This thesis introduces a novel spectral response (SR) measurement technique using polychromatic filters (filters with very broad spectral transmittances) to determine SR of large area PV devices. Conventionally, SR of a photovoltaic (PV) device is determined by illuminating the device under test (DUT) with a series of monochromatic beams at different wavelengths as described in the international standard IEC 60904-8, or beams of limited spectral content using narrow band pass filters or monochromator. One significant problem associated with the application of the narrow band pass filters for a large-area SR measurement is that low light intensity produced on the measurement plane particularly in certain wavelength ranges: the ultraviolet and infrared. This can produce weak signal responses from a tested PV device. In addition, the imperfection of the filter s mounting position can shift the peak wavelength of the filter s transmittance at angle of incidence greater than 10°. This can cause stray light on the measurement plane. The proposed SR measurement method is called the 'polychromatic SR fitting method' or, in short, it is known as the 'polychromatic method'. The advantage of this method is that higher beam intensity can be produced on the measurement plane as a result of large spectral transmittance of the polychromatic filters. This can improve the signal strength of a tested PV device. This new SR measurement method works by comparing the variations in the currents which are measured at different spectra to the currents which are calculated at the same spectral conditions using the SR model. Validations of this method for a large- and small-area SR determinations show that it is potentially feasible as a new technique for determining SR of a PV device with deviations within ±2% across the wavelength bands.

These studies investigated the impact of intensity and body temperature on performance and cardiovascular regulation during high intensity and prolonged exercise. In study 1, polyphenol antioxidant supplementation proved to have no effect on exercise performance and related variables (gross efficiency, perceived exertion, maximal power) during exercise in the heat. Furthermore, there were no differences between the cardiovascular or thermoregulatory responses between control and antioxidant treatments. Study 2 utilized an integrative approach to investigate a classic topic in exercise physiology, namely, is the cardiac output to oxygen consumption relationship linear across a wide range of exercise intensities? The slope of the CO vs. VO2 relationship was significantly reduced from 70 to 100% of VO2max when compared to the slope from 40 to 70% of VO2max (2.0 ± 0.4 vs. 4.4 ± 0.3 l/min, p = 0.025). This finding, in combination with the plateau and eventual reduction in stroke volume at high intensity exercise compared to moderate intensity exercise (146.0 ± 16.6 vs. 138.5 ± 14.9 ml/beat, p = 0.015), argues in favor of a cardiac limitation to high intensity exercise. This study also showed that the pattern of oxygen extraction at the whole body level (arterial venous O2 difference) and the muscle level (deoxygenated hemoglobin) is not similar and that muscle specific differences exist regarding oxygen extraction. Study 3 determined that hyperthermia (elevation of skin temperature by 4.3°C and core temperature by 0.8°C) did not reduce SV independent of the increase in HR. Even under conditions of moderate hyperthermia the reduction in SV is due to the increase in HR and temporally unrelated to increases in cutaneous blood flow. In summary, antioxidant supplementation had no effect on performance, cardiovascular, or thermoregulatory responses to exercise in the heat in well trained subjects. High intensity exercise is associated with a reduced rate of increase in the CO vs. VO2 relationship. Finally, hyperthermia does not reduce SV during exercise when HR is maintained at normal levels. / text

In normal tissues, blood supply is closely matched to tissue demand for wide ranges of oxygen demand and arterial pressure. This suggests that multiple mechanisms regulate blood flow. Theoretical models can be used to analyze these interacting mechanisms. One proposed mechanism for metabolic flow regulation involves the saturation-dependent release of ATP by red blood cells, which triggers an upstream conducted response signal and arteriolar vasodilation. To analyze this mechanism, oxygen and ATP levels are calculated along a flow pathway of seven representative segments, including two vasoactive arteriolar segments. The conducted response signal is dependent on ATP concentration. Arteriolar tone depends on the conducted response signal, local wall shear stress and wall tension. Arteriolar diameters are calculated based on vascular smooth muscle mechanics. The model can account for increases in perfusion consistent with experimental findings at low and moderate oxygen consumption rates despite the opposing effects of the myogenic and shear-dependent responses. Autoregulation, the maintenance of nearly constant blood flow as arterial pressure varies, is assessed in the presence or absence of the myogenic, shear-dependent and/or metabolic responses. The model results indicate that the combined effects of myogenic and metabolic regulation overcome the vasodilatory effect of the shear-dependent response to generate autoregulatory behavior. Capillary recruitment has been shown to increase the capacity for oxygen delivery during exercise. In the model, capillary density is assumed to depend on small arteriole diameter. The model predicts a significant increase in the range over which perfusion can be regulated when recruitment is included. Oscillations in diameter and tone are predicted under certain conditions, suggesting a novel mechanism for vasomotion. The conditions that give rise to oscillations are analyzed. It is shown that the appearance of oscillations depends in a complex way on a number of system parameters. In summary, the theoretical model provides a quantitative assessment of the myogenic, shear-dependent and metabolic responses that affect blood flow regulation and identifies a role for capillary recruitment and vasomotion in the control of blood flow.

