New decoupling zmethod for spiral phase array HTS coil

published_or_final_versio

Use of functional MRI to evaluate correlation between acupoints and the somatic sensory cortex activities

published_or_final_versio

Design of superconducting MRI surface coil by using method of moment

A method of moment with an enhanced model to design high-temperature superconductor (HTS) RF surface coils for magnetic resonant image (MRI) is presented. The resonant frequency and quality factor (Q) of HTS RF spiral coils are simulated using this method. The agreements of resonant frequencies and Qs between the simulation and measurement are excellent with differences less than 1% and 3%, respectively. The 0.2-μ m-thick YBaCuO (YBCO) thin films are deposited onto single side of 0.508-mm-thick LaAlO 3 (LAO) and sapphire substrate and patterned into a spiral shape. To accurately analyze the resonant frequency and Q of a coil, an enhanced two-fluid model is employed. HTS RF coils with diameter of 65 mm for 0.2T and 1.5T MRI systems are designed and fabricated with the measured Q of 19 K and 23 K, respectively. In addition, the shift of resonant frequency due to the mutual coupling between two HTS spiral coils is predicted by this method, which is important for design of HTS coil arrays in an MRI system.published_or_final_versio

Structure of charge density waves in La1.875 Ba0.125 CuO4

Although charge density wave (CDW) correlations exist in several families of cuprate superconductors, they exhibit substantial variation in CDW wave vector and correlation length, indicating a key role for CDW-lattice interactions. We investigated this interaction in La1.875Ba0.125CuO4 using single-crystal x-ray diffraction to collect a large number of CDW peak intensities and determined the Cu and La/Ba atomic distortions induced by the formation of CDW order. Within the CuO2 planes, the distortions involve a periodic modulation of the Cu-Cu spacing along the direction of the ordering wave vector. The charge ordering within the copper-oxygen layer induces an out-of-plane breathing modulation of the surrounding lanthanum layers, which leads to a related distortion on the adjacent copper-oxygen layer. Our result implies that the CDW-related structural distortions do not remain confined to a single layer but rather propagate an appreciable distance through the crystal. This leads to overlapping structural modulations, in which CuO2 planes exhibit distortions arising from the orthogonal CDWs in adjacent layers as well as distortions from the CDW within the layer itself. We attribute this striking effect to the weak c-axis charge screening in cuprates and suggest this effect could help couple the CDWs between adjacent planes in the crystal

A fMRI Study of Correlation Between Acupoints and Brain Cortical Sites Involved in Language Functions

published_or_final_versio

防护林带:湍流的数学模型与计算机模拟

虽然防护林用于减小风速、控制热量和水汽传递及污染物扩散、改善气候与环境、增加作物产量等已经有几百年了,但直到近几十年,人们才开始系统地研究防护林空气动力学的遮蔽机制.在本综述中,我们考察了绕防护林带的流动与湍流控制机制,最新的模型与数值模拟研究情况;通过数值模拟与实验数据的比较,来了解防护林带结构与防风效果之间的关系;讨论数值分析如何及为什么能够得到所需要的结果.本文将从多孔隙防护林带流动基本方程组的推导开始,讨论数值模型及模拟过程,对附体与分离流动进行预测;分析了遮蔽机制与动量交换;对风向、防护林密度、宽度和三维性对流动与湍流的影响作了系统的论述.还对热流和土壤水分蒸发的新模型及数值模拟作了简述.最后,我们对网络工作站、群和高性能分布式并行计算机及其对防护林带模型预报能力的提高作了讨论

Stacking disorder in α−RuCl_{3} investigated via x-ray three-dimensional difference pair distribution function analysis

The van der Waals layered magnet α − RuCl_{3} offers tantalizing prospects for the realization of Majorana quasiparticles. Efforts to understand this are, however, hampered by inconsistent magnetic and thermal transport properties likely coming from the formation of structural disorder during crystal growth, postgrowth processing, or upon cooling through the first order structural transition. Here, we investigate structural disorder in α − RuCl_{3} using x-ray diffuse scattering and three-dimensional difference pair distribution function analysis. We develop a quantitative model that describes disorder in α − RuCl_{3} in terms of rotational twinning and intermixing of the high- and low-temperature structural layer stacking. This disorder may be important to consider when investigating the detailed magnetic and electronic properties of this widely studied material

