This research deals with an investigation of the adsorption of two acids, namely, 5-amino- 2-chlorotoluene-4-sulfonic and chlorhydric acids from their solution onto weakly basic resin. The screening of res-ins, kineti...This research deals with an investigation of the adsorption of two acids, namely, 5-amino- 2-chlorotoluene-4-sulfonic and chlorhydric acids from their solution onto weakly basic resin. The screening of res-ins, kinetics, and isotherm were studied. The results indicate that the D301R is more appropriate for the removal of acids from solution. The adsorption of acids obeys Langmuir isotherm and the first-order kinetics model. Sorptive affinity of the two acids on D301R was found to be in the order of 5-amino-2-chlorotoluene-4-sulfonic acid> chlorhydric acid. Thermodynamic parameters for the adsorption of acids were calculated and discussed. The maxi-mum removal of acids was observed around 97% and 76% at 25℃ for 5-amino-2-chlorotoluene-4-sulfonic acid and chlorhydric acid , respectively.展开更多
Parkinson's disease is primarily caused by the loss of dopaminergic neurons in the substantia nigra compacta.Ferroptosis,a novel form of regulated cell death characterized by iron accumulation and lipid peroxidati...Parkinson's disease is primarily caused by the loss of dopaminergic neurons in the substantia nigra compacta.Ferroptosis,a novel form of regulated cell death characterized by iron accumulation and lipid peroxidation,plays a vital role in the death of dopaminergic neurons.However,the molecular mechanisms underlying ferroptosis in dopaminergic neurons have not yet been completely elucidated.NADPH oxidase 4 is related to oxidative stress,however,whether it regulates dopaminergic neuronal ferroptosis remains unknown.The aim of this study was to determine whether NADPH oxidase 4 is involved in dopaminergic neuronal ferroptosis,and if so,by what mechanism.We found that the transcriptional regulator activating transcription factor 3 increased NADPH oxidase 4 expression in dopaminergic neurons and astrocytes in an 1-methyl-4-phenyl-1,2,3,6 tetrahydropyridine-induced Parkinson's disease model.NADPH oxidase 4 inhibition improved the behavioral impairments observed in the Parkinson's disease model animals and reduced the death of dopaminergic neurons.Moreover,NADPH oxidase 4 inhibition reduced lipid peroxidation and iron accumulation in the substantia nigra of the Parkinson's disease model animals.Mechanistically,we found that NADPH oxidase 4 interacted with activated protein kinase Cαto prevent ferroptosis of dopaminergic neurons.Furthermore,by lowering the astrocytic lipocalin-2 expression,NADPH oxidase 4 inhibition reduced 1-methyl-4-phenyl-1,2,3,6 tetrahydropyridine-induced neuroinflammation.These findings demonstrate that NADPH oxidase 4 promotes ferroptosis of dopaminergic neurons and neuroinflammation,which contribute to dopaminergic neuron death,suggesting that NADPH oxidase 4 is a possible therapeutic target for Parkinson's disease.展开更多
Objective To study the adsorption of 5-Amino-2-chlorotoluene-4-sulfonic (CLT) and chlorhydric (HCl) acids from wastewater by weakly basic resin. Methods The kinetics and isotherm were studied. Thermodynamic parameters...Objective To study the adsorption of 5-Amino-2-chlorotoluene-4-sulfonic (CLT) and chlorhydric (HCl) acids from wastewater by weakly basic resin. Methods The kinetics and isotherm were studied. Thermodynamic parameters for the adsorption of acids were calculated and discussed. Results The adsorption of CLT and HCl acids followed Langmuir isotherm and the first-order kinetics model. Conclusion The adsorptive affinity of the two acids on D301R is in the order of CLT acid 〉 HCl acid. CLT and HCl acids can be separated.展开更多
Multiple sclerosis(MS)is the most common chronic disease of the central nervous system(CNS)in young adults and represents the first cause of severe handicap,originally non-traumatic(Oh et al.,2018).MS is chara cterize...Multiple sclerosis(MS)is the most common chronic disease of the central nervous system(CNS)in young adults and represents the first cause of severe handicap,originally non-traumatic(Oh et al.,2018).MS is chara cterized by the infiltration of auto reactive lymphocytes specific to myelin through the blood-brain barrier,which results in the appearance of inflammatory demyelinating lesions caused by the death of the central nervous system myelinating cells,oligodendrocytes(Oh et al.,2018).There is a prevalence sexual with a ratio of three times more affected women than men.展开更多
