Damages of sensory hair cells(HCs)are mainly responsible for sensorineural hearing loss,while the pathological mechanism remains not fully understood due to the many potential deafness genes unidentified.ftr82,a membe...Damages of sensory hair cells(HCs)are mainly responsible for sensorineural hearing loss,while the pathological mechanism remains not fully understood due to the many potential deafness genes unidentified.ftr82,a member of the largely TRIMs family in fish,has been found specifically expressed in the otic vesicle while its function is still unclear.Here,we investigate the roles of ftr82 in HC development and hearing function utilizing the zebrafish model.The results of in situ hybridization illustrate that ftr82 is always restricted to localize in otic vesicles at different stages.The defects of HCs are observed both in ftr82 morphants and mutants,including significantly decreased crista HCs,shortened cilia as well as remarkably reduced functional HCs in neuromasts,which could be successfully rescued by co-injection of exogenous ftr82 mRNA.The behavior assay of startle response indicates that larvae lacking of ftr82 exhibits lower sensitivity to external sound stimuli.Further research reveals that the loss of HCs is mainly caused by cell apoptosis mediated by caspase-3 activation.Our study demonstrates that ftr82 is a crucial hearing-related gene that regulates the HC morphogenesis and auditory function performing,which provides new insight into the rapid identification of the deafness gene.展开更多
With the introduction of technologies such as structural optimization and error correction,the performance of the MEMS quad-mass gyroscope(QMG)has significantly improved,while noise has gradually become a critical fac...With the introduction of technologies such as structural optimization and error correction,the performance of the MEMS quad-mass gyroscope(QMG)has significantly improved,while noise has gradually become a critical factor limiting its performance.For ease of analysis,this paper categorizes noise into two types:noise at the signal detection end and noise at the excitation end.Firstly,a closed-loop noise model for QMG is established,and the effects of these two types of noise on the dynamic and static performance of QMG are investigated.Additionally,the correlation between structural parameters and noise transmission is analyzed,and the dual impact of DC Bias Voltage optimization on improving QMG performance is explored.Based on the above analysis,a force-to-rebalance(FTR)dual-loop control method incorporating SID and normalized least mean squares(NLMS)is proposed and applied to the MEMS QMG,where SID and NLMS are respectively employed to mitigate the influence of detection-end and driveend noise on the bias performance.Compared to the traditional method,the proposed approach reduces the bias instability(BI)of the MEMS QMG from 0.407°/h to 0.024°/h and the angular random walk(ARW)from 0.137°/√h to 0.006°/√h,achieving improvements of 16.96 times and 22.83 times,respectively.Furthermore,the system achieves a threshold of 0.0001°/s.展开更多
Vertebrate interferon(IFN)expression is fine-tuned in order to avoid excessive tissue injury under normal conditions and during virus infection.FinTRIM(fish novel TRIM,FTR)proteins are reported to regulate the fish IF...Vertebrate interferon(IFN)expression is fine-tuned in order to avoid excessive tissue injury under normal conditions and during virus infection.FinTRIM(fish novel TRIM,FTR)proteins are reported to regulate the fish IFN response.Here,we identify a novel finTRIM gene from yellow catfish(Pelteobagrus fulvidraco),which is sequentially named PfFTR100 according to the nomenclature rule in zebrafish.Genome-wide analyses reveal that FTR100 is unique to Otomorpha fish,with a single copy in spite of additional genome duplication in some fish species.Considering that few of the 99 finTRIM genes identified in zebrafish are conserved in main fish branches and most,such as FTR100,are unique to distinct branches due to lineage-specific expansion of finTRIM genes,we develop a nomenclature for newly cloned finTRIM genes from different fish species.PfFTR100 mRNA is not induced by virus infection,with a relatively high expression level comparable to that of cellular IFN and some IFN-stimulated genes(ISGs)in virally-infected tissues.However,ectopically-expressed PfFTR100 protein is attenuated in virally-infected cells through the proteasomal-dependent pathway.Overexpression of PfFTR100 promotes SVCV replication by downregulating the constitutive and inducible IFN response via a mechanism by which PfFTR100 targets IRF3 and IRF7 to attenuate their mRNA levels rather than their protein levels.Our results indicate that yellow catfish FTR100 is essential for homeostatic regulation of fish tonic IFN response.展开更多
基金supported by grants from the National Natural Science Foundation of China(2018YFA0801004,81870359)the Natural Science Foundation of the Jiangsu Higher Education Institutions of China(22KJB320020)the“Innovation and Entrepreneurship Doctor”Project of Jiangsu Province.
