9 research outputs found

    Using WhatsApp and Facebook social groups for smoking relapse prevention: A pilot pragmatic randomized controlled tria

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    Podium Presentation 5: Paper Session 21 SMOKING AND SOCIAL MEDIA: abstract & oral presentation: no. PA21-2BACKGROUND AND OBJECTIVES: Quit attempters often have episodes of smoking relapse before they can eventually quit. Social media is becoming popular for smoking cessation and relapse prevention, but its effectiveness has not been fully explored. Our randomized controlled trial (RCT) tested the effect of group discussion and reminders via the WhatsApp or Facebook social group to prevent smoking relapse in quitters who had stopped smoking recently. METHODS: A single-blinded, pragmatic parallel three-arm pilot cluster RCT. Recent quitters, who had completed an 8-week treatment and reported abstinence for at least 7 days, were randomly allocated to WhatsApp (n = 42), Facebook (n = 40), and Control group (n = 54). The 2 intervention groups participated in a 2-month group discussion moderated by a trained smoking cessation counselor and received a self-help booklet on smoking cessation. The Control group only received the booklet. FINDINGS: Fewer subjects in the WhatsApp group (14.3%) reported smoking in the past 7 days than the Control group (44.4%) at 2- (odds ratio (OR) = 0.21, 95%CI 0.08-0.58) and 6-month follow-up (35.7% versus 61.1%, OR = 0.35, 95%CI 0.15-0.82). Facebook group showed a lower smoking rate at 2- (30.0 % versus 44.4%, OR = 0.54, 95%CI 0.23-1.27) and 6-month follow-up (52.5 % versus 61.1%, OR = 0.70, 95%CI 0.31-1.61), but the difference was not significant. WhatsApp social groups had more moderators’ posts (Median: 60 versus 31.5; Mann-Whitney U test: p=.05) and subjects’ posts (Median: 35 versus 6; Mann-Whitney U test: p=.07) than Facebook counterparts. CONCLUSIONS: The intervention via WhatsApp social group was effective in reducing relapse, probably because of enhanced discussion and social support. Inactive discussion in the Facebook social group might have attributed to the lower effectiveness. Funding: The work was funded by Tung Wah Group of Hospitals. The organization was funded by the Tobacco Control Office of the Department of Health. Corresponding Author: Yee Tak Derek Cheung, The University of Hong Kong, Hong Kong, [email protected]

    Prostaglandin E2 modulates dendritic cell function during chlamydial genital infection

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    Inflammatory responses mediated by antigen-presenting dendritic cells (DCs), can be modulated by the presence of prostaglandins (PG), including prostaglandin E2 (PGE2). PGE2 modifies the production of an immune response by altering DC function through PGE2 receptors. PGE2 is produced by epithelial cells lining the murine female reproductive tract during Chlamydia muridarum infection and likely manipulates the antichlamydial immune response during antigen uptake in the genital mucosa. Our data demonstrate that the PGE2 present locally in the genital tract upon chlamydial genital infection enhanced the recruitment of CD11b+ conventional DCs, but not CD45R+ plasmacytoid DCs, to infected genital tract tissue and draining lymph nodes in vivo. Furthermore, exposure to PGE2in vitro during infection of murine bone-marrow-derived conventional DCs (cDCs) boosted interleukin-10 mRNA and protein while not influencing interleukin-12p40 production. Infection of cDCs markedly increased mRNA production of the costimulatory molecules CD86, CD40 and a member of the C-type lectin family, DEC-205, but addition of PGE2 increased other costimulatory molecules and C-type lectins. Also, exposure of PGE2 to infected cDCs increased FcÎłRIII and FcÎłRIIb, suggesting that PGE2 enhances the uptake and presentation of C. muridarum and augments production of the antichlamydial adaptive immune response. Taken together, the data suggest that exposure of infected cDCs to PGE2 drives production of a diverse adaptive immune response with implications for regulating tissue inflammation

    Irreversible Modification of the Anion Transporter

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    From: The red cell membrane. - p. 329-367, p. I-VI
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