PURPOSE: To determine the role of TGF-beta1, and its receptors, in bladder tumor, their expressions at various stages of chemically-induced rat bladder carcinogenesis were investigated. MATERIALS AND METHODS: Forty female Sprague-Dawley rats (200-250g) were given drinking water containing 0.05% N-butyl-N-(4-hydroxybutyl) nitrosamine (BBN), and twenty rats, used as a control group, were given tap water. After 10, 20, 25 and 30 weeks of the administration, the bladders of the rats were harvested. The control and BBN-treated rat bladders were analyzed for the expressions of TGF-beta1, and its receptors (RI, RII and RIII), in the mRNA by a real-time quantitative polymerase chain reaction. The protein expression was determined by immunohistochemistry. RESULTS: The expressions of the TGF-beta1 increased in the mRNA with the BBN treatment, while those of the TGF-beta receptors decreased. The up-regulation of TGF-beta1 was statistically significant after 25 weeks of BBN treatment, but down-regulations of RI, RII, and RIII were significant after 20, 25, and 30 weeks of BBN treatment, respectively (p<0.05). The immunohistochemical analysis demonstrated that the TGF-beta1, and its receptors, were localized in the tumor cytoplasm, and their intensities reflected the expression in the mRNA of these tissues. CONCLUSIONS: These data suggest that the enhanced expression of TGF-beta1, as well as the loss of the expressions of RI, RII, and RIII, at the various stages, contributes to the carcinogenesis of the bladder and tumor progression.
Animals ; Carcinogenesis* ; Cytoplasm ; Drinking Water ; Female ; Humans ; Immunohistochemistry ; Polymerase Chain Reaction ; Rats* ; Rats, Sprague-Dawley ; Receptors, Transforming Growth Factor beta ; RNA, Messenger ; Transforming Growth Factor beta ; Transforming Growth Factor beta1 ; Up-Regulation ; Urinary Bladder Neoplasms ; Urinary Bladder* ; Water

BACKGROUND: Vancomycin-resistant enterococci (VRE) infection is an emerging nosocomial problem. VRE usually multidrug-resistant, poses therapeutic dilemmas. The gene that encodes the resistance against vancomycin may spread the resistance to Staphylococcus aureus. However, there are no well-organized studies on the clinical manifestations and the factors that contribute to mortality in Korea. Herein, this study was focused on the clinical manifestations and mortality risks of patients with VRE infection during 8 years (1994-2001) in a university hospital. Understanding of the epidemiology and clinical manifestations of VRE would help develop control strategy of VRE outbreak in a hospital. METHOD: Sixty seven cases that had the VRE infection in Korea University Guro Hospital from January 1, 1994to December 12, 2001, were reviewed. We analyzed the risk factors of VRE infection and death by using univariable and multivariable statistic analyses. RESULTS: VRE infections have recently been increasing. Most of VRE infections were caused by Enterococcus faecium (85.1%) and Enterococcus faecalis (10.4%). Among 67 cases, 40 cases (59.7%) expressed VanA phenotype, 23 cases (34.3%) expressed VanB phenotype, and 3 cases expressed VanC phenotype (6%). The risk factors for death were renal dysfunction, central venous catheter insertion, and tracheostomy by using univariable analysis. The risk factor for death was renal dysfunction by using multivariable analysis. CONCLUSION: VRE has been increasing during the late 1990s in Korea. The VRE infection occurs especially in the patients who have renal dysfunction, long-term hospitalization, and ICU care. The implementation of careful isolation, infection control measures, prudent use of antibiotics, especially vancomycin, and periodic screening of patients populations are required to control VRE infection.
Anti-Bacterial Agents ; Central Venous Catheters ; Enterococcus faecalis ; Enterococcus faecium ; Epidemiology ; Hospitalization ; Humans ; Infection Control ; Korea ; Mass Screening ; Mortality ; Phenotype ; Risk Factors* ; Staphylococcus aureus ; Tracheostomy ; Vancomycin

