增强现实中虚拟物体的投影注册算法研究

研究增强现实的关键技术之一的虚拟物体注册技术,使增强现实系统中的增强信息更具有真实感,结合三色基准注册技术,借助三维空间中的坐标系变换和立体投影变换算法,建立增强现实系统中虚拟物体投影注册模型,提出并推导增强现实系统的虚拟物体立体视觉投影注册算法,该算法能够很好地实现已知几何描述的虚拟物体从其自身坐标系到增强现实系统坐标系的转换,并能够生成具有视差的左右眼立体图像,本算法结合视点的三然基准算法完整地实现了用于增强现实的三维注册。     

Selective Smoothed Finite Element Method

The paper examines three selective schemes for the smoothed finite element method (SFEM) which was formulated by incorporating a cell-wise strain smoothing operation into the standard compatible finite element method (FEM). These selective SFEM schemes were formulated based on three selective integration FEM schemes with similar properties found between the number of smoothing cells in the SFEM and the number of Gaussian integration points in the FEM. Both scheme 1 and scheme 2 are free of nearly incompressible locking, but scheme 2 is more general and gives better results than scheme 1. In addition, scheme 2 can be applied to anisotropic and nonlinear situations, while scheme 1 can only be applied to isotropic and linear situations. Scheme 3 is free of shear locking. This scheme can be applied to plate and shell problems. Results of the numerical study show that the selective SFEM schemes give more accurate results than the FEM schemes.     

Optical properties of NdxGd1−xAl3(BO3)4 crystal

The optical properties of Nd x Gd 1-x Al\-3(BO\-3)\-4 (NGAB) crystal are reported. The refractive index of it were mesured by V_prism method. The absorption spectra and the flourescence specra of NGAB were also obtained. The optical parameters of NGAB were calculated following J_O theory, the three optical parameters are Ω 2 =1 805×10 -20 , Ω 4=1 85×10 -20 , Ω 6=3 793×10 -20 (RMS=1 4×10 -7 ) and β c( 4F 3/2 → 4I 11/2 ) is about 0 53.     

Angiotensin-converting enzyme 2 is an essential regulator of heart function

Cardiovascular diseases are predicted to be the most common cause of death worldwide by 2020. Here we show that angiotensin-converting enzyme 2 (ace2) maps to a defined quantitative trait locus (QTL) on the X chromosome in three different rat models of hypertension. In all hypertensive rat strains, ACE2 messenger RNA and protein expression were markedly reduced, suggesting that ace2 is a candidate gene for this QTL. Targeted disruption of ACE2 in mice results in a severe cardiac contractility defect, increased angiotensin II levels, and upregulation of hypoxia-induced genes in the heart. Genetic ablation of ACE on an ACE2 mutant background completely rescues the cardiac phenotype. But disruption of ACER, a Drosophila ACE2 homologue, results in a severe defect of heart morphogenesis. These genetic data for ACE2 show that it is an essential regulator of heart function in vivo.     

沥青混合料水稳定性分析

根据沥青混合料的强度形成原理和破坏机理以及沥青混合料与水相互作用机理，着重从集料性质、沥青性质、混合料类型、集料粒径和面层压实层厚度等方面分析了影响沥青混合料水稳定性的因素，提出了应在集料选择、沥青选择、沥青混合料设计、加热与拌和、碾压工艺、环境等方面采取措施来改善沥青混合料的水稳定性。     

Inactivation of the apoptosis effector Apaf-1 in malignant melanoma

Metastatic melanoma is a deadly cancer that fails to respond to conventional chemotherapy and is poorly understood at the molecular level. p53 mutations often occur in aggressive and chemoresistant cancers but are rarely observed in melanoma. Here we show that metastatic melanomas often lose Apaf-1, a cell-death effector that acts with cytochrome c and caspase-9 to mediate p53-dependent apoptosis. Loss of Apaf-1 expression is accompanied by allelic loss in metastatic melanomas, but can be recovered in melanoma cell lines by treatment with the methylation inhibitor 5-aza-2'-deoxycytidine (5aza2dC). Apaf-1-negative melanomas are invariably chemoresistant and are unable to execute a typical apoptotic programme in response to p53 activation. Restoring physiological levels of Apaf-1 through gene transfer or 5aza2dC treatment markedly enhances chemosensitivity and rescues the apoptotic defects associated with Apaf-1 loss. We conclude that Apaf-1 is inactivated in metastatic melanomas, which leads to defects in the execution of apoptotic cell death. Apaf-1 loss may contribute to the low frequency of p53 mutations observed in this highly chemoresistant tumour type.     

