Two-dimensional Transport Induced Linear Magneto-Resistance in Topological Insulator Bi2_2Se3_3 Nanoribbons

We report the study of a novel linear magneto-resistance (MR) under perpendicular magnetic fields in Bi2Se3 nanoribbons. Through angular dependence magneto-transport experiments, we show that this linear MR is purely due to two-dimensional (2D) transport, in agreement with the recently discovered linear MR from 2D topological surface state in bulk Bi2Te3, and the linear MR of other gapless semiconductors and graphene. We further show that the linear MR of Bi2Se3 nanoribbons persists to room temperature, underscoring the potential of exploiting topological insulator nanomaterials for room temperature magneto-electronic applications.Comment: ACS Nano, in pres

Discovery of delayed spin-up behavior following two large glitches in the Crab pulsar, and the statistics of such processes

Glitches correspond to sudden jumps of rotation frequency ($\nu$) and its derivative ($\dot{\nu}$) of pulsars, the origin of which remains not well understood yet, partly because the jump processes of most glitches are not well time-resolved. There are three large glitches of the Crab pulsar, detected in 1989, 1996 and 2017, which were found to have delayed spin-up processes before the normal recovery processes. Here we report two additional glitches of the Crab pulsar occurred in 2004 and 2011 for which we discovered delayed spin up processes, and present refined parameters of the largest glitch occurred in 2017. The initial rising time of the glitch is determined as $<0.48$ hour. We also carried out a statistical study of these five glitches with observed spin-up processes. The two glitches occurred in 2004 and 2011 have delayed spin-up time scales ($\tau_{1}$) of $1.7\pm0.8$\,days and $1.6\pm0.4$\,days, respectively. We find that the $\Delta{\nu}$ vs. $|\Delta{\dot\nu}|$ relation of these five glitches is similar to those with no detected delayed spin-up process, indicating that they are similar to the others in nature except that they have larger amplitudes. For these five glitches, the amplitudes of the delayed spin-up process ($|\Delta{\nu}_{\rm d1}|$) and recovery process ($\Delta{\nu}_{\rm d2}$), their time scales ($\tau_{1}$, $\tau_{2}$), and permanent changes in spin frequency ($\Delta{\nu}_{\rm p}$) and total frequency step ($\Delta{\nu}_{\rm g}$) have positive correlations. From these correlations, we suggest that the delayed spin-up processes are common for all glitches, but are too short and thus difficult to be detected for most glitches.Comment: 25 pages, 8 figure

Bioinformatics in China: A Personal Perspective

Biochemical Research MethodsMathematical &amp; Computational BiologySCI(E)PubMed3EDITORIAL MATERIAL4e1000020

Parent-of-origin-specific allelic associations among 106 genomic loci for age at menarche.

Age at menarche is a marker of timing of puberty in females. It varies widely between individuals, is a heritable trait and is associated with risks for obesity, type 2 diabetes, cardiovascular disease, breast cancer and all-cause mortality. Studies of rare human disorders of puberty and animal models point to a complex hypothalamic-pituitary-hormonal regulation, but the mechanisms that determine pubertal timing and underlie its links to disease risk remain unclear. Here, using genome-wide and custom-genotyping arrays in up to 182,416 women of European descent from 57 studies, we found robust evidence (P < 5 × 10(-8)) for 123 signals at 106 genomic loci associated with age at menarche. Many loci were associated with other pubertal traits in both sexes, and there was substantial overlap with genes implicated in body mass index and various diseases, including rare disorders of puberty. Menarche signals were enriched in imprinted regions, with three loci (DLK1-WDR25, MKRN3-MAGEL2 and KCNK9) demonstrating parent-of-origin-specific associations concordant with known parental expression patterns. Pathway analyses implicated nuclear hormone receptors, particularly retinoic acid and γ-aminobutyric acid-B2 receptor signalling, among novel mechanisms that regulate pubertal timing in humans. Our findings suggest a genetic architecture involving at least hundreds of common variants in the coordinated timing of the pubertal transition

