Different from terrestrial equipments (tanks and wheeled vehicles) and airborne crafts (planes or helicopters), the R & M (repair and maintenance) issues about naval vessels are profoundly related to their gigantic size, numerous operators, and thousands of various spare parts which individually have small quantity demand for logistic support. That is why the R & M of naval vessels is much more complicated. According to the Defense White Paper of 2009, the whole military force is going to be downsized. Meanwhile, the rescuing and relieving tasks for natural disasters have also been officially assigned to them. Therefore, the attendance rate of ships is increasing, which causes lower reliability and higher failure rate and consequently the rising R & M load. The dynamical complexity existing among the variables associated with R & M of naval vessels, which are non-linear, interconnecting and time-delaying, makes the system dynamics a very suitable theory for analyzing this kind of issue systematically. During the study, a model was built based on system dynamics. After reviewing related literatures and discussing with professionals in this field, the associated variables were defined and their casual diagrams were also established. We developed the stock-flow diagrams of three subsystems-- R & M process, man power, and material supply. Afterward these three subsystems were integrated into an R & M dynamical system model. Policy influence simulation and scenario design was carried out after basic tests confirming its validity. The results indicated that a higher R & M capacity could obviously reduce the number of ships stalled in shipyard and effectively increasing the discharge rate. Therefore we recommended the associated authority to boost R & M capacity by aggressive actions such as increasing the ratio of recruitment, building R & M knowledge management system and strengthening the education and training. For the follow-up research, we suggest more interviews with industrial personnel and experts, collecting R & M data for each type of naval vessel, deliberating the factors influencing the R & M from different aspects and appropriately defining system boundary in order to establish a model which is more similar to the real world. Therefore its simulated results can approach to the reality further, and the scenario analysis with conclusions induced from policy influence simulation can be more specific for the authorities. Keywords: repair and maintenance of naval vessels, system dynamics, strategy

Abstract Deinococcus radiodurans is highly resistant to radiation when it grown in tryptone-glucose-yeast extraxt (TGY) medium. It oxidized glucose slowly mainly by the pentose phosphate pathway (PPP) and showed little glycolytic Embden-Meyerhof pathway (EMP) activity. The addition of 10 µM Mn(II) into the stationary phase cultures, could induced new round of cell division (Mn-CD effect) and the EMP activity. Glucose metabolized by Mn-CD cells at a EMP:PPP=6:1 ratio. In analyzing the metabolites for DNA repair, we found that after the addition of Mn(II) , the concentrations of PPP metabolites such as insione monophosphate (IMP)¡Buridine monophosphate (UMP) and NAD (nicotine adenine dinucleotide) were greatly reduced. This event is also occurred when replacing the glucose by fructose, sodium acetate, or removing glucose from the TGY culture medium. Besides, we also found that the TGY and TFY grown cells contained more PPP metabolites than those of TAY and TY cells. This finding suggested that glucose and fructose were metabolized by the PPP pathway in D. radiodurans. Finally, the concentrations of IMP¡BUMP and NAD in the cells were greatly decreased after UV irradiation. This indicated that these metabolites were probably employed to repair the DNA damage causing by UV irradiation.

Thesis (Ph. D.)--University of Texas at Austin, 2000. / Vita. Includes bibliographical references (leaves 158-166). Available also in a digital version from Dissertation Abstracts.

published_or_final_version / Civil Engineering / Doctoral / Doctor of Philosophy

published_or_final_version / Biological Sciences / Master / Master of Philosophy

Home environments pose a number of challenges for environmental justice. Healthy homes in healthy neighborhoods are often inaccessible due to socioeconomic factors, environmental racism, and/or environmental gentrification. Publicly funded home repair programs increasingly strive to both improve environmental health conditions and to reduce energy bills for low-income homeowners. Such programs have been intended to stimulate reinvestment in neighborhoods experiencing blight and more recently to reduce gentrification pressure in neighborhoods experiencing rapid reinvestment. While such programs do not represent a silver-bullet solution to the accessibility of healthy housing, the question remains: “What is the potential of low-income home repair programs to serve as a leverage point for environmental justice in urban home environments facing gentrification pressure?” This question is investigated through performance evaluation case studies of three municipally funded, low-income home repair programs in Austin, Texas intended to ameliorate gentrification and advance outcomes related to environmental justice. The findings suggest that as a site of intervention, dialogue, community connection, and resource-mobilization, home repair programs have potential as leverage points in regenerative community development that advances environmental justice performance outcomes. Actors in home environments can increase their performance with the support of the home ecology paradigm (HEP), a synthetic research paradigm that draws from sustainability science, environmental justice, and social learning literature to renew an action research paradigm established by Ellen Swallow Richards in the late 1800s to advance healthy community design and development. Guided by a vision of environmental justice, equipped with tools supporting holistic, multi-scalar systems-thinking and regenerative dialogue assessments, and engaged in a practice of resilient leadership, such actors can more deftly dance with the co-evolving systems of their home environments. In so doing, they increase their potential to directly enhance the material, social, and ecological conditions of life in the present, while also cultivating the capacity of these living systems to adapt resiliently to future disruptions. Furthermore, beyond producing life-enhancing performance outcomes, the HEP also appears to support actors in an engaged praxis that enhances their moment-by-moment experience of life and the vitality of living systems in the present.

