Spinal cord injury represents a severe form of central nervous system trauma for which effective treatments remain limited.Microglia is the resident immune cells of the central nervous system,play a critical role in s...Spinal cord injury represents a severe form of central nervous system trauma for which effective treatments remain limited.Microglia is the resident immune cells of the central nervous system,play a critical role in spinal cord injury.Previous studies have shown that microglia can promote neuronal survival by phagocytosing dead cells and debris and by releasing neuroprotective and anti-inflammatory factors.However,excessive activation of microglia can lead to persistent inflammation and contribute to the formation of glial scars,which hinder axonal regeneration.Despite this,the precise role and mechanisms of microglia during the acute phase of spinal cord injury remain controversial and poorly understood.To elucidate the role of microglia in spinal cord injury,we employed the colony-stimulating factor 1 receptor inhibitor PLX5622 to deplete microglia.We observed that sustained depletion of microglia resulted in an expansion of the lesion area,downregulation of brain-derived neurotrophic factor,and impaired functional recovery after spinal cord injury.Next,we generated a transgenic mouse line with conditional overexpression of brain-derived neurotrophic factor specifically in microglia.We found that brain-derived neurotrophic factor overexpression in microglia increased angiogenesis and blood flow following spinal cord injury and facilitated the recovery of hindlimb motor function.Additionally,brain-derived neurotrophic factor overexpression in microglia reduced inflammation and neuronal apoptosis during the acute phase of spinal cord injury.Furthermore,through using specific transgenic mouse lines,TMEM119,and the colony-stimulating factor 1 receptor inhibitor PLX73086,we demonstrated that the neuroprotective effects were predominantly due to brain-derived neurotrophic factor overexpression in microglia rather than macrophages.In conclusion,our findings suggest the critical role of microglia in the formation of protective glial scars.Depleting microglia is detrimental to recovery of spinal cord injury,whereas targeting brain-derived neurotrophic factor overexpression in microglia represents a promising and novel therapeutic strategy to enhance motor function recovery in patients with spinal cord injury.展开更多
Border-associated macrophages are located at the interface between the brain and the periphery, including the perivascular spaces, choroid plexus, and meninges. Until recently, the functions of border-associated macro...Border-associated macrophages are located at the interface between the brain and the periphery, including the perivascular spaces, choroid plexus, and meninges. Until recently, the functions of border-associated macrophages have been poorly understood and largely overlooked. However, a recent study reported that border-associated macrophages participate in stroke-induced inflammation, although many details and the underlying mechanisms remain unclear. In this study, we performed a comprehensive single-cell analysis of mouse border-associated macrophages using sequencing data obtained from the Gene Expression Omnibus(GEO) database(GSE174574 and GSE225948). Differentially expressed genes were identified, and enrichment analysis was performed to identify the transcription profile of border-associated macrophages. CellChat analysis was conducted to determine the cell communication network of border-associated macrophages. Transcription factors were predicted using the ‘pySCENIC' tool. We found that, in response to hypoxia, borderassociated macrophages underwent dynamic transcriptional changes and participated in the regulation of inflammatory-related pathways. Notably, the tumor necrosis factor pathway was activated by border-associated macrophages following ischemic stroke. The pySCENIC analysis indicated that the activity of signal transducer and activator of transcription 3(Stat3) was obviously upregulated in stroke, suggesting that Stat3 inhibition may be a promising strategy for treating border-associated macrophages-induced neuroinflammation. Finally, we constructed an animal model to investigate the effects of border-associated macrophages depletion following a stroke. Treatment with liposomes containing clodronate significantly reduced infarct volume in the animals and improved neurological scores compared with untreated animals. Taken together, our results demonstrate comprehensive changes in border-associated macrophages following a stroke, providing a theoretical basis for targeting border-associated macrophages-induced neuroinflammation in stroke treatment.展开更多
Strokes include both ischemic stroke,which is mediated by a blockade or reduction in the blood supply to the brain,and hemorrhagic stroke,which comprises intracerebral hemorrhage and subarachnoid hemorrhage and is cha...Strokes include both ischemic stroke,which is mediated by a blockade or reduction in the blood supply to the brain,and hemorrhagic stroke,which comprises intracerebral hemorrhage and subarachnoid hemorrhage and is characterized by bleeding within the brain.Stroke is a lifethreatening cerebrovascular condition characterized by intricate pathophysiological mechanisms,including oxidative stress,inflammation,mitochondrial dysfunction,and neuronal injury.Critical transcription factors,such as nuclear factor erythroid 2-related factor 2 and nuclear factor kappa B,play central roles in the progression of stroke.Nuclear factor erythroid 2-related factor 2 is sensitive to changes in the cellular redox status and is crucial in protecting cells against oxidative damage,inflammatory responses,and cytotoxic agents.It plays a significant role in post-stroke neuroprotection and repair by influencing mitochondrial function,endoplasmic reticulum stress,and lysosomal activity and regulating metabolic pathways and cytokine expression.Conversely,nuclear factor-kappa B is closely associated with mitochondrial dysfunction,the generation of reactive oxygen species,oxidative stress exacerbation,and inflammation.Nuclear factor-kappa B contributes to neuronal injury,apoptosis,and immune responses following stroke by modulating cell adhesion molecules and inflammatory mediators.The interplay between these pathways,potentially involving crosstalk among various organelles,significantly influences stroke pathophysiology.Advancements in single-cell sequencing and spatial transcriptomics have greatly improved our understanding of stroke pathogenesis and offer new opportunities for the development of targeted,individualized,cell typespecific treatments.In this review,we discuss the mechanisms underlying the involvement of nuclear factor erythroid 2-related factor 2 and nuclear factor-kappa B in both ischemic and hemorrhagic stroke,with an emphasis on their roles in oxidative stress,inflammation,and neuroprotection.展开更多
The fast solution of linear equations has always been one of the hot spots in scientific computing.A kind of the diagonal matrix splitting iteration methods are provided,which is different from the classical matrix sp...The fast solution of linear equations has always been one of the hot spots in scientific computing.A kind of the diagonal matrix splitting iteration methods are provided,which is different from the classical matrix splitting methods.Taking the decomposition of the diagonal elements for coefficient matrix as the key point,some new preconditioners are constructed.Taking the tri-diagonal coefficient matrix as an example,the convergence domains and optimal relaxation factor of the new method are analyzed theoretically.The presented new iteration methods are applied to solve linear algebraic equations,even 2D and 3D diffusion problems with the fully implicit discretization.The results of numerical experiments are matched with the theoretical analysis,and show that the iteration numbers are reduced greatly.The superiorities of presented iteration methods exceed some classical iteration methods dramatically.展开更多
The significant variation in plant regeneration efficiency between indica and japonica rice poses a major challenge for crop improvement.However,the molecular basis for this divergence remains largely unclear.In this ...The significant variation in plant regeneration efficiency between indica and japonica rice poses a major challenge for crop improvement.However,the molecular basis for this divergence remains largely unclear.In this study,we investigated the role of Oryza sativa AUXIN RESPONSE FACTOR 13(OsARF13),a transcription factor involved in callus-related processes.We observed that OsARF13 expression is significantly higher in japonica rice callus than in indica rice callus.This differential expression might be associated with an allelic variation in the promoter region of OsARF13,where a deletion commonly found in indica rice corresponds to the loss of a conserved auxin-responsive element(AuxRE)motif.To functionally characterize OsARF13,we generated CRISPR/Cas9-mediated knockout mutants.These mutants exhibited a substantial reduction in callus fresh weight,demonstrating that OsARF13 is required for efficient callus induction.Transcriptome analysis of the osarf13 mutant further showed that OsARF13 influences the expression of genes involved in hormone signal transduction and stress responses.Our findings suggest that OsARF13 is a key component of the regulatory network governing callus induction and that natural variation in its promoter might provide a potential explanation for the differential regenerative capacity between japonica and indica rice subspecies.展开更多
