Hailey-Hailey disease on sun-exposed areas.
Explore the source record for details and available documents.
Biomedical subjects
Publications and source records attributed to T J Yoon.
Explore the source record for details and available documents.
We previously isolated a lectin of the Korean mistletoe (Viscum album coloratum). The cDNA clones that encode the A- or the B-chain of the Korean mistletoe lectin were cloned by reverse transcriptase polymerase chain reaction (RT-PCR). The mRNAs that were extracted from the Korean mistletoe were amplified, ligated into the pGEM-T easy vector, and screened with a Korean mistletoe lectin-specific probe. The probe was prepared by PCR amplification of the Korean mistletoe DNA using a primer set designed on the basis of amino acid sequences of the Korean mistletoe lectin that we had purified and reported. Unlike a recent report, which states that the European mistletoe lectin gene has no isoforms, several different clones of the A- and B-chains of the Korean mistletoe lectin were cloned from the same primer set. Three clones of each were selected for sequencing. The sizes of the A-chains were 762, 762, and 768 bp, respectively. The B-chain sizes were 798, 789, and 789 bp, respectively. Each of the clones showed significant variation in the amino acids sequence, including the N-linked glycosylation sites of the lectin. The sequence analysis of each of the Korean lectin clones, in comparison with the European mistletoe lectin and the other type II ribosome binding proteins, is discussed in the text. In addition, Southern blot analysis of the Korean mistletoe genomic DNA, restricted by different enzymes and hybridized with the lectin DNA, showed multi-bands, supporting the existence of multicopy genes or a gene family. These data suggest that heterogeneity of the mistletoe lectin is not only introduced by post-translational modifications, but also by expression of isotypes of the lectin genes.
2- or 6-(1-hydroxyiminoalkyl)-5,8-dimethoxy-1, 4-naphthoquinone(2- or 6-hyim-DMNQ) derived from the roots of Lithospermum erythrorhizon was synthesized for the evaluation of antitumor activities. Among those derivatives, 2-hyim-DMNQ-S33 was found to be a potent anticancer agent. This compound suppressed the proliferation of Radiation Induced Fibrosarcoma (RIF) cells in a dose-dependent manner. 2-hyim-DMNQ-S33 significantly prolonged the survival time by 239% as compared with Sarcoma 180 tumor-bearing control mice in vivo. We found that the compound significantly suppressed phosphorylation of extracellular signal-regulated kinase (pERK) and activated c-jun-N-terminal kinase (JNK) and protein kinase C (PKC)-alpha following 4 h-treatment. These findings indicate that 2-hyim-DMSQ-S33 exerts antitumor activities by regulating pERK, JNK and PKC-alpha.
The adjuvant effect of lectins (KML-C) isolated from Korean mistletoe (Viscum album coloratum) on induction of humoral and cellular immune responses against keyhole limpet hemocyanine (KLH) was examined. When mice were immunized subcutaneously (s.c.) with KLH (20 micrograms/mouse) admixed with or without 50 ng/mouse of KML-C (KLH + KML-C), mice immunized with KLH + KML-C showed significantly higher antibody titers against KLH than those immunized with KLH alone, showing the highest titer 5 weeks after immunization. Furthermore, boost immunization with KLH + KML-C at 2-week interval elicited much higher activity than single immunization to enhance antibody responses against KLH. The assay for determining isotypes of antibodies revealed that KML-C augmented KLH-specific antibody titers of IgG1, IgG2a and IgG2b. The culture supernatants obtained from the splenocytes of mice treated with KLH + KML-C also showed a higher level of both KLH-specific Th-1 (IL-2 and IFN-gamma) and Th-2 type cytokine (IL-4). In an in vitro analysis of T lymphocyte proliferation to KLH on week 4, the splenocytes of mice treated with KLH + KML-C showed a significantly higher proliferating activity than those treated with KLH alone. In addition, mice immunized twice with KLH + KML-C and followed by intrafootpad (i.f.) injection of KLH (50 micrograms/site) 14 weeks after the primary immunization induced a higher delayed-type hypersensitivity (DTH) reaction than mice treated with KLH alone. These results suggest that KML-C is a potent immunoadjuvant to enhance cellular and humoral immune responses.
BACKGROUND: Quinolone antibiotics are popularly prescribed antibiotics because of their wide antibacterial spectrum and lowered bacterial resistance. Quinolone antibiotics are one of the well-known photosensitizers that induce phototoxicity. Their role in photocarcinogenesis has been suggested in some studies. MATERIAL AND METHODS: Mice were treated with two quinolone antibiotics (ciprofloxacin, which is less phototoxic, and pefloxacin, which is more phototoxic) to study the effect of the antibiotics on sunburn and immune suppression by ultraviolet A (UVA) irradiation. The effects of a combined treatment with UVA and these quinolone antibiotics were measured on back skin swellings, sunburn cell formations, depletion of epidermal Langerhans cells, and local and systemic suppression of contact hypersensitivity. RESULTS: Mice treated with both UVA and quinolone showed significantly increased back skin swellings and decreased epidermal Langerhans cells than mice treated with UVA only. Sunburn cells were increased significantly in mice treated with pefloxacin and 50 J/cm2 of UVA. Combination of pefloxacin and UVA suppressed local contact hypersensitivity significantly, but not systemic contact hypersensitivity. CONCLUSION: Phototoxic quinolones augmented the effect of UVA by increasing sunburn and apoptosis, depleting Langerhans cells and suppressing local immune response. By affecting apoptosis and immune suppression, they may facilitate photocarcinogenesis caused by UVA.
