<?xml version="1.0" encoding="UTF-8"?>
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<title>Honors College Theses</title>
<link href="http://hdl.handle.net/1957/8" rel="alternate"/>
<subtitle>The University Honors College requires a senior thesis for receipt of OSU’s most prestigious degree, the Honors Baccalaureate.</subtitle>
<id>http://hdl.handle.net/1957/8</id>
<updated>2013-06-19T17:13:56Z</updated>
<dc:date>2013-06-19T17:13:56Z</dc:date>
<entry>
<title>The effect of TCDD on cytokine production during the progression of insulitis in NOD mice</title>
<link href="http://hdl.handle.net/1957/39038" rel="alternate"/>
<author>
<name>Pham, Tuan</name>
</author>
<id>http://hdl.handle.net/1957/39038</id>
<updated>2013-06-07T21:42:21Z</updated>
<published>2013-06-07T00:00:00Z</published>
<summary type="text">The effect of TCDD on cytokine production during the progression of insulitis in NOD mice
Pham, Tuan
2,3,7,8-Tetrachlorodibenzo-p-dioxin (TCDD) is a potent immunosuppressant, and suppresses many disease models including graft-versus-host (GVH), experimental autoimmune encephalomyelitis (EAE) and a model of type 1 diabetes in non-obese diabetic (NOD) mice (1-3).  In this study, we show that the inflammation of the pancreas due to insulitis is not a systemic autoimmune response.  When treatment with TCDD was terminated at 15 weeks of age, the pro-inflammatory cytokines IFN-gamma and IL-17 were not detectable in serum.  Likewise, the tissue protective cytokine IL-22 was also not detectable in serum.   Taken together, this suggests that the autoimmune response due to insulitis is localized to the pancreas.
</summary>
<dc:date>2013-06-07T00:00:00Z</dc:date>
</entry>
<entry>
<title>Parasitic Worms: Their Role in Medicin[e] in Modern Europe</title>
<link href="http://hdl.handle.net/1957/39010" rel="alternate"/>
<author>
<name>Aronstein, Laurie E.</name>
</author>
<id>http://hdl.handle.net/1957/39010</id>
<updated>2013-06-06T20:30:23Z</updated>
<published>2013-06-06T00:00:00Z</published>
<summary type="text">Parasitic Worms: Their Role in Medicin[e] in Modern Europe
Aronstein, Laurie E.
Little is known about the role that worms played in the lives of modern Europeans.  This research strove to combine a multitude of primary sources to shape a cohesive depiction of the role of parasitic worms in modern Europe 1700-1800.  The Scientific Revolution played a key role in changing the face of science in the eighteenth century.  The microscope opened a new world of discovery, which natural philosophers took advantage of.  Several natural philosopher's works combined to quite the spontaneous generation controversy, although it was not completely laid to rest until Pasteur's experiments in 1862.  Eighteenth century physicians were able to shift their focus from the question of how worms arose in the human body to how they survived and recording the symptoms, treatments, and the demographic of individuals afflicted with worms.  Worms was for the majority a childhood disease, and as such, from journals and diaries one is able to piece together an oblique picture of how adults and children dealt with death.
</summary>
<dc:date>2013-06-06T00:00:00Z</dc:date>
</entry>
<entry>
<title>The Effects of Orbital Spaceflight on Bone Architecture in Ovariectomized Rats</title>
<link href="http://hdl.handle.net/1957/38980" rel="alternate"/>
<author>
<name>Almog, Roy</name>
</author>
<id>http://hdl.handle.net/1957/38980</id>
<updated>2013-06-05T17:19:24Z</updated>
<published>2013-06-05T00:00:00Z</published>
<summary type="text">The Effects of Orbital Spaceflight on Bone Architecture in Ovariectomized Rats
Almog, Roy
</summary>
<dc:date>2013-06-05T00:00:00Z</dc:date>
</entry>
<entry>
<title>Dissecting DNA Damage Responses in Arabidopsis: A High-Throughput Sequencing Approach</title>
<link href="http://hdl.handle.net/1957/38846" rel="alternate"/>
<author>
<name>Brar, Anantnoor K.</name>
</author>
<author>
<name>Wilcox, Buck W. L.</name>
</author>
<author>
<name>Curtis, Marc</name>
</author>
<author>
<name>Hays, John B.</name>
</author>
<id>http://hdl.handle.net/1957/38846</id>
<updated>2013-05-31T20:37:50Z</updated>
<published>2013-05-31T00:00:00Z</published>
<summary type="text">Dissecting DNA Damage Responses in Arabidopsis: A High-Throughput Sequencing Approach
Brar, Anantnoor K.; Wilcox, Buck W. L.; Curtis, Marc; Hays, John B.
Cells are constantly bombarded with mutagens, both endogenous and exogenous in origin. Endogenous sources of mutation include reactive oxygen species formed during aerobic respiration, replication errors by DNA polymerase, and spontaneous deamination and depurination (Jackson 2009). Exogenous sources of mutation include UV and ionizing radiation, aflatoxins, and polycyclic aromatic hydrocarbons (i.e. compounds found in diesel exhaust and cigarette smoke). As a result, thousands of DNA lesions are created every day. Lesions can stall and impede DNA transcription and replication if they are not removed by DNA repair mechanisms or bypassed by replication. Phosphoinositide 3-kinase (PI3-K) related protein kinases (PIKKs) regulate the DNA damage response in cells (Cimprich 2008). Commonly referred to as the “sentries to the gate of genome stability,” ataxia-telangiectasia mutated (ATM) and ATM and RAD3-related (ATR) promote signaling, cell cycle arrest, and DNA repair in the face of DNA damage. Arabidopsis thaliana plants lacking ATR, when irradiated with UVB, incur elevated stem cell death in growing root tips (Furukawa 2010). Programmed cell death (PCD) is an important protective mechanism that restores tissue homeostasis in stem cell niches and prevents the accumulation of irreparably damaged cells in tissues, albeit with a delay in growth. Without ATR to stabilize damaged replication forks, double strand breaks (DSBs) occur where there is persistent ssDNA, and ATM or ATR (partially redundant in this signaling capacity) initiate repair or PCD if DSBs accumulate. In plants lacking both ATR and ATM, UV-B irradiation results in less stem cell death than in wild type plants. In attempts to cross atr[superscript -/-] plants with an EMS-mutagenized line, we discovered a root terminating phenotype which appears to be dependent on ATR and an unknown gene (ursu). We are using Illumina high-throughput genome sequencing and bioinformatic techniques to map the location of this additional gene.
</summary>
<dc:date>2013-05-31T00:00:00Z</dc:date>
</entry>
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