To meet some special requirements such as paper filler,ceramic titanium white and synthetic 4A zeolite, the raising whiteness of calcined kaolin has become more and more important. The calcined experiments were carrie...To meet some special requirements such as paper filler,ceramic titanium white and synthetic 4A zeolite, the raising whiteness of calcined kaolin has become more and more important. The calcined experiments were carried out with and without additive to increase the whiteness of calcined kaolin. Results show that additive of chloride (A) or oxides can obviously increase the whiteness of calcined kaolin. Meantime,the mechanisms of enhancing the whiteness of calcined kaolin were discussed.展开更多
A kind of enhancing mechanism of structural whiteness dependence on amorphous photonic crystal (APC) structure is introduced in this paper. In the glaze system composed of albite, kaolin, talc, calcite, quartz, titani...A kind of enhancing mechanism of structural whiteness dependence on amorphous photonic crystal (APC) structure is introduced in this paper. In the glaze system composed of albite, kaolin, talc, calcite, quartz, titanium dioxide and zinc oxide, the APC structure will be produced by using quartz as a variable to induce the phase separation. Under different polarities between Ti, Zn etc. and Siion, the separated spheres with the core-shell structure can be obtained and then make up opal-like APCs in the glaze layer. In addition to inner and outer layers of core-shell spheres, the calculated results of refractive indices clearly show the great difference between the particles and the matrix. As a result of different refractive indices, the multiple scatting of visible light plays a key rote in the structural whiteness. However, due to the decrease of the cationic content, APCs with the reverse opal structure would be formed in the interface between glaze and body. Ultimately, the glaze appearance reveals extremely high structural whiteness due to the special APC structure.展开更多
Intracerebral hemorrhage is the most dangerous subtype of stroke,characterized by high mortality and morbidity rates,and frequently leads to significant secondary white matter injury.In recent decades,studies have rev...Intracerebral hemorrhage is the most dangerous subtype of stroke,characterized by high mortality and morbidity rates,and frequently leads to significant secondary white matter injury.In recent decades,studies have revealed that gut microbiota can communicate bidirectionally with the brain through the gut microbiota–brain axis.This axis indicates that gut microbiota is closely related to the development and prognosis of intracerebral hemorrhage and its associated secondary white matter injury.The NACHT,LRR,and pyrin domain-containing protein 3(NLRP3)inflammasome plays a crucial role in this context.This review summarizes the dysbiosis of gut microbiota following intracerebral hemorrhage and explores the mechanisms by which this imbalance may promote the activation of the NLRP3 inflammasome.These mechanisms include metabolic pathways(involving short-chain fatty acids,lipopolysaccharides,lactic acid,bile acids,trimethylamine-N-oxide,and tryptophan),neural pathways(such as the vagus nerve and sympathetic nerve),and immune pathways(involving microglia and T cells).We then discuss the relationship between the activated NLRP3 inflammasome and secondary white matter injury after intracerebral hemorrhage.The activation of the NLRP3 inflammasome can exacerbate secondary white matter injury by disrupting the blood–brain barrier,inducing neuroinflammation,and interfering with nerve regeneration.Finally,we outline potential treatment strategies for intracerebral hemorrhage and its secondary white matter injury.Our review highlights the critical role of the gut microbiota–brain axis and the NLRP3 inflammasome in white matter injury following intracerebral hemorrhage,paving the way for exploring potential therapeutic approaches.展开更多
Neurodevelopmental processes represent a finely tuned interplay between genetic and environmental factors,shaping the dynamic landscape of the developing brain.A major component of the developing brain that enables th...Neurodevelopmental processes represent a finely tuned interplay between genetic and environmental factors,shaping the dynamic landscape of the developing brain.A major component of the developing brain that enables this dynamic is the white matter(WM),known to be affected in neurodevelopmental disorders(NDDs)(Rokach et al.,2024).WM formation is mediated by myelination,a multifactorial process driven by neuro-glia interactions dependent on proper neuronal functionality(Simons and Trajkovic,2006).Another key aspect of neurodevelopmental abnormalities involves neuronal dynamics and function,with recent advances significantly enhancing our understanding of both neuronal and glial mitochondrial function(Devine and Kittler,2018;Rojas-Charry et al.,2021).Energy homeostasis in neurons,attributed largely to mitochondrial function,is critical for proper functionality and interactions with oligodendrocytes(OLs),the cells forming myelin in the brain’s WM.We herein discuss the interplay between these processes and speculate on potential dysfunction in NDDs.展开更多
Beer is a prominent fermented food product and is regarded as the one of most widely consumed beverage globally.There is a dearth of studies examining the impact of different types of beer with intricate components as...Beer is a prominent fermented food product and is regarded as the one of most widely consumed beverage globally.There is a dearth of studies examining the impact of different types of beer with intricate components as a comprehensive intervention on human health and immune status.This study used a 14-day continuous drinking intervention consisting of 5 beers,namely white beer,India pale ale(IPA),Pilsner,non-alcoholic beer,and premium lager beer.Surprisingly,our findings indicate that consuming white beer has little impact on the gut microbiota and physiological condition of mice,whereas consuming other types of beer leads to an increase in Lactobacillus and a decrease in Lachnospiraceae.In addition,we devised an extended feeding experiment to investigate the comparative safety and health benefits of consuming white beer.The research showed that when mice drank excessive quantities of white beer over 42 days,the intestines of the mice had more Prevotellaceae and the Firmicutes to Bacteroidetes ratio(F/B ratio)had a decline from 1.29 to 0.38.The levels of acetic acid,propionic acid,and isobutyric acid increased from 1.0,0.27,and 0.015 mg/g to 1.28,0.38,and 0.037 mg/g,respectively(P<0.05).There were no significant changes observed in the levels of most measured cytokines in the colon tissue of mice that consumed beer,however,there was an increase in the concentration of the inflammatory factor tumor nesrosis factor-α(TNF-α)from 135.86 pg/mL in the control group to 189.78 pg/mL in the white beer group(P<0.01).These results give us real-world proof that we can use to study how different beers affect the host’s health and satisfaction in future research.展开更多
