Biomedical subjects
Publications and source records attributed to J Rowinski.
Directly measured and derived geometric and densitometric parameters were obtained by means of the automated image analyzer Quantimet 720-D in Feulgen-stained HeLa cells synchronized by selective mitotic detachment. These data indicate substantial alteration of nuclear morphology during the entire cell cycle, even during the G1 and G2 phases, and the late G1-early S and late S-G2 transitions.
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The effect of inhibitors of RNA synthesis (Cordycepin, Actinomycin D) and protein synthesis (Cycloheximide) on the development and growth of mouse blastocysts in vitro was explored. Blastocysts exposed in vitro for 24 hours to 50 mu-g/ml Cordycepin, 0.005 mu-g/ml Actinomycin D, or 0.1 mu-g/ml Cycloheximde grew and began to attach to the dish in the similar manner as did the controls. Cell number, 3-H-thymidine-labeling index and mitotic index in treated blastocysts were also similar to controls. Cell number, 3-H-thymidine-labeling index and mitotic index in treated blastocysts were also similar to controls. Control blastocysts grown in vitro for six days attached to the dish, trophoblastic layer was spread and inner cell mass continued to grow and formed an egg-cylinder like structure. Blastocysts grown in constant presence of 50 mu-g/ml of Cordycepin in themedium or those exposed to inhibitor only for the first 24 hours failed to develop inner cell mass derivatives in culture, although the growth of trophoblastic cells was as in controls. The same results were obtained if blastocysts were exposed to 0.005 mu-g/ml of Actinomycin D or to 0.1 mu-g/ml of Cycloheximide either continuously or for the first 24 hours. Higher concentrations of Actinomycin D (0.05 mu-g/ml) or Cycloheximde (1 mu-g/ml) were toxic for the blastocysts causing their degeneration within 24-48 hours. Our results suggested that appropriate concentrations of RNA or protein synthesis inhibitors could prevent the development of inner cell mass derivatives with essentially no effect on the development of primary trophoblast. This would indicate that the process of differentiation of inner cell mass cells is much more sensitive to metabolic inhibitors than the differentiation of giant trophoblastic cells.
Fibroblasts underlying human uterine cervical dysplasia, carcinoma in situ, and invasive carcinoma are agglutinable by concanavalin A (Con A) but not by wheat germ agglutinin, except at very high concentration. Studies with low levels of Con A show that maximal agglutination is obtained with fibroblasts from invasive carcinoma, while the fibroblasts underlying dysplasia give minimal agglutination reactions. Fibroblasts underlying carcinoma in situ give agglutination reactions halfway between those obtained with fibroblasts underlying dysplasia and invasive carcinoma. An epithelial-like cell line obtained from a case of dysplasia shows agglutinability by Con A very similar to that obtained with fibroblasts underlying dysplasia. These epithelial-like cells are also not agglutinable by wheat germ agglutinin. Treatment of the cervical cells, both epithelial and fibroblasts, with neuraminidase leads to slight increase in agglutination by both Con A and wheat germ agglutinin. Marked increase in agglutination is not obtained even after treatment with high concentration of neuraminidase (10 units/10(6) cells). Marked agglutinability, however, is observed after trypsin treatment. The results suggest that, while the fibroblasts obtained from normal cervix are not agglutinable by Con A, surface alterations necessary for Con A-specific agglutination exist in fibroblasts during the early stage of development of uterine cervical epithelial neoplasia (dysplasia) and increase with the progression through carcinoma in situ to invasive carcinoma. Loss of cell surface sialic acids may result in a slight increase in agglutinability, but some other mechanism(s) is likely to be involved in alteration of surface properties that lead to marked agglutinability of the human uterine cervical cells obtained from cancer precursor lesions.
Nuclear chromatin properties in control, SV40-infected and polyoma-infected cultures of mouse embryo fibroblasts were studied using quantitative image analysis. Distribution of Feulgen-DNA-content per nucleus was found to be similar in all three groups of cultures. No differences in nuclear area, mean optical density of chromatin and area of chromatin at different optical density thresholds were measurable between control and SV40-infected fibroblasts. Polyoma-infected fibroblasts were found to have smaller nuclei, more dense and less homogeneous chromatin than non-infected cells. The changes of chromatin in polyoma-infected cells occur in G1, middle S and G2 nuclei. The results are interpreted as an early manifestation of the cytopathic effect of polyoma virus.