Our faculty are dedicated researchers, working to improve the health of our patients through clinical trials and research studies.


Research Project

Principal Investigator

Funding Source


Developmental Alterations in Cardiac Protein Turnover

  • J Akar


To study the effect of BEEF in patients with congestive heart failure

Calcium Entry and Vascular Smooth Muscle Excitation

  • KL Byron
  • L Cribbs


To identify non-selective cation currents in arterial smooth muscle cells and determine their roles in vasopressin-induced action potential generation.

T-Type Ca Channels in Development and Cell Proliferation

  • L Cribbs


To understand the role of T-type Ca channels in the cardiovascular system with particular focus on instances where they appear to predominate and have unique functions over high voltage-activated, L-type channels.

Altered Mechanotransduction Signaling in Type 2 Diabetes and Diabetic Cardiomyopathy

  • A Goodman
  • L Cribbs

American Heart Association

To determine what mechanotransduction signaling molecules are differentially regulated in the heart as a result of diabetes and to look specifically at the regulation of PYK2 in the diabetic milieu

Antiplatelet Effect of PAR-1 Inhibitors

  • WP Jeske

Caden Biosciences

To determine whether a specific series of small molecules modulate platelet-activation response.

Novel Heparin Antagonists

  • WP Jeske
  • JM Walenga
  • J Fareed
  • D Hoppensteadt
  • M Bakhos


To create a comparative neutralization profile of unfractionated heparin by PolyMedix's novel site-directed antagonists

Beta-Adrenergic Receptor Function in Atrial Myocytes

  • SL Lipsius
  • AM Samarel


To test the hypothesis that the ECM-integrin-cytoskeletal complex remodels beta-adrenergic receptor function in atrial myocytes.

Serotonin Therapy for Parkinson's Disease and Neurodegenerative Disorders

  • J Martin

Hines VA Hospital

To develop and produce adeno-associated virus vector genetic constructs for the purpose of developing a novel model of progressive neuronal degeneration as seen in Parkinson's disease. (subcontract with Hines VA Hospital for which Dr. William Wolf is principal investigator)

Human Adult Bone Marrow-Derived Stem Cell Therapy for Recovery from Ischemic Stroke

  • J Martin

Illinois Department of Public Health

To develop and produce adeno-associated virus vector genetic constructs. (subcontract with Hines VA Hospital for which Dr. Gwendolyn Kartje is principal investigator)

Cardioprotection against Endotoxins

  • R Mestril


To study the mechanism by which hsp70 protects cardiomyocytes against endotoxin-induced injury.

Mechanical Activity and Myocyte Remodeling

  • AM Samarel
  • J Martin


To investigate the role of focal adhesion proteins and costameric components in cardiomyocyte remodeling in response to linear and transverse stretch. (subcontract with the University of Illinois at Chicago, a component of a P01 (Integrated mechanisms of cardiac maladaptation) for which Dr. John Solaro is principal investigator and Dr. Brenda Russell is project leader)

T3 Rx During Post-infarction LV Remodeling

  • AM Samarel
  • KK Henderson

T3 Therapeutics and King Pharmaceuticals

To develop a post-myocardial infarction model to facilitate study of the use of T3 in the treatment of congestive heart failure.

HIT Registry

  • JM Walenga
  • WP Jeske
  • MM Prechel

Mitsubishi Pharmaceuticals

To create and maintain the Loyola Registry of Heparin-Induced Thrombocytopenia (HIT) in Cardiovascular Surgery Patients, the only available database of its kind in existence.

PiCT Evaluation

  • JM Walenga
  • D Hoppensteadt


To compare the performance of Pefakit PiCT (Pentapharm) to Heptest (Haemachem).

Differentiation of LMWHs

  • JM Walenga
  • WP Jeske
  • MM Prechel
  • D Hoppensteadt


Pharmacologic characterization and differentiation of low molecular weight heparins and heparin-derived oligosaccharides.



Research in the Division of Dermatology is rapidly growing, due in large part to collaboration between the division and the Department of Pathology. Together, they have participated in several clinical trials and studies on topics such as:

  • Dendritic cell-based immunotherapy of melanoma
  • Protein kinase C signaling in apoptosis and skin cancer
  • Melanocytic cells with relation to vitiligo
  • KSHV infection of endothelial cells
  • Pathogenesis of Kaposi’s sarcoma

Over the past five years, the division has published approximately 70 peer-reviewed articles, abstracts and book chapters.