Biological aging is a complex physiological process characterized by a decline in tissue function and the loss of cellular capabilities,which increase an individual's risk of various diseases[1].While genetic fact...Biological aging is a complex physiological process characterized by a decline in tissue function and the loss of cellular capabilities,which increase an individual's risk of various diseases[1].While genetic factors and lifestyle are key influences on biological aging,environmental factors also play a significant role.Given the rapid aging of the global population,elucidating the factors that influence biological aging is crucial for promoting healthy aging.展开更多
This systematic review synthesizes empirical research on external risk factors for adolescent smartphone addiction.Scopus and Web of Science were searched for English peer-reviewed empirical articles from 2008 onward;...This systematic review synthesizes empirical research on external risk factors for adolescent smartphone addiction.Scopus and Web of Science were searched for English peer-reviewed empirical articles from 2008 onward;28 met inclusion criteria(excluding non-adolescents,generic internet addiction,non-empirical work,or non-English).Thematic synthesis organized findings into three external risk domains—family,school,and peers—considering cultural/contextual mechanisms.Family dynamics(parental phubbing,harsh parenting,dysfunction),school stressors,and adverse peer relationships were identified as accumulating,direct and indirect contributors to smartphone addiction.These operate within a techno-ecological framework,where digital technologies amplify vulnerabilities and create new pathways for maladaptive use.Evidence favors an ecological,multi-level perspective.Future research should use longitudinal designs,standardize measures across cultures,and examine understudied regions—especially Africa—to guide culturally sensitive interventions.展开更多
Varicocele(VC)is widely recognized as a prevalent and clinically significant cause of male infertility.However,the comprehensive pathogenic mechanisms underlying VC development and progression remain incompletely unde...Varicocele(VC)is widely recognized as a prevalent and clinically significant cause of male infertility.However,the comprehensive pathogenic mechanisms underlying VC development and progression remain incompletely understood,creating an important knowledge gap in the field of andrology.This review establishes that VC pathogenesis centers on abnormal vascular remodeling and integrates multiple contributing elements,including anatomical abnormalities,biochemical disturbances,genetic factors,low body mass index(BMI),age,and specific sports habits,while secondary varicoceles are primarily induced by compressive pathologies.Through a systematic synthesis of current evidence and recent advances,this review aims to elucidate the complex pathogenic network of VC and provide valuable insights to guide future research directions and inform the development of targeted clinical applications.展开更多
Investigated theoretically is a photonic-crystal surface-emitting GaN laser based on surface-etched holes with a porous-GaN cladding layer.The porous GaN has a low refractive index,supporting effective confinement to ...Investigated theoretically is a photonic-crystal surface-emitting GaN laser based on surface-etched holes with a porous-GaN cladding layer.The porous GaN has a low refractive index,supporting effective confinement to the resonant mode,and the porous GaN is derived from as-grown GaN,eliminating the lattice mismatch issues typically associated with GaN platforms.Studied systematically is how the photoniccrystal lattice constant,air hole radius,etching depth,and porous-GaN refractive index affect the performance of the laser.The results show that the laser exhibits optimal overall performance when the lattice constant is 216 nm and the hole radius is 60 nm.The etching depth can be chosen between 30 and 100 nm,and the porous-GaN refractive index is preferably in the range of 1.7–1.9.The research achieves a quality factor as high as 1.9×10^(4),with a photonic-crystal-layer confinement factor of 4.24%and an active-layer confinement factor of 21.8%,along with a low threshold gain of 77 cm^(−1).展开更多
BACKGROUND Ischemic stroke is one of the leading global causes of disability and death.Despite advances in modern medical technology that improve acute treatment and rehabilitation measures,post-stroke anxiety and dep...BACKGROUND Ischemic stroke is one of the leading global causes of disability and death.Despite advances in modern medical technology that improve acute treatment and rehabilitation measures,post-stroke anxiety and depression(PSD)do not receive sufficient attention.AIM To systematically evaluate risk factors and early identification markers for PSD for more precise screening and intervention strategies in clinical practice.METHODS This retrospective study analyzed clinical data from 112 patients with ischemic stroke admitted between January 2022 and December 2024.Based on assessments using the Hamilton Rating Scale for Anxiety(HAMA)and Hamilton Rating Scale for Depression(HAMD)at 2 weeks(±3 days)post-stroke,patients were classified into the PSD group(HAMA≥7 and/or HAMD≥7)and the non-PSD group(HAMA<7 and HAMD<7).Observation indicators included psychological assessment,demographic and clinical characteristics,stroke-related clinical indicators,neuroimaging assessments,and laboratory biomarkers.Multivariate logistic regression analysis was used to identify independent risk factors for PSD,and receiver operating characteristic curve analysis was used to evaluate the diagnostic value of potential biomarkers.RESULTS Of the 112 patients,46(41.1%)were diagnosed with PSD.Multivariate analysis identified five independent risk factors:Female gender[Odds ratio(OR)=2.32,95%confidence interval(CI):1.56-3.45],history of mental disorders prior to stroke(OR=3.17,95%CI:1.89-5.32),infarct location in the frontal lobe or limbic system(OR=2.86,95%CI:1.73-4.71),stroke severity with National Institutes of Health Stroke Scale≥8 at admission(OR=2.54,95%CI:1.62-3.99),and low social support(Social Support Rating Scale<35,OR=2.18,95%CI:1.42-3.36).Subgroup analysis showed that depression patients more commonly had left hemisphere lesions(68.4%vs 45.2%),while anxiety patients more frequently presented with right hemisphere lesions(59.5%vs 39.5%).The PSD group exhibited larger infarct volumes(8.7 cm^(3) vs 5.3 cm^(3)),more severe white matter hyperintensities,and more pronounced frontal lobe atrophy.Analysis of inflammatory markers showed significantly elevated levels of interleukin-6(7.8 pg/mL vs 4.5 pg/mL)and tumor necrosis factor-alpha(15.6 pg/mL vs 9.8 pg/mL)in the PSD group,while hypothalamicpituitary-adrenal axis function assessment revealed higher cortisol levels(386.5±92.3 nmol/L vs 328.7±75.6 nmol/L)and flattened diurnal rhythm in the PSD group.CONCLUSION PSD is a complex neuropsychiatric consequence of stroke involving disruption of the frontal-limbic circuitry,neuroinflammatory responses,and dysfunction of the hypothalamic-pituitary-adrenal axis.展开更多
BACKGROUND:The central nervous system is a critical target of severe heatstroke,with oxidative stress and multi-organelle damage being the key pathogenic mechanisms.However,research on endogenous antioxidant defense r...BACKGROUND:The central nervous system is a critical target of severe heatstroke,with oxidative stress and multi-organelle damage being the key pathogenic mechanisms.However,research on endogenous antioxidant defense remains limited.In this study,we aimed to characterize neuronal oxidative damage as a key heatstroke pathological mechanism and assess the neuroprotective effects of nuclear factor E2-related factor 2(NRF2).METHODS:After developing in vivo and in vitro heatstroke models,we employed histological staining,cell viability and apoptosis assays,oxidative stress indicators determination,organelle ultrastructural observation,and molecular expression analysis to investigate the mechanisms of brain injury and changes in the NRF2 pathway following heatstroke.We pretreated mice and SH-SY5Y cells with tert-butylhydroquinone(TBHQ) to activate NRF2 expression.Furthermore,we utilized NRF2 knockout(KO) mice and NRF2 siRNA transfection to suppress NRF2 expression,thereby examining the effects of NRF2 both in vivo and in vitro.RESULTS:We found that heatstroke induced neuronal damage,elevated oxidative stress levels,and caused structural damage to both the mitochondria and the endoplasmic reticulum(ER).Notably,NRF2 activation was insufficient post-heatstroke.Pretreatment with TBHQ effectively activated the NRF2 signaling pathway and mitigated the resulting damage.In contrast,these injuries were exacerbated in NRF2 KO mice and SH-SY5Y cells transfected with NRF2 siRNA.CONCLUSION:This preliminary research shows that the NRF2 antioxidant signaling pathway exerts a protective effect against oxidative stress,mitigating both mitochondrial and ER structural damage in neuronal cells during heatstroke.Therefore,targeting the NRF2 pathway is a promising therapeutic strategy for heatstroke-induced neuronal injury.展开更多
