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Humboldt Gletscher is a 100-km wide, slow-moving glacier in north Greenland which holds a 19-cm global sea level equivalent. Humboldt has been the fourth largest contributor to sea level rise since 1972 but the cause of its mass loss has not been elucidated. Multi-beam echo sounding data collected in 2019 indicate a seabed 200 m deeper than previously known. Conductivity temperature depth data reveal the presence of warm water of Atlantic origin at 0°C at the glacier front and a warming of the ocean waters by 0.9 ± 0.1°C since 1962. Using an ocean model, we reconstruct grounded ice undercutting by the ocean, combine it with calculated retreat caused by ice thinning to floatation, and are able to fully explain the observed retreat. Two thirds of the retreat are caused by undercutting of grounded ice, which is a physical process not included in most ice sheet models.

Zachariae Isstrøm (ZI) and Nioghalvfjerdsfjorden (79N) are marine-terminating glaciers in northeast Greenland that hold an ice volume equivalent to a 1.1-m global sea level rise. ZI lost its floating ice shelf, sped up, retreated at 650 m/y, and experienced a 5-gigaton/y mass loss. Glacier 79N has been more stable despite its exposure to the same climate forcing. We analyze the impact of ocean thermal forcing on the glaciers. A three-dimensional inversion of airborne gravity data reveals an 800-m-deep, broad channel that allows subsurface, warm, Atlantic Intermediate Water (AIW) (+1.[Formula: see text]C) to reach the front of ZI via two sills at 350-m depth. Subsurface ocean temperature in that channel has warmed by 1.3[Formula: see text]C since 1979. Using an ocean model, we calculate a rate of ice removal at the grounding line by the ocean that increased from 108 m/y to 185 m/y in 1979-2019. Observed ice thinning caused a retreat of its flotation line to increase from 105 m/y to 217 m/y, for a combined grounding line retreat of 13 km in 41 y that matches independent observations within 14%. In contrast, the limited access of AIW to 79N via a narrower passage yields lower grounded ice removal (53 m/y to 99 m/y) and thinning-induced retreat (27 m/y to 50 m/y) for a combined retreat of 4.4 km, also within 12% of observations. Ocean-induced removal of ice at the grounding line, modulated by bathymetric barriers, is therefore a main driver of ice sheet retreat, but it is not incorporated in most ice sheet models.

The retreat and acceleration of Greenland glaciers since the mid-1990s have been attributed to the enhanced intrusion of warm Atlantic Waters (AW) into fjords, but this assertion has not been quantitatively tested on a Greenland-wide basis or included in models. Here, we investigate how AW influenced retreat at 226 marine-terminating glaciers using ocean modeling, remote sensing, and in situ observations. We identify 74 glaciers in deep fjords with AW controlling 49% of the mass loss that retreated when warming increased undercutting by 48%. Conversely, 27 glaciers calving on shallow ridges and 24 in cold, shallow waters retreated little, contributing 15% of the loss, while 10 glaciers retreated substantially following the collapse of several ice shelves. The retreat mechanisms remain undiagnosed at 87 glaciers without ocean and bathymetry data, which controlled 19% of the loss. Ice sheet projections that exclude ocean-induced undercutting may underestimate mass loss by at least a factor of 2.

Bathymetry (seafloor depth), is a critical parameter providing the geospatial context for a multitude of marine scientific studies. Since 1997, the International Bathymetric Chart of the Arctic Ocean (IBCAO) has been the authoritative source of bathymetry for the Arctic Ocean. IBCAO has merged its efforts with the Nippon Foundation-GEBCO-Seabed 2030 Project, with the goal of mapping all of the oceans by 2030. Here we present the latest version (IBCAO Ver. 4.0), with more than twice the resolution (200 × 200 m versus 500 × 500 m) and with individual depth soundings constraining three times more area of the Arctic Ocean (∼19.8% versus 6.7%), than the previous IBCAO Ver. 3.0 released in 2012. Modern multibeam bathymetry comprises ∼14.3% in Ver. 4.0 compared to ∼5.4% in Ver. 3.0. Thus, the new IBCAO Ver. 4.0 has substantially more seafloor morphological information that offers new insights into a range of submarine features and processes; for example, the improved portrayal of Greenland fjords better serves predictive modelling of the fate of the Greenland Ice Sheet.

