Impacts of marine heatwaves on top predator distributions are variable but predictable.

Marine heatwaves cause widespread environmental, biological, and socio-economic impacts, placing them at the forefront of 21st-century management challenges. However, heatwaves vary in intensity and evolution, and a paucity of information on how this variability impacts marine species limits our ability to proactively manage for these extreme events. Here, we model the effects of four recent heatwaves (2014, 2015, 2019, 2020) in the Northeastern Pacific on the distributions of 14 top predator species of ecological, cultural, and commercial importance. Predicted responses were highly variable across species and heatwaves, ranging from near total loss of habitat to a two-fold increase. Heatwaves rapidly altered political bio-geographies, with up to 10% of predicted habitat across all species shifting jurisdictions during individual heatwaves. The variability in predicted responses across species and heatwaves portends the need for novel management solutions that can rapidly respond to extreme climate events. As proof-of-concept, we developed an operational dynamic ocean management tool that predicts predator distributions and responses to extreme conditions in near real-time.

UV radiation increases carcinogenic risks for oral tissues compared to skin.

People can expose their oral cavities to UV (290-400 nm) by simply opening their mouths while outdoors. They can also have their oral cavities exposed to UV indoors to different UV-emitting devices used for diagnoses, treatments and procedures like teeth whitening. Because the World Health Organization declared UV radiation as a complete human carcinogen in 2009, we asked if oral tissues are at a similar or higher carcinogenic risk compared to skin tissue. To understand the UVB (290-320 nm)-related carcinogenic risks to these tissues, we measured initial DNA damage in the form of cyclobutane pyrimidine dimers (CPD), the repair rate of CPD (24 h) and the number of apoptotic dead cells over time resulting from increasing doses of erythemally weighted UV radiation. We used commercially available 3D-engineered models of human skin (EpiDerm™), gingival (EpiGingival™) and oral (EpiOral™) tissues and developed an analytical approach for our tri-labeling fluorescent procedure to identify total DNA, CPD and apoptotic cells so we can simultaneously quantify DNA repair rates and dead cells. Both DNA repair and apoptotic cell numbers are significantly lower in oral cells compared with skin cells. The combined results suggest UVB-exposed oral tissues are at a significantly higher carcinogenic risk than skin tissues.