Geometry optimization of p-C_(6)H_(4)-connected cyclo[20]carbon(p-C_(6)H_(4)-C_(20))was carried out at M062X/6-311G(d,p)level,three kinds of bond orders(Mayer,Laplacian,and Wiberg),electron-hole distributions,localize...Geometry optimization of p-C_(6)H_(4)-connected cyclo[20]carbon(p-C_(6)H_(4)-C_(20))was carried out at M062X/6-311G(d,p)level,three kinds of bond orders(Mayer,Laplacian,and Wiberg),electron-hole distributions,localized orbital locators(LOL),and infrared(IR)spectrum were also performed at the same level.Based on TD-DFT M062X/6-311G(d,p)method,the first 20 excited states and ultraviolet(UV)spectra of p-C_(6)H_(4)-C_(20) were calculated.Calculation results of π-electron delocalization analyses prove thatπ-electron delocalization of p-C_(6)H_(4)-C_(20) is more likely to occur on shorter C-C bonds rather than longer C-C bonds,and inside/outside of the ring plane rather than above/below the ring plane.Two absorption peaks of p-C_(6)H_(4)-C_(20) locate at about 319 nm and 236 nm,respectively.展开更多
Neuromyelitis optica spectrum disorders are neuroinflammatory demyelinating disorders that lead to permanent visual loss and motor dysfunction.To date,no effective treatment exists as the exact causative mechanism rem...Neuromyelitis optica spectrum disorders are neuroinflammatory demyelinating disorders that lead to permanent visual loss and motor dysfunction.To date,no effective treatment exists as the exact causative mechanism remains unknown.Therefore,experimental models of neuromyelitis optica spectrum disorders are essential for exploring its pathogenesis and in screening for therapeutic targets.Since most patients with neuromyelitis optica spectrum disorders are seropositive for IgG autoantibodies against aquaporin-4,which is highly expressed on the membrane of astrocyte endfeet,most current experimental models are based on aquaporin-4-IgG that initially targets astrocytes.These experimental models have successfully simulated many pathological features of neuromyelitis optica spectrum disorders,such as aquaporin-4 loss,astrocytopathy,granulocyte and macrophage infiltration,complement activation,demyelination,and neuronal loss;however,they do not fully capture the pathological process of human neuromyelitis optica spectrum disorders.In this review,we summarize the currently known pathogenic mechanisms and the development of associated experimental models in vitro,ex vivo,and in vivo for neuromyelitis optica spectrum disorders,suggest potential pathogenic mechanisms for further investigation,and provide guidance on experimental model choices.In addition,this review summarizes the latest information on pathologies and therapies for neuromyelitis optica spectrum disorders based on experimental models of aquaporin-4-IgG-seropositive neuromyelitis optica spectrum disorders,offering further therapeutic targets and a theoretical basis for clinical trials.展开更多
BACKGROUND:Adeno-associated virus(AAV)gene therapy has been proven to be reliable and safe for the treatment of osteoarthritis in recent years.However,given the complexity of osteoarthritis pathogenesis,single gene ma...BACKGROUND:Adeno-associated virus(AAV)gene therapy has been proven to be reliable and safe for the treatment of osteoarthritis in recent years.However,given the complexity of osteoarthritis pathogenesis,single gene manipulation for the treatment of osteoarthritis may not produce satisfactory results.Previous studies have shown that nuclear factorκB could promote the inflammatory pathway in osteoarthritic chondrocytes,and bone morphogenetic protein 4(BMP4)could promote cartilage regeneration.OBJECTIVE:To test whether combined application of AAV-p65shRNA and AAV-BMP4 will yield the synergistic effect on chondrocytes regeneration and osteoarthritis treatment.METHODS:Viral particles containing AAV-p65-shRNA and AAV-BMP4 were prepared.Their efficacy in inhibiting inflammation in chondrocytes and promoting chondrogenesis was assessed in vitro and in vivo by transfecting AAV-p65-shRNA or AAV-BMP4 into cells.The experiments were divided into five groups:PBS group;osteoarthritis group;AAV-BMP4 group;AAV-p65shRNA group;and BMP4-p65shRNA 1:1 group.Samples were collected at 4,12,and 24 weeks postoperatively.Tissue staining,including safranin O and Alcian blue,was applied after collecting articular tissue.Then,the optimal ratio between the two types of transfected viral particles was further investigated to improve the chondrogenic potential of mixed cells in vivo.RESULTS AND CONCLUSION:The combined application of AAV-p65shRNA and AAV-BMP4 together showed a synergistic effect on cartilage regeneration and osteoarthritis treatment.Mixed cells transfected with