fields and offer a unique model for understanding the molecular mechanisms of Alzheimer’s disease from a perspective of accelerated brain aging.展开更多
The aging process is an inexorable fact throughout our lives and is considered a major factor in develo ping neurological dysfunctions associated with cognitive,emotional,and motor impairments.Aging-associated neurode...The aging process is an inexorable fact throughout our lives and is considered a major factor in develo ping neurological dysfunctions associated with cognitive,emotional,and motor impairments.Aging-associated neurodegenerative diseases are characterized by the progressive loss of neuronal structure and function.展开更多
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 regulat...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.展开更多
Cerium oxide/silicon rubber was prepared via mechanical blending.Mechanical and frictional properties,as well as thermal stability after thermo-oxidative ageing were investigated in this rubber composite.3D surface pr...Cerium oxide/silicon rubber was prepared via mechanical blending.Mechanical and frictional properties,as well as thermal stability after thermo-oxidative ageing were investigated in this rubber composite.3D surface profilometry,scanning electron microscopy(SEM)and thermogravimetry analysis(TGA)were used to study the friction surface characteristics,friction mechanism and thermal stability,respectively.Additionally,swelling experiments were carried out to investigate the variation of crosslinking density.After thermo-oxidative ageing,the tear strength of cerium oxide/silicon rubber decreases.However,in the early ageing stage,improvements in tensile strength,elongation at break,and frictional performance are caused by crosslinking density increments.Moreover,the addition of cerium oxide remarkably improves the re-cross linking degree during ageing process,which in turn decreases the number of holes on the friction surface and endows the silicon rubber with better mechanical and frictional properties,as well as thermo-oxidative ageing resistance.展开更多
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 w...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).展开更多
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...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.展开更多
基金National Natural Science Foundation of China(No.12372130)。
文摘With an increased utilization of carbon fiber reinforced polymers(CFRPs)in high temperature environments,investigating their effects on materials becomes exceedingly important.This study presents a comparative investigation of thermo-oxidative aging effects on the flexural performance of two carbon fiber reinforced composite laminates(CFRCLs):a quasi-isotropic plain-woven CFRCL and a quasi-isotropic unidirectional layup CFRCL(designated as PW-CFRCL and UD-CFRCL,respectively).The CFRCLs were subjected to thermo-oxidative aging for specific durations,and their flexural strength was evaluated through three-point bending tests.The flexural strength of the laminates decreased with the prolonged aging duration.Despite having lower fiber content,PW-CFRCLs showed higher flexural strength than UD-CFRCLs.After eight days of aging,the flexural strength of PW-CFRCLs decreased by merely 4%-5%,while that of UD-CFRCLs decreased by 11%-14%.After 32 days of aging,the thinner PW-CFRCL with the lowest fiber content exhibited the highest flexural strength(595.52 MPa),followed by the thinner UD-CFRCL(549.83 MPa),then the thicker PW-CFRCL(445.29 MPa)and finally,the thicker UD-CFRCL(393.90 MPa).The decline in flexural properties of the laminates was primarily attributed to matrix cracking and interface debonding resulting from matrix oxidation.To validate the universality of this result,the finite element method was employed,showing a good correlation with the experimental findings.
基金financial support from the National Natural Science Foundation of China (No. 51721091)the financial supports from the National Natural Science Foundation of China (Nos. 51873125 and 52073184)Research Foundation (International Program) of Science and Technology Department of Sichuan Province (No. 2019YFH0027)
文摘The changes of crosslinking network of perfluorinated elastomer(FFKM)cured by TAIC and DBPH under thermo-oxidative aging conditions were investigated.Two competitive processes including post-curing and network destruction occur simultaneously,which directly affect the storage modulus and crosslinking density.With the increase of aging temperature,the network destruction becomes dominant.FTIR and XPS characterizations further reveal that the network destruction happens preferentially on the crosslink points of TAIC structure,and the post-curing is mainly caused by the decomposition of residual curing agent DBPH.Unlike the easier breaking of TAIC structure in the crosslinking network,both the backbone and the pendent groups of FFKM itself are much more stable.To further figure out the destruction mechanism,TGAFTIR-GC-MS test was also conducted and a schematic degradation process of TAIC structure was proposed.It is found that the destruction of TAIC crosslinking points happens first on the unstable exocyclic C―N bonds and the intermediate ring radicals could eventually decompose into volatile hydrogen isocyanate(HCNO)under extreme condition.
