Traumatic optic neuropathy is a form of optic neuropathy resulting from trauma.Its pathophysiological mechanisms involve primary and secondary injury phases,leading to progressive retinal ganglion cell loss and axonal...Traumatic optic neuropathy is a form of optic neuropathy resulting from trauma.Its pathophysiological mechanisms involve primary and secondary injury phases,leading to progressive retinal ganglion cell loss and axonal degeneration.Contributing factors such as physical trauma,oxidative stress,neuroinflammation,and glial scar formation exacerbate disease progression and retinal ganglion cell death.Multiple forms of cell death—including apoptosis,pyroptosis,necroptosis,and ferroptosis—are involved at different disease stages.Although current treatments,such as corticosteroid therapy and surgical interventions,have limited efficacy,cell-based therapies have emerged as a promising approach that simultaneously promotes neuroprotection and retinal ganglion cell regeneration.This review summarizes recent advances in cell-based therapies for traumatic optic neuropathy.In the context of cell replacement therapy,retinal ganglion cell-like cells derived from embryonic stem cells and induced pluripotent stem cells—via chemical induction or direct reprogramming—have demonstrated the ability to integrate into the host retina and survive for weeks to months,potentially improving visual function.Mesenchymal stem cells derived from various sources,including bone marrow,umbilical cord,placenta,and adipose tissue,have been shown to enhance retinal ganglion cell survival,stimulate axonal regeneration,and support partial functional recovery.Additionally,neural stem/progenitor cells derived from human embryonic stem cells offer neuroprotective effects and function as“neuronal relays,”facilitating reconnection between damaged regions of the optic nerve and the visual pathway.Beyond direct cell transplantation,cell-derived products,such as extracellular vesicles and cell-extracted solutions,have demonstrated promising neuroprotective effects in traumatic optic neuropathy.Despite significant progress,several challenges remain,including limited integration of transplanted cells,suboptimal functional vision recovery,the need for precise timing and delivery methods,and an incomplete understanding of the role of the retinal microenvironment and glial cell activation in neuroprotection and neuroregeneration.Furthermore,studies with longer observation periods and deeper mechanistic insights into the therapeutic effects of cell-based therapies remain scarce.Two Phase I clinical trials have confirmed the safety and potential benefits of cell-based therapy for traumatic optic neuropathy,with reported improvements in visual acuity.However,further studies are needed to validate these findings and establish significant therapeutic outcomes.In conclusion,cell-based therapies hold great promise for treating traumatic optic neuropathy,but critical obstacles must be overcome to achieve functional optic nerve regeneration.Emerging bioengineering strategies,such as scaffold-based transplantation,may improve cell survival and axonal guidance.Successful clinical translation will require rigorous preclinical validation,standardized protocols,and the integration of advanced imaging techniques to optimize therapeutic efficacy.展开更多
Recent studies have shown that fibrotic scar formation following cerebral ischemic injury has varying effects depending on the microenvironment.However,little is known about how fibrosis is induced and regulated after...Recent studies have shown that fibrotic scar formation following cerebral ischemic injury has varying effects depending on the microenvironment.However,little is known about how fibrosis is induced and regulated after cerebral ischemic injury.Sonic hedgehog signaling participates in fibrosis in the heart,liver,lung,and kidney.Whether Shh signaling modulates fibrotic scar formation after cerebral ischemic stroke and the underlying mechanisms are unclear.In this study,we found that Sonic Hedgehog expression was upregulated in patients with acute ischemic stroke and in a middle cerebral artery occlusion/reperfusion injury rat model.Both Sonic hedgehog and Mitofusin 2 showed increased expression in the middle cerebral artery occlusion rat model and in vitro fibrosis cell model induced by transforming growth factor-beta 1.Activation of the Sonic hedgehog signaling pathway enhanced the expression of phosphorylated Smad 3 and Mitofusin 2 proteins,promoted the formation of fibrotic scars,protected synapses or promoted synaptogenesis,alleviated neurological deficits following middle cerebral artery occlusion/reperfusion injury,reduced cell apoptosis,facilitated the transformation of meninges fibroblasts into myofibroblasts,and enhanced the proliferation and migration of meninges fibroblasts.The Smad3 phosphorylation inhibitor SIS3 reversed the effects induced by Sonic hedgehog signaling pathway activation.Bioinformatics analysis revealed significant correlations between Sonic hedgehog and Smad3,between Sonic hedgehog and Mitofusin 2,and between Smad3 and Mitofusin 2.These findings suggest that Sonic hedgehog signaling may influence Mitofusin 2 expression by regulating Smad3 phosphorylation,thereby modulating the formation of early fibrotic scars following cerebral ischemic stroke and affecting prognosis.The Sonic Hedgehog signaling pathway may serve as a new therapeutic target for stroke treatment.展开更多
Short-chain fatty acids,metabolites produced by the fermentation of dietary fiber by gut microbiota,have garnered significant attention due to their correlation with neurodegenerative diseases,particularly Parkinson’...Short-chain fatty acids,metabolites produced by the fermentation of dietary fiber by gut microbiota,have garnered significant attention due to their correlation with neurodegenerative diseases,particularly Parkinson’s disease.In this review,we summarize the changes in short-chain fatty acid levels and the abundance of short-chain fatty acid-producing bacteria in various samples from patients with Parkinson’s disease,highlighting the critical role of gut homeostasis imbalance in the pathogenesis and progression of the disease.Focusing on the nervous system,we discuss the molecular mechanisms by which short-chain fatty acids influence the homeostasis of both the enteric nervous system and the central nervous system.We identify key processes,including the activation of G protein-coupled receptors and the inhibition of histone deacetylases by short-chain fatty acids.Importantly,structural or functional disruptions in the enteric nervous system mediated by these fatty acids may lead to abnormalα-synuclein expression and gastrointestinal dysmotility,which could serve as an initiating event in Parkinson’s disease.Furthermore,we propose that short-chain fatty acids help establish communication between the enteric nervous system and the central nervous system via the vagal nerve,immune circulation,and endocrine signaling.This communication may shed light on their potential role in the transmission ofα-synuclein from the gut to the brain.Finally,we elucidate novel treatment strategies for Parkinson’s disease that target short-chain fatty acids and examine the challenges associated with translating short-chain fatty acid-based therapies into clinical practice.In conclusion,this review emphasizes the pivotal role of short-chain fatty acids in regulating gut-brain axis integrity and their significance in the pathogenesis of Parkinson’s disease from the perspective of the nervous system.Moreover,it highlights the potential value of short-chain fatty acids in early intervention for Parkinson’s disease.Future research into the molecular mechanisms of short-chain fatty acids and their synergistic interactions with other gut metabolites is likely to advance the clinical translation of innovative short-chain fatty acid-based therapies for Parkinson’s disease.展开更多