AAV-p65shRNA and AAV-BMP4 at a 1:1 ratio produced the most extracellular matrix synthesis(P<0.05).In vivo results also revealed that the combination of the two viruses had the highest regenerative potential for osteoarthritic cartilage(P<0.05).In the present study,we also discovered that the combined therapy had the maximum effect when the two viruses were administered in equal proportions.Decreasing either p65shRNA or BMP4 transfected cells resulted in less collagen II synthesis.This implies that inhibiting inflammation by p65shRNA and promoting regeneration by BMP4 are equally important for osteoarthritis treatment.These findings provide a new strategy for the treatment of early osteoarthritis by simultaneously inhibiting cartilage inflammation and promoting cartilage repair.展开更多
Microglial activation that occurs rapidly after closed head injury may play important and complex roles in neuroinflammation-associated neuronal damage and repair.We previously reported that induced neural stem cells ...Microglial activation that occurs rapidly after closed head injury may play important and complex roles in neuroinflammation-associated neuronal damage and repair.We previously reported that induced neural stem cells can modulate the behavior of activated microglia via CXCL12/CXCR4 signaling,influencing their activation such that they can promote neurological recovery.However,the mechanism of CXCR4 upregulation in induced neural stem cells remains unclear.In this study,we found that nuclear factor-κB activation induced by closed head injury mouse serum in microglia promoted CXCL12 and tumor necrosis factor-αexpression but suppressed insulin-like growth factor-1 expression.However,recombinant complement receptor 2-conjugated Crry(CR2-Crry)reduced the effects of closed head injury mouse serum-induced nuclear factor-κB activation in microglia and the levels of activated microglia,CXCL12,and tumor necrosis factor-α.Additionally,we observed that,in response to stimulation(including stimulation by CXCL12 secreted by activated microglia),CXCR4 and Crry levels can be upregulated in induced neural stem cells via the interplay among CXCL12/CXCR4,Crry,and Akt signaling to modulate microglial activation.In agreement with these in vitro experimental results,we found that Akt activation enhanced the immunoregulatory effects of induced neural stem cell grafts on microglial activation,leading to the promotion of neurological recovery via insulin-like growth factor-1 secretion and the neuroprotective effects of induced neural stem cell grafts through CXCR4 and Crry upregulation in the injured cortices of closed head injury mice.Notably,these beneficial effects of Akt activation in induced neural stem cells were positively correlated with the therapeutic effects of induced neural stem cells on neuronal injury,cerebral edema,and neurological disorders post–closed head injury.In conclusion,our findings reveal that Akt activation may enhance the immunoregulatory effects of induced neural stem cells on microglial activation via upregulation of CXCR4 and Crry,thereby promoting induced neural stem cell–mediated improvement of neuronal injury,cerebral edema,and neurological disorders following closed head injury.展开更多
Electromagnetic interference,which necessitates the rapid advancement of substances with exceptional capabilities for bsorbing electromagnetic waves,is of urgent concern in contemporary society.In this work,CoFe_(2)O_...Electromagnetic interference,which necessitates the rapid advancement of substances with exceptional capabilities for bsorbing electromagnetic waves,is of urgent concern in contemporary society.In this work,CoFe_(2)O_(4)/residual carbon from coal gasification fine slag(CFO/RC)composites were created using a novel hydrothermal method.Various mechanisms for microwave absorption,including conductive loss,natural resonance,interfacial dipole polarization,and magnetic flux loss,are involved in these composites.Consequently,compared with pure residual carbon materials,this composite offers superior capabilities in microwave absorption.At 7.76GHz,the CFO/RC-2 composite achieves an impressive minimum reflection loss(RL_(min))of-43.99 dB with a thickness of 2.44 mm.Moreover,CFO/RC-3 demonstrates an effective absorption bandwidth(EAB)of up to 4.16 GHz,accompanied by a thickness of 1.18mm.This study revealed the remarkable capability of the composite to diminish electromagnetic waves,providing a new generation method for microwave absorbing materials of superior quality.展开更多
基金Supported by the Natural Science Foundation of Jilin Province (No.990337).