Coherent spin manipulation without magnetic fields in strained semiconductors

A consequence of relativity is that in the presence of an electric field, the spin and momentum states of an electron can be coupled; this is known as spin-orbit coupling. Such an interaction opens a pathway to the manipulation of electron spins within non-magnetic semiconductors, in the absence of applied magnetic fields. This interaction has implications for spin-based quantum information processing and spintronics, forming the basis of various device proposals. For example, the concept of spin field-effect transistors is based on spin precession due to the spin-orbit coupling. Most studies, however, focus on non-spin-selective electrical measurements in quantum structures. Here we report the direct measurement of coherent electron spin precession in zero magnetic field as the electrons drift in response to an applied electric field. We use ultrafast optical techniques to spatiotemporally resolve spin dynamics in strained gallium arsenide and indium gallium arsenide epitaxial layers. Unexpectedly, we observe spin splitting in these simple structures arising from strain in the semiconductor films. The observed effect provides a flexible approach for enabling electrical control over electron spins using strain engineering. Moreover, we exploit this strain-induced field to electrically drive spin resonance with Rabi frequencies of up to approximately 30 MHz.     

Beta-catenin/TCF4 transactivates miR-30e during intestinal cell differentiation

The Wnt/beta-catenin/TCF4 pathway plays critical roles in the maintenance of small intestinal epithelium; however, downstream targets of the beta-catenin/TCF4 complex are not extensively characterized. We identified miR-30e as an immediate target activated by the beta-catenin/TCF4 complex. miR-30e was detected in the peri-nuclear region of the intestinal crypt IEC-6 cells. Bioinformatics analysis revealed clustered beta-catenin/TCF4 binding sites within the miR-30e promoter region. This promoter region was cloned into pGL3-control luciferase reporter vector, with the enhancer region removed. Transfection of pCMV-SPORT6-beta-catenin expression vector dose-dependently increased luciferase activity, and co-transfection of pCMV-SPORT6-TCF4 expression vector further enhanced the promoter activity. Dexamethasone-induced IEC-6 cells differentiation caused a 2.5-fold increase in miR-30e expression, and upon beta-catenin siRNA transfection, miR-30e increased 1.3-fold. Electrophoretic mobility shift assay and chromatin immunoprecipitation assay confirmed the binding between beta-catenin/TCF4 complexes from IEC-6 nuclear extracts and the putative sequences in the miR-30e promoter. These results demonstrate that beta-catenin/TCF4 transactivates miR-30e during intestinal cell differentiation.     

Spatial dependence model with feature difference

This paper presents a new spatial dependence model with an adjustment of feature difference. The model accounts for the spatial autocorrelation in both the outcome variables and residuals. The feature difference adjustment in the model helps to emphasize feature changes across neighboring units, while suppressing unobserved covariates that are present in the same neighborhood. The prediction at a given unit incorporates components that depend on the differences between the values of its main features and those of its neighboring units. In contrast to conventional spatial regression models, our model does not require a comprehensive list of global covariates necessary to estimate the outcome variable at the unit, as common macro-level covariates are differenced away in the regression analysis. Using the real estate market data in Hong Kong, we applied Gibbs sampling to determine the posterior distribution of each model parameter. The result of our empirical analysis confirms that the adjustment of feature difference with an inclusion of the spatial error autocorrelation produces better out-of-sample prediction performance than other conventional spatial dependence models. In addition, our empirical analysis can identify components with more significant contributions.     

Inhibition of E coli ATPase activity by a troponin component, TN-I, and by mitochondrial ATPase inhibitor.

The enzymic activity of Mg2+- or Ca2+-stimulated ATPase from Escherichia coli was inhibited by one of the troponin components, TN-I, and by mitochondrial ATPase inhibitor (F1-inhibitor). The inhibitory ability of component TN-I against Mg2+-stimulated AtPase activity was lost after digestion of component TN-I with trypsin. The Mg2+-stimulated ATPase activity inhibited by component TN-I was completely restored by the addition of another troponin component TN-C.