The suppression of ablative Rayleigh–Taylor instability(ARTI)by a spatially modulated laser in inertial confinement fusion(ICF)is studied through numerical simulations.The results show that in the acceleration phase ...The suppression of ablative Rayleigh–Taylor instability(ARTI)by a spatially modulated laser in inertial confinement fusion(ICF)is studied through numerical simulations.The results show that in the acceleration phase of ICF implosion,the growth of ARTI can be suppressed by using a short-wavelength spatially modulated laser.The ARTI growth rate decreases as the wavelength of the spatially modulated laser decreases,and ARTI is completely suppressed after a certain wavelength has been reached.A spatially uniform laser is introduced to keep the state of motion of the implosion fluid consistent,and it is found that the proportion of the spatially modulated laser required for complete suppression of ARTI decreases as the wavelength continues to decrease.We also optimize the spatial intensity distribution of the spatially modulated laser.In addition,as the duration of the spatially modulated laser decreases,the proportion required for completely suppressing ARTI increases,but the required energy decreases.When the perturbation wavenumber decreases,the wavelength of the spatially modulated laser required for complete suppression of ARTI becomes longer.In the case of multimode perturbation,ARTI can also be significantly suppressed by a spatially modulated laser,and the perturbation amplitude can be reduced to less than 10% of that without a spatially modulated laser.We believe that the conclusions drawn from our simulations can provide the basis for new approaches to control ARTI in ICF.展开更多
Understanding the properties of warm dense hydrogen is of key importance for the modeling of compact astrophysical objects and to understand and further optimize inertial confinement fusion applications.The workhorse ...Understanding the properties of warm dense hydrogen is of key importance for the modeling of compact astrophysical objects and to understand and further optimize inertial confinement fusion applications.The workhorse of warm dense matter theory is thermal density functional theory(DFT),which,however,suffers from two limitations:(i)its accuracy can depend on the utilized exchange-correlation functional,which has to be approximated,and(ii)it is generally limited to single-electron properties such as the density distribution.Here,we present a new ansatz combining time-dependent DFT results for the dynamic structure factor S_(ee)(q,ω)with static DFT results for the density response.This allows us to estimate the electron-electron static structure factor S_(ee)(q)of warm dense hydrogen with high accuracy over a broad range of densities and temperatures.In addition to its value for the study of warm dense matter,our work opens up new avenues for the future study of electronic correlations exclusively within the framework of DFT for a host of applications.展开更多
Type 2 diabetes mellitus has central complications:Diabetes,a metabolic disorder primarily characterized by hyperglycemia due to insufficient insulin secretion,or impaired insulin signaling,has significant central com...Type 2 diabetes mellitus has central complications:Diabetes,a metabolic disorder primarily characterized by hyperglycemia due to insufficient insulin secretion,or impaired insulin signaling,has significant central complications.Type 2 diabetes mellitus(T2DM),the most prevalent type of diabetes,affects more than 38 million individuals in the United States(approximately 1 in 10)and is defined by chronic hyperglycemia and insulin resistance,which refers to a reduced cellular response to insulin.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
Self-Centering Piston-Based Braced Frames(SC-PBBFs)are designed to curtail structural damage under severe ground motions.The self-centering mechanism in this bracing mitigates structural damage during an earthquake,th...Self-Centering Piston-Based Braced Frames(SC-PBBFs)are designed to curtail structural damage under severe ground motions.The self-centering mechanism in this bracing mitigates structural damage during an earthquake,thereby reducing post-earthquake repair costs and contributing to seismic resilience.However,non-structural components,particularly those sensitive to floor acceleration,remain vulnerable,resulting in prolonged func-tional recovery times.This paper aims to address this limitation by introducing a novel structural archetype,the Self-Centering Viscous-Based Braced Frame(SC-VBBF),which integrates superelastic shape memory alloy(SMA)bars,viscous dampers(VDs),and friction springs(FSs).A streamlined analytical approach relies on the strength decoupling of VD from other components using aλfactor to design SC-VBBFs.To evaluate the effectiveness of the hybrid brace,a set of 4-,8-,and 12-story archetypes equipped with SC-PBBs and SC-VBBFs are simulated in OpenSees and analyzed under various earthquake types,including crustal,subcrustal,and subduction events.The results demonstrate the superior performance of the SC-VBBF withλ≤0.5 system compared to SC-PBBFs in mitigating floor accelerations under design-level earthquakes and improving seismic resilience.展开更多
For diverse neurodegenerative disorders,microglial cells are activated.Furthermore,dysfunctional and hyperactivated microglia initiate mitochondrial autophagy,oxidative stress,and pathological protein accumulation,end...For diverse neurodegenerative disorders,microglial cells are activated.Furthermore,dysfunctional and hyperactivated microglia initiate mitochondrial autophagy,oxidative stress,and pathological protein accumulation,ending with neuroinflammation that exacerbates damage to dopaminergic neurons and contributes significantly to the pathology of neurodegenerative disorder.Microglial overactivation is closely associated with the secretion of pro-inflammatory cytokines,the phagocytosis of injured neurons,and the modulation of neurotoxic environments.This review summarizes the role of microglia neurodegenerative diseases,such as Alzheimer's disease,Parkinson's disease,multiple sclerosis,multiple system atrophy,amyotrophic lateral sclerosis,frontotemporal dementia,progressive supranuclear palsy,cortical degeneration,Lewy body dementia,and Huntington's disease.It also discusses novel forms of cell death such as ferroptosis,cuproptosis,disulfidptosis,and parthanatos(poly(adenosine diphosphate ribose)polymerase 1-dependent cell death),as well as the impact of regulatory factors related to microglial inflammation on microglial activation and neuroinflammation.The aim is to identify potential targets for microglial cell therapy in neurodegenerative diseases.展开更多