Endocrinology & Metabolism

The division conducts both bench and clinical research and works closely with other divisions and departments at Loyola to achieve its research goals. Currently, the division’s research concentrates on:

  • Role of blood glucose control in preventing cardiovascular and cerebral vascular disease in people with diabetes
  • Impact of alcohol on reproduction
  • Osteoporosis, Vitamin D Deficiency
  • Role of testosterone on bone disorders and brain and lipid metabolism
  • Improved treatments for Paget’s disease
  • Growth hormone therapy


Gastroenterology & Nutrition

The overall mission of the research activities in the Division is to conduct original scientific investigations in diseases and disorders of the digestive system, including the gastrointestinal (GI) tract, liver and pancreas. Research within the division can be broadly divided into basic science research and clinical investigation. The areas of interest include:

Faculty Specific Research Interests:

Gail Hecht, MD
Dr. Hecht's research is focused on understanding how effector proteins expressed by enteropathogenic E. coli and are translocated into intestinal epithelial cells alter host cell physiology including tight junction barrier function, active ion transport processes, and the innate immune response.

Ongoing Research:
Enteropathogenic E. coli (EPEC) is a leading cause of infant death in developing countries and share many virulence factors with the closely related enterohemorrhagic E. coli (EHEC). Unlike other pathogens where toxins play a critical role in diarrhea we have found multiple mechanisms contributing to ion and water movement including alterations in ion absorption and tight junction (TJ) permeability. TJs consist primarily of paired tetraspan proteins including occludin and claudins, which regulate paracellular solute and water permeability in the intestine. Our goal is to determine the precise molecular basis of TJ disruption by EPEC. EPEC encode a type III secretion system or molecular syringe that directly injects effector proteins into the host cell. Three of these effector proteins, EspF, Map and EspG, are the focus of our current project. We have a series of point mutants that disrupt the functions of these effector proteins and are testing whether individual effector functions contribute to distinct pathways of TJ disruption or whether the three effectors work together in a coordinated manner. Our current hypothesis suggests that there is coordination between the effectors to disrupt cell polarity leading to TJ disruption. Disruption of cell polarity is in part beneficial to the bacteria as it allows one of its receptors, the β1 integrin, to be relocalized from basolateral domains to the apical cell surface where it can bind to Intimin on the bacteria.  Cell polarity is governed by a delicate balance between two opposing proteins, Par1b and Par3.  We have found that overexpression of eukaryotic Par1b is protective against EPEC-mediated TJ disruption.  The mechanisms by which Par1b and Par3 are altered and their relation to TJs are a major focus of this project.  It is our hope that understanding the mechanism of TJ alteration will lead to the development of novel therapeutic agents.

The second project in the lab examines the mechanisms by which EPEC attenuates the host inflammatory response.  Unlike Salmonella, EPEC infection does not induce a robust inflammatory response.  This is due to a number of effector proteins that interfere with the NF-B pathway.  Two of these effectors, NleH1 and NleH2, are highly homologous and are the focus of our work.  NF-B is a transcription factor whose transit to the nucleus is typically impeded by the cytoplasmic inhibitor IB.  Upon inflammatory stimulation, such as through toll-like receptors (TLRs), IB is phosphorylated, ubiquitinated and degraded. We reported that EPEC NleH1 and NleH2 block the ubiquitination of IκBα preventing its degradation and subsequent release of NF-B.  This process is specifically due to a kinase site K159 and K169 in NleH1/2 as mutation of these sites ablates the effect of NleH1 and 2 on IκBα ubiquitination.  This work was carried out using cell transfection as we created point mutations in the critical lysine residues in EPEC for each effector expressed in DnleH1/2 background. We are currently characterizing these mutants in a murine model of EPEC infection.  In addition to impact on NF-B signaling, we found that NleH1/2 also alter the MAP kinase signaling cascade, which is also involved in inflammation. There are three primary map kinase pathways and we are currently examining the impact of NleH1/2 on each of these arms.  In addition to understanding how EPEC attenuates the inflammatory response, we hope this work will lead to the production of novel anti-inflammatory agents.

