No abstract available.
Hemangioma* ; Injections, Intralesional* ; Propranolol ; Triamcinolone*

Author list should be corrected.

No abstract available.
Dapsone* ; Herpesvirus 4, Human* ; Hypersensitivity*

No abstract available.
Dermatitis, Contact* ; Prurigo*

Members of the genus Acinetobacter are recognized as newer pathogens of the nosocomial infection with an increasing frequency in recent years. Strains that belonged to A. calcoaceticus-A. baumannii complex (genomic species 1, 2, 3, and 13TU) were major groups associated with nosocomial infection. Phenotypic identification was unreliable and laborious method to classify Acinetobacter strains into 19 genomic species. Rapid and reliable identification of clinical isolates is essential to diagnosis and epidemiology of Acinetobacter. We investigated the suitability of amplified ribosomal DNA restriction analysis (ARDRA) to identify genomic species of 131 Acinetobacter isolates. The 16S rRNA genes (ribosomal DNA) were enzymatically amplified and the amplified PCR products were restricted independently with the enzymes, AluI, CfoI, and MboI. Genomic species of Acinetobacter was classified by the combinations of restriction patterns. The analysis was showed that restriction profiles were characteristic for each genomic species. One hundred fourteen isolates were identified as A. baumannii, twelve were identified as genomic species 13TU, and one was identified as genomic species 3. Four isolates were found to be unknown organisms. All of the isolates which were identified to A. baumannii by phenotypic tests were completely discriminated into A. baumannii and genomic species 13TU by ARDRA. This study demonstrates that ARDRA is a rapid and simple techniques for the identification of Acinetobacter species according to the genomic species.
Acinetobacter baumannii* ; Acinetobacter calcoaceticus* ; Acinetobacter* ; Cross Infection ; Diagnosis ; DNA, Ribosomal* ; Epidemiology ; Genes, rRNA ; Polymerase Chain Reaction

BACKGROUND: UVB irradiation induces acute inflammation through expressions of IL-6, IL-8, and TNF-alpha, in keratinocytes. Curcumin, extracted from the rhizomes of Curcuma longa, has been described as having anti-inflammatory properties; however, it still unknown as to whether curcumin inhibits the UVB-induced expressions of IL-6, IL-8, and TNF-alpha in HaCaT cell lines. OBJECTIVE: In this study we investigated the effects of curcumin on the expression of IL-6, IL-8, and TNF-alpha in HaCaT cells, as well as the photoprotective effect of curcumin ointment in UVB-irradiated hair less mice. METHODS: HaCaT cells were irradiated with various doses of UVB (0, 100, 200, 300 mJ/cm2). Total RNA was extracted from the cells and gene expression was confirmed by RT-PCR, EMSA, and Western blot analysis. In addition we examined whether the ointment containing curcumin prevents the photo damaging events in hairless mice. RESULTS: UVB-irradiated HaCaT cells clearly showed an increased expression of IL-6, IL-8, and TNF-alpha in a UVB dose-dependent manner (0, 100, 200, 300 mJ/cm2). Interestingly, pretreatment of curcumin (40 uM) dramatically reduced the expressions of UVB-induced IL-6, IL-8, and TNF-alpha. In addition, activation of NF-kappaB and MAPKs (p38, JNK, ERK) by UVB were partially attenuated by pretreatment of curcumin in HaCaT cells. Furthermore, the application of ointment containing curcumin partially protected the erythema and skin atrophy in UVB-irradiated hairless nude mice. CONCLUSION: Collectively, these results indicate that curcumin may be applied as a promising anti-inflammatory natural agent through modulation of inflammatory cytokines such as IL-6, IL-8, and TNF-alpha.
Atrophy ; Blotting, Western ; Curcuma ; Curcumin ; Cytokines ; Erythema ; Gene Expression ; Hair ; Inflammation ; Interleukin-6 ; Interleukin-8 ; Keratinocytes ; NF-kappa B ; Rhizome ; RNA ; Skin ; Tumor Necrosis Factor-alpha

PURPOSE: This study was designed to investigate effect of the etoposide on expression of cell cycle regulatory proteins and apoptosis-related proteins in human skin fibroblast (HSF). MATERIALS AND METHODS: HSF cells were treated with etoposide. After treatment, expression patterns of cell cycle regulatory proteins and apoptosis-related proteins were analyzed by using Immunoprecipitation-Western blot method and RT-PCR. RESULTS: Immediately after etoposide treatment, E2F-1 was up- regulated following MDM2 down-regulation. After E2F-1 up-regulation, p53 and p21WAF1 level was markedly increased without or with mRNA up-regulation, respectively. Consistent with these results, cell cycles arrested in mainly G1 phase 24 hr after etoposide treatment. However, HSF cells progressed into apoptosis 72 hr after etoposide treatment. In this process, caspase-3 activation and Bax up-regulation were observed. CONCLUSION: In early response of etoposide treatment, E2F-1 plays an important role in p53 accumulation through MDM2 down- regulation. The increased p53 induce an increase of p21WAF1 level through p21WAF1 mRNA up-regulation. However, after long term treatment of etoposide, HSF cells resulted in apoptotic cell death through caspase-3 activation and Bax up-regulation.
Apoptosis ; Caspase 3 ; Cell Cycle Proteins ; Cell Cycle* ; Cell Death ; Down-Regulation ; Etoposide ; Fibroblasts* ; G1 Phase ; Genes, p53 ; Humans* ; RNA, Messenger ; Skin* ; Up-Regulation