Aconitines are a group of highly bioactive and toxic compounds found in aconitum species.[1]It is clinically used to treat rheumatism,rheumatoid arthritis,osteoarthritis,and cancer.[2]In folk medicine,aconitine is oft...Aconitines are a group of highly bioactive and toxic compounds found in aconitum species.[1]It is clinically used to treat rheumatism,rheumatoid arthritis,osteoarthritis,and cancer.[2]In folk medicine,aconitine is often soaked in white wine to make medicinal wine,which is used to treat rheumatism,joint pain,and other diseases.[3]Improper use of aconitine can cause adverse effects in the nervous system and digestive system,as well as cardiovascular dysfunction,especially arrhythmia.[4]Because of its high toxicity when it is improperly handled,aconitine has attracted widespread attention.展开更多
β-glucocerebrosidase in health and disease:Mutations in theβ-glucocerebrosidase(GBA)gene do cause the rare lysosomal storage disorder Gaucher’s disease(GD)with an estimated global prevalence of 1:200,000(Imbalzano ...β-glucocerebrosidase in health and disease:Mutations in theβ-glucocerebrosidase(GBA)gene do cause the rare lysosomal storage disorder Gaucher’s disease(GD)with an estimated global prevalence of 1:200,000(Imbalzano et al.,2024).GBA is a membrane-bound lysosomalenzyme responsible for glucosylceramide and glucosylsphingosine hydrolysis.When this enzyme is mutated and dysfunctional,its substrates progressively accumulate within cells.展开更多
White-nose syndrome(WNS)has caused recent catastrophic declines among multiple species of bats in eastern North America.The disease's name derives from a visually apparent white growth of the newly discovered fung...White-nose syndrome(WNS)has caused recent catastrophic declines among multiple species of bats in eastern North America.The disease's name derives from a visually apparent white growth of the newly discovered fungus Geomyces destructans on the skin(including the muzzle)of hibernating bats.Colonization of skin by this fungus is associated with characteristic cutaneous lesions that are the only consistent pathological finding related to WNS.However,the role of G.destructans in WNS remains controversial because evidence to implicate the fungus as the primary cause of this disease is lacking.The debate is fuelled,in part,by the assumption that fungal infections in mammals are most commonly associated with immune system dysfunction.Additionally,the recent discovery that G.destructans commonly colonizes the skin of bats of Europe,where no unusual bat mortality events have been reported,has generated further speculation that the fungus is an opportunistic pathogen and that other unidentified factors are the primary cause of WNS.展开更多
The Shanghai High Repetition Rate XFEL and Extreme Light Facility(SHINE)is currently under construction as one of the world’s most advanced hard X-ray free-electron laser facilities.The timing system,as an essential ...The Shanghai High Repetition Rate XFEL and Extreme Light Facility(SHINE)is currently under construction as one of the world’s most advanced hard X-ray free-electron laser facilities.The timing system,as an essential part of the free-electron laser facility,provides precise timing of trigger pulse signals for a range of devices to ensure that particles are generated and accelerated to the designed energy while enabling the precise measurement of beam parameters.To precisely distribute and synchronize the 1.003086 MHz(1300/1296)timing signals over a distance of approximately 3.1 km based on White Rabbit technology,three technical routes have been proposed.This paper begins with a description of the design and development process of the timing system for the SHINE project,which culminates with the determination of the design scheme.During the installation and commissioning of the timing system,the jitter accuracy of the timing signal was tested and found to be less than 10 ps,which meets the requirements of the project.Furthermore,the precise clock synchronization signal provided by the timing system supported the joint debugging of various related systems and realization of beam acquisition.展开更多
Biopolymeric nanocomposites have attracted considerable attention because of their biocompatibility,biodegradability,and unique physicochemical properties.It is essential to manufacture three-dimensional(3D)biocompati...Biopolymeric nanocomposites have attracted considerable attention because of their biocompatibility,biodegradability,and unique physicochemical properties.It is essential to manufacture three-dimensional(3D)biocompatible micro/nanostructures using biopolymeric nanocomposites.Herein,we demonstrate the high-fidelity fabrication of biocompatible 3D features with sub-50 nm resolution using femtosecond laser direct writing(FsLDW)of a biopolymeric nanocomposite composed of egg white and sulfonated graphene(S-graphene).The biopolymer nanocomposite acts as a negative photoresist suitable for water-based lithography.The introduction of S-graphene not only dramatically lowered the laser power threshold but also significantly modulated the morphology of the 3D features constructed by FsLDW.Microstructures with porous,rough,or smooth morphologies were obtained by optimizing the S-graphene concentration and laser scanning speed.The fabricated egg-white/S-graphene microstructures exhibited biocompatibility and environmental degradability.Egg white/S-graphene was also employed to fabricate diffractive gratings with superior optical quality.This study provides a promising method to manufacture biocompatible 3D features with controllable morphology,which has potential applications in biological and photonic fields.展开更多
Chronic cerebral hypoperfusion can lead to neuronal necrosis,trigger inflammatory responses,promote white matter damage,and ultimately result in cognitive impairment.Consequently,chronic cerebral hypoperfusion is an i...Chronic cerebral hypoperfusion can lead to neuronal necrosis,trigger inflammatory responses,promote white matter damage,and ultimately result in cognitive impairment.Consequently,chronic cerebral hypoperfusion is an important factor influencing the onset and progression of vascular dementia.The myelin sheath is a critical component of white matter,and damage and repair of the white matter are closely linked to myelin sheath integrity.This article reviews the role of microglia in vascular dementia,focusing on their effects on myelin sheaths and the potential therapeutic implications.The findings suggest that ischemia and hypoxia cause disruption of the blood-brain barrier and activate microglia,which may worsen blood-brain barrier damage through the release of matrix-degrading enzymes.Microglia-mediated metabolic reprogramming is recognized as an important driver of inflammation.Damage to the blood-brain barrier and subsequent inflammation can lead to myelin injury and accelerate the progression of vascular dementia.Early activation of microglia is a protective response that contributes to the maintenance of blood-brain barrier integrity through sensing,debris-clearing,and defensive mechanisms.However,prolonged activation can trigger a shift in microglia toward the pro-inflammatory M1 phenotype,resulting in myelin damage and cognitive impairment.Triggering receptor expressed on myeloid cells 2 and triggering receptor expressed on myeloid cells 1 have been identified as potential biomarkers for vascular dementia,as both are closely linked to cognitive decline.Although effective clinical treatments for myelin damage in the central nervous system are currently lacking,researchers are actively working to develop targeted therapies.Several drugs,including nimodipine,dopaminergic agents,simvastatin,biotin,and quetiapine,have been evaluated for clinical use in treating microglial and myelin damage.Future research will face challenges in developing targeted therapeutic strategies for vascular dementia,requiring further investigation into the timing,duration,and specific mechanisms of microglial activation,as well as the exploration of new drug combinations and additional therapeutic targets.展开更多
