本文给出一种基于全局异步局部同步(Global Asynchronous Local Synchronous)的四核数字信号处理器(Digital Signal Processor)内部互联设计方案.全局异步局部同步的设计模式可以使四个DSP核心根据任务需要工作在不同的频率域,从而降低...本文给出一种基于全局异步局部同步(Global Asynchronous Local Synchronous)的四核数字信号处理器(Digital Signal Processor)内部互联设计方案.全局异步局部同步的设计模式可以使四个DSP核心根据任务需要工作在不同的频率域,从而降低芯片的总功耗且避免了全局时钟树设计.多核之间采用DMA通道进行数据交换,在占用较小CPU负担的同时,获得较大数据带宽.本文给出一种任务队列的任务调度机制,用于完成多核之间任务的自助申请调度以及数据流的控制.以MP3的解码程序为例,对任务在多核上的分割方法和调度策略进行详细的阐述.展开更多
An asynchronous wrapper with novel handshake circuits for data communication in globally asynchronous locally synchronous （GALS） systems is proposed. The handshake circuits include two communication ports and a loca...An asynchronous wrapper with novel handshake circuits for data communication in globally asynchronous locally synchronous （GALS） systems is proposed. The handshake circuits include two communication ports and a local clock generator. Two approaches for the implementation of communication ports are presented, one with pure standard cells and the others with Mttller-C elements. The detailed design methodology for GALS systems is given and the circuits are validated with VHDL and circuits simulation in standard CMOS technology.展开更多
Salinity severely reduces plant growth and limits agricultural productivity.Dynamic changes and rearrangement of the plant cell wall is an important response to salt stress,but relatively little is known about the bio...Salinity severely reduces plant growth and limits agricultural productivity.Dynamic changes and rearrangement of the plant cell wall is an important response to salt stress,but relatively little is known about the biological importance of specific cell wall components in the response.Here,we demonstrate a specific function ofβ-1,4-galactan in salt hypersensitivity.We found that salt stress induces the accumulation ofβ-1,4-galactan in root cell walls by up regulating the expression of GALACTAN SYNTHASE 1(GALS1),which encodes aβ-1,4-galactan synthase.The accumulation ofβ-1,4-galactan negatively affects salt tolerance.Exogenous application of D-galactose(D-Gal)causes an increase inβ-1,4-galactan levels in the wild type and GALS1 mutants,especially in GALS1 overexpressors,which correlated with the aggravated salt hypersensitivity.Furthermore,we discovered that the BARLEY B RECOMBINANT/BASIC PENTACYSTEINE transcription factors BPC1/BPC2 positively regulate plant salt tolerance by repressing GALS1 expression andβ-1,4-galactan accumulation.Genetic analysis suggested that GALS1 is genetically epistatic to BPC1/BPC2 with respect to the control of salt sensitivity as well as accumulation ofβ-1,4-galactan.Taken together,our results reveal a new regulatory mechanism by whichβ-1,4-galactan regulated by the BPC1/BPC2-GALS1 module aggravates salt sensitivity in Arabidopsis thaliana.展开更多
Plant growth and development are significantly hampered in saline environments,limiting agricultural productivity.Thus,it is crucial to unravel the mechanism underlying plant responses to salt stress.β-1,4-Galactan(g...Plant growth and development are significantly hampered in saline environments,limiting agricultural productivity.Thus,it is crucial to unravel the mechanism underlying plant responses to salt stress.β-1,4-Galactan(galactan),which forms the side chains of pectic rhamnogalacturonan I,enhances plant sensitivity to high-salt stress.Galactan is synthesized by GALACTAN SYNTHASE1(GALS1).We previously showed that Na Cl relieves the direct suppression of GALS1 transcription by the transcription factors BPC1 and BPC2 to induce the excess accumulation of galactan in Arabidopsis(Arabidopsis thaliana).However,how plants adapt to this unfavorable environment remains unclear.Here,we determined that the transcription factors CBF1,CBF2,and CBF3 directly interact with the GALS1 promoter and repress its expression,leading to reduced galactan accumulation and enhanced salt tolerance.Salt stress enhances the binding of CBF1/CBF2/CBF3 to the GALS1 promoter by inducing CBF1/CBF2/CBF3 transcription and accumulation.Genetic analysis suggested that CBF1/CBF2/CBF3 function upstream of GALS1 to modulate salt-induced galactan biosynthesis and the salt response.CBF1/CBF2/CBF3 and BPC1/BPC2 function in parallel to regulate GALS1 expression,thereby modulating the salt response.Our results reveal a mechanism in which salt-activated CBF1/CBF2/CBF3 inhibit BPC1/BPC2-regulated GALS1 expression to alleviate galactan-induced salt hypersensitivity,providing an activation/deactivation fine-tune mechanism for dynamic regulation of GALS1 expression under salt stress in Arabidopsis.展开更多
