基于VMF分布模型的MIMO多天线系统性能研究

基于3维环境的空间统计信道,提出MIMO天线阵列下的VMF分布模型.研究MIMO多天线ULA,UYA和UCA在移动台和基站的拓扑结构,得到VMF(Von Mises Fisher)分布模型下ULA,UYA和UCA的空间衰落相关性(SFC)函数的表达式,比较不同天线阵列对平均仰角(MEOA)的灵敏度.研究表明,MIMO天线阵列的SFC由集中参数、平均方位角(MAOA)及平均仰角(MEOA)决定,该模型的信道性能结果与理论一致.     

Radixin deficiency causes conjugated hyperbilirubinemia with loss of Mrp2 from bile canalicular membranes

The ezrin-radixin-moesin (ERM) family of proteins crosslink actin filaments and integral membrane proteins. Radixin (encoded by Rdx) is the dominant ERM protein in the liver of wildtype mice and is concentrated at bile canalicular membranes (BCMs). Here we show that Rdx(-/-) mice are normal at birth, but their serum concentrations of conjugated bilirubin begin to increase gradually around 4 weeks, and they show mild liver injury after 8 weeks. This phenotype is similar to human conjugated hyperbilirubinemia in Dubin-Johnson syndrome, which is caused by mutations in the multidrug resistance protein 2 (MRP2, gene symbol ABCC2), although this syndrome is not associated with overt liver injury. In wildtype mice, Mrp2 concentrates at BCMs to secrete conjugated bilirubin into bile. In the BCMs of Rdx(-/-) mice, Mrp2 is decreased compared with other BCM proteins such as dipeptidyl peptidase IV (CD26) and P-glycoproteins. In vitro binding studies show that radixin associates directly with the carboxy-terminal cytoplasmic domain of human MRP2. These findings indicate that radixin is required for secretion of conjugated bilirubin through its support of Mrp2 localization at BCMs.     

Disaccharidase rhythm in rat small intestine; no relationship with mitosis rhythm

Summary Same circadian difference in the specific activities of sucrase and maltase was observed in the purified brush border fraction as in the crude homogenate of the mucosa of rat small intestine, suggesting that the disaccharidase rhythm is not due to the mitosis rhythm of epithelial cells.     

Nucleosynthetic signatures of the first stars

The chemically most primitive stars provide constraints on the nature of the first stellar objects that formed in the Universe; elements other than hydrogen, helium and traces of lithium present within these objects were generated by nucleosynthesis in the very first stars. The relative abundances of elements in the surviving primitive stars reflect the masses of the first stars, because the pathways of nucleosynthesis are quite sensitive to stellar masses. Several models have been suggested to explain the origin of the abundance pattern of the giant star HE0107-5240, which hitherto exhibited the highest deficiency of heavy elements known. Here we report the discovery of HE1327-2326, a subgiant or main-sequence star with an iron abundance about a factor of two lower than that of HE0107-5240. Both stars show extreme overabundances of carbon and nitrogen with respect to iron, suggesting a similar origin of the abundance patterns. The unexpectedly low Li and high Sr abundances of HE1327-2326, however, challenge existing theoretical understanding: no model predicts the high Sr abundance or provides a Li depletion mechanism consistent with data available for the most metal-poor stars.     

跌落水流时台阶式溢洪道消力池跃前断面压力修正系数

台阶式溢洪道与平底消力池连接,在跌落水流流况下,比较跃前断面压力修正系λ=1和λ>1两种情况,当λ=1时消能率普遍偏大,其消能率的相对误差最大可达7%左右,随Hdam/yc增大,误差减小。当坝坡相同、坝高一定时,台阶个数与消能率无关,并不影响其误差的大小。λ值与yp/y1呈现非常好的线性相关性,其相关系数r=0.9999以上。     

IGFBP-4 is an inhibitor of canonical Wnt signalling required for cardiogenesis

Insulin-like growth-factor-binding proteins (IGFBPs) bind to and modulate the actions of insulin-like growth factors (IGFs). Although some of the actions of IGFBPs have been reported to be independent of IGFs, the precise mechanisms of IGF-independent actions of IGFBPs are largely unknown. Here we report a previously unknown function for IGFBP-4 as a cardiogenic growth factor. IGFBP-4 enhanced cardiomyocyte differentiation in vitro, and knockdown of Igfbp4 attenuated cardiomyogenesis both in vitro and in vivo. The cardiogenic effect of IGFBP-4 was independent of its IGF-binding activity but was mediated by the inhibitory effect on canonical Wnt signalling. IGFBP-4 physically interacted with a Wnt receptor, Frizzled 8 (Frz8), and a Wnt co-receptor, low-density lipoprotein receptor-related protein 6 (LRP6), and inhibited the binding of Wnt3A to Frz8 and LRP6. Although IGF-independent, the cardiogenic effect of IGFBP-4 was attenuated by IGFs through IGFBP-4 sequestration. IGFBP-4 is therefore an inhibitor of the canonical Wnt signalling required for cardiogenesis and provides a molecular link between IGF signalling and Wnt signalling.