Last updated: 03/27/2006

The DDNC Research laboratory is located in the Biomedical Research Building (BRB) of the University at Buffalo - SUNY, South Campus, a relatively new, well equipped research facility, including 58 separate research modules. Our laboratory, located on the fourth floor (Rooms 422 and 426) of the BRB, occupies approximately 1,250 sq. feet of space.  Equipment and facilities needed to undertake our research are available in our laboratory and in adjacent laboratories. There is also a large shared equipment work area equipped with hoods, isotope and chemical storage areas, dark rooms, cold rooms and space for many pieces of major equipment, including ultracentrifuges, gamma and beta counters, FPLC, HPLC and low temperature freezers.  All research laboratories are located in close proximity on six floors (about 10 lab for each floor), which fosters continuing interaction, discussion and exchange of information between staff, postdoctoral fellows, graduate students and technologists.

Our research program is focused on molecular immunology. Ongoing research projects include:

• Pathogenesis of heparin-induced thrombocytopenia and thrombosis at the molecular-immunology level.
• Biological mechanisms, associated with the ability of the CXC chemokines PF4, of inhibiting/enhancing the proliferation of specific T lymphocyte subsets.
• Pathogenesis of:
  • Inflammatory Bowel Disease (IBD)
  • Nonalcoholic Steatohepatitis (NASH)

Members of Molecular Immunology Lab

Gian Paolo Visentin, M.D. – Associate Professor.  He received his formal training in Clinical Pathology with a strong scientific research foundation in: biochemistry, hematology, immunology, immunohematology and analytical chemistry.  He is responsible for the overall administration and direction of all the research projects.  He has had extensive previous experience in the study of heparin-induced thrombocytopenia and thrombosis (HIT/T) and has, more recently, focused his attention on acquiring the experimental tools required to dissect the immune response associated with HIT/T, IBD and NASH at a molecular level. 

Chao Yan Liu, M.D. – Senior Research Scientist.  Formerly Assistant Professor of Pathology and Chief of Molecular Pathology Laboratory, at the Institute of Radiation Medicine, Beijing (China).  A well trained scientist in molecular pathology, with strong background in basic science biomedical research.  She plays a pivotal role in the execution of many of our experiments, especially those involving the generation, molecular and phenotypic analysis of T cell subsets with special emphasis to regulatory T cells.

Cuiling Shu, M.D., Ph.D. – Research Assistant Professor.  A research scientist with a proven record of success and experience such as gene cloning, protein expression, assay development, and monoclonal antibody production, as well as extensive knowledge of immunology and molecular biology.  She has been in charge of 3 national (China) scientific projects.  Dr. Shu recently joined to our research program focused on the molecular immune pathogenesis of Inflammatory Bowel Disease and Nonalcoholic Steatohepatitis. 

Qi-Hong Sun, M.D., Ph.D. – Research Assistant Professor.  A fully trained research scientist with over ten years of research experience.  His research interests are on the structure and function of cell adhesion molecules, tumor metastasis, and organ fibrosis.   As an Adjunct Professor and Director of the Department of Immunology, Beijing Institute of Radiation Medicine, Beijing (China), he is involved in an international cooperative project aimed to generate and characterize a large number of novel antibodies targeting liver proteins for proteomics (HUPO-HLPP).

April L. Ulmer, M.D. – Pediatric Gastroenterology Fellow.  Dr. Ulmer received her residency training in Internal Medicine and Pediatrics from Geisinger Medical Center in Danville, Pennsylvania.  She joined our department in July, 2004.  Dr. Ulmer is presently a second year fellow with the Digestive Diseases and Nutrition Center at Women’s and Children’s Hospital of Buffalo.  She is completing the research requirement of her fellowship training in the DDNC research laboratory.  Dr. Ulmer’s interests include the genetic basis of inflammatory bowel disease, and her present research focuses on identifying polymorphisms in toll-like receptors that may lead to the development of inflammatory bowel disease.

