频率分析是听觉系统的最基本的功能之一。先前的研究发现,在外周和较低位的中枢听觉结构内神经元的频率调谐曲线(FTC)的带宽均比较宽,而在进入较高位的中枢后,FTC变的越来越锐化(sharpness),频率分析也越来越精确(Suga,1995;Phillips et al.,1988),这提示听中枢有锐化神经元FT的能力和机制。后来的研究者沿用双声刺激方法在猫的听皮质(AC)(Sutter et al.,1991;1999)以及蝙蝠的丘脑(Suga et al.,1997)记录到位于兴奋性FTC单边或/和双边的抑制性FTC。并通过在蝙蝠听皮质采用离子电泳的方法,
Recent efforts in large-scale sequencing of leukemia genomes have revealed numerous novel mutations that can potentially contribute to *** functional significance of these genetic and epigenetic aberrations are beginn...
详细信息
Recent efforts in large-scale sequencing of leukemia genomes have revealed numerous novel mutations that can potentially contribute to *** functional significance of these genetic and epigenetic aberrations are beginning to be *** it is widely accepted that genetic mutations contribute to carcinogenesis,epigenetic mechanisms are increasingly recognized to also play causative roles in cancer ***,these efforts have led to advances in the understanding of leukemia biology as well as clinical applications of next-generation sequencing *** define cooperating genetic,epigenetic and transcriptional abnormalities that are associated with primary MLL chromosomal translocations during the development of leukemia,we have used a combined genomic and functional characterization strategy to explore key events which is critical for transformation but independent of the well-studied MLL fusion pathway:1)Using whole-genome and targeted sequencing of 241 acute leukemia patients,we identified loss-of-function mutations in SETD2(encoding a histone H3K36 methyltransferase),with 22%of patients with MLL rearrangements carrying SETD2mutations.2)Using genome-wide expression and transcription regulatory network analysis of AML patients,we revealed a monocytic expression signature that includes the monocyte fate-determining factor ***,our study defines critical genetic,epigenetic and transcriptional events that cooperate with MLL translocation to drive leukemic transformation.
血管钙化是机体钙磷代谢失衡所致的钙盐沉积于组织间的被动过程,是高血压、糖尿病、慢性肾病、动脉粥样硬化及衰老等的共同的病理生理过程。机体内外环境因素刺激引起内质网功能紊乱可导致错误的或未折叠蛋白质在内质网内聚集,诱发内质网应激(ERS)或未折叠蛋白反应(unfolded protein response,UPR),持续内质网应激则导致细胞凋亡、最终引起疾病的发生和发展。文献报道血管平滑肌细胞凋亡是血管钙化的启动或始动环节。近年来大量文献及我们课题组的工作报道血管钙化时内质网应激反应被激活并启动细胞凋亡。而且内质网应激参与了慢性肾功能衰竭血管钙化、维生素D3加尼古丁诱导的血管钙化及血管瓣膜的钙化。
暂无评论