Nerve trauma commonly results in chronic neuropathic pain. This is by triggering the release of proinflammatory mediators from local and invading cells that induce inflammation and nociceptive neuron hyperexcitability...Nerve trauma commonly results in chronic neuropathic pain. This is by triggering the release of proinflammatory mediators from local and invading cells that induce inflammation and nociceptive neuron hyperexcitability. Even without apparent inflammation, injury sites are associated with increased inflammatory markers. This review focuses on how it might be possible to reduce neuropathic pain by reducing inflammation. Physiologically, pain is resolved by a combination of the out-migration of pro-inflammatory cells from the injury site, the down-regulation of the genes underlying the inflammation, up-regulating genes for anti-inflammatory mediators, and reducing nociceptive neuron hyperexcitability. While various techniques reduce chronic neuropathic pain, the best are effective on < 50% of patients, no technique reliably or permanently eliminates neuropathic pain. This is because most techniques are predominantly aimed at reducing pain, not inflammation. In addition, while single factors reduce pain, increasing evidence indicates significant and longer-lasting pain relief requires multiple factors acting simultaneously. Therefore, it is not surprising that extensive data indicate that the application of platelet-rich plasma provides more significant and longer-lasting pain suppression than other techniques, although its analgesia is neither complete nor permanent. However, several case reports indicate that platelet-rich plasma can induce permanent neuropathic pain elimination when the platelet concentration is significantly increased and is applied to longer nerve lengths. This review examines the primary triggers of the development and maintenance of neuropathic pain and techniques that reduce chronic neuropathic pain. The application of plateletrich plasma holds great promise for providing complete and permanent chronic neuropathic pain elimination.展开更多
BACKGROUND Post-transplant tertiary hyperparathyroidism(PT-tHPT)is a well-recognized complication following kidney transplantation,characterized by persistent excessive secretion of parathyroid hormone(PTH)despite imp...BACKGROUND Post-transplant tertiary hyperparathyroidism(PT-tHPT)is a well-recognized complication following kidney transplantation,characterized by persistent excessive secretion of parathyroid hormone(PTH)despite improved renal function.It is potentially associated with an increased risk of cardiovascular events,renal osteodystrophy,pathologic fractures,graft loss,and mortality.AIM To evaluate the incidence,risk factors,and outcomes of PT-tHPT amongst kidney transplant recipients.METHODS A total of 887 transplant recipients who underwent transplantation between 2000 and 2020 were evaluated.Univariable and multivariable logistic regression was performed to determine the predictors of tertiary hyperparathyroidism.Graft and recipient outcomes were assessed using multivariable Cox regression.A separate multivariable Cox regression was performed to determine the effect of treatment strategies on outcomes.RESULTS PT-tHPT,defined as elevated PTH(>65 ng/L)and persistent hypercalcemia(>2.60 mmol/L),was diagnosed in 14%of recipients.Risk factors for PT-tHPT included older age[odds ratio(OR)=1.36,P<0.001],Asian ethnicity(OR=0.33,P=0.006),total ischemia time(OR=1.03,P=0.048 per hour),pre-transplant serum calcium(OR=1.38,P<0.001)per decile increase,pre-transplant PTH level(OR=1.31,P<0.001)per decile increase,longer dialysis duration(OR=1.12,P=0.002)per year,history of acute rejection(OR=2.37,P=0.012),and slope of estimated glomerular filtration rate change(OR=0.91,P=0.001).There were a 3.4-fold higher risk of death-censored graft loss and a 1.9-fold greater risk of recipient death with PT-tHPT.The three treatment strategies of conservative management,calcimimetic and parathyroidectomy did not significantly change the graft or patient outcome.CONCLUSION Pretransplant elevated calcium and PTH levels,older age and dialysis duration are associated with PT-tHPT.While PT-tHPT significantly affects graft and recipient survival,the treatment strategies did not affect survival.展开更多
Long-term exposure to ambient fine particulate matter(PM2.5)may increase the risk of neurotoxicity in human populations.However,research studies on the underlying mechanisms of chronic PM2.5-induced depression-like be...Long-term exposure to ambient fine particulate matter(PM2.5)may increase the risk of neurotoxicity in human populations.However,research studies on the underlying mechanisms of chronic PM2.5-induced depression-like behaviors,and potential therapeutical strategies,remain scarce.In the present study,after long-term exposure to real-world PM2.5 for 15 weeks,male mice displayed depression-like behaviors,which were revealed using the open field and sucrose preference tests.Mechanistically,chronic PM2.5 exposure promoted astrocytic A1 polarization and disrupted reduction-oxidation balance in the mouse hippocampus.Furthermore,PM2.5-exposed mice displayed pathological damage to hippocampal neurons as well as the inhibition of nuclear factor erythroid 2-related factor 2 signaling.Astrocytic ablation of nuclear factor erythroid 2-related factor 2 exacerbated PM2.5-induced hippocampal neuronal injury in mice via the disruption of astrocyte-to-microglia communication;this finding was confirmed in mice with bilateral and unilateral hippocampal astrocytic Nfe2l2 knockdown.Importantly,the upregulation of nuclear factor erythroid 2-related factor 2 activation by procyanidin significantly ameliorated PM2.5-induced depression-like behaviors through the remodeling of astrocyte-to-microglia communication.Together,our findings shed light on the important role of hippocampal astrocytic nuclear factor erythroid 2-related factor 2 activation for maintaining astrocyte-to-microglia communication,and indicate potential research avenues for therapeutic strategies against PM2.5-induced depresson-like behaviors.展开更多
BACKGROUND:Acute pain is a sudden experience secondary to injuries and varies in perception among individuals.In trauma patients,it can negatively aff ect respiratory function,immune response,and wound healing,making ...BACKGROUND:Acute pain is a sudden experience secondary to injuries and varies in perception among individuals.In trauma patients,it can negatively aff ect respiratory function,immune response,and wound healing,making it a signifi cant public health concern.This study is to determine the prevalence and factors associated with acute pain among emergency trauma patients.METHODS:A multicenter cross-sectional study was conducted.Data were collected via interviewer-administered questionnaires and patient chart review.The data were analyzed via the statistical package for social science version 25.Bivariable and multivariable logistic regression analyses were used.Variables with a P-value<0.05 were considered statistically signifi cant.RESULTS:A total of 397 patients were included in the study,for a response rate of 96.8%.The prevalence of pain during admission was 91.9%(95%confi dence intervals[95%CIs]:88.8%-94.4%).Blunt trauma(adjusted odds ratio[aOR]=2.82;95%CI:1.23-6.45),analgesia before admission to the emergency department(aOR=2.71;95%CI:1.16-6.36),documentation of pain severity in the chart(aOR=2.71;95%CI:1.16-6.36),analgesia provided within two hours after admission(aOR=7.60;95%CI:2.79-20.68),use of non-pharmacological pain management methods(aOR=3.09;95%CI:1.35-7.08)and availability of analgesia(aOR=3.95;95%CI:1.36-11.43)were associated with acute pain experience.CONCLUSION:The prevalence of acute pain among emergency trauma patients was high in the study area.Analgesia should be administered prior to admission,and non-pharmacological pain management should be implemented.Moreover,training on pain assessment and management should be provided for healthcare providers in the emergency department.展开更多
Understory bryophytes play unique and disproportionately important roles in water retention,biogeochemical cycling,and biodiversity conservation,and serve as bioindicators of environmental health in forest ecosystems....Understory bryophytes play unique and disproportionately important roles in water retention,biogeochemical cycling,and biodiversity conservation,and serve as bioindicators of environmental health in forest ecosystems.However,biogeographical research on the biomass of forest bryophytes is inadequately studied and has been limited to elevational gradients.We conducted a systematic cross-regional survey of bryophyte biomass across 413 forest sites in Sichuan Province,China.We analyzed how each environmental variable,including climatic and atmospheric factors,overstory covers,and soil nutrients,relates to bryophyte biomass and quantified their relative contributions.The results indicate that,largely similar to previous local investigations and experiments,at a large scale,bryophytes are abundant in forests with lower temperature,nitrogen deposition,vapor pressure deficit,and tree and herb covers,as well as higher light availability.Moreover,bryophyte biomass is positively associated with soil carbon and nitrogen content.These environmental variables are closely related and jointly influence bryophyte biomass,with mean annual temperature being the most significant factor(accounting for 83%of the relative contribution).The biogeographical patterns of bryophyte biomass contribute to deepening our understanding of their adaptations to multiple environmental variables and enable us to predict their responses to global climate change.These patterns also provide essential evidence for establishing more accurate terrestrial vegetation ecosystem models.展开更多
