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<title>Brock Theses</title>
<link>http://hdl.handle.net/10464/4</link>
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<rdf:li rdf:resource="http://hdl.handle.net/10464/4375"/>
<rdf:li rdf:resource="http://hdl.handle.net/10464/4374"/>
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<dc:date>2013-05-25T22:02:31Z</dc:date>
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<item rdf:about="http://hdl.handle.net/10464/4377">
<title>The Association between Tobacco Control Policies and Marijuana Use among Ontario Undergraduate Students</title>
<link>http://hdl.handle.net/10464/4377</link>
<description>The Association between Tobacco Control Policies and Marijuana Use among Ontario Undergraduate Students
Macintosh, James
Background: Research indicates a steady increase in marijuana use and that it is concurrent with tobacco. There is speculation this concurrency reaches beyond use, to where policies aimed at reducing one may result in the reduction of the other. Purpose: To investigate the association between tobacco control policies and marijuana use among young adult undergraduates. Methods: A stratified sample of Ontario universities resulted in a sample of 4,966 participants. Results: Campuses with a moderately strong policy was found to be significantly associated with decreased marijuana use compared to campuses with a weak tobacco control policy. (OR=0.52, 95% CI: 0.36-0.76). Conclusions: The findings show tobacco control strategies are related to decreased odds of marijuana use among Ontario undergraduates. These findings are important to both policy makers and researchers interested in health strategies pertaining to marijuana and tobacco use and/or how health policies aimed at reducing one risk behaviour can affect another.
</description>
<dc:date>2013-05-15T00:00:00Z</dc:date>
</item>
<item rdf:about="http://hdl.handle.net/10464/4375">
<title>Managerial Risk-Taking and CEO Excess Compensation</title>
<link>http://hdl.handle.net/10464/4375</link>
<description>Managerial Risk-Taking and CEO Excess Compensation
Jafri, Syed Rahat Ali
This paper examines risk taking and CEO excess compensation problems in U.S firms to determine their impact on shareholders wealth. Literature suggests a positive effect of CEO incentive risk and strong corporate governance on CEO risk taking. Furthermore, the strong governance mitigates excess compensation problem. Controlling for governance quality and incentive risk, I provide empirical evidence of a significant association between risk taking and CEO excess compensation. When I also control for pay-performance sensitivity (delta) and feedback effects of incentive compensation on CEO risk taking, I find that higher use of incentive pay encourages risk taking, and due to a high exposure to risk CEOs draws excess compensation. Furthermore, I find that the excess compensation problem is more serious with CEOs taking high risk than with those taking low risk. Finally, I find that CEO risk taking also has structural impacts on CEO compensation
</description>
<dc:date>2013-05-14T00:00:00Z</dc:date>
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<item rdf:about="http://hdl.handle.net/10464/4374">
<title>Linking Ethical Leadership and Employees’ In-Role Performance: Exploring the Mediating Roles of Psychological Capital and Follower-Leader Relational Capital</title>
<link>http://hdl.handle.net/10464/4374</link>
<description>Linking Ethical Leadership and Employees’ In-Role Performance: Exploring the Mediating Roles of Psychological Capital and Follower-Leader Relational Capital
Zafar, Asma
This study investigates the mediating impact of psychological capital and follower-leader relational capital on the relationship between ethical leadership and in-role performance through the lenses of social exchange theory, social information processing theory, and psychological resources theory. Analysis of data collected from a sample of 171 employees and 24 supervisors from Pakistan reveals that ethical leadership has a positive effect on followers’ in-role job performance, yet this effect is fully explained through the role of psychological capital and partially through follower-leader relational capital. Significant implications of these findings for further research and practice are discussed.
</description>
<dc:date>2013-05-14T00:00:00Z</dc:date>
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<item rdf:about="http://hdl.handle.net/10464/4373">
<title>Cellular Mechanisms of Resveratrol's Interaction with Mitochondrial Reactive Oxygen Species Metabolism</title>
<link>http://hdl.handle.net/10464/4373</link>
<description>Cellular Mechanisms of Resveratrol's Interaction with Mitochondrial Reactive Oxygen Species Metabolism
Robb, Ellen
Resveratrol, a polyphenol found naturally in red wines, has attracted great interest in both the scientific community and the general public for its reported ability to protect against many of the diseases facing Western society today.  While the purported health effects of resveratrol are well characterized, details of the cellular mechanisms that give rise to these observations are unclear. &#13;
Here, the mitochondrial antioxidant enzyme Mn superoxide dismutase (MnSOD) was identified as a proximal target of resveratrol in vitro and in vivo.  MnSOD protein and activity levels increase significantly in cultured cells treated with resveratrol, and in the brain tissue of mice given resveratrol in a high fat diet.  Preventing the increase in MnSOD levels eliminates two of resveratrol’s more interesting effects in the context of human health: inhibition of proliferative cell growth and cytoprotection.  Thus, the induction of MnSOD is a critical step in the molecular mechanism of resveratrol. 	Mitochondrial morphology is a malleable property that is capable of impeding cell cycle progression and conferring resistance against stress induced cell death.       Using confocal microscopy and a novel ‘cell free’ fusion assay it was determined that concurrent with changes in MnSOD protein levels, resveratrol treatment leads to a more fused mitochondrial reticulum.  This observation may be important to resveratrol’s ability to slow proliferative cell growth and confer cytoprotection. &#13;
Resveratrol's biological activities, including the ability to increase MnSOD levels, are strikingly similar to what is observed with estrogen treatment.  Resveratrol fails to increase MnSOD levels, slow proliferative cell growth and confer cytoprotection in the presence of an estrogen receptor antagonist.  Resveratrol's effects can be replicated with the specific estrogen receptor beta agonist diarylpropionitrile, and are absent in myoblasts lacking estrogen receptor beta. Four compounds that are structurally similar to resveratrol and seven phytoestrogens predicted to bind to estrogen receptor beta were screened for their effects on MnSOD, proliferative growth rates and stress resistance in cultured mammalian cells.  Several of these compounds were able to mimic the effects of resveratrol on MnSOD levels, proliferative cell growth and stress resistance in vitro.  &#13;
	Thus, I hypothesize that resveratrol interacts with estrogen receptor beta to induce the upregulation of MnSOD, which in turn affects cell cycle progression and stress resistance.  These results have important implications for the understanding of RES’s biological activities and potential applications to human health.
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<dc:date>2013-05-14T00:00:00Z</dc:date>
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