目的:颈前路减压融合术是治疗退行性颈椎病的经典手术方式,钉板的使用增加了融合率及稳定性的同时,间接导致了邻近椎体退变和术后吞咽困难的发生。文章通过Meta分析方法比较ROI-C^(TM)自锁系统和传统融合器联合钉板内固定治疗退行性颈...目的:颈前路减压融合术是治疗退行性颈椎病的经典手术方式,钉板的使用增加了融合率及稳定性的同时,间接导致了邻近椎体退变和术后吞咽困难的发生。文章通过Meta分析方法比较ROI-C^(TM)自锁系统和传统融合器联合钉板内固定治疗退行性颈椎病患者的临床结果和并发症情况,为颈前路减压融合术中内固定方式的选择提供循证学支持。方法:检索中国知网、万方、维普、PubMed、Cochrane Library、Web of Science和Embase数据库,检索关于颈前路减压融合术中应用ROI-C^(TM)自锁系统与融合器联合钉板内固定治疗退行性颈椎病的中英文文献。检索时间范围为各数据库建库至2023年7月。由2名研究者严格按照纳入与排除标准选择文献,采用Cochrane偏倚风险工具对随机对照试验进行质量评价,NOS量表对队列研究进行质量评价。采用RevMan 5.4软件进行Meta分析。结局指标包括手术时间、术中出血量、日本骨科协会(Japanese Orthopaedic Association Scores,JOA)评分、颈椎功能障碍指数、C_(2)-C_(7)Cobb角、融合率、邻近椎体退变发生率、融合器沉降率和吞咽困难发生率。结果:共纳入13项研究,其中回顾性队列研究11项,随机对照试验2项,共1136例患者,ROI-C组569例,融合器联合钉板组567例。Meta分析结果显示:ROI-C组与融合器联合钉板组在手术时间(MD=-15.52,95%CI:-18.62至-12.42,P<0.00001),术中出血量(MD=-24.53,95%CI:-32.46至-16.61,P<0.00001),术后邻近节段退变率(RR=0.40,95%CI:0.27-0.60,P<0.00001)和术后总吞咽困难发生率(RR=0.18,95%CI:0.13-0.26,P<0.00001)均具有显著性差异。两者在术后JOA评分、颈椎功能障碍指数、C_(2)-C_(7)Cobb角、融合率和融合器沉降率方面无显著性差异(P≥0.05)。结论:在颈椎前路减压融合术中应用ROI-C^(TM)自锁系统与传统融合器联合钉板内固定治疗退行性颈椎病均可达到满意的临床效果,ROI-C^(TM)自锁系统操作更加简单,相比融合器联合钉板内固定能明显减少手术时间及术中出血量,在减少术后吞咽困难及邻近节段退变发生率等方面具有明显优势,对于跳跃型颈椎病及邻椎病翻修患者,更加推荐使用ROI-C^(TM)自锁系统。但鉴于其可能存在较高的沉降率,对于多节段且合并融合器沉降高危因素如骨质疏松、椎体终板破损的退行性颈椎病患者,仍建议使用融合器联合钉板内固定。展开更多
Two-terminal(2-T)perovskite(PVK)/CuIn(Ga)Se_(2)(CIGS)tandem solar cells(TSCs)have been considered as an ideal tandem cell because of their best bandgap matching regarding to Shockley–Queisser(S–Q)limits.However,the ...Two-terminal(2-T)perovskite(PVK)/CuIn(Ga)Se_(2)(CIGS)tandem solar cells(TSCs)have been considered as an ideal tandem cell because of their best bandgap matching regarding to Shockley–Queisser(S–Q)limits.However,the nature of the irregular rough morphology of commercial CIGS prevents people from improving tandem device performances.In this paper,D-homoserine lactone hydrochloride is proven to improve coverage of PVK materials on irregular rough CIGS surfaces and also passivate bulk defects by modulating the growth of PVK crystals.In addition,the minority carriers near the PVK/C60 interface and the incompletely passivated trap states caused interface recombination.A surface reconstruction with 2-thiopheneethylammonium iodide and N,N-dimethylformamide assisted passivates the defect sites located at the surface and grain boundaries.Meanwhile,LiF is used to create this field effect,repelling hole carriers away from the PVK and C60 interface and thus reducing recombination.As a result,a 2-T PVK/CIGS tandem yielded a power conversion efficiency of 24.6%(0.16 cm^(2)),one of the highest results for 2-T PVK/CIGS TSCs to our knowledge.This validation underscores the potential of our methodology in achieving superior performance in PVK/CIGS tandem solar cells.展开更多
Repetitive traumatic brain injury impacts adult neurogenesis in the hippocampal dentate gyrus,leading to long-term cognitive impairment.However,the mechanism underlying this neurogenesis impairment remains unknown.In ...Repetitive traumatic brain injury impacts adult neurogenesis in the hippocampal dentate gyrus,leading to long-term cognitive impairment.However,the mechanism underlying this neurogenesis impairment remains unknown.In this study,we established a male mouse model of repetitive traumatic brain injury and performed long-term evaluation of neurogenesis of the hippocampal dentate gyrus after repetitive traumatic