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        Genetic architecture and candidate genes detected for chicken internal organ weight with a 600 K single nucleotide polymorphism array

        Taocun Dou,Manman Shen,Meng Ma,Liang Qu,Yongfeng Li,Yuping Hu,Jian Lu,Jun Guo,Xingguo Wang,Kehua Wang 아세아·태평양축산학회 2019 Animal Bioscience Vol.32 No.3

        Objective: Internal organs indirectly affect economic performance and well-being of animals. Study of internal organs during later layer period will allow full utilization of layer hens. Hence, we conducted a genome-wide association study (GWAS) to identify potential quantitative trait loci or genes that potentially contribute to internal organ weight. Methods: A total of 1,512 chickens originating from White Leghorn and Dongxiang Blue-Shelled chickens were genotyped using high-density Affymetrix 600 K single nucleotide polymorphism (SNP) array. We conducted a GWAS, linkage disequilibrium analysis, and heritability estimated based on SNP information by using GEMMA, Haploview and GCTA software. Results: Our results displayed that internal organ weights show moderate to high (0.283 to 0.640) heritability. Variance partitioned across chromosomes and chromosome lengths had a linear relationship for liver weight and gizzard weight (R2 = 0.493, 0.753). A total of 23 highly significant SNPs that associated with all internal organ weights were mainly located on Gallus gallus autosome (GGA) 1 and GGA4. Six SNPs on GGA2 affected heart weight. After the final analysis, five top SNPs were in or near genes 5-Hydroxytryptamine receptor 2A, general transcription factor IIF polypeptide 2, WD repeat and FYVE domain containing 2, non-SMC condensin I complex subunit G, and sonic hedgehog, which were considered as candidate genes having a pervasive role in internal organ weights. Conclusion: Our findings provide an understanding of the underlying genetic architecture of internal organs and are beneficial in the selection of chickens.

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        Omi inhibition ameliorates neuron apoptosis and neurological deficit after subarachnoid hemorrhage in rats

        Du Yuanfeng,Yang Dingbo,Dong Xiaoqiao,Du Quan,Wang Ding,Shen Yongfeng,Yu Wenhua 한국유전학회 2021 Genes & Genomics Vol.43 No.12

        Background Subarachnoid hemorrhage (SAH) is a severe neurological emergency, resulting in cognitive impairments and threatening human's health. Currently, SAH has no efective treatment. It is urgent to search for an efective therapy for SAH. Objective To explore the expression of Omi protein after subarachnoid hemorrhage in rats. Methods SAH rat model was established by injecting blood into the prechiasmatic cistern. Neurological defcit was assessed by detecting neurological defcit scores and brain tissue water contents. Apoptotic cells were evaluated by TUNEL staining and IHC staining. Omi and Cleaved caspase 3 expressions in nerve cells were determined by double staining using IF. Apoptosis-related proteins were measured by Western blotting assay. Results SAH rat model was successfully established, showing more apoptotic cells and high neurological defcit scores in SAH rat. In SAH rat model, Omi expression in nerve cells was elevated and the upregulation of Omi mainly occurred in cytoplasm, accompanied by the degradation of XIAP and the increased cleaved caspase 3/9 and cleaved PARP. Once treated with UCF-101, a specifc inhibitor of Omi, the increased cell apoptosis, left/right brain moisture contents and neurological defcits were notably reversed in SAH rat brain. Of note, SAH-induced the increases of apoptosis-related protein in nerve cells were also rescued by the administration of UCF-101. Conclusions UCF-101-mediated Omi inhibition decreased the degradation of XIAP and subsequently inhibited the activation of apoptosis-related proteins, decreased nerve cell apoptosis, leading to the improvement on early brain injury in SAH rat. UCF-101-based Omi inhibition may be used to treat SAH with great potential application.

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