Univ., Diss.--Freiburg, 2006.

Abridged and revised Thesis (Ph. D.)--Albert-Ludwigs-Universität, Freiburg, 2006: P. 12. / Includes bibliographical references and sources (p. 801-851) and indexes.

Master of Science / Department of Journalism and Mass Communications / Major Professor Not Listed / This exploratory research utilized focus groups from college students to learn how and why people are using current mobile dating applications to form and maintain relationships. Additionally, the author asked participants about their perception of a new mobile application that is still in the conceptual stages called Flick. The results revealed seven key themes to the gratifications people receive from mobile dating apps: (Theme 1: Dating Applications as Games and Entertainment; Theme 2: Perceptions of App Functions Vary by Gender; Theme 3: Dating Applications to Embrace Hookup Culture/Casual Sex; Theme 4: Dating Applications as the Lottery Ticket for Love/Relationship Seeking; Theme 5: Dating Applications as Self-Validation; Theme 6: Dating Applications for Social Means; Theme 7: Dating Applications as Trendiness) Lastly, the overall perceptions of Flick were very positive from all sessions. However, when it comes to the dating component of the application, the users were much more uncertain. Due to this finding, the author has decided to take the branding and purpose of Flick to only focus on the business and friend components.

Under en lång tid har Harlequin-romaner och romantiska fantasier varit populära bland kvinnor. Den klassiska berättelsen om hjältinnan som finner kärleken med den perfekta mannen är specifikt riktad mot kvinnor. Det har forskats kring dessa romantiska fantasier, men det saknas forskning om hur dessa romantiska fantasier representerar maskuliniteten bland de manliga karaktärerna. Målet med det här arbetet är att försöka fylla en del av det tomrummet. Med hjälp av William Labovs narrativa modell och en kvalitativ textanalys har jag analyserat två filmer inom genren chick flick, Bridget Jones’s Diary (2001) och Bridget Jones: Edge of Reason (2004). Min analys visar att maskuliniteterna som framställs i romantiska berättelser följer väldigt stereotypiska maskulina drag. Exempelvis använder sig de manliga karaktärerna ofta av fysiskt våld för att visa sin manliga dominans och genom att vinna i ett slagsmål vill de visa vem som är den bästa mannen för Bridget Jones. / Harlequin novels and romantic fantasies have been popular with women for a number of years. The classic story of the heroine finding her true love with the perfect man is directed specifically to women, for their enjoyment. While there have been studies about the romantic fantasies themselves, there’s a distinct lack of research on how these romantic fantasies portray the male characters and their masculinity. This study is a step towards filling that gap. Using a combination of William Labov’s narrative model, as well as a qualitative textanalysis, to examine two chick flicks, Bridget Jones’s Diary (2001) and Bridget Jones: Edge of Reason (2004), I have found that the masculinities portrayed in romantic fantasies follow very stereotypical male behavior. For example, the male characters will often resort to physical violence to prove their male dominance and by winning a fight they want to prove that they are the right man for Bridget Jones.

CYP2D6 metabolizes codeine to morphine, the active analgesic metabolite. Variation in brain CYP2D6 activity may affect brain morphine levels after codeine administration and thereby influence analgesia. We investigate the effect of inhibiting brain CYP2D on codeine-induced analgesia. METHODS: Rats received intracerebroventricular (i.c.v.) injections of CYP2D inhibitors or vehicle controls. Rats were then given subcutaneous codeine injections and analgesia was measured with the tail-flick test. Morphine and codeine concentrations in brain and plasma were measured. CYP2D activity in brain and liver were assessed in vitro. RESULTS: Compared to vehicle treatment, i.c.v. inhibitor treatments resulted in lower codeine-induced analgesia, lower morphine levels in brain but not in plasma after codeine injections, and lower CYP2D activity in brain membranes but not in liver microsomes. CONCLUSIONS: Inhibiting brain CYP2D reduces codeine’s metabolism to morphine, resulting in less analgesia. Variation in brain CYP2D6 activity may influence response to codeine and other CYP2D6 substrates.

