Hugo Pedrozo

Bio [2005]
Hugo was born in Barranquilla, Colombia, and moved to the U.S. at the age of 18 to pursue a higher education. He obtained his bachelor's, M.S., and Ph.D., all of them in the biological sciences, in San Antonio, Texas. Hugo's Ph.D. degree is in human physiology and cell and molecular biology. His dissertation dealt with the biochemical mechanisms responsible for changes in biomineralization in response to altered gravity forces. After a three-year postdoc and two years as an instructor in the Department of Orthopaedics at the University of Texas Health Sciences Center at San Antonio, Hugo pursued a career in industry. He is currently employed by the orthopaedic division of Johnson & Johnson as a senior scientist. At J&J, Hugo is part of a concept development team whose goal is to come up with new technologies applicable to orthopaedics, more specifically in tissue engineering and drug delivery systems. Hugo's general interest is to investigate the roots of robustness present in physiological and developmental systems, in addition to concerted attacks, vulnerabilities, and error propagation within otherwise "healthy" systems.

Project Title
Modeling Trabecular Bone with a 3D Reaction-Diffusion Automaton

Project

In this project we developed a three-dimensional (3D) model of trabecular bone utilizing a reaction-diffusion paradigm similar to that used to generate two-dimensional models of animal pigmentation. The basic setup consists of a four-cell array in 3D space with an "agent" allowed to reciprocally carry information among them. The strength (weight) of the agent at each cell in all three axes was arbitrarily manipulated to obtain a structure that closely resembled healthy trabecular bone. Subsequently, the weights of the agent at each position in the 3D lattice were varied to obtain the appearance of osteoporotic trabecular bone. Several parameters were measured to determine the effect of agent weight on bone formation in our model. These parameters were bone density, inner surface area, total pore length, and connectivity or pore size. In all cases the initial placement of the active cells was random, and the effect of initial density on the formation of our bone model was tested by varying the probability of a random cell existing in a particular location in the matrix.