基金financially supported by the National Natural Science Foundation of China(Nos.51790504 and U19A2096)the Programme of Introducing Talents of Discipline to Universities(No.B13040)State Key Laboratory of Polymer Materials Engineering(No.sklpme2019-2-07)。
文摘The aging of natural rubber(NR)at high temperatures will seriously affect its service lifetime in many key applications.In the present work,the changes in microstructure and mechanical properties of semi-efficient vulcanized NR/carbon black(CB)vulcanizates during thermooxidative aging at high temperatures(150-200℃)and a moderate temperature(95℃)were compared.At high temperatures,a two-stage aging behavior,which was characteristic of a first rapid decline and then a continuous rise in the crosslinking density(ve),was identified and was found to be closely related to the depletion behavior of antioxidants.The surface cracking behavior observed in the second stage of high-temperature aging was discussed in terms of the grafting reaction of macromolecular radicals on CB particles and thermal expansion.In contrast,the aging of NR at moderate temperatures was much mild,which featured a continuous increase in ve and an oxidation mechanism dominated by peroxy radicals attacking double bonds.In general,the mechanical properties of NR vulcanizates during high-temperature aging depended on the competition effects of structural evolution in the crosslinked network and oxidation-induced chain scission.
基金The work was supported by National Key R&D Plan Project(2017YFD0601200)Hunan Key R&D Plan Project(2017SK2334)of College of Materials Science and Engineering,Central South University of Forestry and Technology.
文摘This study investigated the characteristics of wood fiber/polycaprolactone composite after an artificial accelerated thermo-oxidative aging treatment.The effect of time,temperature and humidity during the treatment on their mechanical,chemical and morphology properties were evaluated.The composite was prepared from melted wood fibers and modified polycaprolactone by a molding process.A temperature and humidity controllable test chamber was used for the thermo-oxidative aging of the composite.The thermo-oxidative aging caused surface of the composite to be much more rougher and even a few cracks and holes appeared on it.According to the spectra of Fourier Transform Infrared(FTIR)and Gel Permeation Chromatography(GPC),C=O in the molecular chain of polycaprolactone was hydrolyzed and C–O was broken after the aging treatment,which resulted in a reduction in average molecular weight of the composite.Moreover,results showed that the mechanical strength decreased a lot with the increase in time,temperature and humidity,and the effect of temperature and humidity was more significant compared with that of time.Controlling the temperature and humidity during thermo-oxidative aging treatment could accelerate the aging of composite,which provided a quick and effective method for evaluating the aging resistance of the composite.
文摘The mechanical, morphological and thermo-oxidative aging properties of the glass fiber reinforced polypropylene (RGF-PP) were studied based on four different maleic anhydride grafted polypropylene (PP-g-MAH) compatibilizers with different content of residual maleic anhydride (MAH). It was shown that PP-g-MAH compatibilizer could significantly improve the mechanical properties of RGF-PP, while from thermal and morphological analysis results, the content of residual MAH had negative influence on long term thermo- oxidative aging properties of RGF-PP with adding PP-g-MAH compatibilizer;the lower the residual content of MAH is, the better the thermo stability of the PP-g-MAH is, and also the better the thermo-oxidative aging properties was obtained.
基金financially supported by the National Key Technology R&D Program of China(No.2011BAE26B05)
文摘Isotactic poly（butene-1） （iPB） with spherical morphology was synthesized successfully with bulk precipitation polymerization without post-treatment of the products. The bulk precipitation polymerization process made it possible for iPB to be used as general plastic due to the acceptable decreased cost compared with the solution polymerization process. The influence of catalyst residues on the aging and thermal stability of iPB synthesized by bulk precipitation polymerization method was investigated by gel permeation chromatography, mechanical performance testing, thermogravimetric analysis and infrared spectroscopic analysis. Commercial iPB and the lab-made iPB with varied catalyst residue contents were studied. The results demonstrated that the catalyst residues played an important role in the aging process of the iPB. A possible mechanism of aging promotion by catalyst residues was proposed.
基金supported by Science Foundation Ireland (Grant 19/FFP/6666),Cure Parkinson’s (Grant CP:GO01)a PhD studentship from the Anatomical Society。
文摘SKI family transcriptional corepressor 1(SKOR1also known as LbxCor1, Fussel15, or CORL1), is a member of the SKI family of proteins and is transcribed from a protein-coding gene located on chromosome 15 in humans, that has a molecular weight of approximately 100 kDa. Skor1 is highly expressed in neurons in the central nervous system of both humans and rodents.
