Diverticulitis is a common gastrointestinal condition in both the United States and Europe. Approximately 200,000 people are hospitalized for cases of diverticulitis in the United States alone on a yearly basis. When small pouches called diverticula develop along the sigmoid colon, the lower part of the colon, this initial condition is known as diverticulosis. Diverticulosis turns into diverticulitis when these diverticula, located in the left lower quadrant (LLQ) of the abdomen, become inflamed usually due to a bacterial infection. A common symptom of diverticulitis is when patients generally have LLQ pain sustained over a period of time. We, the Surgical Outcomes Research Center (SORCE), are conducting the Diverticulitis Evaluation of Patient Burden, Utilization, and Trajectory (DEBUT) study to investigate the impact of diverticulitis treatment options on patients and to improve the understanding about how physicians and patients decide to have elective surgery for diverticulitis. Currently, the optimal timing for elective (non-emergency) colectomy surgery to treat diverticulitis is unclear, and diverticulitis affects individuals in many different ways. Through our patient-centered research approach in DEBUT, we hope to determine the impact of treatment decisions on a patient's quality of life, work, and clinical symptoms. These patient-reported outcomes are measured over time among patients who do and do not undergo elective colectomy surgery to treat diverticulitis. Our goals are to better understand how physicians and patients decide to undergo elective colectomy surgery to treat diverticulitis as well as provide higher quality evidence that can help patients and their physicians to make better-informed decisions about the timing of surgery for diverticulitis. Results gained from this study may eventually help inform current medical recommendations for diverticulitis treatment and give current healthcare professionals the tools necessary to develop more effective guidelines for treating patients with diverticulitis.

Abnormalities in TGF-ß signaling are thought to cause aortic aneurysms and dissection in people with inherited syndromic illnesses such as Marfan's and Loeys-Dietz Syndrome. However, the mechanisms linking changes in TGF-ß signaling to aortic disease evolution are poorly understood. We developed a mouse model in which the type II TGF-ß receptor was deleted to characterize and study the effects of this perturbation in TGF-ß signaling. My research focused specifically on characterizing any histologic changes in the aorta in 7-8 week old mice, 1 week after deleting the TGF-ß receptor. To quantify changes in aortic architecture, we employed methods such as H&E staining and fluorescence microscopy. Our results showed that the ascending aortas of the mice with the TGF-ß receptor knockout had significantly larger medial thickness and medial area, with p-values of 0.0001 and less than 0.0001, respectively. However, we did not find a significant difference in elastic breaks between the two experimental groups, although previous research has shown increased elastic breaks in aortas of mice with the TGF-ß receptor deletion when measured at a later point (14 weeks post-deletion). Together, these results suggest that there are subtle but significant aortic changes as early as one week following receptor deletion. This suggests that losing TGF-ß signaling causes early and immediate changes in the aortic smooth muscle cells and matrix proteins that are quantifiable by histology. More research is needed to understand the precise mechanisms behind why these changes occur and how they might be related to the development of aneurysms.