Comparison of the meteorology and surface energy balance at Storbreen and Midtdalsbreen, two glaciers in southern Norway

We compare 5 years of meteorological records from automatic weather stations (AWSs) on Storbreen and Midtdalsbreen, two glaciers in southern Norway, located approximately 120 km apart. The records are obtained from identical AWSs with an altitude difference of 120 m and cover the period September 2001 to September 2006. Air temperature at the AWS locations is found to be highly correlated, even with the seasonal cycle removed. The most striking difference between the two sites is the difference in wind climate. Midtdalsbreen is much more under influence of the large-scale circulation with wind speeds on average a factor 1.75 higher. On Storbreen, weaker katabatic winds are dominant. The main melt season is from May to September at both locations. During the melt season, incoming and net solar radiation are larger on Midtdalsbreen, whereas incoming and net longwave radiation are larger on Storbreen, primarily caused by thicker clouds on the latter. The turbulent fluxes are a factor 1.7 larger on Midtdalsbreen, mainly due to the higher wind speeds. Inter-daily fluctuations in the surface energy fluxes are very similar at the AWS sites. On average, melt energy is a factor 1.3 larger on Midtdalsbreen, a result of both larger net radiation and larger turbulent fluxes. The relative contribution of net radiation to surface melt is larger on Storbreen (76%) than on Midtdalsbreen (66%). As winter snow depth at the two locations is comparable in most years, the larger amount of melt energy results in an earlier disappearance of the snowpack on Midtdalsbreen and 70% more ice melt than on Storbreen. We compare the relative and absolute values of the energy fluxes on Storbreen and Midtdalsbreen with reported values for glaciers at similar latitudes. Furthermore, a comparison is made with meteorological variables measured at two nearby weather stations, showing that on-site measurements are essential for an accurate calculation of the surface energy balance and melt rate

Arrest of mammalian fibroblasts in G1 in response to actin inhibition is dependent on retinoblastoma pocket proteins but not on p53

p53 and the retinoblastoma (RB) pocket proteins are central to the control of progression through the G1 phase of the cell cycle. The RB pocket protein family is downstream of p53 and controls S-phase entry. Disruption of actin assembly arrests nontransformed mammalian fibroblasts in G1. We show that this arrest requires intact RB pocket protein function, but surprisingly does not require p53. Thus, mammalian fibroblasts with normal pocket protein function reversibly arrest in G1 on exposure to actin inhibitors regardless of their p53 status. By contrast, pocket protein triple knockout mouse embryo fibroblasts and T antigen–transformed rat embryo fibroblasts lacking both p53 and RB pocket protein function do not arrest in G1. Fibroblasts are very sensitive to actin inhibition in G1 and arrest at drug concentrations that do not affect cell adhesion or cell cleavage. Interestingly, G1 arrest is accompanied by inhibition of surface ruffling and by induction of NF2/merlin. The combination of failure of G1 control and of tetraploid checkpoint control can cause RB pocket protein–suppressed cells to rapidly become aneuploid and die after exposure to actin inhibitors, whereas pocket protein–competent cells are spared. Our results thus establish that RB pocket proteins can be uniquely targeted for tumor chemotherapy

Structural brain imaging studies offer clues about the effects of the shared genetic etiology among neuropsychiatric disorders

Malalties; GenèticaEnfermedades; GenéticaDiseases; GeneticsGenomewide association studies have found significant genetic correlations among many neuropsychiatric disorders. In contrast, we know much less about the degree to which structural brain alterations are similar among disorders and, if so, the degree to which such similarities have a genetic etiology. From the Enhancing Neuroimaging Genetics through Meta-Analysis (ENIGMA) consortium, we acquired standardized mean differences (SMDs) in regional brain volume and cortical thickness between cases and controls. We had data on 41 brain regions for: attention-deficit/hyperactivity disorder (ADHD), autism spectrum disorder (ASD), bipolar disorder (BD), epilepsy, major depressive disorder (MDD), obsessive compulsive disorder (OCD), and schizophrenia (SCZ). These data had been derived from 24,360 patients and 37,425 controls. The SMDs were significantly correlated between SCZ and BD, OCD, MDD, and ASD. MDD was positively correlated with BD and OCD. BD was positively correlated with OCD and negatively correlated with ADHD. These pairwise correlations among disorders were correlated with the corresponding pairwise correlations among disorders derived from genomewide association studies (r = 0.494). Our results show substantial similarities in sMRI phenotypes among neuropsychiatric disorders and suggest that these similarities are accounted for, in part, by corresponding similarities in common genetic variant architectures

