Source File Set Search for Clone-and-Own Reuse Analysis

Clone-and-own approach is a natural way of source code reuse for software developers. To assess how known bugs and security vulnerabilities of a cloned component affect an application, developers and security analysts need to identify an original version of the component and understand how the cloned component is different from the original one. Although developers may record the original version information in a version control system and/or directory names, such information is often either unavailable or incomplete. In this research, we propose a code search method that takes as input a set of source files and extracts all the components including similar files from a software ecosystem (i.e., a collection of existing versions of software packages). Our method employs an efficient file similarity computation using b-bit minwise hashing technique. We use an aggregated file similarity for ranking components. To evaluate the effectiveness of this tool, we analyzed 75 cloned components in Firefox and Android source code. The tool took about two hours to report the original components from 10 million files in Debian GNU/Linux packages. Recall of the top-five components in the extracted lists is 0.907, while recall of a baseline using SHA-1 file hash is 0.773, according to the ground truth recorded in the source code repositories.Comment: 14th International Conference on Mining Software Repositorie

Role of the Schizosaccharomyces pombe F-box DNA helicase in processing recombination intermediates.

In an effort to identify novel genes involved in recombination repair, we isolated fission yeast Schizosaccharomyces pombe mutants sensitive to methyl methanesulfonate (MMS) and a synthetic lethal with rad2. A gene that complements such mutations was isolated from the S. pombe genomic library, and subsequent analysis identified it as the fbh1 gene encoding the F-box DNA helicase, which is conserved in mammals but not conserved in Saccharomyces cerevisiae. An fbh1 deletion mutant is moderately sensitive to UV, MMS, and ¿ rays. The rhp51 (RAD51 ortholog) mutation is epistatic to fbh1. fbh1 is essential for viability in stationary-phase cells and in the absence of either Srs2 or Rqh1 DNA helicase. In each case, lethality is suppressed by deletion of the recombination gene rhp57. These results suggested that fbh1 acts downstream of rhp51 and rhp57. Following UV irradiation or entry into the stationary phase, nuclear chromosomal domains of the fbh1¿ mutant shrank, and accumulation of some recombination intermediates was suggested by pulsed-field gel electrophoresis. Focus formation of Fbh1 protein was induced by treatment that damages DNA. Thus, the F-box DNA helicase appears to process toxic recombination intermediates, the formation of which is dependent on the function of Rhp51

SO(2,1) Covariant IIB Superalgebra

We propose a type IIB super-Poincare algebra with SO(2,1) covariant central extension. Together with SO(2,1) and SO(9,1) generators, a SO(2,1) triplet (momenta), a Majorana-spinor doublet (supercharges) and a Rarita-Schwinger central charge generate a group, G. We consider a coset G/H where H=(SO(2) x Lorentz), and the SL(2,R) 2-form doublet is obtained by the coset construction. It is shown that U(1) connections, whose strengths are associated with 2-forms, are recognized as coordinates of the enlarged space. We suggest that this is the fundamental algebra governing the superstring theories which explains the IIB SL(2,R) duality and geometrical origin of U(1) fields.Comment: 12 pages, Latex; <[email protected], [email protected], [email protected]

Preferential recruitment of CCR6-expressing Th17 cells to inflamed joints via CCL20 in rheumatoid arthritis and its animal model