A networks-on-chip （NoC） cost-effective design method was given based on the globallyasynchronous locally-synchronous （GALS） interconnect structure. In this method, the synchronous mode was used to transmit data a...A networks-on-chip （NoC） cost-effective design method was given based on the globallyasynchronous locally-synchronous （GALS） interconnect structure. In this method, the synchronous mode was used to transmit data among routers, network interface （NI）, and intellectual property （IP） via a synchronous circuit. Compared with traditional methods of implementing GALS, this method greatly reduces the transmission latency and is compatible with existing very large scale integration （VLSI） design tools. The platform designed based on the method can support two kinds of packetizing mechanisms, any topology, several kinds of traffic, and many configurable parameters such as the number of virtual channels, thus the platform is universal. An NoC evaluation methodology is given with a case study showing that the platform and evaluation methodology work well.展开更多
Complex genetic architecture is the major cause of heterogeneity in epilepsy,which poses challenges for accurate diagnosis and precise treatment.A large number of epilepsy candidate genes have been identified from cli...Complex genetic architecture is the major cause of heterogeneity in epilepsy,which poses challenges for accurate diagnosis and precise treatment.A large number of epilepsy candidate genes have been identified from clinical studies,particularly with the widespread use of next-generation sequencing.Validating these candidate genes is emerging as a valuable yet challenging task.Drosophila serves as an ideal animal model for validating candidate genes associated with neurogenetic disorders such as epilepsy,due to its rapid reproduction rate,powerful genetic tools,and efficient use of ethological and electrophysiological assays.Here,we systematically summarize the advantageous techniques of the Drosophila model used to investigate epilepsy genes,including genetic tools for manipulating target gene expression,ethological assays for seizure-like behaviors,electrophysiological techniques,and functional imaging for recording neural activity.We then introduce several typical strategies for identifying epilepsy genes and provide new insights into gene-gene interactions in epilepsy with polygenic causes.We summarize well-established precision medicine strategies for epilepsy and discuss prospective treatment options,including drug therapy and gene therapy for genetic epilepsy based on the Drosophila model.Finally,we also address genetic counseling and assisted reproductive technology as potential approaches for the prevention of genetic epilepsy.展开更多
End-stage liver diseases,such as cirrhosis and liver cancer caused by hepatitis B,are often combined with hepatic encephalopathy(HE);ammonia poisoning is posited as one of its main pathogenesis mechanisms.Ammonia is c...End-stage liver diseases,such as cirrhosis and liver cancer caused by hepatitis B,are often combined with hepatic encephalopathy(HE);ammonia poisoning is posited as one of its main pathogenesis mechanisms.Ammonia is closely related to autophagy,but the molecular mechanism of ammonia’s regulatory effect on autophagy in HE remains unclear.Sialylation is an essential form of glycosylation.In the nervous system,abnormal sialylation affects various physiological processes,such as neural development and synapse formation.ST3 β-galactoside α2,3-sialyltransferase 6(ST3GAL6)is one of the significant glycosyltransferases responsible for addingα2,3-linked sialic acid to substrates and generating