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Biomedical subjects

D Y Zhou

Publications and source records attributed to D Y Zhou.

10 recordsLinked to original sources
PubMed1991

Study of molecular markers of resistance to m-AMSA in a human breast cancer cell line. Decrease of topoisomerase II and increase of both topoisomerase I and acidic glutathione S transferase.

Resistance to 0.8 microM 4'-(9-acridinylamino)methanesulphon-m-anisidide (m-AMSA) was induced by stepwise increases of drug concentration in the human tumor cell line CALc18 originating from a breast adenocarcinoma. The resistant cell line CALc18/AMSA exhibited a resistance index of 10 and a cross-resistance to other topoisomerase II inhibitors. A 3-fold decrease in the levels of topoisomerase II decatenating activity was found in CALc18/AMSA cells. By contrast, topoisomerase I activity was increased by about 3-fold in resistant cells. Interestingly this line was hypersensitive to camptothecin, a specific inhibitor of topoisomerase I. Restriction endonuclease patterns of the topoisomerase I and topoisomerase II loci were found to be identical in CALc18/AMSA and CALc18 with no evidence of gene amplification and rearrangements. Alkaline elution of m-AMSA-treated cells showed that DNA single strand breaks and DNA-protein crosslinks were decreased in CALc18/AMSA. The DNA lesions also obtained in m-AMSA-treated nuclei indicated that no drug uptake modification occurred in both cells. Moreover, the in vitro m-AMSA-induced DNA cleavage per unit of decatenating activity and the inhibitory effects of antitumoral drugs on decatenation were not found to be different with topoisomerase II from sensitive or resistant cells. However the specific cleavage induced by m-AMSA/per mg of crude protein from resistant cells was 2 to 3 times decreased. Multidrug resistance gene transcripts were not detected while levels of acidic glutathione S transferase mRNA were found to be 8 to 10-fold greater in resistant than in sensitive cell line with no amplification of the gene. In conclusion, the diminution of topoisomerase II activity and the increase of both topoisomerase I and acidic glutathione S transferase transcripts could contribute to the resistant phenotype of these breast cancer cells.

Adenocarcinoma↗
PubMed1990

Quantitative morphological study of Langerhans cells by computerized image analysis.

ATPase-stained normal and topical nitrogen mustard treated Langerhans cells (LC) in guinea pig epidermis were studied quantitatively and morphologically by computerized image analysis. Significant correlation and linear regression were found between the perimeter and square root of its area for both cytoplasm and nucleus; a theoretical basis was thus given for morphological identification of LC. The directly measured and derived geometric parameters indicated not only substantial alteration of cytoplasm morphology of post-treated LC such as cytoplasmatosis and dendrites reduction but also a potential change of nuclear size and functional status. We conclude that quantitative morphological analysis is an objective, precise and practical method for LC research.

Animals↗
PubMed1990

Chemotaxis of polymorphonuclear leukocytes towards LTB4 in patients with psoriasis in vitro.

The random migration and chemotaxis of polymorphonuclear leukocytes (PMN) in agarose were studied in 21 patients with psoriasis and 10 healthy controls. Different concentrations of LTB4 were used as chemoattractants. The random migration and chemotaxis towards lower concentrations of LTB4 were enhanced and that towards higher concentrations of LTB4 reduced in psoriasis. The differences of body involvement, sex, and family history of psoriasis had no influence on PMN migration.

Adult↗