The prevalence of antimicrobial resistance (AMR) phenotypes and genotypic characteristics (Class 1 integron and AMR gene cassettes) in commensal Escherichia coli (EC) and vancomycin resistant Enterococcus faecium (EF) isolated from humans and swine in a semi-closed, integrated farrow-to-fork population were evaluated in a crosssectional study. Our objective was to establish baseline antimicrobial resistance patterns and to evaluate the stability of isolate recovery phenotype within multiple grab samples per collection day and over multiple biweekly samples collected during a period of several months. This data will serve as a baseline for continuing longitudinal studies within the population. These continuing studies should produce the first comprehensive epidemiological data to document the transmission dynamics of antimicrobial resistance in the farrow-to-fork continuum. Outcome variables assessed included: phenotypic resistance in EC, pan-susceptibility, multi-resistance and genotypic resistance. Potential predictor variables included: 1) host species, 2) unit, 3) unit type, 4) housing cohort by species, and 5) time of day. There were significant differences (p<0.05) between host species with swine at higher odds for both single and multiple resistance. There were also differences in resistance based on unit location, unit-type, and housing cohort within both humans and swine. Our study found no significant differences (p>0.05) in resistance between swine workers and non-swine workers with the sole exception of resistance to cephalothin, with non-swine workers at 1.89 higher odds for resistance (p=0.02). A total of 17 VRE were isolated from human wastewater samples, and to the author’s knowledge these represent the first environmentally isolated VRE in the U.S. Several unique multi-resistance phenotypes were observed and future evaluation of AMR phenotype in continuing longitudinal studies provides a unique opportunity to study phenotypic patterns and dissemination through the study population.

Insulin resistacne and hyperinsulinemia are important risk factors for development of type 2 diabetes mellitus and hypertension. Recently, accumulating evidence has shown that endothelial dysfunction, increases in peripheral vessel resistnce and overactivation of the sympathetic neruvous system contribute to the development of insulin resistance-associated hypertension. The signigicance of cardiovascular regulatory center in the brain stem in pathophysiology of the insulin resistance-induced hypertension, however, has not been explored. Previously studies have proved that increases in superoxide anion (O2£»−) production in peripheral tissue and suppression of nitric oxide (NO) expression in the endothial cell are involved in insulin resistance and hypertension. The nucleus tractus solitarius (NTS) and rostral ventrolateral medulla (RVLM) are involved in neural regulation of blood pressure by serving respectively as the primary baroreceptor afferent terminal sites and the location of sympathetic premotor neurons for cardiovascular regulation in the brain stem. Clinically, the peroxisome proliferator-activated receptor (PPAR) agonist is commonly prescribed for the treatment of type 2 diabetes mellitus by activate PPAR£^ to enhance peripheral tissue insulin sensitizing ability, to maintain blood glucose homeostasis. Intriguingly, both animal and human studies revealed that PPAR£^ agonist also possesses blood pressure lowering effect, although the underlying mechanism is not clear. We therefore investigated in the present study the role of NO and O2£»− in the NTS and RVLM in the pathophysiology of the high fructose diet-induced insulin resistacne and hypertension, and to evaluate the potential central antihypertensive effect of PPAR£^ agonist in rats subjected to high fructose diet. The normotensive male Wistar Kyoto rats (WKY) were divided into 4 groups, including 3 experimental group that received 60% high fructose diet for 8 weeks and one control group that received regular chow diet for the same period of time. Within the 3 experimental groups, two of them received oral administration of rosiglitazone or pioglitazone (10 mg/kg/day) at the last two weeks (from week 6 to week 8) and the third group received saline ingestion. Systemic blood pressure was measured by tail vein sphygmomanometer very week and venous blood was drawn every other week to measure blood sugar and insulin level. At the end of the experiment, oral glucose tolerance test (OGTT) was tested and O2£»− and NO production in the NTS and RVLM were quantified. In adult male WKY rats I found that high fructose diet induced insulin resistance, hypertriglycemia and hypertension. Oral administration of rosiglitazone or pioglitazone significantly blunted the hypertension, hypertriglyceridemia, and ameliorated insulin resistance induced by high fructose diet. The high fructose diet also increased tissue level of O2£»− in the NTS and RVLM. PPAR£^ agonist treatment for two weeks did not affect the induced oxidative stress in these two nuclei. NO production was also increased in the NTS and RVLM after high fructose diet for 6 weeks. Oral treatment of rosiglitazone or pioglitazone significantly attenuated NO production after high fructose diet. At the molecular level, protein expressions of the NADPH oxdase subunits (p40phox, p47phox and gp91phox) and superoxide dismutase (cupper/zinc SOD, mitochondrial SOD, extracellular SOD) were not altered in the NTS or RVLM after high fructose diet alone or in addition with rosiglitazone or pioglitazone treatment. In the RVLM, there was a significant increase in neuronal NO synthase (nNOS) expression with concomitant decrease in inducible NOS (iNOS) expression. Oral treatment of PPAR£^ agonist for two weeks significantly suppressed the induced nNOS upregulation and attenuated the induced downregulation of iNOS expression in the RVLM. Together these results suggest that overproduction of O2£»− and NO in the NTS and RVLM may related to the development of insulin resistance-associated hypertension. Oral treatment of PPAR£^ agonist, including rosiglitazone and pioglitazone, may provide antihypertensive protection by superssing the induced-nNOS expression and increasing the induced-iNOS expression in the RVLM.

