Seung-Keun Oh

Recombinant human growth hormone decreases lung and liver tissue lipid peroxidation and increases antioxidant activity after thermal injury in rats.

The combination of increased oxidant with decreased endogenous polypeptide and protein antioxidant activity corresponds to a decrease in cellular energetics and cell membrane lipid peroxidation. Providing large doses of growth hormone has been shown to preserve cell mass and organ function after burn injury. The role of growth hormone in oxidant injury has not been defined. We determined whether growth hormone altered the degree of lung and liver lipid peroxidation and the activity of glutathione and catalase in lung and liver tissue after burn injury. Four groups of 40 rats each were studied for 48 hours, with 1 group receiving a 20% full-thickness burn, 1 group treated with growth hormone after 20% full-thickness burn injury, a control group, and a growth hormone alone-treated group. We found increased lipid peroxidation, measured as malondialdehyde, in lung and liver tissue, and a decrease in glutathione and catalase activities during the 48-hour post-burn period. The addition of growth hormone prevented the lipid peroxidation and significantly increased tissue glutathione and catalase activities with respect to control values. Growth hormone alone also increased endogenous antioxidant levels. We conclude that growth hormone given after burn injury decreases oxidant stress by producing a significant increase in the endogenous antioxidants glutathione and catalase.

Flow cytometric analysis of primary tumors and their corresponding metastatic nodes in breast cancer.

Human breast carcinoma is biologically heterogeneous, and its clinical course may vary from one which is indolent to one which rapidly progresses. Although it is the metastasis rather than the primary tumor that ultimately overwhelms the patients, studies concerning the DNA pattern have focused on the primary tumors. This study was undertaken to identify heterogeneities between primary tumors and metastases, and to evaluate the prognostic significance of the ploidy pattern and the S-phase fraction (SPF) of metastatic nodes in axillary node positive patients. Seventy-four frozen specimens of the primary and corresponding metastatic nodes from 37 patients have been analyzed by flow cytometry and the SPF calculated. The results of ploidy pattern analysis in primaries revealed 25 diploidy (67.6%) and 12 aneuploidy (32.4%), while those in metastasis showed 17 diploidy (46.0%) and 20 aneuploidy (54.0%). The aneuploidy group in metastatic nodes had the poorer histological grade (85.0% vs. 15.0%, p = 0.02), and more mean metastatic nodes (5.75 ± 2.10 vs. 3.05 ± 1.56, p = 0.018), and more frequent lymphatic vessel invasion (65.0% vs. 11.8%, p = 0.031) than its counterpart. Decreased expression of ER (70.6% vs. 25.0% p = 0.006) and increased expression of c-erbB2 (65.0% vs. 23.5%, p = 0.012) were observed in the aneuploidy of metastatic nodes. The group with higher SPF in metastatic nodes had more metastatic nodes (5.47 ± 2.31 vs. 4.00 ± 1.78, p = 0.042), and the higher incidence of lymphatic vessel invasion (57.9% vs. 22.2%, p = 0.027), and poor histological grade (71.4% vs. 37.5%, p = 0.039). In conclusion, the cell populations in metastatic nodes revealed DNA pattern which differed from that of primary tumors. The ploidy pattern and SPF in metastatic nodes might be considered as discriminate measure for risk factors in breast cancer patients with positive axillary node.