CYP2D6 metabolizes codeine to morphine, the active analgesic metabolite. Variation in brain CYP2D6 activity may affect brain morphine levels after codeine administration and thereby influence analgesia. We investigate the effect of inhibiting brain CYP2D on codeine-induced analgesia. METHODS: Rats received intracerebroventricular (i.c.v.) injections of CYP2D inhibitors or vehicle controls. Rats were then given subcutaneous codeine injections and analgesia was measured with the tail-flick test. Morphine and codeine concentrations in brain and plasma were measured. CYP2D activity in brain and liver were assessed in vitro. RESULTS: Compared to vehicle treatment, i.c.v. inhibitor treatments resulted in lower codeine-induced analgesia, lower morphine levels in brain but not in plasma after codeine injections, and lower CYP2D activity in brain membranes but not in liver microsomes. CONCLUSIONS: Inhibiting brain CYP2D reduces codeine’s metabolism to morphine, resulting in less analgesia. Variation in brain CYP2D6 activity may influence response to codeine and other CYP2D6 substrates.

INTRODUCTION: Smoking is one of the single greatest causes of numerous preventable diseases. We were interested in developing an animal model of nicotine metabolism that can be used to examine the effects of potential CYP2A6 inhibitors on nicotine metabolism and nicotine-mediated behaviours. Pharmacogenetic studies have demonstrated that in humans, smoking behaviour is associated with rates of nicotine metabolism by the CYP2A6 enzyme. Mouse CYP2A5 shares structural and functional similarities to human CYP2A6 and has been implicated in nicotine self-administration behaviours in mice, therefore the mouse represents a potential animal model for studying nicotine metabolism. METHODS: We characterized nicotine and cotinine metabolism in two commonly used mouse strains (DBA/2 and C57Bl/6). We also examined the association between nicotine self-administration behaviours and nicotine metabolism, and the impact of direct manipulation (i.e. inhibition) of nicotine metabolism on nicotine pharmacodynamics (hot-plate and tail-flick tests) in mice. Finally, we studied the effect of selegiline (a known cytochrome P450 mechanism-based inhibitor) on nicotine metabolism in mice and in human CYP2A6. RESULTS: Nicotine metabolism in mice in vitro was mediated by CYP2A5, and this enzyme was responsible for over 70% and 90% of the metabolism of nicotine to cotinine and cotinine to 3-hydroxycotinine as shown by immuno-inhibition studies, respectively. A polymorphism in CYP2A5 between mouse strains, known to alter the probe substrate coumarin’s metabolism, did not affect nicotine metabolism but dramatically altered cotinine metabolism. Nicotine self-administration behaviour in mice was associated with level of hepatic CYP2A5 proteins and rates of nicotine metabolism in male mice. In inhibition studies, the CYP2A5/6 inhibitor methoxsalen inhibited both in vitro and in vivo nicotine metabolism in mice and substantially increased the anti-nociceptive effect of nicotine. Finally, selegiline was found to be an inhibitor of CYP2A5 decreasing nicotine metabolism in vitro and in vivo in mice. Moreover, we showed that selegiline is a mechanism-based inhibitor of CYP2A6 inhibiting nicotine metabolism irreversibly. CONCLUSION: The above data suggested that the mouse model may be suitable for examining the impact of inhibition (and genetic variation) on nicotine metabolism and nicotine-mediated behaviours and may potentially be used to screen for novel inhibitors of nicotine metabolism.