文摘In modern ZnO varistors,traditional aging mechanisms based on increased power consumption are no longer relevant due to reduced power consumption during DC aging.Prolonged exposure to both AC and DC voltages results in increased leakage current,decreased breakdown voltage,and lower nonlinearity,ultimately compromising their protective performance.To investigate the evolution in electrical properties during DC aging,this work developed a finite element model based on Voronoi networks and conducted accelerated aging tests on commercial varistors.Throughout the aging process,current-voltage characteristics and Schottky barrier parameters were measured and analyzed.The results indicate that when subjected to constant voltage,current flows through regions with larger grain sizes,forming discharge channels.As aging progresses,the current focus increases on these channels,leading to a decline in the varistor’s overall performance.Furthermore,analysis of the Schottky barrier parameters shows that the changes in electrical performance during aging are non-monotonic.These findings offer theoretical support for understanding the aging mechanisms and condition assessment of modern stable ZnO varistors.
基金supported by ANID FONDECYT No.1221178Centro Ciencia&Vida,FB210008,Financiamiento Basal para Centros Científicos y Tecnológicos de Excelencia de ANID to CTR.
文摘Aging is a physiological and complex process produced by accumulative age-dependent cellular damage,which significantly impacts brain regions like the hippocampus,an essential region involved in memory and learning.A crucial factor contributing to this decline is the dysfunction of mitochondria,particularly those located at synapses.Synaptic mitochondria are specialized organelles that produce the energy required for synaptic transmission but are also important for calcium homeostasis at these sites.In contrast,non-synaptic mitochondria primarily involve cellular metabolism and long-term energy supply.Both pools of mitochondria differ in their form,proteome,functionality,and cellular role.The proper functioning of synaptic mitochondria depends on processes such as mitochondrial dynamics,transport,and quality control.However,synaptic mitochondria are particularly vulnerable to age-associated damage,characterized by oxidative stress,impaired energy production,and calcium dysregulation.These changes compromise synaptic transmission,reducing synaptic activity and cognitive decline during aging.In the context of neurodegenerative diseases such as Alzheimer’s,Parkinson’s,and Huntington’s,the decline of synaptic mitochondrial function is even more pronounced.These diseases are marked by pathological protein accumulation,disrupted mitochondrial dynamics,and heightened oxidative stress,accelerating synaptic dysfunction and neuronal loss.Due to their specialized role and location,synaptic mitochondria are among the first organelles to exhibit dysfunction,underscoring their critical role in disease progression.This review delves into the main differences at structural and functional levels between synaptic and non-synaptic mitochondria,emphasizing the vulnerability of synaptic mitochondria to the aging process and neurodegeneration.These approaches highlight the potential of targeting synaptic mitochondria to mitigate age-associated cognitive impairment and synaptic degeneration.This review emphasizes the distinct vulnerabilities of hippocampal synaptic mitochondria,highlighting their essential role in sustaining brain function throughout life and their promise as therapeutic targets for safeguarding the cognitive capacities of people of advanced age.
基金supported by grants from Natural Science Foundation of Jilin Province(No.23JQ08,No.YDZJ202502 CXJD077,No.JLARS-2025-0802-09 and No.YDZJ202501ZY TS706).
文摘As the aging population continues to grow,age-related health issues are becoming increasingly prominent,attracting widespread attention and concern from society.While research on the mechanisms of aging is relatively extensive,studies on the association between aging and related diseases remain limited.G.lucidum,a traditional medicinal fungus,has garnered significant attention due to its diverse bioactive properties.Recent studies have revealed that G.lucidum and its active components exhibit significant potential in anti-aging and regulating dysregulation of glucose and lipid metabolism.However,a comprehensive and detailed review of recent research findings has yet to be thoroughly explored.This paper summarizes and elucidates the latest advances in the pathological mechanisms of aging-related glucose and lipid metabolism disorders by retrieving data from databases such as X-mol and PubMed,provides a detailed account of the regulatory effects of G.lucidum’s primary active components on aging and lipid metabolism,and explores their potential mechanisms.Additionally,it discusses the application prospects of G.lucidum in the fields of anti-aging and metabolic regulation,aiming to provide a reference for research on aging-mediated lipid metabolism disorders and to lay a theoretical foundation for the further development and application of G.lucidum.