BACKGROUND: Vancomycin-resistant enterococci (VRE) infection is an emerging nosocomial problem. VRE usually multidrug-resistant, poses therapeutic dilemmas. The gene that encodes the resistance against vancomycin may spread the resistance to Staphylococcus aureus. However, there are no well-organized studies on the clinical manifestations and the factors that contribute to mortality in Korea. Herein, this study was focused on the clinical manifestations and mortality risks of patients with VRE infection during 8 years (1994-2001) in a university hospital. Understanding of the epidemiology and clinical manifestations of VRE would help develop control strategy of VRE outbreak in a hospital. METHOD: Sixty seven cases that had the VRE infection in Korea University Guro Hospital from January 1, 1994to December 12, 2001, were reviewed. We analyzed the risk factors of VRE infection and death by using univariable and multivariable statistic analyses. RESULTS: VRE infections have recently been increasing. Most of VRE infections were caused by Enterococcus faecium (85.1%) and Enterococcus faecalis (10.4%). Among 67 cases, 40 cases (59.7%) expressed VanA phenotype, 23 cases (34.3%) expressed VanB phenotype, and 3 cases expressed VanC phenotype (6%). The risk factors for death were renal dysfunction, central venous catheter insertion, and tracheostomy by using univariable analysis. The risk factor for death was renal dysfunction by using multivariable analysis. CONCLUSION: VRE has been increasing during the late 1990s in Korea. The VRE infection occurs especially in the patients who have renal dysfunction, long-term hospitalization, and ICU care. The implementation of careful isolation, infection control measures, prudent use of antibiotics, especially vancomycin, and periodic screening of patients populations are required to control VRE infection.
Anti-Bacterial Agents ; Central Venous Catheters ; Enterococcus faecalis ; Enterococcus faecium ; Epidemiology ; Hospitalization ; Humans ; Infection Control ; Korea ; Mass Screening ; Mortality ; Phenotype ; Risk Factors* ; Staphylococcus aureus ; Tracheostomy ; Vancomycin

Benzo[a]pyrene (B[a]P) is a polycyclic aromatic hydrocarbon and ubiquitous environmental toxin with known harmful effects to human health. Abnormal phenotypes of keratinocytes are closely associated with their exposure to B[a]P. Resorcinol is a component of argan oil with reported anticancer activities, but its mechanism of action and potential effect on B[a]P damage to the skin is unknown. In this study, we investigated the effects of resorcinol on B[a]P-induced abnormal keratinocyte biology and its mechanisms of action in human epidermal keratinocyte cell line HaCaT. Resorcinol suppressed aryl hydrocarbon receptor (AhR) activity as evidenced by the inhibition of B[a]P-induced xenobiotic response element (XRE)-reporter activation and cytochrome P450 1A1 (CYP1A1) expression. In addition, resorcinol attenuated B[a]P-induced nuclear translocation of AhR, and production of ROS and pro-inflammatory cytokines. We also found that resorcinol increased nuclear factor (erythroid-derived 2)-like 2 (Nrf2) activity. Antioxidant response element (ARE)-reporter activity and expression of ARE-dependent genes NAD(P)H dehydrogenase [quinone] 1 (NQO1), heme oxygenase-1 (HO-1) were increased by resorcinol. Consistently, resorcinol treatment induced nuclear localization of Nrf2 as seen by Western analysis. Knockdown of Nrf2 attenuated the resorcinol effects on ARE signaling, but knockdown of AhR did not affect resorcinol activation of Nrf2. This suggests that activation of antioxidant activity by resorcinol is not mediated by AhR. These results indicate that resorcinol is protective against effects of B[a]P exposure. The mechanism of action of resorcinol is inhibition of AhR and activation of Nrf2-mediated antioxidant signaling. Our findings suggest that resorcinol may have potential as a protective agent against B[a]P-containing pollutants.