glycan structures.We found that the expression of ST3GAL6 was upregulated in the brains of mice with HE and in astrocytes after ammonia induction,and the expression levels of α2,3-sialylated glycans and autophagy-related proteins microtubule-associated protein light chain 3(LC3)and Beclin-1 were upregulated in ammonia-induced astrocytes.These findings suggest that ST3GAL6 is related to autophagy in HE.Therefore,we aimed to determine the regulatory relationship between ST3GAL6 and autophagy.We found that silencing ST3GAL6 and blocking or degrading α2,3-sialylated glycans by way of Maackia amurensis lectin-II(MAL-II)and neuraminidase can inhibit autophagy.In addition,silencing the expression of ST3GAL6 can downregulate the expression of heat shock proteinβ8(HSPB8)and Bcl2-associated athanogene 3(BAG3).Notably,the overexpression of HSPB8 partially restored the reduced autophagy levels caused by silencing ST3GAL6 expression.Our results indicate that ST3GAL6 regulates autophagy through the HSPB8-BAG3 complex.展开更多
Background:This study aimed to construct and characterize a humanized influenza mouse model expressing hST6GAL1.Methods:Humanized fragments,consisting of the endothelial cell-specific K18 promoter,human ST6GAL1-encodi...Background:This study aimed to construct and characterize a humanized influenza mouse model expressing hST6GAL1.Methods:Humanized fragments,consisting of the endothelial cell-specific K18 promoter,human ST6GAL1-encoding gene,and luciferase gene,were microinjected into the fertilized eggs of mice.The manipulated embryos were transferred into the oviducts of pseudopregnant female mice.The offspring were identified using PCR.Mice exhibiting elevated expression of the hST6GAL1 gene were selectively bred for propagation,and in vivo analysis was performed for screening.Expression of the humanized gene was tested by performing immunohistochemical(IHC)analysis.Hematologic and biochemical analyses using the whole blood and serum of humanized hST6GAL1 mice were performed.Results:Successful integration of the human ST6GAL1 gene into the mouse genome led to the overexpression of human SiaT ST6GAL1.Seven mice were identified as carrying copies of the humanized gene,and the in vivo analysis indicated that hST6GAL1gene expression in positive mice mirrored influenza virus infection characteristics.The IHC results revealed that hST6GAL1 was expressed in the lungs of humanized mice.Moreover,the hematologic and biochemical parameters of the positive mice were within the normal range.Conclusion:A humanized influenza mouse model expressing the hST6GAL1 gene was successfully established and characterized.展开更多
文摘本文给出一种基于全局异步局部同步(Global Asynchronous Local Synchronous)的四核数字信号处理器(Digital Signal Processor)内部互联设计方案.全局异步局部同步的设计模式可以使四个DSP核心根据任务需要工作在不同的频率域,从而降低芯片的总功耗且避免了全局时钟树设计.多核之间采用DMA通道进行数据交换,在占用较小CPU负担的同时,获得较大数据带宽.本文给出一种任务队列的任务调度机制,用于完成多核之间任务的自助申请调度以及数据流的控制.以MP3的解码程序为例,对任务在多核上的分割方法和调度策略进行详细的阐述.
文摘An asynchronous wrapper with novel handshake circuits for data communication in globally asynchronous locally synchronous （GALS） systems is proposed. The handshake circuits include two communication ports and a local clock generator. Two approaches for the implementation of communication ports are presented, one with pure standard cells and the others with Mttller-C elements. The detailed design methodology for GALS systems is given and the circuits are validated with VHDL and circuits simulation in standard CMOS technology.
基金This study was supported by grants from the National Natural Science Foundation of China(31871534 and 32001445)the Natural Science Foundation of Jiangsu Province(BK20200557)+2 种基金the China Postdoctoral Science Foundation(2019M651846)the Six Talent Peaks Program of Jiangsu Province(2016-NY-079)and the Natural Science Foundation of Guangdong Province(2018A030313686).H.V.S.was supported through the Joint BioEnergy Institute(http://www.jbei.org)by the U.S.Department of Energy,Office of Science,Office of Biological and Environmental Research,through contract DE-AC02-05CH11231 between Lawrence Berkeley National Laboratory and the U.S.Department of Energy.
