Diagnosing the extreme surface melt event over southwestern Greenland in 2007

Abstract. Analysis of passive microwave brightness temperatures from the space-borne Special Sensor Microwave Imager (SSM/I) documents a record surface snowmelt over high elevations (above 2000 m) of the Greenland ice sheet during summer of 2007. To interpret this record, results from the SSM/I are examined in conjunction with fields from the National Centers for Environmental Prediction/National Center for Atmospheric Research reanalysis and output from a regional climate model. The record surface melt reflects unusually warm conditions, seen in positive summertime anomalies of surface air temperatures, downwelling longwave radiation, 1000–500 hPa atmospheric thickness, and the net surface energy flux, linked in turn to southerly airflow over the ice sheet. Low snow accumulation may have contributed to the record through promoting anomalously low surface albedo

Prevention of “Humanized” Diabetogenic CD8 T-Cell Responses in HLA-Transgenic NOD Mice by a Multipeptide Coupled-Cell Approach

OBJECTIVE: Type 1 diabetes can be inhibited in standard NOD mice by autoantigen-specific immunotherapy targeting pathogenic CD8+ T-cells. NOD.beta2m(null).HHD mice expressing human HLA-A2.1 but lacking murine major histocompatibility complex class I molecules develop diabetes characterized by CD8 T-cells recognizing certain autoantigenic peptides also targeted in human patients. These include peptides derived from the pancreatic beta-cell proteins insulin (INS1/2 A(2-10) and INS1 B(5-14)) and islet-specific glucose-6-phosphatase catalytic subunit-related protein (IGRP(265-273) and IGRP(228-236)). Hence, NOD.beta2m(null).HHD mice represent a model system for developing potentially clinically translatable interventions for suppressing diabetogenic HLA-A2.1-restricted T-cell responses. RESEARCH DESIGN AND METHODS: Starting at 4-6 weeks of age, NOD.beta2m(null).HHD female mice were injected intravenously with syngeneic splenocytes to which various admixtures of the four above-mentioned peptides were bound by the cross-linking agent ethylene carbodiimide (ECDI). RESULTS: Treatment with such cells bearing the complete cocktail of INS and IGRP epitopes (designated INS/IGRP-SPs) significantly inhibited diabetes development in NOD.beta2m(null).HHD recipients compared with controls receiving splenocytes coupled with an irrelevant HLA-A2.1-restricted Flu16 peptide. Subsequent analyses found syngeneic splenocytes bearing the combination of the two ECDI-coupled IGRPs but not INS peptides (IGRP-SPs or INS-SPs) effectively inhibited diabetes development in NOD.beta2m(null).HHD mice. This result was supported by enzyme-linked immunospot (ELISPOT) analyses indicating combined INS/IGRP-SPs diminished HLA-A2.1-restricted IGRP but not INS autoreactive CD8+ T-cell responses in NOD.beta2m(null).HHD mice. CONCLUSIONS: These data support the potential of a cell therapy approach targeting HLA-A2.1-restricted IGRP autoreactive CD8 T-cells as a diabetes intervention approach in appropriate human patients

New climate models reveal faster and larger increases in Arctic precipitation than previously projected

As the Arctic continues to warm faster than the rest of the planet, evidence mounts that the region is experiencing unprecedented environmental change. The hydrological cycle is projected to intensify throughout the twenty-first century, with increased evaporation from expanding open water areas and more precipitation. The latest projections from the sixth phase of the Coupled Model Intercomparison Project (CMIP6) point to more rapid Arctic warming and sea-ice loss by the year 2100 than in previous projections, and consequently, larger and faster changes in the hydrological cycle. Arctic precipitation (rainfall) increases more rapidly in CMIP6 than in CMIP5 due to greater global warming and poleward moisture transport, greater Arctic amplification and sea-ice loss and increased sensitivity of precipitation to Arctic warming. The transition from a snow- to rain-dominated Arctic in the summer and autumn is projected to occur decades earlier and at a lower level of global warming, potentially under 1.5 °C, with profound climatic, ecosystem and socio-economic impacts

The large‐scale freshwater cycle of the Arctic

This paper synthesizes our understanding of the Arctic\u27s large‐scale freshwater cycle. It combines terrestrial and oceanic observations with insights gained from the ERA‐40 reanalysis and land surface and ice‐ocean models. Annual mean freshwater input to the Arctic Ocean is dominated by river discharge (38%), inflow through Bering Strait (30%), and net precipitation (24%). Total freshwater export from the Arctic Ocean to the North Atlantic is dominated by transports through the Canadian Arctic Archipelago (35%) and via Fram Strait as liquid (26%) and sea ice (25%). All terms are computed relative to a reference salinity of 34.8. Compared to earlier estimates, our budget features larger import of freshwater through Bering Strait and larger liquid phase export through Fram Strait. While there is no reason to expect a steady state, error analysis indicates that the difference between annual mean oceanic inflows and outflows (∼8% of the total inflow) is indistinguishable from zero. Freshwater in the Arctic Ocean has a mean residence time of about a decade. This is understood in that annual freshwater input, while large (∼8500 km3), is an order of magnitude smaller than oceanic freshwater storage of ∼84,000 km3. Freshwater in the atmosphere, as water vapor, has a residence time of about a week. Seasonality in Arctic Ocean freshwater storage is nevertheless highly uncertain, reflecting both sparse hydrographic data and insufficient information on sea ice volume. Uncertainties mask seasonal storage changes forced by freshwater fluxes. Of flux terms with sufficient data for analysis, Fram Strait ice outflow shows the largest interannual variability

Toll-Like Receptor 7 Is Required for Lacrimal Gland Autoimmunity and Type 1 Diabetes Development in Male Nonobese Diabetic Mice.

