The relationships between competition, innovation, and regulation have long been studied in an attempt to understand and evaluate the effect of regulation on the wealth and growth of nations. Recent empirical work has emerged taking advantage of the still ongoing proliferation of ever more disaggregated data to shed more light on these relationships and at the same time uncover new puzzles in need of explanations. This thesis is an attempt to address the discrepancies between some of these newly discovered phenomena and current theory. In Chapter 1 I introduce an insight of Friedrich Hayek - that competition allows a thousand flowers to bloom, and discovers the best among them - into a conventional model of Schumpeterian innovation. I show how the model can account for two seemingly contradictory empirical phenomena, a positive relationship between competition and industry-level productivity growth, and an inverted-U relationship between competition and firm-level innovation. In Chapter 2 I extend the model to investigate the effects of patent protection on competition and innovation, and to understand the interaction between patent policy and product-market regulation. I calibrate the model to show that patent protection in the U.S. is depressing competition, innovation, growth, and welfare. Using patent and citation data, I further provide empirical evidence supporting the implications of the model. In Chapter 3 I investigate the impact of regulatory entry barriers to new firms on aggregate output and total factor productivity. Following recent work by Thomas J. Holmes and John J. Stevens, I extend a standard model of monopolistic competition to account for the existence of both niche markets and mass markets within industries. Calibrating the model using U.S. manufacturing data, I show this extension goes a long way towards explaining the large gap between empirical estimates of the impact of barriers to entry and the quantitative predictions of current models.

The relationships between competition, innovation, and regulation have long been studied in an attempt to understand and evaluate the effect of regulation on the wealth and growth of nations. Recent empirical work has emerged taking advantage of the still ongoing proliferation of ever more disaggregated data to shed more light on these relationships and at the same time uncover new puzzles in need of explanations. This thesis is an attempt to address the discrepancies between some of these newly discovered phenomena and current theory. In Chapter 1 I introduce an insight of Friedrich Hayek - that competition allows a thousand flowers to bloom, and discovers the best among them - into a conventional model of Schumpeterian innovation. I show how the model can account for two seemingly contradictory empirical phenomena, a positive relationship between competition and industry-level productivity growth, and an inverted-U relationship between competition and firm-level innovation. In Chapter 2 I extend the model to investigate the effects of patent protection on competition and innovation, and to understand the interaction between patent policy and product-market regulation. I calibrate the model to show that patent protection in the U.S. is depressing competition, innovation, growth, and welfare. Using patent and citation data, I further provide empirical evidence supporting the implications of the model. In Chapter 3 I investigate the impact of regulatory entry barriers to new firms on aggregate output and total factor productivity. Following recent work by Thomas J. Holmes and John J. Stevens, I extend a standard model of monopolistic competition to account for the existence of both niche markets and mass markets within industries. Calibrating the model using U.S. manufacturing data, I show this extension goes a long way towards explaining the large gap between empirical estimates of the impact of barriers to entry and the quantitative predictions of current models.

The purpose of this thesis was to investigate the role of lactate in the regulatory volume response of mammalian skeletal muscle to hypertonic challenge-induced cell shrinkage. It was demonstrated that adult mice skeletal muscle single fibres responded to increased extracellular osmolarity in a dose-dependent manner when exposed to NaCl or sucrose challenge. This regulatory response to sucrose and NaCl however was abolished when cells were pre-treated with bumetanide, a specific sodium-potassium-chloride cotransport (NKCC) inhibitor, demonstrating that the NKCC is primarily responsible for eliciting a regulatory volume increase (RVI). When cells were exposed to NaLac treatment, bumetanide incubation did not significantly diminish the ability of the cells to recover volume. Furthermore, these cells lost less volume compared to NaCl or sucrose control. Inhibiting the single muscle fibres with either monocarboxylate transport (MCT) inhibitor phloretin or pCMBS resulted in significantly greater volume loss and impaired volume recovery. Combined MCT inhibition of phloretin or pCMBS with NKCC inhibition (bumetanide) led to unexpected findings, whereby the cells lost very little volume. These data suggest that while skeletal muscle fibres may utilize the NKCC to regulate volume, the ability for these cells to employ the most efficient means of volume regulation involves the inclusion of lactate as well via MCT uptake. / NSERC

No description available.

No description available.