brain injury.Our results showed that repetitive traumatic brain injury inhibited neural stem cell proliferation and development,delayed neuronal maturation,and reduced the complexity of neuronal dendrites and spines.Mice with repetitive traumatic brain injuryalso showed deficits in spatial memory retrieval.Moreover,following repetitive traumatic brain injury,neuroinflammation was enhanced in the neurogenesis microenvironment where C1q levels were increased,C1q binding protein levels were decreased,and canonical Wnt/β-catenin signaling was downregulated.An inhibitor of C1 reversed the long-term impairment of neurogenesis induced by repetitive traumatic brain injury and improved neurological function.These findings suggest that repetitive traumatic brain injury–induced C1-related inflammation impairs long-term neurogenesis in the dentate gyrus and contributes to spatial memory retrieval dysfunction.展开更多
Several studies have shown that activation of unfolded protein response and endoplasmic reticulum(ER)stress plays a crucial role in severe cerebral ischemia/reperfusion injury.Autophagy occurs within hours after cereb...Several studies have shown that activation of unfolded protein response and endoplasmic reticulum(ER)stress plays a crucial role in severe cerebral ischemia/reperfusion injury.Autophagy occurs within hours after cerebral ischemia,but the relationship between ER stress and autophagy remains unclear.In this study,we established experimental models using oxygen-glucose deprivation/reoxygenation in PC12 cells and primary neurons to simulate cerebral ischemia/reperfusion injury.We found that prolongation of oxygen-glucose deprivation activated the ER stress pathway protein kinase-like endoplasmic reticulum kinase(PERK)/eukaryotic translation initiation factor 2 subunit alpha(e IF2α)-activating transcription factor 4(ATF4)-C/EBP homologous protein(CHOP),increased neuronal apoptosis,and induced autophagy.Furthermore,inhibition of ER stress using inhibitors or by si RNA knockdown of the PERK gene significantly attenuated excessive autophagy and neuronal apoptosis,indicating an interaction between autophagy and ER stress and suggesting PERK as an essential target for regulating autophagy.Blocking autophagy with chloroquine exacerbated ER stress-induced apoptosis,indicating that normal levels of autophagy play a protective role in neuronal injury following cerebral ischemia/reperfusion injury.Findings from this study indicate that cerebral ischemia/reperfusion injury can trigger neuronal ER stress and promote autophagy,and suggest that PERK is a possible target for inhibiting excessive autophagy in cerebral ischemia/reperfusion injury.展开更多
Netrin-1 and its receptors play crucial roles in inducing axonal growth and neuronal migration during neuronal development.Their profound impacts then extend into adulthood to encompass the maintenance of neuronal sur...Netrin-1 and its receptors play crucial roles in inducing axonal growth and neuronal migration during neuronal development.Their profound impacts then extend into adulthood to encompass the maintenance of neuronal survival and synaptic function.Increasing amounts of evidence highlight several key points:(1)Diminished Netrin-1 levels exacerbate pathological progression in animal models of Alzheimer’s disease and Parkinson’s disease,and potentially,similar alterations occur in humans.