INTRODUCTION: Smoking is one of the single greatest causes of numerous preventable diseases. We were interested in developing an animal model of nicotine metabolism that can be used to examine the effects of potential CYP2A6 inhibitors on nicotine metabolism and nicotine-mediated behaviours. Pharmacogenetic studies have demonstrated that in humans, smoking behaviour is associated with rates of nicotine metabolism by the CYP2A6 enzyme. Mouse CYP2A5 shares structural and functional similarities to human CYP2A6 and has been implicated in nicotine self-administration behaviours in mice, therefore the mouse represents a potential animal model for studying nicotine metabolism. METHODS: We characterized nicotine and cotinine metabolism in two commonly used mouse strains (DBA/2 and C57Bl/6). We also examined the association between nicotine self-administration behaviours and nicotine metabolism, and the impact of direct manipulation (i.e. inhibition) of nicotine metabolism on nicotine pharmacodynamics (hot-plate and tail-flick tests) in mice. Finally, we studied the effect of selegiline (a known cytochrome P450 mechanism-based inhibitor) on nicotine metabolism in mice and in human CYP2A6. RESULTS: Nicotine metabolism in mice in vitro was mediated by CYP2A5, and this enzyme was responsible for over 70% and 90% of the metabolism of nicotine to cotinine and cotinine to 3-hydroxycotinine as shown by immuno-inhibition studies, respectively. A polymorphism in CYP2A5 between mouse strains, known to alter the probe substrate coumarin’s metabolism, did not affect nicotine metabolism but dramatically altered cotinine metabolism. Nicotine self-administration behaviour in mice was associated with level of hepatic CYP2A5 proteins and rates of nicotine metabolism in male mice. In inhibition studies, the CYP2A5/6 inhibitor methoxsalen inhibited both in vitro and in vivo nicotine metabolism in mice and substantially increased the anti-nociceptive effect of nicotine. Finally, selegiline was found to be an inhibitor of CYP2A5 decreasing nicotine metabolism in vitro and in vivo in mice. Moreover, we showed that selegiline is a mechanism-based inhibitor of CYP2A6 inhibiting nicotine metabolism irreversibly. CONCLUSION: The above data suggested that the mouse model may be suitable for examining the impact of inhibition (and genetic variation) on nicotine metabolism and nicotine-mediated behaviours and may potentially be used to screen for novel inhibitors of nicotine metabolism.

An ultra-low dose of a drug is approximately 1000-fold lower than the dose range traditionally used to induce a therapeutic effect. The purpose of the present thesis was to broaden the knowledge of the ultra-low dose effect, that was previously identified in the opioid receptor system, by looking at whether opioids and cannabinoids interact at the ultra-low dose level, whether cannabinoid receptors themselves demonstrate the ultra-low dose antagonist effect, and whether the opioid ultra-low dose effect is maintained in a model of persistent, unavoidable pain. For experiment 1, separate groups of Long Evans rats were tested for antinociception following an injection of vehicle, the cannabinoid agonist WIN 55 212-2 (WIN), the opioid antagonist naltrexone (an ultra-low or a high dose), or a combination of WIN and naltrexone doses. Ultra-low dose naltrexone elevated WIN-induced tail flick thresholds without extending its duration of action. In experiment 2, antinociception was tested in rats following either acute or sub-chronic (7 days) injections of vehicle, WIN, ultra-low doses of the CB1 receptor antagonist rimonabant (SR 141716), or a combination of WIN and ultra-low dose rimonabant. Following the chronic experiment, striatal tissue was rapidly extracted and subjected to co-immunoprecipitation to analyse CB1 receptor coupling to G-protein subtypes. Ultra-low dose rimonabant extended the duration of WIN-induced antinociception, and attenuated the development of WIN-induced tolerance. Animals chronically treated with WIN alone had CB1 receptors predominately coupling to Gs proteins, whereas all other groups had CB1 receptors predominately coupling to Gi proteins. For experiment 3, all animals were subjected to the formalin test following either acute or sub-chronic injections of vehicle, the opiate morphine, ultra-low doses naltrexone, or a combination of morphine and ultra-low dose naltrexone. Ultra-low dose naltrexone had no significant effect on morphine-induced pain ratings in either the acute, or sub-chronic drug treatments. This thesis provides evidence that the ultra-low dose effect, including the agonist-induced G-protein coupling switch, extends to another receptor type. This effect may, therefore, be part of a generalized principle that applies to many G-protein coupled receptors. / Thesis (Ph.D, Psychology) -- Queen's University, 2007-11-05 09:31:30.162 / A portion of this research was supported by a Canadian Institutes of Health Research (CIHR) Proof of Principle Grant to M.C. Olmstead and J.J. Paquette.

In this thesis, I do a reparative reading of contemporary Swedish comics, that uses feminine signifiers, both in their imagery and writing. A crucial point of departure, in this thesis, is how literature can ”do” theory and be seen as a way of creating knowledge. I explore what the comics does to me, as a reader, and how. I experiment with the form and style of academic writing in order to clearly define my position and situate the production of knowledge. By focusing on the affects and nourishment, that the comics contain, I try to imagine a feminist other, with the help of my figuration: Nietzsche Minaj, and my imaginary utopian place: ”mitt flick(tionella) rum”. I conclude, that the comics both reproduce and transform feminine signifiers, while challenging the idea of dichotomies, in the spirit of gurlesque theory.