Wildfires are a natural hazard that present an increasing risk to communities in fire-prone areas. This study examines the impacts of the municipal-level built environment upon fire damages in California, a particularly fire-vulnerable state. This study uses a multivariate linear regression model to isolate the effects of the human built environment upon reported monetary wildfire damages. Reported monetary losses from wildfires for the years 2007 to 2010 are examined against relevant built environment variables, while statistically controlling for biophysical and socio-economic variables. The fully-specified regression model indicates that wildfire property damage is driven primarily by the built environment. Socioeconomic and biophysical variables contribute comparatively little explanatory power to the model. Findings from this study will be of particular interest to fire management officials, land developers, and urban planners interested in creating a more fire-resilient future for cities within California.

The objective of this thesis is to develop a nondestructive evaluation method that could accurately locate and size damage in structures. The method is to be based on pre-damage and post-damage strain energies of beam and column elements. The method should apply to 1-D as well as 2-D and 3-D structures with single or multiple damage locations. To achieve the objectives listed above, the following four tasks are addressed: (1) the development of the theoretical foundations of the nondestructive evaluation theory; (2) the validation of the accuracy of the theory using exact structural deformational data generated from the static analysis of F. E. models in SAP2000; (3) the validation of the practical feasibility of the theory using approximated structural deformational data generated from the modal analyses of F.E. models in SAP2000; and (4) the application of the methodology to an existing structure. The numerical simulations of damage indicate that the proposed NDE method can clearly locate damage in the structures and provide an accurate quantitative value of damage severities, even when only a few lower frequencies and mode shapes are known. The field data analysis results indicate that the developed NDE method can locate damage and provide conservative values for damage severity estimations.

Astronauts in space flight missions are exposed to increased iron (Fe) stores and galactic cosmic radiation, both of which independently induce oxidative stress. Oxidative stress can result in protein, lipid, and DNA oxidation. Recent evidence has linked oxidative stress to bone loss with aging and estrogen deficiency. Whether the increased iron stores and radiation that astronauts face are exacerbating their extreme bone loss while in space is unclear. We hypothesized that elevated iron levels (induced by feeding a high iron diet) and gamma radiation exposure would independently increase markers of oxidative stress and markers of oxidative damage and result in loss of bone mass, with the combined treatment having additive or synergistic effects. Male Sprague-Dawley rats (15-weeks old, n=32) were randomized to receive an adequate (45 mg Fe/kg diet) or high (650 mg Fe/kg diet) Fe diet for 4 weeks and either 3 Gy (8 fractions, 0.375 Gy each) of 137Cs radiation (γRAD) or sham exposure every other day over 16 days starting on day 14. Serum Fe and catalase and liver Fe and glutathione peroxidase (GPX) were assessed by standard techniques. Immunostaining for 8-hydroxy-2-deoxyguanosine (8-OHdG, marker of DNA adducts) quantified the number of cells with oxidative damage in cortical bone. Bone histomorphometry assessed bone cell activity and cancellous bone microarchitecture in the metaphyseal region. Ex vivo pQCT quantified volumetric bone mineral density (vBMD); bone mechanical strength was assessed by 3-pt bending at the midshaft tibia and compression of the femoral neck. High Fe diet increased liver Fe and decreased volume per total volume (BV/TV). γRAD decreased osteoid surface per bone surface (OS/BS) and osteocyte density. The combined treatment increased serum catalase, liver GPX, and serum iron and decreased cancellous vBMD and trabecular number (Tb.N). High Fe diet and γRAD independently increased number of osteocytes stained positive for 8-OHdG, with the combined treatment exhibiting twice as many osteocytes positively stained compared to the control. Higher serum Fe levels were associated with higher oxidative damage (r =0.38) and lower proximal tibial cancellous vBMD (r =–0.38). Higher serum catalase levels were associated with higher oxidative damage (r =0.48), lower BV/TV (r =–0.40) and lower cancellous vBMD (r =–0.39). High dietary iron and fractionated 137Cs γRAD leads to a moderate elevation in iron stores and results in oxidative damage in bone and are associated with decreased cancellous bone density. Moderate elevations in iron stores are not only found in astronauts, but also naturally occur in healthy human populations. This healthy population with elevated iron stores may also have increased levels of oxidative stress in the body. Elevated levels of oxidative stress not only increase one’s risk for accelerated bone loss, but also the risk of developing other chronic diseases such as insulin resistance, hypertension, dyslipidemia, and metabolic syndrome.

Within the scope of this thesis, a reliability based risk assessment, based on Monte Carlo simulation was used to analyse the safety levels of Esenk&ouml / y Fishery Harbor main breakwater, Sea of Marmara, Turkey. In the past, in reliability-based risk assessment methodology in Turkey, the design conditions were only wave characteristics, tidal range, storm surge, wave set-up and the structural system parameters. However in this study, the tsunami risk which was considered as a major design parameter is included in the computations. In this study, development of a structural stability criterion in coastal engineering was suggested to achieve a common definition of reliability including the tsunami risk. The model introduced in this study is a practical technique in the reliability-based risk assessment of breakwaters subject to tsunami risk. In order to determine the occurrence probability of design condition, which is a function of storm waves, tidal range, storm surge and tsunami height, the Monte Carlo simulation, was applied. From the reliability-based risk assessment model applied to Esenk&ouml / y Fishery Harbor as a pilot study in Turkey it was found that, inclusion of the tsunami risk increases the failure risk of the structure, and as lifetime of the structure increases, the impact of tsunami risk on the failure mechanism is more reflected. For Esenk&ouml / y Fishery Harbor main breakwater, tsunami was not the key design parameter when compared to storm waves. However, in regions with great seismic activity, tsunami risk may be very noteworthy depending on the frequency and the magnitude of the tsunami.

