- Bick RJ, Grigore AM, Poindexter BJ, Schnee PM, Nussmeier NA, Gregoric ID, Shah NA, Myers TJ, Buja LM and Frazier OH. Left Ventricular unloading with an assist device results in receptor relocalization as well as increased beta-adrenergic receptor numbers. Are these changes indications for outcome? J. Cardiac Surg., 20:1-5, 2005
- Bick RJ, Poindexter, BJ, Davis, RA, Schiess MC. Determination of the site of action of calcitonin gene-related peptide in the alteration of intracellular calcium levels in adult and neonatal rodent myocytes. Peptides, 26(11):2231-2238, 2005
Tuzun, E, Bick, R, Conger, J, Clubb, F, Gregoric, I, Frazier, H, Radovancevic, R. Assessment of ventricular reverse modeling in an ovine model of non-ischemic heart failure. Amer. Soc. Aritif. Implant. Org. Journal, 51(2), 63-67, 2005- Poindexter, BJ, Buja, LM, Bhat, S, Milner, SM, Bick, RJ. Localization of the antimicrobial peptides human beta defensins, human neutrophil defensin, and LL-37 in normal and burned skin. Burns, 32(4), 402-407, 2006
- Schnee, P.M., Shah, N., Bergheim, M., Poindexter, B.J., Buja, L.M., Myers, T.J., Radovancevic, B., Frazier, O.H., Bick, R.J. Reversal of myocyte hypertrophy by ventricular unloading; Cardiac improvement without adrenergic receptor up-regulation and relocalization. Medscape General Medicine http://www.medscape.com/viewarticle/ 530973_print, 8(2):45, 2006
- Kanellis, J, Bick, R, Garcia, G, Truong, L.D, Tsao, CC, Poindexter, B, Feng, L, Johnson, R, Sheikh-Hamad, D. Stanniocalcin-1 Inhibits MCP1-Mediated Chemotaxis in Murine Macrophage-Like RAW264.7 cells. Submitted November 2006, Amer. J. Physiol., Renal Physiol.
- Merritt, T.M., Bick, R., Poindexter, B.J. and Hecht, J.T. Unique matrix structure in the rER cisternae of pseudoachondroplasia chondrocytes. Amer. J. Pathol., 170(1), 293-300, 2007
- Chakraborty, A., Brooks, H., Zhang, P., Smith, C., McReynolds, M., Hoying, J., Bick, R., Truong, L., Poindexter, B., Lan, H., Elbjeirami, W., Sheikh-Hamad, D. Stanniocalcin-1 regulates endothelial gene expression and modulates trans-endothelial migration of leukocytes. American Journal of Physiology; Renal, 292(2):F895-904, 2007
- Klein, G.L, Enkhbataar, P., Traber, D.L., Buja, L.M., Jonkam, C.C., Poindexter, B.J., Bick, R.J. Cardiovascular distribution of the calcium sensing receptor before and after burns. In Press, Burns, April 2007 doi:10.1016/j.burns.2007.04.010
- Bick, R.J., Bhat, S., Poindexter, B.J., Buja, L.M., Lawyer, C.H. and Milner, S.M. Nuclear localization of HBD-1 in human keratinocytes. August 10th, 2007, J. Burns and Wounds
Roger Bick, MMedEd, MBS
Professor
Director of Imaging Core Facility
Course Director of Histology for MSI
Co-Director, Clinical Applications for MSI
Department of Pathology & Laboratory Medicine
(713) 500 - 5406
Roger.J.Bick@uth.tmc.edu
Heart failure, Parkinson's Disease, Burns, Microscopy
http://www.uth.tmc.edu/pathology/histology/index.html
Education
East Hertfordshire College, National Certificate in Elective Biology, 1971
South Bank Polytechnic, London, National Certificate in Physiology/Pharmacology, 1974
Masters in Medical Education, University of Dundee, 2005
Research Interests:
Cardiac repair and recovery. Assist devices were originally thought to be solely a bridge to heart transplantation, sustaining and supporting the patient until and organ became available. However the implantation of LVADs allowed some hearts to initiate repair and recovery pathways, such that mechanical well-being was reestablished. Our work with Dr. O. H. “Bud” Frazier and his group at Texas Heart Institute examines the repair mechanisms and structural recoveries in core samples taken at the time of LVAD implantation and explantation/transplant using biochemical and fluorescence imaging.
Neurodegeneration. As our population ages, the number of patients that develop Parkinson’s (PD) and Alzheimer’s disease has dramatically increased. We are concentrating on PD and conducting research to investigate the inflammatory links in the initiation and development of this chronic disease. Cytokines have been shown by this lab to induce the protein aggregations associated with non-reversible degeneration. We use a cultured glial cell line and lipopolysaccharide treated rat brains to evaluate the effects of cytokines, both individually and in combination, on neuronal cell death and protein perturbations. Our studies also use CSF from patients that present to the department of neurology and we collaborate with Dr. Mya Schiess, Vice Chair and Director of Movement Disorders. Neurology fellows rotate through the imaging core lab to get an understanding of cell based problems in neurodegeneration. As an offshoot to this research, we are also looking at neuropeptides and their modulation of ion movements leading to muscle cell tetanus.
Other collaborations. With Dr. Gordon Klein at UTMB, Dept. of Pediatrics and Pediatric Gastroenterology. Researching the localization and effects of the calcium sensing receptor in burn injury and heart failure
With Dr. Stephen Milner at John’s Hopkins, Dept. of Plastic Surgery and Regional Burns Unit. Roles and up-regulation of defensins in burn injury
With Dr. David Sheikh-Hamad, Dept. of Medicine, Renal Unit, Baylor College of Medicine and Ben Taub Hospital. Role of the calcium channel blocker Stanniocalcin-1 in heart failure and chemotaxis
With Dr. Jacqui Hecht, Dept. of Pediatrics, UTMSH and Shriners Hospital. Cartilage malformations in achondroplastic disease