Stars getting close enough to black holes(BHs)can be torn apart by strong tidal forces,producing electromagnetic flares.To date,more than 100 tidal disruption events(TDEs)have been observed,each involving invariably n...Stars getting close enough to black holes(BHs)can be torn apart by strong tidal forces,producing electromagnetic flares.To date,more than 100 tidal disruption events(TDEs)have been observed,each involving invariably normal gaseous stars whose debris falls onto the BH,sustaining the flares over years.White dwarfs(WDs),which are the most prevalent compact stars and a million times denser-and therefore tougher-than gaseous stars,can only be disrupted by intermediate-mass black holes(IMBHs)of 10^(2)–10^(5) solar masses.WD-TDEs are considered to generate more powerful and short-lived flares,but their evidence has been lacking.Here we report observations of a fast and luminous X-ray transient EP250702a detected by Einstein Probe.Its one-day-long X-ray peak as luminous as 10^(47−49) erg s^(−1) showed strong recurrent flares with hard spectra extending to several tens of MeV gamma-rays,as detected by Fermi/GBM and Konus-Wind,indicating relativistic jet emission.The jet's X-rays dropped sharply from 3×10^(49) erg s^(−1) to around 1044 erg s^(−1) within 20 days(10 days in the source rest frame).These characteristics are inconsistent with any previously known transient phenomena.We suggest that this fast-evolving event over the unprecedentedly short timescale arises likely from disruption of a WD by an IMBH.At late times,a soft component progressively dominates the X-ray spectrum,reaching a luminosity as high as 1044 erg s^(−1),which is consistent with being extreme super-Eddington emission from an accretion disk expected to form in an IMBH-WD TDE.WD-TDEs open a new window for investigating the elusive IMBHs and their surrounding stellar environments,and they are prime sources of gravitational waves in the band of space-based interferometers.展开更多
Regulatory T cells are crucial immunomodulatory cells that play essential roles in both ischemic stroke and intracerebral hemorrhage.These cells are vital in post-stroke inflammation since they suppress immune respons...Regulatory T cells are crucial immunomodulatory cells that play essential roles in both ischemic stroke and intracerebral hemorrhage.These cells are vital in post-stroke inflammation since they suppress immune responses and promote tissue repair.This review thoroughly examines the dynamic changes in the number and function of regulatory T cells and highlights their distinct roles at various stages of stroke progression.In the acute phase(within 5-7 days),regulatory T cells exert neuroprotective effects primarily by reducing inflammation.In the chronic phase(7 days post-onset),these cells support neuroregeneration and functional recovery.The review also explores the emerging role of regulatory T cells in the brain-gut axis,a key mediator of the systemic immune responses following stroke,and discusses its relevance in modulating post-stroke inflammation and repair.Various strategies aimed at enhancing regulatory T cell responses include adoptive transfer of regulatory T cells,administration of pharmacological agents,and induction of mucosal tolerance.All these approaches can potentially enhance the immunomodulatory and repair functions of regulatory T cells.Nevertheless,despite the promising preclinical results,the translation of regulatory T cell-based therapies into clinical practice is associated with challenges related to optimal timing,dosage,and long-term efficacy.Overall,targeting regulatory T cells is a novel and promising immunoregulatory approach for mitigating stroke-induced injury and promoting neural repair.展开更多
Cerebral small vessel disease is a major vascular contributor to cognitive impairment and dementia.However,there remains a lack of effective preventative or therapeutic regimens for cerebral small vessel disease.In th...Cerebral small vessel disease is a major vascular contributor to cognitive impairment and dementia.However,there remains a lack of effective preventative or therapeutic regimens for cerebral small vessel disease.In this study,we investigated the potential therapeutic effects of MCC950,a selective NOD-like receptor family pyrin domain-containing protein 3 inhibitor,on cerebral small vessel disease pathogenesis and cognitive decline in spontaneously hypertensive rats.Our results showed that chronic administration of MCC950(10 mg/kg)to spontaneously hypertensive rats inhibited NOD-like receptor family pyrin domain-containing protein 3 inflammasome activation,thereby considerably suppressing the production of pyroptosis executive protein gasdermin D and pro-inflammatory factors,including interleukin-1βand-18.A decrease in astrocytic and microglial activation was also observed.We also found that MCC950 significantly inhibited autophagy.More importantly,behavioral assessment indicated that MCC950 administration ameliorated impaired neurocognitive function,which was associated with improvements in neuropathological hallmarks in the cerebral small vessel disease brain,such as blood‒brain barrier breakdown,white matter damage,and endothelial dysfunction.Thus,our findings revealed that the NOD-like receptor family pyrin domain-containing protein 3 inflammasome is a key contributor to the onset or progression of cerebral small vessel disease and suggested the potential of NOD-like receptor family pyrin domain-containing protein 3-based therapy as a potential novel strategy for treating cerebral small vessel disease.展开更多
Blue calico,which dates back more than 800 years,is a traditional blue-and-white-printed fabric in Nantong,a city in East China's Jiangsu Province.Blue calico is renowned for its simple,yet elegant,patterns,the st...Blue calico,which dates back more than 800 years,is a traditional blue-and-white-printed fabric in Nantong,a city in East China's Jiangsu Province.Blue calico is renowned for its simple,yet elegant,patterns,the striking beauty of its blue-and-white harmony and,especially,for its printing and dyeing being performed by hand.展开更多
