The airborne glacier and ice surface topography interferometer (GLISTIN-A) is a single-pass radar interferometer developed for accurate high-resolution swath mapping of dynamic ice surfaces. We present the first validation results of the operational sensor, collected in 2013 over glaciers in Alaska and followed by more exhaustive collections from Greenland in 2016 and 2017. In Alaska, overlapping flight-tracks were mosaicked to mitigate potential residual trends across-track and the resultant maps are validated with lidar. Furthermore, repeat acquisitions of Columbia Glacier collected with a three day separation indicate excellent stability and repeatability. Commencing 2016, GLISTIN-A has circumnavigated Greenland for 4 consecutive years. Due to flight hour limitations, overlapping swaths were not flown. In 2016, comparison with airborne lidar data finds that residual systematic errors exhibit evenly distributed small slopes (all less than 10 millidegrees) and nadir biases were typically less than 1 m. Similarly 2017 data exhibited up to meter-scale nadir biases and evenly distributed residual slopes with a standard deviation of ~10 millidegrees). All satisfied the science accuracy requirements of the Greenland campaigns (3 m accuracy across an 8 km swath).

Abstract Background Notch4 is a member of the Notch family of receptors that is primarily expressed in the vascular endothelial cells. Genetic deletion of Notch4 does not result in an overt phenotype in mice, thus the function of Notch4 remains poorly understood. Methods We examined the requirement for Notch4 in the development of breast cancer vasculature. Orthotopic transplantation of mouse mammary tumor cells wild type for Notch4 into Notch4 deficient hosts enabled us to delineate the contribution of host Notch4 independent of its function in the tumor cell compartment. Results Here, we show that Notch4 expression is required for tumor onset and early tumor perfusion in a mouse model of breast cancer. We found that Notch4 expression is upregulated in mouse and human mammary tumor vasculature. Moreover, host Notch4 deficiency delayed the onset of MMTV-PyMT tumors, wild type for Notch4, after transplantation. Vessel perfusion was decreased in tumors established in Notch4-deficient hosts. Unlike in inhibition of Notch1 or Dll4, vessel density and branching in tumors developed in Notch4-deficient mice were unchanged. However, final tumor size was similar between tumors grown in wild type and Notch4 null hosts. Conclusion Our results suggest a novel role for Notch4 in the establishment of tumor colonies and vessel perfusion of transplanted mammary tumors.