PURPOSE: We performed this study to evaluate the process of radiation induced apoptosis in A431 skin epithelial cancer cell line. MATERIALS AND METHODS: Low to high dose radiation (0, 2, 5, 10, 25 Gy) was given to A431 cells by Cs-137 cell irradiator. Apoptosis was evaluated by cell morphology, dye exclusion test, and DNA laddering. RESULTS: Cell viability decreased as the radiation dose increased. Number of apoptotic bodies increased as radiation dose increased. It increased most significantly at 12 hours after irradiation. Lactate dehydrogenase activity in culture medium increased according to radiation dose and time after irradiation. CONCLUSION:: Radiation-induced apoptosis which was the main course of cell death in A431 cells could be analyzed quantitatively by counting apoptotic bodies under microscope. Apoptosis increased as radiation dose increased.
Apoptosis* ; Cell Death ; Cell Line ; Cell Survival ; DNA ; L-Lactate Dehydrogenase ; Skin

No abstract available.
Humans ; Hyalin* ; Hyaline Membrane Disease* ; Infant, Newborn

PURPOSE: The purpose of this study was to evaluate the relationship between radiation-induced activation of DNA repair genes and radiation induced apoptosis in A431 cell line. MATERALS AND METHODS: Five and 25 Gys of gamma radiation were given to A431 cells by a Cs-137 cell irradiator. Apoptosis was evaluated by flow cytometry using annexin V-fluorescein isothiocyanate and propidium iodide staining. The expression of DNA repair genes was evaluated by both Northern and Western blot analyses. RESULTS: The number of apoptotic cells increased with the increased radiation dose. It increased most significantly at 12 hours after irradiation. Expression of p53, p21, and hRAD50 reached the highest level at 12 hours after 5 Gy irradiation. In response to 25 Gy irradiation, hRAD50 and p21 were expressed maximally at 12 hours, but p53 and GADD45 genes showed the highest expression level after 12 hours. CONCLUSION: Induction of apoptosis and DNA repair by ionizing radiation were closely correlated. The peak time of inducing apoptosis and DNA repair was 12 hours in this study model. hRAD50, a recently discovered DNA repair gene, was also associated with radiation-induced apoptosis.
Apoptosis* ; Blotting, Western ; Cell Line* ; DNA Repair* ; DNA* ; Flow Cytometry ; Gamma Rays ; Humans* ; Propidium ; Radiation, Ionizing

No abstract available.

No abstract available.
Animals ; Chitosan* ; Eating* ; Mice*

No abstract available.
Animals ; Chitosan* ; Rats* ; Water*

No abstract available.
Animals ; Colloids* ; Mice*

PURPOSE: To evaluate differential points of patterns of clustered microcalcification between malignant(n=17) and benign(n=46) lesions on mammogram MATERIALS AND METHODS: We retrospectively and prospectively evaluated mammograms of surgically confirmed 63 patients showing clustered microcalcifications. Area, density, number, size, shape of calcification were evaluated along with associated mass and parenchymal distortion. RESULTS: Malignant calcifications were more variable in size(14/17, 77% vs 25/46, 53%) and shape(l 1/17, 64. 8% vs 13/46, 28.2%) than benign counterparts. Pepper, fine granular, branching, comma, tadpole and wormiform calcification were observed in malignant lesion with statistical significance. The malignant calcifications showed more faint(12/17, 70.5% vs 23/46, 50%), irregular margin(17/17, 100% vs 19/46, 42%) and they were usually associated with parenchymal distortion(16/17, 94% vs 9/46, 20%) and ill-defined masses(10/17, 58.9% vs 12/46, 26.1%). CONCLUSION: Clustered microcalcifications with variable size and shape, faint or irregular margin, parenchymal distortion, ill-defined masses seen on mammography, suggest malignancy.
Humans ; Larva ; Mammography ; Prospective Studies ; Retrospective Studies

No abstract available.
Apnea*

No abstract available.