Software systems are now pervasive throughout our world. The reliability of these systems is an urgent necessity. A large degree of research effort on increasing software reliability is dedicated to requirements, architecture, design, implementation and testing---activities that are performed before system deployment. While such approaches have become substantially more advanced, software remains buggy and failures remain expensive. We take a radically different approach to reliability from previous approaches, namely contract-driven data structure repair for runtime error recovery, where erroneous executions of deployed software are corrected on-the-fly using rich behavioral contracts. Our key insight is to transform the software contract---which gives a high level description of the expected behavior---to an efficient implementation which repairs the erroneous data structures in the program state upon an error. To improve efficiency, scalability, and effectiveness of repair, in addition to rich behavioral contracts, we leverage the current erroneous state, dynamic behavior of the program, as well as repair history and abstraction. A core technical problem our approach to repair addresses is construction of structurally complex data that satisfy desired properties. We present a novel structure generation technique based on dynamic programming---a classic optimization approach---to utilize the recursive nature of the structures. We use our technique for constraint-based testing. It provides better scalability than previous work. We applied it to test widely-used web browsers and found some known and unknown bugs. Our use of dynamic programming in structure generation opens a new future direction to tackle the scalability problem of data structure repair. This research advances our ability to develop correct programs. For programs that already have contracts, error recovery using our approach can come at a low cost. The same contracts can be used for systematically testing code before deployment using existing as well as our new techniques. Thus, we enable a novel unification of software verification and error recovery. / text

Thesis (M.S.)--Massachusetts Institute of Technology, Dept. of Civil Engineering, 1980. / MICROFICHE COPY AVAILABLE IN ARCHIVES AND ENGINEERING. / Bibliography: leaves 151-153. / by Paul J. Haven. / M.S.

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M. Tech. Civil Engineering.. / Investigates the feasibility of recycling construction waste for re-use as raw material in rehabilitation of roads in Bethal (Govan Mbeki Municipality). Specific Objectives: (a) To identify the causes of roads failure within the study area.(b) To assess feasibility of reuse of construction waste and propose method of road rehabilitation.(c) To recycle unsuitable material through characterisation of the construction waste. (d) To compare the cost implications when recycled construction waste is used with that of normal roads' rehabilitation.

When one thinks of motor vehicle accident damage repairs, one often thinks of unscrupulous operators and a scurrilous industry. While this is regrettably often the case, there is a counterpoint, being the significant number of motor body repair firms that have invested significant sums in establishing accredited and certified motor body repair outlets, and who offer a premium service. The industry is one that is regulated by the South African Motor Body Repair Association, a body that seeks to dictate a standard of repairs by dictating membership eligibility relative to investment in equipment. Most unfortunately, this stipulation does not adequately take into account the flow of work that there may be from the motor vehicle insurance industry, and many repairers find themselves having to resort to nefarious means to ensure that business comes their way. The author of this report is a co-owner of an advanced major structural motor body repairer. Rather than stooping to unethical practices, the owners have sought to undertake a position appraisal and gap analysis with the intention of uncovering the strategic alternatives available to their firm. The firm has implemented the strategic choices highlighted by this report to good effect and has enjoyed enhanced revenue streams and business competitiveness as a result of undertaking this exercise. This report serves to document the highlights of that process. / Thesis (MBA)-University of Natal, Durban, 2002.