基金supported by grants from Collaborative Research Fund(Ref:C4032-21GF)General Research Grant(Ref:14114822)+1 种基金Group Research Scheme(Ref:3110146)Area of Excellence(Ref:Ao E/M-402/20)。
文摘Mitochondrial dysfunction and oxidative stress are widely regarded as primary drivers of aging and are associated with several neurodegenerative diseases.The degeneration of motor neurons during aging is a critical pathological factor contributing to the progression of sarcopenia.However,the morphological and functional changes in mitochondria and their interplay in the degeneration of the neuromuscular junction during aging remain poorly understood.A defined systematic search of the Pub Med,Web of Science and Embase databases(last accessed on October 30,2024)was conducted with search terms including'mitochondria','aging'and'NMJ'.Clinical and preclinical studies of mitochondrial dysfunction and neuromuscular junction degeneration during aging.Twentyseven studies were included in this systematic review.This systematic review provides a summary of morphological,functional and biological changes in neuromuscular junction,mitochondrial morphology,biosynthesis,respiratory chain function,and mitophagy during aging.We focus on the interactions and mechanisms underlying the relationship between mitochondria and neuromuscular junctions during aging.Aging is characterized by significant reductions in mitochondrial fusion/fission cycles,biosynthesis,and mitochondrial quality control,which may lead to neuromuscular junction dysfunction,denervation and poor physical performance.Motor nerve terminals that exhibit redox sensitivity are among the first to exhibit abnormalities,ultimately leading to an early decline in muscle strength through impaired neuromuscular junction transmission function.Parg coactivator 1 alpha is a crucial molecule that regulates mitochondrial biogenesis and modulates various pathways,including the mitochondrial respiratory chain,energy deficiency,oxidative stress,and inflammation.Mitochondrial dysfunction is correlated with neuromuscular junction denervation and acetylcholine receptor fragmentation,resulting in muscle atrophy and a decrease in strength during aging.Physical therapy,pharmacotherapy,and gene therapy can alleviate the structural degeneration and functional deterioration of neuromuscular junction by restoring mitochondrial function.Therefore,mitochondria are considered potential targets for preserving neuromuscular junction morphology and function during aging to treat sarcopenia.
基金supported by the Swedish ResearchCouncil and the Swedish Brain Foundation,theCancer Research Funds of Radiumhemmet,theStrategic Research Area in Cancer(StratCan),the Strategic Research Area in Neuroscience(StratNeuro),the Swedish Cancer Society,theSwedish Childhood Cancer Foundation,theKarolinska Institutet Foundation,the InnoHKinitiative of the Innovation and TechnologyCommission of the Hong Kong SpecialAdministrative Region Government(to BJ).Openaccess funding is provided by the KarolinskaInstitute.
文摘In recent years,rising life expectancy has led to a significant increase in the prevalence of neurodegenerative disorders,including Alzheimer’s disease(AD),Parkinson’s disease,and age-related cognitive decline.Additionally,other neurological conditions such as glioblastoma,the most common and aggressive brain tumor in adults have been more frequently reported in aging populations.The brain itself is highly vulnerable to age-related changes,particularly disruptions in homeostatic regulation,which further contribute to its functional decline and heightened susceptibility to disease.This has led to a surge of interest in understanding the cellular and molecular mechanisms driving these changes.
文摘Regenerative medicine is a promising therapeutic avenue for previously incurable diseases.As the risk of chronic and degenerative diseases significantly increases with age,the elderly population represents a major cohort for stem cell-based therapies.However,the regenerative potential of stem cells significantly decreases with advanced age and deteriorating health status of the donor.Therefore,the efficacy of autologous stem cell therapy is significantly compromised in older patients.To overcome these limitations,alternative strategies have been used to restore the age-and disease-depleted function of stem cells.These methods aim to restore the therapeutic efficacy of aged stem cells for autologous use.This article explores the effect of donor age and health status on the regenerative potential of stem cells.It further highlights the limitations of stem cell-based therapy for autologous treatment in the elderly.A comprehensive insight into the potential strategies to address the“age”and“disease”compromised regenerative potential of autologous stem cells is also presented.The information provided here serves as a valuable resource for physicians and patients for optimization of stem cellbased autologous therapy for aged patients.