This report shows that interleukin (IL) 17–producing T helper type 17 (Th17) cells predominantly express CC chemokine receptor (CCR) 6 in an animal model of rheumatoid arthritis (RA). Th17 cells induced in vivo in normal mice via homeostatic proliferation similarly express CCR6, whereas those inducible in vitro by transforming growth factor β and IL-6 additionally need IL-1 and neutralization of interferon (IFN) γ and IL-4 for CCR6 expression. Forced expression of RORγt, a key transcription factor for Th17 cell differentiation, induces not only IL-17 but also CCR6 in naive T cells. Furthermore, Th17 cells produce CCL20, the known ligand for CCR6. Synoviocytes from arthritic joints of mice and humans also produce a large amount of CCL20, with a significant correlation (P = 0.014) between the amounts of IL-17 and CCL20 in RA joints. The CCL20 production by synoviocytes is augmented in vitro by IL-1β, IL-17, or tumor necrosis factor α, and is suppressed by IFN-γ or IL-4. Administration of blocking anti-CCR6 monoclonal antibody substantially inhibits mouse arthritis. Thus, the joint cytokine milieu formed by T cells and synovial cells controls the production of CCL20 and, consequently, the recruitment of CCR6+ arthritogenic Th17 cells to the inflamed joints. These results indicate that CCR6 expression contributes to Th17 cell function in autoimmune disease, especially in autoimmune arthritis such as RA

T cell self-reactivity forms a cytokine milieu for spontaneous development of IL-17+ Th cells that cause autoimmune arthritis

This report shows that highly self-reactive T cells produced in mice as a result of genetically altered thymic T cell selection spontaneously differentiate into interleukin (IL)-17–secreting CD4+ helper T (Th) cells (Th17 cells), which mediate an autoimmune arthritis that clinically and immunologically resembles rheumatoid arthritis (RA). The thymus-produced self-reactive T cells, which become activated in the periphery via recognition of major histocompatibility complex/self-peptide complexes, stimulate antigen-presenting cells (APCs) to secrete IL-6. APC-derived IL-6, together with T cell–derived IL-6, drives naive self-reactive T cells to differentiate into arthritogenic Th17 cells. Deficiency of either IL-17 or IL-6 completely inhibits arthritis development, whereas interferon (IFN)-γ deficiency exacerbates it. The generation, differentiation, and persistence of arthritogenic Th17 cells per se are, however, insufficient for producing overt autoimmune arthritis. Yet overt disease is precipitated by further expansion and activation of autoimmune Th17 cells, for example, via IFN-γ deficiency, homeostatic proliferation, or stimulation of innate immunity by microbial products. Thus, a genetically determined T cell self-reactivity forms a cytokine milieu that facilitates preferential differentiation of self-reactive T cells into Th17 cells. Extrinsic or intrinsic stimuli further expand these cells, thereby triggering autoimmune disease. Intervention in these events at cellular and molecular levels is useful to treat and prevent autoimmune disease, in particular RA

A role for fungal β-glucans and their receptor Dectin-1 in the induction of autoimmune arthritis in genetically susceptible mice

A combination of genetic and environmental factors can cause autoimmune disease in animals. SKG mice, which are genetically prone to develop autoimmune arthritis, fail to develop the disease under a microbially clean condition, despite active thymic production of arthritogenic autoimmune T cells and their persistence in the periphery. However, in the clean environment, a single intraperitoneal injection of zymosan, a crude fungal β-glucan, or purified β-glucans such as curdlan and laminarin can trigger severe chronic arthritis in SKG mice, but only transient arthritis in normal mice. Blockade of Dectin-1, a major β-glucan receptor, can prevent SKG arthritis triggered by β-glucans, which strongly activate dendritic cells in vitro in a Dectin-1–dependent but Toll-like receptor-independent manner. Furthermore, antibiotic treatment against fungi can prevent SKG arthritis in an arthritis-prone microbial environment. Multiple injections of polyinosinic-polycytidylic acid double-stranded RNA also elicit mild arthritis in SKG mice. Thus, specific microbes, including fungi and viruses, may evoke autoimmune arthritis such as rheumatoid arthritis by stimulating innate immunity in individuals who harbor potentially arthritogenic autoimmune T cells as a result of genetic anomalies or variations

LL55: Selective Early Lymphoid Expression of a Murine cDNA Clone Which Encodes a Putative RNA-Binding Protein

