Thesis (Ph. D.)--Ohio State University, 2004. / Title from first page of PDF file. Document formatted into pages; contains xv, 150 p.; also includes graphics (some col.). Includes abstract and vita. Advisor: Jonathan P. Pelz, Dept. of Physics. Includes bibliographical references (p. 144-150).

Thesis (M.S.)--University of Missouri-Columbia, 2003. / Typescript. Includes bibliographical references (leaves 69-72). Also available on the Internet.

Thesis (M.S.)--University of Missouri-Columbia, 2003. / Typescript. Includes bibliographical references (leaves 69-72). Also available on the Internet.

Thesis (M.S.)--Youngstown State University, 2009. / Includes bibliographical references (leaves 65-67). Also available via the World Wide Web in PDF format.

Buildings consume 40 % of Europe’s total energy consumption and causes 33 % of the CO2 emissions. (Pol and Lippert, 2010) Existing old buildings, especially those constructed with limited energy standards before 1960, are in need of refurbishment and energy efficiency. (Economidou, 2011) The thesis is a part of the EU project GrowSmarter, where smart solutions for sustainable cities are to be implemented in the lighthouse cities Stockholm, Cologne and Barcelona. (European Commission, 2014) The purpose of this thesis is to look into the experiences, success factors and barriers from the CONCERTO initiative, BEEM-UP project and EPC model, focusing on energy efficient refurbishment. The intent is that e.g. authorities, municipalities, companies and building owners, who are planning on performing energy efficient refurbishment measures, can access identified success factors and barriers in previous projects of different scale and methods. The conclusions of this study are that the communication and cooperation between stakeholders in a project, knowledge transfer and training of installers are important factors for successful projects. Information and involvement of tenants facilitates work execution, improves results after refurbishment and increases energy knowledge and awareness. The data quantity and quality is another influencing factor on building performance and the difference between calculated and measured energy savings. Stakeholder approach, energy performance regulations, ownership structure and financial status/possibilities for the building owner can affect project results. / GrowSmarter

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The small dispersion limit of the focusing nonlinear Schroödinger equation (fNLS) exhibits a rich structure with rapid oscillations at microscopic scales. Due to the non self-adjoint scattering problem associated to fNLS, very few rigorous results exist in the semiclassical limit. The asymptotics for reectionless WKB-like initial data was worked out in [KMM03] and for the family q(x, 0) = sech^(1+(i/∈)μ in [TVZ04]. In both studies the authors observed sharp breaking curves in the space-time separating regions with disparate asymptotic behaviors. In this paper we consider another exactly solvable family of initial data, specifically the family of centered square pulses, q(x; 0) = qx[-L,L] for real amplitudes q. Using Riemann- Hilbert techniques we obtain rigorous pointwise asymptotics for the semiclassical limit of fNLS globally in space and up to an O(1) maximal time. In particular, we find breaking curves emerging in accord with the previous studies. Finally, we show that the discontinuities in our initial data regularize by the immediate generation of genus one oscillations emitted into the support of the initial data. This is the first case in which the genus structure of the semiclassical asymptotics for fNLS have been calculated for non-analytic initial data.

The blood-brain barrier (BBB) is located at the level of the cerebral microvasculature and is critical to maintain central nervous system (CNS) homeostasis. The tight junction (TJ) protein complexes between endothelial cells at the BBB are primarily responsible for limiting paracellular diffusion of substances from the blood to the CNS. The BBB’s functional integrity is compromised in a number of disease states which affect the CNS, suggesting BBB dysfunction causes or contributes to many diseases of the CNS. A common component of most of these diseases is oxidative stres. Oxidative stress is associated with hypoxia-reoxygenation (HR) and peripheral inflammatory pain (PIP). Both HR and PIP have been shown to compromise BBB functional integrity. Using in vivo rat models of HR and PIP, we examined the role of ROS on BBB permeability as well as the TJ protein occludin using the free radical scavenger tempol. First, we subjected rats to HR with or without pre-treatment with tempol (200 mg/kg). We showed that tempol prevents up-regulation of the cellular stress marker heat shock protein 70 at the BBB during HR. Next we showed tempol reverses HR-mediated BBB permeability increase to ¹⁴C-sucrose, a marker of BBB paracellular permeability. Tempol also attenuated changes in the structure and localization of occludin, suggesting ROS produced during HR alter occludin and lead to disruption of BBB. We then investigated whether ROS production have similar effects on occludin and BBB permeability during PIP by administering 3% λ-carrageenan into the hind paw of rats. We found tempol attenuated carrageenan-induced increase in paw edema and thermal hyperalgesia. Tempol also attenuated up-regulation of the cellular stress marker NF-κB in cerebral microvessels. Tempol significantly decreased BBB permeability to ¹⁴C sucrose during PIP. We found PIP reduces disulfide bonds in occludin oligomeric assemblies thought to be important in maintaining the structural integrity of the BBB. Tempol significantly inhibited disulfide bond reduction, suggesting ROS mediate BBB disruption during inflammatory pain by reducing occludin disulfide bonding. Taken together, these findings show the involvement of ROS during HR and PIP contributes to BBB dysfunction by altering the structure of high molecular weight occludin oligomeric assemblies.

P-glycoprotein (Pgp; ABCB1) is a well known transporter involved in energy-dependent-drug efflux activity. At the brain capillary endothelium, its luminal membrane location is ideal for its ascribed role in the physiological efflux of a wide array of structurally and functionally diverse compounds from the brain. This is a critical issue in regards to the delivery of central nervous system (CNS)-acting therapeutics. Moreover, a dysregulation of Pgp has been implicated in specific CNS disease states, including Alzheimer's disease, epilepsy, and brain cancer where an upregulation of Pgp has been well established as a mediator of multi-drug resistance. Inflammation is a common component in all of these conditions. Previously our laboratory has reported changes in BBB molecular and functional properties during inflammatory pain (Huber et al. 2001). This has led us to investigate the effects of peripheral inflammatory pain on Pgp efflux transport properties at the BBB, in vivo. In the present study we examined the effects of lambda-carrageenan-induced inflammatory pain (i.e. hyperalgesia; CIP) on the molecular and functional properties of Pgp at the BBB. Western blots using enriched fractions of isolated rat brain microvessels revealed that Pgp expression at the BBB was increased by CIP and that this increase occurred predominantly within the membrane region of the cell. Additionally, both in situ brain perfusions and whole body antinociceptive profiling of the Pgp substrate and opioid analgesic, [3H] morphine, indicate that changes in Pgp at the BBB, mediated by peripheral inflammation, can impact brain uptake of morphine. To further elucidate the mechanism(s) behind the rapid upregulation (3 h) of Pgp at this region, we explored regulation of Pgp at the plasma membrane. Our findings show that CIP induces a movement of Pgp within these domains and that Pgp co-localizes with caveolin-1 and clathrin, key structural proteins associated with caveolae and clathrin-pit lipid rafts, respectively. Our data indicate for the first time that peripheral inflammatory pain induces functional and molecular changes in Pgp, a critical efflux transporter, at the BBB in vivo and that these alterations may be mediated in part via a proteolipidic re-organization mechanism.