Cloaked Facebook pages: Exploring fake Islamist propaganda in social media

This research analyses cloaked Facebook pages that are created to spread political propaganda by cloaking a user profile and imitating the identity of a political opponent in order to spark hateful and aggressive reactions. This inquiry is pursued through a multi-sited online ethnographic case study of Danish Facebook pages disguised as radical Islamist pages, which provoked racist and anti-Muslim reactions as well as negative sentiments towards refugees and immigrants in Denmark in general. Drawing on Jessie Daniels’ critical insights into cloaked websites, this research furthermore analyses the epistemological, methodological and conceptual challenges of online propaganda. It enhances our understanding of disinformation and propaganda in an increasingly interactive social media environment and contributes to a critical inquiry into social media and subversive politics

Deficiency of the Fanconi anemia E2 ubiqitin conjugase UBE2T only partially abrogates Alu-mediated recombination in a new model of homology dependent recombination

The primary function of the UBE2T ubiquitin conjugase is in the monoubiquitination of the FANCI-FANCD2 heterodimer, a central step in the Fanconi anemia (FA) pathway. Genetic inactivation of UBE2T is responsible for the phenotypes of FANCT patients; however, a FANCT patient carrying a maternal duplication and a paternal deletion in the UBE2T loci displayed normal peripheral blood counts and UBE2T protein levels in B-lymphoblast cell lines. To test whether reversion by recombination between UBE2T AluYa5 elements could have occurred in the patient's hematopoietic stem cells despite the defects in homologous recombination (HR) in FA cells, we constructed HeLa cell lines containing the UBE2T AluYa5 elements and neighboring intervening sequences flanked by fluorescent reporter genes. Introduction of a DNA double strand break in the model UBE2T locus in vivo promoted single strand annealing (SSA) between proximal Alu elements and deletion of the intervening color marker gene, recapitulating the reversion of the UBE2T duplication in the FA patient. To test whether UBE2T null cells retain HR activity, the UBE2T genes were knocked out in HeLa cells and U2OS cells. CRISPR/Cas9-mediated genetic knockout of UBE2T only partially reduced HR, demonstrating that UBE2T-independent pathways can compensate for the recombination defect in UBE2T/FANCT null cells

Complementation of hypersensitivity to DNA interstrand crosslinking agents demonstrates that XRCC2 is a Fanconi anaemia gene

Background Fanconi anemia (FA) is a heterogeneous inherited disorder clinically characterized by progressive bone marrow failure, congenital anomalies, and a predisposition to malignancies. Objective Determine, based on correction of cellular phenotypes, whether XRCC2 is a FA gene. Methods Cells (900677) from a previously identified patient with biallelic mutation of XRCC2, among other mutations, were genetically complemented with wild-type XRCC2. Results Wild-type XRCC2 corrects each of three phenotypes characteristic of FA cells, all related to the repair of DNA interstrand crosslinks, including increased sensitivity to mitomycin C (MMC), chromosome breakage, and G2-M accumulation in the cell cycle. Further, the p.R215X mutant of XRCC2, which is harbored by the patient, is unstable. This provides an explanation for the pathogenesis of this mutant, as does the fact that 900677 cells have reduced levels of other proteins in the XRCC2-RAD51B-C-D complex. Also, FANCD2 monoubiquitination and foci formation, but not assembly of RAD51 foci, are normal in 900677 cells. Thus, XRCC2 acts late in the FA-BRCA pathway as also suggested by hypersensitivity of 900677 cells to ionizing radiation. These cells also share milder sensitivities toward olaparib and formaldehyde with certain other FA cells. Conclusions XRCC2/FANCU is a FA gene, as is another RAD51 paralog gene, RAD51C/FANCO. Notably, similar to a subset of FA genes that act downstream of FANCD2, biallelic mutation of XRCC2/FANCU has not been associated with bone marrow failure. Taken together, our results yield important insights into phenotypes related to FA and its genetic origins