Our Research Laboratories
The Cooney Lab (Sepsis and Nutrition)
Dr Cooney’s research program is focused on several areas in surgical metabolism including: anabolic failure after injury or infection, mechanisms of diabetes resolution after bariatric surgery and more recently the regulation of intestinal inflammation.
- Anabolic Failure: The metabolic response to injury and infection results in the reprioritization of protein metabolism and loss of muscle mass. The development of “Growth Hormone Resistance” is a major cause of anabolic failure. Dr. Cooney’ laboratory lead a NIH funded research program examining the molecular mechanisms of hepatic GH resistance for the last 16 years.
- Resolution of Diabetes: Dr Cooney’s laboratory has used a combination of animal models, cell culture studies and translational studies in morbidly obese patients having gastric bypass surgery to improve our understanding of how bariatric surgery procedures improve insulin sensitivity and diabetes before significant weight loss occurs. Ongoing studies include proteomic analysis of pre- and post-RYGB patients, animals studies of intestinal glucose transport and L cell function.
- Regulation of Intestinal Inflammation: Several clinically important conditions including necrotizing enterocolitis (NEC) and inflammatory bowel disease (IBD) result in potentially life threatening intestinal inflammation. Our laboratory is working to understand the mechanisms by which short chain fatty acids (SCFAs) and other potential mediators cause inflammation of the intestinal epithelium. In addition, we are working to understand how diet, specific nutrients and other factors can be used to attenuate and potentially treat intestinal inflammation.
The Gahtan Lab (Vascular Surgery)
The Vascular Surgery Reseach Laboratory dominantly studies the role of thrombospondin-1 (TSP-1) in peripheral arterial disease and the process of intimal hyperplasia. TSP-1, a matricellular glycoprotein that was first discovered during the 1970s, is released by platelets during the formation of a hemostatic plug. In addition, macrophages, monocytes, fibroblasts, vascular smooth muscle cells, tumor cells, and endothelial cells also secrete or their function is modulated by TSP-1. The lab mostly focuses on the effects of thrombospondin-1 on vascular smooth muscle cells in vitro and the effects of TSP-1 in vivo on intimal hyperplasia. The laboratory mostly studies intracellular signaling cascade regulated by TSP-1, the role of statin drugs on TSP-1 inducible IH and vascular smooth muscle cell migration. Collaborations with the Syracuse Biomaterials Institute are also ongoing. The lab has a PhD faculty on site, an experienced senior laboratory technician, and postdoctoral fellows. The lab is currently funded through a VA Merit Award. Clinical research interests include clinical and functional outcomes after vascular reconstruction, noninvasive vascular imaging, and surveillance techniques and protocols.
The Nieman Lab (Cardiopulmonary and Critical Care)
The Cardiopulmonary and Critical Care Laboratory has a research focus on the pathogenesis and treatment of the acute respiratory distress syndrome (ARDS), ventilator induced lung injury (VILI) and multiple organ dysfunction syndrome (MODS). There are four main areas of research:
- understanding the pathogenesis of systemic inflammation as it relates to the development of ARDS
- investigating the role played by toxic ascites in propagating systemic inflammation and multiple organ dysfunction syndrome (MODS)
- determining the impact of mechanical ventilation, in the form of ventilator induced lung injury (VILI), in ARDS pathogenesis
- using this knowledge in discovering methods to prevent the development of ARDS by preemptive application of direct peritoneal resuscitation and protective mechanical ventilation
The Wang Lab (Surfactant Biology)
Dr Wang's Laboratory focuses on the physiology of surfactant proteins and their role in pathophysiology using both animal disease models (sepsis, bacterial pneumonia and urinary tract infection) and human patients.
Surfactant proteins A and D (SP-A and SP-D) are members of C-type lectin family, which play a critical role in host defense, inflammation and lung homeostasis. Surfactant protein B (SP-B) is a key component of pulmonary surfactant and is essential for normal lung function. To explore the cellular and molecular mechanisms of surfactant proteins in the variety of pulmonary diseases we have generated humanized transgenic mice which carry genetic variant of human surfactant protein gene, then these humanized transgenic mice as well as gene deficient (knockout) mice are used in our work. In another project, we investigate the role of intronic cis-acting elements and trans-acting factors on RNA splicing of surfactant proteins in lung development and diseases.