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Rising global sea levels are one of many impacts associated with current anthropogenic global warming. The Antarctic Ice Sheet (AIS) has the potential to contribute several meters of sea level rise over the next few centuries. To predict future sea level rise contributions from ice sheets, both global and regional climate model (RCM) outputs are used as forcing in ice sheet model simulations. While the impact of different global models on future projections is well-studied, the effect of different regional models on the evolution of the AIS is mostly unknown. In our study, we present the impact of the choice of present-day reference RCM forcing on the evolution of the AIS. We used the Parallel Ice Sheet Model (PISM) to study the AIS in a quasi-equilibrium state and under future projections, combining present-day RCM output with global climate model projections. Our study suggests differences in projected Antarctic sea level contributions due to the choice of different present-day surface mass balance (SMB) and temperature baseline forcings of 10.6 mm in the year 2100 and 70.0 mm in 2300 under the RCP8.5 scenario. Those uncertainties are an order of magnitude smaller than what is estimated from uncertainties related to ice sheet and climate models. However, we observe an increase in RCM-induced uncertainties over time and for higher-emission scenarios. Additionally, our study shows that the complex relationship between the selected RCM baseline climatology and its impact on future sea level rise is closely related to the stability of West Antarctic Ice Sheet (WAIS), particularly the dynamic response of Thwaites and Pine Island glaciers. On millennial timescale, the choice of the RCM reference leads to ice volume differences up to 2.3 m and can result in the long-term collapse of the West Antarctic Ice Sheet.

Rising global sea levels are one of many impacts associated with current anthropogenic global warming. The Antarctic Ice Sheet (AIS) has the potential to contribute several meters of sea level rise over the next few centuries. To predict future sea level rise contributions from ice sheets, both global and regional climate model (RCM) outputs are used as forcing in ice sheet model simulations. While the impact of different global models on future projections is well-studied, the effect of different regional models on the evolution of the AIS is mostly unknown. In our study, we present the impact of the choice of present-day reference RCM forcing on the evolution of the AIS. We used the Parallel Ice Sheet Model (PISM) to study the AIS in a quasi-equilibrium state and under future projections, combining present-day RCM output with global climate model projections. Our study suggests differences in projected Antarctic sea level contributions due to the choice of different present-day surface mass balance (SMB) and temperature baseline forcings of 10.6 mm in the year 2100 and 70.0 mm in 2300 under the RCP8.5 scenario. Those uncertainties are an order of magnitude smaller than what is estimated from uncertainties related to ice sheet and climate models. However, we observe an increase in RCM-induced uncertainties over time and for higher-emission scenarios. Additionally, our study shows that the complex relationship between the selected RCM baseline climatology and its impact on future sea level rise is closely related to the stability of West Antarctic Ice Sheet (WAIS), particularly the dynamic response of Thwaites and Pine Island glaciers. On millennial timescale, the choice of the RCM reference leads to ice volume differences up to 2.3 m and can result in the long-term collapse of the West Antarctic Ice Sheet. [ABSTRACT FROM AUTHOR]

To determine the cutaneous effects of in utero and lactational exposure to the AHR ligand 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD), pregnant C57BL/6J mice were exposed by gavage to a vehicle or 5 μg TCDD/kg body weight at embryonic day 12 and epidermal barrier formation and function were studied in their offspring from postnatal day 1 (P1) through adulthood. TCDD-exposed pups were born with acanthosis. This effect was AHR-dependent and subsided by P6 with no evidence of subsequent inflammatory dermatitis. The challenge of adult mice with MC903 showed similar inflammatory responses in control and treated animals, indicating no long-term immunosuppression to this chemical. Chloracne-like sebaceous gland hypoplasia and cyst formation were observed in TCDD-exposed P21 mice, with concomitant microbiome dysbiosis. These effects were reversed by P35. CYP1A1 and CYP1B1 expression in the skin was increased in the exposed mice until P21, then declined. Both CYP proteins co-localized with LRIG1-expressing progenitor cells at the infundibulum. CYP1B1 protein also co-localized with a second stem cell niche in the isthmus. These results indicate that this exposure to TCDD causes a chloracne-like effect without inflammation. Transient activation of the AhR, due to the shorter half-life of TCDD in mice, likely contributes to the reversibility of these effects.

Antea Group and KULeuven were awarded a project in Flanders to identify the regions exporting high sediment loads to unnavigable watercourses and the sedimentation zones within them. Two types of models are applied: hydrological sediment export models (SEM) and hydraulic sediment transport models (STM). The influence of erosion control measures on sediment export as well as river engineering measures needs to be taken into account. A concept will be developed to connect the SEM and STM, enabling the sediment to be routed from upstream to the sedimentation zones. Results of the study will be used by the Flemish government to plan erosion control measures, estimate future sedimentation volumes, steer sedimentation and optimize river engineering and dredging works. Finally, model results could also be used to obtain better insights to the re-suspension risks of contaminated sediment in watercourses.

Diurnal oscillation of intracellular redox potential is known to couple metabolism with the circadian clock, yet the responsible mechanisms are not well understood. We show here that chemical activation of NRF2 modifies circadian gene expression and rhythmicity, with phenotypes similar to genetic NRF2 activation. Loss of Nrf2 function in mouse fibroblasts, hepatocytes and liver also altered circadian rhythms, suggesting that NRF2 stoichiometry and/or timing of expression are important to timekeeping in some cells. Consistent with this concept, activation of NRF2 at a circadian time corresponding to the peak generation of endogenous oxidative signals resulted in NRF2-dependent reinforcement of circadian amplitude. In hepatocytes, activated NRF2 bound specific enhancer regions of the core clock repressor gene Cry2, increased Cry2 expression and repressed CLOCK/BMAL1-regulated E-box transcription. Together these data indicate that NRF2 and clock comprise an interlocking loop that integrates cellular redox signals into tissue-specific circadian timekeeping.