Operation Red Campus”: An Experimental Analysis of CRNC Advertisements Targeting the Millennial Generation

Using an experimental survey design, this study evaluated an advertising campaign developed by the College Republican National Committee targeting Millennials in the 2014 midterm elections. Three particular advertisements from “Operation Red Campus” were selected and tested using a pre-survey and two post-surveys. Due to data constraints, only the results of the first post-survey were used in this analysis. This campaign was designed in response to the Republican Party’s continued problems of low youth turnout and poor party perceptions. This thesis analyzes the effectiveness of the strategies employed by the CRNC to target 18-24-year-olds with this campaign, adding to the limited body of literature on the subject. Following the pre-survey, respondents were exposed to randomized clips of one of the randomized CRNC advertisements or a control advertisement for the television show from which they were based. I hypothesized that respondents would be able to identify that the ads in the treatment condition were political in nature and that those exposed to the treatments would exude more positive views of the Republican Party and less positive views of Democrats. Findings showed that while the CRNC advertisements did significantly decrease Democratic favorability, there was no significant change among Republicans. Additionally, the results showed that the ads produced no change in voting behavior toward Democrats but significantly changed voting behaviors away from the Republican Party. The implications of these findings are analyzed and discussed

Insights into the Genetic Architecture Underlying Plasma Lipids and Related Phenotypes from Genome-wide Human Genetic Variation.

Complex traits are multifactorial, often with risk contributions from numerous common and rare genetic mutations. The considerable challenges in understanding complex human phenotypes have prompted genome-wide association studies (GWAS), which generally compare large samples of unrelated individuals to test the relationship between genetic markers or nearby linked alleles and modulation of a trait or disease risk. Heritable levels of plasma lipids can influence heart disease risk, highlighting lipid-associated genetic variants as effective therapeutic targets. In collaboration with the Global Lipids Genetics Consortium, I present a follow-up study of approximately 100,000 individuals genotyped on a custom Metabochip array in the largest meta-analysis for lipids to-date. I report 62 novel genetic loci associated with lipids and present downstream bioinformatics analyses to support the role of these loci in lipid regulation. Many of the GWAS-identified lipid loci are non-protein-coding, suggesting a role in transcriptional regulation. This regulatory role can involve altering the DNA sequence at which proteins bind, ultimately affecting gene expression levels in particular cell types. I developed an open source tool called GREGOR (Genomic Regulatory Elements and Gwas Overlap AlgoRithm) to evaluate enrichment of GWAS variants in tissue-specific regulatory features defined by experimental approaches such as chromatin immunoprecipitation followed by high-throughput DNA sequencing (ChIP-seq). I report strong evidence for enrichment in DNase hypersensitive sites of biologically relevant tissues for 5 phenotypes including lipids, coronary artery disease, blood pressure, body mass index, and type 2 diabetes. In addition, I evaluate regulatory feature overlap of linked variants at a set of individual lipid-associated loci to predict the functionality of particular variants, and present experimental results to support my computational predictions. Lastly, I perform discovery and genotyping of structural variation (SV) from low-pass whole genome sequence data of 2,202 Norwegian cases with early-onset myocardial infarction (MI) and matched controls. I use complementary and established SV detection algorithms to call deletions, duplications, and inversions, and perform association analyses with MI disease risk and lipid levels. I observe a deletion in strong linkage disequilibrium with a known MI-associated single variant at the WDR12 locus, suggesting its plausibility as a functional variant at that locus.PhDBioinformaticsUniversity of Michigan, Horace H. Rackham School of Graduate Studieshttp://deepblue.lib.umich.edu/bitstream/2027.42/120821/1/schellen_1.pd

Analysis of parasite-specific T cells and cellular interactions in the spleen during <em>Plasmodium berghei</em> induced experimental cerebral malaria

