Today is Saturday, Aug. 15, 2020

Department of



Research Faculty

Charles Caldwell, PhDCharles C. Caldwell, PhD
Professor, Department of Surgery 

The goal of our lab is to manipulate the immune response to sepsis in a manner that reduces tissue injury and mortality.  A key aspect of the high mortality associated with sepsis is the inappropriate immune response to the systemic infection.  The process of inflammation is instrumental to an organism’s response to invading microorganisms or repair of damaged tissues.  This process is initiated by components of the innate immune system and is tempered by a number of regulatory mechanisms.  If this hyper-inflammatory process is prolonged and/or exaggerated, significant inflammatory tissue and organ damage may ensue.  In contrast, suppression of the immune response prior to complete pathogen eradication can lead to bacterial overgrowth and organ failure. Our lab has three interlocking research interests: 1) elucidation of underlying mechanisms that mediate inflammation during sepsis, 2) determination of the septic patients' immune status, and 3) intervention with molecular analogs to alter the immune response.  Specifically, during sepsis, we are currently investigating 1) the role of T cells and neutrophil-derived microparticles and 2) the use of flow cytometry to determine patient immune status in a time-constrained environment.

Michael J. Edwards, MD

Michael J. Edwards, MD
Professor, Department of Surgery

Dr. Edwards is responsible for the professional development of all trainees in the department of surgery.

Michael D. Goodman, MD

Michael D. Goodman, MD
Associate Professor, Department of Surgery

Our lab is focused on the physiologic response to 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 murine and porcine 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 platelets and platelet-derived microparticles after traumatic injuries, including hemorrhagic shock, traumatic brain injury, and burns.

Erich Gulbins, MD, PhDErich Gulbins, MD, PhD
Chair, Department of Molecular Biology, University of Duisburg-Essen
Professor, Department of Surgery, University of Cincinnati

My laboratory studies the role of the acid sphingomyelinase/ceramide system in biomedicine. Currently, my lab is investigating the function of the acid sphingomyelinase/ceramide/acid ceramidase/sphingosine system in bacterial infections, tumor biology and cellular stress responses. In particular, we investigate the role of the acid sphingomyelinase, ceramide, acid ceramidase and sphingosine in pulmonary and systemic infections with Pseudomonas aeruginosa, Staphylococcus aureus and Mycobacteria (BCG). Mechanistic insights are applied to cystic fibrosis, ventilation-associated pneumonia and bacterial sepsis. Novel strategies to prevent these illnesses or treatments options are actively developed. Many cellular signalling events that are activated in response to bacterial pathogens are also involved in the response of the microenvironment to a malignant tumor. The group therefore studies the role of the acid sphingomyelinase/ceramide/acid ceramidase system in cells of the microenvironment of malignant tumors for their growth and treatment response. Finally, we are interested in understanding the role of sphingolipids in cellular stress responses. We study the signalling events initiated in mammalian cells by various forms of stress and applies these basic studies to the regulation of cell death.

Dr. Michael HelmrathMichael A. Helmrath, MD, FACS
Professor of Surgery
Richard and Geralyn Azizkhan Chair of Pediatric Surgery
Director of Surgical Research
Surgical Director, Intestinal Rehabilitation Center

Our lab’s research focus is on developing strategies to improve the outcomes in children with intestinal failure. Understanding the biology of intestinal stem cells is a key to unravel the mechanism involved during the disease process. To that end, our team developed in vitro culture techniques to maintain and expand individual human intestinal stem cell derived from human tissue samples and pluripotent stem cells as well as surgical animal models. As part of the Intestinal Stem Cell Consortium (ISCC, NIH), our lab is actively involved in the intestinal stem cell field. Our current projects include: (1) Modeling a human gut; (2) Regional patterning of intestinal stem cells; (3) Mechanisms of intestinal adaptation following ileo-cecal resection; (4) Nutritional approaches to enhance intestinal adaptation response; and (5) Intestinal failure program.

Alex B. Lentsch, PhDAlex 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, MDAmy 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 small and large animals as well as in vitro models to study endothelial cell barrier function.

Timothy A. Pritts, MD, PhDTimothy A. Pritts, MD, PhD
Professor of Surgery

Our laboratory studies the impact of different resuscitation strategies for 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.  This work has influenced resuscitation strategies for massive transfusion at our trauma center and in the United States military. Some of our most recent efforts have examined the red blood cell storage lesion in packed red blood cells.  This lesion is a series of biochemical and physical changes in erythrocytes that leads to degradation of the quality of the red blood cell unit and harm to the recipient.  Our goal is to maximize the quality of erythrocytes transfused during resuscitation.  Additional work has focused 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.  Aspects of this work include the effect of aged, as compared to fresh, blood components as well as hypotensive resuscitative strategies on the host response to hemorrhagic shock.