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Friedreich ataxia (FRDA) is the most common inherited ataxia disorder, caused by a GAA repeat expansion mutation within the first intron of the FXN gene. The subsequent deficiency of frataxin protein leads to neurological disability, increased risk of diabetes mellitus, cardiomyopathy and premature death. The exact FRDA disease mechanism is not yet clear, despite some understanding of epigenetic, transcriptional and DNA repair system effects that lead to frataxin reduction. Previous studies have shown that mismatch repair (MMR) genes can affect other trinucleotide repeat disorders by destabilisation of the repeats. Furthermore, it has been proposed that frataxin deficiency might lead to cell malignancy by an as yet undefined mode of action. Therefore, the principle aim of this thesis was to use human and genetically altered mouse cells and tissues to understand the effects of MMR proteins on GAA repeat instability and FXN transcription, and also to identify potential changes in MMR transcription that might cause malignancy in FXN-defective human cells. Firstly, by using FXN and MMR genetically altered mice, MMR proteins were shown to be involved in both intergenerational and somatic GAA repeat instability, although their effects in the two systems were different. Thus, Msh2 or Msh3 were both found to protect against intergenerational transmission of GAA contractions, while loss of Msh2 or Msh3 reduced somatic GAA repeat expansions and increased levels of FXN transcription in brain and cerebellum tissues. Loss of Msh6 induced both intergenerational GAA repeat expansions and contractions, while the frequency of somatic GAA repeat expansions was reduced. Curiously, the level of FXN transcription was also reduced in Msh6-deficient brain and cerebellum tissues. On the other hand, Pms2 was found to protect against both intergenerational and somatic GAA repeat expansions, with loss of Pms2 causing increased GAA repeat expansions and decreased levels of FXN transcription in brain and cerebellum tissues. Finally, loss of Mlh1 led to a reduced frequency of both intergenerational and somatic GAA repeat expansions, but the level of FXN transcription was also reduced in brain and cerebellum tissues. Furthermore, upregulation of MMR mRNA expression was detected in human FRDA fibroblast cells, but downregulation was seen in FRDA cerebellum tissues, suggesting tissue-dependent control of FXN and MMR expression. In summary, these studies indicate that the MMR system can affect GAA repeat expansion instability and FXN transcription through different mechanisms of action. Furthermore, frataxin deficiency can also affect the levels of MMR mRNA expression in a tissue-dependent manner. These findings will assist future investigations aimed at identifying novel FRDA therapies.

When the DNA of Escherichia coli is damaged a set of events termed "SOS functions" occur to aid cellular survival. The recA and lexA proteins are involved in the regulation of these functions. To determine the role of the lexA protein, amber mutations, designated spr-55(amber), were isolated in the lexA-3 gene. The lack of the lexA-3 gene product abolished sensitivity to ultraviolet light and resulted in the constitutive synthesis of recA protein. Introduction of amber suppressor mutations restored the original lexA-3 phenotype. It was concluded that spr mutations inactivate lexA protein resulting in the constitutive expression of the SOS functions. These data provide evidence that the lexA protein is the repressor for the recA gene. The repair of phage lambda (λ⁺) by ultraviolet light was determined in the strains carrying alleles of the spr, uvrA, and recA genes. The survival of the phage was more in the spr-51 uvrA⁺ strain as compared to wild type. These results were not dependent on the recA genotype. Introduction of the uvrA-6 mutation into the spr-51 uvrA⁺ recA⁺ strains resulted in the same relative decrease of phage survival. These results suggest that lexA protein is involved in the regulation of uvrA-dependent excision repair and that inactivation of lexA leads to the constitutive expression of excision repair. New mutant forms of lexaA protein were isolated. The lexA⁺, lexA-3, lexA-10, and lexA-27 proteins displayed identical mobilities in the Weber and Osborn gel system. The lexA-10 and lexA-27 genes showed different phenotypes and encoded proteins of different mobilities in the Laemmli gel system. It was concluded that the differences in mobilities observed in the Laemmli gel system are due to alterations in charge or amino acid, not in size; furthermore; the molecular weight of lexA⁺ protein was determined to be 24 kilodaltons.

DNA repair in Gossypium barbadense L. cotyledonary tissue was examined in vivo during early germination. DNA strand breaks were initiated by applying ethyl methanesulfonate (EMS) during seed imbibition. Strand rejoining was monitored through a period of EMS induced DNS synthesis by means of velocity sedimentation analysis. There was an absence of DNA molecular weight increase as disclosed by the sedimentation profiles. It is presumed velocity sedimentation evaluation was insensitive for detecting in vivo restoration of cotyledonous DNA strand breaks. The altered DNA synthesis response perceived within treated seedling cotyledons perhaps reflects, but does not establish the operation of a cellular mutagenic repair system. EMS induced morphological mutant cotton plants arising during the course of this investigation were cytologically identified as possessing duplicate-deficient chromosomes.