Lung Transplant Outcomes: Institutional Review
Principal Investigator: Scott B. Johnson, MD
Under this umbrella protocol, we are teasing out few of the factors that may affect the outcomes after a lung transplant through a retrospective chart review.
Outcomes after re-do lung transplants
Contributors: Scott B. Johnson, MD, Daniel T. DeArmond MD, Nitin A Das, Charles Huynh MS-3, JinWen Sui MS-4
The purpose of this retrospective chart review is to evaluate the outcomes after second lung transplants in terms of survival, complications and incidence of rejections. This is an important question as it impacts judicious utilization of valuable resources.
VATS vs. open lobectomy: comparison of outcomes in high adoption rate hospitals
Contributors: Daniel T. DeArmond, MD, Nitin A. Das, Stewart R. Miller PhD, Sajed Mohammed PhD
Summary: This study utilizes the Texas Discharge Database to evaluate factors that affect outcomes after VATS (minimally invasive) lobectomy as compared to Open (thoracotomy) in terms of major morbidity and in-hospital mortality.
Interleukin – 18 in Left Ventricular Hypertrophy, Aortic Aneurysms and Heart Transplants
Contributors: A. J. Carpenter, MD, PhD in collaboration with Bysani Chandrasekar, DVM. Ph.D (Columbia University, Missouri)
Dr. Carpenter is collaborating with Dr. Chandra to elucidate relationship between interleukin-18 and various cardiac morbidities. Past studies have shown increase in graft stenosis associated with high levels of IL-18 which was blocked by IL-18 binding proteins in rodents. Future studies are focusing on finding association between LVH, aortic aneurysms and cardiac remodeling.
TRAF3-IP2 in Chronic Hyperglycemia
Contributors: A. J. Carpenter, MD, PhD, Nitin A. Das, Bysani Chandrasekar, DVM. Ph.D (Columbia University, Missouri)
Summary: Chronic hyperglycemia increases TRAF3IP2 expression in all layers of the vessel wall, contributing to heightened inflammation, excessive accumulation of SMCs, and luminal occlusion. Our goal is to target increased TRAF3IP2 expression by either genetic or interventional approach to block chronic hyperglycemia-mediated injury-induced vascular inflammation, endothelial dysfunction, and intimal hyperplasia. If we are able to identify TRAF3IP2 as a master regulator of diabetes-induced neointima formation, we could develop inhibitors to target its expression and inhibit neointimal hyperplasia and extend the life of these CAB grafts.