文摘This research deals with an investigation of the adsorption of two acids, namely, 5-amino- 2-chlorotoluene-4-sulfonic and chlorhydric acids from their solution onto weakly basic resin. The screening of res-ins, kinetics, and isotherm were studied. The results indicate that the D301R is more appropriate for the removal of acids from solution. The adsorption of acids obeys Langmuir isotherm and the first-order kinetics model. Sorptive affinity of the two acids on D301R was found to be in the order of 5-amino-2-chlorotoluene-4-sulfonic acid> chlorhydric acid. Thermodynamic parameters for the adsorption of acids were calculated and discussed. The maxi-mum removal of acids was observed around 97% and 76% at 25℃ for 5-amino-2-chlorotoluene-4-sulfonic acid and chlorhydric acid , respectively.
基金supported by the National Natural Science Foundation of China,Nos.82271444(to JP),82271268(to BZ),and 82001346(to YL)the National Key Research and Development Program of China,No.2022YFE0210100(to BZ)。
文摘Parkinson's disease is primarily caused by the loss of dopaminergic neurons in the substantia nigra compacta.Ferroptosis,a novel form of regulated cell death characterized by iron accumulation and lipid peroxidation,plays a vital role in the death of dopaminergic neurons.However,the molecular mechanisms underlying ferroptosis in dopaminergic neurons have not yet been completely elucidated.NADPH oxidase 4 is related to oxidative stress,however,whether it regulates dopaminergic neuronal ferroptosis remains unknown.The aim of this study was to determine whether NADPH oxidase 4 is involved in dopaminergic neuronal ferroptosis,and if so,by what mechanism.We found that the transcriptional regulator activating transcription factor 3 increased NADPH oxidase 4 expression in dopaminergic neurons and astrocytes in an 1-methyl-4-phenyl-1,2,3,6 tetrahydropyridine-induced Parkinson's disease model.NADPH oxidase 4 inhibition improved the behavioral impairments observed in the Parkinson's disease model animals and reduced the death of dopaminergic neurons.Moreover,NADPH oxidase 4 inhibition reduced lipid peroxidation and iron accumulation in the substantia nigra of the Parkinson's disease model animals.Mechanistically,we found that NADPH oxidase 4 interacted with activated protein kinase Cαto prevent ferroptosis of dopaminergic neurons.Furthermore,by lowering the astrocytic lipocalin-2 expression,NADPH oxidase 4 inhibition reduced 1-methyl-4-phenyl-1,2,3,6 tetrahydropyridine-induced neuroinflammation.These findings demonstrate that NADPH oxidase 4 promotes ferroptosis of dopaminergic neurons and neuroinflammation,which contribute to dopaminergic neuron death,suggesting that NADPH oxidase 4 is a possible therapeutic target for Parkinson's disease.
基金The study was supported by the Nature Science Foundation of Jilin Province (No. 990337).
文摘Objective To study the adsorption of 5-Amino-2-chlorotoluene-4-sulfonic (CLT) and chlorhydric (HCl) acids from wastewater by weakly basic resin. Methods The kinetics and isotherm were studied. Thermodynamic parameters for the adsorption of acids were calculated and discussed. Results The adsorption of CLT and HCl acids followed Langmuir isotherm and the first-order kinetics model. Conclusion The adsorptive affinity of the two acids on D301R is in the order of CLT acid 〉 HCl acid. CLT and HCl acids can be separated.
基金supported by a grant from the French Multiple Sclerosis Society(ARSEP,Grant Number:R20163LL)(to AMG)。
文摘Multiple sclerosis(MS)is the most common chronic disease of the central nervous system(CNS)in young adults and represents the first cause of severe handicap,originally non-traumatic(Oh et al.,2018).MS is chara cterized by the infiltration of auto reactive lymphocytes specific to myelin through the blood-brain barrier,which results in the appearance of inflammatory demyelinating lesions caused by the death of the central nervous system myelinating cells,oligodendrocytes(Oh et al.,2018).There is a prevalence sexual with a ratio of three times more affected women than men.
