Two long-term slow slip events(SSEs) in Lower Cook Inlet, Alaska, were identified by Li SS et al.(2016). The earlier SSE lasted at least 9 years with M_(w) ~7.8 and had an average slip rate of ~82 mm/year. The latter ...Two long-term slow slip events(SSEs) in Lower Cook Inlet, Alaska, were identified by Li SS et al.(2016). The earlier SSE lasted at least 9 years with M_(w) ~7.8 and had an average slip rate of ~82 mm/year. The latter SSE, occurring in a similar area, lasted approximately 2 years with M_(w) ~7.2 and an average slip rate of ~91 mm/year. To test whether these SSEs triggered earthquakes near the slow slip area, we calculated the Coulomb stressing rate changes on receiver faults by using two fault geometry definitions: nodal planes of focal mechanism solutions of past earthquakes, and optimally oriented fault planes. Regions in the shallow slab(30–60 km) that experienced a significant increase in the Coulomb stressing rate due to slip by the SSEs showed an increase in seismicity rates during SSE periods. No correlation was found in the volumes that underwent a significant increase in the Coulomb stressing rate during the SSE within the crust and the intermediate slab. We modeled variations in seismicity rates by using a combination of the Coulomb stress transfer model and the framework of rate-and-state friction. Our model indicated that the SSEs increased the Coulomb stress changes on adjacent faults,thereby increasing the seismicity rates even though the ratio of the SSE stressing rate to the background stressing rate was small. Each long-term SSE in Alaska brought the megathrust updip of the SSE areas closer to failure by up to 0.1–0.15 MPa. The volumes of significant Coulomb stress changes caused by the Upper and Lower Cook Inlet SSEs did not overlap.展开更多
Background: New normality is uncertain in every sense, specifically in education and for many health disciplines. Being immersed in COVID-19 pandemics brought serious consequences for mental health, and is very import...Background: New normality is uncertain in every sense, specifically in education and for many health disciplines. Being immersed in COVID-19 pandemics brought serious consequences for mental health, and is very important to handle emotions and stress coping strategies to obtain positive outcomes. Objective: To identify the most frequent emotions, as well as the adaptation strategies to the new normality faced by the students of nursing. Methods: Qualitative and phenomenological research, with the participation of 20 students from both genders in the middle term of nursing career at Faculty of Higher Studies Iztacala, National Autonomous University of Mexico, from August to November 2021. Information was collected from a focal group for ten sessions;analysis was according to De Souza Minayo, and there was a signed informed consent letter from participants. Results: Four categories emerged with sub-categories. Category I Maximized emotions. Sub-categories: 1) Frustration, anger, disappointment;2) Personal disappointment, hopelessness, uncertainty;3) Depression. Category II Support elements close to the new normality. Sub-categories: 1) Family communication;2) Education for mental and physical health. Category III Stressing situations that exceeded the student. Sub-category: Disease in lovely ones. Category IV Stress coping strategies. Sub-categories: 1) Friends and relatives that help to get better;2) Family values. Informers pointed out to have maximized emotion, and having no self-control on its negative outcomes occurred;in addition, the situation was not favorable at home with several losses of loved ones, as well as a poor economy that threatened students to give up studies. Conclusion: Emotions facing this new normality are very important and should be attended to, their proper handling will result in a new learning of socio-emotional abilities, stress coping strategies development, better adaptation and informed decisions taken.展开更多
This article describes the effective channel length degradation under hot carrier stressing. The extraction is based on the IDs-Vcs characteristics by maximum transconductance （maximum slope of IDs ＆ VGS） in the li...This article describes the effective channel length degradation under hot carrier stressing. The extraction is based on the IDs-Vcs characteristics by maximum transconductance （maximum slope of IDs ＆ VGS） in the linear region. The transconductance characteristics are determine for the several devices of difference drawn channel length. The effective channel length of submicron LDD （Lightly Doped Drain） NMOSFETs （Metal Oxide Semiconductor Field Effect Transistor） under hot carrier stressing was measured at the stress time varying from zero to 10,000 seconds. It is shown that the effective channel length was increased with time. This is caused by charges trapping in the oxide during stress. The increased of effective channel length （△Leff） is seem to be increased sharply as the gate channel length is decrease.展开更多
This paper analyzes the influence of fatigue loading on the residual stress profile in high strength steel wires. To this end, different sinusoidal loads with diverse values of maximum loading level and number of cycl...This paper analyzes the influence of fatigue loading on the residual stress profile in high strength steel wires. To this end, different sinusoidal loads with diverse values of maximum loading level and number of cycles were simulated on wires in which several residual stress profiles had been previously introduced, some of them with a tensile state and others with a compressive state. An analysis was made of the evolution with time of such residual stress laws by comparing them at key instants of loading, that is, at initial instant, at maximum load, at minimum load and at final instant. Numerical results show only a minor influence of fatigue loading on the residual stress profile.展开更多
China Network Communications Group Corporation (CNC) proposed and reaffirmed for many times the strategic objective of transferring to a broadband communication and multimedia service provider since the beginning of t...China Network Communications Group Corporation (CNC) proposed and reaffirmed for many times the strategic objective of transferring to a broadband communication and multimedia service provider since the beginning of this year. CNC, insisting on self-innovation, is going to forge itself into a domestically high-class and internationally influential innovative company within five years.展开更多
How to put forward advisory suggestions regarded as feasible, workable and acceptable by the State leaders through the integration of the goodwill cherished by our scientists with the blueprint masterminded by the hos...How to put forward advisory suggestions regarded as feasible, workable and acceptable by the State leaders through the integration of the goodwill cherished by our scientists with the blueprint masterminded by the hosts of various R&D projects? It seems to me a problem worthy of our serious consideration. Here I would like to suggest that under the leading group of national S&T affairs, a new organ functionally similar to the State R&D Center be set up. Acting as a counselling team to the group, it must be small in payroll and include by strategists spe-展开更多
In order to investigate the ratcheting behavior of T225NG alloy, a series of ratcheting tests under uniaxial long-cyclic stressing were performed. The results show that the ratcheting strain of this alloy can get into...In order to investigate the ratcheting behavior of T225NG alloy, a series of ratcheting tests under uniaxial long-cyclic stressing were performed. The results show that the ratcheting strain of this alloy can get into shakedown after tens （or hundreds） of thousand cycles. After the ratcheting strain is saturated under the condition that stress amplitude is half of peak stress, it will bring about subsequent fatigue failure, and relationship between fatigue life and one of peak stress and saturated ratcheting （SR） strain meets power law. As the alloy is under stress jiggling with stress amplitude that is 1%-2.5% of peak stress, the ratcheting strain still become remarkable and goes into shakedown after several hundreds of thousand cycles but there exists little accessional strain caused by creep effect. It is notable that, when the peak stress is 85%-100% of yield stress, the long-cyclic stressing will lead SR strain to be from 1.4% to 2.5% even if the initial ratio of ratcheting strain is zero. Based on ratcheting threshold property of peak stress and monotonicity of relationship between the peak stress and SR strain, a saturated ratcheting model （SRM） is developed to predict SR strain and to estimate saturated creep strain also. In addition, the classes of ratcheting evolutions of metals are discussed.展开更多
