540 research outputs found

    Talking about Public Health: An Analysis of a Municipal Public Health Twitter Feed

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    Social media has become an increasingly popular tool used by experts and laypeople alike to obtain, share, and create health information. Public health authorities have also begun to use web 2.0 platforms to share information and foster engagement with the public. Existing public health research about Twitter has explored its uses as a tool of health promotion, however communication on the Twitter platform has not yet been explored from a critical public health perspective. The purpose of this study is to analyze how talk about public health occurs online via Twitter. Using both content and discourse analysis of communication on Toronto Public Health\u27s official Twitter feed, this study explores emergent themes of biomedicalization; how biomedical power is affirmed; and assesses whether Twitter can be a useful platform to facilitate a dialogue between citizen and state. The immediacy and transparency, characteristic of the Twitter platform, do support dialogues that question and responsibilize the health authority, however biomedical power is most often affirmed rather than challenged. This study argues that while Twitter may be an effective tool to facilitate engagement, it does little to reshape the existing power dynamic between citizen and state

    miRNA expression profiles and molecular networks in resting and LPS-activated BV-2 microglia-Effect of cannabinoids.

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    Mammalian microRNAs (miRNAs) play a critical role in modulating the response of immune cells to stimuli. Cannabinoids are known to exert beneficial actions such as neuroprotection and immunosuppressive activities. However, the underlying mechanisms which contribute to these effects are not fully understood. We previously reported that the psychoactive cannabinoid Δ9-tetrahydrocannabinol (THC) and the non-psychoactive cannabidiol (CBD) differ in their anti-inflammatory signaling pathways. Using lipopolysaccharide (LPS) to stimulate BV-2 microglial cells, we examined the role of cannabinoids on the expression of miRNAs. Expression was analyzed by performing deep sequencing, followed by Ingenuity Pathway Analysis to describe networks and intracellular pathways. miRNA sequencing analysis revealed that 31 miRNAs were differentially modulated by LPS and by cannabinoids treatments. In addition, we found that at the concentration tested, CBD has a greater effect than THC on the expression of most of the studied miRNAs. The results clearly link the effects of both LPS and cannabinoids to inflammatory signaling pathways. LPS upregulated the expression of pro-inflammatory miRNAs associated to Toll-like receptor (TLR) and NF-κB signaling, including miR-21, miR-146a and miR-155, whereas CBD inhibited LPS-stimulated expression of miR-146a and miR-155. In addition, CBD upregulated miR-34a, known to be involved in several pathways including Rb/E2f cell cycle and Notch-Dll1 signaling. Our results show that both CBD and THC reduced the LPS-upregulated Notch ligand Dll1 expression. MiR-155 and miR-34a are considered to be redox sensitive miRNAs, which regulate Nrf2-driven gene expression. Accordingly, we found that Nrf2-mediated expression of redox-dependent genes defines a Mox-like phenotype in CBD treated BV-2 cells. In summary, we have identified a specific repertoire of miRNAs that are regulated by cannabinoids, in resting (surveillant) and in LPS-activated microglia. The modulated miRNAs and their target genes are controlled by TLR, Nrf2 and Notch cross-talk signaling and are involved in immune response, cell cycle regulation as well as cellular stress and redox homeostasis

    Pathways and gene networks mediating the regulatory effects of cannabidiol, a nonpsychoactive cannabinoid, in autoimmune T cells.

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    BackgroundOur previous studies showed that the non-psychoactive cannabinoid, cannabidiol (CBD), ameliorates the clinical symptoms in mouse myelin oligodendrocyte glycoprotein (MOG)35-55-induced experimental autoimmune encephalomyelitis model of multiple sclerosis (MS) as well as decreases the memory MOG35-55-specific T cell (TMOG) proliferation and cytokine secretion including IL-17, a key autoimmune factor. The mechanisms of these activities are currently poorly understood.MethodsHerein, using microarray-based gene expression profiling, we describe gene networks and intracellular pathways involved in CBD-induced suppression of these activated memory TMOG cells. Encephalitogenic TMOG cells were stimulated with MOG35-55 in the presence of spleen-derived antigen presenting cells (APC) with or without CBD. mRNA of purified TMOG was then subjected to Illumina microarray analysis followed by ingenuity pathway analysis (IPA), weighted gene co-expression network analysis (WGCNA) and gene ontology (GO) elucidation of gene interactions. Results were validated using qPCR and ELISA assays.ResultsGene profiling showed that the CBD treatment suppresses the transcription of a large number of proinflammatory genes in activated TMOG. These include cytokines (Xcl1, Il3, Il12a, Il1b), cytokine receptors (Cxcr1, Ifngr1), transcription factors (Ier3, Atf3, Nr4a3, Crem), and TNF superfamily signaling molecules (Tnfsf11, Tnfsf14, Tnfrsf9, Tnfrsf18). "IL-17 differentiation" and "IL-6 and IL-10-signaling" were identified among the top processes affected by CBD. CBD increases a number of IFN-dependent transcripts (Rgs16, Mx2, Rsad2, Irf4, Ifit2, Ephx1, Ets2) known to execute anti-proliferative activities in T cells. Interestingly, certain MOG35-55 up-regulated transcripts were maintained at high levels in the presence of CBD, including transcription factors (Egr2, Egr1, Tbx21), cytokines (Csf2, Tnf, Ifng), and chemokines (Ccl3, Ccl4, Cxcl10) suggesting that CBD may promote exhaustion of memory TMOG cells. In addition, CBD enhanced the transcription of T cell co-inhibitory molecules (Btla, Lag3, Trat1, and CD69) known to interfere with T/APC interactions. Furthermore, CBD enhanced the transcription of oxidative stress modulators with potent anti-inflammatory activity that are controlled by Nfe2l2/Nrf2 (Mt1, Mt2a, Slc30a1, Hmox1).ConclusionsMicroarray-based gene expression profiling demonstrated that CBD exerts its immunoregulatory effects in activated memory TMOG cells via (a) suppressing proinflammatory Th17-related transcription, (b) by promoting T cell exhaustion/tolerance, (c) enhancing IFN-dependent anti-proliferative program, (d) hampering antigen presentation, and (d) inducing antioxidant milieu resolving inflammation. These findings put forward mechanism by which CBD exerts its anti-inflammatory effects as well as explain the beneficial role of CBD in pathological memory T cells and in autoimmune diseases