文摘Damages of sensory hair cells(HCs)are mainly responsible for sensorineural hearing loss,while the pathological mechanism remains not fully understood due to the many potential deafness genes unidentified.ftr82,a member of the largely TRIMs family in fish,has been found specifically expressed in the otic vesicle while its function is still unclear.Here,we investigate the roles of ftr82 in HC development and hearing function utilizing the zebrafish model.The results of in situ hybridization illustrate that ftr82 is always restricted to localize in otic vesicles at different stages.The defects of HCs are observed both in ftr82 morphants and mutants,including significantly decreased crista HCs,shortened cilia as well as remarkably reduced functional HCs in neuromasts,which could be successfully rescued by co-injection of exogenous ftr82 mRNA.The behavior assay of startle response indicates that larvae lacking of ftr82 exhibits lower sensitivity to external sound stimuli.Further research reveals that the loss of HCs is mainly caused by cell apoptosis mediated by caspase-3 activation.Our study demonstrates that ftr82 is a crucial hearing-related gene that regulates the HC morphogenesis and auditory function performing,which provides new insight into the rapid identification of the deafness gene.
基金supported in part by the National Natural Science Foundation of China under Grants 61971466in part by the Equipment Pre-Research Foundation of China under Grant 80917020506.
文摘With the introduction of technologies such as structural optimization and error correction,the performance of the MEMS quad-mass gyroscope(QMG)has significantly improved,while noise has gradually become a critical factor limiting its performance.For ease of analysis,this paper categorizes noise into two types:noise at the signal detection end and noise at the excitation end.Firstly,a closed-loop noise model for QMG is established,and the effects of these two types of noise on the dynamic and static performance of QMG are investigated.Additionally,the correlation between structural parameters and noise transmission is analyzed,and the dual impact of DC Bias Voltage optimization on improving QMG performance is explored.Based on the above analysis,a force-to-rebalance(FTR)dual-loop control method incorporating SID and normalized least mean squares(NLMS)is proposed and applied to the MEMS QMG,where SID and NLMS are respectively employed to mitigate the influence of detection-end and driveend noise on the bias performance.Compared to the traditional method,the proposed approach reduces the bias instability(BI)of the MEMS QMG from 0.407°/h to 0.024°/h and the angular random walk(ARW)from 0.137°/√h to 0.006°/√h,achieving improvements of 16.96 times and 22.83 times,respectively.Furthermore,the system achieves a threshold of 0.0001°/s.
基金supported by grants from the National Key R&D Program of China(2022YFF1000302)the Strategic Priority Research Program of the Chinese Academy of Sciences(XDA24010308)+1 种基金the National Natural Science Foundation(31972826 and 32102838)the Freshwater Ecology and Biotechnology Laboratory(2019FBZ04).
文摘Vertebrate interferon(IFN)expression is fine-tuned in order to avoid excessive tissue injury under normal conditions and during virus infection.FinTRIM(fish novel TRIM,FTR)proteins are reported to regulate the fish IFN response.Here,we identify a novel finTRIM gene from yellow catfish(Pelteobagrus fulvidraco),which is sequentially named PfFTR100 according to the nomenclature rule in zebrafish.Genome-wide analyses reveal that FTR100 is unique to Otomorpha fish,with a single copy in spite of additional genome duplication in some fish species.Considering that few of the 99 finTRIM genes identified in zebrafish are conserved in main fish branches and most,such as FTR100,are unique to distinct branches due to lineage-specific expansion of finTRIM genes,we develop a nomenclature for newly cloned finTRIM genes from different fish species.PfFTR100 mRNA is not induced by virus infection,with a relatively high expression level comparable to that of cellular IFN and some IFN-stimulated genes(ISGs)in virally-infected tissues.However,ectopically-expressed PfFTR100 protein is attenuated in virally-infected cells through the proteasomal-dependent pathway.Overexpression of PfFTR100 promotes SVCV replication by downregulating the constitutive and inducible IFN response via a mechanism by which PfFTR100 targets IRF3 and IRF7 to attenuate their mRNA levels rather than their protein levels.Our results indicate that yellow catfish FTR100 is essential for homeostatic regulation of fish tonic IFN response.