Non-invasive cardiac stress imaging plays a central role in the assessment of patients with known or suspected coronary artery disease.The current guidelines suggest estimation of the myocardial ischaemic burden as a ...Non-invasive cardiac stress imaging plays a central role in the assessment of patients with known or suspected coronary artery disease.The current guidelines suggest estimation of the myocardial ischaemic burden as a criterion for revascularisation on prognostic grounds despite the lack of standardised reporting of the magnitude of ischaemia on various non-invasive imaging methods.Future studies should aim to accurately describe the relationship between myocardial ischaemic burden as assessed by cardiovascular magnetic resonance imaging and mortality.展开更多
Ischemic stroke is a major cause of neurological deficits and high disability rate.As the primary immune cells of the central nervous system,microglia play dual roles in neuroinflammation and tissue repair following a...Ischemic stroke is a major cause of neurological deficits and high disability rate.As the primary immune cells of the central nervous system,microglia play dual roles in neuroinflammation and tissue repair following a stroke.Their dynamic activation and polarization states are key factors that influence the disease process and treatment outcomes.This review article investigates the role of microglia in ischemic stroke and explores potential intervention strategies.Microglia exhibit a dynamic functional state,transitioning between pro-inflammatory(M1)and anti-inflammatory(M2)phenotypes.This duality is crucial in ischemic stroke,as it maintains a balance between neuroinflammation and tissue repair.Activated microglia contribute to neuroinflammation through cytokine release and disruption of the blood-brain barrier,while simultaneously promoting tissue repair through anti-inflammatory responses and regeneration.Key pathways influencing microglial activation include Toll-like receptor 4/nuclear factor kappa B,mitogen-activated protein kinases,Janus kinase/signal transducer and activator of transcription,and phosphoinositide 3-kinase/protein kinase B/mammalian target of rapamycin pathways.These pathways are targets for various experimental therapies aimed at promoting M2 polarization and mitigating damage.Potential therapeutic agents include natural compounds found in drugs such as minocycline,as well as traditional Chinese medicines.Drugs that target these regulatory mechanisms,such as small molecule inhibitors and components of traditional Chinese medicines,along with emerging technologies such as single-cell RNA sequencing and spatial transcriptomics,offer new therapeutic strategies and clinical translational potential for ischemic stroke.展开更多
Stroke,particularly ischemic stroke,is the leading cause of long-term disability and mortality worldwide.It occurs due to the occlusion of the cerebral arteries,which significantly reduces the delivery of blood,oxygen...Stroke,particularly ischemic stroke,is the leading cause of long-term disability and mortality worldwide.It occurs due to the occlusion of the cerebral arteries,which significantly reduces the delivery of blood,oxygen,and essential nutrients to brain tissues.This deprivation triggers a cascade of cellular events that ultimately leads to neuronal death.Recent studies have clarified the multifactorial pathogenesis of ischemic stroke,highlighting the roles of energy failure,excitotoxicity,oxidative stress,neuroinflammation,and apoptosis.This review aimed to provide a comprehensive insight into the fundamental mechanisms driving neuronal death triggered by ischemia and to examine the progress of neuroprotective therapeutic approaches designed to mitigate neuronal loss and promote neurological recovery after a stroke.Additionally,we explored widely accepted findings regarding the potential pathways implicated in neuronal death during ischemic stroke,including the interplay of apoptosis,autophagy,pyroptosis,ferroptosis,and necrosis,which collectively influence neuronal fate.We also discussed advancements in neuroprotective therapeutics,encompassing a range of interventions from pharmacological modulation to stem cell-based therapies,aimed at reducing neuronal injury and enhancing functional recovery following ischemic stroke.Despite these advancements,challenges remain in translating mechanistic insights into effective clinical therapies.Although neuroprotective strategies have shown promise in preclinical models,their efficacy in human trials has been inconsistent,often due to the complex pathology of ischemic stroke and the timing of interventions.In conclusion,this review synthesizes mechanistic insights into the intricate interplay of molecular and cellular pathways driving neuronal death post-ischemia.It sheds light on cutting-edge advancements in potential neuroprotective therapeutics,underscores the promise of regenerative medicine,and offers a forward-looking perspective on potential clinical breakthroughs.The ongoing evolution of precision-targeted interventions is expected to significantly enhance preventative strategies and improve clinical outcomes.展开更多
The cure rate for chronic neurodegenerative diseases remains low,creating an urgent need for improved intervention methods.Recent studies have shown that enhancing mitochondrial function can mitigate the effects of th...The cure rate for chronic neurodegenerative diseases remains low,creating an urgent need for improved intervention methods.Recent studies have shown that enhancing mitochondrial function can mitigate the effects of these diseases.This paper comprehensively reviews the relationship between mitochondrial dysfunction and chronic neurodegenerative diseases,aiming to uncover the potential use of targeted mitochondrial interventions as viable therapeutic options.We detail five targeted mitochondrial intervention strategies for chronic neurodegenerative diseases that act by promoting mitophagy,inhibiting mitochondrial fission,enhancing mitochondrial biogenesis,applying mitochondria-targeting antioxidants,and transplanting mitochondria.Each method has unique advantages and potential limitations,making them suitable for various therapeutic situations.Therapies that promote mitophagy or inhibit mitochondrial fission could be particularly effective in slowing disease progression,especially in the early stages.In contrast,those that enhance mitochondrial biogenesis and apply mitochondria-targeting antioxidants may offer great benefits during the middle stages of the disease by improving cellular antioxidant capacity and energy metabolism.Mitochondrial transplantation,while still experimental,holds great promise for restoring the function of damaged cells.Future research should focus on exploring the mechanisms and effects of these intervention strategies,particularly regarding their safety and efficacy in clinical settings.Additionally,the development of innovative mitochondria-targeting approaches,such as gene editing and nanotechnology,may provide new solutions for treating chronic neurodegenerative diseases.Implementing combined therapeutic strategies that integrate multiple intervention methods could also enhance treatment outcomes.展开更多
Stroke is a major cause of death and disability worldwide.It is characterized by a highly interconnected and multiphasic neuropathological cascade of events,in which an intense and protracted inflammatory response pla...Stroke is a major cause of death and disability worldwide.It is characterized by a highly interconnected and multiphasic neuropathological cascade of events,in which an intense and protracted inflammatory response plays a crucial role in worsening brain injury.Neuroinflammation,a key player in the pathophysiology of stroke,has a dual role.In the acute phase of stroke,neuroinflammation exacerbates brain injury,contributing to neuronal damage and blood–brain barrier disruption.This aspect of neuroinflammation is associated with poor neurological outcomes.Conversely,in the recovery phase following stroke,neuroinflammation facilitates brain repair processes,including neurogenesis,angiogenesis,and synaptic plasticity.The transition of neuroinflammation from a harmful to a reparative role is not well understood.Therefore,this review seeks to explore the mechanisms underlying this transition,with the goal of informing the development of therapeutic interventions that are both time-and context-specific.This review aims to elucidate the complex and dual role of neuroinflammation in stroke,highlighting the main actors,biomarkers of the disease,and potential therapeutic approaches.展开更多
