Trishla
Mehta
Sponsor: Raul Aranovich, Ph.D. Linguistics Chinook Jargon, the trade language used by Indigenous tribes in the Pacific Northwest, both before and after contact with European fur traders, lacks a deep analysis of its usage pre- contact. Past research has delved into proving Chinook Jargon was used pre-contact, with current research focusing on proving the contributions of specific language families in the Pacific Northwest. In attempting to study the usage of terms from the Salish language family, it was found that primary records of Chinook Jargon may conflict with each other regarding the words in a fluent speaker's lexicon. For example, where one dictionary uses a Salish-origin term for "grandmother", one record of storytelling texts uses a different, unsourced form for "grandmother". These texts comprise some of the first documentations of Chinook Jargon, and the last records prior to the extinction of a list of Indigenous languages. Research is now comparing a larger set of data to understand the source of these inconsistencies, and identify potential dialectical forms of Chinook Jargon. Etymological analysis provides insight on language formation, phonological shifts, and prevents the academic homogenization of Indigenous cultures. CTCF as a Mediator of TET1-Dependent Gene Regulation in Airway Epithelial Cells
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Trishla Mehta
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Asthma is a chronic inflammatory airway disease that is exacerbated by environmental allergens and pollutants such as diesel exhaust particles (DEP) and house dust mite (HDM). Epigenetic regulation plays a critical role in shaping airway immune responses, yet the mechanisms underlying these effects remain incompletely understood. TET1, a DNA-modifying enzyme with both enzymatic and non-enzymatic functions, has been shown to protect against allergen- and pollutant-induced lung inflammation. Prior studies in mouse models and human bronchial epithelial cells (HBECs) demonstrate that loss of TET1 results in increased airway inflammation, altered chromatin accessibility, and dysregulated expression of inflammatory cytokines and antioxidant genes. Notably, TET1-dependent chromatin changes overlap with predicted CTCF binding sites, a key regulator of three-dimensional chromatin organization, suggesting a functional interaction. In this project, I propose to test the hypothesis that TET1 regulates inflammatory and antioxidant gene expression through modulation of CTCF binding in airway epithelial cells. Using siRNA-mediated knockdown of CTCF in HBECs followed by DEP or HDM exposure, I will assess changes in gene and protein expression and compare these results to existing TET1 knockdown datasets. This work aims to identify a novel epigenomic mechanism contributing to airway inflammation and asthma. Gender and Acculturation: The Influence on Mexican Heritage Mother-Infant Interaction Nadya Mejia
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UC Davis / VM: Anat Physio & Cell Biology / 2026
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Trishla Mehta