Germinal matrix hemorrhage in preterm neonates often leads to white matter injury,contributing to long-term neurodevelopmental impairments.As resident brain immune cells,microglia play a complex role in injury respons...Germinal matrix hemorrhage in preterm neonates often leads to white matter injury,contributing to long-term neurodevelopmental impairments.As resident brain immune cells,microglia play a complex role in injury response,including inflammation and repair.Although colony-stimulating factor 1 receptor inhibitors such as PLX5622 enable the selective depletion of microglia,their therapeutic potential in neonatal germinal matrix hemorrhage remains underexplored.Here,we used a collagenase-induced germinal matrix hemorrhage model in postnatal day 5 mice,and intraperitoneally administered PLX562272 hours post-germinal matrix hemorrhage to achieve targeted,temporary microglial depletion during the peak injury response.We then assessed the effects of this delayed intervention on oligodendrocyte lineage cell maturation,white matter integrity,and neurobehavioral outcomes.Additionally,RNA sequencing data from a germinal matrix hemorrhage rat model were analyzed using weighted gene co-expression network analysis to identify the critical phases for interventions.RNA sequencing data revealed a critical period in which key synaptic functions declined while immune responses intensified post-germinal matrix hemorrhage,thus pinpointing the critical response phases for potential interventions.Delayed PLX5622 treatment effectively depleted activated microglia,protecting against white matter injury and enhancing oligodendrocyte lineage cell maturation and myelination in subcortical white matter regions.Moreover,magnetic resonance imaging analysis revealed reduced brain lesion volumes in treated mice.Behaviorally,PLX5622-treated mice exhibited significant improvements in motor coordination and reduced hyperactivity compared with vehicle-treated germinal matrix hemorrhage model mice.These findings suggest that,when timed to avoid interference with initial oligodendrocyte lineage cell proliferation,targeted microglial depletion with PLX5622 significantly mitigates white matter damage and improves neurobehavioral outcomes in neonatal germinal matrix hemorrhage.The present study highlights the therapeutic potential of selectively modulating microglial reactivity to support neurodevelopment in preterm infants with brain injury.展开更多
Myelin,made by oligodendrocytes(OLs)in the central nervous system(CNS),is essential for neural transmission.In particular,myelin facilitates communication across the long connections between different brain regions th...Myelin,made by oligodendrocytes(OLs)in the central nervous system(CNS),is essential for neural transmission.In particular,myelin facilitates communication across the long connections between different brain regions that form the white matter.Myelinated segments also provide metabolic intermediates to axons,supporting their demanding energetic needs.Genetic disorders that disrupt myelin formation result in progressive neurologic degeneration.展开更多
White matter injury is a key factor impacting stroke recovery.Physical exercise can promote white matter repair.Immune cells,especially regulatory T(Treg)cells,contribute to strengthening white matter integrity,yet li...White matter injury is a key factor impacting stroke recovery.Physical exercise can promote white matter repair.Immune cells,especially regulatory T(Treg)cells,contribute to strengthening white matter integrity,yet little is known about the underlying mechanism.To examine this,we established a transient middle cerebral artery occlusion male mouse model.We found that physical exercise elevated brain Treg cells,thereby enhancing neurological recovery,reducing neuroinflammation,promoting myelin debris clearance,and accelerating white matter repair.Depletion of Treg cells caused a decrease in these positive effects of physical exercise.Mechanistically,the rise in osteopontin triggered by physical exercise is dampened when Treg cells are depleted.In addition,Treg-conditioned medium reduced oxygen-glucose deprivation/re-oxygenation-induced microglial inflammation and enhanced phagocytosis,which could be blocked by osteopontin antibodies.Importantly,although Treg infusion could mimic the protective effects of physical exercise,osteopontin blockade partially countered the effects of physical exercise and Treg cells.Finally,our sequencing data revealed a marked upregulation of C-X-C motif chemokine ligand 12(CXCL12)mRNA expression subsequent to physical exercise,which was confirmed at the protein level.Stimulation of Treg cells with stroke brain lysates increased C-X-C motif chemokine receptor 4(CXCR4)expression,indicating a potential role for the CXCL12-CXCR4 axis in recruiting Treg cells.These findings suggest that physical exercise promotes white matter repair after ischemic stroke by Treg cells.展开更多
Spinal cord injury(SCI)interrupts the flow of information between the brain and the spinal cord,thus leading to a loss of sensory information and motor paralysis of the body below the lesion.Surprisingly,most SCIs are...Spinal cord injury(SCI)interrupts the flow of information between the brain and the spinal cord,thus leading to a loss of sensory information and motor paralysis of the body below the lesion.Surprisingly,most SCIs are incomplete and spare supraspinal pathways,especially those located within the peripheral white matter of the spinal cord,which includes reticulospinal pathways originating from the medullary reticular formation.Whereas there is abundant literature about the motor cortex,its corticospinal pathway,and its capacity to modulate functional recovery after SCI,less is known about the medullary reticular formation and its reticulospinal pathway.展开更多
Myelination,the continuous ensheathment of neuronal axons,is a lifelong process in the nervous system that is essential for the precise,temporospatial conduction of action potentials between neurons.Myelin also provid...Myelination,the continuous ensheathment of neuronal axons,is a lifelong process in the nervous system that is essential for the precise,temporospatial conduction of action potentials between neurons.Myelin also provides intercellular metabolic support to axons.Even minor disruptions in the integrity of myelin can impair neural performance and increase susceptibility to neurological diseases.In fact,myelin degeneration is a well-known neuropathological condition that is associated with normal aging and several neurodegenerative diseases,including multiple sclerosis and Alzheimer’s disease.In the central nervous system,compact myelin sheaths are formed by fully mature oligodendrocytes.However,the entire oligodendrocyte lineage is susceptible to changes in the biological microenvironment and other risk factors that arise as the brain ages.In addition to their well-known role in action potential propagation,oligodendrocytes also provide intercellular metabolic support to axons by transferring energy metabolites and delivering exosomes.Therefore,myelin degeneration in the aging central nervous system is a significant contributor to the development of neurodegenerative diseases.Interventions that mitigate age-related myelin degeneration can improve neurological function in aging individuals.In this review,we investigate the changes in myelin that are associated with aging and their underlying mechanisms.We also discuss recent advances in understanding how myelin degeneration in the aging brain contributes to neurodegenerative diseases and explore the factors that can prevent,slow down,or even reverse age-related myelin degeneration.Future research will enhance our understanding of how reducing age-related myelin degeneration can be used as a therapeutic target for delaying or preventing neurodegenerative diseases.展开更多
文摘To meet some special requirements such as paper filler,ceramic titanium white and synthetic 4A zeolite, the raising whiteness of calcined kaolin has become more and more important. The calcined experiments were carried out with and without additive to increase the whiteness of calcined kaolin. Results show that additive of chloride (A) or oxides can obviously increase the whiteness of calcined kaolin. Meantime,the mechanisms of enhancing the whiteness of calcined kaolin were discussed.
