Complexity Analysis of Reed-Solomon Decoding over GF(2^m) Without Using Syndromes

For the majority of the applications of Reed-Solomon (RS) codes, hard decision decoding is based on syndromes. Recently, there has been renewed interest in decoding RS codes without using syndromes. In this paper, we investigate the complexity of syndromeless decoding for RS codes, and compare it to that of syndrome-based decoding. Aiming to provide guidelines to practical applications, our complexity analysis differs in several aspects from existing asymptotic complexity analysis, which is typically based on multiplicative fast Fourier transform (FFT) techniques and is usually in big O notation. First, we focus on RS codes over characteristic-2 fields, over which some multiplicative FFT techniques are not applicable. Secondly, due to moderate block lengths of RS codes in practice, our analysis is complete since all terms in the complexities are accounted for. Finally, in addition to fast implementation using additive FFT techniques, we also consider direct implementation, which is still relevant for RS codes with moderate lengths. Comparing the complexities of both syndromeless and syndrome-based decoding algorithms based on direct and fast implementations, we show that syndromeless decoding algorithms have higher complexities than syndrome-based ones for high rate RS codes regardless of the implementation. Both errors-only and errors-and-erasures decoding are considered in this paper. We also derive tighter bounds on the complexities of fast polynomial multiplications based on Cantor's approach and the fast extended Euclidean algorithm.Comment: 11 pages, submitted to EURASIP Journal on Wireless Communications and Networkin

PROGRAM INSPECTION AND TESTING TECHNIQUES FOR CODE CLONES AND REFACTORINGS IN EVOLVING SOFTWARE

Developers often perform copy-and-paste activities. This practice causes the similar code fragment (aka code clones) to be scattered throughout a code base. Refactoring for clone removal is beneficial, preventing clones from having negative effects on software quality, such as hidden bug propagation and unintentional inconsistent changes. However, recent research has provided evidence that factoring out clones does not always reduce the risk of introducing defects, and it is often difficult or impossible to remove clones using standard refactoring techniques. To investigate which or how clones can be refactored, developers typically spend a significant amount of their time managing individual clone instances or clone groups scattered across a large code base. To address the problem, this research proposes two techniques to inspect and validate refactoring changes. First, we propose a technique for managing clone refactorings, Pattern-based clone Refactoring Inspection (PRI), using refactoring pattern templates. By matching the refactoring pattern templates against a code base, it summarizes refactoring changes of clones, and detects the clone instances not consistently factored out as potential anomalies. Second, we propose Refactoring Investigation and Testing technique, called RIT. RIT improves the testing efficiency for validating refactoring changes. RIT uses PRI to identify refactorings by analyzing original and edited versions of a program. It then uses the semantic impact of a set of identified refactoring changes to detect tests whose behavior may have been affected and modified by refactoring edits. Given each failed asserts, RIT helps developers focus their attention on logically related program statements by applying program slicing for minimizing each test. For debugging purposes, RIT determines specific failure-inducing refactoring edits, separating from other changes that only affect other asserts or tests

Large offspring syndrome, a bovine model for the human loss-of-imprinting overgrowth syndrome Beckwith-Wiedemann

Title from PDF of title page (University of Missouri--Columbia, viewed on September 6, 2013).The entire thesis text is included in the research.pdf file; the official abstract appears in the short.pdf file; a non-technical public abstract appears in the public.pdf file.Thesis advisor: Dr. Rocio Melissa RiveraIncludes bibliographical references.Vita.M.S. University of Missouri--Columbia 2013.Dissertations, Academic -- University of Missouri--Columbia -- Animal sciences."May 2013"Beckwith-Wiedemann syndrome (BWS) is a human loss-of-imprinting syndrome primarily characterized by macrosomia, macroglossia, and abdominal wall defects. BWS has been associated with misregulation of two clusters of imprinted genes. Children conceived with the use of assisted reproductive technologies (ART) appear to have an increased incidence of BWS. As in humans, ART can also induce a similar overgrowth syndrome in ruminants which is referred to as large offspring syndrome (LOS). The main goal of our study is to determine if LOS shows similar loss-of-imprinting at loci known to be misregulated in BWS. To test this, Bos taurus indicus × Bos taurus taurus F1 hybrids were generated by artificial insemination (AI; control) or by ART. Seven of the 27 conceptuses in the ART group were in the > 97th percentile body weight when compared to controls. Further, other characteristics reported in BWS were observed in the ART group, such as large tongue, umbilical hernia, and ear malformations. KCNQ1OT1 (the most-often misregulated imprinted gene in BWS) was biallelically-expressed in various organs in two out of seven overgrown conceptuses from the ART group, but shows monoallelic expression in all tissues of the AI conceptuses. Furthermore, biallelic expression of KCNQ1OT1 is associated with loss of methylation at the KvDMR1 on the maternal allele and with down-regulation of the maternally-expressed gene CDKN1C. In conclusion, our results show phenotypic and epigenetic similarities between LOS and BWS, and we propose the use of LOS as an animal model to investigate the etiology of BWS