文摘Geometry optimization of p-C_(6)H_(4)-connected cyclo[20]carbon(p-C_(6)H_(4)-C_(20))was carried out at M062X/6-311G(d,p)level,three kinds of bond orders(Mayer,Laplacian,and Wiberg),electron-hole distributions,localized orbital locators(LOL),and infrared(IR)spectrum were also performed at the same level.Based on TD-DFT M062X/6-311G(d,p)method,the first 20 excited states and ultraviolet(UV)spectra of p-C_(6)H_(4)-C_(20) were calculated.Calculation results of π-electron delocalization analyses prove thatπ-electron delocalization of p-C_(6)H_(4)-C_(20) is more likely to occur on shorter C-C bonds rather than longer C-C bonds,and inside/outside of the ring plane rather than above/below the ring plane.Two absorption peaks of p-C_(6)H_(4)-C_(20) locate at about 319 nm and 236 nm,respectively.
文摘Neuromyelitis optica spectrum disorders are neuroinflammatory demyelinating disorders that lead to permanent visual loss and motor dysfunction.To date,no effective treatment exists as the exact causative mechanism remains unknown.Therefore,experimental models of neuromyelitis optica spectrum disorders are essential for exploring its pathogenesis and in screening for therapeutic targets.Since most patients with neuromyelitis optica spectrum disorders are seropositive for IgG autoantibodies against aquaporin-4,which is highly expressed on the membrane of astrocyte endfeet,most current experimental models are based on aquaporin-4-IgG that initially targets astrocytes.These experimental models have successfully simulated many pathological features of neuromyelitis optica spectrum disorders,such as aquaporin-4 loss,astrocytopathy,granulocyte and macrophage infiltration,complement activation,demyelination,and neuronal loss;however,they do not fully capture the pathological process of human neuromyelitis optica spectrum disorders.In this review,we summarize the currently known pathogenic mechanisms and the development of associated experimental models in vitro,ex vivo,and in vivo for neuromyelitis optica spectrum disorders,suggest potential pathogenic mechanisms for further investigation,and provide guidance on experimental model choices.In addition,this review summarizes the latest information on pathologies and therapies for neuromyelitis optica spectrum disorders based on experimental models of aquaporin-4-IgG-seropositive neuromyelitis optica spectrum disorders,offering further therapeutic targets and a theoretical basis for clinical trials.
文摘BACKGROUND:Adeno-associated virus(AAV)gene therapy has been proven to be reliable and safe for the treatment of osteoarthritis in recent years.However,given the complexity of osteoarthritis pathogenesis,single gene manipulation for the treatment of osteoarthritis may not produce satisfactory results.Previous studies have shown that nuclear factorκB could promote the inflammatory pathway in osteoarthritic chondrocytes,and bone morphogenetic protein 4(BMP4)could promote cartilage regeneration.OBJECTIVE:To test whether combined application of AAV-p65shRNA and AAV-BMP4 will yield the synergistic effect on chondrocytes regeneration and osteoarthritis treatment.METHODS:Viral particles containing AAV-p65-shRNA and AAV-BMP4 were prepared.Their efficacy in inhibiting inflammation in chondrocytes and promoting chondrogenesis was assessed in vitro and in vivo by transfecting AAV-p65-shRNA or AAV-BMP4 into cells.The experiments were divided into five groups:PBS group;osteoarthritis group;AAV-BMP4 group;AAV-p65shRNA group;and BMP4-p65shRNA 1:1 group.Samples were collected at 4,12,and 24 weeks postoperatively.Tissue staining,including safranin O and Alcian blue,was applied after collecting articular tissue.Then,the optimal ratio between the two types of transfected viral particles was further investigated to improve the chondrogenic potential of mixed cells in vivo.RESULTS AND CONCLUSION:The combined application of AAV-p65shRNA and AAV-BMP4 together showed a synergistic effect on cartilage regeneration and osteoarthritis treatment.Mixed cells transfected with AAV-p65shRNA and AAV-BMP4 at a 1:1 ratio produced the most extracellular matrix synthesis(P<0.05).In vivo results also revealed that the combination of the two viruses had the highest regenerative potential for osteoarthritic cartilage(P<0.05).In the present study,we also discovered that the combined therapy had the maximum effect when the two viruses were administered in equal proportions.Decreasing either p65shRNA or BMP4 transfected cells resulted in less collagen II synthesis.This implies that inhibiting inflammation by p65shRNA and promoting regeneration by BMP4 are equally important for osteoarthritis treatment.These findings provide a new strategy for the treatment of early osteoarthritis by simultaneously inhibiting cartilage inflammation and promoting cartilage repair.