基金the National Natural Science Foundation of China (Grant No. 21661017)the Natural Science Foundation of Jiangxi Province (Grant No. 20161B AB203081)the Foundation of Jiangxi Provincial Department of Education (Grant Nos. GJJ170795 and GJJ180718).
文摘A kind of enhancing mechanism of structural whiteness dependence on amorphous photonic crystal (APC) structure is introduced in this paper. In the glaze system composed of albite, kaolin, talc, calcite, quartz, titanium dioxide and zinc oxide, the APC structure will be produced by using quartz as a variable to induce the phase separation. Under different polarities between Ti, Zn etc. and Siion, the separated spheres with the core-shell structure can be obtained and then make up opal-like APCs in the glaze layer. In addition to inner and outer layers of core-shell spheres, the calculated results of refractive indices clearly show the great difference between the particles and the matrix. As a result of different refractive indices, the multiple scatting of visible light plays a key rote in the structural whiteness. However, due to the decrease of the cationic content, APCs with the reverse opal structure would be formed in the interface between glaze and body. Ultimately, the glaze appearance reveals extremely high structural whiteness due to the special APC structure.
基金supported by the Guangdong Basic and Applied Basic Research Foundation,No.2023A1515030045(to HS)Presidential Foundation of Zhujiang Hospital of Southern Medical University,No.yzjj2022ms4(to HS)。
文摘Intracerebral hemorrhage is the most dangerous subtype of stroke,characterized by high mortality and morbidity rates,and frequently leads to significant secondary white matter injury.In recent decades,studies have revealed that gut microbiota can communicate bidirectionally with the brain through the gut microbiota–brain axis.This axis indicates that gut microbiota is closely related to the development and prognosis of intracerebral hemorrhage and its associated secondary white matter injury.The NACHT,LRR,and pyrin domain-containing protein 3(NLRP3)inflammasome plays a crucial role in this context.This review summarizes the dysbiosis of gut microbiota following intracerebral hemorrhage and explores the mechanisms by which this imbalance may promote the activation of the NLRP3 inflammasome.These mechanisms include metabolic pathways(involving short-chain fatty acids,lipopolysaccharides,lactic acid,bile acids,trimethylamine-N-oxide,and tryptophan),neural pathways(such as the vagus nerve and sympathetic nerve),and immune pathways(involving microglia and T cells).We then discuss the relationship between the activated NLRP3 inflammasome and secondary white matter injury after intracerebral hemorrhage.The activation of the NLRP3 inflammasome can exacerbate secondary white matter injury by disrupting the blood–brain barrier,inducing neuroinflammation,and interfering with nerve regeneration.Finally,we outline potential treatment strategies for intracerebral hemorrhage and its secondary white matter injury.Our review highlights the critical role of the gut microbiota–brain axis and the NLRP3 inflammasome in white matter injury following intracerebral hemorrhage,paving the way for exploring potential therapeutic approaches.
文摘Neurodevelopmental processes represent a finely tuned interplay between genetic and environmental factors,shaping the dynamic landscape of the developing brain.A major component of the developing brain that enables this dynamic is the white matter(WM),known to be affected in neurodevelopmental disorders(NDDs)(Rokach et al.,2024).WM formation is mediated by myelination,a multifactorial process driven by neuro-glia interactions dependent on proper neuronal functionality(Simons and Trajkovic,2006).Another key aspect of neurodevelopmental abnormalities involves neuronal dynamics and function,with recent advances significantly enhancing our understanding of both neuronal and glial mitochondrial function(Devine and Kittler,2018;Rojas-Charry et al.,2021).Energy homeostasis in neurons,attributed largely to mitochondrial function,is critical for proper functionality and interactions with oligodendrocytes(OLs),the cells forming myelin in the brain’s WM.We herein discuss the interplay between these processes and speculate on potential dysfunction in NDDs.
基金financially supported by the National Key R&D Program of China(2022YFA1304103)Agricultural Scientific and Technological Innovation Project of Shandong Academy of Agricultural Sciences(CXGC2024A04)SKLMT Frontiers&Challenges Project.
文摘Beer is a prominent fermented food product and is regarded as the one of most widely consumed beverage globally.There is a dearth of studies examining the impact of different types of beer with intricate components as a comprehensive intervention on human health and immune status.This study used a 14-day continuous drinking intervention consisting of 5 beers,namely white beer,India pale ale(IPA),Pilsner,non-alcoholic beer,and premium lager beer.Surprisingly,our findings indicate that consuming white beer has little impact on the gut microbiota and physiological condition of mice,whereas consuming other types of beer leads to an increase in Lactobacillus and a decrease in Lachnospiraceae.In addition,we devised an extended feeding experiment to investigate the comparative safety and health benefits of consuming white beer.The research showed that when mice drank excessive quantities of white beer over 42 days,the intestines of the mice had more Prevotellaceae and the Firmicutes to Bacteroidetes ratio(F/B ratio)had a decline from 1.29 to 0.38.The levels of acetic acid,propionic acid,and isobutyric acid increased from 1.0,0.27,and 0.015 mg/g to 1.28,0.38,and 0.037 mg/g,respectively(P<0.05).There were no significant changes observed in the levels of most measured cytokines in the colon tissue of mice that consumed beer,however,there was an increase in the concentration of the inflammatory factor tumor nesrosis factor-α(TNF-α)from 135.86 pg/mL in the control group to 189.78 pg/mL in the white beer group(P<0.01).These results give us real-world proof that we can use to study how different beers affect the host’s health and satisfaction in future research.
基金supported by grants from the National Natural Science Foundation of China(82360387)the Key Laboratory of Emergency Medicine of Yunnan Province(202449CE340015).
文摘Aconitines are a group of highly bioactive and toxic compounds found in aconitum species.[1]It is clinically used to treat rheumatism,rheumatoid arthritis,osteoarthritis,and cancer.[2]In folk medicine,aconitine is often soaked in white wine to make medicinal wine,which is used to treat rheumatism,joint pain,and other diseases.[3]Improper use of aconitine can cause adverse effects in the nervous system and digestive system,as well as cardiovascular dysfunction,especially arrhythmia.[4]Because of its high toxicity when it is improperly handled,aconitine has attracted widespread attention.
