Due to the presence of turbid media, such as microdust and water vapor in the environment, outdoor pictures taken under hazy weather circumstances are typically degraded. To enhance the quality of such images, this wo...Due to the presence of turbid media, such as microdust and water vapor in the environment, outdoor pictures taken under hazy weather circumstances are typically degraded. To enhance the quality of such images, this work proposes a new hybrid λ2-λ0 penalty model for image dehazing. This model performs a weighted fusion of two distinct transmission maps, generated by imposing λ2 and λ0 norm penalties on the approximate regression coefficients of the transmission map. This approach effectively balances the sparsity and smoothness associated with the λ0 and λ2 norms, thereby optimizing the transmittance map. Specifically, when the λ2 norm is penalized in the model, an updated guided image is obtained after implementing λ0 penalty. The resulting optimization problem is effectively solved using the least square method and the alternating direction algorithm. The dehazing framework combines the advantages of λ2 and λ0 norms, enhancing sparse and smoothness, resulting in higher quality images with clearer details and preserved edges.展开更多
Mitochondrial dysfunction is a significant pathological alte ration that occurs in Parkinson's disease(PD),and the Thr61lle(T61I)mutation in coiled-coil helix coiled-coil helix domain containing 2(CHCHD2),a crucia...Mitochondrial dysfunction is a significant pathological alte ration that occurs in Parkinson's disease(PD),and the Thr61lle(T61I)mutation in coiled-coil helix coiled-coil helix domain containing 2(CHCHD2),a crucial mitochondrial protein,has been reported to cause Parkinson's disease.FIFO-ATPase participates in the synthesis of cellular adenosine triphosphate(ATP)and plays a central role in mitochondrial energy metabolism.However,the specific roles of wild-type(WT)CHCHD2 and T611-mutant CHCHD2 in regulating F1FO-ATPase activity in Parkinson's disease,as well as whether CHCHD2 or CHCHD2 T61I affects mitochondrial function through regulating F1FO-ATPase activity,remain unclea r.Therefore,in this study,we expressed WT CHCHD2 and T61l-mutant CHCHD2 in an MPP^(+)-induced SH-SY5Y cell model of PD.We found that CHCHD2 protected mitochondria from developing MPP^(+)-induced dysfunction.Under normal conditions,ove rexpression of WT CHCHD2 promoted F1FO-ATPase assembly,while T61I-mutant CHCHD2 appeared to have lost the ability to regulate F1FO-ATPase assembly.In addition,mass spectrometry and immunoprecipitation showed that there was an interaction between CHCHD2 and F1FO-ATPase.Three weeks after transfection with AAV-CHCHD2 T61I,we intraperitoneally injected 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine into mice to establish an animal model of chronic Parkinson's disease and found that exogenous expression of the mutant protein worsened the behavioral deficits and dopaminergic neurodegeneration seen in this model.These findings suggest that WT CHCHD2 can alleviate mitochondrial dysfunction in PD by maintaining F1F0-ATPase structure and function.展开更多
Web 2.0的出现使信息构建(IA)的内容发生了深刻变化,IA已进入"信息构建2.0"(IA2.0)阶段。在IA2.0阶段,IA作为一门学科、一种角色和一类社团的协调统一体而存在,它强调真正"以用户为中心"和"丰富的用户体验&qu...Web 2.0的出现使信息构建(IA)的内容发生了深刻变化,IA已进入"信息构建2.0"(IA2.0)阶段。在IA2.0阶段,IA作为一门学科、一种角色和一类社团的协调统一体而存在,它强调真正"以用户为中心"和"丰富的用户体验"的核心理念,以满足新环境下的用户需求。Web2.0网站的IA,是IA2.0的典型应用,也是IA2.0阶段研究的主要内容,本文将其称为网站IA2.0。文中设计了一个网站IA2.0模型,并进行了简单的实例分析。展开更多
文摘Due to the presence of turbid media, such as microdust and water vapor in the environment, outdoor pictures taken under hazy weather circumstances are typically degraded. To enhance the quality of such images, this work proposes a new hybrid λ2-λ0 penalty model for image dehazing. This model performs a weighted fusion of two distinct transmission maps, generated by imposing λ2 and λ0 norm penalties on the approximate regression coefficients of the transmission map. This approach effectively balances the sparsity and smoothness associated with the λ0 and λ2 norms, thereby optimizing the transmittance map. Specifically, when the λ2 norm is penalized in the model, an updated guided image is obtained after implementing λ0 penalty. The resulting optimization problem is effectively solved using the least square method and the alternating direction algorithm. The dehazing framework combines the advantages of λ2 and λ0 norms, enhancing sparse and smoothness, resulting in higher quality images with clearer details and preserved edges.
基金supported by the National Natural Science Foundation of China(Youth Program),No.81901282(to XC)the National Natural Science Foundation of China,Nos.81401416(to PX),81870992(to PX),81870856(to XC and MZ)+3 种基金Guangdong Basic and Applied Basic Research Foundation the Science Foundation,No.2019A1515011189(to XC)Central Government Guiding Local Science and Technology Development Projects,No.ZYYD2022C17(to PX)Key Project of Guangzhou Health Commission,No.2019-ZD-09(to PX)Science and Technology Planning Project of Guangzhou,Nos.202102020029(to XC),202102010010(to PX)。
文摘Mitochondrial dysfunction is a significant pathological alte ration that occurs in Parkinson's disease(PD),and the Thr61lle(T61I)mutation in coiled-coil helix coiled-coil helix domain containing 2(CHCHD2),a crucial mitochondrial protein,has been reported to cause Parkinson's disease.FIFO-ATPase participates in the synthesis of cellular adenosine triphosphate(ATP)and plays a central role in mitochondrial energy metabolism.However,the specific roles of wild-type(WT)CHCHD2 and T611-mutant CHCHD2 in regulating F1FO-ATPase activity in Parkinson's disease,as well as whether CHCHD2 or CHCHD2 T61I affects mitochondrial function through regulating F1FO-ATPase activity,remain unclea r.Therefore,in this study,we expressed WT CHCHD2 and T61l-mutant CHCHD2 in an MPP^(+)-induced SH-SY5Y cell model of PD.We found that CHCHD2 protected mitochondria from developing MPP^(+)-induced dysfunction.Under normal conditions,ove rexpression of WT CHCHD2 promoted F1FO-ATPase assembly,while T61I-mutant CHCHD2 appeared to have lost the ability to regulate F1FO-ATPase assembly.In addition,mass spectrometry and immunoprecipitation showed that there was an interaction between CHCHD2 and F1FO-ATPase.Three weeks after transfection with AAV-CHCHD2 T61I,we intraperitoneally injected 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine into mice to establish an animal model of chronic Parkinson's disease and found that exogenous expression of the mutant protein worsened the behavioral deficits and dopaminergic neurodegeneration seen in this model.These findings suggest that WT CHCHD2 can alleviate mitochondrial dysfunction in PD by maintaining F1F0-ATPase structure and function.