Identification of the Allosteric Regulatory Site of Insulysin

Background: Insulin degrading enzyme (IDE) is responsible for the metabolism of insulin and plays a role in clearance of the Ab peptide associated with Alzheimer's disease. Unlike most proteolytic enzymes, IDE, which consists of four structurally related domains and exists primarily as a dimer, exhibits allosteric kinetics, being activated by both small substrate peptides and polyphosphates such as ATP.Principal Findings: the crystal structure of a catalytically compromised mutant of IDE has electron density for peptide ligands bound at the active site in domain 1 and a distal site in domain 2. Mutating residues in the distal site eliminates allosteric kinetics and activation by a small peptide, as well as greatly reducing activation by ATP, demonstrating that this site plays a key role in allostery. Comparison of the peptide bound IDE structure (using a low activity E111F IDE mutant) with unliganded wild type IDE shows a change in the interface between two halves of the clamshell-like molecule, which may enhance enzyme activity by altering the equilibrium between closed and open conformations. in addition, changes in the dimer interface suggest a basis for communication between subunits.Conclusions/Significance: Our findings indicate that a region remote from the active site mediates allosteric activation of insulysin by peptides. Activation may involve a small conformational change that weakens the interface between two halves of the enzyme.United States Public Health ServicesUniv Kentucky, Dept Mol & Cellular Biochem, Lexington, KY 40536 USAUniv Kentucky, Struct Biol Ctr, Lexington, KY USAUniversidade Federal de São Paulo, Dept Biophys, Escola Paulista Med, São Paulo, BrazilUniversidade Federal de São Paulo, Dept Biophys, Escola Paulista Med, São Paulo, BrazilUnited States Public Health Services: NS38041United States Public Health Services: DA02243United States Public Health Services: DA016176United States Public Health Services: P20 RR20171United States Public Health Services: T32 DA016176Web of Scienc

A Hidden Markov Model for Copy Number Variant prediction from whole genome resequencing data

Motivation: Copy Number Variants (CNVs) are important genetic factors for studying human diseases. While high-throughput whole genome re-sequencing provides multiple lines of evidence for detecting CNVs, computational algorithms need to be tailored for different type or size of CNVs under different experimental designs. Results: To achieve optimal power and resolution of detecting CNVs at low depth of coverage, we implemented a Hidden Markov Model that integrates both depth of coverage and mate-pair relationship. The novelty of our algorithm is that we infer the likelihood of carrying a deletion jointly from multiple mate pairs in a region without the requirement of a single mate pairs being obvious outliers. By integrating all useful information in a comprehensive model, our method is able to detect medium-size deletions (200-2000bp) at low depth (<10× per sample). We applied the method to simulated data and demonstrate the power of detecting medium-size deletions is close to theoretical values. Availability: A program implemented in Java, Zinfandel, is available at http://www.cs.columbia.edu/~itsik/zinfandel

Essential Roles of BCCIP in Mouse Embryonic Development and Structural Stability of Chromosomes

BCCIP is a BRCA2- and CDKN1A(p21)-interacting protein that has been implicated in the maintenance of genomic integrity. To understand the in vivo functions of BCCIP, we generated a conditional BCCIP knockdown transgenic mouse model using Cre-LoxP mediated RNA interference. The BCCIP knockdown embryos displayed impaired cellular proliferation and apoptosis at day E7.5. Consistent with these results, the in vitro proliferation of blastocysts and mouse embryonic fibroblasts (MEFs) of BCCIP knockdown mice were impaired considerably. The BCCIP deficient mouse embryos die before E11.5 day. Deletion of the p53 gene could not rescue the embryonic lethality due to BCCIP deficiency, but partially rescues the growth delay of mouse embryonic fibroblasts in vitro. To further understand the cause of development and proliferation defects in BCCIP-deficient mice, MEFs were subjected to chromosome stability analysis. The BCCIP-deficient MEFs displayed significant spontaneous chromosome structural alterations associated with replication stress, including a 3.5-fold induction of chromatid breaks. Remarkably, the BCCIP-deficient MEFs had a ∼20-fold increase in sister chromatid union (SCU), yet the induction of sister chromatid exchanges (SCE) was modestly at 1.5 fold. SCU is a unique type of chromatid aberration that may give rise to chromatin bridges between daughter nuclei in anaphase. In addition, the BCCIP-deficient MEFs have reduced repair of irradiation-induced DNA damage and reductions of Rad51 protein and nuclear foci. Our data suggest a unique function of BCCIP, not only in repair of DNA damage, but also in resolving stalled replication forks and prevention of replication stress. In addition, BCCIP deficiency causes excessive spontaneous chromatin bridges via the formation of SCU, which can subsequently impair chromosome segregations in mitosis and cell division