基金funded by the AFM-Telethon Foundation (#28703)by the Italian Ministry of Education, University and Research (Grant P2022Y2A3L funded in the framework of NRRP, Mission 4.2, Investment 1.1 “progetti di ricerca di Rilevante Interesse Nazionale - PRIN”, funded by the European Union Next Generation EU, CUP C53D23007520001+2 种基金Grant P20227YB93, CUP C53D23003030001) (to MC)the activities of the National Center for Gene Therapy and Drugs based on RNA Technology, funded in the framework of the National Recovery and Resilience Plan (NRRP), Mission 4 “Education and Research”, Component 2 “From Research to Business”, Investment 1.4 “Strengthening research structures for supporting the creation of National Centres, national R&D leaders on some Key Enabling Technologies”funded by the European Union-Next Generation EU, Project CN00000041, CUP B93D21010860004, Spoke n. 5 “Inflammatory and infectious diseases” (to MC)
文摘β-glucocerebrosidase in health and disease:Mutations in theβ-glucocerebrosidase(GBA)gene do cause the rare lysosomal storage disorder Gaucher’s disease(GD)with an estimated global prevalence of 1:200,000(Imbalzano et al.,2024).GBA is a membrane-bound lysosomalenzyme responsible for glucosylceramide and glucosylsphingosine hydrolysis.When this enzyme is mutated and dysfunctional,its substrates progressively accumulate within cells.
文摘White-nose syndrome(WNS)has caused recent catastrophic declines among multiple species of bats in eastern North America.The disease's name derives from a visually apparent white growth of the newly discovered fungus Geomyces destructans on the skin(including the muzzle)of hibernating bats.Colonization of skin by this fungus is associated with characteristic cutaneous lesions that are the only consistent pathological finding related to WNS.However,the role of G.destructans in WNS remains controversial because evidence to implicate the fungus as the primary cause of this disease is lacking.The debate is fuelled,in part,by the assumption that fungal infections in mammals are most commonly associated with immune system dysfunction.Additionally,the recent discovery that G.destructans commonly colonizes the skin of bats of Europe,where no unusual bat mortality events have been reported,has generated further speculation that the fungus is an opportunistic pathogen and that other unidentified factors are the primary cause of WNS.
基金supported by SHINE and Shanghai Municipal Science and Technology Major Project(No.2017SHZDZX02).
文摘The Shanghai High Repetition Rate XFEL and Extreme Light Facility(SHINE)is currently under construction as one of the world’s most advanced hard X-ray free-electron laser facilities.The timing system,as an essential part of the free-electron laser facility,provides precise timing of trigger pulse signals for a range of devices to ensure that particles are generated and accelerated to the designed energy while enabling the precise measurement of beam parameters.To precisely distribute and synchronize the 1.003086 MHz(1300/1296)timing signals over a distance of approximately 3.1 km based on White Rabbit technology,three technical routes have been proposed.This paper begins with a description of the design and development process of the timing system for the SHINE project,which culminates with the determination of the design scheme.During the installation and commissioning of the timing system,the jitter accuracy of the timing signal was tested and found to be less than 10 ps,which meets the requirements of the project.Furthermore,the precise clock synchronization signal provided by the timing system supported the joint debugging of various related systems and realization of beam acquisition.
基金financially supported by the National Key Research and Development Program of China(Nos.2024YFB4607402 and 2016YFC1100502)the National Natural Science Foundation of China(Nos.51673208 and 61975213)。
文摘Biopolymeric nanocomposites have attracted considerable attention because of their biocompatibility,biodegradability,and unique physicochemical properties.It is essential to manufacture three-dimensional(3D)biocompatible micro/nanostructures using biopolymeric nanocomposites.Herein,we demonstrate the high-fidelity fabrication of biocompatible 3D features with sub-50 nm resolution using femtosecond laser direct writing(FsLDW)of a biopolymeric nanocomposite composed of egg white and sulfonated graphene(S-graphene).The biopolymer nanocomposite acts as a negative photoresist suitable for water-based lithography.The introduction of S-graphene not only dramatically lowered the laser power threshold but also significantly modulated the morphology of the 3D features constructed by FsLDW.Microstructures with porous,rough,or smooth morphologies were obtained by optimizing the S-graphene concentration and laser scanning speed.The fabricated egg-white/S-graphene microstructures exhibited biocompatibility and environmental degradability.Egg white/S-graphene was also employed to fabricate diffractive gratings with superior optical quality.This study provides a promising method to manufacture biocompatible 3D features with controllable morphology,which has potential applications in biological and photonic fields.
基金supported by the Natural Science Foundation of Beijing,No.7232279(to XW)the National Natural Science Foundation of China,No.U21A20400(to QW)Key Project of Beijing University of Chinese Medicine,Nos.2022-JYB-JBZR-004(to XW),2024-JYB-JBZD-043(to CL).
文摘Chronic cerebral hypoperfusion can lead to neuronal necrosis,trigger inflammatory responses,promote white matter damage,and ultimately result in cognitive impairment.Consequently,chronic cerebral hypoperfusion is an important factor influencing the onset and progression of vascular dementia.The myelin sheath is a critical component of white matter,and damage and repair of the white matter are closely linked to myelin sheath integrity.This article reviews the role of microglia in vascular dementia,focusing on their effects on myelin sheaths and the potential therapeutic implications.The findings suggest that ischemia and hypoxia cause disruption of the blood-brain barrier and activate microglia,which may worsen blood-brain barrier damage through the release of matrix-degrading enzymes.Microglia-mediated metabolic reprogramming is recognized as an important driver of inflammation.Damage to the blood-brain barrier and subsequent inflammation can lead to myelin injury and accelerate the progression of vascular dementia.Early activation of microglia is a protective response that contributes to the maintenance of blood-brain barrier integrity through sensing,debris-clearing,and defensive mechanisms.However,prolonged activation can trigger a shift in microglia toward the pro-inflammatory M1 phenotype,resulting in myelin damage and cognitive impairment.Triggering receptor expressed on myeloid cells 2 and triggering receptor expressed on myeloid cells 1 have been identified as potential biomarkers for vascular dementia,as both are closely linked to cognitive decline.Although effective clinical treatments for myelin damage in the central nervous system are currently lacking,researchers are actively working to develop targeted therapies.Several drugs,including nimodipine,dopaminergic agents,simvastatin,biotin,and quetiapine,have been evaluated for clinical use in treating microglial and myelin damage.Future research will face challenges in developing targeted therapeutic strategies for vascular dementia,requiring further investigation into the timing,duration,and specific mechanisms of microglial activation,as well as the exploration of new drug combinations and additional therapeutic targets.