With the gradual advancement of research methods and technologies,various biological processes have been identified as playing roles in the pathogenesis of neurodegenerative diseases.However,current descriptions of th...With the gradual advancement of research methods and technologies,various biological processes have been identified as playing roles in the pathogenesis of neurodegenerative diseases.However,current descriptions of these biological processes do not fully explain the onset,progression,and development of these conditions.Therefore,exploration of the pathogenesis of neurodegenerative diseases remains a valuable area of research.This review summarizes the potential common pathogeneses of Alzheimer’s disease,Parkinson’s disease,amyotrophic lateral sclerosis,Huntington’s disease,frontotemporal lobar dementia,and Lewy body disease.Research findings have indicated that several common biological processes,including aging,genetic factors,progressive neuronal dysfunction,neuronal death and apoptosis,protein misfolding and aggregation,neuroinflammation,mitochondrial dysfunction,axonal transport defects,and gut microbiota dysbiosis,are involved in the pathogenesis of these six neurodegenerative diseases.Based on current information derived from diverse areas of research,these biological processes may form complex pathogenic networks that lead to distinctive types of neuronal death in neurodegenerative diseases.Furthermore,promoting the regeneration of damaged neurons may be achievable through the repair of affected neural cells if the underlying pathogenesis can be prevented or reversed.Hence,these potential common biological processes may represent only very small,limited elements within numerous intricate pathogenic networks associated with neurodegenerative diseases.In clinical treatment,interfering with any single biological process has proven insufficient to completely halt the progression of neurodegenerative diseases.Therefore,future research on the pathogenesis of neurodegenerative diseases should focus on uncovering the complex pathogenic networks,rather than isolating individual biological processes.Based on this,therapies that aim to block or reverse various targets involved in the potential pathogenic mechanisms of neurodegenerative diseases may be promising directions,as current treatment methods that focus on halting a single pathogenic factor have not achieved satisfactory efficacy.展开更多
Lysosomal storage disorders and their impact upon the central nervous system:Lysosomal storage disorders(LSDs)are a group of over 70 rare inherited metabolic disorders(Platt et al.,2018).They are caused by dysfunction...Lysosomal storage disorders and their impact upon the central nervous system:Lysosomal storage disorders(LSDs)are a group of over 70 rare inherited metabolic disorders(Platt et al.,2018).They are caused by dysfunction of lysosomes,organelles that contain enzymes responsible for digesting macromolecules.In functional lysosomes,these enzymes break down complex substrates,and the resulting fragments are recycled.Individual LSDs are caused by mutations in genes that encode lysosomal enzymes or other proteins crucial for lysosome function(Platt et al.,2018).展开更多
Estrogen deficiency after menopause accelerates bone loss by stimulating osteoclast formation and activity,but the molecular pathways that link estrogen signaling to osteoclast regulation remain incompletely defined.H...Estrogen deficiency after menopause accelerates bone loss by stimulating osteoclast formation and activity,but the molecular pathways that link estrogen signaling to osteoclast regulation remain incompletely defined.Here,we identify the sialyltransferase ST3GAL-I as a key mediator of RANKL-induced osteoclastogenesis.RANKL activates c-FOS to drive ST3GAL1 transcription,whereas estrogen-bound ERαcompetes with TRAF6 and suppresses this c-FOS–dependent induction.In a clinical cohort of pre-menopausal and post-menopausal women with or without osteoporosis,serum total andα-2,3-linked sialic acid levels increased with age and were highest in post-menopausal osteoporotic patients.Single-cell RNA sequencing of human bone revealed that osteoclasts form a prominent cluster only after menopause,where FOS,CTSK,and ST3GAL1 are strongly co-expressed,and the estrogen-responsive gene PGR is down-regulated.Additionally,in vivo experiments showed that sialidase treatment in estrogen-deficient models effectively reduced osteoclast-mediated bone loss,mimicking the effects of estradiol.These findings define a direct molecular link between loss of estrogen and activation of a FOS–ST3GAL1 sialylation pathway in osteoclasts,providing mechanistic insight into the enhanced bone resorption characteristic of post-menopausal osteoporosis.展开更多
This letter reports a gravitational redshift measurement experiment using a satellite-based compact passive hydrogen maser(PHM)in a lunar distant retrograde orbit(DRO).In March 2024,the Chinese Academy of Sciences lau...This letter reports a gravitational redshift measurement experiment using a satellite-based compact passive hydrogen maser(PHM)in a lunar distant retrograde orbit(DRO).In March 2024,the Chinese Academy of Sciences launched the DRO-A/B twin satellites,which entered a DRO in July 2024.This orbit has a geocentric distance of approximately 300,000–450,000 kilometers and a 2:1 resonance ratio.Employing microwave dual one-way ranging(DOWR),satellite-ground time-frequency comparisons were successfully achieved in April 2025 using the PHM aboard the DRO-A satellite.This study validated the in-orbit performance of the compact PHM and supported tests of the Einstein Equivalence Principle.The gravitational redshift measurement result is(8.74±4.17)×10^(−3).As the world’s first fundamental physics experiment to deploy PHMs in a lunar DRO,this study provides significant new engineering approaches for testing gravitational theories in cislunar space.展开更多
Cells actively sense and transduce microenvironmental mechanical inputs into chemical signals via cytoskeletal rearrangements.During these mechanosensation and mechanotransduction processes,the role of the actin cytos...Cells actively sense and transduce microenvironmental mechanical inputs into chemical signals via cytoskeletal rearrangements.During these mechanosensation and mechanotransduction processes,the role of the actin cytoskeleton is well-understood,whereas the role of the tubulin cytoskeleton remains largely elusive.Here,we report the dynamic changes in microtubules in response to microenvironmental stiffness during chondrocyte mitosis.Mechanical stiffness was found to be coupled with microtubule generation,directing microtubule dynamics in mitotic chondrocytes.Refilin B was found to be a key regulator of microtubule assembly in chondrocytes in response to mechanical stiffness.It was found to play its role in microtubule formation via the p-Smad3 signaling pathway.Additionally,integrin-linked kinase(ILK),triggered by mechanical stiffness,was found to play an indispensable role in the process of microtubule dynamics mediated by refilin B.Our data emphasizes stiffness-mediated dynamic changes in the microtubules of chondrocytes in a quiescent state(G0)and at anaphase,which improves our understanding of the mechanical regulation of microtubule assembly during the chondrocyte cell cycle and provides insights into microenvironment mechanics during tissue maintenance,wound healing,and disease occurrence.展开更多
Predicting the behavior of renewable energy systems requires models capable of generating accurate forecasts from limited historical data,a challenge that becomes especially pronounced when commissioning new facil-iti...Predicting the behavior of renewable energy systems requires models capable of generating accurate forecasts from limited historical data,a challenge that becomes especially pronounced when commissioning new facil-ities where operational records are scarce.This review aims to synthesize recent progress in data-efficient deep learning approaches for addressing such“cold-start”forecasting problems.It primarily covers three interrelated domains—solar photovoltaic(PV),wind power,and electrical load forecasting—where data scarcity and operational variability are most critical,while also including representative studies on hydropower and carbon emission prediction to provide a broader systems perspective.To this end,we examined trends from over 150 predominantly peer-reviewed studies published between 2019 and mid-2025,highlighting advances in zero-shot and few-shot meta-learning frameworks that enable rapid model adaptation with minimal labeled data.Moreover,transfer learning approaches combined with spatiotemporal graph neural networks have been employed to transfer knowledge from existing energy assets to new,data-sparse environments,effectively capturing hidden dependencies among geographic features,meteorological dynamics,and grid structures.Synthetic data generation has further proven valuable for expanding training samples and mitigating overfitting in cold-start scenarios.In addition,large language models and explainable artificial intelligence(XAI)—notably conversational XAI systems—have been used to interpret and communicate complex model behaviors in accessible terms,fostering operator trust from the earliest deployment stages.By consolidating methodological advances,unresolved challenges,and open-source resources,this review provides a coherent overview of deep learning strategies that can shorten the data-sparse ramp-up period of new energy infrastructures and accelerate the transition toward resilient,low-carbon electricity grids.展开更多