Neuronal cell death is a common outcome of multiple pathophysiological processes and a key factor in neurological dysfunction after subarachnoid hemorrhage.Neuronal ferroptosis in particular plays an important role in...Neuronal cell death is a common outcome of multiple pathophysiological processes and a key factor in neurological dysfunction after subarachnoid hemorrhage.Neuronal ferroptosis in particular plays an important role in early brain injury.Bromodomain-containing protein 4,a member of the bromo and extraterminal domain family of proteins,participated in multiple cell death pathways,but the mechanisms by which it regulates ferroptosis remain unclear.The primary aim of this study was to investigate how bromodomain-containing protein 4 affects neuronal ferroptosis following subarachnoid hemorrhage in vivo and in vitro.Our findings revealed that endogenous bromodomain-containing protein 4 co-localized with neurons,and its expression was decreased 48 hours after subarachnoid hemorrhage of the cerebral cortex in vivo.In addition,ferroptosis-related pathways were activated in vivo and in vitro after subarachnoid hemorrhage.Targeted inhibition of bromodomain-containing protein 4 in neurons increased lipid peroxidation and intracellular ferrous iron accumulation via ferritinophagy and ultimately led to neuronal ferroptosis.Using cleavage under targets and tagmentation analysis,we found that bromodomain-containing protein 4 enrichment in the Raf-1 promoter region decreased following oxyhemoglobin stimulation in vitro.Furthermore,treating bromodomain-containing protein 4-knockdown HT-22 cell lines with GW5074,a Raf-1 inhibitor,exacerbated neuronal ferroptosis by suppressing the Raf-1/ERK1/2 signaling pathway.Moreover,targeted inhibition of neuronal bromodomain-containing protein 4 exacerbated early and long-term neurological function deficits after subarachnoid hemorrhage.Our findings suggest that bromodomain-containing protein 4 may have neuroprotective effects after subarachnoid hemorrhage,and that inhibiting ferroptosis could help treat subarachnoid hemorrhage.展开更多
Ischemia–reperfusion injury is a common pathophysiological mechanism in retinal degeneration.PANoptosis is a newly defined integral form of regulated cell death that combines the key features of pyroptosis,apoptosis,...Ischemia–reperfusion injury is a common pathophysiological mechanism in retinal degeneration.PANoptosis is a newly defined integral form of regulated cell death that combines the key features of pyroptosis,apoptosis,and necroptosis.Oligomerization of mitochondrial voltage-dependent anion channel 1 is an important pathological event in regulating cell death in retinal ischemia–reperfusion injury.However,its role in PANoptosis remains largely unknown.In this study,we demonstrated that voltage-dependent anion channel 1 oligomerization-mediated mitochondrial dysfunction was associated with PANoptosis in retinal ischemia–reperfusion injury.Inhibition of voltage-dependent anion channel 1 oligomerization suppressed mitochondrial dysfunction and PANoptosis in retinal cells subjected to ischemia–reperfusion injury.Mechanistically,mitochondria-derived reactive oxygen species played a central role in the voltagedependent anion channel 1-mediated regulation of PANoptosis by promoting PANoptosome assembly.Moreover,inhibiting voltage-dependent anion channel 1 oligomerization protected against PANoptosis in the retinas of rats subjected to ischemia–reperfusion injury.Overall,our findings reveal the critical role of voltage-dependent anion channel 1 oligomerization in regulating PANoptosis in retinal ischemia–reperfusion injury,highlighting voltage-dependent anion channel 1 as a promising therapeutic target.展开更多
In this study,a novel polysaccharide GPA-G 2-H was derived from ginseng.Furthermore,the coherent study of its structural characteristics,fermented characteristics in vitro,as well as antioxidant mechanism of fermented...In this study,a novel polysaccharide GPA-G 2-H was derived from ginseng.Furthermore,the coherent study of its structural characteristics,fermented characteristics in vitro,as well as antioxidant mechanism of fermented product FGPA-G 2-H on Aβ25-35-induced PC 12 cells were explored.The structure of GPA-G 2-H was determined by means of zeta potential analysis,FTIR,HPLC,XRD,GC-MS and NMR.The backbone of GPA-G 2-H was mainly composed of→4)-α-D-Glcp-(1→with branches substituted at O-3.Notably,GPA-G 2-H was degraded by intestinal microbiota in vitro with total sugar content and pH value decreasing,and short-chain fatty acids(SCFAs)increasing.Moreover,GPA-G 2-H significantly promoted the proliferation of Lactobacillus,Muribaculaceae and Weissella,thereby making positive alterations in intestinal microbiota composition.Additionally,FGPA-G 2-H activated the Nrf 2/HO-1 signaling pathway,enhanced HO-1,NQO 1,SOD and GSH-Px,while inhabited Keap 1,MDA and LDH,which alleviated Aβ-induced oxidative stress in PC 12 cells.These provide a solid theoretical basis for the further development of ginseng polysaccharides as functional food and antioxidant drugs.展开更多
Carbon fiber-reinforced carbon aerogel(C/CA)composites are one of the most promising candidates for applications requiring both thermal insulation and load bearing capabilities.The preparation of anti-oxidation coatin...Carbon fiber-reinforced carbon aerogel(C/CA)composites are one of the most promising candidates for applications requiring both thermal insulation and load bearing capabilities.The preparation of anti-oxidation coatings on C/CA to address its susceptibility to oxidation is a feasible approach to promote its application in oxidative environments.However,the currently reported coatings on C/CA mainly focus on improving the ablation performance and coating preparation process typically necessitating high-temperature heat treatment.This procedure can increase its thermal conductivity and reduce its thermal insulation ability.In this study,a series of ceramic-resin coatings were fabricated on C/CA through a simple slurry brushing-drying approach at room temperature.The effects of phenolic resin content on the coating structure,residual stress,thermal shock,and oxidation behaviors were investigated.Due to the adhesive properties and curing-induced shrinkage,the PR-7.5 coating(containing 7.5%(in mass)phenolic resin in the slurry)exhibits bonding strength close to fracture strength of the substrate and residual compressive stress of 0.853 GPa,which is beneficial for resisting thermal shock cracking.However,excessive resin content(PR-10.0 containing 10.0%(in mass)phenolic resin in the slurry)induces tensile stress due to uneven curing shrinkage,thereby leading to thermal shock cracking.Meanwhile,oxidation tests reveal significantly reduced weight losses for PR-7.5(17.46%at 800℃/100 min,8.15%at 1000℃/120 min,3.15%at 1200℃/120 min)versus uncoated C/CA’s 44.60%loss at 800℃/20 min.This work provides a brand-new and simple approach to improving the anti-oxidation performance of C/CA and expands its application in mild oxidative environments.展开更多
Protein aggregates,mitochondrial import stress and neurodegenerative disorders:A salient hallmark of several neurodegenerative diseases,including Parkinson’s disease,is the abundance of protein aggregates(Goiran et a...Protein aggregates,mitochondrial import stress and neurodegenerative disorders:A salient hallmark of several neurodegenerative diseases,including Parkinson’s disease,is the abundance of protein aggregates(Goiran et al.,2022).This molecular event is believed to lead to activation of stress pathways ultimately resulting in cellular dysfunction(Eldeeb et al.,2022).Accordingly,many lines of research investigations focused on dampening the formation of protein aggregates or augmenting the clearance of protein aggregates as a potential therapeutic strategy to counteract the progression of neurodegenerative diseases,albeit with little success(Costa-Mattioli and Walter,2020).Cell stress cues such as the accumulation of protein aggregates lead to the activation of stress response pathways that aid cells in responding to the damage.Despite the notion that the transient activation of these pathways helps cells cope with stressors,persistent activation can induce unwanted apoptosis of cells and reduce overall tissue strength as well as lead to an accumulation of aggregation-prone proteins(Hetz and Papa,2018).Mutations in proteins involved in stress signaling termination can cause conditions like ataxia and early-onset dementia(Conroy et al.,2014).Therefore,it is crucial for stress response signaling to be turned off once conditions have improved.Nevertheless,the mechanisms by which cells silence these signals are still elusive.展开更多
