We propose to address the open set domain adaptation problem by aligning images at both the pixel space and the feature space.Our approach,called Open Set Translation and Adaptation Network(OSTAN),consists of two main...We propose to address the open set domain adaptation problem by aligning images at both the pixel space and the feature space.Our approach,called Open Set Translation and Adaptation Network(OSTAN),consists of two main components:translation and adaptation.The translation is a cycle-consistent generative adversarial network,which translates any source image to the“style”of a target domain to eliminate domain discrepancy in the pixel space.The adaptation is an instance-weighted adversarial network,which projects both(labeled)translated source images and(unlabeled)target images into a domain-invariant feature space to learn a prior probability for each target image.The learned probability is applied as a weight to the unknown classifier to facilitate the identification of the unknown class.The proposed OSTAN model significantly outperforms the state-of-the-art open set domain adaptation methods on multiple public datasets.Our experiments also demonstrate that both the image-to-image translation and the instance-weighting framework can further improve the decision boundaries for both known and unknown classes.展开更多
Compared with traditional solid-state drives(SSDs),open-channel SSDs(OCSSDs)expose their internal physical layout and provide a host-based flash translation layer(FTL)that allows host-side software to control the inte...Compared with traditional solid-state drives(SSDs),open-channel SSDs(OCSSDs)expose their internal physical layout and provide a host-based flash translation layer(FTL)that allows host-side software to control the internal operations such as garbage collection(GC)and input/output(I/O)scheduling.In this paper,we comprehensively survey research works built on OCSSDs in recent years.We show how they leverage the features of OCSSDs to achieve high throughput,low latency,long lifetime,strong performance isolation,and high resource utilization.We categorize these efforts into five groups based on their optimization methods:adaptive interface customizing,rich FTL co-designing,internal parallelism exploiting,rational I/O scheduling,and efficient GC processing.We discuss the strengths and weaknesses of these efforts and find that almost all these efforts face a dilemma between performance effectiveness and management complexity.We hope that this survey can provide fundamental knowledge to researchers who want to enter this field and further inspire new ideas for the development of OCSSDs.展开更多
Objective Cisplatin(CDDP)-based chemotherapy is a first-line,drug regimen for muscle-invasive bladder cancer(BC)and metastatic bladder cancer.Clinically,resistance to CDDP restricts the clinical benefit of some bladde...Objective Cisplatin(CDDP)-based chemotherapy is a first-line,drug regimen for muscle-invasive bladder cancer(BC)and metastatic bladder cancer.Clinically,resistance to CDDP restricts the clinical benefit of some bladder cancer patients.AT-rich interaction domain 1A(ARID1A)gene mutation occurs frequently in bladder cancer;however,the role of CDDP sensitivity in BC has not been studied.Methods We established ARID1A knockout BC cell lines using CRISPR/Cas9 technology.IC50 determination,flow cytometry analysis of apoptosis,and tumor xenograft assays were performed to verify changes in the CDDP sensitivity of BC cells losing ARID1A.qRT-PCR,Western blotting,RNA interference,bioinformatic analysis,and ChIP-qPCR analysis were performed to further explore the potential mechanism of ARID1A inactivation in CDDP sensitivity in BC.Results It was found that ARID1A inactivation was associated with CDDP resistance in BC cells.Mechanically,loss of ARID1A promoted the expression of eukaryotic translation initiation factor 4A3(EIF4A3)through epigenetic regulation.Increased expression of EIF4A3 promoted the expression of hsa_circ_0008399(circ0008399),a novel circular RNA(circRNA)identified in our previous study,which,to some extent,showed that ARID1A deletion caused CDDP resistance through the inhibitory effect of circ0008399 on the apoptosis of BC cells.Importantly,EIF4A3-IN-2 specifically inhibited the activity of EIF4A3 to reduce circ0008399 production and restored the sensitivity of ARID1A inactivated BC cells to CDDP.Conclusion Our research deepens the understanding of the mechanisms of CDDP resistance in BC and elucidates a potential strategy to improve the efficacy of CDDP in BC patients with ARID1A deletion through combination therapy targeting EIF4A3.展开更多
Translation factor SelB is the key component for the specific decoding of UGA codons with selenocysteine at the ribosome. SelB binds selenocysteyl-tRNASec, guanine nucleotides and a secondary structure of the selenopr...Translation factor SelB is the key component for the specific decoding of UGA codons with selenocysteine at the ribosome. SelB binds selenocysteyl-tRNASec, guanine nucleotides and a secondary structure of the selenoprotein mRNA following the UGA at the 3' side. A comparison of the amino acid sequences of SelB species from E. coli,Desulfomicrobium baculatum, Clostridium thermoaceticum and Haemophilus influenzae showed that the proteins consist of at least four structural domains from which the Nterminal three are well conserved and share homology with elongation factor Tu whereas the C-terminal one is more variable and displays no similarity to any protein known. With the aid of the coordinates of EF-Tu the N-terminal part has been modelled into a 3D structure which exhibits intriguing features concerning its interaction with guanine nucleotides and other components of the translational apparatus. Cloning and expression of fragments of SelB and biochemical analysis of the purified truncated proteins showed that the C-terminal 19 kDa protein fragment is able to specifically bind to the selenoprotein mRNA. SelB, thus, is a translation factor functionally homologous to EF-Tu hooked up to the mRNA with its C-terminal end. The formation by SelB of a quaternary complex in vivo has been proven by overexpression of truncated genes of SelB and by demonstration that fragments comprising the mRNA or the tRNA binding domain inhibit selenocysteine insertion展开更多
基金supported by the National Natural Science Foundation of China under Grant Nos.62032011 and 61772257.