I offer suggestions to increase the probability of success of an international research project.Collaborative studies often produce more innovative and transformative scientific results than work done by a single inve...I offer suggestions to increase the probability of success of an international research project.Collaborative studies often produce more innovative and transformative scientific results than work done by a single investigator or an isolated team.My advice is intended for early-career scientists.The product of the collaboration may be high-impact research publications,enhanced geophysical monitoring capabilities in a foreign country,or an advanced training course.Choosing the right international partner is the most important step.Keeping an open mind and being receptive to suggestions to modify the initial concept is critical.Other key steps include having a mutually agreed upon plan with achievable goals and well-defined expected outcomes.International cooperation is a richly rewarding experience that accelerates progress in the Earth Sciences.展开更多
After spinal cord injury,impairment of the sensorimotor circuit can lead to dysfunction in the motor,sensory,proprioceptive,and autonomic nervous systems.Functional recovery is often hindered by constraints on the tim...After spinal cord injury,impairment of the sensorimotor circuit can lead to dysfunction in the motor,sensory,proprioceptive,and autonomic nervous systems.Functional recovery is often hindered by constraints on the timing of interventions,combined with the limitations of current methods.To address these challenges,various techniques have been developed to aid in the repair and reconstruction of neural circuits at different stages of injury.Notably,neuromodulation has garnered considerable attention for its potential to enhance nerve regeneration,provide neuroprotection,restore neurons,and regulate the neural reorganization of circuits within the cerebral cortex and corticospinal tract.To improve the effectiveness of these interventions,the implementation of multitarget early interventional neuromodulation strategies,such as electrical and magnetic stimulation,is recommended to enhance functional recovery across different phases of nerve injury.This review concisely outlines the challenges encountered following spinal cord injury,synthesizes existing neurostimulation techniques while emphasizing neuroprotection,repair,and regeneration of impaired connections,and advocates for multi-targeted,task-oriented,and timely interventions.展开更多
The interleukin-17 family is the key group of cytokines and displays a broad spectrum of biological functions,including regulating the inflammatory cascade in various autoimmune and inflammatory diseases,such as multi...The interleukin-17 family is the key group of cytokines and displays a broad spectrum of biological functions,including regulating the inflammatory cascade in various autoimmune and inflammatory diseases,such as multiple sclerosis,neuromyelitis optica spectrum disorder,myasthenia gravis,Guillain–Barre syndrome,acute disseminated encephalomyelitis,diabetes,inflammatory skin diseases,joint inflammation,and cancer.Although the function of the interleukin-17 family has attracted increasing research attention over many years,the expression,function,and regulation mechanisms of different interleukin-17 members are complicated and still only partially understood.Currently,the interleukin-17A pathway is considered a critical therapeutic target for numerous immune and chronic inflammatory diseases,with several monoclonal antibodies against interleukin-17A having been successfully used in clinical practice.Whether other interleukin-17 members have the potential to be targeted in other diseases is still debated.This review first summarizes the recent advancements in understanding the physicochemical properties,physiological functions,cellular origins,and downstream signaling pathways of different members and corresponding receptors of the interleukin-17 family.Subsequently,the function of interleukin-17 in various immune diseases is discussed,and the important role of interleukin-17 in the pathological process of immune diseases is demonstrated from multiple perspectives.Then,the current status of targeted interleukin-17 therapy is summarized,and the effectiveness and safety of targeted interleukin-17 therapy are analyzed.Finally,the clinical application prospects of targeting the interleukin-17 pathway are discussed.展开更多
The China-ASEAN Free Trade Area(CAFTA)3.0Upgrade Protocol added a section on“Supply Chain Connectivity,”which emphasizes that all parties recognize the lessons learned from the COVID-19 pandemic and cooperate to enh...The China-ASEAN Free Trade Area(CAFTA)3.0Upgrade Protocol added a section on“Supply Chain Connectivity,”which emphasizes that all parties recognize the lessons learned from the COVID-19 pandemic and cooperate to enhance the resilience of the regional supply chain.This is an inevitable trend amid the current accelerated restructuring of the global supply chain,the complex and severe international economic and trade situation,and the impact on the regional industrial chain.It also represents a fundamental shift and consensus on the logic of supply chain cooperation between China and ASEAN countries—a transformation from“Efficiency First”to“Resilience First.”展开更多
Dear Editor,Idiopathic orbital inflammation(IOI),also known as orbital inflammatory pseudotumor,is a relatively common orbital disorder[1].Its pathogenesis remains unclear,often regarded as a nonspecific immune-mediat...Dear Editor,Idiopathic orbital inflammation(IOI),also known as orbital inflammatory pseudotumor,is a relatively common orbital disorder[1].Its pathogenesis remains unclear,often regarded as a nonspecific immune-mediated response[2].IOI presents with symptoms such as pain,photophobia,proptosis,eyelid swelling,edema,conjunctival congestion,and diplopia,with possible vision loss occurring in some cases.Based on the soft tissue structures involved,IOI can be classified into subtypes such as myositis,optic neuritis,dacryoadenitis,diffuse orbital inflammation,and orbital inflammatory masses[2].展开更多
基金supported by the National Key Research and Development Program of China,No.2022YFA1105502(to PG)the National Natural Science Foundation of China,Nos.82271123(to PG),32200618(to ZT)。