Vector-transmitted parasitic infections are a global health problem. Diseases such as malaria are a major health threat and economic burden for developing countries. In Sub-Saharan Africa malaria causing Plasmodium parasites may evoke life threatening complications, which mainly affect children under the age of five years. Pathogenesis of cerebral malaria is a multifactorial complex process that involves inflammatory mediators such as effector T cells and IFN-γ. Time, origin and cellular and molecular factors involved in early immune responses priming effector T cells responsible for the pathogenesis of cerebral malaria have been less investigated. In our study we were able to determine the presence of parasite specific cytotoxic T cells in spleen and brain during Plasmodium berghei infection. This enabled us to analyse cellular interactions involved in the priming of T cells directed against the parasite. The place of essential T cell priming during Plasmodium infections was determined in splenectomised mice, in which effector responses were reduced and experimental cerebral malaria (ECM) pathology was absent. Depletion of antigen- presenting cells, involved in maintaining the organized splenic structure, abrogated T cell priming and resulted in the loss of effector responses. Without either macrophages, DCs or B cells lytic activity and IFN-γ production by parasite-specific T cells was diminished and in the absence of effector responses ECM progression was suppressed. In detail, we provide evidence that macrophages, B cells and dendritic cells, as well as CD4+ T cells together with TLR-9 and IL-12 signalling comprise complex interactions affecting T cell generation during blood stage malaria leading to neuropathology. Taken together our study suggests, that early immune responses during P. berghei infection are generated in the spleen and that distinct cells and cytokines drive gen-eration of parasite-specific T cells leading to subsequent pathology.Durch Vektoren übertragene Parasiteninfektionen stellen weltweit eine große Herausforderung dar. Krankheiten, wie z.B. Malaria bergen große gesundheitliche, aber auch ökonomische Risiken. Malaria, ausgelöst durch eine Plasmodium- Infektion, ist eine schwerwiegende Krankheit mit zum Teil lebensgefährlichen Komplikationen, die insbesondere Kinder unter fünf Jahren betreffen. Die Pathogenese von zerebraler Malaria ist ein multifaktorieller und komplexer Entzündungsprozess, bei dem Effektor T-Zellen und IFN-γ eine wichtige Rolle spielen. Obwohl T-Zellen stark in die Entwicklung zerebraler Malaria involviert sind, ist über Ursprung, zeitliche Abfolge und zelluläre und molekulare Prozesse der frühen Immunantwort, die für die Aktivierung von Effektor T-Zellen verantwortlich sind, bisher wenig bekannt. Wir konnten die Existenz von Parasiten-spezifischen zytotoxischen T-zellen in der Milz und im Gehirn während einer Plasmodium berghei ANKA Infektion in einem Mausmodell nachweisen. Das Entfernen der Milz ging mit einem reduziertem Risiko der zerebrale Malaria und einer verminderten Entzündungsreaktion einher. Dies zeigte, dass Effektor T-Zellen in der Milz generiert werden. Durch die Depletion Antigen-präsentierender Zellen, welche strukturgebend für die Milzarchitektur sind, wurde die Generierung und Aktivierung von Effektor T- Zellen verhindert und inflammatorische Reaktionen unterbunden. In Abwesenheit von Makrophagen, dendritischen Zellen, oder B-Zellen war die zytotoxische Aktivität und die INF-γ Antwort reduziert und neuropathologische Symptome blieben aus. Dies deutet darauf hin, dass komplexe Interaktionen von Makrophagen, B- Zellen, und dendritische Zellen, sowie CD4+ T Helfer Zellen zusammen mit TLR-9 und IL-12 Signalwegen, die T-Zell-Generierung in einer Plasmodium-Infektion und somit die Pathogenese von zerebraler Malaria stark beeinflussen. Zusammengefasst liefert dieses Projekt Hinweise dafür, dass die frühe Immunantwort gegen den Parasiten in der Milz hervorgerufen wird, wobei spezifisch Immunzellen und Zytokine an der Bildung von Effektor T-Zellen beteiligt sind, welche wiederum zu der Entstehung von neurologischen Schäden führen

Prospectus, April 4, 2007

https://spark.parkland.edu/prospectus_2007/1027/thumbnail.jp

Prospectus, April 11, 2007

https://spark.parkland.edu/prospectus_2007/1009/thumbnail.jp

Charge Transfer Parameters of Nix_{x}Mny_{y}Co1−x−y_{1-x-y} Cathodes Evaluated by a Transmission Line Modeling Approach

The performance of lithium‐ion batteries can be analyzed and improved by appropriate electrochemical models. A challenging yet crucial part is the parameterization of these models. Until now, the literature has incompletely investigated and cited the charge transfer process parameters describing the lithium transfer between the active material particles in the electrode and the liquid electrolyte. Herein, a novel approach is presented for obtaining these charge transfer parameters. The well‐established experimental methods of electrochemical impedance spectroscopy and focused ion beam tomography are applied. By introducing both experimental results into a transmission line model, a reliable determination of the charge transfer parameters j$_{0}$, k, and r$_{CT}$ can be achieved. The new approach is validated by comparing the results of four cathodes, all containing the state‐of‐the‐art active material Ni$_{x}$Mn$_{y}$Co$_{1-x-y}$ (NMC), but with different microstructures and/or stoichiometries

Changes in benthic ecosystems and ocean circulation in the Southeast Atlantic across Eocene Thermal Maximum 2

Eocene Thermal Maximum 2 (ETM2) occurred -1.8 Myr after the Paleocene-Eocene Thermal Maximum (PETM) and, like the PETM, was characterized by a negative carbon isotope excursion and warming. We combined benthic foraminiferal and sedimentological records for Southeast Atlantic Sites 1263 (1500 m paleodepth) and 1262 (3600 m paleodepth) to show that benthic foraminiferal diversity and accumulation rates declined more precipitously and severely at the shallower site during peak ETM2. As the sites are in close proximity, differences in surface productivity cannot have caused this differential effect. Instead, we infer that changes in ocean circulation across ETM2 may have produced more pronounced warming at intermediate depths (Site 1263). The effects of warming include increased metabolic rates, a decrease in effective food supply and increased deoxygenation, thus potentially explaining the more severe benthic impacts at Site 1263. In response, bioturbation may have decreased more at Site 1263 than at Site 1262, differentially affecting bulk carbonate records. We use a sediment-enabled Earth system model to test whether a reduction in bioturbation and/or the likely reduced carbonate saturation of more poorly ventilated waters can explain the more extreme excursion in bulk δ C and sharper transition in wt % CaCO at Site 1263. We find that both enhanced acidification and reduced bioturbation during the ETM2 peak are needed to account for the observed features. Our combined ecological and modeling analysis illustrates the potential role of ocean circulation changes in amplifying local environmental changes and driving temporary, but drastic, loss of benthic biodiversity and abundance. 13

Prospectus, May 30, 2007

https://spark.parkland.edu/prospectus_2007/1013/thumbnail.jp

Prospectus, February 7, 2007

https://spark.parkland.edu/prospectus_2007/1003/thumbnail.jp