文摘Salinity severely reduces plant growth and limits agricultural productivity.Dynamic changes and rearrangement of the plant cell wall is an important response to salt stress,but relatively little is known about the biological importance of specific cell wall components in the response.Here,we demonstrate a specific function ofβ-1,4-galactan in salt hypersensitivity.We found that salt stress induces the accumulation ofβ-1,4-galactan in root cell walls by up regulating the expression of GALACTAN SYNTHASE 1(GALS1),which encodes aβ-1,4-galactan synthase.The accumulation ofβ-1,4-galactan negatively affects salt tolerance.Exogenous application of D-galactose(D-Gal)causes an increase inβ-1,4-galactan levels in the wild type and GALS1 mutants,especially in GALS1 overexpressors,which correlated with the aggravated salt hypersensitivity.Furthermore,we discovered that the BARLEY B RECOMBINANT/BASIC PENTACYSTEINE transcription factors BPC1/BPC2 positively regulate plant salt tolerance by repressing GALS1 expression andβ-1,4-galactan accumulation.Genetic analysis suggested that GALS1 is genetically epistatic to BPC1/BPC2 with respect to the control of salt sensitivity as well as accumulation ofβ-1,4-galactan.Taken together,our results reveal a new regulatory mechanism by whichβ-1,4-galactan regulated by the BPC1/BPC2-GALS1 module aggravates salt sensitivity in Arabidopsis thaliana.
基金supported by grants from the National Natural Science Foundation of China(32001445)。
文摘Plant growth and development are significantly hampered in saline environments,limiting agricultural productivity.Thus,it is crucial to unravel the mechanism underlying plant responses to salt stress.β-1,4-Galactan(galactan),which forms the side chains of pectic rhamnogalacturonan I,enhances plant sensitivity to high-salt stress.Galactan is synthesized by GALACTAN SYNTHASE1(GALS1).We previously showed that Na Cl relieves the direct suppression of GALS1 transcription by the transcription factors BPC1 and BPC2 to induce the excess accumulation of galactan in Arabidopsis(Arabidopsis thaliana).However,how plants adapt to this unfavorable environment remains unclear.Here,we determined that the transcription factors CBF1,CBF2,and CBF3 directly interact with the GALS1 promoter and repress its expression,leading to reduced galactan accumulation and enhanced salt tolerance.Salt stress enhances the binding of CBF1/CBF2/CBF3 to the GALS1 promoter by inducing CBF1/CBF2/CBF3 transcription and accumulation.Genetic analysis suggested that CBF1/CBF2/CBF3 function upstream of GALS1 to modulate salt-induced galactan biosynthesis and the salt response.CBF1/CBF2/CBF3 and BPC1/BPC2 function in parallel to regulate GALS1 expression,thereby modulating the salt response.Our results reveal a mechanism in which salt-activated CBF1/CBF2/CBF3 inhibit BPC1/BPC2-regulated GALS1 expression to alleviate galactan-induced salt hypersensitivity,providing an activation/deactivation fine-tune mechanism for dynamic regulation of GALS1 expression under salt stress in Arabidopsis.
基金Supported by the National Natural Science Foundation of China (No.90607009)the National High-Tech Research and Development(863) Program(No.2008AA01Z107)the National Key Basic Research and Development(973) Program of China(No.2007CB310701)
文摘A networks-on-chip （NoC） cost-effective design method was given based on the globallyasynchronous locally-synchronous （GALS） interconnect structure. In this method, the synchronous mode was used to transmit data among routers, network interface （NI）, and intellectual property （IP） via a synchronous circuit. Compared with traditional methods of implementing GALS, this method greatly reduces the transmission latency and is compatible with existing very large scale integration （VLSI） design tools. The platform designed based on the method can support two kinds of packetizing mechanisms, any topology, several kinds of traffic, and many configurable parameters such as the number of virtual channels, thus the platform is universal. An NoC evaluation methodology is given with a case study showing that the platform and evaluation methodology work well.
基金supported by the Guangdong Basic and Applied Basic Research Foundation,No.2022A1515111123(to JQ)。
文摘Complex genetic architecture is the major cause of heterogeneity in epilepsy,which poses challenges for accurate diagnosis and precise treatment.A large number of epilepsy candidate genes have been identified from clinical studies,particularly with the widespread use of next-generation sequencing.Validating these candidate genes is emerging as a valuable yet challenging task.Drosophila serves as an ideal animal model for validating candidate genes associated with neurogenetic disorders such as epilepsy,due to its rapid reproduction rate,powerful genetic tools,and efficient use of ethological and electrophysiological assays.Here,we systematically summarize the advantageous techniques of the Drosophila model used to investigate epilepsy genes,including genetic tools for manipulating target gene expression,ethological assays for seizure-like behaviors,electrophysiological techniques,and functional imaging for recording neural activity.We then introduce several typical strategies for identifying epilepsy genes and provide new insights into gene-gene interactions in epilepsy with polygenic causes.We summarize well-established precision medicine strategies for epilepsy and discuss prospective treatment options,including drug therapy and gene therapy for genetic epilepsy based on the Drosophila model.Finally,we also address genetic counseling and assisted reproductive technology as potential approaches for the prevention of genetic epilepsy.