文摘Traumatic optic neuropathy is a form of optic neuropathy resulting from trauma.Its pathophysiological mechanisms involve primary and secondary injury phases,leading to progressive retinal ganglion cell loss and axonal degeneration.Contributing factors such as physical trauma,oxidative stress,neuroinflammation,and glial scar formation exacerbate disease progression and retinal ganglion cell death.Multiple forms of cell death—including apoptosis,pyroptosis,necroptosis,and ferroptosis—are involved at different disease stages.Although current treatments,such as corticosteroid therapy and surgical interventions,have limited efficacy,cell-based therapies have emerged as a promising approach that simultaneously promotes neuroprotection and retinal ganglion cell regeneration.This review summarizes recent advances in cell-based therapies for traumatic optic neuropathy.In the context of cell replacement therapy,retinal ganglion cell-like cells derived from embryonic stem cells and induced pluripotent stem cells—via chemical induction or direct reprogramming—have demonstrated the ability to integrate into the host retina and survive for weeks to months,potentially improving visual function.Mesenchymal stem cells derived from various sources,including bone marrow,umbilical cord,placenta,and adipose tissue,have been shown to enhance retinal ganglion cell survival,stimulate axonal regeneration,and support partial functional recovery.Additionally,neural stem/progenitor cells derived from human embryonic stem cells offer neuroprotective effects and function as“neuronal relays,”facilitating reconnection between damaged regions of the optic nerve and the visual pathway.Beyond direct cell transplantation,cell-derived products,such as extracellular vesicles and cell-extracted solutions,have demonstrated promising neuroprotective effects in traumatic optic neuropathy.Despite significant progress,several challenges remain,including limited integration of transplanted cells,suboptimal functional vision recovery,the need for precise timing and delivery methods,and an incomplete understanding of the role of the retinal microenvironment and glial cell activation in neuroprotection and neuroregeneration.Furthermore,studies with longer observation periods and deeper mechanistic insights into the therapeutic effects of cell-based therapies remain scarce.Two Phase I clinical trials have confirmed the safety and potential benefits of cell-based therapy for traumatic optic neuropathy,with reported improvements in visual acuity.However,further studies are needed to validate these findings and establish significant therapeutic outcomes.In conclusion,cell-based therapies hold great promise for treating traumatic optic neuropathy,but critical obstacles must be overcome to achieve functional optic nerve regeneration.Emerging bioengineering strategies,such as scaffold-based transplantation,may improve cell survival and axonal guidance.Successful clinical translation will require rigorous preclinical validation,standardized protocols,and the integration of advanced imaging techniques to optimize therapeutic efficacy.
基金supported by the National Natural Science Foundation of China,Nos.82171456(to QY)and 81971229(to QY)the Natural Science Foundation of Chongqing,Nos.CSTC2021JCYJ-MSXMX0263(to QY)and CSTB2023NSCQ-MSX1015(to XL)Doctoral Innovation Project of The First Affiliated Hospital of Chongqing Medical University,Nos.CYYY-BSYJSCXXM-202318(to JW)and CYYY-BSYJSCXXM-202327(to HT).
文摘Recent studies have shown that fibrotic scar formation following cerebral ischemic injury has varying effects depending on the microenvironment.However,little is known about how fibrosis is induced and regulated after cerebral ischemic injury.Sonic hedgehog signaling participates in fibrosis in the heart,liver,lung,and kidney.Whether Shh signaling modulates fibrotic scar formation after cerebral ischemic stroke and the underlying mechanisms are unclear.In this study,we found that Sonic Hedgehog expression was upregulated in patients with acute ischemic stroke and in a middle cerebral artery occlusion/reperfusion injury rat model.Both Sonic hedgehog and Mitofusin 2 showed increased expression in the middle cerebral artery occlusion rat model and in vitro fibrosis cell model induced by transforming growth factor-beta 1.Activation of the Sonic hedgehog signaling pathway enhanced the expression of phosphorylated Smad 3 and Mitofusin 2 proteins,promoted the formation of fibrotic scars,protected synapses or promoted synaptogenesis,alleviated neurological deficits following middle cerebral artery occlusion/reperfusion injury,reduced cell apoptosis,facilitated the transformation of meninges fibroblasts into myofibroblasts,and enhanced the proliferation and migration of meninges fibroblasts.The Smad3 phosphorylation inhibitor SIS3 reversed the effects induced by Sonic hedgehog signaling pathway activation.Bioinformatics analysis revealed significant correlations between Sonic hedgehog and Smad3,between Sonic hedgehog and Mitofusin 2,and between Smad3 and Mitofusin 2.These findings suggest that Sonic hedgehog signaling may influence Mitofusin 2 expression by regulating Smad3 phosphorylation,thereby modulating the formation of early fibrotic scars following cerebral ischemic stroke and affecting prognosis.The Sonic Hedgehog signaling pathway may serve as a new therapeutic target for stroke treatment.
基金supported by the National Key R&D Program of China,No.2021YFC2501200(to PC).
文摘Short-chain fatty acids,metabolites produced by the fermentation of dietary fiber by gut microbiota,have garnered significant attention due to their correlation with neurodegenerative diseases,particularly Parkinson’s disease.In this review,we summarize the changes in short-chain fatty acid levels and the abundance of short-chain fatty acid-producing bacteria in various samples from patients with Parkinson’s disease,highlighting the critical role of gut homeostasis imbalance in the pathogenesis and progression of the disease.Focusing on the nervous system,we discuss the molecular mechanisms by which short-chain fatty acids influence the homeostasis of both the enteric nervous system and the central nervous system.We identify key processes,including the activation of G protein-coupled receptors and the inhibition of histone deacetylases by short-chain fatty acids.Importantly,structural or functional disruptions in the enteric nervous system mediated by these fatty acids may lead to abnormalα-synuclein expression and gastrointestinal dysmotility,which could serve as an initiating event in Parkinson’s disease.Furthermore,we propose that short-chain fatty acids help establish communication between the enteric nervous system and the central nervous system via the vagal nerve,immune circulation,and endocrine signaling.This communication may shed light on their potential role in the transmission ofα-synuclein from the gut to the brain.Finally,we elucidate novel treatment strategies for Parkinson’s disease that target short-chain fatty acids and examine the challenges associated with translating short-chain fatty acid-based therapies into clinical practice.In conclusion,this review emphasizes the pivotal role of short-chain fatty acids in regulating gut-brain axis integrity and their significance in the pathogenesis of Parkinson’s disease from the perspective of the nervous system.Moreover,it highlights the potential value of short-chain fatty acids in early intervention for Parkinson’s disease.Future research into the molecular mechanisms of short-chain fatty acids and their synergistic interactions with other gut metabolites is likely to advance the clinical translation of innovative short-chain fatty acid-based therapies for Parkinson’s disease.
基金supported by the National Natural Science Foundation of China(NSFC)(Nos.12074399,12204500,and 12004403)the Key Projects of Intergovernmental International Scientific and Technological Innovation Cooperation(No.2021YFE0116700)+1 种基金the Shanghai Natural Science Foundation(No.20ZR1464400)the Shanghai Sailing Program(No.22YF1455300).
