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- 검색키워드
- 저자 : Zhaowei Jiang (검색결과 3 건)
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Zhaowei Cai,Zhilan Xiao,Yufang Wang,Huazhen Liu,Kangdi Zhang,Xiaoning Zhen,Xiaoling Jiang 한국유전학회 2020 Genes & Genomics Vol.42 No.11
Background Down syndrome (DS), caused by trisomy 21, is the most common human chromosomal disorder. Hippocampalabnormalities have been believed to be responsible for the DS developmental cognitive deficits. Cumulative evidences indicatedthat non-coding RNAs (ncRNAs) participated in brain development and function. Currently, few was known whetherdysregulated ncRNAs existed in DS whether the dysregulated ncRNAs played important pathology roles in DS. Objective The purpose of this study was generating an overview map of the dysregulated ncRNAs in DS, including themicroRNA (miRNA), long ncRNA (lncRNA) and circular RNA (circRNAs). DS mouse models are invaluable tools forfurther mechanism and therapy studies. Methods The well-studied DS mouse model Dp(16)1/Yey was used in this study as it contains the trisomy of the whole humanchromosome 21 syntenic region on mouse chromosomes 16. Hippocampi were isolated from pups of seven-days-old. Librariesfor miRNA, lncRNA and circRNAs were constructed separately, and the next generation sequencing method was utilized. Results Differentially expressed (DE) miRNAs, lncRNAs and circRNAs were reported. Relative few regulating relationshipwere found between the DE miRNAs and DE mRNAs. LncRNAs originated from the trisomic regions expressed in clusters,but not all of them were 1.5-fold increased expressed. Dramatic DE circular RNAs were found in the DS hippocampus. The host genes of the DE circRNAs were enriched on functions which were well-known impaired in DS, e.g. long-termpotentiation,glutamatergic synapse, and GABAergic synapse. Conclusions We generated the first DS developmental hippocampal ncRNA transcriptome map. This work laid foundationsfor further investigations on role of ncRNAs in hippocampal functions.
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Experimental study on fatigue behavior of innovative hollow composite bridge slabs
Yang Chen,Zhaowei Jiang,Qing Xu,Chong Ren 국제구조공학회 2023 Steel and Composite Structures, An International J Vol.46 No.6
In order to study the fatigue performance of the flat steel plate-lightweight aggregate concrete hollow composite bridge slab subjected to fatigue load, both static test on two specimens and fatigue test on six specimens were conducted. The effects of the arrangement of the steel pipes, the amplitude of the fatigue load and the upper limit as well as lower limit of fatigue load on failure performance were investigated. Besides, for specimens in fatigue test, strains of the concrete, residual deflection, bending stiffness, residual bearing capacity and dynamic response were analyzed. Test results showed that the specimens failed in the fracture of the bottom flat steel plate regardless of the arrangement of the steel pipes. Moreover, the fatigue loading cycles of composite slab were mainly controlled by the amplitude of the fatigue load, but the influences of upper limit and lower limit of fatigue load on fatigue life was slight. The fatigue life of the composite bridge slabs can be determined by the fatigue strength of bottom flat steel plate, which can be calculated by the method of allowable stress amplitude in steel structure design code.
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Zhou Zuolin,Zhi Chunchun,Chen Die,Cai Zhaowei,Jiang Xiaoling 한국유전학회 2023 Genes & Genomics Vol.45 No.10
Background Down syndrome (DS), the most frequently occurring human chromosomal disorder, is caused by trisomy 21. The exact molecular effects of trisomy on certain cell populations in the brain remain poorly understood. Objective The purpose of this study was to investigate the effects of trisomy on the transcriptomes of various types of neurons and nonneuronal cells in the hippocampus. Methods A total of 8993 nuclei from the WT and 6445 nuclei from the Dp16 hippocampus were analyzed by single-nucleus RNA sequencing (snRNA-seq). Cell clustering was achieved by the Seurat program. Results Hippocampal cells were grouped into multiple neuronal and nonneuronal populations. Only a limited number of trisomic genes were upregulated (q < 0.001) over 1.25-fold in a specific type of hippocampal cell. Specifically, deregulation of genes associated with synaptic signaling and organization was observed in multiple cell populations, including excitatory neurons, oligodendrocytes, and microglia. This observation suggests the potential importance of synapse deficits in DS. Interestingly, GO annotation of the upregulated genes suggested potential activation of the immune system by hippocampal excitatory neurons. Fewer trisomic genes were altered in nonneuronal cells than in neurons. Notably, microglial transcriptome analysis revealed significantly (q < 0.001) increased expression of C1qb and C1qc, which suggested potential involvement of complement-mediated synapse loss mediated by microglia in DS. Conclusion The trisomy-related hippocampal deficits should be driven by a small amount, not all, of the trisomic genes in a specific type of cell. Our work may help to narrow down both the molecular and cellular targets for future gene therapies in DS.
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