For teachers of freshman English composition, the most time-consuming aspect of teaching is responding to student papers (Anson, 2012; Straub, 2000b). Teachers respond in various ways, but most teachers agree that they should offer written feedback to students (Beach & Friedrich, 2006). However, little research has been conducted to determine how teachers’ written feedback practices reflect their beliefs about the purpose of such feedback. This qualitative study explores the relationship between English composition teachers’ beliefs about written feedback and their actual written feedback practices. The participants were a sample of four instructors of freshman English composition at a mid-sized metropolitan public university. Interviews, classroom observations, course documents, and samples of teachers’ written comments were analyzed to determine teachers’ written response practices and their beliefs related to the purposes of freshman writing and their roles as writing teachers. Results suggest that teachers were aware of their beliefs, and their written response practices were consistent with their beliefs. Teachers utilized different approaches to respond to student writing, but those approaches are consistent with current recommendations for responding to student writing. Three major themes emerged from the study. First, teachers must be given the opportunity to reflect about and articulate their beliefs about written response so they will know why they respond in the way they do. Second, teachers work within the boundaries of their specific writing program to organize their written responses to student writing. Third, teachers must respond to student writing from varying perspectives as readers of the text. The findings support studies which indicate that written response is a sociocultural practice and teacher beliefs are just one aspect of the complex nature of teacher written response. The study should add to the fields of response theory and the formation of teacher beliefs.

Building fragility describes the likelihood of damage to a building due to random ground motions. Conventional methods for computing building fragilities are either based on statistical extrapolation of detailed analyses on one or two specific buildings or make use of Monte Carlo simulation with these models. However, the Monte Carlo technique usually requires a relatively large number of simulations in order to obtain a sufficiently reliable estimate of the fragilities, and it quickly becomes impractical to simulate the required thousands of dynamic time-history structural analyses for physics-based analytical models. An alternative approach for carrying out the structural simulation is explored in this work. The use of Response Surface Methodology in connection with the Monte Carlo simulations simplifies the process of fragility computation. More specifically, a response surface is sought to predict the structural response calculated from complex dynamic analyses. Computational cost required in a Monte Carlo simulation will be significantly reduced since the simulation is performed on a polynomial response surface function, rather than a complex dynamic model. The methodology is applied to the fragility computation of an unreinforced masonry (URM) building located in the New Madrid Seismic Zone. Different rehabilitation schemes for this structure are proposed and evaluated through fragility curves. Response surface equations for predicting peak drift are generated and used in the Monte Carlo simulation. Resulting fragility curves show that the URM building is less likely to be damaged from future earthquakes when rehabilitation is properly incorporated. The thesis concludes with a discussion of an extension of the methodology to the problem of computing fragilities for a collection of buildings of interest. Previous approaches have considered uncertainties in material properties, but this research incorporates building parameters such as geometry, stiffness, and strength variabilities as well as nonstructural parameters (age, design code) over an aggregation of buildings in the response surface models. Simulation on the response surface yields the likelihood of damage to a group of buildings under various earthquake intensity levels. This aspect is of interest to governmental agencies or building owners who are responsible for planning proper mitigation measures for collections of buildings.

My dissertation focuses on the design and incentives of survey techniques. As many institutions use surveys to allocate funding or determine policy, ensuring surveys provide accurate information is essential. Though incentives certainly play a role in whether survey participants report information truthfully, economists have largely overlooked the issue while statisticians tend to focus on estimators without directly modeling incentive constraints. One of the chapters models and analyzes the incentives of a commonly used survey technique, randomized response, while the other two chapters of my dissertation design two response techniques which improve upon others found in the literature by obtaining more precise estimates and/or incentivizing participants better. In Chapter One "A Game Theoretic Analysis of the Randomized Response Technique," I explicitly model the decision of participants to truthfully respond in the randomized response survey as a game. Randomized response techniques are used to determine the proportion of a population that belongs to a stigmatized group and introduce noise so the surveyor cannot perfectly infer whether a participant belongs to a stigmatized group, regardless of how a participant responds. The interviewer wants to reduce noise as much as possible while maintaining enough noise to ensure participants respond truthfully. Unlike prior literature, I find that the incentives of a participant depend on the number of participants; therefore, the amount of noise required under randomized response decreases when the number of participants increases as adding respondents relaxes truth-telling constraints. However, adding respondents only relaxes incentive constraints to a limit, so some noise remains even when there are a large number of participants. I improve upon the original randomized response technique in two ways in Chapter 2: "Eliciting Private Information using Correlation: A Modification of Randomized Response." In standard randomized response techniques, participants receive questions independently by using a randomization device such as a die. With my technique, participants receive perfectly correlated questions which reduces the variance of the surveyor's estimator while still protecting the privacy of the subjects. Unlike with the randomized response technique, adding correlation allows the surveyor to use a dominant strategy mechanism though it provides limited information. In addition to correlation, my technique provides the surveyor with private information on the distribution of questions asked. Because of the private information, participants become more uncertain of which question is more associated with the stigmatizing characteristic giving them a stronger incentive to respond truthfully. My final chapter, Chapter 3 "A Response Technique with Dominant Strategies in Forced Responses," improves upon a randomized response technique commonly used in practice. In the forced response technique, a fraction of survey participants are directly asked whether they belong to the stigmatizing group while the remaining participants either simply state "yes" or "no" according to a privately observed command. Unlike the original randomized response technique, the surveyor must worry whether participants obey the command in addition to answering truthfully. Psychologically, participants may feel more inclined to disobey than to lie. Therefore, I design a technique where obeying the command is a dominant strategy by providing the surveyor with private information. The paper then discusses a more general response technique with private information and suggests restrictions on the mechanisms to ensure the surveyor does not have an incentive to try to "trick" respondents into believing they have more privacy protection than they actually do. The chapter concludes with a discussion on privacy measures.

