Mayer-Rokitansky-Küster-Hauser (MRKH) is a rare Disorder of Sexual Development (DSD) that results in the lack of a uterus and vagina in women. Receiving this diagnosis during adolescence can cause various forms of psychological distress in patients and families.<br/>Specifically, this condition could affect a women’s gender identity, body image, romantic relationships, family relationships, and psychological wellbeing. Parents are also put in a stressful<br/>position as they now have to navigate the healthcare system, disclosure, and the relationship with their child. This study aims to expand the knowledge of psychosocial adjustment by studying body<br/>image, gender identity, and mental health in individuals living with MRKH as well as parental disclosure, parental support systems, and parental perceptions of their child’s mental health.

The goal of this project was to design and create a genetic construct that would allow for <br/>tumor growth to be induced in the center of the wing imaginal disc of Drosophila larvae, the <br/>R85E08 domain, using a heat shock. The resulting transgene would be combined with other <br/>transgenes in a single fly that would allow for simultaneous expression of the oncogene and, in <br/>the surrounding cells, other genes of interest. This system would help establish Drosophila as a <br/>more versatile and reliable model organism for cancer research. Furthermore, pilot studies were <br/>performed, using elements of the final proposed system, to determine if tumor growth is possible <br/>in the center of the disc, which oncogene produces the best results, and if oncogene expression <br/>induced later in development causes tumor growth. Three different candidate genes were <br/>investigated: RasV12, PvrACT, and Avli.

Early life exposures play a significant role in shaping health and disease susceptibility. Maternal obesity influences the offspring’s long-term risk of colorectal cancer, yet the understanding of the impact on developmental programming of intestinal stem cells and later risk of colorectal cancer remains limited. This has highlighted the growing need for a model that studies the influence of the maternal environment on the developing colon. The goal is to optimize a platform that generates human colon organoids (hCOs) from embryonic stem cells (hESCs) reliably and reproducibly and use it as a model to study colonic developmental patterning in an obesogenic environment. The organoids are derived by multi-step directed differentiation trajectory of embryonic stem cells, definitive endoderm, mid/hind gut, to fetal colon. The protocol was optimized to ensure consistent production of colonic organoids in contrast to small intestinal or urothelial cells which follow similar differentiation paths. To model an obesogenic environment on the platform, both the intrinsic and extrinsic properties of the developing colon were leveraged: 1) pharmacologically activating the transcription factor Peroxisome Proliferator-Activated Receptors Delta (PPARd) to mimic the cell-autonomous response to a pro-obesity maternal high fat diet, and 2) exposing the developing colon organoids to pro-inflammatory cytokine IL-17a to mimic the pre-pathological inflammatory state. The hESC-to-HCO model demonstrates the utility of ESC-derived organoids in studying the impact of maternal environmental factors on colonic development, generating a platform to explore factors that affect human development and maturation.