Radiologist evaluation of an X-ray tube-based diffraction-enhanced imaging prototype using full-thickness breast specimens.

Rationale And Objectives: Conventional mammographic image contrast is derived from x-ray absorption, resulting in breast structure visualization due to density gradients that attenuate radiation without distinction between transmitted, scattered, or refracted x-rays. Diffraction-enhanced imaging (DEI) allows for increased contrast with decreased radiation dose compared to conventional mammographic imaging because of monochromatic x-rays, its unique refraction-based contrast mechanism, and excellent scatter rejection. However, a lingering drawback to the clinical translation of DEI has been the requirement for synchrotron radiation.

Characterization of diffraction-enhanced imaging contrast in breast cancer.

Diffraction-enhanced imaging (DEI) is a new x-ray imaging modality that has been shown to enhance contrast between normal and cancerous breast tissues. In this study, diffraction-enhanced imaging in computed tomography (DEI-CT) mode was used to quantitatively characterize the refraction contrasts of the organized structures associated with invasive human breast cancer. Using a high-sensitivity Si (3 3 3) reflection, the individual features of breast cancer, including masses, calcifications and spiculations, were observed.

Superantigen-primed T cells exposed to 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) replicate poorly following recall encounter.

The current study investigated the effect of tetrachlorodibenzo-p-dioxin (TCDD) on the ability of staphylococcal enterotoxin A (SEA)-primed T cells to divide by dual-labeling the cells with 5,6-carboxyfluorescein diacetate succinimidyl ester (CFSE) and antibodies against the specific T cell receptors. C57BL/6 wild-type mice were injected ip with TCDD (10 microg/kg body weight) followed by hind footpad injections of SEA (10 microg/footpad). The draining popliteal lymph nodes (PLN) were harvested 1-4 days posttreatment, labeled with CFSE and cultured for 1-4 days without further stimulation or in the presence of the recall antigen.