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The Bering Glacier–Bagley Icefield system in Alaska is currently surging (2011). Large-scale elevation changes and small-scale elevation-change characteristics are investigated to understand surge progression, especially mass transport from the pre-surge reservoir area to the receiving area and propagation of the kinematic surge wave as manifested in heavy crevassing characteristic of rapid, brittle deformation. This analysis is based on airborne laser altimeter data collected over Bering Glacier in September 2011. Results include the following: (1) Maximal crevasse depth is 60 m, reached in a rift that separates two deformation domains, indicative of two different flow regimes. Otherwise surge crevasse depth reaches 20–30 m. (2) Characteristic parameters of structural provinces are derived by application of geostatistical classification. Parameters include significance and spacing of crevasses, surface roughness and crevasse-edge curvature (indicative of crevasse age). A classification based on these parameters serves to objectively discriminate structural provinces, indicative of surge progression down-glacier and up-glacier. (3) Elevation changes from 2011 and 2010 altimetry show 40–70 m surface lowering in the reservoir area in lower central Bering Glacier and 20–40m thickening near the front in Tashalich arm. Combining elevation changes with results of crevasse profilometry and pattern analysis, the rapid progression of the surge can be mathematically–physically reconstructed.

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Syndrome individual with differential genotoxin sensitivity and a DNA damage response defect, SUMMARY Purpose: Roberts Syndrome (RBS) is a rare recessively-transmitted developmental disorder characterized by growth retardation, craniofacial abnormalities and truncation of limbs. All affected individuals to date have mutations in the ESCO2 (Establishment of cohesion 2) gene, a key regulator of the cohesin complex, which is involved in sister chromatid cohesion and DNA double-strand break (dsb) repair.Here we characterize DNA damage responses (DDRs) for the first time in a RBSaffected family. Methods and Materials: Lymphoblastoid cell lines (LCLs) were established from an RBS family, including the proband, and parents carrying ESCO2 mutations. Various DDR assays were performed on these cells, including clonogenic, chromosome break and apoptosis assays, checkpoint activation indicators and measures of DNA breakage and repair. Results: Cells derived from the RBS-affected individual showed sensitivity to ionizing radiation (IR) and Mitomycin C (MMC) -induced DNA damage. In this ESCO2 compound heterozygote, other DNA damage responses were also defective, including enhanced IR-induced clastogenicity and apoptosis, increased DNA dsb induction and a reduced capacity for repairing IR -induced DNA dsbs as measured by γ-H2AX foci and the comet assay.Conclusions: in addition to its developmental features, RBS can be, like ataxia telangiectasia, considered a DNA damage response-defective syndrome, which contributes to its cellular, molecular and clinical phenotype.