Background Environmental hypoxia is a common phenomenon in aquaculture,which causes gill tissue injury in fish.Glutathione(GSH)is a vital antioxidant in animal tissues,and its levels decrease under hypoxic conditions....Background Environmental hypoxia is a common phenomenon in aquaculture,which causes gill tissue injury in fish.Glutathione(GSH)is a vital antioxidant in animal tissues,and its levels decrease under hypoxic conditions.However,the effects of glutathione on fish under hypoxic stress remain poorly understood.This study aimed to investigate the impact of glutathione on gill tissue damage in fish under hypoxic stress and explore the underlying mechanisms.Methods Six experimental diets with varying glutathione concentrations.The actual glutathione levels in these diets,measured by high-performance liquid chromatography,were 0.00,145.95,291.90,437.85,583.80,and 729.75 mg/kg,respectively.Fish were fed these diets for 70 d,after which a 96-h hypoxic stress experiment was conducted.The experiment was set up with normoxic and hypoxic groups,in which the dissolved oxygen in the group was 6 mg/L,and that in the group was 1 mg/L.Results This research revealed that glutathione could enhance the growth performance and antioxidant capability of juvenile grass carp while mitigating the structural damage to gill tissues induced by hypoxia stress.Mechanistic investigations further indicated that glutathione mitigated hypoxia-induced oxidative injury in gill tissues and improved their antioxidant capacity.In addition,glutathione attenuated gill apoptosis induced by hypoxia stress.Glutathione also inhibited the initiation,nucleation,elongation,and degradation phases of autophagy,thereby attenuating hypoxia-induced gill autophagy.Moreover,glutathione was found to alleviate hypoxia-induced endoplasmic reticulum stress(ERS)in gills,a response potentially linked to the suppression of PERK,IRE1,and ATF6 signaling pathways.Finally,based on the ROS and PC contents in gill tissue,the optimum glutathione supplementation levels for juvenile grass carp under hypoxia stress were 437.10 and 495.00 mg/kg,respectively.Conclusions In conclusion,our experimental results demonstrated the effectiveness of glutathione in alleviating gill tissue damage caused by hypoxic stress.This study confirms the feasibility and effectiveness of dietary glutathione addition to alleviate hypoxic stress in fish.展开更多
Global population pressures have necessitated increased focus on protecting and developing resilient plant species that can maintain productivity despite environmental challenges.Environmental degradation,driven by cl...Global population pressures have necessitated increased focus on protecting and developing resilient plant species that can maintain productivity despite environmental challenges.Environmental degradation,driven by climate change and anthropogenic activities,poses significant threats to global food security through various forms of physical stress.Major environmental constraints affecting agricultural yields worldwide include salinity,water scarcity,nutritional imbalances(encompassing mineral toxicity and deficiencies),and extreme temperatures.Crop yield is influenced by multiple abiotic factors,including agronomic conditions,climatic variables,and soil nutrient availability.Plants develop various survival mechanisms at molecular,cellular,and physiological levels in response to stress.Abiotic stress,whether occurring individually or in combination,significantly impacts crop growth and productivity.For instance,drought stress reduces leaf area,plant height,and overall crop development.Cold stress inhibits plant development and crop efficiency,leading to diminished productivity.Salinity stress not only induces water stress in plants but also negatively affects cytosolic metabolism,cell development,membrane function,and increases reactive oxygen species(ROS)production.Elevated CO_(2)concentrations may enhance global precipitation patterns,potentially resulting in increased rainfall that can adversely affect crop development.Plants under excessive water stress exhibit reduced amylose content but increased crude protein levels.This affects both quality and quantity of crop production by inhibiting seed germination and causing growth impairment through combined effects of elevated osmotic potential and ion toxicity.Plants have evolved various escape-avoidance and tolerance mechanisms in response to abiotic stress,including physiological adaptations and integrated cellular or molecular responses.This review paper examines the impact of abiotic stress on morpho-physiological,biochemical,and molecular activities across various crops.Additionally,it analyzes crop interactions with abiotic stress regarding response and adaptation mechanisms,providing a fundamental framework for species selection and development of stress-tolerant varieties in the future.展开更多
Bread wheat(Triticum aestivum L.)is a staple hexaploid crop with numerous wild relatives.However,domestication and modern breeding have significantly narrowed its genetic diversity,diminishing its capacity to adapt to...Bread wheat(Triticum aestivum L.)is a staple hexaploid crop with numerous wild relatives.However,domestication and modern breeding have significantly narrowed its genetic diversity,diminishing its capacity to adapt to climate change.Wild relatives of wheat serve as a vital reservoir of genetic diversity,offering traits thatenhance its resistance to various biotic and abiotic stresses.Over recent decades,remarkable progress has been made in utilizing superior genes from wild relatives to bolster wheat's defenses against diseases and pests,though the exploration of genes conferring abiotic stress tolerance has lagged behind.In this review,we summarize key advancements in the utilization of wild relatives for wheat enhancement over the past century,emphasizing both theoretical and technological innovations.Furthermore,we evaluate the potential contributions of wild relatives to address production challenges posed by climate change.We also explore strategies for isolating superior genes and developing prebreeding germplasm to support the future development of climate-resilient wheat varieties.展开更多
基金supported by the National Natural Science Foundation of China (Grant No. 42104001)。
文摘Two long-term slow slip events(SSEs) in Lower Cook Inlet, Alaska, were identified by Li SS et al.(2016). The earlier SSE lasted at least 9 years with M_(w) ~7.8 and had an average slip rate of ~82 mm/year. The latter SSE, occurring in a similar area, lasted approximately 2 years with M_(w) ~7.2 and an average slip rate of ~91 mm/year. To test whether these SSEs triggered earthquakes near the slow slip area, we calculated the Coulomb stressing rate changes on receiver faults by using two fault geometry definitions: nodal planes of focal mechanism solutions of past earthquakes, and optimally oriented fault planes. Regions in the shallow slab(30–60 km) that experienced a significant increase in the Coulomb stressing rate due to slip by the SSEs showed an increase in seismicity rates during SSE periods. No correlation was found in the volumes that underwent a significant increase in the Coulomb stressing rate during the SSE within the crust and the intermediate slab. We modeled variations in seismicity rates by using a combination of the Coulomb stress transfer model and the framework of rate-and-state friction. Our model indicated that the SSEs increased the Coulomb stress changes on adjacent faults,thereby increasing the seismicity rates even though the ratio of the SSE stressing rate to the background stressing rate was small. Each long-term SSE in Alaska brought the megathrust updip of the SSE areas closer to failure by up to 0.1–0.15 MPa. The volumes of significant Coulomb stress changes caused by the Upper and Lower Cook Inlet SSEs did not overlap.