文摘The suppression of ablative Rayleigh–Taylor instability(ARTI)by a spatially modulated laser in inertial confinement fusion(ICF)is studied through numerical simulations.The results show that in the acceleration phase of ICF implosion,the growth of ARTI can be suppressed by using a short-wavelength spatially modulated laser.The ARTI growth rate decreases as the wavelength of the spatially modulated laser decreases,and ARTI is completely suppressed after a certain wavelength has been reached.A spatially uniform laser is introduced to keep the state of motion of the implosion fluid consistent,and it is found that the proportion of the spatially modulated laser required for complete suppression of ARTI decreases as the wavelength continues to decrease.We also optimize the spatial intensity distribution of the spatially modulated laser.In addition,as the duration of the spatially modulated laser decreases,the proportion required for completely suppressing ARTI increases,but the required energy decreases.When the perturbation wavenumber decreases,the wavelength of the spatially modulated laser required for complete suppression of ARTI becomes longer.In the case of multimode perturbation,ARTI can also be significantly suppressed by a spatially modulated laser,and the perturbation amplitude can be reduced to less than 10% of that without a spatially modulated laser.We believe that the conclusions drawn from our simulations can provide the basis for new approaches to control ARTI in ICF.
基金partially supported by the Center for Advanced Systems Understanding (CASUS), financed by Germany’s Federal Ministry of Education and Research and the Saxon State Government out of the State Budget approved by the Saxon State Parliamentthe European Union’s Just Transition Fund (JTF) within the project Röntgenlaser Optimierung der Laserfusion (ROLF), Contract No. 5086999001, co-financed by the Saxon State Government out of the State Budget approved by the Saxon State Parliament+3 种基金the European Research Council (ERC) under the European Union’s Horizon 2022 Research and Innovation Programme (Grant Agreement No. 101076233, “PREXTREME”)Computations were performed on a Bull Cluster at the Center for Information Services and High-Performance Computing (ZIH) at Technische Universität Dresden and at the Norddeutscher Verbund für Hoch- und Höchstleistungsrechnen (HLRN) under Grant No. mvp00024support by the National Natural Science Foundation of China under Grant No. 12274171support by the Advanced Materials–National Science and Technology Major Project (Grant No. 2024ZD0606900)
文摘Understanding the properties of warm dense hydrogen is of key importance for the modeling of compact astrophysical objects and to understand and further optimize inertial confinement fusion applications.The workhorse of warm dense matter theory is thermal density functional theory(DFT),which,however,suffers from two limitations:(i)its accuracy can depend on the utilized exchange-correlation functional,which has to be approximated,and(ii)it is generally limited to single-electron properties such as the density distribution.Here,we present a new ansatz combining time-dependent DFT results for the dynamic structure factor S_(ee)(q,ω)with static DFT results for the density response.This allows us to estimate the electron-electron static structure factor S_(ee)(q)of warm dense hydrogen with high accuracy over a broad range of densities and temperatures.In addition to its value for the study of warm dense matter,our work opens up new avenues for the future study of electronic correlations exclusively within the framework of DFT for a host of applications.
基金supported by grants from NIH T32(DK007260,to WC)the Steno North American Fellowship awarded by the Novo Nordisk Foundation(NNF23OC0087108,to WC)+6 种基金STI2030-Major Projects(2021ZD0202700,to HY)the National Natural Science Foundation of China(32241004,to HY)the Natural Science Foundation of Zhejiang Province of China(LR24C090001,to HY)Key R&D Program of Zhejiang Province(2024SSYS0017,to HY)CAMS Innovation Fund for Medical Sciences(2019-12M-5-057,to HY)Fundamental Research Funds for the Central Universities(226-2022-00193,to HY)the Non-profit Central Research Institute Fund of Chinese Academy of Medical Sciences(2023-PT310-01,to HY)。
文摘Type 2 diabetes mellitus has central complications:Diabetes,a metabolic disorder primarily characterized by hyperglycemia due to insufficient insulin secretion,or impaired insulin signaling,has significant central complications.Type 2 diabetes mellitus(T2DM),the most prevalent type of diabetes,affects more than 38 million individuals in the United States(approximately 1 in 10)and is defined by chronic hyperglycemia and insulin resistance,which refers to a reduced cellular response to insulin.
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Self-Centering Piston-Based Braced Frames(SC-PBBFs)are designed to curtail structural damage under severe ground motions.The self-centering mechanism in this bracing mitigates structural damage during an earthquake,thereby reducing post-earthquake repair costs and contributing to seismic resilience.However,non-structural components,particularly those sensitive to floor acceleration,remain vulnerable,resulting in prolonged func-tional recovery times.This paper aims to address this limitation by introducing a novel structural archetype,the Self-Centering Viscous-Based Braced Frame(SC-VBBF),which integrates superelastic shape memory alloy(SMA)bars,viscous dampers(VDs),and friction springs(FSs).A streamlined analytical approach relies on the strength decoupling of VD from other components using aλfactor to design SC-VBBFs.To evaluate the effectiveness of the hybrid brace,a set of 4-,8-,and 12-story archetypes equipped with SC-PBBs and SC-VBBFs are simulated in OpenSees and analyzed under various earthquake types,including crustal,subcrustal,and subduction events.The results demonstrate the superior performance of the SC-VBBF withλ≤0.5 system compared to SC-PBBFs in mitigating floor accelerations under design-level earthquakes and improving seismic resilience.
基金funded by the Science and Technology Research of Henan Province,No.242103810041(to JY)。
文摘For diverse neurodegenerative disorders,microglial cells are activated.Furthermore,dysfunctional and hyperactivated microglia initiate mitochondrial autophagy,oxidative stress,and pathological protein accumulation,ending with neuroinflammation that exacerbates damage to dopaminergic neurons and contributes significantly to the pathology of neurodegenerative disorder.Microglial overactivation is closely associated with the secretion of pro-inflammatory cytokines,the phagocytosis of injured neurons,and the modulation of neurotoxic environments.This review summarizes the role of microglia neurodegenerative diseases,such as Alzheimer's disease,Parkinson's disease,multiple sclerosis,multiple system atrophy,amyotrophic lateral sclerosis,frontotemporal dementia,progressive supranuclear palsy,cortical degeneration,Lewy body dementia,and Huntington's disease.It also discusses novel forms of cell death such as ferroptosis,cuproptosis,disulfidptosis,and parthanatos(poly(adenosine diphosphate ribose)polymerase 1-dependent cell death),as well as the impact of regulatory factors related to microglial inflammation on microglial activation and neuroinflammation.The aim is to identify potential targets for microglial cell therapy in neurodegenerative diseases.