基金supported by the National Natural Science Foundation of China(No.82370592)the Discipline Construction Project of the Health System in Pudong New Area(No.PWZbr2022-15)the Pudong New Area Special Fund for Livelihood Research Project of Science and Technology Development Fund(No.PKJ2021-Y12),China.
文摘End-stage liver diseases,such as cirrhosis and liver cancer caused by hepatitis B,are often combined with hepatic encephalopathy(HE);ammonia poisoning is posited as one of its main pathogenesis mechanisms.Ammonia is closely related to autophagy,but the molecular mechanism of ammonia’s regulatory effect on autophagy in HE remains unclear.Sialylation is an essential form of glycosylation.In the nervous system,abnormal sialylation affects various physiological processes,such as neural development and synapse formation.ST3 β-galactoside α2,3-sialyltransferase 6(ST3GAL6)is one of the significant glycosyltransferases responsible for addingα2,3-linked sialic acid to substrates and generating glycan structures.We found that the expression of ST3GAL6 was upregulated in the brains of mice with HE and in astrocytes after ammonia induction,and the expression levels of α2,3-sialylated glycans and autophagy-related proteins microtubule-associated protein light chain 3(LC3)and Beclin-1 were upregulated in ammonia-induced astrocytes.These findings suggest that ST3GAL6 is related to autophagy in HE.Therefore,we aimed to determine the regulatory relationship between ST3GAL6 and autophagy.We found that silencing ST3GAL6 and blocking or degrading α2,3-sialylated glycans by way of Maackia amurensis lectin-II(MAL-II)and neuraminidase can inhibit autophagy.In addition,silencing the expression of ST3GAL6 can downregulate the expression of heat shock proteinβ8(HSPB8)and Bcl2-associated athanogene 3(BAG3).Notably,the overexpression of HSPB8 partially restored the reduced autophagy levels caused by silencing ST3GAL6 expression.Our results indicate that ST3GAL6 regulates autophagy through the HSPB8-BAG3 complex.
基金National Key Research and Development Program of China,Grant/Award Number:2021YFC2301403 and 2022YFF0711000。
文摘Background:This study aimed to construct and characterize a humanized influenza mouse model expressing hST6GAL1.Methods:Humanized fragments,consisting of the endothelial cell-specific K18 promoter,human ST6GAL1-encoding gene,and luciferase gene,were microinjected into the fertilized eggs of mice.The manipulated embryos were transferred into the oviducts of pseudopregnant female mice.The offspring were identified using PCR.Mice exhibiting elevated expression of the hST6GAL1 gene were selectively bred for propagation,and in vivo analysis was performed for screening.Expression of the humanized gene was tested by performing immunohistochemical(IHC)analysis.Hematologic and biochemical analyses using the whole blood and serum of humanized hST6GAL1 mice were performed.Results:Successful integration of the human ST6GAL1 gene into the mouse genome led to the overexpression of human SiaT ST6GAL1.Seven mice were identified as carrying copies of the humanized gene,and the in vivo analysis indicated that hST6GAL1gene expression in positive mice mirrored influenza virus infection characteristics.The IHC results revealed that hST6GAL1 was expressed in the lungs of humanized mice.Moreover,the hematologic and biochemical parameters of the positive mice were within the normal range.Conclusion:A humanized influenza mouse model expressing the hST6GAL1 gene was successfully established and characterized.
基金supported by The Research Grants Council of The HongKong SAR Government (7488/05M) the Research Fund for the Control of Infectious Diseases of the Health, Welfare and Food Bureauof the Hong Kong SAR Government, the Li Ka Shing Foundation+1 种基金the Providence Foundation in memory of The late Dr. Lui Hac Minhgrants from The National Natural Science Foundation of China(30571674, 30771988)~~