BACKGROUND: Vitiligo on hairy areas like the scalp and eyebrows is frequently associated with leukotrichia and repigmentation by photochemotherapy is usually difficult because of a deficient melanocyte reservoir. Although epidermal grafting to supply melanocytes is very effective for stable vitiligo, hair growth inhibits successful transfer of melanocytes from grafted epidermis in dense hair-bearing regions. OBJECTIVE: To investigate the effectiveness of preoperative chemical epilation to improve the results of epidermal graft by suction blister on hairy areas. METHODS: Two patients who had vitiligo with leukotrichia on the face and scalp were treated with epidermal grafting using suction blister after chemical epilation. Two weeks after the graft they were treated with topical psolaren plus ultraviolet A (PUVA) therapy. RESULTS: Epidermal grafting was performed successfully, and successful repigmentation of the skin with significant improvement of leukotrichia was observed in each of two patients. CONCLUSION: Chemical epilation followed by epidermal grafting is a safe, easy, and effective treatment for vitiligo affecting hairy regions.
The mistletoe lectins are major active components in the extract of European mistletoes that have been widely used in adjuvant chemotherapy of cancer. This study was performed to investigate the mechanism of anticancer and antimetastatic activity of the purified Korean mistletoe lectin (Viscum album L. coloratum agglutinin, VCA). C57BL6 mice inoculated with B16-BL6 melanoma cells and treated with VCA were assessed for survival and metastasis. The induction of apoptosis of B16-BL6 cells by VCA was investigated by morphological changes, DNA fragmentation characteristics, and cell cycle analysis. The antiangiogenic activity of VCA was also measured by the CAM (choriallantoic membrane) assay. Length of survival of mice was increased and lung metastasis was inhibited by VCA. Treatment of cells with VCA resulted in growth suppression, nuclear morphological changes, DNA fragmentation, and an increased fraction of cells in sub-G1 consistent with apoptosis. Antiangiogenesis of VCA was assessed by CAM assay, where vessel growth induced by fat emulsion was decreased. These results suggest that VCA inhibits tumor growth and metastasis by increasing apoptosis and inhibiting angiogenesis.
Papular elastorrhexis is a rare disease developing asymptomatic skin-colored small papules in adolescence with histopathological loss of elastic fibers. There has been no established treatment for this disease. A 4-year-old Korean boy had multiple, hard, whitish papules on his chest and back for one year. Histopathologic examination revealed focal loss of elastic fibers in the dermis, and X-ray examination showed no bony abnormalities. His skin lesions were improved by intralesional injections of triamcinolone but recurred after four months.
Two Korean men complained of painful erythematous swellings of the proximal nail folds. When we removed the overlying nail plates, we observed new ones growing under the old ones. These painful swellings disappeared after the affected nails were extracted. We found typical onychomadesis in another finger during the follow-up, suggesting that the initial condition marked the onset of onychomadesis. Because both patients had plaster casts removed recently and histories of trauma, it was hypothesized that trauma might be responsible for this peculiar condition.
We have examined uncoupling protein-2 (UCP2) gene expression in the adipose tissue of obese and normal rats and mice, and also in differentiated rat adipocytes in primary culture. Expression of the UCP2 gene was examined in rat and mouse adipose tissues using both RT-PCR and Northern blotting. Although the RT-PCR was not quantitative, the band corresponding to the UCP2 mRNA was stronger in white adipose tissue than in brown fat, regardless of the body weight of the rats. In agreement with the RT-PCR data, there was a higher level of UCP2 mRNA in the white adipocytes than in brown adipocytes, the level being greater in obese mice. Fibroblastic preadipocytes were obtained from the inguinal fat pad of suckling rats. Lipid droplets developed inside the cells upon differentiation and adipsin and UCP2 mRNAs were detected by Northern blotting. Both mRNAs were evident in the adipocytes at 4, 6, and 10 d after the induction of differentiation. There was no indication that the expression of UCP2 was markedly affected by the addition of leptin, dexamethasone or isoprenaline.