基金supported by the National Natural Science Foundation of China (Nos. 52175322, 52271031)the Natural Science Foundation of Jilin Province, China (No. SKL202302015)。
文摘The effects of artificial aging(T6)on the creep resistance with tensile stresses in the range of 50−80 MPa at 175℃were investigated for an extruded Mg−1.22Al−0.31Ca−0.44Mn(wt.%)alloy.The Guinier-Preston(G.P.)zones primarily precipitate in the sample aged at 200℃for 1 h(T6-200℃/1h),while the Al_(2)Ca phases mainly precipitate in the sample aged at 275℃for 8 h(T6-275℃/8h).The T6-200℃/1h sample exhibits excellent creep resistance,with a steady-state creep rate one order of magnitude lower than that of the T6-275℃/8h sample.The abnormally high stress exponent(~8.2)observed in the T6-200℃/1h sample is associated with the power-law breakdown mechanism.TEM analysis illuminates that the creep mechanism for the T6-200℃/1h sample is cross-slip between basal and prismatic dislocations,while the T6-275℃/8h sample exhibits a mixed mechanism of dislocation cross-slip and climb.Compared with the Al_(2)Ca phase,the dense G.P.zones effectively impede dislocation climb and glide during the creep process,demonstrating superior creep resistance of the T6-200℃/1h sample.
基金supported by the NIA/NIH(1K01AG060040).Studies performed by JN were funded by the NICHD/NIH(5R00HD096117)Microscopy Core Facility supported,in part,with funding from NIH-NCI Cancer Center Support Grant P30 CA016059.
文摘Alzheimer’s disease is initially thought to be caused by age-associated accumulation of plaques,in recent years,research has increasingly associated Alzheimer’s disease with lysosomal storage and metabolic disorders,and the explanation of its pathogenesis has shifted from amyloid and tau accumulation to oxidative stress and impaired lipid and glucose metabolism aggravated by hypoxic conditions.However,the underlying mechanisms linking those cellular processes and conditions to disease progression have yet to be defined.Here,we applied a disease similarity approach to identify unknown molecular targets of Alzheimer’s disease by using transcriptomic data from congenital diseases known to increase Alzheimer’s disease risk,namely Down syndrome,Niemann-Pick type C disease,and mucopolysaccharidoses I.We uncovered common pathways,hub genes,and miRNAs across in vitro and in vivo models of these diseases as potential molecular targets for neuroprotection and amelioration of Alzheimer’s disease pathology,many of which have never been associated with Alzheimer’s disease.We then investigated common molecular alterations in brain samples from a Niemann-Pick type C disease mouse model by juxtaposing them with brain samples of both human and mouse models of Alzheimer’s disease.Detailed phenotypic,molecular,chronological,and biological aging analyses revealed that the Npc1tm(I1061T)Dso mouse model can serve as a potential short-lived in vivo model for brain aging and Alzheimer’s disease research.This research represents the first comprehensive approach to congenital disease association with neurodegeneration and a new perspective on Alzheimer’s disease research while highlighting shortcomings and lack of correlation in diverse in vitro models.Considering the lack of an Alzheimer’s disease mouse model that recapitulates the physiological hallmarks of brain aging,the short-lived Npc1^(tm(I1061T)Dso) mouse model can further accelerate the research in these fields and offer a unique model for understanding the molecular mechanisms of Alzheimer’s disease from a perspective of accelerated brain aging.
文摘The aging process is an inexorable fact throughout our lives and is considered a major factor in develo ping neurological dysfunctions associated with cognitive,emotional,and motor impairments.Aging-associated neurodegenerative diseases are characterized by the progressive loss of neuronal structure and function.
基金supported by the Key Projects of Medical Science and Technology of Henan Province,No.SBGJ202002099(to JY)。
文摘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.
基金Project supported by the Development Plan for Academics in Huanshui,the Natural Science Foundation of the Henan Province(182300410169,182102210201)the Support Project of Scientific and Technological Innovation Talents of Universities in Henan Province(19HASTIT023).
文摘Cerium oxide/silicon rubber was prepared via mechanical blending.Mechanical and frictional properties,as well as thermal stability after thermo-oxidative ageing were investigated in this rubber composite.3D surface profilometry,scanning electron microscopy(SEM)and thermogravimetry analysis(TGA)were used to study the friction surface characteristics,friction mechanism and thermal stability,respectively.Additionally,swelling experiments were carried out to investigate the variation of crosslinking density.After thermo-oxidative ageing,the tear strength of cerium oxide/silicon rubber decreases.However,in the early ageing stage,improvements in tensile strength,elongation at break,and frictional performance are caused by crosslinking density increments.Moreover,the addition of cerium oxide remarkably improves the re-cross linking degree during ageing process,which in turn decreases the number of holes on the friction surface and endows the silicon rubber with better mechanical and frictional properties,as well as thermo-oxidative ageing resistance.
基金funded by CONAHCYT grant(252808)to GFCONAHCYT’s“Estancias Posdoctorales por México”program(662350)to HTB。
文摘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).
基金supported by the National Natural Science Foundation of China,No.81921006(to GHL)。
文摘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.