文摘Background: New normality is uncertain in every sense, specifically in education and for many health disciplines. Being immersed in COVID-19 pandemics brought serious consequences for mental health, and is very important to handle emotions and stress coping strategies to obtain positive outcomes. Objective: To identify the most frequent emotions, as well as the adaptation strategies to the new normality faced by the students of nursing. Methods: Qualitative and phenomenological research, with the participation of 20 students from both genders in the middle term of nursing career at Faculty of Higher Studies Iztacala, National Autonomous University of Mexico, from August to November 2021. Information was collected from a focal group for ten sessions;analysis was according to De Souza Minayo, and there was a signed informed consent letter from participants. Results: Four categories emerged with sub-categories. Category I Maximized emotions. Sub-categories: 1) Frustration, anger, disappointment;2) Personal disappointment, hopelessness, uncertainty;3) Depression. Category II Support elements close to the new normality. Sub-categories: 1) Family communication;2) Education for mental and physical health. Category III Stressing situations that exceeded the student. Sub-category: Disease in lovely ones. Category IV Stress coping strategies. Sub-categories: 1) Friends and relatives that help to get better;2) Family values. Informers pointed out to have maximized emotion, and having no self-control on its negative outcomes occurred;in addition, the situation was not favorable at home with several losses of loved ones, as well as a poor economy that threatened students to give up studies. Conclusion: Emotions facing this new normality are very important and should be attended to, their proper handling will result in a new learning of socio-emotional abilities, stress coping strategies development, better adaptation and informed decisions taken.
文摘This article describes the effective channel length degradation under hot carrier stressing. The extraction is based on the IDs-Vcs characteristics by maximum transconductance （maximum slope of IDs ＆ VGS） in the linear region. The transconductance characteristics are determine for the several devices of difference drawn channel length. The effective channel length of submicron LDD （Lightly Doped Drain） NMOSFETs （Metal Oxide Semiconductor Field Effect Transistor） under hot carrier stressing was measured at the stress time varying from zero to 10,000 seconds. It is shown that the effective channel length was increased with time. This is caused by charges trapping in the oxide during stress. The increased of effective channel length （△Leff） is seem to be increased sharply as the gate channel length is decrease.
文摘This paper analyzes the influence of fatigue loading on the residual stress profile in high strength steel wires. To this end, different sinusoidal loads with diverse values of maximum loading level and number of cycles were simulated on wires in which several residual stress profiles had been previously introduced, some of them with a tensile state and others with a compressive state. An analysis was made of the evolution with time of such residual stress laws by comparing them at key instants of loading, that is, at initial instant, at maximum load, at minimum load and at final instant. Numerical results show only a minor influence of fatigue loading on the residual stress profile.
文摘China Network Communications Group Corporation (CNC) proposed and reaffirmed for many times the strategic objective of transferring to a broadband communication and multimedia service provider since the beginning of this year. CNC, insisting on self-innovation, is going to forge itself into a domestically high-class and internationally influential innovative company within five years.
文摘How to put forward advisory suggestions regarded as feasible, workable and acceptable by the State leaders through the integration of the goodwill cherished by our scientists with the blueprint masterminded by the hosts of various R&D projects? It seems to me a problem worthy of our serious consideration. Here I would like to suggest that under the leading group of national S&T affairs, a new organ functionally similar to the State R&D Center be set up. Acting as a counselling team to the group, it must be small in payroll and include by strategists spe-
文摘In order to investigate the ratcheting behavior of T225NG alloy, a series of ratcheting tests under uniaxial long-cyclic stressing were performed. The results show that the ratcheting strain of this alloy can get into shakedown after tens （or hundreds） of thousand cycles. After the ratcheting strain is saturated under the condition that stress amplitude is half of peak stress, it will bring about subsequent fatigue failure, and relationship between fatigue life and one of peak stress and saturated ratcheting （SR） strain meets power law. As the alloy is under stress jiggling with stress amplitude that is 1%-2.5% of peak stress, the ratcheting strain still become remarkable and goes into shakedown after several hundreds of thousand cycles but there exists little accessional strain caused by creep effect. It is notable that, when the peak stress is 85%-100% of yield stress, the long-cyclic stressing will lead SR strain to be from 1.4% to 2.5% even if the initial ratio of ratcheting strain is zero. Based on ratcheting threshold property of peak stress and monotonicity of relationship between the peak stress and SR strain, a saturated ratcheting model （SRM） is developed to predict SR strain and to estimate saturated creep strain also. In addition, the classes of ratcheting evolutions of metals are discussed.
文摘Non-invasive cardiac stress imaging plays a central role in the assessment of patients with known or suspected coronary artery disease.The current guidelines suggest estimation of the myocardial ischaemic burden as a criterion for revascularisation on prognostic grounds despite the lack of standardised reporting of the magnitude of ischaemia on various non-invasive imaging methods.Future studies should aim to accurately describe the relationship between myocardial ischaemic burden as assessed by cardiovascular magnetic resonance imaging and mortality.
基金supported by the National Natural Science Foundation of China,82471345(to LC)the Key Research and Development Program for Social Development by the Jiangsu Provincial Department of Science and Technology.No.BE2022668(to LC).