    Measurement of Transverse Polarization of Electrons Emitted in Free Neutron Decay

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    The final analysis of the experiment determining both components of the transverse polarization of electrons (σT1\sigma_{T_{1}}, σT2\sigma_{T_{2}}) emitted in the β\beta-decay of polarized, free neutrons is presented. The T-odd, P-odd correlation coefficient quantifying σT2\sigma_{T_{2}}, perpendicular to the neutron polarization and electron momentum, was found to be R=R= 0.004±0.012±\pm0.012\pm0.005. This value is consistent with time reversal invariance, and significantly improves both earlier result and limits on the relative strength of imaginary scalar couplings in the weak interaction. The value obtained for the correlation coefficient associated with σT1\sigma_{T_{1}}, N=N= 0.067±0.011±\pm0.011\pm0.004, agrees with the Standard Model expectation, providing an important sensitivity test of the experimental setup. The present result sets constraints on the imaginary part of scalar and tensor couplings in weak interaction. Implications for parameters of the leptoquark exchange model and minimal supersymmetric model (MSSM) with R-parity violation are discussed

    Alcohol use disorder increases the risk of nonfatal and fatal cardiovascular disease : an 11-year follow-up of a Polish population-based cohort. The HAPIEE study

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    INTRODUCTION Self‑reported alcohol intake is an inaccurate measure, especially in heavy drinkers. The simple 4‑item CAGE questionnaire assessing alcohol use disorder was found to be positively associated with alcohol consumption and mortality. OBJECTIVES This study aimed to investigate the relationship between alcohol use disorder assessed with the CAGE questionnaire and the incidence of cardiovascular disease (CVD) in a population‑based Polish sample. PATIENTS AND METHODS A cohort study with an 11‑year follow‑up was conducted. A random sample of 10 728 residents of Kraków aged 45 to 69 years completed baseline examination, including the CAGE questionnaire. Information on new cases of CVD was obtained from further questionnaires and confirmed by clinical diagnosis. Data on mortality and causes of death were obtained from the local registry, the Central Statistical Office, and the participants’ families. The effect of the CAGE score on the risk of CVD was assessed using Cox proportional hazard models. RESULTS The analysis included 7112 individuals who completed the CAGE questionnaire and were free of CVD at baseline. No alcohol use disorder was reported in 94% of the participants. There was a positive association between the CAGE score and the risk of CVD. In the fully adjusted model, compared with participants scoring 0, the hazard ratios among those scoring 3 and 4 points were 2.19 (95% CI, 1.43–3.37) and 2.79 (95% CI, 1.65–4.73), respectively. The association was somewhat stronger for fatal CVD. CONCLUSIONS We found a strong, graded association between the CAGE score and the risk of CVD incidence, which was independent of other risk factors for CVD. The CAGE questionnaire might be considered as an additional tool to identify individuals at high risk of CVD

    Study of three-nucleon dynamics in the dp breakup collisions using the Wasa detector

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    An experiment to investigate the ^{1}H(d,pp)n breakup reaction using a deuteron beam of 300, 340, 380 and 400 MeV and the WASA detector has been performed at the Cooler Synchrotron COSY-Jülich. As a first step, the data collected at the beam energy of 340 MeV are analysed, with a focus on the proton–proton coincidences registered in the Forward Detector. Elastically scattered deuterons are used for precise determination of the luminosity. The main steps of the analysis, including energy calibration, particle identification (PID) and efficiency studies, and their impact on the final accuracy of the result, are discussed
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