ABSTRACT
Introduction: In early 2020, North American jurisdictions required households (e.g., romantic couples) to isolate together to help mitigate the spread of COVID-19. This study provides a first look at the interplay of depressive symptoms and conflict behaviors among isolating couples, including tests of predictions of the stress generation hypothesis. Methods: Mixed-gender couples residing in Canada (N = 711) completed online measures across two waves. We used the actor-partner interdependence mediation model, with Wave 1 depressive symptoms as the predictor, Wave 1 conflict enactment as the mediator, and Wave 2 depressive symptoms as the outcome. Results: Depressive symptoms showed stability across Wave 1 and 2. Wave 1 depressive symptoms showed associations with Wave 1 conflict enactment. For men (but not women), Wave 1 conflict enactment was associated with their own and their partner's Wave 2 depressive symptoms. For both partners, Wave 1 conflict enacted by men mediated the association between Wave 1 depressive symptoms and Wave 2 depressive symptoms. Discussion: Our study confirms and extends the stress generation hypothesis to the pandemic context, showing that depressive symptoms may partially contribute to conflict for isolating couples and that conflict behaviors enacted by men toward their partner can exacerbate depressive symptoms in both partners.
ABSTRACT
Despite current aggressive regimens, the majority of patients with MYCN amplification die due to drug-resistant disease, and further intensification ofchemotherapy will not significantly improve this outcome. We propose an entirely novel strategy to oppose MYCN oncogenic function in NB: by blockingthe metabolic reprogramming driven by MYCN. Based on our data and the recent literature, our guiding hypotheses are that: a) lipid metabolism is requiredfor NB tumorigenesis, and b) targeting MYCN-driven lipogenesis will effectively block NB tumor growth. We have demonstrated that lipid metabolism is aselective metabolic dependency of MYCN-driven tumors. MYCN drives both fatty acid (FA) synthesis and FA uptake to maintain NB cell survival. TargetingFA uptake effectively blocks NB in vivo tumor growth.