EGFR TKIs are standard therapy for advanced NSCLC. In order to define their role in early disease, we implemented a phase II trial of neoadjuvant gefitinib in clinical stage I NSCLC. Tumour shrinkage was seen in 43% of patients, with 11% achieving RECIST partial response (PR). Analysis of molecular markers showed EGFR TKD mutations in 17% of cases, being the only associated with PR. For the first time we defined the histopathological response of NSCLC to these agents, characterized by reduction in tumour cellularity and proliferative index as well as presence of non-mucinous BAC histology. Clinical PR tumours also presented large areas of stromal fibrosis with presence of focal residual tumour. In a characterization of intracellular signalling response, EGFR dephosphorylation in the residues Y1068 and Y1173 was not concordant and only the former was significantly reduced. pAkt Ser473/Akt and Thr308/Akt ratios were significantly reduced but observed among both, clinical responders and resistant patients. Interestingly, reduction in pEGFR Y1068 was significantly associated with increase in tumour cellularity (p=0.047), Ki-67 index (p=0.018) and tumour growth (p=0.019) with a residual perinuclear localization been detected, suggesting a novel mechanism of resistance involving receptor internalization. Finally, we determined that the EGFR protein remains stable up to one hour of post resection ischemia but two to three tumour samples are necessary for an adequate tumour representation. Furthermore, EGFR cytoplasmic compartment presented the best association with clinical response in our cohort. Taking all together, we were able to generate the first clinical trial exploring the use of an EGFR TKI in early NSCLC, characterizing for the first time the histopathological and signalling responses to these agents with an evidence of a potential novel mechanism of resistance. Finally, we observed that multiple samples collection for an adequate tumour representation, and assessment of the cytoplasmic compartment, are warrant.

EGFR TKIs are standard therapy for advanced NSCLC. In order to define their role in early disease, we implemented a phase II trial of neoadjuvant gefitinib in clinical stage I NSCLC. Tumour shrinkage was seen in 43% of patients, with 11% achieving RECIST partial response (PR). Analysis of molecular markers showed EGFR TKD mutations in 17% of cases, being the only associated with PR. For the first time we defined the histopathological response of NSCLC to these agents, characterized by reduction in tumour cellularity and proliferative index as well as presence of non-mucinous BAC histology. Clinical PR tumours also presented large areas of stromal fibrosis with presence of focal residual tumour. In a characterization of intracellular signalling response, EGFR dephosphorylation in the residues Y1068 and Y1173 was not concordant and only the former was significantly reduced. pAkt Ser473/Akt and Thr308/Akt ratios were significantly reduced but observed among both, clinical responders and resistant patients. Interestingly, reduction in pEGFR Y1068 was significantly associated with increase in tumour cellularity (p=0.047), Ki-67 index (p=0.018) and tumour growth (p=0.019) with a residual perinuclear localization been detected, suggesting a novel mechanism of resistance involving receptor internalization. Finally, we determined that the EGFR protein remains stable up to one hour of post resection ischemia but two to three tumour samples are necessary for an adequate tumour representation. Furthermore, EGFR cytoplasmic compartment presented the best association with clinical response in our cohort. Taking all together, we were able to generate the first clinical trial exploring the use of an EGFR TKI in early NSCLC, characterizing for the first time the histopathological and signalling responses to these agents with an evidence of a potential novel mechanism of resistance. Finally, we observed that multiple samples collection for an adequate tumour representation, and assessment of the cytoplasmic compartment, are warrant.

Measures of data quality are important for the evaluation and improvement of survey design and procedures. A detailed investigation of the sources, magnitude and impact of errors is necessary to identify how survey design and procedures may be improved and how resources allocated more efficiently among various aspects of the survey operation. A major part of this thesis is devoted to the overview of statistical theory and methods for measuring the contribution of response variability to the overall error of a survey. A very common practice in surveys is to select groups (clusters) of elements together instead of independent selection of elements. In practice cluster samples tend to produce higher sampling variance for statistics than element samples of the same size. Their frequent use stems from the desirable cost features that they have. Most data collection and sample designs involve some overlapping between interviewer workload and the sampling units (clusters). For those cases, a proportion of the measurement variance, which is due to interviewers, is reflected to some degree in the sampling variance calculations. The prime purpose in this thesis is to determine a variance formula that decomposes the total variance into sampling and measurement variance components for two commonly used data collection and sample designs. Once such a decomposition is obtained, determining an optimum allocation in existence of measurement errors would be possible.

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