文摘Ischemic stroke is a major cause of neurological deficits and high disability rate.As the primary immune cells of the central nervous system,microglia play dual roles in neuroinflammation and tissue repair following a stroke.Their dynamic activation and polarization states are key factors that influence the disease process and treatment outcomes.This review article investigates the role of microglia in ischemic stroke and explores potential intervention strategies.Microglia exhibit a dynamic functional state,transitioning between pro-inflammatory(M1)and anti-inflammatory(M2)phenotypes.This duality is crucial in ischemic stroke,as it maintains a balance between neuroinflammation and tissue repair.Activated microglia contribute to neuroinflammation through cytokine release and disruption of the blood-brain barrier,while simultaneously promoting tissue repair through anti-inflammatory responses and regeneration.Key pathways influencing microglial activation include Toll-like receptor 4/nuclear factor kappa B,mitogen-activated protein kinases,Janus kinase/signal transducer and activator of transcription,and phosphoinositide 3-kinase/protein kinase B/mammalian target of rapamycin pathways.These pathways are targets for various experimental therapies aimed at promoting M2 polarization and mitigating damage.Potential therapeutic agents include natural compounds found in drugs such as minocycline,as well as traditional Chinese medicines.Drugs that target these regulatory mechanisms,such as small molecule inhibitors and components of traditional Chinese medicines,along with emerging technologies such as single-cell RNA sequencing and spatial transcriptomics,offer new therapeutic strategies and clinical translational potential for ischemic stroke.
基金supported by the National Natural Science Foundation of China,Nos.82171387 and 31830111(both to SL).
文摘Stroke,particularly ischemic stroke,is the leading cause of long-term disability and mortality worldwide.It occurs due to the occlusion of the cerebral arteries,which significantly reduces the delivery of blood,oxygen,and essential nutrients to brain tissues.This deprivation triggers a cascade of cellular events that ultimately leads to neuronal death.Recent studies have clarified the multifactorial pathogenesis of ischemic stroke,highlighting the roles of energy failure,excitotoxicity,oxidative stress,neuroinflammation,and apoptosis.This review aimed to provide a comprehensive insight into the fundamental mechanisms driving neuronal death triggered by ischemia and to examine the progress of neuroprotective therapeutic approaches designed to mitigate neuronal loss and promote neurological recovery after a stroke.Additionally,we explored widely accepted findings regarding the potential pathways implicated in neuronal death during ischemic stroke,including the interplay of apoptosis,autophagy,pyroptosis,ferroptosis,and necrosis,which collectively influence neuronal fate.We also discussed advancements in neuroprotective therapeutics,encompassing a range of interventions from pharmacological modulation to stem cell-based therapies,aimed at reducing neuronal injury and enhancing functional recovery following ischemic stroke.Despite these advancements,challenges remain in translating mechanistic insights into effective clinical therapies.Although neuroprotective strategies have shown promise in preclinical models,their efficacy in human trials has been inconsistent,often due to the complex pathology of ischemic stroke and the timing of interventions.In conclusion,this review synthesizes mechanistic insights into the intricate interplay of molecular and cellular pathways driving neuronal death post-ischemia.It sheds light on cutting-edge advancements in potential neuroprotective therapeutics,underscores the promise of regenerative medicine,and offers a forward-looking perspective on potential clinical breakthroughs.The ongoing evolution of precision-targeted interventions is expected to significantly enhance preventative strategies and improve clinical outcomes.
基金partly supported by the Yan’an University Qin Chuanyuan“Scientist+Engineer”Team Special Fund,No.2023KXJ-012(to YL)Yan’an University Transformation of Scientific and Technological Achievements Fund,No.2023CGZH-001(to YL)+2 种基金College Students Innovation and Entrepreneurship Training Program,Nos.D2023158,202410719056(to XS,JM)Yan’an University Production and Cultivation Project,No.CXY202001(to YL)Kweichow Moutai Hospital Research and Talent Development Fund Project,No.MTyk2022-25(to XO)。
文摘The cure rate for chronic neurodegenerative diseases remains low,creating an urgent need for improved intervention methods.Recent studies have shown that enhancing mitochondrial function can mitigate the effects of these diseases.This paper comprehensively reviews the relationship between mitochondrial dysfunction and chronic neurodegenerative diseases,aiming to uncover the potential use of targeted mitochondrial interventions as viable therapeutic options.We detail five targeted mitochondrial intervention strategies for chronic neurodegenerative diseases that act by promoting mitophagy,inhibiting mitochondrial fission,enhancing mitochondrial biogenesis,applying mitochondria-targeting antioxidants,and transplanting mitochondria.Each method has unique advantages and potential limitations,making them suitable for various therapeutic situations.Therapies that promote mitophagy or inhibit mitochondrial fission could be particularly effective in slowing disease progression,especially in the early stages.In contrast,those that enhance mitochondrial biogenesis and apply mitochondria-targeting antioxidants may offer great benefits during the middle stages of the disease by improving cellular antioxidant capacity and energy metabolism.Mitochondrial transplantation,while still experimental,holds great promise for restoring the function of damaged cells.Future research should focus on exploring the mechanisms and effects of these intervention strategies,particularly regarding their safety and efficacy in clinical settings.Additionally,the development of innovative mitochondria-targeting approaches,such as gene editing and nanotechnology,may provide new solutions for treating chronic neurodegenerative diseases.Implementing combined therapeutic strategies that integrate multiple intervention methods could also enhance treatment outcomes.
基金supported by European Union-NextGeneration EU under the Italian University and Research(MUR)National Innovation Ecosystem grant ECS00000041-VITALITY-CUP E13C22001060006(to MdA)。
文摘Stroke is a major cause of death and disability worldwide.It is characterized by a highly interconnected and multiphasic neuropathological cascade of events,in which an intense and protracted inflammatory response plays a crucial role in worsening brain injury.Neuroinflammation,a key player in the pathophysiology of stroke,has a dual role.In the acute phase of stroke,neuroinflammation exacerbates brain injury,contributing to neuronal damage and blood–brain barrier disruption.This aspect of neuroinflammation is associated with poor neurological outcomes.Conversely,in the recovery phase following stroke,neuroinflammation facilitates brain repair processes,including neurogenesis,angiogenesis,and synaptic plasticity.The transition of neuroinflammation from a harmful to a reparative role is not well understood.Therefore,this review seeks to explore the mechanisms underlying this transition,with the goal of informing the development of therapeutic interventions that are both time-and context-specific.This review aims to elucidate the complex and dual role of neuroinflammation in stroke,highlighting the main actors,biomarkers of the disease,and potential therapeutic approaches.
基金supported by the National Natural Science Foundation of China,Nos.82371310(to YJ),82271306(to JP)the Sichuan Science and Technology Support Program,Nos.2023YFH0069(to JP),2023NSFSC0028(to YJ),2023NSFSC1559(to YJ),2022YFS0615(to JP),2022NSFSC1421(to JP)+1 种基金Scientific Research Project of Sichuan Provincial Health Commission,No.23LCYJ040(to YJ)Youth Foundation of Southwestern Medical University and Southwest Medical University Project,Nos.2020ZRQNA038(to JP),2021ZKZD013(to JP),2021LZXNYD-P01(to YJ),2023QN014(to JP).