Sjögren syndrome (SS) is an immunologically complex, chronic autoimmune disease targeting lacrimal and salivary glands. Nonobese diabetic (NOD) mice spontaneously develop inflammation of lacrimal and salivary glands with histopathological features similar to SS in humans including focal lymphocytic infiltrates in the affected glands. The innate immune signals driving lymphocytic infiltration of these glands are not well-defined. Here we evaluate the role of Toll-like receptor (TLR) 7 in the development of SS-like manifestations in NOD mice. We created a Tlr7 knockout NOD mouse strain and performed histological and gene expression studies to characterize the effects of TLR7 on autoimmunity development. TLR7 was required for male-specific lacrimal gland inflammation but not for female-specific salivary gland inflammation. Moreover, TLR7 was required for type 1 diabetes development in male but not female NOD mice. RNA sequencing demonstrated that TLR7 was associated with a type I interferon (IFN) response and a type I IFN-independent B cell response in the lacrimal glands. Together these studies identify a previously unappreciated pathogenic role for TLR7 in lacrimal gland autoimmunity and T1D development in male NOD mice adding to the growing body of evidence supporting sex differences in mechanisms of autoimmune disease in NOD mice

Arctic sea-ice change: a grand challenge of climate science

Over the period of modern satellite observations, Arctic sea-ice extent at the end of the melt season (September) has declined at a rate of >11% per decade, and there is evidence that the rate of decline has accelerated during the last decade.While climate models project further decreases in seaice mass and extent through the 21st century, the model ensemble mean trend over the period of instrumental records is smaller than observed. Possible reasons for the apparent discrepancy between observations and model simulations include observational uncertainties, vigorous unforced climate variability in the high latitudes, and limitations and shortcomings of the models stemming in particular from gaps in understanding physical process. The economic significance of a seasonally sea-ice-free future Arctic, the increased connectivity of a warmer Arctic with changes in global climate, and large uncertainties in magnitude and timing of these impacts make the problem of rapid sea-ice loss in the Arctic a grand challenge of climate science. Meaningful prediction/projection of the Arctic sea-ice conditions for the coming decades and beyond requires determining priorities for observations and model development, evaluation of the ability of climate models to reproduce the observed sea-ice behavior as a part of the broader climate system, improved attribution of the causes of Arctic sea-ice change, and improved understanding of the predictability of sea-ice conditions on seasonal through centennial timescales in the wider context of the polar climate predictability

Record winter winds in 2020/21 drove exceptional Arctic sea ice transport

AbstractThe volume of Arctic sea ice is in decline but exhibits high interannual variability, which is driven primarily by atmospheric circulation. Through analysis of satellite-derived ice products and atmospheric reanalysis data, we show that winter 2020/21 was characterised by anomalously high sea-level pressure over the central Arctic Ocean, which resulted in unprecedented anticyclonic winds over the sea ice. This atmospheric circulation pattern drove older sea ice from the central Arctic Ocean into the lower-latitude Beaufort Sea, where it is more vulnerable to melting in the coming warm season. We suggest that this unusual atmospheric circulation may potentially lead to unusually high summer losses of the Arctic’s remaining store of old ice.</jats:p

Energy input is primary controller of methane bubbling in subarctic lakes

Emission of methane (CH4) from surface waters is often dominated by ebullition (bubbling), a transport mode with high‐spatiotemporal variability. Based on new and extensive CH4 ebullition data, we demonstrate striking correlations (r2 between 0.92 and 0.997) when comparing seasonal bubble CH4 flux from three shallow subarctic lakes to four readily measurable proxies of incoming energy flux and daily flux magnitudes to surface sediment temperature (r2 between 0.86 and 0.94). Our results after continuous multiyear sampling suggest that CH4 ebullition is a predictable process, and that heat flux into the lakes is the dominant driver of gas production and release. Future changes in the energy received by lakes and ponds due to shorter ice‐covered seasons will predictably alter the ebullitive CH4 flux from freshwater systems across northern landscapes. This finding is critical for our understanding of the dynamics of radiatively important trace gas sources and associated climate feedback

Interleukin-27 Is Essential for Type 1 Diabetes Development and Sjögren Syndrome-like Inflammation.

Human genetic studies implicate interleukin-27 (IL-27) in the pathogenesis of type 1 diabetes (T1D), but the underlying mechanisms remain largely unexplored. To further define the role of IL-27 in T1D, we generated non-obese diabetic (NOD) mice deficient in IL-27 or IL-27Rα. In contrast to wild-type NOD mice, both NOD.Il27-/- and NOD.Il27ra-/- strains are completely resistant to T1D. IL-27 from myeloid cells and IL-27 signaling in T cells are critical for T1D development. IL-27 directly alters the balance of regulatory T cells (Tregs) and T helper 1 (Th1) cells in pancreatic islets, which in turn modulates the diabetogenic activity of CD8 T cells. IL-27 also directly enhances the effector function of CD8 T cells within pancreatic islets. In addition to T1D, IL-27 signaling in T cells is also required for lacrimal and salivary gland inflammation in NOD mice. Our study reveals that IL-27 contributes to autoimmunity in NOD mice through multiple mechanisms and provides substantial evidence to support its pathogenic role in human T1D

Deletion of Vβ3

In both humans and NOD mice, type 1 diabetes (T1D) develops from the autoimmune destruction of pancreatic beta cells by T cells. Interactions between both helper CD