Selected Publications

• Visentin GP, Ford SE, Scott JP, Aster RH. (1994) Antibodies from Patients with Heparin- Induced Thrombocytopenia/Thrombosis are Specific for Platelet Factor 4 Complexed with Heparin or Bound to Endothelial Cells. J Clin Invest 93:81-88.
• Visentin GP , Aster RH. (1995) Heparin-induced thrombocytopenia and thrombosis.  Curr Opin Hematol 2:351-357.
• Visentin GP, Malik M, Cyganiak KA, Aster RH. (1996) Patients Treated with Unfractionated Heparin During Open Heart Surgery are at High Risk to Form Antibodies Reactive with Heparin: Platelet Factor 4 Complexes. J Lab Clin Med 128(4):376-83.
• Sun QH, DeLisser HM, Zukowski MM, Paddock C, Albelda SM, Newman PJ. (1996) Individually distinct Ig homology domains in PECAM-1 regulate homophilic binding and modulate receptor affinity. J Biol Chem 271(19):11090-8. 
• Suh JS, Malik MI, Aster RH, Visentin GP. (1997) Characterization of the Humoral Immune Response in Heparin-Induced Thrombocytopenia. Am J Hematol 54(3):196-201.
• Suh JS, Aster RH, Visentin GP. (1998) Antibodies from Patients with Heparin-induced Trombocytopenia/Thrombosis Recognize Different Epitopes on Heparin : Platelet Factor 4. Blood 91:916-922.
• Sun QH, Paddock C, Visentin GP , Zukowski MM, Muller WA, Newman PJ. (1988) Cell surface glycosaminoglycans do not serve as ligands for PECAM-1. PECAM-1 is not a heparin-binding protein. J Biol Chem 273(19):11483-90.
• Peterson JA, Visentin GP , Newman PJ, Aster RH. (1998) A recombinant soluble form of the integrin alpha IIb beta 3 (GPIIb-IIIa) assumes an active, ligand-binding conformation and is recognized by GPIIb-IIIa-specific monoclonal, allo-, auto-, and drug-dependent platelet antibodies. Blood 92:2053-63.  
• Gentilini G, Kirschbaum NE, Augustine JA, Aster RH, Visentin GP. (1999) Inhibition of Human Umbilical Vein Endothelial Cell (HUVEC) Proliferation by the CXC Chemokine Platelet Factor 4 (PF4) Is Associated with Impaired Down-Regulation of p21Cip1/WAF1. Blood 93:25-33.
• Bacsi S, De Palma R, Visentin GP , Gorski J, Aster RH. (1999) Complexes of Heparin and Platelet Factor 4 Specifically Stimulate T Cells from Patients with Heparin-Induced Thrombocytopenia/Thrombosis. Blood 94:1-9.
• Visentin GP. (1999) Heparin-induced Thrombocytopenia: Molecular Pathogenesis. Thromb Haemost 82:448-56.
• Bacsi S, Geoffrey R, Visentin GP, DePalma R, Aster RH, Gorski J. (2001) Identification of T cells responding to a self-protein modified by an external agent. Human Immunology 62:113-24.
• Visentin GP, Moghaddam M, Berry SE, McFarland JG, Aster RH. (2001) Heparin is Not Required for Detection of Antibodies Associated with Heparin-induced Thrombocytopenia/Thrombosis. J Lab Clin Med 138(1):22-31.
• Ruiz C, Liu CY, Sun QH, Sigaud-Fiks M, Fressinaud E, Muller JY, Nurden P, Nurden AT, Newman PJ, Valentin N. (2001) A point mutation in the cysteine-rich domain of glycoprotein (GP) IIIa results in the expression of a GPIIb-IIIa (alphaIIbbeta3) integrin receptor locked in a high-affinity state and a Glanzmann thrombasthenia-like phenotype. Blood 98(8):2432-41.
• Sun QH, Liu CY, Wang R, Paddock C, Newman PJ. (2002) Disruption of the long-range GPIIIa Cys(5)-Cys(435) disulfide bond results in the production of constitutively active GPIIb-IIIa (alpha(IIb)beta(3) integrin complexes. Blood 100(6):2094-101.
• Visentin GP , Liu CY, Aster RH. (2003) Molecular Immunopathogenesis of heparin-induced thrombocytopenia. In: Heparin-Induced Thrombocytopenia, third edition. Marcel Dekker, New York, 179-196.
• Liu CY, Battaglia M, Lee SH, Sun QH, Aster RH, Visentin GP. (2005) Platelet Factor 4 (PF4) Differentially Modulates CD4⁺CD25⁺ (Regulatory) vs. CD4⁺CD25^- (Non-Regulatory) T Cells. The Journal of Immunology, 174:2680–86.