文摘Neuronal cell death is a common outcome of multiple pathophysiological processes and a key factor in neurological dysfunction after subarachnoid hemorrhage.Neuronal ferroptosis in particular plays an important role in early brain injury.Bromodomain-containing protein 4,a member of the bromo and extraterminal domain family of proteins,participated in multiple cell death pathways,but the mechanisms by which it regulates ferroptosis remain unclear.The primary aim of this study was to investigate how bromodomain-containing protein 4 affects neuronal ferroptosis following subarachnoid hemorrhage in vivo and in vitro.Our findings revealed that endogenous bromodomain-containing protein 4 co-localized with neurons,and its expression was decreased 48 hours after subarachnoid hemorrhage of the cerebral cortex in vivo.In addition,ferroptosis-related pathways were activated in vivo and in vitro after subarachnoid hemorrhage.Targeted inhibition of bromodomain-containing protein 4 in neurons increased lipid peroxidation and intracellular ferrous iron accumulation via ferritinophagy and ultimately led to neuronal ferroptosis.Using cleavage under targets and tagmentation analysis,we found that bromodomain-containing protein 4 enrichment in the Raf-1 promoter region decreased following oxyhemoglobin stimulation in vitro.Furthermore,treating bromodomain-containing protein 4-knockdown HT-22 cell lines with GW5074,a Raf-1 inhibitor,exacerbated neuronal ferroptosis by suppressing the Raf-1/ERK1/2 signaling pathway.Moreover,targeted inhibition of neuronal bromodomain-containing protein 4 exacerbated early and long-term neurological function deficits after subarachnoid hemorrhage.Our findings suggest that bromodomain-containing protein 4 may have neuroprotective effects after subarachnoid hemorrhage,and that inhibiting ferroptosis could help treat subarachnoid hemorrhage.
基金supported by the National Natural Science Foundation of China,Nos.82172196(to KX),82372507(to KX)the Natural Science Foundation of Hunan Province,China,No.2023JJ40804(to QZ)the Key Laboratory of Emergency and Trauma(Hainan Medical University)of the Ministry of Education,China,No.KLET-202210(to QZ)。
文摘Ischemia–reperfusion injury is a common pathophysiological mechanism in retinal degeneration.PANoptosis is a newly defined integral form of regulated cell death that combines the key features of pyroptosis,apoptosis,and necroptosis.Oligomerization of mitochondrial voltage-dependent anion channel 1 is an important pathological event in regulating cell death in retinal ischemia–reperfusion injury.However,its role in PANoptosis remains largely unknown.In this study,we demonstrated that voltage-dependent anion channel 1 oligomerization-mediated mitochondrial dysfunction was associated with PANoptosis in retinal ischemia–reperfusion injury.Inhibition of voltage-dependent anion channel 1 oligomerization suppressed mitochondrial dysfunction and PANoptosis in retinal cells subjected to ischemia–reperfusion injury.Mechanistically,mitochondria-derived reactive oxygen species played a central role in the voltagedependent anion channel 1-mediated regulation of PANoptosis by promoting PANoptosome assembly.Moreover,inhibiting voltage-dependent anion channel 1 oligomerization protected against PANoptosis in the retinas of rats subjected to ischemia–reperfusion injury.Overall,our findings reveal the critical role of voltage-dependent anion channel 1 oligomerization in regulating PANoptosis in retinal ischemia–reperfusion injury,highlighting voltage-dependent anion channel 1 as a promising therapeutic target.
基金Supported by the National Key Research and Development Program of Traditional Chinese Medicine Modernization Project,China(No.2023YFC3504000)the Science and Technology Development Project of Jilin Province,China(No.20240404043ZP)the Science and Technology Innovation Cooperation Project of Changchun Science and Technology Bureau and Chinese Academy of Sciences,China(No.23SH14)。
文摘In this study,a novel polysaccharide GPA-G 2-H was derived from ginseng.Furthermore,the coherent study of its structural characteristics,fermented characteristics in vitro,as well as antioxidant mechanism of fermented product FGPA-G 2-H on Aβ25-35-induced PC 12 cells were explored.The structure of GPA-G 2-H was determined by means of zeta potential analysis,FTIR,HPLC,XRD,GC-MS and NMR.The backbone of GPA-G 2-H was mainly composed of→4)-α-D-Glcp-(1→with branches substituted at O-3.Notably,GPA-G 2-H was degraded by intestinal microbiota in vitro with total sugar content and pH value decreasing,and short-chain fatty acids(SCFAs)increasing.Moreover,GPA-G 2-H significantly promoted the proliferation of Lactobacillus,Muribaculaceae and Weissella,thereby making positive alterations in intestinal microbiota composition.Additionally,FGPA-G 2-H activated the Nrf 2/HO-1 signaling pathway,enhanced HO-1,NQO 1,SOD and GSH-Px,while inhabited Keap 1,MDA and LDH,which alleviated Aβ-induced oxidative stress in PC 12 cells.These provide a solid theoretical basis for the further development of ginseng polysaccharides as functional food and antioxidant drugs.
基金National Natural Science Foundation of China(52272075,52472053)Research Fund of Youth Innovation Promotion Association of CAS,China(2021190)Defense Industrial Technology Development Program(JCKY2021130B007)。
文摘Carbon fiber-reinforced carbon aerogel(C/CA)composites are one of the most promising candidates for applications requiring both thermal insulation and load bearing capabilities.The preparation of anti-oxidation coatings on C/CA to address its susceptibility to oxidation is a feasible approach to promote its application in oxidative environments.However,the currently reported coatings on C/CA mainly focus on improving the ablation performance and coating preparation process typically necessitating high-temperature heat treatment.This procedure can increase its thermal conductivity and reduce its thermal insulation ability.In this study,a series of ceramic-resin coatings were fabricated on C/CA through a simple slurry brushing-drying approach at room temperature.The effects of phenolic resin content on the coating structure,residual stress,thermal shock,and oxidation behaviors were investigated.Due to the adhesive properties and curing-induced shrinkage,the PR-7.5 coating(containing 7.5%(in mass)phenolic resin in the slurry)exhibits bonding strength close to fracture strength of the substrate and residual compressive stress of 0.853 GPa,which is beneficial for resisting thermal shock cracking.However,excessive resin content(PR-10.0 containing 10.0%(in mass)phenolic resin in the slurry)induces tensile stress due to uneven curing shrinkage,thereby leading to thermal shock cracking.Meanwhile,oxidation tests reveal significantly reduced weight losses for PR-7.5(17.46%at 800℃/100 min,8.15%at 1000℃/120 min,3.15%at 1200℃/120 min)versus uncoated C/CA’s 44.60%loss at 800℃/20 min.This work provides a brand-new and simple approach to improving the anti-oxidation performance of C/CA and expands its application in mild oxidative environments.