Ascorbate(Asc),commonly known as vitamin C,is a vital molecule for plant growth,development,and stress resilience.It is also known to play a crucial role in various physiological processes,including photosynthesis,cel...Ascorbate(Asc),commonly known as vitamin C,is a vital molecule for plant growth,development,and stress resilience.It is also known to play a crucial role in various physiological processes,including photosynthesis,cell division,and differentiation.This article thoroughly explores the processes governing the metabolism of Asc in plants and its roles in physiological functions.It lays down a robust theoretical groundwork for delving into Asc production,transportation,functions,and its potential applications in stress alleviation and horticulture.Furthermore,recent studies indicate that Asc plays a role in regulating fruit development and affecting postharvest storage characteristics,thereby influencing fruit ripening and resilience to stress.Hence,there is a growing importance in studying the synthesis and utilization of Asc in plants.Although the critical role of Asc in controlling plant redox signals has been extensively studied,the precise mechanisms by which it manages cellular redox homeostasis to maintain the equilibrium between reactive oxygen scavenging and cell redox signaling remain elusive.This gap in knowledge presents fresh opportunities to explore how the production of Asc in plants is regulated and how plants react to environmental stressors.Furthermore,this article delves into the potential for a comprehensive investigation into the essential function of Asc in fruits,the development of Asc-rich fruits,and the enhancement of postharvest storage properties.展开更多
Anthocyanins are important flavonoid pigments in the coloration of fruits.To identify candidate genes involved in anthocyanin accumulation,metabolic and transcriptome analyses were conducted in‘Nanguo'pear and it...Anthocyanins are important flavonoid pigments in the coloration of fruits.To identify candidate genes involved in anthocyanin accumulation,metabolic and transcriptome analyses were conducted in‘Nanguo'pear and its red sport cultivar‘Nanhong'pear.The results showed that‘Nanhong'pear had significantly higher anthocyanin and flavonol contents.Additionally,transcriptomic analysis showed that there were significant differences in the expression of genes involved in phenylpropanoid and flavonoid biosynthesis pathways between the two cultivars,with PuGSTF12 being the most upregulated gene in the‘Nanhong'cultivar.Further analysis identified a novel MYB transcription factor(PuMYB93),and its silencing repressed PuGSTF12 expression and anthocyanin accumulation,suggesting it plays an essential role in the regulation of anthocyanin biosynthesis.Moreover,yeast one-hybrid analysis,electrophoretic mobility shift assay,andβ-glucuronidase assay indicated that PuMYB93 can directly bind to the PuGSTF12 promoter to positively regulate its expression.Additionally,PuGSTF12 silencing suppressed the coloration of PuMYB93-OE peels,suggesting that PuGSTF12 act downstream of PuMYB93.Overall,the findings of this study show that PuMYB93 promotes anthocyanin transport in pears by regulating PuGSTF12 expression to further enhance anthocyanin accumulation.展开更多
Environment serves as the pivotal medium to produce fermented food,with fluctuations in environmental factors exerting a profound impact on the modulation of fermentation microbial communities.Such shifts are crucial ...Environment serves as the pivotal medium to produce fermented food,with fluctuations in environmental factors exerting a profound impact on the modulation of fermentation microbial communities.Such shifts are crucial for the distinctiveness of fermented food flavor and the variability in quality.Chinese liquor(Baijiu)is one of the typical representatives of spontaneous fermented food.In this review,the multifaceted relationship between regional environmental attributes and the fermentation dynamics of Baijiu was examined,with a spotlight on the strong-flavor,sauce-flavor,and light-flavor varieties.It reveals the influence of regional environmental factors and brewing environmental factors on microbial function and metabolism,which results in the formation of unique flavor characteristics of Baijiu.The 9 main factors affecting the microecology of Baijiu fermentation were further explored,including environmental sensitivity,microbial interactions,biogeographic patterns,and key abiotic factors such as temperature and humidity.Environmental factor management is crucial for controlling microbial community in fermentation.Intelligent detection of the fermentation system is combined with artificial intelligence to realize the digitalization of Baijiu fermentation,with a view to further studying the environmental mechanism or quantitative control relationship of natural fermentation,improving the environmental stability of natural fermentation,and promoting the mechanization and intelligence of fermentation production.展开更多
The pathophysiology of many ailments,including neurological,gastrointestinal,and metabolic disorders,is well known to be influenced by intestinal dysbiosis.Clinical research has provided evidence suggesting a strong c...The pathophysiology of many ailments,including neurological,gastrointestinal,and metabolic disorders,is well known to be influenced by intestinal dysbiosis.Clinical research has provided evidence suggesting a strong correlation between dysbiosis of the gut microbiome and colorectal cancer(CRC)development.The active reprogramming of metabolic pathways to boost glycolysis,fatty acid production,lipogenesis,and glutaminolysis constitutes a major metabolic shift in cancer development,including CRC.The complex combination of different factors leads to CRC,making it an environmental disease.These factors include food and lifestyle choices,genetics and family history,age,underlying intestinal diseases,and dysbiosis of the gut microbiota.One of the primary risk factors for carcinoma development is diet,which impacts an individual’s gut microbiome.In addition to impacting CRC formation,the gut microbiome also has immunomodulatory effects,including various immunological interactions and the underlying mechanisms governing them.Microbial interactions in CRC have been extensively studied,yet numerous unresolved queries exist on how gut bacteria can influence treatment.Microbiome-driven immunotherapies,focusing on probiotics,prebiotics,and synbiotics,represent a promising therapeutic avenue.However,large-scale treatment utilization in CRC patients is limited by several issues,including variations in the microbial makeup of each patient’s gut and a lack of established methods.The study highlights the impact of several risk factors,including dysbiosis of the gut microbiome and different approaches to halting and treating CRC progression with a focus on diet changes and modulation of the gut flora.Given the foregoing,we propose that if research gaps are addressed and immunotherapy is paired with microbial interventions,microbiota-based therapeutics could potentially impede the growth of tumors and treat CRC.展开更多
基金supported by the National Natural Science Foundation of China,Nos.82072165 and 82272256(both to XM)the Key Project of Xiangyang Central Hospital,No.2023YZ03(to RM)。
文摘Spinal cord injury represents a severe form of central nervous system trauma for which effective treatments remain limited.Microglia is the resident immune cells of the central nervous system,play a critical role in spinal cord injury.Previous studies have shown that microglia can promote neuronal survival by phagocytosing dead cells and debris and by releasing neuroprotective and anti-inflammatory factors.However,excessive activation of microglia can lead to persistent inflammation and contribute to the formation of glial scars,which hinder axonal regeneration.Despite this,the precise role and mechanisms of microglia during the acute phase of spinal cord injury remain controversial and poorly understood.To elucidate the role of microglia in spinal cord injury,we employed the colony-stimulating factor 1 receptor inhibitor PLX5622 to deplete microglia.We observed that sustained depletion of microglia resulted in an expansion of the lesion area,downregulation of brain-derived neurotrophic factor,and impaired functional recovery after spinal cord injury.Next,we generated a transgenic mouse line with conditional overexpression of brain-derived neurotrophic factor specifically in microglia.We found that brain-derived neurotrophic factor overexpression in microglia increased angiogenesis and blood flow following spinal cord injury and facilitated the recovery of hindlimb motor function.Additionally,brain-derived neurotrophic factor overexpression in microglia reduced inflammation and neuronal apoptosis during the acute phase of spinal cord injury.Furthermore,through using specific transgenic mouse lines,TMEM119,and the colony-stimulating factor 1 receptor inhibitor PLX73086,we demonstrated that the neuroprotective effects were predominantly due to brain-derived neurotrophic factor overexpression in microglia rather than macrophages.In conclusion,our findings suggest the critical role of microglia in the formation of protective glial scars.Depleting microglia is detrimental to recovery of spinal cord injury,whereas targeting brain-derived neurotrophic factor overexpression in microglia represents a promising and novel therapeutic strategy to enhance motor function recovery in patients with spinal cord injury.
