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
根据美国Second Life Library 2.0虚拟社区的建设现状,分析图书馆虚拟社区的营销模式,认为虚拟社区改变了用户被动服务的地位,获得了主动权。对此,图书馆需采用聚众为媒的策略,为虚拟社区中的用户营造良好的使用体验,引导用户成为创建...根据美国Second Life Library 2.0虚拟社区的建设现状,分析图书馆虚拟社区的营销模式,认为虚拟社区改变了用户被动服务的地位,获得了主动权。对此,图书馆需采用聚众为媒的策略,为虚拟社区中的用户营造良好的使用体验,引导用户成为创建服务的合作者和品牌传播的中间人。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.
