Humanities (HIST Group Presentation)

 

Moderator: Jama Grove

New Directions in Historiography
Cambry Bates, Christine Goodman, Wendy Jimenez, Brenlyee Meaux, and Mallory Stout
Research Advisor: Dr. Jama Grove, Department of History

“New Directions in Historiography” will explore a diverse range of topics, each of which has been subjected to extensive historical and scholarly analysis. Panel participants will provide an overview of the available historical literature on each topic, analyze the assumptions embedded within that scholarship, and argue for the need for re-interpretation from a fresh perspective. In each instance, presenters will propose a fresh route for research and analysis that can enlarge or deepen our understanding of historical topics. Although the topics under discussion are wide-ranging, each presenter aims to dispel myths within existing historical depictions, separate myth from reality, and empower people who have been wrongly portrayed in existing scholarship.

Cambry Bates will question our contemporary use of “witch hunt” as shorthand for irrational persecution by examining the Salem Witch Trials with attention to the legal and judicial frameworks through which people sought to bring witches to justice. Christine Goodman will examine the ways that insurrection against the United States became legitimized and perpetuated by notions that groups such as the United Daughters of the Confederacy infused into the American understanding of the US Civil War. Wendy Jimenez analyzes the Divine Feminine through the figure of Malintzin to reveal how Mexican people transform this national symbol according to their own race, class, and gender in ways that support or subvert patriarchal notions of machismo. Mallory Stout draws out the ways that eugenics is often associated with Nazi Germany, while the ideology originated in US scholarship and continued to shape American culture and practice, although these practices were often stripped of the label, long after the pseudo-scientific field of eugenics was discredited on the international stage. Brenlyee Meaux will analyze the deficiencies in existing scholarship of sex work in Storyville, New Orleans, and how the rise in female scholars, and particularly women of color, in the past decades have incorporated a more complex understanding of the intersection of race, gender, and power in sex work.

 

Posters

Moderator: Scott Chirhart

An Improved Estimation Method under Restricted Parameter Space

Kedran Young
Research Advisor: Dr. Yeil Kwon, Department of Mathematics, University of Central Arkansas

In a binomial model, the sample proportion \hat p= x/n, where x stands for the number of successes out of n trials with the dichotomous outcomes (success/failure), is considered one of the best estimators for p (a true success probability). The sample proportion has many desirable properties such as unbiasedness, minimum variance, and convergence to true probability p when the sample size n goes to infinity. However, when we estimate p for infrequent events, the sample proportion might not be the best since the sample proportion is the optimized estimator under the parameter space 0<p<1. In particular, the sample proportion tends to be inaccurate with a small sample. If we focus on a parameter space appropriately restricted for infrequent events, we may find an improved estimator for p.

In this research, an alternative estimation method for p is proposed under the parameter space restriction for infrequent events. The proposed estimator may be regarded as a generalized form of the Laplace estimator for p. By estimating the additional parameters, the proposed estimator can be expected to achieve a meaningful improvement. The simulation study reveals that the proposed estimator is expected to have a smaller mean squared error (MSE) than the sample proportion, especially for the small sample. Furthermore, the proposed estimator is applied to Major League Baseball (MLB) data to predict the home run rate, demonstrating the proposed estimator's performance in estimating small values of p.

The Effect of Proton Radiation on α-Synuclein in Human Neuronal-like Cells

Cara Armstrong
Research Advisors: Drs. Lynn Harrison1, Kara Lind1, Xiaohong Lu2, Urska Cvek3, Matthew Maynard4, and Phong Huynh5

Department of Physiology1, Department of Pharmacology, Toxicology, and Neuroscience2, Department of Computer Science3, Louisiana State University Health Sciences Center, Willis Knighton Cancer Center Radiation Oncology4, and Xavier University5

Astronauts have exposure to low doses of high energy ionizing radiation in space, and NASA is concerned that exposure increases the risk of developing neurodegenerative disease. Parkinson’s disease (PD) is a neurodegenerative disease characterized by high levels of oxidative stress and aggregates of mutated/damaged alpha-synuclein (α-SYN) protein in brain cells. The SNCA gene encodes the α-SYN protein. The pathology of PD and the destruction of dopaminergic neurons are related to α-SYN aggregates. Oxidative stress influences the progression of PD by threatening the guanine nucleobase. When adenine is inserted instead of cytosine during DNA replication, mutations occur. Transcriptional mutagenesis is the production of mutant RNA transcripts due to RNA polymerase inserting the wrong ribonucleotide during transcription. Transcriptional mutagenesis could generate mutated α-SYN after radiation. The mutation may occur in replication or differentiated brain cells when RNA polymerase encounters oxidative DNA damage in the transcribed DNA strand.

The predominant type of radiation in galactic cosmic rays is proton radiation. Proteus One radiotherapy unit proton radiation simulated space radiation. Different proton dosages stimulated oxidative stress to test the correlation between aggregates of damaged α-SYN and oxidative stress. Neuroblastoma cell line (SHSY5Y) was differentiation into neuronal-like cells using retinoic acid. Replicating and differentiated cells were irradiated with 0, 0.5, and 2 Gy of protons. RNA was isolated at 1, 5, and 20 hours post-irradiation. Quantitative real-time PCR processed the transcript level of the SNCA gene and other genes that encode oxidative DNA repair proteins. Protein was isolated from irradiated cells to examine DNA repair and α-SYN protein levels. The SNCA DNA sequence was examined and found that positions in the sequence could produce mutant transcripts by transcriptional mutagenesis. The TANGO computer algorithm predicted an increase in the potential for α-SYN protein aggregation for some mutant proteins. Wild type or one mutant α-SYN protein vectors were created and transfected into SHSY5Y cells to induce aggregate formation.

The real-time PCR showed that the SNCA transcript increased two-fold between replicating and differentiated. There were no signs of increased expression with irradiation because there was a slight difference in SNCA transcript expression levels between 0.5 and 2gy.

Deprenyl induces synergistic developmental delay in C. elegans ced-9(gf) mutants

Payton Lii
Research Advisor: Dr. Katherine Weeks, Department of Chemistry

Deprenyl (Selegiline) is a monoamine oxidase B inhibitor used to treat Parkinson’s Disease by inhibiting the metabolism of the neurotransmitter dopamine. Deprenyl produces a neuroprotective effect in vitro by increasing the expression of the anti-apoptotic gene bcl2 in cultured mammalian neurons. Deprenyl also increases the lifespan of rats by an unknown mechanism. Here we characterize deprenyl-induced developmental delay in C. elegans, a novel effect of this compound, and begin to deduce its mechanism of action. The nematode BCL2 ortholog (CED-9) regulates developmental rates of C. elegans, and our lab identified CED-9 as a potential candidate for the deprenyl-induced developmental delay that we observed. Populations of wild type (N2) and ced-9 gain of function (gf) C. elegans were synchronized to the same age and exposed to either vehicle (water) or 1.0 mM deprenyl. Developmental rates and lifespan of the organisms in each condition were scored. The deprenyl and ced-9(gf) combination have a synergistic effect on developmental delay with no apparent change in average lifespan, suggesting that deprenyl treatment either further increases CED-9 activity in the ced-9(gf) mutant or works independently of CED-9 activity to delay C. elegans development.