Cancer is considered to occur through abnormal growth and differentiation processes, in which oncogenes and tumor suppressor genes are deeply related. Cellular responses to DNA-damaging agents are believed to be critical determinants of human tumorigenesis. Cell cycle arrests and DNA repair following DNA damage require the coordination of multiple gene products that, as a whole, serve to maintain the integrity of the genome. Within the cell cycle, both G1-S and G2-M phase transitions are under constant surveillance by checkpoint genes for the protection of cells from either exogenous or endogenous DNA-damaging agents. p53 tumor suppressor gene mediates cell cycle perturbations in response to DNA damage, and play a role in cell death, genetic stability, and cancer susceptibility. Recently, gene therapy with p53 tumor suppressor gene is expected as a new effective therapeutic strategy in many kinds of cancer. By using retroviral vector system, we transduced p53 tumor suppressor gene into human osteosarcoma cells, and analysed its growth suppression and apoptosis inducing effects. Combined effects of p53 gene therapy with chemotherapeutic agent or radiation were also analysed. Titer of ecotrophic p53 retrovirus was 5.0x10/ml, and that of amphotrophic p53 retrovirus was 2.0x10/ml when NIH3T3 cells were used as target cells. Human osteosarcoma cells infected with amphotrophic p53 retroviruses showed increased p21waf1 gene expression, which acts as a major cyclin-dependent kinase inhibitor in DNA damage responses. In normal DMEM media, human skin fibroblasts infected with amphotrophic p53wt retroviruses showed very slow growing (1.7 fold increase in doubling time) and very low saturation density (50% decrease in cell density). In media containing chemotherapeutic agent, human osteosarcoma cells infected with p53wt retroviruses died rapidly; 75% of them died within 4 days and all of them died within 10 days of incubation with chemotherapeutic agent. Their DNAs were extracted and electrophoresed in agarose gel, and we identified DNA ladders characteristic of apoptotic cell death. When human osteosarcoma cells infected with p53 retroviruses were irradiated with ultraviolet light, more than 95% of cancer cells died within 1 day; whereas mock infected cells showed only less than 5% of cell death. These findings suggest that retroviral vector mediated p53 tumor suppressor gene transfer into cancer cells can suppress tumor cell growth and decrease tumor cell density effectively. These findings also suggest that effective induction of tumor cell apoptosis can be obtained when p53 gene therapy is used in combination with chemotherapy or radiotherapy.
Apoptosis ; Carcinogenesis ; Cell Count ; Cell Cycle ; Cell Cycle Checkpoints ; Cell Death ; DNA ; DNA Damage ; DNA Repair ; Drug Therapy ; Fibroblasts ; Gene Expression ; Genes, p53 ; Genes, Tumor Suppressor* ; Genetic Therapy* ; Genome ; Humans ; Oncogenes ; Osteosarcoma ; Phase Transition ; Phosphotransferases ; Radiotherapy ; Retroviridae* ; Sepharose ; Skin ; Ultraviolet Rays ; Zidovudine

No abstract available.
Blister*

BACKGROUND: The wound healing process is delayed by bacterial infection. Thus, proper prevention and treatment of infection are very important parts of wound healing. Silver has been used for wound dressing material due to its antimicrobial activities. Recently, a new nanochemistry technique made silver particles <20 nm in diameter, and this nanocrystalline silver can be used for dressing material. However, the antimicrobial effects of Nanosilver-coated gauze for bacterial skin infections are not well known. OBJECTIVE: We investigated the antimicrobial activities of 3 Nanosilver-coated gauzes (1500A, 800A and 100A) against known pathogens: Methicillin susceptible Staphylococcus aureus (MSSA), Methicillin resistant Staphylococcus aureus (MRSA) and Pseudomonas aeruginosa (P. aeruginosa). METHODS: The antimicrobial effects of Nanosilver-coated gauze on MSSA, MRSA and P. aeruginosa were tested using a disk diffusion method. RESULTS: Nanosilver-coated gauzes of 1500A and 800A thicknesses showed antimicrobial activities against MSSA, implying susceptibility, while the 100A Nanosilver-coated gauze showed intermediate activity. For MRSA and P. aeruginosa, 1500A Nanosilver-coated gauze showed antimicrobial activities, but 800A and 100A Nanosilver-coated gauzes were not effective. CONCLUSION: The results suggest that a 1500A thick Nanosilver-coated gauze has antimicrobial activities against MSSA, MRSA and P. aeruginosa in culture. Therefore, nanocrystalline silver may be a promising alternative dressing material for successful control of cutaneous infections.
Bacteria ; Bacterial Infections ; Bandages ; Diffusion ; Methicillin ; Methicillin Resistance ; Methicillin-Resistant Staphylococcus aureus ; Pseudomonas aeruginosa ; Silver ; Skin ; Staphylococcus aureus ; Wound Healing