The thesis describes the establishment of a laser damage facility in the ultra violet. The laser is a pulsed excimer laser (25 n sec) capable of an output energy of 1 Joule at wavelengths of 193, 245, 308, 337 and 351 nm. The problems involved in making reliable damage threshold measurements are addressed, such as energy calibration, beam attenuation, damage detection and temporal and spatial beam profiling. A computer controlled frame store and video system enabling single shot spatial profiling and peak fluence measurements to be performed is described. Such a system is essential if reliable results are to be obtained from lasers whose spatial output cannot be described by a Gaussian. Using the damage facility, work has been performed on single crystal Caf2 laser windows ascertaining the bulk and surface damage thresholds as a function of crystal purity, surface finishing and polishing procedures. The results of a T.E.M. study give an insight into the fundamental damage mechanism of this material to be electron avalanche breakdown. The role of transient primary defects in the bulk breakdown of CaF2 has been investigated using dye laser probe techniques, and indicate that the presence of U.V. generated self trapped excitons, acting as sinks for the conduction band electrons, greatly enhances the damage threshold. Work on coatings using a LIMA (Laser-induced ion mass analyser) is reported and the potential of this machine as a laser damage diagnostic tool is explored.

No description available.

No description available.

A substantial number of whiplash injuries are reported for motor vehicle accidents which produce little or no structural damage to the automobile. These injuries are predominantly associated with rear-end type accidents affecting passengers of the struck vehicle. Since passengers of the striking vehicles are not reporting as many injuries for the same accidents, occupant and vehicle dynamics experienced during low speed-rear impacts were proposed to be a major source of the whiplash claims. A review of previous research revealed that little information exists for this type of accident. In general, vehicle safety research and government regulations have been directed towards occupant mortality - not injury - in frontal collisions. Occupant dynamics research has been limited to sled testing, using modified seat structures, or out-of-date vehicle models. Full scale, rear impact, crash testing has concentrated on high impact speeds (above 30 km/h) where significant structural deformation occurs. A research program was designed to investigate the occupant and vehicle dynamics during low speed - rear impacts. Experimental research was undertaken to document the structural performance of vehicles, noting the impact speeds necessary to initiate the crush mechanisms in the rear portion of the vehicle. To facilitate this testing, a pendulum impactor, based on the government test procedures, was designed and built to consistently reproduce impact speeds below 20 km/h. A total of 56 rear impact tests were conducted with 1977-1982 Volkswagen Rabbits. The vehicle wheels were locked to represent a vehicle stopped in traffic - the most commonly reported whiplash producing accident. An anthropometric test dummy was used to represent a front seat passenger during the tests. High speed video recordings of the tests were digitized to provide kinematic information on the occupant and vehicle response. Accelerometers were incorporated into the last 24 tests to monitor the acceleration levels at the bumper mount, seat mount and within the dummy. Information obtained from this testing suggested that permanent structural damage was only visible when an impact speed between 14 and 15 km/h was experienced by the vehicle. Very little frame deformation occurs for impact speeds below this value. Below this threshold, the vehicle frame can be considered rigid; vehicle response being dominated by the compliance of the bumper and suspension systems as well as sliding of the locked wheels. The accompanying occupant response was a differential rebound of the head and shoulders off the seatback and head restraint. This relative motion between the head and torso was evident in each test and increases the potential for injury. Typical occupant response observed consisted of an initial loading and deflection of the seatback due to the occupant's inertia followed by the release of this stored spring energy as the occupant was catapulted forward. It is this elastic behaviour of the seatback which is the likely cause of whiplash injury. Resulting head velocities were found to be in the order of 1.5 - 2 times the resulting vehicle speed. Initial occupant postures which increased the distance between the torso and seatback tended to increase the dynamic loading experienced by the passenger. Analytical modelling of the vehicle was initiated as the groundwork for full occupant-vehicle simulation. A finite element model of the vehicle frame, bumper, and suspension was created. Previously obtained empirical information suggested that a non-linear bumper and suspension system connected to a rigid frame would be an acceptable approximation. A parametric analysis of bumper stiffness and braking conditions was conducted in a 30 simulation matrix. General kinematic trends of the tests were observed in the simulations, however, limitations in the material properties introduced a much stiffer response than that experimentally observed. Results from this study show that little protection is offered to an occupant during a rear end collision. Impact energy management within the vehicle may not be adequate to prevent injury. Improved occupant protection requires the highly elastic behaviour of the vehicle frame and seatback to be attenuated. This will eliminate the amplification of vehicle motion through the seatback to the occupant. / Applied Science, Faculty of / Mechanical Engineering, Department of / Graduate

