Michael D. Goodman, MD

Professor, Department of Surgery

Our lab is focused on the systemic responses to injury, and more specifically, traumatic brain injury. The primary theme of this line of research focuses on the effects of brain injury on coagulation and inflammation and examines the interaction of these two responses. A secondary theme of this work, done in collaboration with the United States Air Force, focuses on the response to hypobaric and hypoxic environments following traumatic brain injury and polytrauma. To this end, we have established models of traumatic brain injury, hemorrhagic shock, and tissue injury to further examine the physiologic responses to secondary insults following primary injuries. Additional laboratory projects are examining the roles of platelet activation and platelet-derived microvesicles after traumatic injuries, including hemorrhagic shock, traumatic brain injury, splenectomy, and a combination of these injuries, which are established in both basic science and translational models.

Alex B. Lentsch, PhD

Professor, Department of Surgery

Our laboratory studies molecular and cellular mechanisms of local and systemic inflammation induced by organ ischemia/reperfusion. Our work in this regard has evolved over the past 20 years, during which we have made several seminal contributions towards our understanding of the induction, propagation, and resolution of the acute inflammatory response to hepatic ischemia/reperfusion. We are currently investigating the divergent roles of CXC chemokines in regulating the recovery and regeneration of damaged liver parenchyma after ischemic insult. Most recently we have found that hepatocytes release exosomes that have proliferative effects during the process of tissue repair. Moreover, the release of these exosomes is regulated by the CXC chemokine receptors, CXCR1 and CXCR2, in a manner completely independent from their known function as chemoattractant receptors. I have also been intimately involved in other trauma-related research labs related to this training program in order to help provide our trainees the best research experience possible.

Amy T. Makley, MD

Associate Professor, Department of Surgery

Our research focuses on understanding the roles of sphingosine-1-phosphate (S1P) and its receptor, S1P receptor 1 (S1PR1) in endothelial barrier function after massive transfusion for hemorrhage. We have identified a loss of endothelial barrier function as a contributor to acute lung injury resulting from hemorrhage and resuscitation and preliminary evidence from our laboratory shows that the transfusion of aged pRBCs causes endothelial cell dysfunction in association with alterations in the S1P / S1PR1 signaling pathway. The goals of our research are to determine the mechanisms by which the S1P / S1PR1 system regulates endothelial cell function and integrity, and elucidate the manner in which this system is altered by exposure to pRBCs following transfusion for hemorrhagic shock. To achieve our goals, we have established models of polytrauma and hemorrhagic shock in simulated and in vitro models to study endothelial cell barrier function.

Timothy A. Pritts, MD, PhD

Professor, Department of Surgery

Our research seeks to advance care for injured and critically ill patients, with a focus on resuscitation strategies and blood product improvement, and care for the wounded warfighter. We study the impact of different resuscitation strategies on the inflammatory, endothelial, and coagulation response to hemorrhagic shock. We have found that the ideal resuscitation fluid is a one to one ratio of packed red blood cells to fresh frozen plasma. Recent efforts have examined the red blood cell storage lesion in packed red blood cells and whole blood. This lesion is a series of biochemical and physical changes in erythrocytes that leads to degradation of the quality of the blood and harm to the recipient. Our goal is to maximize the quality of erythrocytes transfused during resuscitation. Additional work focusses on the special needs of the injured warfighter. Through our partnership with the US military, we have worked together to advance our understanding of how to provide optimal care in austere and challenging environments, especially in the far-forward critical care transport setting.

Basilia Zingarelli, MD, PhD

Professor, Department of Pediatrics, Critical Care Medicine, CCHMC

The Zingarelli Laboratory is focused on the investigation of the pathophysiologic mechanisms of sepsis, trauma and hemorrhagic shock, which are leading causes of morbidity and mortality in intensive care units. A particular goal of her research has been to define the mechanisms of metabolic recovery and innate immune responses mediated by the nuclear hormone receptors peroxisome proliferator activated receptors (PPARs) and by the AMP activated protein kinase (AMPK), which are major regulators of the glucose and lipid metabolism. In dissecting the dysmetabolic mechanisms of organ injury, the Zingarelli laboratory has discovered that key molecules of the mitochondrial retrograde signaling, such as humanin, may contribute to the regulation of metabolic recovery of damaged organs. Research efforts also focus on understanding the role of aging on the clinical course of infections, severe hemorrhage and trauma. The laboratory employs a multidisciplinary approach combining in vivo and in vitro experimental models in genetically modified rodents and cell lines. These models are also utilized as a translational research platform to screen novel pharmacological compounds that can modulate the molecular mechanisms of organ function. The goal is to identify specific therapeutic interventions for pediatric, adult and elderly patients.

Jonathan Beyeler, MD

General Surgery Resident

Goodman Lab – Dr. Beyeler is studying coagulation response to traumatic brain injury. 

Catherine Kapcar, DO

Clinical Fellow, Critical Care Medicine, Cincinnati Children’s Hospital

Zingarelli Lab – We focus on sepsis-associated myocardial dysfunction (SAMD) - a major contributor to pediatric septic shock morbidity and mortality. My project, titled Mechanisms of Circulating Myocardial Depressants in Human iPSC-Cardiomyocytes, focuses on advancing our understanding of the pathophysiological mechanisms underlying myocardial depression in septic shock and explores potential therapeutic targets to improve outcomes of patients with SAMD.

Darren Turner, MD

General Surgery Resident

Morales Lab – The subject of Dr. Turner’s research involves large animal studies which look at the systemic effects of cardiac pulmonary bypass.  Moving forward, he is researching the outcomes of using para oriole, pulsatile flow, ventricular system devices versus perioral, continuous flow ventricular system devices as a bridge to heart transplant in pediatric patients.

Gregory Wetmore, MD

General Surgery Resident

Goodman and Pritts Labs – Dr. Wetmore is looking at UCHL1 as a novel marker of hemorrhagic shock.  He is also looking into the direct role of red blood cells in the contribution to clot formation.