14 research outputs found

    Social Media Advocacy

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    Our research project’s purpose is to inform the local community on the ethics and effectiveness as well as the exploitive power of using social media to promote international and domestic causes. We will educate the public and professionals on the responsible use of social media in advocacy and the consequences of its misuse. We will achieve this goal by researching social media movements and their lasting effects in academic journals and major news outlets. We will then share these findings in a presentation, educating our audience and providing them with the knowledge necessary for responsible use. The presentation will compare, contrast and analyze four international campaigns conducted over social media, resulting in various outcomes. The campaigns are the ALS Ice Bucket Challenge, Kony 2012, the #FirstWorldProblems Hashtag Killer by Water is Life ,and #bringbackourgirls

    Hair cortisol as a hypothalamic-pituitary-adrenal axis biomarker in pregnant women with asthma: a retrospective observational study

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    Background: Cortisol is a hormone involved in many physiological functions including fetal maturation and epigenetic programming during pregnancy. This study aimed to use hair cortisol as a biomarker of chronic inhaled corticosteroid (ICS) exposure and assess the potential effects of asthma on the hypothalamic-pituitary-adrenal (HPA) axis in pregnant women. We hypothesized that pregnant women with asthma treated with ICS would exhibit lower hair cortisol concentrations, indicative of adrenal suppression, compared to women with asthma not using ICS and women who do not have asthma. Methods: We performed an observational retrospective cohort study. Hair samples were analyzed from pregnant women with asthma, with (n = 56) and without (n = 31) ICS treatment, and pregnant women without asthma (n = 31). Hair samples were segmented based on the growth rate of 1 cm/month and analyzed by enzyme immunoassay to provide cortisol concentrations corresponding to preconception, trimesters 1–3, and postpartum. Hair cortisol concentrations were compared within and among the groups using non-parametric statistical tests. Results: Hair cortisol concentrations increased across trimesters for all three groups, but this increase was dampened in women with asthma (P = 0.03 for Controls vs. ICS Treated and Controls vs. No ICS). ICS Treated women taking more than five doses per week had hair cortisol concentrations 47 % lower in third trimester than Controls. Linear regression of the third trimester hair cortisol results identified asthma as a significant factor when comparing consistent ICS use or asthma as the predictor (F(1, 25) = 9.7, P = 0.005, R2 adj = 0.257). Conclusions: Hair cortisol successfully showed the expected change in cortisol over the course of pregnancy and may be a useful biomarker of HPA axis function in pregnant women with asthma. The potential impact of decreased maternal cortisol in women with asthma on perinatal outcomes remains to be determined.Medicine, Faculty ofOther UBCNon UBCPediatrics, Department ofReviewedFacult

    Childhood ADHD and Involvement in Early Pregnancy: Mechanisms of Risk

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    Objective: ADHD is associated with risky sexual behavior and early pregnancy, but few studies have examined mechanisms of risk linking childhood ADHD to early pregnancy. The present study utilized data from the Multimodal Treatment Study of ADHD to examine potential mechanisms that may account for the association between childhood ADHD and becoming pregnant or causing a pregnancy by age 18. Method: Participants were 579 children with ADHD and 289 comparison peers followed over 16 years. Results: Relative to the comparison group, those with childhood ADHD were at more than two times increased risk of early pregnancy. Univariately, persistence of ADHD symptoms, delinquency/substance use, and academic performance/achievement during adolescence each mediated the association between childhood ADHD and early pregnancy. When considered together, only delinquency/substance use remained a significant mediator of this relationship. Conclusion: Findings point toward specific targets of intervention for youth with ADHD to prevent early pregnancy

    Mechanisms driving neutrophil-induced t-cell immunoparalysis in ovarian cancer

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    T-cell activation and expansion in the tumor microenvironment (TME) are critical for antitumor immunity. Neutrophils in theTME acquire a complement-dependent T-cell suppressor phenotype that is characterized by inhibition of T-cell proliferation and activation through mechanisms distinct from those of myeloid-derived suppressor cells. In this study, we used ascites fluid supernatants (ASC) from patients with ovarian cancer as an authentic component of the TME to evaluate the effects of ASC on neutrophil function and mechanisms for neutrophil-driven immune suppression. ASC prolonged neutrophil life span, decreased neutrophil density, and induced nuclear hypersegmentation. Mass cytometry analysis showed that ASC induced 15 distinct neutrophil clusters. ASC stimulated complement deposition and signaling in neutrophils, resulting in surface mobilization of granule constituents, including NADPH oxidase. NADPH oxidase activation and phosphatidylserine signaling were required for neutrophil suppressor function, although we did not observe a direct role of extracellular reactive oxygen species in inhibiting T-cell proliferation. Postoperative surgical drainage fluid also induced a complement-dependent neutrophil suppressor phenotype, pointing to this effect as a general response to injury. Like circulating lymphocytes, ASC-activated neutrophils caused complement-dependent suppression of tumorassociated lymphocytes. ASC-activated neutrophils adhered to T cells and caused trogocytosis of T-cell membranes. These injury and signaling cues resulted in T-cell immunoparalysis characterized by impaired NFAT translocation, IL2 production, glucose uptake, mitochondrial function, and mTOR activation. Our results demonstrate that complement-dependent priming of neutrophil effector functions in the TME induces a T-cell nonresponsiveness distinct from established checkpoint pathways and identify targets for immunotherapy
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