文摘Protein aggregates,mitochondrial import stress and neurodegenerative disorders:A salient hallmark of several neurodegenerative diseases,including Parkinson’s disease,is the abundance of protein aggregates(Goiran et al.,2022).This molecular event is believed to lead to activation of stress pathways ultimately resulting in cellular dysfunction(Eldeeb et al.,2022).Accordingly,many lines of research investigations focused on dampening the formation of protein aggregates or augmenting the clearance of protein aggregates as a potential therapeutic strategy to counteract the progression of neurodegenerative diseases,albeit with little success(Costa-Mattioli and Walter,2020).Cell stress cues such as the accumulation of protein aggregates lead to the activation of stress response pathways that aid cells in responding to the damage.Despite the notion that the transient activation of these pathways helps cells cope with stressors,persistent activation can induce unwanted apoptosis of cells and reduce overall tissue strength as well as lead to an accumulation of aggregation-prone proteins(Hetz and Papa,2018).Mutations in proteins involved in stress signaling termination can cause conditions like ataxia and early-onset dementia(Conroy et al.,2014).Therefore,it is crucial for stress response signaling to be turned off once conditions have improved.Nevertheless,the mechanisms by which cells silence these signals are still elusive.
基金financially supported by the Sichuan Science and Technology Program(2024YFNH0016,2024NSFSC2072)the earmarked fund for CARS(CARS-45)+2 种基金the National Science Fund for Distinguished Young Scholars of China(32425056)the National Key Research and Development Program of China(2023YFD2400600)Sichuan Innovation Team of National Modern Agricultural Industry Technology System(SCCXTD-2024-15)。
文摘Background Environmental hypoxia is a common phenomenon in aquaculture,which causes gill tissue injury in fish.Glutathione(GSH)is a vital antioxidant in animal tissues,and its levels decrease under hypoxic conditions.However,the effects of glutathione on fish under hypoxic stress remain poorly understood.This study aimed to investigate the impact of glutathione on gill tissue damage in fish under hypoxic stress and explore the underlying mechanisms.Methods Six experimental diets with varying glutathione concentrations.The actual glutathione levels in these diets,measured by high-performance liquid chromatography,were 0.00,145.95,291.90,437.85,583.80,and 729.75 mg/kg,respectively.Fish were fed these diets for 70 d,after which a 96-h hypoxic stress experiment was conducted.The experiment was set up with normoxic and hypoxic groups,in which the dissolved oxygen in the group was 6 mg/L,and that in the group was 1 mg/L.Results This research revealed that glutathione could enhance the growth performance and antioxidant capability of juvenile grass carp while mitigating the structural damage to gill tissues induced by hypoxia stress.Mechanistic investigations further indicated that glutathione mitigated hypoxia-induced oxidative injury in gill tissues and improved their antioxidant capacity.In addition,glutathione attenuated gill apoptosis induced by hypoxia stress.Glutathione also inhibited the initiation,nucleation,elongation,and degradation phases of autophagy,thereby attenuating hypoxia-induced gill autophagy.Moreover,glutathione was found to alleviate hypoxia-induced endoplasmic reticulum stress(ERS)in gills,a response potentially linked to the suppression of PERK,IRE1,and ATF6 signaling pathways.Finally,based on the ROS and PC contents in gill tissue,the optimum glutathione supplementation levels for juvenile grass carp under hypoxia stress were 437.10 and 495.00 mg/kg,respectively.Conclusions In conclusion,our experimental results demonstrated the effectiveness of glutathione in alleviating gill tissue damage caused by hypoxic stress.This study confirms the feasibility and effectiveness of dietary glutathione addition to alleviate hypoxic stress in fish.
基金financially supported by the National Key R&D Program of China(2022YFE0113400)the Jiangsu Provincial Fund for Realizing Carbon Emission Peaking and Neutralization,China(BE2022305)+1 种基金the National Natural Science Fundation of China(32102411)the Project funded by China Postdoctoral Science Foundation(2022M722698)。
文摘Global population pressures have necessitated increased focus on protecting and developing resilient plant species that can maintain productivity despite environmental challenges.Environmental degradation,driven by climate change and anthropogenic activities,poses significant threats to global food security through various forms of physical stress.Major environmental constraints affecting agricultural yields worldwide include salinity,water scarcity,nutritional imbalances(encompassing mineral toxicity and deficiencies),and extreme temperatures.Crop yield is influenced by multiple abiotic factors,including agronomic conditions,climatic variables,and soil nutrient availability.Plants develop various survival mechanisms at molecular,cellular,and physiological levels in response to stress.Abiotic stress,whether occurring individually or in combination,significantly impacts crop growth and productivity.For instance,drought stress reduces leaf area,plant height,and overall crop development.Cold stress inhibits plant development and crop efficiency,leading to diminished productivity.Salinity stress not only induces water stress in plants but also negatively affects cytosolic metabolism,cell development,membrane function,and increases reactive oxygen species(ROS)production.Elevated CO_(2)concentrations may enhance global precipitation patterns,potentially resulting in increased rainfall that can adversely affect crop development.Plants under excessive water stress exhibit reduced amylose content but increased crude protein levels.This affects both quality and quantity of crop production by inhibiting seed germination and causing growth impairment through combined effects of elevated osmotic potential and ion toxicity.Plants have evolved various escape-avoidance and tolerance mechanisms in response to abiotic stress,including physiological adaptations and integrated cellular or molecular responses.This review paper examines the impact of abiotic stress on morpho-physiological,biochemical,and molecular activities across various crops.Additionally,it analyzes crop interactions with abiotic stress regarding response and adaptation mechanisms,providing a fundamental framework for species selection and development of stress-tolerant varieties in the future.
基金supported by the Biological Breeding-National Science and Technology Major Project(2023ZD04071)the National Key Research and Development Program of China(2023YFF1000600)and the National Natural Science Foundation of China(32272084,32372089,and 31971887).
文摘Bread wheat(Triticum aestivum L.)is a staple hexaploid crop with numerous wild relatives.However,domestication and modern breeding have significantly narrowed its genetic diversity,diminishing its capacity to adapt to climate change.Wild relatives of wheat serve as a vital reservoir of genetic diversity,offering traits thatenhance its resistance to various biotic and abiotic stresses.Over recent decades,remarkable progress has been made in utilizing superior genes from wild relatives to bolster wheat's defenses against diseases and pests,though the exploration of genes conferring abiotic stress tolerance has lagged behind.In this review,we summarize key advancements in the utilization of wild relatives for wheat enhancement over the past century,emphasizing both theoretical and technological innovations.Furthermore,we evaluate the potential contributions of wild relatives to address production challenges posed by climate change.We also explore strategies for isolating superior genes and developing prebreeding germplasm to support the future development of climate-resilient wheat varieties.