文摘Stars getting close enough to black holes(BHs)can be torn apart by strong tidal forces,producing electromagnetic flares.To date,more than 100 tidal disruption events(TDEs)have been observed,each involving invariably normal gaseous stars whose debris falls onto the BH,sustaining the flares over years.White dwarfs(WDs),which are the most prevalent compact stars and a million times denser-and therefore tougher-than gaseous stars,can only be disrupted by intermediate-mass black holes(IMBHs)of 10^(2)–10^(5) solar masses.WD-TDEs are considered to generate more powerful and short-lived flares,but their evidence has been lacking.Here we report observations of a fast and luminous X-ray transient EP250702a detected by Einstein Probe.Its one-day-long X-ray peak as luminous as 10^(47−49) erg s^(−1) showed strong recurrent flares with hard spectra extending to several tens of MeV gamma-rays,as detected by Fermi/GBM and Konus-Wind,indicating relativistic jet emission.The jet's X-rays dropped sharply from 3×10^(49) erg s^(−1) to around 1044 erg s^(−1) within 20 days(10 days in the source rest frame).These characteristics are inconsistent with any previously known transient phenomena.We suggest that this fast-evolving event over the unprecedentedly short timescale arises likely from disruption of a WD by an IMBH.At late times,a soft component progressively dominates the X-ray spectrum,reaching a luminosity as high as 1044 erg s^(−1),which is consistent with being extreme super-Eddington emission from an accretion disk expected to form in an IMBH-WD TDE.WD-TDEs open a new window for investigating the elusive IMBHs and their surrounding stellar environments,and they are prime sources of gravitational waves in the band of space-based interferometers.
基金supported by National Key R&D Program:Key Special Project on Research for the Prevention and Treatment of Common Diseases-2022 Annual Project,Nos.2022YFC2504900,2022YFC2504902(both to ZL).
文摘Regulatory T cells are crucial immunomodulatory cells that play essential roles in both ischemic stroke and intracerebral hemorrhage.These cells are vital in post-stroke inflammation since they suppress immune responses and promote tissue repair.This review thoroughly examines the dynamic changes in the number and function of regulatory T cells and highlights their distinct roles at various stages of stroke progression.In the acute phase(within 5-7 days),regulatory T cells exert neuroprotective effects primarily by reducing inflammation.In the chronic phase(7 days post-onset),these cells support neuroregeneration and functional recovery.The review also explores the emerging role of regulatory T cells in the brain-gut axis,a key mediator of the systemic immune responses following stroke,and discusses its relevance in modulating post-stroke inflammation and repair.Various strategies aimed at enhancing regulatory T cell responses include adoptive transfer of regulatory T cells,administration of pharmacological agents,and induction of mucosal tolerance.All these approaches can potentially enhance the immunomodulatory and repair functions of regulatory T cells.Nevertheless,despite the promising preclinical results,the translation of regulatory T cell-based therapies into clinical practice is associated with challenges related to optimal timing,dosage,and long-term efficacy.Overall,targeting regulatory T cells is a novel and promising immunoregulatory approach for mitigating stroke-induced injury and promoting neural repair.
基金supported by the National Natural Science Foundation of China,No.82201626(to CC)the Natural Science Foundation of LiaoningProvince,No.2022-MS-442(to CC)the Dalian Municipal Medical Key Specialty Climbing Project,No.2024ZZ040(to MZ).
文摘Cerebral small vessel disease is a major vascular contributor to cognitive impairment and dementia.However,there remains a lack of effective preventative or therapeutic regimens for cerebral small vessel disease.In this study,we investigated the potential therapeutic effects of MCC950,a selective NOD-like receptor family pyrin domain-containing protein 3 inhibitor,on cerebral small vessel disease pathogenesis and cognitive decline in spontaneously hypertensive rats.Our results showed that chronic administration of MCC950(10 mg/kg)to spontaneously hypertensive rats inhibited NOD-like receptor family pyrin domain-containing protein 3 inflammasome activation,thereby considerably suppressing the production of pyroptosis executive protein gasdermin D and pro-inflammatory factors,including interleukin-1βand-18.A decrease in astrocytic and microglial activation was also observed.We also found that MCC950 significantly inhibited autophagy.More importantly,behavioral assessment indicated that MCC950 administration ameliorated impaired neurocognitive function,which was associated with improvements in neuropathological hallmarks in the cerebral small vessel disease brain,such as blood‒brain barrier breakdown,white matter damage,and endothelial dysfunction.Thus,our findings revealed that the NOD-like receptor family pyrin domain-containing protein 3 inflammasome is a key contributor to the onset or progression of cerebral small vessel disease and suggested the potential of NOD-like receptor family pyrin domain-containing protein 3-based therapy as a potential novel strategy for treating cerebral small vessel disease.
文摘Blue calico,which dates back more than 800 years,is a traditional blue-and-white-printed fabric in Nantong,a city in East China's Jiangsu Province.Blue calico is renowned for its simple,yet elegant,patterns,the striking beauty of its blue-and-white harmony and,especially,for its printing and dyeing being performed by hand.
基金supported by the National Key Research and Development Program of China,No.2022YFC2704801(to CZhu)the National Natural Science Foundation of China,Nos.U21A20347(to CZhu),82203969(to YX),82371472(to XZ)+3 种基金Health Commission of Henan Province,Nos.SBGJ202303039(to XZ),SBGJ202301009(to CZhu),YQRC2024018(to XZ),YQRC2024019(to YX)Henan Science and Technology Department,Nos.242102311054(to XZ),241111521300(to CZhu),GZS2023003(to XW)Swedish Research Council,Nos.2022-01019(to CZhu),2021-01950(to XW)Swedish Governmental Grants to Scientists Working in Healthcare,Nos.ALFGBG-1005209(to CZhu),ALFBG-1005257(to XW),ALFGBG-965197(to CZhu).