Clinical neuropsychologists are often called upon to make decisions on the genuineness of cognitive deficits following a head injury. This is a difficult task, particularly when deficits are subtle, as there are few reliable tools to aid the clinician in his or her decision making process. In the present study, normal participants instructed to feign brain injury (M) , traumatically brain-injured individuals (BI) , and normal controls (C), completed a series of computer-administered implicit memory (IM) tasks. Results were compared to those for the Victoria Symptom Validity Test (VSVT; Slick, Hopp, Strauss, & Pinch, 1994; Slick, Hopp, Strauss, & Thompson, 1997), a commercially available forced-choice recognition task. All IM tasks included items which had been previously presented once, twice or four times, as well as foils (items not previously presented). Previous exposure to test items was expected to be associated with increased accuracy (Hits) and decreased Response Latency. Participants in the BI and C groups were expected to perform equally well and better than the M group participants with respect to Hits. Response Latency on incorrect items (Misses) was also expected to discriminate M participants from BI and C participants because the conscious decision to provide an incorrect response was expected to increase decision making time. Results with respect to overall Hits were confirmed (M=127.87, M=129.72, and M=107.10 for the BI, C, and M groups, respectively) . Increased accuracy with repetition of items in the priming phase was not confirmed, likely because both BI and C participants performed close to ceiling levels. Discriminant function analysis based on total Hit rates, resulted in correct classification of 85 percent (46 out of 54) of the participants. This was comparable to the results for Hard items combined on the VSVT. Response Latency measures did not effectively discriminate among groups, while results did indicate a main effect of Presentation Level (priming) on Response Latency with participants, independent of Group Membership, tending to respond most quickly (Hits only) to items presented 4 times during the priming phase and least quickly to items presented only once. Overall, results suggest that further investigation of IM tasks for the detection of conscious malingering is warranted as these tasks appear to tap the dimensions on which the general population hold misconceptions about the effects of brain injury, i.e., overall ability/performance and response latency. / Graduate

Male factor infertility is a contributing factor in up to 50% of infertile couples. Increasing numbers of couples undergoing assisted reproductive technology (ART) treatment and reports of a possible decline in male fertility suggest that lifestyle, occupational and environmental exposures might impair semen quality. Sperm DNA contains both DNA strand breaks and base damage that has been associated with poor semen quality but few studies have examined the role of double strand breaks (DSBs), a toxic lesion, or DNA damage such as N7-methyldeoxyguanosine (N7-MedG) arising from alkylating agents that can be toxic and mutagenic. The aim of this research was to examine the relationships between exposures, DNA damage and male fertility. Men were recruited from couples attending for ART treatment and they provided information on lifestyle, occupational and environmental exposures as well as a sperm sample. Semen concentration and motility was determined by standard techniques in the neat sample and the prepared sample that underwent density gradient centrifugation for ART treatment. DSBs were measured in individual sperm cells by the neutral Comet assay and N7-MedG levels in sperm DNA by an immunoslot blot assay. Information on ART outcomes (% fertilisation, % cleavage and clinical pregnancy) was collected and associations between DNA damage, exposures, semen quality and ART outcomes were determined. Expression of individual DNA repair proteins was also examined in individual oocytes. Men in manual work had significantly lower semen volumes and higher % immotile sperm. Exposure to dry cleaning fluids and having a fever were associated with a decrease in sperm number and while non-ionizing radiation was associated with an increase in % immotile sperm, X-ray exposure was correlated to a decrease in % progressively motile sperm. Semen parameters were significantly and negatively correlated with DSBs in neat and prepared sperm, and N7-MedG levels in neat sperm. Density gradient centrifugation improved sperm sample quality and decreased DSBs and N7-MedG levels significantly. Successful fertilization of oocytes was negatively associated with DSB levels in neat and prepared sperm and with N7-MedG levels in neat sperm. Lower DSB levels in men were associated with an increased chance of an achieving clinical pregnancy especially in ICSI couples. N7-MedG levels were significantly correlated with driving a car and exposure to detergent or printing inks and dyestuffs. DSBs were correlated negatively with exercise and positively with eating nuts and almonds or exposure to non-ionizing radiation. DNA repair gene expression in individual oocytes showed significant intra and inter-individual variability. Sperm DNA damage can reduce male fertility, but the causes of such damage remain to be identified. The variable ability of individual oocytes to repair this damage may well affect the chance for a successful pregnancy.

