基于能量原理和Kalman滤波器的实时模型修正策略

为了实时监测结构的安全状态,提出了一种计算速度快、易收敛的模型修正策略.首先通过计算瞬时能量来建立结构单元刚度和结构响应之间的关系;然后,将结构瞬时能量代入Kalman滤波器中,根据每一时间步能量预测值和实际测量值的差异进行修正,得到结构的真实刚度;最后,以美国地震工程模拟中心数据库(NEES)中的美国某州际公路指示牌支撑桁架为例进行数值验证,结果表明:无噪声干扰情况下,刚度发生20%,40%,60%,80%损伤的杆件和未发生损伤的杆件均能在0.4 s内从初始刚度收敛到各自的真实刚度;在5%随机噪声干扰下,利用该策略修正得到的刚度误差均小于12%;每一时间步所消耗的CPU时间远小于采样周期.因此,利用能量原理和Kalman滤波器能够快速有效地对未知刚度的结构进行实时模型修正.     

Nephrocystin-5, a ciliary IQ domain protein, is mutated in Senior-Loken syndrome and interacts with RPGR and calmodulin

Nephronophthisis (NPHP) is the most frequent genetic cause of chronic renal failure in children. Identification of four genes mutated in NPHP subtypes 1-4 (refs. 4-9) has linked the pathogenesis of NPHP to ciliary functions. Ten percent of affected individuals have retinitis pigmentosa, constituting the renal-retinal Senior-Loken syndrome (SLSN). Here we identify, by positional cloning, mutations in an evolutionarily conserved gene, IQCB1 (also called NPHP5), as the most frequent cause of SLSN. IQCB1 encodes an IQ-domain protein, nephrocystin-5. All individuals with IQCB1 mutations have retinitis pigmentosa. Hence, we examined the interaction of nephrocystin-5 with RPGR (retinitis pigmentosa GTPase regulator), which is expressed in photoreceptor cilia and associated with 10-20% of retinitis pigmentosa. We show that nephrocystin-5, RPGR and calmodulin can be coimmunoprecipitated from retinal extracts, and that these proteins localize to connecting cilia of photoreceptors and to primary cilia of renal epithelial cells. Our studies emphasize the central role of ciliary dysfunction in the pathogenesis of SLSN.     

Hatching chronology of Blue Grouse in northeastern Oregon

Hatching chronology of Blue Grouse ( Dendragapus obscurus ) in northeastern Oregon was determined from 431 immatures examined from 1981 to 1985. Young hatched from 1 May through 8 July; median hatching dates for the five years ranged from 27 May to 5 June. Peak hatching in Oregon occurred from one to four weeks earlier than in most portions of the range of Blue Grouse but were similar to north central Washington and Idaho. Variations in hatching dates possibly were related to rainfall.       

Change in compatibility after microinjection of cytoplasm in amoebae

Summary A cytoplasmic fraction from D32, a clone of amoebae derived fromAmoeba proteus injected with cytoplasm fromA. discoides, inhibited cell division inA. proteus but not inA. discoides indicating a permanent change with respect to compatibility.     

Selective inhibition of cotranslational translocation of vascular cell adhesion molecule 1

Increased expression of vascular cell adhesion molecule 1 (VCAM1) is associated with a variety of chronic inflammatory conditions, making its expression and function a target for therapeutic intervention. We have recently identified CAM741, a derivative of a fungus-derived cyclopeptolide that acts as a selective inhibitor of VCAM1 synthesis in endothelial cells. Here we show that the compound represses the biosynthesis of VCAM1 in cells by blocking the process of cotranslational translocation, which is dependent on the signal peptide of VCAM1. CAM741 does not inhibit targeting of the VCAM1 nascent chains to the translocon channel but prevents translocation to the luminal side of the endoplasmic reticulum (ER), through a process that involves the translocon component Sec61beta. Consequently, the VCAM1 precursor protein is synthesized towards the cytosolic compartment of the cells, where it is degraded. Our results indicate that the inhibition of cotranslational translocation with low-molecular-mass compounds, using specificity conferred by signal peptides, can modulate the biosynthesis of certain secreted and/or membrane proteins. In addition, they highlight cotranslational translocation at the ER membrane as a potential target for drug discovery.     

Combining naturally occurring polyphenols with TNF-related apoptosis-inducing ligand: a promising approach to kill resistant cancer cells?

TNF-related apoptosis-inducing ligand (TRAIL) and its receptors are attractive targets for anticancer therapy owing to their ability to trigger apoptosis selectively in cancer cells but not in normal cells. To date, many combinatorial strategies, such as chemotherapy or radiotherapy, have given encouraging results for overcoming TRAIL resistance in preclinical models. In this review, we provide an overview of the molecular mechanisms underlying sensitization to TRAIL-induced apoptosis by polyphenols. These naturally occurring compounds can restore tumor cell sensitivity to TRAIL-induced cell death with no apparent toxicity towards normal cells. Both extrinsic and intrinsic pathways can be modulated by polyphenols, the activation of which largely depends on the cell type, the particular polyphenolic compound, and the conditions of treatment. The large variety of polyphenol cellular targets could prove useful in circumventing TRAIL resistance. The relevance of these combined treatments for cancer therapy is discussed in the light of recent preclinical studies.     

The effect of plant growth substances and natural products on RNA and DNA synthesis in leukocytes.

The effect of auxins, cytokinins, gibberellins and phenolics on the incorporation of uridine and thymidine into the nucleic acids of human leukocytes was examined. Both the stimulation and inhibition of the incorporation of the precursors was noted. The auxins consistently promoted the incorporation of uridine.