Single cell gel electrophoresis (SCGE), more commonly known as the Comet assay, is an uncomplicated, affordable and versatile method for investigating DNA damage and repair. Existing comet–assay based methods were modified and applied in this study in order to examine the effects of different perturbations on the DNA repair capacity of different samples. Mitochondrial functioning has a vast effect on overall cell physiology and does not simply involve the production of energy in the form of ATP that sustains common biological processes, but is also associated with important cellular occurrences such as apoptosis and ROS production. It is suggested that a change in mitochondrial function may lead to extensive ROS production which may negatively affect macromolecules, including proteins involved in DNA repair pathways, and impaired energy formation which in turn may hamper the proper occurrence of energy driven processes. Complex I and ?III knock–down systems established in 143B cells are used to investigate the effect that perturbations of the energy metabolism may have on DNA repair capacity. Metallothioneins (MTs) are known to play an imperative role in trace element homeostasis and detoxification of metals and are effective ROS scavengers. The prooxidant environment that heavy metal imbalance causes may result in mutagenesis and transformation through DNA damage. It is suggested that an imbalance in the metal homeostasis caused by MT knock–out may create an environment favourable for DNA damage formation and at the same time impair DNA repair pathways. Because of the multi–functionality and involvement of metallothioneins in such a wide variety of biological processes, it was considered interesting and essential to extend the investigation on the effect of the absence of metallothioneins on DNA repair. A metallothionein I and ?II knock–out mouse model is employed to determine the effect of MT knock–out on DNA repair capacity. It was clear from the results obtained that transfection of cells, as used to investigate a perturbation in the energy metabolism in 143B cells, has an impairing effect on DRC. It was also confirmed that metallothioneins play an important and diverse role in cell biology since the absence thereof inhibits both BER and NER. / Thesis (M.Sc. (Biochemistry))--North-West University, Potchefstroom Campus, 2011.

Single cell gel electrophoresis (SCGE), more commonly known as the Comet assay, is an uncomplicated, affordable and versatile method for investigating DNA damage and repair. Existing comet–assay based methods were modified and applied in this study in order to examine the effects of different perturbations on the DNA repair capacity of different samples. Mitochondrial functioning has a vast effect on overall cell physiology and does not simply involve the production of energy in the form of ATP that sustains common biological processes, but is also associated with important cellular occurrences such as apoptosis and ROS production. It is suggested that a change in mitochondrial function may lead to extensive ROS production which may negatively affect macromolecules, including proteins involved in DNA repair pathways, and impaired energy formation which in turn may hamper the proper occurrence of energy driven processes. Complex I and ?III knock–down systems established in 143B cells are used to investigate the effect that perturbations of the energy metabolism may have on DNA repair capacity. Metallothioneins (MTs) are known to play an imperative role in trace element homeostasis and detoxification of metals and are effective ROS scavengers. The prooxidant environment that heavy metal imbalance causes may result in mutagenesis and transformation through DNA damage. It is suggested that an imbalance in the metal homeostasis caused by MT knock–out may create an environment favourable for DNA damage formation and at the same time impair DNA repair pathways. Because of the multi–functionality and involvement of metallothioneins in such a wide variety of biological processes, it was considered interesting and essential to extend the investigation on the effect of the absence of metallothioneins on DNA repair. A metallothionein I and ?II knock–out mouse model is employed to determine the effect of MT knock–out on DNA repair capacity. It was clear from the results obtained that transfection of cells, as used to investigate a perturbation in the energy metabolism in 143B cells, has an impairing effect on DRC. It was also confirmed that metallothioneins play an important and diverse role in cell biology since the absence thereof inhibits both BER and NER. / Thesis (M.Sc. (Biochemistry))--North-West University, Potchefstroom Campus, 2011.