No description available.

The current prevailing notion is that the limbic system is inextricably linked to emotion, and indeed, most textbooks, research articles, and scientific lectures tout the limbic system as being the predominant purveyor of emotional processing in the brain. Yet, more than a half-century of research has produced surprisingly little evidence in support of such a notion, suggesting that the concept of an emotional limbic system is overly simplistic. The primary objective of this thesis is to determine whether the limbic system is necessary for one aspect of emotion, namely, its conscious experience. Neurological patients with focal damage to different regions of the limbic system - including the hippocampus, amygdala, insular cortex, anterior cingulate cortex (ACC), and ventromedial prefrontal cortex (vmPFC) - underwent multiple emotion induction procedures using affectively-laden film clips. For comparison, two other groups of participants were tested: patients with brain damage outside of the limbic system and healthy participants without brain damage. Two emotion inductions aimed at eliciting diffuse emotional states of positive or negative affect, and five emotion inductions aimed at eliciting specific emotional states of happiness, sadness, anger, disgust, or fear. Immediately following the end of each film clip, the return of emotion back to its baseline state was tracked over a three minute "emotion recovery" time period. The results of the experiment revealed three main findings. First, limbic system damage did not disrupt the experience of emotion during the film clips, with patients reporting high levels of the induced target emotion at a magnitude comparable to both comparison groups. Second, patients with bilateral damage circumscribed to either the hippocampus or the vmPFC demonstrated an abnormally slow rate of emotion recovery, indicating that these limbic regions are important for the successful downregulation of emotion. Third, patients with large bilateral lesions affecting multiple limbic structures (including the medial temporal lobes and insular cortices) showed an abnormally rapid rate of emotion recovery, with the induced emotion returning to baseline levels within 60 seconds following the end of each film. Based on these findings, it is concluded that the limbic system is not necessary for the experience of emotion, but is necessary for sustaining and regulating that experience after the emotion-inducing stimulus is no longer directly accessible to consciousness.

No description available.

archives@tulane.edu / BRCA1 faithfully repairs damaged DNA by promoting homology-directed repair (HDR). Loss of Brca1 and other HDR genes are incompatible with embryonic viability and cause severe genomic instability. Cells lacking BRCA1 are sensitive to cellular stresses such as DNA damage caused by ionizing radiation (IR). Homozygous loss of Brca1 is embryonic lethal in mice, and the few tissue-specific knockouts generated develop abnormally. Therefore, we created an inducible Cre mouse model to study Brca1 loss in all adult mouse tissues allowing for examination of viability, longevity, and stress response in the absence of HDR and the importance of HDR in different tissues of an adult mouse. After validating the inducible Cre system using a reporter allele in mice, we generated mice with alleles of the inducible Cre system and floxed Brca1 alleles. Cre was induced in adult mice at ten weeks of age, resulting in extensive, widespread deletion of Brca1. Contrary to the embryonic lethality observed in all previously tested germline Brca1 knockout mouse models, adult mice with Brca1 deletion displayed no overt phenotypes. Brca1Δ/Δ mice showed extensive, widespread deletion of Brca1 and survived up to 1 year after Brca1 recombination. Targeted, high-depth sequencing of recombined tissues indicated mutations accumulated in both the mammary gland and the intestine. However, only the mammary gland had an HDR deficiency signature. Next, we examined Brca1Δ/Δ mice survival after exposure to ionizing radiation and mitomycin C (MMC). Surprisingly, Brca1Δ/Δ mice responses are DNA damage specific. Brca1Δ/Δ mice deficient for HDR showed no increased sensitivity to IR but died four to eight days following MMC exposure. Our results show that BRCA1 is not required for long-term viability or DNA double-strand break repair, but BRCA1 is essential for DNA crosslink repair to maintain viability in an adult mouse. / 1 / JoyOlayiwola