Analyses and Comparison of Imputation-Based Association Methods

Genotype imputation methods have become increasingly popular for recovering untyped genotype data. An important application with imputed genotypes is to test genetic association for diseases. Imputation-based association test can provide additional insight beyond what is provided by testing on typed tagging SNPs only. A variety of effective imputation-based association tests have been proposed. However, their performances are affected by a variety of genetic factors, which have not been well studied. In this study, using both simulated and real data sets, we investigated the effects of LD, MAF of untyped causal SNP and imputation accuracy rate on the performances of seven popular imputation-based association methods, including MACH2qtl/dat, SNPTEST, ProbABEL, Beagle, Plink, BIMBAM and SNPMStat. We also aimed to provide a comprehensive comparison among methods. Results show that: 1). imputation-based association tests can boost signals and improve power under medium and high LD levels, with the power improvement increasing with strengthening LD level; 2) the power increases with higher MAF of untyped causal SNPs under medium to high LD level; 3). under low LD level, a high imputation accuracy rate cannot guarantee an improvement of power; 4). among methods, MACH2qtl/dat, ProbABEL and SNPTEST perform similarly and they consistently outperform other methods. Our results are helpful in guiding the choice of imputation-based association test in practical application

A phasing and imputation method for pedigreed populations that results in a single-stage genomic evaluation

<p>Abstract</p> <p>Background</p> <p>Efficient, robust, and accurate genotype imputation algorithms make large-scale application of genomic selection cost effective. An algorithm that imputes alleles or allele probabilities for all animals in the pedigree and for all genotyped single nucleotide polymorphisms (SNP) provides a framework to combine all pedigree, genomic, and phenotypic information into a single-stage genomic evaluation.</p> <p>Methods</p> <p>An algorithm was developed for imputation of genotypes in pedigreed populations that allows imputation for completely ungenotyped animals and for low-density genotyped animals, accommodates a wide variety of pedigree structures for genotyped animals, imputes unmapped SNP, and works for large datasets. The method involves simple phasing rules, long-range phasing and haplotype library imputation and segregation analysis.</p> <p>Results</p> <p>Imputation accuracy was high and computational cost was feasible for datasets with pedigrees of up to 25 000 animals. The resulting single-stage genomic evaluation increased the accuracy of estimated genomic breeding values compared to a scenario in which phenotypes on relatives that were not genotyped were ignored.</p> <p>Conclusions</p> <p>The developed imputation algorithm and software and the resulting single-stage genomic evaluation method provide powerful new ways to exploit imputation and to obtain more accurate genetic evaluations.</p

Positive Evolutionary Selection of an HD Motif on Alzheimer Precursor Protein Orthologues Suggests a Functional Role

HD amino acid duplex has been found in the active center of many different enzymes. The dyad plays remarkably different roles in their catalytic processes that usually involve metal coordination. An HD motif is positioned directly on the amyloid beta fragment (Aβ) and on the carboxy-terminal region of the extracellular domain (CAED) of the human amyloid precursor protein (APP) and a taxonomically well defined group of APP orthologues (APPOs). In human Aβ HD is part of a presumed, RGD-like integrin-binding motif RHD; however, neither RHD nor RXD demonstrates reasonable conservation in APPOs. The sequences of CAEDs and the position of the HD are not particularly conserved either, yet we show with a novel statistical method using evolutionary modeling that the presence of HD on CAEDs cannot be the result of neutral evolutionary forces (p<0.0001). The motif is positively selected along the evolutionary process in the majority of APPOs, despite the fact that HD motif is underrepresented in the proteomes of all species of the animal kingdom. Position migration can be explained by high probability occurrence of multiple copies of HD on intermediate sequences, from which only one is kept by selective evolutionary forces, in a similar way as in the case of the “transcription binding site turnover.” CAED of all APP orthologues and homologues are predicted to bind metal ions including Amyloid-like protein 1 (APLP1) and Amyloid-like protein 2 (APLP2). Our results suggest that HDs on the CAEDs are most probably key components of metal-binding domains, which facilitate and/or regulate inter- or intra-molecular interactions in a metal ion-dependent or metal ion concentration-dependent manner. The involvement of naturally occurring mutations of HD (Tottori (D7N) and English (H6R) mutations) in early onset Alzheimer's disease gives additional support to our finding that HD has an evolutionary preserved function on APPOs