Cytotoxic lectins (KML-C) were isolated from an extract of Korean mistletoe [Viscum album C. (coloratum)] by affinity chromatography on a hydrolysed Sepharose 4B column, and the chemical and biological properties of KML-C were examined, partly by comparing them with a lectin (EML-1) from European mistletoe[Viscum album L. (loranthaceae)]. The hemagglutinating activity of KML-C was inhibited by N-acetyl-D-galactosamine and D-galactose at the minimum concentrations of 6.3 and 12.5 microM/ml, respectively. Further biochemical analyses indicated that KML-C consists of four chains (Mr = 27.5, 30, 31 and 32.5 kDa) which, in some of the molecules, are disulfide-linked, and that the chains of KML-C are distributed over a broad range of isoelectric points (pI), 8.0 to 9.0, whereas the range for EML-1 is 6.6-7.0. A difference was also observed between the N-terminal sequences of KML-C and EML-1. The isolated lectins showed strong cytotoxicity against various human and murine tumor cells, and the cytotoxic activity of KML-C was higher than that of EML-1. Tumor cells treated with KML-C exhibited typical patterns of apoptotic cell death, such as apparent morphological changes and DNA fragmentation, and its apoptosis-inducing activity was blocked by addition of Zn2+, an inhibitor of Ca2+/Mg2+ -dependent endonucleases, in a dose-dependent manner. These results suggest that KML-C is a novel lectin related to the cytotoxicity of Korean mistletoe, and that its cytotoxic activity against tumor cells is due to apoptosis mediated by Ca2+/Mg2+ -dependent endonucleases.
A 29-year-old Korean woman had erythematous papular patches on her face for six months. The eruptions recurred in a cyclic fashion along with her menstruation. The patient responded positively to an intradermal skin test for estrogen and showed marked improvement with the antiestrogen drug, Tamoxifen. We concluded that sensitivity to her own estrogen caused this dermatitis, that an intradermal skin test with progesterone and estrogen should be carried out routinely in patients with cyclic premenstrual flares, and that tamoxifen can be used as a specific therapy. To the best of our knowledge, this woman is the first patient with estrogen dermatitis reported in Korea.
The association of exposure to bleomycin with the development of scleroderma-like cutaneous abnormalities has been reported. We experienced a case of scleroderma involving the hands, feet, and forearms after bleomycin chemotherapy. The present report supports the possible causal relation of bleomycin with scleroderma. Regarding the widespread use of bleomycin, this complication is thought to be under appreciated.
We examined the inhibitory effect of an aqueous extract (referred to as KM-110) from Viscum album coloratum, a Korean mistletoe, on tumour metastasis produced by highly metastatic murine tumour cells, B16-BL6 melanoma, colon 26-M3.1 carcinoma and L5178Y-ML25 lymphoma cells, using experimental and spontaneous metastasis models in syngeneic mice. In experimental metastasis of B16-BL6 and colon 26-M3.1 cells, intravenous (i.v.) administration of KM-110 (100 micrograms/mouse) 1 day after tumour inoculation significantly inhibited lung metastasis of both tumour cells. The administration of KM-110 also exhibited a therapeutic effect on liver and spleen metastasis of L5178Y-ML25 lymphoma cells. Furthermore, in spontaneous metastasis of B16-BL6 melanoma cells, multiple administration of KM-110 into tumour-bearing mice resulted in significant inhibition of lung metastasis by tumour cells, as well as the suppressive activity to the growth of primary tumour. In in vivo analysis for tumour-induced angiogenesis, the i.v. administration of KM-110 suppressed tumour growth and inhibited the number of blood vessels oriented towards the tumour mass. In a bioassay, the culture supernatant (KM-110-treated medium) of murine peritoneal macrophages that had been stimulated with KM-110 (1-10 micrograms/ml) for 30 min followed by 24 h incubation in fresh medium showed a strong tumour necrosis factor-alpha (TNF-alpha) activity. In addition, KM-110-treated medium significantly inhibited the growth of in vitro cultures of rat lung endothelial (RLE) cells. These results suggested that the extract of Korean mistletoe inhibits tumour metastasis caused by haematogenous as well as non-haematogenous tumour cells, and that its antimetastatic effect results from the suppression of tumour growth and the inhibition of tumour-induced angiogenesis by inducing TNF-alpha.
We here demonstrated the prophylactic effect of an extract (KM-110) from Viscum album coloratum, a Korean mistletoe, on tumor metastasis produced by highly metastatic tumor cells, colon 26-M3.1 carcinoma, B16-BL6 melanoma and L5178Y-ML25 lymphoma cells, using experimental models in mice. Intravenous (i.v.) administration of KM-110 (100 microg/mouse) 2 days before tumor inoculation significantly inhibited lung metastasis of B16-BL6 and colon 26-M3.1 cells, and liver and spleen metastasis of L5178Y-ML25 cells. The prophylactic effect of KM-110 on tumor metastasis was evident with various administration routes, i.e. subcutaneous, oral, intranasal as well as i.v., and was dependent upon the dose of KM-110 administered. Furthermore, mice given KM-110 (100 microg) 2 days before tumor inoculation showed significantly prolonged survival rates compared with the untreated mice. In a time course analysis of NK activity, i.v. administration of KM-110 (100 microg) significantly augmented NK cytotoxicity to Yac-a tumor cells from 1 to 3 days after KM-110 treatment. Furthermore, depletion NK cells by injection of rabbit anti-asialo GM1 serum completely abolished the inhibitory effect of KM-110 on lung metastasis of colon 26-M3.1 cells. These results suggest that KM-110 possesses immunopotentiating activity which enhances the host defense system against tumors, and that its prophylactic effect on tumor metastasis is mediated by NK cell activation.