Specific expression of various RNA-binding protein (RNP) molecules is one of the critical factors that determine the development in Drosophila melanogaster and Caenorhabditis elegans. In the present study, we found a complementary DNA clone, LL55 encoding a putative RNP. Structural comparison of nucleotide and amino acid sequences demonstrate that LL55 encoding a nuclear protein with two RNA-binding consensus motifs and the common arginine-serine repeats, is similar to the sex-determining transformer-2 (tra-2) gene of Drosophila melanogaster. The expression of 2.3 kilobase (kb) and 1.5 kb LL55 messenger RNA (mRNA) is ubiquitous in murine organs and tissues, but it is selective in the early development of fetal life. It appears as early as day 10.5 and increases until day 15 of gestation in accordance with the expression of λ5 mRNA which is involved in murine pre-B cell generation. Taking account of the selective expression and the specific regulation of RNP molecules, the finding of LL55 RNP provides a new outlook for the generation and function of the immune system

Experimental infection of dogs with a feline endogenous retrovirus RD-114

<p>Abstract</p> <p>Background</p> <p>The feline endogenous retrovirus RD114 is contained in the genome of cats. The virus may contaminate live canine vaccines based on cultured feline cells. The <it>in vivo </it>infectivity, acute and subacute pathogenicity, and viral proliferation of the RD114 virus were evaluated by experimental infection of dogs.</p> <p>Methods</p> <p>Nine specific pathogen free dogs were divided into three groups, with each group consisting of one female and two male dogs. Dogs were subcutaneously inoculated in the neck with either 1 ml RD114 stock virus (group A), inactivated RD114 virus suspension (group B), or cell culture medium (group C) as a negative control. To assess blood cell counts and biochemical properties, blood samples from each group were collected 5 days before inoculation, just prior to inoculation, and 1, 3, 7 and 10 days post-inoculation.</p> <p>Result</p> <p>During the experimental period of 51 days, none of the dogs inoculated with RD114 virus showed any clinical signs, significant increases in rectal temperature or abnormal blood biochemical characteristics including C-reactive protein when compared with the negative controls. We were not able to re-isolate the RD114 virus from buffy coat cells of group A dogs. Additionally, we could not detect RD114 provirus in the genomic DNA isolated from peripheral blood leukocytes, lymph node, spleen and sternal bone marrow cells.</p> <p>Conclusions</p> <p>Signs of RD114 virus proliferation were not found after subcutaneous infection of dogs. Although the potential risk caused by infection with RD114 virus in dogs could not be assessed in this study, we suspect that RD114 virus has little or no virulence in dogs.</p

Beneficial Effect of Food Substitute Containing L-Arginine, ω-3 Poly Unsaturated Fatty Acid, and Ribonucleic Acid in Preventing or Improving Metabolic Syndrome: A Study in 15 Overweight Patients and a Study of Fatty Acid Metabolism in Animals

This study was conducted to investigate whether or not a food substitute (Dr. BAANs®) containing three bioactive components L-arginine, ω-3 polyunsaturated fatty acid, and ribonucleic acid, supplied orally to 15 overweight patients, may have efficacy to prevent or improve the metabolic syndrome of these patients. To provide supporting data for this clinical study, the in vivo fatty acid metabolism of obese mice was analyzed using 125I labeled 15-(p-iodophenyl)-9-methylpentadecanoic acid (9MPA) in the tissues’ lipid pool. After 3 months of intervention, the results showed that there were improvements observed in liver functions, lipid profiles and metabolic syndrome marker. Significant differences were also found in the values of blood pressure, body weight, percentage of body fat, and body mass index. In the animal study, the tissue uptake of 125I-9MPA at 10 min after injection was higher in obese mice than in the control mice and the treatment with Dr. BAANs® in obese mice decreased the uptake significantly. The final product metabolite of p-iodophenylacetic acid in obese mice was increased significantly by the treatment. In conclusion, this food substitute may have a beneficial effect for the prevention or improvement of metabolic syndrome