7,095 research outputs found

    A statistical framework for the design of microarray experiments and effective detection of differential gene expression

    Full text link
    Four reasons why you might wish to read this paper: 1. We have devised a new statistical T test to determine differentially expressed genes (DEG) in the context of microarray experiments. This statistical test adds a new member to the traditional T-test family. 2. An exact formula for calculating the detection power of this T test is presented, which can also be fairly easily modified to cover the traditional T tests. 3. We have presented an accurate yet computationally very simple method to estimate the fraction of non-DEGs in a set of genes being tested. This method is superior to an existing one which is computationally much involved. 4. We approach the multiple testing problem from a fresh angle, and discuss its relation to the classical Bonferroni procedure and to the FDR (false discovery rate) approach. This is most useful in the analysis of microarray data, where typically several thousands of genes are being tested simultaneously.Comment: 9 pages, 1 table; to appear in Bioinformatic

    A Sharp upper bound for the spectral radius of a nonnegative matrix and applications

    Get PDF
    In this paper, we obtain a sharp upper bound for the spectral radius of a nonnegative matrix. This result is used to present upper bounds for the adjacency spectral radius, the Laplacian spectral radius, the signless Laplacian spectral radius, the distance spectral radius, the distance Laplacian spectral radius, the distance signless Laplacian spectral radius of a graph or a digraph. These results are new or generalize some known results.Comment: 16 pages in Czechoslovak Math. J., 2016. arXiv admin note: text overlap with arXiv:1507.0705

    Elucidating the roles of SOD3 correlated genes and reactive oxygen species in rare human diseases using a bioinformatic-ontology approach

    Get PDF
    Superoxide Dismutase 3 (SOD3) scavenges extracellular superoxide giving a hydrogen peroxide metabolite. Both Reactive Oxygen Species diffuse through aquaporins causing oxidative stress and biomolecular damage. SOD3 is differentially expressed in cancer and this research utilises Gene Expression Omnibus data series GSE2109 with 2,158 cancer samples. Genome-wide expression correlation analysis was conducted with SOD3 as the seed gene. Categorical SOD3 Pearson Correlation gene lists incrementing in correlation strength by 0.01 from ρ≥|0.34| to ρ≥|0.41| were extracted from the data. Positively and negatively SOD3 correlated genes were separated for each list and checked for significance against disease overlapping genes in the ClinVar and Orphanet databases via Enrichr. Disease causal genes were added to the relevant gene list and checked against Gene Ontology, Phenotype Ontology, and Elsevier Pathways via Enrichr before the significant ontologies containing causal and non-overlapping genes were reviewed with a literature search for possible disease and oxidative stress associations. 12 significant individually discriminated disorders were identified: Autosomal Dominant Cutis Laxa (p = 6.05x10-7), Renal Tubular Dysgenesis of Genetic Origin (p = 6.05x10-7), Lethal Arteriopathy Syndrome due to Fibulin-4 Deficiency (p = 6.54x10-9), EMILIN-1-related Connective Tissue Disease (p = 6.54x10-9), Holt-Oram Syndrome (p = 7.72x10-10), Multisystemic Smooth Muscle Dysfunction Syndrome (p = 9.95x10-15), Distal Hereditary Motor Neuropathy type 2 (p = 4.48x10-7), Congenital Glaucoma (p = 5.24x210-9), Megacystis-Microcolon-Intestinal Hypoperistalsis Syndrome (p = 3.77x10-16), Classical-like Ehlers-Danlos Syndrome type 1 (p = 3.77x10-16), Retinoblastoma (p = 1.9x10-8), and Lynch Syndrome (p = 5.04x10-9). 35 novel (21 unique) genes across 12 disorders were identified: ADNP, AOC3, CDC42EP2, CHTOP, CNN1, DES, FOXF1, FXR1, HLTF, KCNMB1, MTF2, MYH11, PLN, PNPLA2, REST, SGCA, SORBS1, SYNPO2, TAGLN, WAPL, and ZMYM4. These genes are proffered as potential biomarkers or therapeutic targets for the corresponding rare diseases discussed.</p

    The naturalness in the BLMSSM and B-LSSM

    Full text link
    In order to interpret the Higgs mass and its decays more naturally, we hope to intrude the BLMSSM and B-LSSM. In the both models, the right-handed neutrino superfields are introduced to better explain the neutrino mass problems. In addition, there are other superfields considered to make these models more natural than MSSM. In this paper, the method of χ2\chi^2 analyses will be adopted in the BLMSSM and B-LSSM to calculate the Higgs mass, Higgs decays and muon g2g-2. With the fine-tuning in the region 0.67%2.5%0.67\%-2.5\% and 0.67%5%0.67\%-5\%, we can obtain the reasonable theoretical values that are in accordance with the experimental results respectively in the BLMSSM and B-LSSM. Meanwhile, the best-fitted benchmark points in the BLMSSM and B-LSSM will be acquired at minimal (χminBL)2=2.34736(\chi^{BL}_{min})^2 = 2.34736 and (χminBL)2=2.47754(\chi^{B-L}_{min})^2 = 2.47754, respectively

    The order analysis for the two loop corrections to lepton MDM

    Full text link
    The experimental data of the magnetic dipole moment(MDM) of lepton(ee, μ\mu) is very exact. The deviation between the experimental data and the standard model prediction maybe come from new physics contribution. In the supersymmetric models, there are very many two loop diagrams contributing to the lepton MDM. In supersymmetric models, we suppose two mass scales MSHM_{SH} and MM with MSHMM_{SH}\gg M for supersymmetric particles. Squarks belong to MSHM_{SH} and the other supersymmetric particles belong to MM. We analyze the order of the contributions from the two loop diagrams. The two loop triangle diagrams corresponding to the two loop self-energy diagram satisfy Ward-identity, and their contributions possess particular factors. This work can help to distinguish the important two loop diagrams giving corrections to lepton MDM.Comment: 12 pages, 3 figure

    Dry computational approaches for wet medical problems

    Get PDF
    This is a report on the 4th international conference in ‘Quantitative Biology and Bioinformatics in Modern Medicine’ held in Belfast (UK), 19–20 September 2013. The aim of the conference was to bring together leading experts from a variety of different areas that are key for Systems Medicine to exchange novel findings and promote interdisciplinary ideas and collaborations
    corecore