文摘We propose to address the open set domain adaptation problem by aligning images at both the pixel space and the feature space.Our approach,called Open Set Translation and Adaptation Network(OSTAN),consists of two main components:translation and adaptation.The translation is a cycle-consistent generative adversarial network,which translates any source image to the“style”of a target domain to eliminate domain discrepancy in the pixel space.The adaptation is an instance-weighted adversarial network,which projects both(labeled)translated source images and(unlabeled)target images into a domain-invariant feature space to learn a prior probability for each target image.The learned probability is applied as a weight to the unknown classifier to facilitate the identification of the unknown class.The proposed OSTAN model significantly outperforms the state-of-the-art open set domain adaptation methods on multiple public datasets.Our experiments also demonstrate that both the image-to-image translation and the instance-weighting framework can further improve the decision boundaries for both known and unknown classes.
基金Project supported by the National Natural Science Foundation of China(No.62025203)。
文摘Compared with traditional solid-state drives(SSDs),open-channel SSDs(OCSSDs)expose their internal physical layout and provide a host-based flash translation layer(FTL)that allows host-side software to control the internal operations such as garbage collection(GC)and input/output(I/O)scheduling.In this paper,we comprehensively survey research works built on OCSSDs in recent years.We show how they leverage the features of OCSSDs to achieve high throughput,low latency,long lifetime,strong performance isolation,and high resource utilization.We categorize these efforts into five groups based on their optimization methods:adaptive interface customizing,rich FTL co-designing,internal parallelism exploiting,rational I/O scheduling,and efficient GC processing.We discuss the strengths and weaknesses of these efforts and find that almost all these efforts face a dilemma between performance effectiveness and management complexity.We hope that this survey can provide fundamental knowledge to researchers who want to enter this field and further inspire new ideas for the development of OCSSDs.
基金This work was supported by grants from the National Natural Science Foundation of China(No.81974396,No.81874091,No.82072840,and No.82102734)the Natural Science Foundation of Hubei Province(No.2020CFB829)the Health Commission of Hubei Province Scientific Research Project(No.WJ2021F081).
文摘Objective Cisplatin(CDDP)-based chemotherapy is a first-line,drug regimen for muscle-invasive bladder cancer(BC)and metastatic bladder cancer.Clinically,resistance to CDDP restricts the clinical benefit of some bladder cancer patients.AT-rich interaction domain 1A(ARID1A)gene mutation occurs frequently in bladder cancer;however,the role of CDDP sensitivity in BC has not been studied.Methods We established ARID1A knockout BC cell lines using CRISPR/Cas9 technology.IC50 determination,flow cytometry analysis of apoptosis,and tumor xenograft assays were performed to verify changes in the CDDP sensitivity of BC cells losing ARID1A.qRT-PCR,Western blotting,RNA interference,bioinformatic analysis,and ChIP-qPCR analysis were performed to further explore the potential mechanism of ARID1A inactivation in CDDP sensitivity in BC.Results It was found that ARID1A inactivation was associated with CDDP resistance in BC cells.Mechanically,loss of ARID1A promoted the expression of eukaryotic translation initiation factor 4A3(EIF4A3)through epigenetic regulation.Increased expression of EIF4A3 promoted the expression of hsa_circ_0008399(circ0008399),a novel circular RNA(circRNA)identified in our previous study,which,to some extent,showed that ARID1A deletion caused CDDP resistance through the inhibitory effect of circ0008399 on the apoptosis of BC cells.Importantly,EIF4A3-IN-2 specifically inhibited the activity of EIF4A3 to reduce circ0008399 production and restored the sensitivity of ARID1A inactivated BC cells to CDDP.Conclusion Our research deepens the understanding of the mechanisms of CDDP resistance in BC and elucidates a potential strategy to improve the efficacy of CDDP in BC patients with ARID1A deletion through combination therapy targeting EIF4A3.
文摘Translation factor SelB is the key component for the specific decoding of UGA codons with selenocysteine at the ribosome. SelB binds selenocysteyl-tRNASec, guanine nucleotides and a secondary structure of the selenoprotein mRNA following the UGA at the 3' side. A comparison of the amino acid sequences of SelB species from E. coli,Desulfomicrobium baculatum, Clostridium thermoaceticum and Haemophilus influenzae showed that the proteins consist of at least four structural domains from which the Nterminal three are well conserved and share homology with elongation factor Tu whereas the C-terminal one is more variable and displays no similarity to any protein known. With the aid of the coordinates of EF-Tu the N-terminal part has been modelled into a 3D structure which exhibits intriguing features concerning its interaction with guanine nucleotides and other components of the translational apparatus. Cloning and expression of fragments of SelB and biochemical analysis of the purified truncated proteins showed that the C-terminal 19 kDa protein fragment is able to specifically bind to the selenoprotein mRNA. SelB, thus, is a translation factor functionally homologous to EF-Tu hooked up to the mRNA with its C-terminal end. The formation by SelB of a quaternary complex in vivo has been proven by overexpression of truncated genes of SelB and by demonstration that fragments comprising the mRNA or the tRNA binding domain inhibit selenocysteine insertion