基金supported by Qingdao Key Medical and Health Discipline ProjectThe Intramural Research Program of the Affiliated Hospital of Qingdao University,No. 4910Qingdao West Coast New Area Science and Technology Project,No. 2020-55 (all to SW)。
文摘Border-associated macrophages are located at the interface between the brain and the periphery, including the perivascular spaces, choroid plexus, and meninges. Until recently, the functions of border-associated macrophages have been poorly understood and largely overlooked. However, a recent study reported that border-associated macrophages participate in stroke-induced inflammation, although many details and the underlying mechanisms remain unclear. In this study, we performed a comprehensive single-cell analysis of mouse border-associated macrophages using sequencing data obtained from the Gene Expression Omnibus(GEO) database(GSE174574 and GSE225948). Differentially expressed genes were identified, and enrichment analysis was performed to identify the transcription profile of border-associated macrophages. CellChat analysis was conducted to determine the cell communication network of border-associated macrophages. Transcription factors were predicted using the ‘pySCENIC' tool. We found that, in response to hypoxia, borderassociated macrophages underwent dynamic transcriptional changes and participated in the regulation of inflammatory-related pathways. Notably, the tumor necrosis factor pathway was activated by border-associated macrophages following ischemic stroke. The pySCENIC analysis indicated that the activity of signal transducer and activator of transcription 3(Stat3) was obviously upregulated in stroke, suggesting that Stat3 inhibition may be a promising strategy for treating border-associated macrophages-induced neuroinflammation. Finally, we constructed an animal model to investigate the effects of border-associated macrophages depletion following a stroke. Treatment with liposomes containing clodronate significantly reduced infarct volume in the animals and improved neurological scores compared with untreated animals. Taken together, our results demonstrate comprehensive changes in border-associated macrophages following a stroke, providing a theoretical basis for targeting border-associated macrophages-induced neuroinflammation in stroke treatment.
基金supported by grants from the Zhejiang Provincial TCM Science and Technology Plan Project,No.2023ZL156(to YH)Ningbo Top Medical and Health Research Program,No.2022020304(to XG)+1 种基金the Natural Science Foundation of Ningbo,No.2023J019(to YH)Key Laboratory of Precision Medicine for Atherosclerotic Diseases of Zhejiang Province,No.2022E10026(to YH)。
文摘Strokes include both ischemic stroke,which is mediated by a blockade or reduction in the blood supply to the brain,and hemorrhagic stroke,which comprises intracerebral hemorrhage and subarachnoid hemorrhage and is characterized by bleeding within the brain.Stroke is a lifethreatening cerebrovascular condition characterized by intricate pathophysiological mechanisms,including oxidative stress,inflammation,mitochondrial dysfunction,and neuronal injury.Critical transcription factors,such as nuclear factor erythroid 2-related factor 2 and nuclear factor kappa B,play central roles in the progression of stroke.Nuclear factor erythroid 2-related factor 2 is sensitive to changes in the cellular redox status and is crucial in protecting cells against oxidative damage,inflammatory responses,and cytotoxic agents.It plays a significant role in post-stroke neuroprotection and repair by influencing mitochondrial function,endoplasmic reticulum stress,and lysosomal activity and regulating metabolic pathways and cytokine expression.Conversely,nuclear factor-kappa B is closely associated with mitochondrial dysfunction,the generation of reactive oxygen species,oxidative stress exacerbation,and inflammation.Nuclear factor-kappa B contributes to neuronal injury,apoptosis,and immune responses following stroke by modulating cell adhesion molecules and inflammatory mediators.The interplay between these pathways,potentially involving crosstalk among various organelles,significantly influences stroke pathophysiology.Advancements in single-cell sequencing and spatial transcriptomics have greatly improved our understanding of stroke pathogenesis and offer new opportunities for the development of targeted,individualized,cell typespecific treatments.In this review,we discuss the mechanisms underlying the involvement of nuclear factor erythroid 2-related factor 2 and nuclear factor-kappa B in both ischemic and hemorrhagic stroke,with an emphasis on their roles in oxidative stress,inflammation,and neuroprotection.
基金The National Natural Science Foundations of China (12202219)the Natural Science Foundations of Ningxia (2024AAC02009, 2023AAC05001)the Ningxia Youth Top Talents Training Project。
文摘The fast solution of linear equations has always been one of the hot spots in scientific computing.A kind of the diagonal matrix splitting iteration methods are provided,which is different from the classical matrix splitting methods.Taking the decomposition of the diagonal elements for coefficient matrix as the key point,some new preconditioners are constructed.Taking the tri-diagonal coefficient matrix as an example,the convergence domains and optimal relaxation factor of the new method are analyzed theoretically.The presented new iteration methods are applied to solve linear algebraic equations,even 2D and 3D diffusion problems with the fully implicit discretization.The results of numerical experiments are matched with the theoretical analysis,and show that the iteration numbers are reduced greatly.The superiorities of presented iteration methods exceed some classical iteration methods dramatically.
基金supported by the National Natural Science Foundation of China(Grant Nos.32201834 and 32201814)the Hainan Provincial Natural Science Foundation of China(Grant No.324RC530)+1 种基金the Hainan Provincial‘Nanhai NewStar’Science and Technology Innovation Platform Project,China(Grant No.NHXXRCXM-202362)the Research Startup Funding from Hainan Institute of Zhejiang University,China(Grant No.0201-6602-A12202).