基金supported by the National Natural Science Foundation of China,No.82160255(to RX)the Natural Science Foundation of Jiangxi Province,No.20212BAB216026(to HL)+2 种基金Science and Technology Plan Project of Health Commission of Jiangxi Province,No.202110016(to HL)Science and Technology Plan Project of Jiangxi Provincial Administration of Traditional Chinese Medicine,No.2022B975(to HL)a grant from Jiangxi Province Key Laboratory of Neurology,No.2024SSY06081(to RX).
文摘With the gradual advancement of research methods and technologies,various biological processes have been identified as playing roles in the pathogenesis of neurodegenerative diseases.However,current descriptions of these biological processes do not fully explain the onset,progression,and development of these conditions.Therefore,exploration of the pathogenesis of neurodegenerative diseases remains a valuable area of research.This review summarizes the potential common pathogeneses of Alzheimer’s disease,Parkinson’s disease,amyotrophic lateral sclerosis,Huntington’s disease,frontotemporal lobar dementia,and Lewy body disease.Research findings have indicated that several common biological processes,including aging,genetic factors,progressive neuronal dysfunction,neuronal death and apoptosis,protein misfolding and aggregation,neuroinflammation,mitochondrial dysfunction,axonal transport defects,and gut microbiota dysbiosis,are involved in the pathogenesis of these six neurodegenerative diseases.Based on current information derived from diverse areas of research,these biological processes may form complex pathogenic networks that lead to distinctive types of neuronal death in neurodegenerative diseases.Furthermore,promoting the regeneration of damaged neurons may be achievable through the repair of affected neural cells if the underlying pathogenesis can be prevented or reversed.Hence,these potential common biological processes may represent only very small,limited elements within numerous intricate pathogenic networks associated with neurodegenerative diseases.In clinical treatment,interfering with any single biological process has proven insufficient to completely halt the progression of neurodegenerative diseases.Therefore,future research on the pathogenesis of neurodegenerative diseases should focus on uncovering the complex pathogenic networks,rather than isolating individual biological processes.Based on this,therapies that aim to block or reverse various targets involved in the potential pathogenic mechanisms of neurodegenerative diseases may be promising directions,as current treatment methods that focus on halting a single pathogenic factor have not achieved satisfactory efficacy.
文摘Lysosomal storage disorders and their impact upon the central nervous system:Lysosomal storage disorders(LSDs)are a group of over 70 rare inherited metabolic disorders(Platt et al.,2018).They are caused by dysfunction of lysosomes,organelles that contain enzymes responsible for digesting macromolecules.In functional lysosomes,these enzymes break down complex substrates,and the resulting fragments are recycled.Individual LSDs are caused by mutations in genes that encode lysosomal enzymes or other proteins crucial for lysosome function(Platt et al.,2018).
基金funded by a grant from the National Natural Science Foundation of China(82572785,82172489,82172449)funding for young investigators of PLA(2022-JCJQ-QT-004)。
文摘Estrogen deficiency after menopause accelerates bone loss by stimulating osteoclast formation and activity,but the molecular pathways that link estrogen signaling to osteoclast regulation remain incompletely defined.Here,we identify the sialyltransferase ST3GAL-I as a key mediator of RANKL-induced osteoclastogenesis.RANKL activates c-FOS to drive ST3GAL1 transcription,whereas estrogen-bound ERαcompetes with TRAF6 and suppresses this c-FOS–dependent induction.In a clinical cohort of pre-menopausal and post-menopausal women with or without osteoporosis,serum total andα-2,3-linked sialic acid levels increased with age and were highest in post-menopausal osteoporotic patients.Single-cell RNA sequencing of human bone revealed that osteoclasts form a prominent cluster only after menopause,where FOS,CTSK,and ST3GAL1 are strongly co-expressed,and the estrogen-responsive gene PGR is down-regulated.Additionally,in vivo experiments showed that sialidase treatment in estrogen-deficient models effectively reduced osteoclast-mediated bone loss,mimicking the effects of estradiol.These findings define a direct molecular link between loss of estrogen and activation of a FOS–ST3GAL1 sialylation pathway in osteoclasts,providing mechanistic insight into the enhanced bone resorption characteristic of post-menopausal osteoporosis.
文摘This letter reports a gravitational redshift measurement experiment using a satellite-based compact passive hydrogen maser(PHM)in a lunar distant retrograde orbit(DRO).In March 2024,the Chinese Academy of Sciences launched the DRO-A/B twin satellites,which entered a DRO in July 2024.This orbit has a geocentric distance of approximately 300,000–450,000 kilometers and a 2:1 resonance ratio.Employing microwave dual one-way ranging(DOWR),satellite-ground time-frequency comparisons were successfully achieved in April 2025 using the PHM aboard the DRO-A satellite.This study validated the in-orbit performance of the compact PHM and supported tests of the Einstein Equivalence Principle.The gravitational redshift measurement result is(8.74±4.17)×10^(−3).As the world’s first fundamental physics experiment to deploy PHMs in a lunar DRO,this study provides significant new engineering approaches for testing gravitational theories in cislunar space.
基金supported by the National Natural Science Foundation of China(grant numbers 81771047 to J.X.,11932014,12372315 to X.L.,and 82273837 to L.S.)Sichuan Science and Technology Innovation Talent Project(2022JDRC0044)。
文摘Cells actively sense and transduce microenvironmental mechanical inputs into chemical signals via cytoskeletal rearrangements.During these mechanosensation and mechanotransduction processes,the role of the actin cytoskeleton is well-understood,whereas the role of the tubulin cytoskeleton remains largely elusive.Here,we report the dynamic changes in microtubules in response to microenvironmental stiffness during chondrocyte mitosis.Mechanical stiffness was found to be coupled with microtubule generation,directing microtubule dynamics in mitotic chondrocytes.Refilin B was found to be a key regulator of microtubule assembly in chondrocytes in response to mechanical stiffness.It was found to play its role in microtubule formation via the p-Smad3 signaling pathway.Additionally,integrin-linked kinase(ILK),triggered by mechanical stiffness,was found to play an indispensable role in the process of microtubule dynamics mediated by refilin B.Our data emphasizes stiffness-mediated dynamic changes in the microtubules of chondrocytes in a quiescent state(G0)and at anaphase,which improves our understanding of the mechanical regulation of microtubule assembly during the chondrocyte cell cycle and provides insights into microenvironment mechanics during tissue maintenance,wound healing,and disease occurrence.