Selected Publications:

Roxas JL, Koutsouris A, Bellmeyer A, Tesfay S, Royan S, Falzari D, Harris A, Cheng H, Rhee KJ, and Hecht G.   Enterohemorrhagic E. coli alters murine intestinal epithelial tight junction protein expression and barrier function in Shiga toxin independent manner.  J Lab Invest.  90:1152-1168, 2010. [PMCID: PMC2912457]

Thanabalasuriar A, Koutsouris A, Weflen A, Hecht G, and Gruenheid S. The bacterial virulence factor NleA is required for the disruption of intestinal tight junctions by enteropathogenic E. coli. Cellular Microbiology, 12:31-41 2010. [PMCID: PMC2850276]

Royan SV, Jones RM, Koutsouris A, Roxas JL, Falzari K, Weflen A, Kim A, Bellmeyer A, Turner JR, Neish  A, Rhee KJ, Viswanathan VK, Hecht GA. Enteropathogenic E. coli non-LEE encoded effectors NleH1 and NleH2 attenuate NF-kB activation. Mol Micro, 78:1232-45, 2010. [PMCID: PMC3325542]

Glotfelty L and Hecht G. Enteropathogenic E. coli effectors EspG1/G2 Disrupt Tight Junctions: New Roles and Mechanisms.  Ann N Y Acad Sci., 1258:149-58, 2012.

Promila Banerjee, MD

- Banerjee, P, Sontag SJ.  Gastroesophageal reflux, laryngopharyngeal reflux, and aspiration.  Asthma, Comorbidities, Co-existing Conditions, and Differential Diagnoses. Editors: Lockey & Ledford 2013
- Sahai A, Banerjee P. EUS Guided Fine Needle Aspiration.  Endosonography   Editors:  R. Hawes & P. Fockens.  Elsevier  2005.

- Dawravoo L, Gandhi P, Schnell T, Sontag SJ, Banerjee, P.  Ulcers in the Immunosuppressed:  Beyond Infections and Aspirin.  American Journal of Gastroenterology Oct. 2012, volume 107 S544.
- Roberts J, Banerjee P, Freeman J, Castell DO.  Patients With GERD and Not Barretts Show Normalized Impedance After PPI Treatment.  American Journal of Gastroenterology Sept 2009
- Gershuny K, Banerjee P, Bolampally S, Bongiorno CP.  Factors Predicting Severity in Clostridium Difficile Infection.  American Journal of Gastroenterology Sept. 2010 

Omar Khan, MD
· Developed Brown Cancer Center Database, now incorporated in the Kentucky Cancer Registry

· Khan O, Sewell J, Shergill, A. “Gastroenterology.” Hospitalist Handbook. Ed. Sanjiv Shah. UCSF:
2007, 157-168.

· Ongoing Projects: Anti-glycan serologies and response to anti-TNF agents in Crohn's Disease,
Predicting risk and severity of recurrent in Crohn's Disease after Ileal resection.
· Khan O, Harrell L. “A Review of Fecal Biomarkers in the Diagnosis of IBD Recurrence.” Inflamm
Bowel Dis Monit 2010; 11(1):15-21.

· Ongoing projects: Quality measures of surveillance endoscopy in high-risk CRC patients, Multicenter
population & clinic-based validation cohort of Lynch Syndrome screening modalities (Syngal,
Kastrinos, Khan
· Poster Presentation: Society of General Internal Medicine Research Methods Precourse, March 2008.
· Oral Presentation: Risk and Familial Susceptibility for Colon Cancer, Digestive Disease Week, 2010.
· Khan O, Kupfer S, Terdiman J. “Performance of Lynch Syndrome Predictive Models in a Multi-Center
US Referral Population.” Am J of Gastroenterology, 2011 Oct; 106(10): 1822-7.

Basabi Rana, PhD
Research in my laboratory focuses on identifying both the positive and negative regulators of growth. In one of the projects and to identify the positive regulators of growth, we have initiated studies at a molecular level to understand the mechanism(s) underlying the trophic effects of the gastrointestinal peptide hormone (gastrin) in cancer cells. These studies identified the oncoprotein beta-catenin and the transcription factor CREB as candidate upstream mediators of gastrin induced growth, involving the cell cycle regulator protein cyclin D1 [1]. Studies are currently underway to determine specifically the role of these molecules in cancer cell proliferation and migration and to identify the upstream signaling pathways involved. These studies are expected to provide a mechanistic insight into the mechanism and identify specific signaling pathways responsible for mediating the trophic effects of gastrin. My future goal with these studies is to determine whether a similar mechanism operates in an in vivo environment.