(2)Genetic mutations of Netrin-1 receptors increase an individuals’susceptibility to neurodegenerative disorders.(3)Therapeutic approaches targeting Netrin-1 and its receptors offer the benefits of enhancing memory and motor function.(4)Netrin-1 and its receptors show genetic and epigenetic alterations in a variety of cancers.These findings provide compelling evidence that Netrin-1 and its receptors are crucial targets in neurodegenerative diseases.Through a comprehensive review of Netrin-1 signaling pathways,our objective is to uncover potential therapeutic avenues for neurodegenerative disorders.展开更多
文摘目的:颈前路减压融合术是治疗退行性颈椎病的经典手术方式,钉板的使用增加了融合率及稳定性的同时,间接导致了邻近椎体退变和术后吞咽困难的发生。文章通过Meta分析方法比较ROI-C^(TM)自锁系统和传统融合器联合钉板内固定治疗退行性颈椎病患者的临床结果和并发症情况,为颈前路减压融合术中内固定方式的选择提供循证学支持。方法:检索中国知网、万方、维普、PubMed、Cochrane Library、Web of Science和Embase数据库,检索关于颈前路减压融合术中应用ROI-C^(TM)自锁系统与融合器联合钉板内固定治疗退行性颈椎病的中英文文献。检索时间范围为各数据库建库至2023年7月。由2名研究者严格按照纳入与排除标准选择文献,采用Cochrane偏倚风险工具对随机对照试验进行质量评价,NOS量表对队列研究进行质量评价。采用RevMan 5.4软件进行Meta分析。结局指标包括手术时间、术中出血量、日本骨科协会(Japanese Orthopaedic Association Scores,JOA)评分、颈椎功能障碍指数、C_(2)-C_(7)Cobb角、融合率、邻近椎体退变发生率、融合器沉降率和吞咽困难发生率。结果:共纳入13项研究,其中回顾性队列研究11项,随机对照试验2项,共1136例患者,ROI-C组569例,融合器联合钉板组567例。Meta分析结果显示:ROI-C组与融合器联合钉板组在手术时间(MD=-15.52,95%CI:-18.62至-12.42,P<0.00001),术中出血量(MD=-24.53,95%CI:-32.46至-16.61,P<0.00001),术后邻近节段退变率(RR=0.40,95%CI:0.27-0.60,P<0.00001)和术后总吞咽困难发生率(RR=0.18,95%CI:0.13-0.26,P<0.00001)均具有显著性差异。两者在术后JOA评分、颈椎功能障碍指数、C_(2)-C_(7)Cobb角、融合率和融合器沉降率方面无显著性差异(P≥0.05)。结论:在颈椎前路减压融合术中应用ROI-C^(TM)自锁系统与传统融合器联合钉板内固定治疗退行性颈椎病均可达到满意的临床效果,ROI-C^(TM)自锁系统操作更加简单,相比融合器联合钉板内固定能明显减少手术时间及术中出血量,在减少术后吞咽困难及邻近节段退变发生率等方面具有明显优势,对于跳跃型颈椎病及邻椎病翻修患者,更加推荐使用ROI-C^(TM)自锁系统。但鉴于其可能存在较高的沉降率,对于多节段且合并融合器沉降高危因素如骨质疏松、椎体终板破损的退行性颈椎病患者,仍建议使用融合器联合钉板内固定。
基金supported by“National Natural Science Foundation of China(U21A20171,U20A20245)”“Hubei Provincial Natural Science Foundation of China(2023AFA010)”+1 种基金“Independent Innovation Projects of the Hubei Longzhong Laboratory(2022ZZ-09)”“Social Public Welfare and Basic Research Special Project of Zhongshan(2020B2015).”。
文摘Two-terminal(2-T)perovskite(PVK)/CuIn(Ga)Se_(2)(CIGS)tandem solar cells(TSCs)have been considered as an ideal tandem cell because of their best bandgap matching regarding to Shockley–Queisser(S–Q)limits.However,the nature of the irregular rough morphology of commercial CIGS prevents people from improving tandem device performances.In this paper,D-homoserine lactone hydrochloride is proven to improve coverage of PVK materials on irregular rough CIGS surfaces and also passivate bulk defects by modulating the growth of PVK crystals.In addition,the minority carriers near the PVK/C60 interface and the incompletely passivated trap states caused interface recombination.A surface reconstruction with 2-thiopheneethylammonium iodide and N,N-dimethylformamide assisted passivates the defect sites located at the surface and grain boundaries.Meanwhile,LiF is used to create this field effect,repelling hole carriers away from the PVK and C60 interface and thus reducing recombination.As a result,a 2-T PVK/CIGS tandem yielded a power conversion efficiency of 24.6%(0.16 cm^(2)),one of the highest results for 2-T PVK/CIGS TSCs to our knowledge.This validation underscores the potential of our methodology in achieving superior performance in PVK/CIGS tandem solar cells.