We reconstruct the mass balance of the Greenland Ice Sheet using a comprehensive survey of thickness, surface elevation, velocity, and surface mass balance (SMB) of 260 glaciers from 1972 to 2018. We calculate mass discharge, D, into the ocean directly for 107 glaciers (85% of D) and indirectly for 110 glaciers (15%) using velocity-scaled reference fluxes. The decadal mass balance switched from a mass gain of +47 ± 21 Gt/y in 1972-1980 to a loss of 51 ± 17 Gt/y in 1980-1990. The mass loss increased from 41 ± 17 Gt/y in 1990-2000, to 187 ± 17 Gt/y in 2000-2010, to 286 ± 20 Gt/y in 2010-2018, or sixfold since the 1980s, or 80 ± 6 Gt/y per decade, on average. The acceleration in mass loss switched from positive in 2000-2010 to negative in 2010-2018 due to a series of cold summers, which illustrates the difficulty of extrapolating short records into longer-term trends. Cumulated since 1972, the largest contributions to global sea level rise are from northwest (4.4 ± 0.2 mm), southeast (3.0 ± 0.3 mm), and central west (2.0 ± 0.2 mm) Greenland, with a total 13.7 ± 1.1 mm for the ice sheet. The mass loss is controlled at 66 ± 8% by glacier dynamics (9.1 mm) and 34 ± 8% by SMB (4.6 mm). Even in years of high SMB, enhanced glacier discharge has remained sufficiently high above equilibrium to maintain an annual mass loss every year since 1998.

The continuous and precise mapping of glacier calving fronts is essential for monitoring and understanding rapid glacier changes in Antarctica and Greenland, which have the potential for significant sea level rise within the current century. This effort has been mostly restricted to the slow and painstaking manual digitalization of the calving front positions in thousands of satellite imagery products. Here, we have developed a machine learning toolkit to automatically detect glacier calving front margins in satellite imagery. The toolkit is based on semantic image segmentation using Convolutional Neural Networks (CNN) with a modified U-Net architecture to isolate the calving fronts from satellite images after having been trained with a dataset of images and their corresponding manually-determined calving fronts. As a case study we train our neural network on a varied set of Landsat images with lowered resolutions from Jakobshavn, Sverdrup, and Kangerlussuaq glaciers, Greenland and test the results on images from Helheim glacier, Greenland to evaluate the performance of the approach. The neural network is able to identify the calving front in new images with a mean deviation of 96.3 m from the true fronts, equivalent to 1.97 pixels on average, while the corresponding error for manually-determined fronts on the same resolution images is 92.5 m (1.89 pixels). We find that the trained neural network significantly outperforms common edge detection techniques, and can be used to continuously map out calving-ice fronts with a variety of data products.

Large uncertainties in model parameterizations and input data sets make projections of future sea level rise contributions of outlet glaciers challenging. Here we introduce a novel technique for weighing large ensemble model simulations that uses information of key observables. The approach is robust to input errors and yields calibrated means and error estimates of a glacier's mass balance. We apply the technique to Jakobshavn Isbræ, using a model that includes a dynamic calving law, and closely reproduce the observed behavior from 1985 to 2018 by forcing the model with ocean temperatures only. Our calibrated projection suggests that the glacier will continue to retreat and contribute about 5.1 mm to eustatic sea level rise by 2100 under present-day climatic forcing. Our analysis shows that the glacier's future evolution will strongly depend on the ambient oceanic setting.

