Implications of surface flooding on airborne estimates of snow depth on sea ice

Snow depth observations from airborne snow radars, such as the NASA's Operation IceBridge (OIB) mission, have recently been used in altimeter-derived sea ice thickness estimates, as well as for model parameterization. A number of validation studies comparing airborne and in situ snow depth measurements have been conducted in the western Arctic Ocean, demonstrating the utility of the airborne data. However, there have been no validation studies in the Atlantic sector of the Arctic. Recent observations in this region suggest a significant and predominant shift towards a snow-ice regime caused by deep snow on thin sea ice. During the Norwegian young sea Ice, Climate and Ecosystems (ICE) expedition (N-ICE2015) in the area north of Svalbard, a validation study was conducted on 19 March 2015. This study collected ground truth data during an OIB overflight. Snow and ice thickness measurements were obtained across a two-dimensional (2-D) 400 m × 60 m grid. Additional snow and ice thickness measurements collected in situ from adjacent ice floes helped to place the measurements obtained at the gridded survey field site into a more regional context. Widespread negative freeboards and flooding of the snowpack were observed during the N-ICE2015 expedition due to the general situation of thick snow on relatively thin sea ice. These conditions caused brine wicking into and saturation of the basal snow layers. This causes the airborne radar signal to undergo more diffuse scattering, resulting in the location of the radar main scattering horizon being detected well above the snow–ice interface. This leads to a subsequent underestimation of snow depth; if only radar-based information is used, the average airborne snow depth was 0.16 m thinner than that measured in situ at the 2-D survey field. Regional data within 10 km of the 2-D survey field suggested however a smaller deviation between average airborne and in situ snow depth, a 0.06 m underestimate in snow depth by the airborne radar, which is close to the resolution limit of the OIB snow radar system. Our results also show a broad snow depth distribution, indicating a large spatial variability in snow across the region. Differences between the airborne snow radar and in situ measurements fell within the standard deviation of the in situ data (0.15–0.18 m). Our results suggest that seawater flooding of the snow–ice interface leads to underestimations of snow depth or overestimations of sea ice freeboard measured from radar altimetry, in turn impacting the accuracy of sea ice thickness estimates.</p

On the reliability of the theoretical internal conversion coefficients

Possible sources of uncertainties in the calculations of the internal conversion coefficients are studied. The uncertainties induced by them are estimated.Comment: 16 pages (including 3 figures inserted by 'epsfig' macro

Sea-ice-free Arctic during the Last Interglacial supports fast future loss

The Last Interglacial (LIG), a warmer period 130-116 ka before present, is a potential analog for future climate change. Stronger LIG summertime insolation at high northern latitudes drove Arctic land summer temperatures 4-5 °C higher than the preindustrial era. Climate model simulations have previously failed to capture these elevated temperatures, possibly because they were unable to correctly capture LIG sea-ice changes. Here, we show the latest version of the fully-coupled UK Hadley Center climate model (HadGEM3) simulates a more accurate Arctic LIG climate, including elevated temperatures. Improved model physics, including a sophisticated sea-ice melt-pond scheme, result in a complete simulated loss of Arctic sea ice in summer during the LIG, which has yet to be simulated in past generations of models. This ice-free Arctic yields a compelling solution to the longstanding puzzle of what drove LIG Arctic warmth and supports a fast retreat of future Arctic summer sea ice

The role of the tissue microenvironment in the regulation of cancer cell motility and invasion

During malignant neoplastic progression the cells undergo genetic and epigenetic cancer-specific alterations that finally lead to a loss of tissue homeostasis and restructuring of the microenvironment. The invasion of cancer cells through connective tissue is a crucial prerequisite for metastasis formation. Although cell invasion is foremost a mechanical process, cancer research has focused largely on gene regulation and signaling that underlie uncontrolled cell growth. More recently, the genes and signals involved in the invasion and transendothelial migration of cancer cells, such as the role of adhesion molecules and matrix degrading enzymes, have become the focus of research. In this review we discuss how the structural and biomechanical properties of extracellular matrix and surrounding cells such as endothelial cells influence cancer cell motility and invasion. We conclude that the microenvironment is a critical determinant of the migration strategy and the efficiency of cancer cell invasion

C4.4A as a candidate marker in the diagnosis of colorectal cancer

C4.4A is a member of the Ly-6 family with restricted expression in non-transformed tissues. C4.4A expression in human cancer has rarely been evaluated. Thus, it became important to explore C4.4A protein expression in human tumour tissue to obtain an estimate on the frequency of expression and the correlation with tumour progression, the study focusing on colorectal cancer. The analysis of C4.4A in human tumour lines by western blot and immunoprecipitation using polyclonal rabbit antibodies that recognize different C4.4A epitopes revealed C4.4A oligomer and heavily glycosylated C4.4A isoform expression that, in some instances, inhibited antibody binding and interaction with the C4.4A ligand galectin-3. In addition, tumour cell lines released C4.4A by vesicle shedding and proteolytic cleavage. C4.4A was expressed in over 80% of primary colorectal cancer and liver metastasis with negligible expression in adjacent colonic mucosa, inflamed colonic tissue and liver. This compares well with EpCAM and CO-029 expression in over 90% of colorectal cancer. C4.4A expression was only observed in about 50% of pancreatic cancer and renal cell carcinoma. By de novo expression in colonic cancer tissue, we consider C4.4A as a candidate diagnostic marker in colorectal cancer, which possibly can be detected in body fluids