Les mitochondries sont des structures uniques dans la cellule mammifère. Ces organites portent leur propre génome (ADN mitochondrial, ADNmt) qui se compose d'une petite molécule qui codifie pour 13 polypeptides de la chaîne de transport d'électrons (ETC), 22 ARNt et 2 gènes d'ARNr pour sa propre synthèse protéique. Le MTDNA est proposé pour être plus susceptible au stress oxydatif que le génome nucléaire (ADNn) parce que non seulement il manque d'histones protectrices, mais aussi en raison de sa proximité avec les complexes ETC qui sont les principaux producteurs de ROS dans les cellules de mammifères. Parmi tous les types de dommages à l'ADNmt, les dommages oxydatifs sont les plus répandus et, de loin, les mieux étudiés. La voie de réparation de l'excision de base (BER) est un mécanisme de réparation d'ADN conservé de façon évolutive qui répare les dommages de base d'ADN non volumineux. Puisque la guanine a le potentiel redox le plus bas de toute autre base dans l'ADN, elle est facilement oxydée à la 8-oxoguanine (8-oxoG) qui est l’altération la plus fréquente induite par les ROS sur les deux, l'ADNc et l'ADNmt. Si la fourche de réplication contourne le 8-oxoG avant son élimination, un A est souvent inséré sur le brin d'ADN opposé et les réplications subséquentes corrigent la transversion de G à T. Lorsqu'il est associé à la cytosine, le 8-oxoG est éliminé de l'ADN par l'ADN glycosylase de 8-oxoguanine (OGG1) qui, de cette manière, initie le procédé BER. OGG1 est une glycosylase de ménage bi fonctionnelle qui, conjointement avec d'autres enzymes BER différentes, est présente dans les compartiments nucléaires et mitochondriaux, soulignant l'importance de maintenir l'intégrité de l'ADNmt pour le fonctionnement cellulaire normal. Il a été démontré que la surexpression d'une version recombinante d'OGG1, spécifiquement destinée aux mitochondries par un signal de ciblage mitochondrial supplémentaire (MTS) (OGG1-MTS), protège les cellules d'un stress oxydatif, probablement en raison d'une efficacité accrue dans la réparation De 8-oxoG dans l'ADNmt. L'objectif principal de notre projet est d'élucider si la perte spécifique de l'activité de réparation 8-oxoG dans les mitochondries (mais pas dans le compartiment nucléaire) a un impact sur les fonctions organelles et / ou sur la viabilité cellulaire et aussi pour dévoiler le mécanisme / s Derrière les effets protecteurs d'OGG1 sur la physiologie mitochondriale et la maintenance d'ADNmt / Mitochondria are unique structures within the mammalian cell. These organelles carry their own genome (mitochondrial DNA, mtDNA) which consists of a small molecule that codifies for 13 polypeptides of the electron transport chain (ETC), 22 tRNA and 2 rRNA genes for its own protein synthesis. MtDNA is proposed to be more susceptible to oxidative stress than the nuclear genome (nDNA) because not only it lacks protective histones but also because of its proximity to ETC complexes which are the main ROS producers in mammalian cells. Among all the types of mtDNA damage, oxidative damage is the most prevalent and, by far, the best studied. Base excision repair (BER) pathway is an evolutionarily conserved DNA repair mechanism that repairs non-bulky DNA base damages. Since guanine has the lowest redox potential of any other bases in DNA, it is readily oxidized to 8-oxoguanine (8-oxoG) that is the most frequent alteration induced by ROS on both, nDNA and mtDNA. If the replication fork bypasses the 8-oxoG before its removal, an A is often inserted on the opposite DNA strand and subsequent replications fix the G to T transversion. When paired with cytosine, 8-oxoG is removed from DNA by the 8-oxoguanine DNA glycosylase (OGG1) that in such a way initiates the BER process. OGG1 is a bifunctional housekeeping glycosylase that, together with other various BER enzymes is present in both nuclear and mitochondrial compartments, highlighting the importance of maintaining mtDNA integrity for normal cellular functioning. It has been demonstrated that the overexpression of a recombinant version of OGG1, specifically targeted to mitochondria by an additional Mitochondrial Targeting Signal (MTS) (OGG1-MTS), protects the cells from an oxidative stress, likely due to an increased efficiency in the repair of 8-oxoG in mtDNA. The main goal of our project is to elucidate if the specific loss of 8-oxoG repair activity in mitochondria (but not in nuclear compartment) has an impact on the organelles’ functions and/or on cell viability and also to unveil the mechanism/s behind the protective effects of OGG1 on mitochondrial physiology and mtDNA maintenance.