研究了微肋管内R407C和R22的流动沸腾换热特性,采用威尔逊图解法对实验数据进行处理,主要分析实验工况、制冷剂物性、微肋管结构等变量的影响。结果表明:制冷剂R407C与R22与换热壁面之间的换热热阻均随热流密度、质流密度、干度、肋片...研究了微肋管内R407C和R22的流动沸腾换热特性,采用威尔逊图解法对实验数据进行处理,主要分析实验工况、制冷剂物性、微肋管结构等变量的影响。结果表明:制冷剂R407C与R22与换热壁面之间的换热热阻均随热流密度、质流密度、干度、肋片螺旋角等的增加而减小;由于制冷剂气液相密度比的差异性,R22传热系数比与R407C的高约18.5%—21.4%。选用关联式对微肋管内R407C流动沸腾换热特性进行预测评估,并对关联式预测精度随干度、质流密度等的变化趋势进行分析。在所选关联式内,Yu and Koyama关联式表现出最佳预测效果,其平均预测误差在±6.5%以内,且干度、质流密度对其预测精度的影响相近;而对于其它关联式,干度对关联式预测精度的影响比重普遍高于质流密度。展开更多
Osteogenesis imperfecta(OI)is a group of diseases caused by defects in type I collagen processing which result in skeletal fragility.While these disorders have been regarded as defects in osteoblast function,the role ...Osteogenesis imperfecta(OI)is a group of diseases caused by defects in type I collagen processing which result in skeletal fragility.While these disorders have been regarded as defects in osteoblast function,the role of matrix-embedded osteocytes in OI pathogenesis remains largely unknown.Homozygous human SP7(c.946 C>T,R316C)mutation results in a recessive form of OI characterized by fragility fractures,low bone mineral density and osteocyte dendrite defects.To better understand how the OI-causing R316C mutation affects the function of SP7,we generated Sp7^(R342C)knock-in mice.Consistent with patient phenotypes,Sp7^(R342C/R342C)mice demonstrate increased cortical porosity and reduced cortical bone mineral density.Sp7^(R342C/R342C)mice show osteocyte dendrite defects,increased osteocyte apoptosis,and intracortical bone remodeling with ectopic intracortical osteoclasts and elevated osteocyte Tnfsf11 expression.展开更多
文摘研究了微肋管内R407C和R22的流动沸腾换热特性,采用威尔逊图解法对实验数据进行处理,主要分析实验工况、制冷剂物性、微肋管结构等变量的影响。结果表明:制冷剂R407C与R22与换热壁面之间的换热热阻均随热流密度、质流密度、干度、肋片螺旋角等的增加而减小;由于制冷剂气液相密度比的差异性,R22传热系数比与R407C的高约18.5%—21.4%。选用关联式对微肋管内R407C流动沸腾换热特性进行预测评估,并对关联式预测精度随干度、质流密度等的变化趋势进行分析。在所选关联式内,Yu and Koyama关联式表现出最佳预测效果,其平均预测误差在±6.5%以内,且干度、质流密度对其预测精度的影响相近;而对于其它关联式,干度对关联式预测精度的影响比重普遍高于质流密度。
基金support from the National Institute of Health(K99AR081897,R00AR081897)M.N.W.acknowledges funding support from the National Institute of Health(P01DK011794,R01DK116716)+1 种基金the Smith Family Foundation Odyssey Award,and the Chen Institute Massachusetts General Hospital Research Scholar(2024-2029)awardμCT and bone histomorphometry were performed by the Center for Skeletal Research at Massachusetts General Hospital,a NIH-funded program(P30AR066261 and AR075042)led by Mary Bouxsein and Marie Demay.
文摘Osteogenesis imperfecta(OI)is a group of diseases caused by defects in type I collagen processing which result in skeletal fragility.While these disorders have been regarded as defects in osteoblast function,the role of matrix-embedded osteocytes in OI pathogenesis remains largely unknown.Homozygous human SP7(c.946 C>T,R316C)mutation results in a recessive form of OI characterized by fragility fractures,low bone mineral density and osteocyte dendrite defects.To better understand how the OI-causing R316C mutation affects the function of SP7,we generated Sp7^(R342C)knock-in mice.Consistent with patient phenotypes,Sp7^(R342C/R342C)mice demonstrate increased cortical porosity and reduced cortical bone mineral density.Sp7^(R342C/R342C)mice show osteocyte dendrite defects,increased osteocyte apoptosis,and intracortical bone remodeling with ectopic intracortical osteoclasts and elevated osteocyte Tnfsf11 expression.
