The escalating need for high-performance artificial intelligence(AI)computing intensifies the"memory bottleneck"of the von Neumann architecture,prompting extensive exploration of computation-in-memory(CIM)so...The escalating need for high-performance artificial intelligence(AI)computing intensifies the"memory bottleneck"of the von Neumann architecture,prompting extensive exploration of computation-in-memory(CIM)solutions.This study is cen-tered on the optimization of a high-efficiency,low-power"L"-shaped split-gate floating-gate(FG)memory for CIM applications.Fabricated on a 55 nm CMOS platform,the memory devices were systematically investigated through wafer acceptance test(WAT),Sentaurus^(TM)simulations and comprehensive evaluations with the DNN+NeuroSim Framework V2.0.Among devices with diverse FG lengths,the 95-nm FG variant exhibits outstanding performance:it achieves a 5.35 V memory window,reaches a maximum conductance of 16.7μS with excellent linearity under the varying voltage and width pulse scheme(VWPS),real-izes 32-state multi-level storage,and attains a 92%training accuracy on the CIFAR-10 dataset using the VGG8 neural network.展开更多
Background Neuroendocrine prostate cancer(NEPC)is an aggressive subtype of castration-resistant prostate cancer(CRPC)that is typically resistant to nearly all current therapies.Methods In this study,single-cell RNA se...Background Neuroendocrine prostate cancer(NEPC)is an aggressive subtype of castration-resistant prostate cancer(CRPC)that is typically resistant to nearly all current therapies.Methods In this study,single-cell RNA sequencing(scRNA-seq)and bioinformatic analysis identified centrosomal protein 55(CEP55)as a critical factor in the transformation from hormone-sensitive prostate cancer(HSPC)to CRPC and,ultimately to,NEPC.Results Subsequent bioinformatics analyses and clinical sample validation showed that CEP55 is significantly upregulated in NEPC tissues relative to HSPC and CRPC.Furthermore,while CEP55 show no significant association with the immune microenvironment or cancer-associated fibroblasts(CAFs),our findings indicated that it directly mediates the plasticity of prostate cancer cells,thereby driving NEPC progression.Specifically,in vivo and in vitro experiments confirmed that CEP55 enhances cell proliferation,migration,invasion and the expression of NEPC biomarkers in prostate cancer.Importantly,although cisplatin is the primary treatment for NEPC clinically,CEP55 has been shown to regulate cisplatin resistance through the phosphorylation of cyclin-dependent kinase 1(CDK1)at the tyrosine 15(Tyr15)site.Conclusions In summary,our study identifies a key gene that influences the neuroendocrine differentiation process in prostate cancer,suggesting its potential as an important therapeutic target.展开更多
基金supported by National Key Research and Development Program of China (2022YFF0605803)Zhejiang key R&D project (2023C01017)+1 种基金the Zhejiang Key Research and Development Project (2024SJCZX0030)Zhejiang Technology Innovation Center of CMOS IC Manufacture Process and Design for supporting us to do this research.
文摘The escalating need for high-performance artificial intelligence(AI)computing intensifies the"memory bottleneck"of the von Neumann architecture,prompting extensive exploration of computation-in-memory(CIM)solutions.This study is cen-tered on the optimization of a high-efficiency,low-power"L"-shaped split-gate floating-gate(FG)memory for CIM applications.Fabricated on a 55 nm CMOS platform,the memory devices were systematically investigated through wafer acceptance test(WAT),Sentaurus^(TM)simulations and comprehensive evaluations with the DNN+NeuroSim Framework V2.0.Among devices with diverse FG lengths,the 95-nm FG variant exhibits outstanding performance:it achieves a 5.35 V memory window,reaches a maximum conductance of 16.7μS with excellent linearity under the varying voltage and width pulse scheme(VWPS),real-izes 32-state multi-level storage,and attains a 92%training accuracy on the CIFAR-10 dataset using the VGG8 neural network.
基金supported by the Guangdong Basic and Applied Basic Research Foundation(Nos:2024A1515012687)the National Natural Science Foundation of China(No.82303052).
文摘Background Neuroendocrine prostate cancer(NEPC)is an aggressive subtype of castration-resistant prostate cancer(CRPC)that is typically resistant to nearly all current therapies.Methods In this study,single-cell RNA sequencing(scRNA-seq)and bioinformatic analysis identified centrosomal protein 55(CEP55)as a critical factor in the transformation from hormone-sensitive prostate cancer(HSPC)to CRPC and,ultimately to,NEPC.Results Subsequent bioinformatics analyses and clinical sample validation showed that CEP55 is significantly upregulated in NEPC tissues relative to HSPC and CRPC.Furthermore,while CEP55 show no significant association with the immune microenvironment or cancer-associated fibroblasts(CAFs),our findings indicated that it directly mediates the plasticity of prostate cancer cells,thereby driving NEPC progression.Specifically,in vivo and in vitro experiments confirmed that CEP55 enhances cell proliferation,migration,invasion and the expression of NEPC biomarkers in prostate cancer.Importantly,although cisplatin is the primary treatment for NEPC clinically,CEP55 has been shown to regulate cisplatin resistance through the phosphorylation of cyclin-dependent kinase 1(CDK1)at the tyrosine 15(Tyr15)site.Conclusions In summary,our study identifies a key gene that influences the neuroendocrine differentiation process in prostate cancer,suggesting its potential as an important therapeutic target.
