Paid paternal leave linked to better mental health outcomes for dads - Northwestern Now News

When genes are "expressed," it is like reading an instruction manual to create things the body needs - such as proteins or RNA. It is an incredibly important process in regulating normal cellular functions. Understanding more about gene expression can reveal insights into the biological processes behind different conditions. One of those conditions we desperately need to learn more about is autism spectrum disorder (ASD), which is a neurodevelopmental condition characterized by difficulties in social communication, alongside restricted or repetitive patterns of behavior and interests. Epidemiological studies have linked advanced paternal age to an increased risk of ASD in offspring. However, the mechanisms underlying this association remain poorly understood.

When our second child was born, my spouse had several weeks of paternity leave under his parental leave policy at work. I’m a certified family life educator, and parental leave comes up regularly in my teaching and community work. So I was aware of the benefits his leave could have for our family – in theory.

We’re sharing this article early to provide faster access to peer-reviewed, accepted research. It is citable and carries a permanent DOI. This version is subject to further edits and will be replaced automatically by the final Version of Record. All legal disclaimers apply. AbstractBunyamwera virus (BUNV) is the prototypical member of the Peribunyaviridae family of arthropod-borne viruses and possesses a genome comprising three segments of negative-sense RNA, named small, medium and large. The medium segment encodes a polyprotein that is processed to form Gn and Gc spikes and a non-structural protein, NSm. The role of NSm during replication in mammalian cells is poorly characterized, although it associates with a Golgi-derived structure called the virus factory (VF), the site of BUNV genome replication and virion assembly. To further define NSm function, we generated an epitope-tagged BUNV and used co-immunoprecipitation and quantitative proteomics to identify host interacting partners.

Scientists co-led by St. Jude Children's Research Hospital have identified a potential therapeutic vulnerability in some forms of osteosarcoma. Published today in the Journal of Experimental Medicine, a combination approach slowed tumor growth and prolonged survival in preclinical models of this pediatric bone cancer. The therapies degraded EP300 (a protein that is co-opted to express oncogenes in many cancers) and inhibited AKT (a well-known cancer drug target), highlighting the combination's clinical potential. Osteosarcoma has lower survival compared to many other cancers, with relapsed and metastatic disease showing especially poor outcomes. As no new treatments have been approved for the disease in the last 40 years, the findings provide a much-needed new therapeutic avenue to explore.