文摘Germinal matrix hemorrhage in preterm neonates often leads to white matter injury,contributing to long-term neurodevelopmental impairments.As resident brain immune cells,microglia play a complex role in injury response,including inflammation and repair.Although colony-stimulating factor 1 receptor inhibitors such as PLX5622 enable the selective depletion of microglia,their therapeutic potential in neonatal germinal matrix hemorrhage remains underexplored.Here,we used a collagenase-induced germinal matrix hemorrhage model in postnatal day 5 mice,and intraperitoneally administered PLX562272 hours post-germinal matrix hemorrhage to achieve targeted,temporary microglial depletion during the peak injury response.We then assessed the effects of this delayed intervention on oligodendrocyte lineage cell maturation,white matter integrity,and neurobehavioral outcomes.Additionally,RNA sequencing data from a germinal matrix hemorrhage rat model were analyzed using weighted gene co-expression network analysis to identify the critical phases for interventions.RNA sequencing data revealed a critical period in which key synaptic functions declined while immune responses intensified post-germinal matrix hemorrhage,thus pinpointing the critical response phases for potential interventions.Delayed PLX5622 treatment effectively depleted activated microglia,protecting against white matter injury and enhancing oligodendrocyte lineage cell maturation and myelination in subcortical white matter regions.Moreover,magnetic resonance imaging analysis revealed reduced brain lesion volumes in treated mice.Behaviorally,PLX5622-treated mice exhibited significant improvements in motor coordination and reduced hyperactivity compared with vehicle-treated germinal matrix hemorrhage model mice.These findings suggest that,when timed to avoid interference with initial oligodendrocyte lineage cell proliferation,targeted microglial depletion with PLX5622 significantly mitigates white matter damage and improves neurobehavioral outcomes in neonatal germinal matrix hemorrhage.The present study highlights the therapeutic potential of selectively modulating microglial reactivity to support neurodevelopment in preterm infants with brain injury.
基金support held by JPA,Collaborative Network Award BRAVEinMS,Grant/Award Number:PA-1604-08492(MG)from the Multiple Sclerosis Society of Canada,Grant/Award Number:1038154(to TEK).
文摘Myelin,made by oligodendrocytes(OLs)in the central nervous system(CNS),is essential for neural transmission.In particular,myelin facilitates communication across the long connections between different brain regions that form the white matter.Myelinated segments also provide metabolic intermediates to axons,supporting their demanding energetic needs.Genetic disorders that disrupt myelin formation result in progressive neurologic degeneration.
基金supported by the National Natural Science Foundation of China,Nos.82172546(to XH),82172547(to ZZ)the Natural ScienceFoundation of Guangdong Province,Nos.2023A1515012695(to XH),2024A1515010419(to ZZ)the Science and Technology Plan Project of Guangzhou,Nos.202201020413(to ZZ),2023A04J1099(to ZZ).
文摘White matter injury is a key factor impacting stroke recovery.Physical exercise can promote white matter repair.Immune cells,especially regulatory T(Treg)cells,contribute to strengthening white matter integrity,yet little is known about the underlying mechanism.To examine this,we established a transient middle cerebral artery occlusion male mouse model.We found that physical exercise elevated brain Treg cells,thereby enhancing neurological recovery,reducing neuroinflammation,promoting myelin debris clearance,and accelerating white matter repair.Depletion of Treg cells caused a decrease in these positive effects of physical exercise.Mechanistically,the rise in osteopontin triggered by physical exercise is dampened when Treg cells are depleted.In addition,Treg-conditioned medium reduced oxygen-glucose deprivation/re-oxygenation-induced microglial inflammation and enhanced phagocytosis,which could be blocked by osteopontin antibodies.Importantly,although Treg infusion could mimic the protective effects of physical exercise,osteopontin blockade partially countered the effects of physical exercise and Treg cells.Finally,our sequencing data revealed a marked upregulation of C-X-C motif chemokine ligand 12(CXCL12)mRNA expression subsequent to physical exercise,which was confirmed at the protein level.Stimulation of Treg cells with stroke brain lysates increased C-X-C motif chemokine receptor 4(CXCR4)expression,indicating a potential role for the CXCL12-CXCR4 axis in recruiting Treg cells.These findings suggest that physical exercise promotes white matter repair after ischemic stroke by Treg cells.
基金supported by Craig H.Neilsen Foundation,Wings for Life Foundation,Canadian Institutes of Health Research,and Fonds de Recherche Québec-Santé(to FB).
文摘Spinal cord injury(SCI)interrupts the flow of information between the brain and the spinal cord,thus leading to a loss of sensory information and motor paralysis of the body below the lesion.Surprisingly,most SCIs are incomplete and spare supraspinal pathways,especially those located within the peripheral white matter of the spinal cord,which includes reticulospinal pathways originating from the medullary reticular formation.Whereas there is abundant literature about the motor cortex,its corticospinal pathway,and its capacity to modulate functional recovery after SCI,less is known about the medullary reticular formation and its reticulospinal pathway.
基金supported by grants from Guangdong Basic and Applied Basic Research Foundation,No.2021A1515110801(to SW)the National Natural Science Foundation of China,No.82301511(to SW)+1 种基金“Double First-Class”Construction Project of NPU,Nos.0515023GH0202320(to JC),0515023SH0201320(to JC)973 Program,No.2011CB504100(to JC).
文摘Myelination,the continuous ensheathment of neuronal axons,is a lifelong process in the nervous system that is essential for the precise,temporospatial conduction of action potentials between neurons.Myelin also provides intercellular metabolic support to axons.Even minor disruptions in the integrity of myelin can impair neural performance and increase susceptibility to neurological diseases.In fact,myelin degeneration is a well-known neuropathological condition that is associated with normal aging and several neurodegenerative diseases,including multiple sclerosis and Alzheimer’s disease.In the central nervous system,compact myelin sheaths are formed by fully mature oligodendrocytes.However,the entire oligodendrocyte lineage is susceptible to changes in the biological microenvironment and other risk factors that arise as the brain ages.In addition to their well-known role in action potential propagation,oligodendrocytes also provide intercellular metabolic support to axons by transferring energy metabolites and delivering exosomes.Therefore,myelin degeneration in the aging central nervous system is a significant contributor to the development of neurodegenerative diseases.Interventions that mitigate age-related myelin degeneration can improve neurological function in aging individuals.In this review,we investigate the changes in myelin that are associated with aging and their underlying mechanisms.We also discuss recent advances in understanding how myelin degeneration in the aging brain contributes to neurodegenerative diseases and explore the factors that can prevent,slow down,or even reverse age-related myelin degeneration.Future research will enhance our understanding of how reducing age-related myelin degeneration can be used as a therapeutic target for delaying or preventing neurodegenerative diseases.