文摘Predicting the behavior of renewable energy systems requires models capable of generating accurate forecasts from limited historical data,a challenge that becomes especially pronounced when commissioning new facil-ities where operational records are scarce.This review aims to synthesize recent progress in data-efficient deep learning approaches for addressing such“cold-start”forecasting problems.It primarily covers three interrelated domains—solar photovoltaic(PV),wind power,and electrical load forecasting—where data scarcity and operational variability are most critical,while also including representative studies on hydropower and carbon emission prediction to provide a broader systems perspective.To this end,we examined trends from over 150 predominantly peer-reviewed studies published between 2019 and mid-2025,highlighting advances in zero-shot and few-shot meta-learning frameworks that enable rapid model adaptation with minimal labeled data.Moreover,transfer learning approaches combined with spatiotemporal graph neural networks have been employed to transfer knowledge from existing energy assets to new,data-sparse environments,effectively capturing hidden dependencies among geographic features,meteorological dynamics,and grid structures.Synthetic data generation has further proven valuable for expanding training samples and mitigating overfitting in cold-start scenarios.In addition,large language models and explainable artificial intelligence(XAI)—notably conversational XAI systems—have been used to interpret and communicate complex model behaviors in accessible terms,fostering operator trust from the earliest deployment stages.By consolidating methodological advances,unresolved challenges,and open-source resources,this review provides a coherent overview of deep learning strategies that can shorten the data-sparse ramp-up period of new energy infrastructures and accelerate the transition toward resilient,low-carbon electricity grids.
文摘I offer suggestions to increase the probability of success of an international research project.Collaborative studies often produce more innovative and transformative scientific results than work done by a single investigator or an isolated team.My advice is intended for early-career scientists.The product of the collaboration may be high-impact research publications,enhanced geophysical monitoring capabilities in a foreign country,or an advanced training course.Choosing the right international partner is the most important step.Keeping an open mind and being receptive to suggestions to modify the initial concept is critical.Other key steps include having a mutually agreed upon plan with achievable goals and well-defined expected outcomes.International cooperation is a richly rewarding experience that accelerates progress in the Earth Sciences.
基金supported by the National Key Research and Development Program of China,No.2023YFC3603705(to DX)the National Natural Science Foundation of China,No.82302866(to YZ).
文摘After spinal cord injury,impairment of the sensorimotor circuit can lead to dysfunction in the motor,sensory,proprioceptive,and autonomic nervous systems.Functional recovery is often hindered by constraints on the timing of interventions,combined with the limitations of current methods.To address these challenges,various techniques have been developed to aid in the repair and reconstruction of neural circuits at different stages of injury.Notably,neuromodulation has garnered considerable attention for its potential to enhance nerve regeneration,provide neuroprotection,restore neurons,and regulate the neural reorganization of circuits within the cerebral cortex and corticospinal tract.To improve the effectiveness of these interventions,the implementation of multitarget early interventional neuromodulation strategies,such as electrical and magnetic stimulation,is recommended to enhance functional recovery across different phases of nerve injury.This review concisely outlines the challenges encountered following spinal cord injury,synthesizes existing neurostimulation techniques while emphasizing neuroprotection,repair,and regeneration of impaired connections,and advocates for multi-targeted,task-oriented,and timely interventions.
基金supported by the National Natural Science Foundational of China(Key Program),No.U24A20692(to CJZ)the National Natural Science Foundational of China,Nos.82101414(to MLJ),82371355(to CJZ)+4 种基金the National Natural Science Foundational of China for Excellent Young Scholars,No.82022019(to CJZ)Sichuan Special Fund for Distinguished Young Scholars,No.24NSFJQ0052(to CJZ)The Innovation and Entrepreneurial Team of Sichuan Tianfu Emei Program,No.CZ2024018(to CJZ)Funding for Distinguished Young Scholars of Sichuan Provincial People’s Hospital,No.30420230005(to CJZ)Funding for Distinguished Young Scholars of University of Electronic Science and Technology of China,No.A1098531023601381(to CJZ)。
文摘The interleukin-17 family is the key group of cytokines and displays a broad spectrum of biological functions,including regulating the inflammatory cascade in various autoimmune and inflammatory diseases,such as multiple sclerosis,neuromyelitis optica spectrum disorder,myasthenia gravis,Guillain–Barre syndrome,acute disseminated encephalomyelitis,diabetes,inflammatory skin diseases,joint inflammation,and cancer.Although the function of the interleukin-17 family has attracted increasing research attention over many years,the expression,function,and regulation mechanisms of different interleukin-17 members are complicated and still only partially understood.Currently,the interleukin-17A pathway is considered a critical therapeutic target for numerous immune and chronic inflammatory diseases,with several monoclonal antibodies against interleukin-17A having been successfully used in clinical practice.Whether other interleukin-17 members have the potential to be targeted in other diseases is still debated.This review first summarizes the recent advancements in understanding the physicochemical properties,physiological functions,cellular origins,and downstream signaling pathways of different members and corresponding receptors of the interleukin-17 family.Subsequently,the function of interleukin-17 in various immune diseases is discussed,and the important role of interleukin-17 in the pathological process of immune diseases is demonstrated from multiple perspectives.Then,the current status of targeted interleukin-17 therapy is summarized,and the effectiveness and safety of targeted interleukin-17 therapy are analyzed.Finally,the clinical application prospects of targeting the interleukin-17 pathway are discussed.
文摘The China-ASEAN Free Trade Area(CAFTA)3.0Upgrade Protocol added a section on“Supply Chain Connectivity,”which emphasizes that all parties recognize the lessons learned from the COVID-19 pandemic and cooperate to enhance the resilience of the regional supply chain.This is an inevitable trend amid the current accelerated restructuring of the global supply chain,the complex and severe international economic and trade situation,and the impact on the regional industrial chain.It also represents a fundamental shift and consensus on the logic of supply chain cooperation between China and ASEAN countries—a transformation from“Efficiency First”to“Resilience First.”
基金Supported by the National Natural Science Foundation of China(No.82388101,No.81930024)the Science and Technology Commission of Shanghai(No.22YS1400400,No.20DZ2270800).
文摘Dear Editor,Idiopathic orbital inflammation(IOI),also known as orbital inflammatory pseudotumor,is a relatively common orbital disorder[1].Its pathogenesis remains unclear,often regarded as a nonspecific immune-mediated response[2].IOI presents with symptoms such as pain,photophobia,proptosis,eyelid swelling,edema,conjunctival congestion,and diplopia,with possible vision loss occurring in some cases.Based on the soft tissue structures involved,IOI can be classified into subtypes such as myositis,optic neuritis,dacryoadenitis,diffuse orbital inflammation,and orbital inflammatory masses[2].