文摘The significant variation in plant regeneration efficiency between indica and japonica rice poses a major challenge for crop improvement.However,the molecular basis for this divergence remains largely unclear.In this study,we investigated the role of Oryza sativa AUXIN RESPONSE FACTOR 13(OsARF13),a transcription factor involved in callus-related processes.We observed that OsARF13 expression is significantly higher in japonica rice callus than in indica rice callus.This differential expression might be associated with an allelic variation in the promoter region of OsARF13,where a deletion commonly found in indica rice corresponds to the loss of a conserved auxin-responsive element(AuxRE)motif.To functionally characterize OsARF13,we generated CRISPR/Cas9-mediated knockout mutants.These mutants exhibited a substantial reduction in callus fresh weight,demonstrating that OsARF13 is required for efficient callus induction.Transcriptome analysis of the osarf13 mutant further showed that OsARF13 influences the expression of genes involved in hormone signal transduction and stress responses.Our findings suggest that OsARF13 is a key component of the regulatory network governing callus induction and that natural variation in its promoter might provide a potential explanation for the differential regenerative capacity between japonica and indica rice subspecies.
基金support from the Shenzhen Science and Technology program(grant number 202208183000115)。
文摘Biological aging is a complex physiological process characterized by a decline in tissue function and the loss of cellular capabilities,which increase an individual's risk of various diseases[1].While genetic factors and lifestyle are key influences on biological aging,environmental factors also play a significant role.Given the rapid aging of the global population,elucidating the factors that influence biological aging is crucial for promoting healthy aging.
基金supported by the 2025 Fujian Provincial Social Science Foundation Project(FJ2025C074).
文摘This systematic review synthesizes empirical research on external risk factors for adolescent smartphone addiction.Scopus and Web of Science were searched for English peer-reviewed empirical articles from 2008 onward;28 met inclusion criteria(excluding non-adolescents,generic internet addiction,non-empirical work,or non-English).Thematic synthesis organized findings into three external risk domains—family,school,and peers—considering cultural/contextual mechanisms.Family dynamics(parental phubbing,harsh parenting,dysfunction),school stressors,and adverse peer relationships were identified as accumulating,direct and indirect contributors to smartphone addiction.These operate within a techno-ecological framework,where digital technologies amplify vulnerabilities and create new pathways for maladaptive use.Evidence favors an ecological,multi-level perspective.Future research should use longitudinal designs,standardize measures across cultures,and examine understudied regions—especially Africa—to guide culturally sensitive interventions.
基金funded by China Postdoctoral Science Foundation(Grant Number:2025M773939)NationalNatural Science Foundation of China(Grant Number:82205131)Sichuan Science and Technology Program(Grant Number:2025ZNSFSC1798).
文摘Varicocele(VC)is widely recognized as a prevalent and clinically significant cause of male infertility.However,the comprehensive pathogenic mechanisms underlying VC development and progression remain incompletely understood,creating an important knowledge gap in the field of andrology.This review establishes that VC pathogenesis centers on abnormal vascular remodeling and integrates multiple contributing elements,including anatomical abnormalities,biochemical disturbances,genetic factors,low body mass index(BMI),age,and specific sports habits,while secondary varicoceles are primarily induced by compressive pathologies.Through a systematic synthesis of current evidence and recent advances,this review aims to elucidate the complex pathogenic network of VC and provide valuable insights to guide future research directions and inform the development of targeted clinical applications.
基金funded by the Natural Science Foundation of Nanjing University of Posts and Telecommunications(Grant No.NY224125)the Open Fund of the State Key Laboratory of Advanced Optical Communication Systems and Networks(SJTU)(Grant No.2023GZKF018)the Postgraduate Research and Practice Innovation Program of Jiangsu Province(Grant Nos.KYCX24_1199 and SJCX24_0286).
文摘Investigated theoretically is a photonic-crystal surface-emitting GaN laser based on surface-etched holes with a porous-GaN cladding layer.The porous GaN has a low refractive index,supporting effective confinement to the resonant mode,and the porous GaN is derived from as-grown GaN,eliminating the lattice mismatch issues typically associated with GaN platforms.Studied systematically is how the photoniccrystal lattice constant,air hole radius,etching depth,and porous-GaN refractive index affect the performance of the laser.The results show that the laser exhibits optimal overall performance when the lattice constant is 216 nm and the hole radius is 60 nm.The etching depth can be chosen between 30 and 100 nm,and the porous-GaN refractive index is preferably in the range of 1.7–1.9.The research achieves a quality factor as high as 1.9×10^(4),with a photonic-crystal-layer confinement factor of 4.24%and an active-layer confinement factor of 21.8%,along with a low threshold gain of 77 cm^(−1).
文摘BACKGROUND Ischemic stroke is one of the leading global causes of disability and death.Despite advances in modern medical technology that improve acute treatment and rehabilitation measures,post-stroke anxiety and depression(PSD)do not receive sufficient attention.AIM To systematically evaluate risk factors and early identification markers for PSD for more precise screening and intervention strategies in clinical practice.METHODS This retrospective study analyzed clinical data from 112 patients with ischemic stroke admitted between January 2022 and December 2024.Based on assessments using the Hamilton Rating Scale for Anxiety(HAMA)and Hamilton Rating Scale for Depression(HAMD)at 2 weeks(±3 days)post-stroke,patients were classified into the PSD group(HAMA≥7 and/or HAMD≥7)and the non-PSD group(HAMA<7 and HAMD<7).Observation indicators included psychological assessment,demographic and clinical characteristics,stroke-related clinical indicators,neuroimaging assessments,and laboratory biomarkers.Multivariate logistic regression analysis was used to identify independent risk factors for PSD,and receiver operating characteristic curve analysis was used to evaluate the diagnostic value of potential biomarkers.RESULTS Of the 112 patients,46(41.1%)were diagnosed with PSD.Multivariate analysis identified five independent risk factors:Female gender[Odds ratio(OR)=2.32,95%confidence interval(CI):1.56-3.45],history of mental disorders prior to stroke(OR=3.17,95%CI:1.89-5.32),infarct location in the frontal lobe or limbic system(OR=2.86,95%CI:1.73-4.71),stroke severity with National Institutes of Health Stroke Scale≥8 at admission(OR=2.54,95%CI:1.62-3.99),and low social support(Social Support Rating Scale<35,OR=2.18,95%CI:1.42-3.36).Subgroup analysis showed that depression patients more commonly had left hemisphere lesions(68.4%vs 45.2%),while anxiety patients more frequently presented with right hemisphere lesions(59.5%vs 39.5%).The PSD group exhibited larger infarct volumes(8.7 cm^(3) vs 5.3 cm^(3)),more severe white matter hyperintensities,and more pronounced frontal lobe atrophy.Analysis of inflammatory markers showed significantly elevated levels of interleukin-6(7.8 pg/mL vs 4.5 pg/mL)and tumor necrosis factor-alpha(15.6 pg/mL vs 9.8 pg/mL)in the PSD group,while hypothalamicpituitary-adrenal axis function assessment revealed higher cortisol levels(386.5±92.3 nmol/L vs 328.7±75.6 nmol/L)and flattened diurnal rhythm in the PSD group.CONCLUSION PSD is a complex neuropsychiatric consequence of stroke involving disruption of the frontal-limbic circuitry,neuroinflammatory responses,and dysfunction of the hypothalamic-pituitary-adrenal axis.