The article presents the text of a presentation made by Sir Michael Wood, International Law Commission (ILC) Special Rapporteur Identification of Customary International Law (CIL), at the Fourth Meeting of the Asian-African Legal Consultative Organization (AALCO) Informal Expert Group on Customary International Law on August 27, 2015. Topics discussed include the meaning of state sovereignty, the methodology of the ILC for identifying CIL, and the role of judicial decisions in relation to CIL.

Objective: Acute agitation in pediatrics is commonly encountered in hospital settings, can contribute to significant physical and psychological distress, and management is highly varied in practice. As such, the development of a standardized pharmacologic guideline is paramount. We aimed to develop a novel clinical pathway (CP) for management of acute agitation for all hospitalized pediatric patients in Canada. Methods: Healthcare professionals in Canada with expertise in treating and managing pediatric agitation formed a working group and developed a CP through conducting a literature review, engaging key partners, and obtaining interdisciplinary consensus (iterative real-time discussions with content experts). Once developed, the preliminary CP was presented to additional internal and external partners via multiple grand rounds and a webinar; feedback from participants guided final CP revisions. Results: The working group created a pediatric inpatient CP to guide pharmacologic management of agitation and serve as an easy-to-use clinical and educational resource with three complementary sections including: 1) a treatment algorithm, 2) a quick reference medication chart, and 3) two supporting documents, which provide a general overview of non-pharmacologic strategies prior to CP implementation and an illustrative scenario to accompany the medication chart to ensure effective utilization. Conclusions: This is the first CP to standardize pharmacological treatment and management of acute agitation in children in inpatient settings in Canada. Although further research is warranted to assess implementation and support process improvement, the CP can be adapted by individual institutions to assist in prompt pharmacological management of pediatric agitation to potentially improve outcomes for patients, families, and healthcare professionals. [ABSTRACT FROM AUTHOR]

APOE4 is the strongest genetic risk factor for late-onset Alzheimer disease. ApoE4 increases brain amyloid-β pathology relative to other ApoE isoforms. However, whether APOE independently influences tau pathology, the other major proteinopathy of Alzheimer disease and other tauopathies, or tau-mediated neurodegeneration, is not clear. By generating P301S tau transgenic mice on either a human ApoE knock-in (KI) or ApoE knockout (KO) background, here we show that P301S/E4 mice have significantly higher tau levels in the brain and a greater extent of somatodendritic tau redistribution by three months of age compared with P301S/E2, P301S/E3, and P301S/EKO mice. By nine months of age, P301S mice with different ApoE genotypes display distinct phosphorylated tau protein (p-tau) staining patterns. P301S/E4 mice develop markedly more brain atrophy and neuroinflammation than P301S/E2 and P301S/E3 mice, whereas P301S/EKO mice are largely protected from these changes. In vitro, E4-expressing microglia exhibit higher innate immune reactivity after lipopolysaccharide treatment. Co-culturing P301S tau-expressing neurons with E4-expressing mixed glia results in a significantly higher level of tumour-necrosis factor-α (TNF-α) secretion and markedly reduced neuronal viability compared with neuron/E2 and neuron/E3 co-cultures. Neurons co-cultured with EKO glia showed the greatest viability with the lowest level of secreted TNF-α. Treatment of P301S neurons with recombinant ApoE (E2, E3, E4) also leads to some neuronal damage and death compared with the absence of ApoE, with ApoE4 exacerbating the effect. In individuals with a sporadic primary tauopathy, the presence of an ε4 allele is associated with more severe regional neurodegeneration. In individuals who are positive for amyloid-β pathology with symptomatic Alzheimer disease who usually have tau pathology, ε4-carriers demonstrate greater rates of disease progression. Our results demonstrate that ApoE affects tau pathogenesis, neuroinflammation, and tau-mediated neurodegeneration independently of amyloid-β pathology. ApoE4 exerts a 'toxic' gain of function whereas the absence of ApoE is protective.