基金supported by the Fundamental Research Program of Shanxi Province of China,No.20210302124277the Science Foundation of Shanxi Bethune Hospital,No.2021YJ13(both to JW)。
文摘Repetitive traumatic brain injury impacts adult neurogenesis in the hippocampal dentate gyrus,leading to long-term cognitive impairment.However,the mechanism underlying this neurogenesis impairment remains unknown.In this study,we established a male mouse model of repetitive traumatic brain injury and performed long-term evaluation of neurogenesis of the hippocampal dentate gyrus after repetitive traumatic brain injury.Our results showed that repetitive traumatic brain injury inhibited neural stem cell proliferation and development,delayed neuronal maturation,and reduced the complexity of neuronal dendrites and spines.Mice with repetitive traumatic brain injuryalso showed deficits in spatial memory retrieval.Moreover,following repetitive traumatic brain injury,neuroinflammation was enhanced in the neurogenesis microenvironment where C1q levels were increased,C1q binding protein levels were decreased,and canonical Wnt/β-catenin signaling was downregulated.An inhibitor of C1 reversed the long-term impairment of neurogenesis induced by repetitive traumatic brain injury and improved neurological function.These findings suggest that repetitive traumatic brain injury–induced C1-related inflammation impairs long-term neurogenesis in the dentate gyrus and contributes to spatial memory retrieval dysfunction.
基金supported by the National Natural Science Foundation of China,Nos.82260245(to YX),81660207(to YX),81960253(to YL),82160268(to YL),U1812403(to ZG)Science and Technology Projects of Guizhou Province,Nos.[2019]1440(to YX),[2020]1Z067(to WH)+1 种基金Cultivation Foundation of Guizhou Medical University,No.[20NSP069](to YX)Excellent Young Talents Plan of Guizhou Medical University,No.(2022)101(to WH)。
文摘Several studies have shown that activation of unfolded protein response and endoplasmic reticulum(ER)stress plays a crucial role in severe cerebral ischemia/reperfusion injury.Autophagy occurs within hours after cerebral ischemia,but the relationship between ER stress and autophagy remains unclear.In this study,we established experimental models using oxygen-glucose deprivation/reoxygenation in PC12 cells and primary neurons to simulate cerebral ischemia/reperfusion injury.We found that prolongation of oxygen-glucose deprivation activated the ER stress pathway protein kinase-like endoplasmic reticulum kinase(PERK)/eukaryotic translation initiation factor 2 subunit alpha(e IF2α)-activating transcription factor 4(ATF4)-C/EBP homologous protein(CHOP),increased neuronal apoptosis,and induced autophagy.Furthermore,inhibition of ER stress using inhibitors or by si RNA knockdown of the PERK gene significantly attenuated excessive autophagy and neuronal apoptosis,indicating an interaction between autophagy and ER stress and suggesting PERK as an essential target for regulating autophagy.Blocking autophagy with chloroquine exacerbated ER stress-induced apoptosis,indicating that normal levels of autophagy play a protective role in neuronal injury following cerebral ischemia/reperfusion injury.Findings from this study indicate that cerebral ischemia/reperfusion injury can trigger neuronal ER stress and promote autophagy,and suggest that PERK is a possible target for inhibiting excessive autophagy in cerebral ischemia/reperfusion injury.
基金supported by the National Natural Science Foundation of China(Youth Science Fund Project),No.81901292(to GC)the National Key Research and Development Program of China,No.2021YFC2502100(to GC)the National Natural Science Foundation of China,No.82071183(to ZZ).
文摘Netrin-1 and its receptors play crucial roles in inducing axonal growth and neuronal migration during neuronal development.Their profound impacts then extend into adulthood to encompass the maintenance of neuronal survival and synaptic function.Increasing amounts of evidence highlight several key points:(1)Diminished Netrin-1 levels exacerbate pathological progression in animal models of Alzheimer’s disease and Parkinson’s disease,and potentially,similar alterations occur in humans.(2)Genetic mutations of Netrin-1 receptors increase an individuals’susceptibility to neurodegenerative disorders.(3)Therapeutic approaches targeting Netrin-1 and its receptors offer the benefits of enhancing memory and motor function.(4)Netrin-1 and its receptors show genetic and epigenetic alterations in a variety of cancers.These findings provide compelling evidence that Netrin-1 and its receptors are crucial targets in neurodegenerative diseases.Through a comprehensive review of Netrin-1 signaling pathways,our objective is to uncover potential therapeutic avenues for neurodegenerative disorders.