基金supported by the National Natural Science Foundation of China (No.82202432)the Guangzhou Science and Technology Plan Project (No.2023A04J2059,2024A03J0242)。
文摘BACKGROUND:The central nervous system is a critical target of severe heatstroke,with oxidative stress and multi-organelle damage being the key pathogenic mechanisms.However,research on endogenous antioxidant defense remains limited.In this study,we aimed to characterize neuronal oxidative damage as a key heatstroke pathological mechanism and assess the neuroprotective effects of nuclear factor E2-related factor 2(NRF2).METHODS:After developing in vivo and in vitro heatstroke models,we employed histological staining,cell viability and apoptosis assays,oxidative stress indicators determination,organelle ultrastructural observation,and molecular expression analysis to investigate the mechanisms of brain injury and changes in the NRF2 pathway following heatstroke.We pretreated mice and SH-SY5Y cells with tert-butylhydroquinone(TBHQ) to activate NRF2 expression.Furthermore,we utilized NRF2 knockout(KO) mice and NRF2 siRNA transfection to suppress NRF2 expression,thereby examining the effects of NRF2 both in vivo and in vitro.RESULTS:We found that heatstroke induced neuronal damage,elevated oxidative stress levels,and caused structural damage to both the mitochondria and the endoplasmic reticulum(ER).Notably,NRF2 activation was insufficient post-heatstroke.Pretreatment with TBHQ effectively activated the NRF2 signaling pathway and mitigated the resulting damage.In contrast,these injuries were exacerbated in NRF2 KO mice and SH-SY5Y cells transfected with NRF2 siRNA.CONCLUSION:This preliminary research shows that the NRF2 antioxidant signaling pathway exerts a protective effect against oxidative stress,mitigating both mitochondrial and ER structural damage in neuronal cells during heatstroke.Therefore,targeting the NRF2 pathway is a promising therapeutic strategy for heatstroke-induced neuronal injury.
文摘Nerve trauma commonly results in chronic neuropathic pain. This is by triggering the release of proinflammatory mediators from local and invading cells that induce inflammation and nociceptive neuron hyperexcitability. Even without apparent inflammation, injury sites are associated with increased inflammatory markers. This review focuses on how it might be possible to reduce neuropathic pain by reducing inflammation. Physiologically, pain is resolved by a combination of the out-migration of pro-inflammatory cells from the injury site, the down-regulation of the genes underlying the inflammation, up-regulating genes for anti-inflammatory mediators, and reducing nociceptive neuron hyperexcitability. While various techniques reduce chronic neuropathic pain, the best are effective on < 50% of patients, no technique reliably or permanently eliminates neuropathic pain. This is because most techniques are predominantly aimed at reducing pain, not inflammation. In addition, while single factors reduce pain, increasing evidence indicates significant and longer-lasting pain relief requires multiple factors acting simultaneously. Therefore, it is not surprising that extensive data indicate that the application of platelet-rich plasma provides more significant and longer-lasting pain suppression than other techniques, although its analgesia is neither complete nor permanent. However, several case reports indicate that platelet-rich plasma can induce permanent neuropathic pain elimination when the platelet concentration is significantly increased and is applied to longer nerve lengths. This review examines the primary triggers of the development and maintenance of neuropathic pain and techniques that reduce chronic neuropathic pain. The application of plateletrich plasma holds great promise for providing complete and permanent chronic neuropathic pain elimination.
文摘BACKGROUND Post-transplant tertiary hyperparathyroidism(PT-tHPT)is a well-recognized complication following kidney transplantation,characterized by persistent excessive secretion of parathyroid hormone(PTH)despite improved renal function.It is potentially associated with an increased risk of cardiovascular events,renal osteodystrophy,pathologic fractures,graft loss,and mortality.AIM To evaluate the incidence,risk factors,and outcomes of PT-tHPT amongst kidney transplant recipients.METHODS A total of 887 transplant recipients who underwent transplantation between 2000 and 2020 were evaluated.Univariable and multivariable logistic regression was performed to determine the predictors of tertiary hyperparathyroidism.Graft and recipient outcomes were assessed using multivariable Cox regression.A separate multivariable Cox regression was performed to determine the effect of treatment strategies on outcomes.RESULTS PT-tHPT,defined as elevated PTH(>65 ng/L)and persistent hypercalcemia(>2.60 mmol/L),was diagnosed in 14%of recipients.Risk factors for PT-tHPT included older age[odds ratio(OR)=1.36,P<0.001],Asian ethnicity(OR=0.33,P=0.006),total ischemia time(OR=1.03,P=0.048 per hour),pre-transplant serum calcium(OR=1.38,P<0.001)per decile increase,pre-transplant PTH level(OR=1.31,P<0.001)per decile increase,longer dialysis duration(OR=1.12,P=0.002)per year,history of acute rejection(OR=2.37,P=0.012),and slope of estimated glomerular filtration rate change(OR=0.91,P=0.001).There were a 3.4-fold higher risk of death-censored graft loss and a 1.9-fold greater risk of recipient death with PT-tHPT.The three treatment strategies of conservative management,calcimimetic and parathyroidectomy did not significantly change the graft or patient outcome.CONCLUSION Pretransplant elevated calcium and PTH levels,older age and dialysis duration are associated with PT-tHPT.While PT-tHPT significantly affects graft and recipient survival,the treatment strategies did not affect survival.
基金National Basic Research Plan Project of China,No.2023YFC3708303the National Natural Science Foundation of China,No.82241084the High-level Talent in Public Health of Beijing,No.Discipline Leaders-03-29(all to XL).
文摘Long-term exposure to ambient fine particulate matter(PM2.5)may increase the risk of neurotoxicity in human populations.However,research studies on the underlying mechanisms of chronic PM2.5-induced depression-like behaviors,and potential therapeutical strategies,remain scarce.In the present study,after long-term exposure to real-world PM2.5 for 15 weeks,male mice displayed depression-like behaviors,which were revealed using the open field and sucrose preference tests.Mechanistically,chronic PM2.5 exposure promoted astrocytic A1 polarization and disrupted reduction-oxidation balance in the mouse hippocampus.Furthermore,PM2.5-exposed mice displayed pathological damage to hippocampal neurons as well as the inhibition of nuclear factor erythroid 2-related factor 2 signaling.Astrocytic ablation of nuclear factor erythroid 2-related factor 2 exacerbated PM2.5-induced hippocampal neuronal injury in mice via the disruption of astrocyte-to-microglia communication;this finding was confirmed in mice with bilateral and unilateral hippocampal astrocytic Nfe2l2 knockdown.Importantly,the upregulation of nuclear factor erythroid 2-related factor 2 activation by procyanidin significantly ameliorated PM2.5-induced depression-like behaviors through the remodeling of astrocyte-to-microglia communication.Together,our findings shed light on the important role of hippocampal astrocytic nuclear factor erythroid 2-related factor 2 activation for maintaining astrocyte-to-microglia communication,and indicate potential research avenues for therapeutic strategies against PM2.5-induced depresson-like behaviors.
文摘BACKGROUND:Acute pain is a sudden experience secondary to injuries and varies in perception among individuals.In trauma patients,it can negatively aff ect respiratory function,immune response,and wound healing,making it a signifi cant public health concern.This study is to determine the prevalence and factors associated with acute pain among emergency trauma patients.METHODS:A multicenter cross-sectional study was conducted.Data were collected via interviewer-administered questionnaires and patient chart review.The data were analyzed via the statistical package for social science version 25.Bivariable and multivariable logistic regression analyses were used.Variables with a P-value<0.05 were considered statistically signifi cant.RESULTS:A total of 397 patients were included in the study,for a response rate of 96.8%.The prevalence of pain during admission was 91.9%(95%confi dence intervals[95%CIs]:88.8%-94.4%).Blunt trauma(adjusted odds ratio[aOR]=2.82;95%CI:1.23-6.45),analgesia before admission to the emergency department(aOR=2.71;95%CI:1.16-6.36),documentation of pain severity in the chart(aOR=2.71;95%CI:1.16-6.36),analgesia provided within two hours after admission(aOR=7.60;95%CI:2.79-20.68),use of non-pharmacological pain management methods(aOR=3.09;95%CI:1.35-7.08)and availability of analgesia(aOR=3.95;95%CI:1.36-11.43)were associated with acute pain experience.CONCLUSION:The prevalence of acute pain among emergency trauma patients was high in the study area.Analgesia should be administered prior to admission,and non-pharmacological pain management should be implemented.Moreover,training on pain assessment and management should be provided for healthcare providers in the emergency department.