Dr. Shimul Shah

Shimul A. Shah, MD
Professor of Surgery and Chief of Solid Organ Transplantation

Our research laboratory, Cincinnati Research in Outcomes and Safety in Surgery (CROSS), is a multidisciplinary group focused on health services research that has grown to include over six surgical faculty and a research team of over twenty residents and students. We have focused on the understanding and management of hospital care services such as pancreatic cancer care, colorectal surgery and liver transplantation and hepatobiliary surgery as it relates to surgical outcomes. Our group has investigated under-utilization and disparities in surgical and cancer care, and authored or co-authored nearly 60 publications since its inception in 2012. More recently, our work has been focused on clinical care and redesign of patient centered care after major surgery with prospective examination of important aspects like enhanced recovery after surgery, opioid use in surgery and utilization barriers for low socioeconomic status patients. We have developed a tele-medical home program for post-liver transplantation patients and published the first pilot program demonstrating its utility and feasibility. Our group has conducted a randomized controlled trial to assess the clinical effectiveness of telehealth versus standard of care starting in October 2016 which was the first of its kind in surgery and transplantation and has the potential to change the way patients are cared for after major surgery.

Dr. Greg Tiao

Gregory M. Tiao, MD, FACS
Professor of Surgery
Frederick C. Ryckman Chair of Pediatric Surgery
Division Director, Pediatric General & Thoracic Surgery
Surgical Director, Pediatric Liver Transplantation
Director, Pediatric Surgery Residency Program

Our lab focuses on the molecular mechanism of biliary atresia, a devastating inflammatory cholangiopathy leading to obstruction of the biliary tree and, without treatment, death within two years of birth. It is the most common cause of pediatric end stage liver disease and remains the number one indication for pediatric liver transplantation in the United States. In the murine model of biliary atresia, rhesus rotavirus (RRV) injected within the first three days of life resulted in cholangiocyte infection and biliary obstruction. Through an ongoing R01 funded project by the NIH, our research team generated and utilized a unique set of rotavirus strains containing single gene substitutions (rotavirus reassortants) to identify a particular gene of rotavirus which is involved in the pathogenesis of murine biliary atresia. This gene/protein has recently been shown to be involved in the activation of natural killer cells. Current research is focused on identifying the epitopes involved in disease pathogenesis. These novel findings might provide insight into understanding the cause of biliary atresia in infants.

Hector R. Wong, MD

Hector R. Wong, MD
Professor, Department of Pediatrics, Critical Care Medicine, CCHMC

Our laboratory is engaged in translational and basic science approaches to sepsis. The translational component consists of a multi-institutional database of children with sepsis and septic shock. The database consists of whole blood-derived RNA, DNA, and serum, and is richly annotated with extensive clinical data. This database has been in existence over a decade and has been leveraged for the derivation of gene expression-based subclasses of children with septic shock having clinically relevant phenotypes, the discovery of stratification biomarkers, and the discovery of novel therapeutic targets. These data are frequently brought back to the laboratory for formal hypothesis testing using both adult and immature models of sepsis. Recently, this work expanded to the related area of intestinal ischemia/reperfusion injury, which was the focus of research for one of the surgical residents in the Wong laboratory (Daly).  The interplay between these translational and basic science efforts provides a rich environment for current and prospective T32 trainees.

Basilia Zingarelli, MD, PhDBasilia Zingarelli, MD, PhD
Professor, Department of Pediatrics, Critical Care Medicine, CCHMC

Our 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. Ongoing projects are primarily funded by two R01 grants from the National Institutes of Health. Dr. Zingarelli has identified putative anti-inflammatory nuclear receptors, the peroxisome proliferator activated receptors (PPARγ, PPARα and PPARδ ), and liver X receptors (LXRs), which regulate gene transcription of several cytotoxic modulators and may be important defense factors. Recent research efforts also focus on understanding the role of aging on the clinical course of infections, severe hemorrhage and trauma. The Zingarelli laboratory is also investigating the role of the PPARγ co-activator-1α (PGC-1α) and the AMP activated kinase (AMPK) in a variety of metabolic processes with particular interest on the molecular mechanisms of autophagy, a process that allows the cell to dispose dysfunctional organelles, and mitochondrial biogenesis, a process that allows the cell to restore energy homeostasis. 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.

Resident publications 2015-2020