Thesis (Honors)--Liberty University Honors Program, 2008. / Includes bibliographical references.

Thesis (Honors)--Liberty University Honors Program, 2008. / Includes bibliographical references.

Thesis (M.Sc.)--York University, 2006. Graduate Programme in Chemistry. / Typescript. Includes bibliographical references (leaves 128-131). Also available on the Internet. MODE OF ACCESS via web browser by entering the following URL: http://gateway.proquest.com/openurl?url_ver=Z39.88-2004&res_dat=xri:pqdiss&rft_val_fmt=info:ofi/fmt:kev:mtx:dissertation&rft_dat=xri:pqdiss:MR29561

Thesis (Ph.D)--Virginia Commonwealth University, 2009. / Prepared for: Dept. of Pharmacology and Toxicology. Title from title-page of electronic thesis. Bibliography: leaves 134-160.

Thesis (MScAgric)--University of Stellenbosch, 2008. / Bibliography. Also available via the Internet.

Thesis (Ph.D.)--East Carolina University, 2008. / Presented to the faculty of the Department of Exercise and Sport Science. Advisor: G. Lynis Dohm. Title from PDF t.p. (viewed Apr. 23, 2010). Includes bibliographical references.

Thesis (M. Phil.)--Hong Kong University of Science and Technology, 2003. / Includes bibliographical references. Also available in electronic version. Access restricted to campus users.

Much of the research on the Palestinian Resistance Movement focuses on the period of its most active international terrorism, roughly between the June 1967 Arab-Israeli war and October 1977. These studies focus largely on the violent acts of the movement’s operatives and the movement’s Marxist political theory during this time. Less has been written, however, about the movement’s development prior to 1967, or the relationship between traditional forms of anti-colonial resistance and tribal violence in Palestinian society and the forms of resistance that manifested within the Palestinian Resistance Movement. This thesis analyzes the development of political critiques and theories on the use of political violence within the organizations of Palestinian Resistance between the nakba in 1948 and the 1967 Arab-Israeli war, tracing them back to the traditional sociopolitical structures that regulated authority and tribal violence in Palestine prior to the twentieth century. Due to a variety of economic and political forces at work in the region, political authority among Arab Palestinians shifted from rural kinship-based networks to urban patronage-based networks between roughly 1858 and 1922. This resulted in a disconnection between those wielding political and economic influence and the population’s center of mass, which remained in the rural hinterlands. This dual structure, which ultimately contributed to the failure of nationalist Palestinian leaders to effectively harness peasant anticolonial resistance during the British Mandate to strategic ends, was a central element in the critique of mid-century Palestinian Resistance Movement thinkers, and informed the theories they generated during this time. As an illustration of Palestinian resistance thought during this period, I analyze the content and editorial perspective of Filasṭīn, a newspaper published by the Arab Nationalist Movement from 1964 to 1967. Through this newspaper, the ANM clearly articulated a position on Arab government and the use of violence for political ends which remained a major influence in the theories of the movement after 1967. / text