The impact of 21st century Arctic sea ice decline on the climate and mass balance of the Greenland ice sheet and Svalbard’s glaciers and ice caps

The Arctic is a region particularly susceptible to rapid climate change. General circulation models (GCMs) suggest a polar amplification of any global warming signal by a factor of about 1.5 due, in part, to sea ice feedbacks. The dramatic recent decline in multi-year sea ice cover lies outside the standard deviation of the CMIP3 ensemble GCM predictions. Sea ice acts as a barrier between cold air and warmer oceans during winter, as well as inhibiting evaporation from the ocean surface water during the summer. An ice free Arctic would likely have an altered hydrological cycle with more evaporation from the ocean surface leading to changes in precipitation distribution and amount. Using the U.K. Met Office Regional Climate Model (RCM), HadRM3, the atmospheric effects of the observed and projected reduction in Arctic sea ice are investigated. The RCM is driven by the atmospheric GCM HadAM3. Both models are forced with sea surface temperature and sea ice for the period 2061-2090 from the CMIP3 HadGEM1 experiments. Here we use an RCM at 50km resolution over the Arctic and 25km over Svalbard, which captures well the present-day pattern of precipitation and provides a detailed picture of the projected changes in the behaviour of the oceanic-atmosphere moisture fluxes and how they affect precipitation. These experiments show that the projected 21stCentury sea ice decline alone causes large impacts to the surface mass balance (SMB) on Svalbard. However Greenland’s SMB is not significantly affected by sea ice decline alone, but responds with a strongly negative shift in SMB when changes to SST are incorporated into the experiments. This is the first study to characterise the impact of changes in future sea ice to Arctic terrestrial cryosphere mass balance.

Propeptide-mediated inhibition of myostatin increases muscle mass through inhibiting proteolytic pathways in aged mice

Mammalian aging is accompanied by a progressive loss of skeletal muscle, a process called sarcopenia. Myostatin, a secreted member of the transforming growth factor-β family of signaling molecules, has been shown to be a potent inhibitor of muscle growth. Here, we examined whether muscle growth could be promoted in aged animals by antagonizing the activity of myostatin through the neutralizing activity of the myostatin propeptide. We show that a single injection of an AAV8 virus expressing the myostatin propeptide induced an increase in whole body weights and all muscles examined within 7 weeks of treatment. Our cellular studies demonstrate that muscle enlargement was due to selective fiber type hypertrophy, which was accompanied by a shift toward a glycolytic phenotype. Our molecular investigations elucidate the mechanism underpinning muscle hypertrophy by showing a decrease in the expression of key genes that control ubiquitin-mediated protein breakdown. Most importantly, we show that the hypertrophic muscle that develops as a consequence of myostatin propeptide in aged mice has normal contractile properties. We suggest that attenuating myostatin signaling could be a very attractive strategy to halt and possibly reverse age-related muscle loss.