基金supported by the National Natural Science Foundation of China(No.31600316)the Sichuan Science and Technology Program(2023NSFSC0198)。
文摘Understory bryophytes play unique and disproportionately important roles in water retention,biogeochemical cycling,and biodiversity conservation,and serve as bioindicators of environmental health in forest ecosystems.However,biogeographical research on the biomass of forest bryophytes is inadequately studied and has been limited to elevational gradients.We conducted a systematic cross-regional survey of bryophyte biomass across 413 forest sites in Sichuan Province,China.We analyzed how each environmental variable,including climatic and atmospheric factors,overstory covers,and soil nutrients,relates to bryophyte biomass and quantified their relative contributions.The results indicate that,largely similar to previous local investigations and experiments,at a large scale,bryophytes are abundant in forests with lower temperature,nitrogen deposition,vapor pressure deficit,and tree and herb covers,as well as higher light availability.Moreover,bryophyte biomass is positively associated with soil carbon and nitrogen content.These environmental variables are closely related and jointly influence bryophyte biomass,with mean annual temperature being the most significant factor(accounting for 83%of the relative contribution).The biogeographical patterns of bryophyte biomass contribute to deepening our understanding of their adaptations to multiple environmental variables and enable us to predict their responses to global climate change.These patterns also provide essential evidence for establishing more accurate terrestrial vegetation ecosystem models.
基金supported by the Lendület/Momentum Programme of the Hungarian Academy of Sciencesthe National Research, Development, and Innovation Office, Hungary (Grant Nos. LP2024/21 and K146791)+2 种基金Bayers fellowship program MEDHA and Department of Botany, University of Calicutthe financial assistance provided in the form of Junior Research Fellowship from the University Grants Commission (UGC), Indiathe financial assistance provided by the Council for Scientific and Industrial Research(CSIR), India
文摘Ascorbate(Asc),commonly known as vitamin C,is a vital molecule for plant growth,development,and stress resilience.It is also known to play a crucial role in various physiological processes,including photosynthesis,cell division,and differentiation.This article thoroughly explores the processes governing the metabolism of Asc in plants and its roles in physiological functions.It lays down a robust theoretical groundwork for delving into Asc production,transportation,functions,and its potential applications in stress alleviation and horticulture.Furthermore,recent studies indicate that Asc plays a role in regulating fruit development and affecting postharvest storage characteristics,thereby influencing fruit ripening and resilience to stress.Hence,there is a growing importance in studying the synthesis and utilization of Asc in plants.Although the critical role of Asc in controlling plant redox signals has been extensively studied,the precise mechanisms by which it manages cellular redox homeostasis to maintain the equilibrium between reactive oxygen scavenging and cell redox signaling remain elusive.This gap in knowledge presents fresh opportunities to explore how the production of Asc in plants is regulated and how plants react to environmental stressors.Furthermore,this article delves into the potential for a comprehensive investigation into the essential function of Asc in fruits,the development of Asc-rich fruits,and the enhancement of postharvest storage properties.
基金supported by the National Natural Science Foundation of China(32372641)the Shandong Provincial Natural Science Foundation,China(ZR2024QC143)the Liaoning Provincial Natural Science Foundation,China(2022-MS-258)。
文摘Anthocyanins are important flavonoid pigments in the coloration of fruits.To identify candidate genes involved in anthocyanin accumulation,metabolic and transcriptome analyses were conducted in‘Nanguo'pear and its red sport cultivar‘Nanhong'pear.The results showed that‘Nanhong'pear had significantly higher anthocyanin and flavonol contents.Additionally,transcriptomic analysis showed that there were significant differences in the expression of genes involved in phenylpropanoid and flavonoid biosynthesis pathways between the two cultivars,with PuGSTF12 being the most upregulated gene in the‘Nanhong'cultivar.Further analysis identified a novel MYB transcription factor(PuMYB93),and its silencing repressed PuGSTF12 expression and anthocyanin accumulation,suggesting it plays an essential role in the regulation of anthocyanin biosynthesis.Moreover,yeast one-hybrid analysis,electrophoretic mobility shift assay,andβ-glucuronidase assay indicated that PuMYB93 can directly bind to the PuGSTF12 promoter to positively regulate its expression.Additionally,PuGSTF12 silencing suppressed the coloration of PuMYB93-OE peels,suggesting that PuGSTF12 act downstream of PuMYB93.Overall,the findings of this study show that PuMYB93 promotes anthocyanin transport in pears by regulating PuGSTF12 expression to further enhance anthocyanin accumulation.
基金financially supported by the National Natural Science Foundation of China(22138004)National Treasure Ecological Research Synergetic Innovation Center.
文摘Environment serves as the pivotal medium to produce fermented food,with fluctuations in environmental factors exerting a profound impact on the modulation of fermentation microbial communities.Such shifts are crucial for the distinctiveness of fermented food flavor and the variability in quality.Chinese liquor(Baijiu)is one of the typical representatives of spontaneous fermented food.In this review,the multifaceted relationship between regional environmental attributes and the fermentation dynamics of Baijiu was examined,with a spotlight on the strong-flavor,sauce-flavor,and light-flavor varieties.It reveals the influence of regional environmental factors and brewing environmental factors on microbial function and metabolism,which results in the formation of unique flavor characteristics of Baijiu.The 9 main factors affecting the microecology of Baijiu fermentation were further explored,including environmental sensitivity,microbial interactions,biogeographic patterns,and key abiotic factors such as temperature and humidity.Environmental factor management is crucial for controlling microbial community in fermentation.Intelligent detection of the fermentation system is combined with artificial intelligence to realize the digitalization of Baijiu fermentation,with a view to further studying the environmental mechanism or quantitative control relationship of natural fermentation,improving the environmental stability of natural fermentation,and promoting the mechanization and intelligence of fermentation production.
文摘The pathophysiology of many ailments,including neurological,gastrointestinal,and metabolic disorders,is well known to be influenced by intestinal dysbiosis.Clinical research has provided evidence suggesting a strong correlation between dysbiosis of the gut microbiome and colorectal cancer(CRC)development.The active reprogramming of metabolic pathways to boost glycolysis,fatty acid production,lipogenesis,and glutaminolysis constitutes a major metabolic shift in cancer development,including CRC.The complex combination of different factors leads to CRC,making it an environmental disease.These factors include food and lifestyle choices,genetics and family history,age,underlying intestinal diseases,and dysbiosis of the gut microbiota.One of the primary risk factors for carcinoma development is diet,which impacts an individual’s gut microbiome.In addition to impacting CRC formation,the gut microbiome also has immunomodulatory effects,including various immunological interactions and the underlying mechanisms governing them.Microbial interactions in CRC have been extensively studied,yet numerous unresolved queries exist on how gut bacteria can influence treatment.Microbiome-driven immunotherapies,focusing on probiotics,prebiotics,and synbiotics,represent a promising therapeutic avenue.However,large-scale treatment utilization in CRC patients is limited by several issues,including variations in the microbial makeup of each patient’s gut and a lack of established methods.The study highlights the impact of several risk factors,including dysbiosis of the gut microbiome and different approaches to halting and treating CRC progression with a focus on diet changes and modulation of the gut flora.Given the foregoing,we propose that if research gaps are addressed and immunotherapy is paired with microbial interventions,microbiota-based therapeutics could potentially impede the growth of tumors and treat CRC.
