The PIN/PEN Merger

The Sound Change Across Kansas: PEN/PIN Merger Isaiah Solorzano, Mary Kohn Department of English College of Arts & Sciences Mergers, a sound change that present themselves in the background of everyday conversations, usually going unnoticed and uninterrupted across speech communities. I am interested in the sound change of short vowels found in word pairs like pen-pin, shown to be changing [1]. In 2014, Strelluf suggested the low-back merger is present in Kansas City due, in part, to a large initial population of South Midland speakers. This study indicates the merger should be advancing [1]. We do not understand, entirely, how or why sound changes. The merged vowel sound /i/ is starting to occupy the space the vowel sound /ɛ/ occupies. This project builds on Strelluf’s insights of sound change, in Kansas City, by 1) empirically exploring data to detect changes in Kansas, and 2) framing issues in a broader sense to understand how this dialect has arose, using a structural and social explanation. The data comes from sociolinguistic interviews which are recorded informal conversations between the researcher and participants. The independent variables include gender, age, class, and ethnic group. The dependent variables include formant frequencies F1 and F2, stress, duration, and other linguistic variables. We use a sample population of 30 subjects. The data has been measured with Forced Alignment and Vowel Extraction (FAVE), an automatic extraction technique [1][2]. I predict that men and the working class are leaders of this change, coinciding with Strelluf, but going against standard hypothesis over mergers in the field today. Strelluf, C. (2014). We have such a normal, non-accented voice: a sociophonetic study of English in Kansas City(Doctoral dissertation, University of Missouri--Columbia). Severance, N., Evanini, K., & Dinkin, A. (2016). Examining the reliability of automated vowel analyses using FAVE. In NorthWest Phonetics & Phonology Conference (pp. 13-15)

Cervical Cancer Development: Implications of HPV16 E6E7-NFX1-123 Regulated Genes

High-risk human papillomavirus (HR HPV) causes nearly all cervical cancers, half of which are due to HPV type 16 (HPV16). HPV16 oncoprotein E6 (16E6) binds to NFX1-123, and dysregulates gene expression, but their clinical implications are unknown. Additionally, HPV16 E7’s role has not been studied in concert with NFX1-123 and 16E6. HR HPVs express both oncogenes, and transformation requires their expression, so we sought to investigate the effect of E7 on gene expression. This study’s goal was to define gene expression profiles across cervical precancer and cancer stages, identify genes correlating with disease progression, assess patient survival, and validate findings in cell models. We analyzed NCBI GEO datasets containing transcriptomic data linked with cervical cancer stage and utilized LASSO analysis to identify cancer-driving genes. Keratinocytes expressing 16E6 and 16E7 (16E6E7) and exogenous NFX1-123 were tested for LASSO-identified gene expression. Ten out of nineteen genes correlated with disease progression, including CEBPD, NOTCH1, and KRT16, and affected survival. 16E6E7 in keratinocytes increased CEBPD, KRT16, and SLPI, and decreased NOTCH1. Exogenous NFX1-123 in 16E6E7 keratinocytes resulted in significantly increased CEBPD and NOTCH1, and reduced SLPI. This work demonstrates the clinical relevance of CEBPD, NOTCH1, KRT16, and SLPI, and shows the regulatory effects of 16E6E7 and NFX1-123