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Artificial extracellular matrix proteins were synthesized using recombinant DNA technology. These proteins were meant to mimic the internal elastic lamina of the tunica intima of muscular arteries for use in the design of small diameter ($<$6 mm) vascular prostheses. These proteins are composed of two blocks, an elastin-like block made up of repeats of the pentapeptide (VPGIG) and a cell binding segment which is composed of the CS5 region of fibronectin. Proteins of the following sequence were designed, synthesized and characterized: (CS5 (VPGIG)$\sb{40})\sb3$ and (CS5(VPGIG)$\sb{20})\sb5$. Successful synthesis and purification were confirmed by NMR spectroscopy and amino acid analysis. These artificial extracellular matrix proteins were designed with both controlled structural integrity and endothelial cell binding ability. The presence of a lower critical solution temperature (LCST) for both proteins suggests that the properties of the elastin like blocks were maintained. The endothelial cell binding ability of the CS5 region of fibronectin was also retained, as demonstrated through human umbilical vein endothelial cell (HUVEC) adhesion and spreading on the proteins, as well as through inhibition of this adhesion through preincubation of the HUVECs with soluble GREDVDY peptide which is known to inhibit $\alpha\sb4\beta\sb1$ integrin binding to CS5. Equivalent numbers of HUVECs adhered to (CS5(VPGIG)$\sb{20})\sb5$ and to fibronectin, although the number of cells well spread on the former was only approximately 55% of the number of those well spread on fibronectin.

The purpose of this research was to determine consequences of repeated impacts during running. Part I. This study investigated midsole hardness influences on mechanics and hematology during a prolonged downhill run. Twenty-four males ran downhill (−12%, 3.4 m·s−1, 30 minutes) wearing soft, medium or hard midsoles (40, 55, or 70 Shore A). Mean peak tibial acceleration (PTA) was calculated every five minutes. Plasma free hemoglobin (PfHb), hemoglobin (Hb), hematocrit (Hct), and creatine kinase (CK) were analyzed pre- and post-exercise. PTA was initially less (p < 0.05) and tended to be less (p = 0.057) In the soft versus the hard group. Hemolysis and muscle damage resulted. Hard midsoles increased shock and may prolong hemolysis and increase muscle damage. Part II. This study investigated impact shock attenuation, joint kinematics, muscle activation and oxygen consumption during a prolonged run. Ten males ran downhill (−12% grade, 3.4 m·s−1 , 30 minutes). Accelerometers sampled shock data. Joint kinematics and oxygen cost (O2) were collected. Electromyography data (EMG) were collected from six muscles. Shock magnitude, high frequency power and attenuation remained constant. Joint geometry was modified while peak joint velocities increased (p < 0.05). EMG timing was altered (p < 0.05; gluteus maximus, tibialis anterior and gastrocnemius). EMG activation increased (p < 0.05; rectus femoris, vastus lateralis) and O2 increased (p < 0.05). Shock may have remained constant by modifying joint geometry, increasing peak joint velocities, varying muscle timing, and increasing muscle activation and energy cost. Part III. This study investigated midsole hardness and surface stiffness influences on impact shock, joint kinematics, muscle activation and oxygen cost. Twelve males ran in six conditions, combinations of midsole hardness (40 and 70 Shore A) and surface stiffness (100 kN·m −1, 200 kN·m−1, 350 kN·m −1). Accelerometers sampled shock data. Joint kinematics and O2 were collected. EMG was collected from six muscles. Shock magnitude, the power of high frequencies, and attenuation increased (p < 0.05) with surface stiffness regardless of midsole. Peak joint velocities increased (p < 0.05) with increasing surface stiffness while O2 decreased (p < 0.05). Muscle activation levels decreased (p < 0.05; gluteus maximus, biceps femoris and gastrocnemius). Shock was attenuated by increasing peak joint velocities without a concomitant increase in energy cost or muscle activation.

This dissertation presents a new approach to stochastic modeling of magnetic resonance images. A rigorous and comprehensive model of MR image formation is derived based on the physics of magnetic resonance image formation, and the model is validated using real MRI data. A general theoretical result about the existence of spatial autoregressive processes is presented. We attempted to obtain an accurate tissue classification map for a set of real MR images based on two doctors' hand tracings of the boundaries of the regions of the different tissues in the images. In accordance with the prior knowledge of the tissue map, we designed a prior model for the distribution of the underlying tissue map. The technique is applied to tissue classification on a set of real MR images by the use of the Bayesian formulation and ICM algorithm.

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