国立情報学研究所で電子化したコンテンツを使用している。

hSMG-1 (human suppressor with morphogenic effect on genitalia) is the most recent addition to the family of phosphatidyl-inositol-3 kinase related kinases (PIKK). This family includes proteins such as Ataxia Telangiectasia Mutated (ATM), DNA Dependent Protein Kinase (DNA-PK), ATM and Rad3 related kinase (ATR) which are involved in stress induced signal transduction, cell cycle checkpoint control and DNA damage repair. hSMG-1 was first described in Caenorhabditis elegans where it was shown to be essential for Nonsense Mediated mRNA Decay (NMD). More recently hSMG-1 has been implicated in NMD and in the DNA damage response in mammalian cells. Three hSMG-1 isoforms have been described in the literature to date. Isoform 1 is 3 657 amino acids long with isoforms 2 (3 521 amino acids) and 3 (3 031 amino acids) N-terminal truncations of isoform 1. To explore the role of hSMG-1 in the DNA damage response three separate antibodies were generated. Each antibody was raised against a different region of hSMG-1, which allowed detection of specific hSMG-1 isoforms. These hSMG-1 antibodies were found to be suitable for immunoprecipitations, immunoblotting and immunofluorescence. The specificity of the antibodies was further confirmed using mass spectrometric analysis which identified the immunoprecipitated band as hSMG-1. Using these antibodies hSMG-1 was found to be located primarily in the cytoplasm, a novel location for a PIKK protein predicted to be involved in the DNA damage response. In addition, it was found that hSMG-1 isoform 2 was the only isoform present in the cytoplasm and is the major cellular isoform. All three isoforms were detected in the nucleus, with isoforms 1 and 3 only present in this cellular compartment, consistent with a proposed role in the DNA damage response. The generation of hSMG-1 specific antibodies allowed the characterisation of endogenous hSMG-1 kinase activity, which was found to be Mn2+ dependent and was stimulated after DNA damage (ionising radiation, ultraviolet radiation and hydrogen peroxide). Endogenous hSMG-1 was also demonstrated to bind to N-terminal hSMG-1 GST fusion proteins, suggesting that hSMG-1 can from multimers. In addition, hSMG-1 was found to associate with p53, a key component of the DNA damage response pathway, which is also targeted by other members of the PIKK family in response to DNA damage. In response to DNA damage hSMG-1 was observed by immunofluorescence to localise to discrete cytoplasmic granules. These sites were subsequently identified as stress granules (SG). During NMD hSMG-1 targets Upf1, a key step leading to the degradation of aberrant mRNA. Upf1 is recruited to the aberrant mRNA by Upf2 and both proteins were detected in SG. DNA damage induced SG were also demonstrated to be sites of phosphorylated hSMG-1 target motifs [phospho S(/T)Q], suggesting that hSMG-1 has kinase activity within SG. The presence of this phosphorylated site in SG parallels the presence of hSMG-1 at all times observed during SG formation and disassociation. Interestingly, not all treatments with genotoxic agents resulted in hSMG-1 inclusion in SG, indicating that hSMG-1 is not a core component of SG. Indeed, hSMG-1 was excluded from SG induced with the mitochondrial poisons clotrimazole (CZ) and sodium arsenite (NaAs), agents commonly used to induce SG. In addition to hSMG-1, Upf1, Upf2 and phospho S(/T)Q motifs were also excluded from CZ and NaAs induced SG. Reducing the cellular levels of hSMG-1 using small interfering RNA (siRNA) abrogated the formation of SG in response to DNA damage, indicating a crucial role for hSMG-1 in the formation of these SG. Surprisingly, a role for ATM in SG formation after DNA damage was suggested. Abrogation of ATM activity with small molecule inhibitors resulted in decreased SG formation after DNA damage. This novel role of ATM was not required for the induction of SG after treatment with CZ or NaAs. This was confirmed by observing SG induction with the same agents in ATM deficient (A-T) cells. Given that hSMG-1 is excluded from CZ or NaAs induced stress granules this indicates that not only is ATM signalling required for SG formation after DNA damage but this ATM-dependent pathway for SG formation involves the recruitment of hSMG-1, as well as the previously described proteins. This suggests that there are at least two distinct signaling pathways responsible for SG formation, one pathway which is both hSMG-1 and ATM dependent and the other which is ATM and hSMG-1 independent. Here I describe a novel and essential role for hSMG-1 and ATM in stress granule formation after exposure to agents that damage DNA and produce physiological stress.

Thesis (MPhysio)--University of South Australia, 1998

Thesis (Ph. D.)--Ohio State University, 2007. / Full text release at OhioLINK's ETD Center delayed at author's request

Thesis (Ph.D.) -- McMaster University, 2000. / Includes bibliographical references (leaves 244-294). Also available via World Wide Web.

Thesis (M. Phil.)--University of Hong Kong, 2007. / Also available in print.