Search

A knowledge of the fundamental optical properties of breast tissues is necessary in order to optimize transillumination imaging techniques for the diagnosis of breast disease. The optical absorption and scattering coefficients have been measured in normal and diseased breast tissues, over the range of wavelengths from 500 to 1100 nm. The tissues were obtained from surgical specimens, and consisted of normal glandular and adipose tissues, fibrocystic disease, fibroadenoma, and ductal carcinoma. Total attenuation coefficients were measured for thin slices of tissue obtained on a microtome. The diffuse reflectance and transmittance were measured for 1.0 mm thick samples of these tissues, using standard integrating sphere techniques. Monte Carlo simulations were performed to derive the scattering and absorption coefficients, as well as the mean cosine of the scattering angle. The results indicate that scatter exceeds absorption by at least two orders of magnitude. The absorption coefficients are strongly affected by the presence of blood, particularly at wavelengths below 600nm. The scattering coefficients lie in the range 30 mm to 90 mm-1 at 500 nm, and fall smoothly with increasing wavelength to between 10 mm and 50 mm at 1100 nm. The scatter coefficient for adipose tissue differs, in that it is invariant with wavelength over this spectral range. The scattered light, for all tissues examined, is highly forward peaked, with the mean cosine of the scattering angle in the range 0.945 to 0.985. This value remains constant with wavelength to within +/-0.01 for any given tissue. The absorption coefficients and scattering properties of each tissue type fall within distinct ranges at each wavelength. Fibrocystic disease and adipose tissue appear to be the most clearly distinguishable groups. The optical properties of carcinoma do not differ significantly from those of normal glandular tissues, although both groups differ from other tissue types. The implications of these results for imaging are yet to be determined. Thesis Master of Science (MS)

Idiopathic pulmonary fibrosis (IPF) is an aggressive and thus far incurable disease, characterized by aberrant fibroblast-mediated extracellular matrix deposition. Our understanding of the disease etiology is incomplete; however, there is consensus that a reduction-oxidation (redox) imbalance plays a role. In this study we use the autofluorescent properties of two redox molecules, NAD(P)H and FAD, to quantify changes in their relative abundance in living lung tissue of mice with experimental lung fibrosis, and in freshly isolated cells from mouse lungs and humans with IPF. Our results identify cell population-specific intracellular redox changes in the lungs in experimental and human fibrosis. We focus particularly on redox changes within collagen producing cells, where we identified a bimodal distribution of NAD(P)H concentrations, establishing NAD(P)H high and NAD(P)H low sub-populations. NAD(P)H high fibroblasts exhibited elevated pro-fibrotic gene expression and decreased collagenolytic protease activity relative to NAD(P)H low fibroblasts. The NAD(P)H high population was present in healthy lungs but expanded with time after bleomycin injury suggesting a potential role in fibrosis progression. We identified a similar increased abundance of NAD(P)H high cells in freshly dissociated lungs of subjects with IPF relative to controls, and similar reductions in collagenolytic activity in this cell population. These data highlight the complexity of redox state changes in experimental and human pulmonary fibrosis and the need for selective approaches to restore redox imbalances in the fibrotic lung.