基金supported by the National Natural Science Foundation of China,Nos.82271397(to MG),82001293(to MG),82171355(to RX),81971295(to RX),and 81671189(to RX)。
文摘Microglial activation that occurs rapidly after closed head injury may play important and complex roles in neuroinflammation-associated neuronal damage and repair.We previously reported that induced neural stem cells can modulate the behavior of activated microglia via CXCL12/CXCR4 signaling,influencing their activation such that they can promote neurological recovery.However,the mechanism of CXCR4 upregulation in induced neural stem cells remains unclear.In this study,we found that nuclear factor-κB activation induced by closed head injury mouse serum in microglia promoted CXCL12 and tumor necrosis factor-αexpression but suppressed insulin-like growth factor-1 expression.However,recombinant complement receptor 2-conjugated Crry(CR2-Crry)reduced the effects of closed head injury mouse serum-induced nuclear factor-κB activation in microglia and the levels of activated microglia,CXCL12,and tumor necrosis factor-α.Additionally,we observed that,in response to stimulation(including stimulation by CXCL12 secreted by activated microglia),CXCR4 and Crry levels can be upregulated in induced neural stem cells via the interplay among CXCL12/CXCR4,Crry,and Akt signaling to modulate microglial activation.In agreement with these in vitro experimental results,we found that Akt activation enhanced the immunoregulatory effects of induced neural stem cell grafts on microglial activation,leading to the promotion of neurological recovery via insulin-like growth factor-1 secretion and the neuroprotective effects of induced neural stem cell grafts through CXCR4 and Crry upregulation in the injured cortices of closed head injury mice.Notably,these beneficial effects of Akt activation in induced neural stem cells were positively correlated with the therapeutic effects of induced neural stem cells on neuronal injury,cerebral edema,and neurological disorders post–closed head injury.In conclusion,our findings reveal that Akt activation may enhance the immunoregulatory effects of induced neural stem cells on microglial activation via upregulation of CXCR4 and Crry,thereby promoting induced neural stem cell–mediated improvement of neuronal injury,cerebral edema,and neurological disorders following closed head injury.
基金financially supported by the Key Project of Natural Science Research in Colleges and Universities of Anhui Province,China(No.2022AH050816)the Open Research Grant of Joint National-Local Engineering Research Centre for Safe and Precise Coal Mining(Nos.EC2023013 and EC2022018)+1 种基金the National Natural Science Foundation of China(No.52200139)the Introduction of Talent in Anhui University of Science and Technology,China(Nos.2021yjrc18 and 2023yjrc79)。
文摘Electromagnetic interference,which necessitates the rapid advancement of substances with exceptional capabilities for bsorbing electromagnetic waves,is of urgent concern in contemporary society.In this work,CoFe_(2)O_(4)/residual carbon from coal gasification fine slag(CFO/RC)composites were created using a novel hydrothermal method.Various mechanisms for microwave absorption,including conductive loss,natural resonance,interfacial dipole polarization,and magnetic flux loss,are involved in these composites.Consequently,compared with pure residual carbon materials,this composite offers superior capabilities in microwave absorption.At 7.76GHz,the CFO/RC-2 composite achieves an impressive minimum reflection loss(RL_(min))of-43.99 dB with a thickness of 2.44 mm.Moreover,CFO/RC-3 demonstrates an effective absorption bandwidth(EAB)of up to 4.16 GHz,accompanied by a thickness of 1.18mm.This study revealed the remarkable capability of the composite to diminish electromagnetic waves,providing a new generation method for microwave absorbing materials of superior quality.
