Shipwreck in the first half of the nineteenth century had been an on-going national tragedy. It was not officially quantified until the 185O's when it was found that 1025 ships a year on average were lost, the consequent destruction of life averaged 830 persons a year, with an annual loss to the country representing some 1.5m. There had been a devastating loss to the maritime strength of Britain since the close of the Napoleonic Wars. The response to this on-going national disaster was slow but eventually emerged principally in three areas: humanitarian, technical and political. The humanitarian driven reform came from amongst other sources by way of incentives to inventors from the Royal Humane Society, the formation and establishment of a lifeboat service and a general up-swelling of opinion by exposure to pamphlets and newspapers against the evils of shipwreck. The technical response came as inventors and builders sought to find new forms of construction in ships, lifeboats, life-saving equipment and safety equipment amongst others. Politically, the increasing use of the select committee to bring facts before the public and parliament served as the basis of much reform in nineteenth century England, the 1836 Inquiry into the causes of shipwreck, the 1839 Inquiry into the losses of timber-laden ships and the 1843 Inquiry into the causes of shipwreck being the major exposers of malpractice. The object of this thesis and the major research question is to assess the principal strengths and directions of these responses as the climate of opinion changed and reforms albeit piecemeal came about. The work begins with an outline of the situation as it affected different parts of the coast and some of the localised responses to shipwreck. Using the 1836 Inquiry as the basis for establishing the causes of the problems, itself a new datum point in maritime history as it was the instigating basis for change, the nature of shipwreck and course of reform is traced through the following two decades up until the unifying 'great' Merchant Shipping Act of 1854.

Bioelectrochmical systems (BES) are engineered electrochemical devices that harness hidden chemical energy of the wastewater in to the form of electricity or hydrogen. Unique microbial communities enrich in these systems for oxidation of organic matter as well as transfer of resulted electron to anode, known them as “electricigens” communities. Exploring novel electricigenesis microbial communities in the nature and understanding their electromicrobiology is one the important aspect for BES systems scale up. Herein, we report first time the electricigenesis property of an anaerobic, fresh water sediment, sulfur reducing bacterium Desulfuromona acetexigens. The electrochemical behavior of D. acetexigens biofilms grown on graphite-rod electrodes in batch-fed mode under an applied potential was investigated with traditional electroanalytical tools, and correlate the electron transfer from biofilms to electrode with a model electricigen Geobacter sulfurreducens electrochemical behavior. Research findings suggest that D. acetexigens has the ability to use electrode as electron acceptor in BES systems through establishing the direct contact with anode by expressing the membrane bound redox proteins, but not due to the secretion of soluble redox mediators. Preliminary results revealed that D. acetexigens express three distinct redox proteins in their membranes for turnover of the electrons from biofilm to electrode, and the 4 whole electricigenesis process observed to be unique in the D. acetexigens compared to that of well-studied model organism G. sulfurreducens.

Objectives: Vitamin D deficiency is highly prevalent and has been linked to increased morbidity and mortality. There has been an increase in testing for vitamin D with a concomitant increase in costs. While individual factors are significantly linked to vitamin D status, prior studies have not yielded a model predictive of vitamin D status or 25(OH)D levels. The purpose of this investigation was to determine if a prediction model of vitamin D could be developed using extensive demographic data and laboratory parameters. Methods: Patient data from 6 Veterans Administration Medical Centers were extracted from medical charts. Results: For the 14,920 available patients, several factors including triglyceride level, race, total cholesterol, body mass index, calcium level, and number of missed appointments were significantly linked to vitamin D status. However, these variables accounted for less than 15% of the variance in vitamin D levels. While the variables correctly classified vitamin D deficiency status for 71% of patients, only 33% of those who were actually deficient were correctly identified as deficient. Conclusion: Given the failure to find a sufficiently predictive model for vitamin D deficiency, we propose that there is no substitute for laboratory testing of 25(OH)D levels. A baseline vitamin D 3 daily replacement of 1000-2000 IU initially with further modification based on biannual testing appears to factor in the wide variation in dose response observed with vitamin D replacement and is especially important in high-risk groups such as ethnic minorities.

Using data from the Health, Aging, and Body Composition study, we examined whether low 25-hydroxyvitamin D (25[OH]D) concentrations were associated with prevalent or incident cognitive impairment. Serum 25(OH)D concentrations were measured in 2,786 older adults and categorized as <20 ng/mL, 20 to <30 ng/mL, or ≥30 ng/mL. Cognitive impairment was defined as a score >1.5 standard deviations below race and education specific means on either digit symbol substitution test or modified mini-mental state test. Logistic regression determined the odds of cognitive impairment at baseline and year 5 by 25(OH)D category. 25(OH)D concentrations were <30 ng/mL in 57.3% of whites and 84.6% of blacks. After excluding participants with baseline cognitive impairment (n = 340), 13% of whites and 13% of blacks developed cognitive impairment by year 5. In whites, 25(OH)D concentrations <30 ng/mL were not associated with prevalent or incident cognitive impairment. Black participants with 25(OH)D concentrations <20 ng/mL had a higher odds of prevalent, but not incident cognitive impairment (OR (95% CI): 2.05 (1.08–3.91), p = 0.03) compared to participants with 25(OH)D concentrations ≥30 ng/mL. Low 25(OH)D concentrations were associated with twofold higher odds of prevalent cognitive impairment in blacks.

Medial calcification refers to mineral deposition in the middle layer of arteries. This mineralization is common in chronic kidney disease patients and causes an increased chance of cardiovascular complications. Calcitriol, the active form of vitamin D, is often administered to these patients to treat an associated condition, secondary hyperparathyroidism. Unfortunately, calcitriol treatment may promote vascular calcification due to increasing serum calcium and phosphate. We examined the effects of calcitriol supplementation on vascular smooth muscle cell (VSMC) calcification, through atomic absorption, scanning electron microscopy, and western blot analysis. Additionally, we examined the effects of the combinations of calcitriol, fibroblast growth factor 23 (FGF-23), and klotho. We determined that calcitriol supplementation alone increased calcification but was not associated with a transition towards an osteoblast-like phenotype. On the other hand, the combination of calcitriol and FGF-23 caused a decrease in calcification, but this decrease was attenuated with the further addition of klotho.

No description available.

Hydroxyproline as a modified amino acid can serve as a carbon and nitrogen source for certain microorganisms. Its primary isomer trans-4-hydroxy-L-proline is found in the root nodule of legume plants. Hydroxyproline (Hyp) catabolism has been characterized in bacteria and animal cells. In bacteria, trans-4-hydroxy-L-proline (trans-4-L-proline) is converted to the central metabolite α-ketoglutarate (α-KG) by four reactions. The Hyp catabolism pathway has been identified in the nitrogen-fixing legume endosymbiont Sinorhizobium meliloti. hypS is one of the transcripts in the 14 hyp gene cluster on the pSymB megaplasmid, and was annotated to encode a putative malate/L-lactate dehydrogenase. In this study, purified HypS was assayed on different substrates and the reaction products were characterized. It was demonstrated that HypS can oxidize L-proline and reduce Δ1-pyrroline-2-carboxylate, but not on L-malate. Noticeably unlike the wild type strain, a hypS- mutant strain failed to grow on D-proline. The ability of D-proline to support grow of an L-proline auxotroph, together with the substrate specificity of HypS, strongly suggests that hypS is involved in the metabolism of D-proline to L-proline in S. meliloti. The possible role of HypS in the catabolism of Hyp or related compounds remains to be determined. / Thesis / Master of Science (MSc)

Mémoire numérisé par la Direction des bibliothèques de l'Université de Montréal.

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