Survey on the Status of Smoking Inside Eating Establishments in the Cities of Kobe and Amagasaki.

BACKGROUND: The Hyogo Prefectural Government has been enforcing a smoking ban ordinance since April 2013. The present survey was conducted to determine the extent to which the smoking ban has been successfully implemented in eating establishments in Kobe City and Amagasaki City.Methods and Results:The Health and Welfare Department of the Hyogo Prefectural Government provided a list of eating establishments in Kobe and Amagasaki City. From these, we chose 1,300 from each city using random number generation. Responses were obtained from 310 establishments in Kobe City (response rate: 23.8%) and 297 in Amagasaki City (22.8%). Overall, 58.1% of the establishments surveyed in Kobe City were aware of the ordinance, a recognition rate significantly higher than that of Amagasaki City, where only 45.5% of eateries were aware of the ordinance (P=0.003). Of the Kobe City eateries, 31.7% had succeeded in implementing a complete ban on smoking. In Amagasaki City, the rate was significantly lower, at just 13.4% (P<0.001). A logistic regression analysis showed that coffee shops, Japanese-style taverns, bars, and eating establishments that served alcohol were the independent significant predictors of low compliance. Kobe City restaurants, women, and families were the independent significant predictors of high compliance with the complete smoking ban. CONCLUSIONS: The rates of recognition and implementation of the complete smoking ban were significantly lower in Amagasaki City than in Kobe City. There needs to be a strong and continuous socialization campaign to promote the ordinance.

Terfenadine antagonism against interleukin-4-modulated gene expression of T cell cytokines.

Here, we investigated whether an anti-allergy drug, terfenadine, affects interleukin-4-modulated cytokine expression in peripheral T cells. Peripheral blood T cells were first stimulated with recombinant interleukin-4 and then tested for modulation of the mRNA of a panel of cytokines using the reverse transcription-polymerase chain reaction followed by Southern blot analysis. It was found that T cells constitutively expressed mRNA specific to T helper 1 cytokines (interleukin-2, interferon-gamma, tumor necrosis factor-alpha), which was markedly downregulated upon stimulation with interleukin-4, whereas mRNA for T helper 2 cytokines such as interleukins 4, 5, and 6 was induced in response to interleukin-4. Interestingly, the interleukin-4-induced expression of all T helper 2 cytokines examined was markedly downregulated by terfenadine. Among T helper 1 cytokines, interleukin-4-mediated suppression of tumor necrosis factor-alpha was not affected by terfenadine, which, however, markedly restored mRNA expression of interferon-gamma or interleukin-2. Electrophoretic mobility shift assays using [32P]-labeled synthetic oligonucleotides encoding the consensus binding motif of activator protein-1 demonstrated that interleukin-4-induced binding of activator protein-1 composed of JunB was interfered by terfenadine. This study indicates that terfenadine, at least partially, interferes with interleukin-4-activated signaling, leading to terfenadine antagonism against the modulatory impact of interleukin-4 on T cell cytokines.

Basal cell carcinoma on the right hallux.

Basal cell carcinomas (BCCs) usually develop in sun-exposed areas. The finger, toe, and nail unit are very rare sites of BCC. We describe a patient with BCC on the right hallux. Clinically, it appeared as a brown-colored small plaque with an irregular border on the nail fold and dorsum of the right hallux. Histopathological findings were consistent with the superficial type of BCC.

Overactivation of IL-4-induced activator protein-1 in atopic dermatitis.

Atopic dermatitis is regarded as mediated by Th2-type immunity. In fact, it frequently coincides with the elevation of immunoglobulin (Ig)-E in patients' sera. Due to the pivotal role of interleukin (IL)-4 in regulation of IgE, we hypothesized if atopic dermatitis represents a hyper-reactive condition in response to IL-4 when it coincides the higher serum level of IgE. To address this possibility, peripheral blood mononuclear cells (PBMC) isolated from patients with atopic dermatitis with the high serum IgE level, from those with psoriasis or from healthy volunteers were stimulated with recombinant IL-4 and analyzed for activation of transcription factors including activator protein (AP)-1 or signal transducers and activators of transcription (STAT)-6 by employing electrophoretic mobility shift assays. Although no significant difference between atopy patients and other groups was observed in the STAT-6 binding activity in IL-4-stimulated PBMC, it over-activated the binding of AP-1 in PBMC of the patients with atopic dermatitis. The AP-1 binding was interfered by the use of an antibody directed against JunB. This is the indication that IL-4-overactivated AP-1 is composed of JunB. Furthermore, semi-quantitative RT-PCR analyses revealed marked down-modulation of a Th1 cytokine, interferon (IFN)-gamma, in IL-4-stimulated PBMC derived from atopy patients, but not that from healthy individuals. Together, our present study indicates that AP-1 is over-activated by IL-4 in PBMC of the atopic patients with the higher IgE level, thereby implying that IL-4-induced over-activation of AP-1 might be one of pathogenic factors in atopic dermatitis.