In an era of highly advertised blockbuster medicines, newly approved pharmaceuticals can pose a hazard to the public if not properly monitored following their approval. Drugs are only given to a limited number of healthy individuals during clinical trials, leaving significant questions as to the risks for the population at large. There are limited opportunities for assessment following the product’s introduction onto the market and adverse effects may not be detected. This paper argues that hurdles in tracking long-term safety and effectiveness can be partially remedied through the aggregation and analysis of information collected through pharmaceutical data mining. Pharmaceutical data mining is a process whereby private organizations compile extensive information on patients’ prescription histories, including: the drug prescribed, recommended dosage, and the patient’s subsequent history with the medication. The Canadian government should collect this information and analyze its meaning to better ensure the long-term safety and effectiveness of drugs.

Ion channel regulation is key to the control of excitability and behaviour. In the bag cell neurons of Aplysia californica, a voltage- and Ca2+-dependent nonselective cation channel drives a ~30-minute afterdischarge, culminating in the release of egg-laying hormone. Using excised, inside-out single channel patch-clamp, this study tested the hypothesis that inositol 1,4,5-trisphosphate (IP3), which is produced during the afterdischarge, and channel-associated protein kinase C (PKC), which is activated throughout the afterdischarge, cause a left-shift (enhancement) in both the voltage- and Ca2+-dependence of the cation channel. Kinetic analysis of bag cell neuron cation channel voltage-dependence revealed that, with depolarization, the channel remained open longer and reopened more often. A cation channel subconductance was also observed, and found to be 13 pS vs. the typical 23 pS full-conductance. The cytoplasmic face of cation channel-containing patches was exposed to 1 mM ATP, as a phosphate source for channel-associated PKC, and/or 5 uM IP3. Apparent PKC-dependent phosphorylation left-shifted voltage-dependence by -3 mV, although this effect was more prominent at negative voltages (between -90 and -30 mV). Conversely, IP3 right-shifted voltage-dependence (change in V1/2 of 6 mV). Cation channel Ca2+-dependence was similar to that previously reported, with a control EC50 of 3-5 uM. This was right-shifted by PKC (EC50 = 30 uM) and even more so by IP3 (apparent EC50 = 20 M). PKC largely rescued the Ca2+ responsiveness in the presence of IP3 (EC50 = 20 uM). Unexpectedly, IP3 plus ATP resulted in an increase in channel unitary conductance at more positive voltages. The multi-faceted regulation of the bag cell neuron cation channel suggests sophisticated modulatory control. Upregulation, such as depolarization and the left-shift in voltage-dependence with PKC, would drive the afterdischarge, while counteracting effects, such as IP3 right-shifting voltage-dependence, as well as PKC and IP3 suppressing Ca2+-dependence, would simultaneously or subsequently attenuate the channel, thus preventing an interminable afterdischarge. / Thesis (Master, Physiology) -- Queen's University, 2008-08-26 13:20:16.528

Adolescents experience heightened emotional arousal and difficulty regulating that arousal. Adolescent girls have emotion regulation difficulties particularly associated with symptoms of depression and anxiety. In adults, the emotion dysregulation associated with depression and anxiety has been linked to not accepting emotions. Emotional non-acceptance is the act of judging certain emotional experiences as inadmissible and trying to avoid, suppress, or ignore those experiences. In adults, non-acceptance is thought to paradoxically lead to amplified emotional arousal and difficulty regulating arousal. Previous research supports this idea for the subjective experience of emotion but not the physiological response. The goal of the current study was to elicit these differences in physiology in order to better understand the effects of emotional non-acceptance on emotion regulation. Eighty-two adolescent girls were asked to perform a spontaneous speech while physiological and subjective responses were measured. These same measures were taken before and after the speech. Trait-like emotional non-acceptance was also measured. Although trait non-acceptance predicted differences in one aspect of physiology, there were no other effects of emotional acceptance or non-acceptance on physiological response. In line with previous research, emotional acceptance and non-acceptance had their effects on the subjective experience of emotion, both in reaction to, and recovery from, the speech. Interestingly, in the current sample, induced non-acceptance had no effects on arousal or regulation. Also, greater effects were found for self-reported positive emotion than any other measure of emotional response. Results support the idea that emotional non-acceptance and acceptance affect the appraisal of emotional experiences but do not affect the emotional arousal itself. Also, the findings of this study suggest that emotional non-acceptance has more qualities of a trait than a state. The implications for the model of emotional acceptance and the effects of puberty on emotion regulation are discussed. / Thesis (Master, Psychology) -- Queen's University, 2009-09-29 14:18:38.431

No description available.

No description available.