超临界压力下航空煤油流动与传热特性试验

本文针对超燃冲压发动机再生冷却系统运行条件,实验研究了大庆RP-3煤油在超临界压力下的流动和传热特性,目的在于研究煤油在各种工况下的流动参数变化以及对流传热规律. 煤油通过二级煤油加热/输运系统加热,试验的煤油压力约2.6M~5.0MPa,油温约300~800 K. 相应的壁面热流密度为10~300 kW/m2. 通过油温与壁温的同步测量,结合非定常传热分析,获得了超临界压力下、亚/超临界温度范围内煤油的流动和传热物理参量的变化曲线

中国科学院高温气体动力学重点实验室研究进展

中国科学院高温气体动力学重点实验室是在钱学森先生和郭永怀先生创立的科研队伍的基础上于1994年组建的, 实验室成立以来一直坚持钱学森先生倡导的 "工程科学"理念, 面向国家安全和国民经济的重大战略需求, 主要研究高温、高超声速极端条件下, 具有分子振动与转动激发、解离、电离等内态变化介质的流动规律,推动气体动力学科的创新与发展; 并通过发展新理论、新方法、新概念和新技术, 突破国家重大需求项目的关键技术, 为作出基础性、前瞻性和战略性的研究成果:建设具有重要国际影响的高温气体动力学研究与人才培养基地.实验室2004年和2005年先后以优良成绩通过中科院和国家重点实验室评估; 2006年获得国家基金委创新群体; 2007年获得中科院/国家外专局国际合作伙伴; 2009年度中科院重点实验室评估排名第一.近年来,实验室以突破高超声速关键技术为目的, 在高焓高超声速气体流动、超声速燃烧与爆轰物理、稀薄气体与非平衡流动、高超声速飞行器气动构型理论等主要研究方向取得了重要进展, 在支撑中国高超声速流动模拟实验技术、高超声速推进技术、气动热预测与防护技术、高超声速飞行器设计技术等重大关键技术的突破方面发挥了重要作用、

An ATP-dependent mechanism mediates intercellular calcium signaling in bone cell network under single cell nanoindentation

To investigate the roles of intercellular gap junctions and extracellular ATP diffusion in bone cell calcium signaling propagation in bone tissue, in vitro bone cell networks were constructed by using microcontact printing and self-assembled monolayer technologies. In the network, neighboring cells were interconnected through functional gap junctions. A single cell at the center of the network was mechanically stimulated by using an AFM nanoindenter. Intracellular calcium ([Ca2+](i)) responses of the bone cell network were recorded and analyzed. In the untreated groups, calcium propagation from the stimulated cell to neighboring cells was observed in 40% of the tests. No significant difference was observed in this percentage when the intercellular gap junctions were blocked. This number, however, decreased to 10% in the extracellular ATP-pathway-blocked group. When both the gap junction and ATP pathways were blocked, intercellular calcium waves were abolished. When the intracellular calcium store in ER was depleted, the indented cell can generate calcium transients, but no [Ca2+](i) signal can be propagated to the neighboring cells. No [Ca2+](i) response was detected in the cell network when the extracellular calcium source was removed. These findings identified the biochemical pathways involved in the calcium signaling propagation in bone cell networks. Published by Elsevier Ltd.