In a second project and to identify the negative regulators of growth, we have focused on the transcription factor Peroxisome Proliferator Activated Receptor (PPAR) gamma. Ligand mediated activation of PPARgamma has been shown to be effective in regulating growth in multiple cancer cells. Our earlier studies revealed that Troglitazone mediated activation of PPARgamma can inhibit growth of the liver cells [2]. Active research is currently underway in my laboratory to determine the role of Troglitazone and other PPARgamma ligands in regulating survival and apoptotic pathways in gastrointestinal cancer cells. Earlier studies from my laboratory also revealed some novel pathways of beta-catenin degradation following activation of PPARgamma [3]. We are now extending these studies to identify the key mediators involved in this pathway of beta catenin degradation. Since beta catenin is mutated or overexpressed in many cancer types, this novel degradation pathway might be effective in regulating these resistant tumors via regulating mutated beta catenin expression.

In a separate project, we are carrying out studies to identify the specific signaling pathways operating in the cancer cells to regulate the expression levels and signaling via beta catenin. This has the potential of opening new possibilities of developing targeted cancer therapies for treating beta catenin dependent resistant tumors. In pilot studies our laboratory recently identified a cross-talk of a Stress Kinase family member in regulating beta catenin pathway in prostate cancer.

Literature Cited:

  1. Pradeep A, Sharma C, Sathyanarayana P, Albanese C, Fleming JV, Wang TC, Wolfe MM, Baker KM, Pestell RG, Rana B: Gastrin-mediated activation of cyclin D1 transcription involves beta-catenin and CREB pathways in gastric cancer cells. Oncogene 2004, 23:3689-3699.
  2. Sharma C, Pradeep A, Pestell RG, Rana B: Peroxisome proliferator-activated receptor gamma activation modulates cyclin D1 transcription via beta-catenin-independent and cAMP-response element-binding protein-dependent pathways in mouse hepatocytes. J Biol Chem 2004, 279:16927-16938.
  3. Sharma C, Pradeep A, Wong L, Rana A, Rana B: Peroxisome proliferator-activated receptor gamma activation can regulate beta-catenin levels via a proteasome-mediated and adenomatous polyposis coli-independent pathway. J Biol Chem 2004, 279:35583-35594.

Mukund Venu, MD
Mukund Venu, Martin E, Saeian K, et al. High prevalence of vitamin A & D Deficiency in Patients Evaluated for Liver Transplantation. Liver Transplantation. 2013 Jun;19(6):627-33.

Mukund Venu, Brown RD, Lepe R, et al. Laboratory diagnosis and non-operative management of biliary complications in living donor liver transplant patients.  Journal of Clinical Gastroenterology. 2007;41(5):501-6.


Hospital Medicine

Research in the field of hospital medicine is focused on the areas of health care quality, patient safety, outcomes research and informatics.  Faculty are encouraged to collaborate with other researchers from faculty colleagues from around the University in these areas.  A cross disciplinary Research In Progress Seminar is being developed which will encourage collaborative research.  Opportunities to develop the research presence of hospital medicine are strongly encouraged.


Pulmonary & Critical Care Medicine

Areas of Current Research include:

  • Mechanisms of weaning failure
  • Patient-ventilator interactions
  • Respiratory muscle pathophysiology
  • Sleep in the ICU
  • Control of breathing
  • Outcome in long-term ventilated patients
  • Lung transplantation
  • COPD rehabilitation
  • Alterations in lung cellular function after acute injury



Members of the division are active researchers and have published their findings  in peer-reviewed articles, abstracts and book chapters. The outcomes of their studies have appeared in various medical publications, including the Journal of Rheumatology, Therapeutic Apheresis, Seminars of Hematology and Oncology, Journal of Heart and Lung Transplantation and Academic Medicine. Research interests include but are not limited to:

  • Rheumatoid arthritis and spondyloarthropathies
  • Management of pulmonary hypertension
  • Study of novel agents to treat rheumatoid arthritis and gout
  • Use of apheresis to reduce acute graft rejection in organ transplant patients
  • Management of idiopathic pulmonary fibrosis and retroperitoneal fibrosis

A complete catalog of all ongoing clinical trials in the Loyola University Health System can be found here.