Ice XII in its second regime of metastability

We present neutron powder diffraction results which give unambiguous evidence for the formation of the recently identified new crystalline ice phase[Lobban et al.,Nature, 391, 268, (1998)], labeled ice XII, at completely different conditions. Ice XII is produced here by compressing hexagonal ice I_h at T = 77, 100, 140 and 160 K up to 1.8 GPa. It can be maintained at ambient pressure in the temperature range 1.5 < T < 135 K. High resolution diffraction is carried out at T = 1.5 K and ambient pressure on ice XII and accurate structural properties are obtained from Rietveld refinement. At T = 140 and 160 K additionally ice III/IX is formed. The increasing amount of ice III/IX with increasing temperature gives an upper limit of T ~ 150 K for the successful formation of ice XII with the presented procedure.Comment: 3 Pages of RevTeX, 3 tables, 3 figures (submitted to Physical Review Letters

Human RTEL1 associates with Poldip3 to facilitate responses to replication stress and R-loop resolution

International audienc

NSD1 mutations generate a genome-wide DNA methylation signature

published_or_final_versio

Alite calcium sulfoaluminate cement: chemistry and thermodynamics

Calcium sulfoaluminate (C$A) cement is a binder of increasing interest to the cement industry and is undergoing rapid development. Current formulations do not contain alite; however, alite calcium sulfoaluminate (a-C$A) cements can combine the favourable characteristics of Portland cement (PC) with those of C$A cement while also having a lower carbon dioxide footprint than the current generation of PC clinkers. This paper presents two results on the formation of a-C$A clinkers. The first is a thermodynamic study demonstrating that the production of a-C$A clinker is possible without the use of mineralisers, doping with foreign elements, or using multiple stages of heating. It is established that a-C$A clinker can be readily produced in a standard process by controlling the oxygen and sulfur dioxide fugacity in the atmosphere. This allows for the stabilisation of ye’elimite to the higher temperatures required for alite stability. The second result establishes that when using fluorine to mineralise a-C$A clinker production, the iron content in the clinker is also an important variable. Although the exact mechanism of alite stabilisation is not known, it is shown that alite formation increases with the combination of calcium fluoride and iron (III) oxide in the mix

DNA Methylation Signature for EZH2 Functionally Classifies Sequence Variants in Three PRC2 Complex Genes.

Weaver syndrome (WS), an overgrowth/intellectual disability syndrome (OGID), is caused by pathogenic variants in the histone methyltransferase EZH2, which encodes a core component of the Polycomb repressive complex-2 (PRC2). Using genome-wide DNA methylation (DNAm) data for 187 individuals with OGID and 969 control subjects, we show that pathogenic variants in EZH2 generate a highly specific and sensitive DNAm signature reflecting the phenotype of WS. This signature can be used to distinguish loss-of-function from gain-of-function missense variants and to detect somatic mosaicism. We also show that the signature can accurately classify sequence variants in EED and SUZ12, which encode two other core components of PRC2, and predict the presence of pathogenic variants in undiagnosed individuals with OGID. The discovery of a functionally relevant signature with utility for diagnostic classification of sequence variants in EZH2, EED, and SUZ12 supports the emerging paradigm shift for implementation of DNAm signatures into diagnostics and translational research

Achieving global biodiversity goals by 2050 requires urgent and integrated actions

Governments are negotiating actions intended to halt biodiversity loss and put it on a path to recovery by 2050. Here, we show that bending the curve for biodiversity is possible, but only if actions are implemented urgently and in an integrated manner. Connecting these actions to biodiversity outcomes and tracking progress remain a challenge

Dengue Virus Infection of Aedes aegypti Requires a Putative Cysteine Rich Venom Protein

Citation: Londono-Renteria, B., Troupin, A., Conway, M. J., Vesely, D., Ledizet, M., Roundy, C. M., . . . Colpitts, T. M. (2015). Dengue Virus Infection of Aedes aegypti Requires a Putative Cysteine Rich Venom Protein. Plos Pathogens, 11(10), 23. doi:10.1371/journal.ppat.1005202Dengue virus (DENV) is a mosquito-borne flavivirus that causes serious human disease and mortality worldwide. There is no specific antiviral therapy or vaccine for DENV infection. Alterations in gene expression during DENV infection of the mosquito and the impact of these changes on virus infection are important events to investigate in hopes of creating new treatments and vaccines. We previously identified 203 genes that were >= 5-fold differentially upregulated during flavivirus infection of the mosquito. Here, we examined the impact of silencing 100 of the most highly upregulated gene targets on DENV infection in its mosquito vector. We identified 20 genes that reduced DENV infection by at least 60% when silenced. We focused on one gene, a putative cysteine rich venom protein (SeqID AAEL000379; CRVP379), whose silencing significantly reduced DENV infection in Aedes aegypti cells. Here, we examine the requirement for CRVP379 during DENV infection of the mosquito and investigate the mechanisms surrounding this phenomenon. We also show that blocking CRVP379 protein with either RNAi or specific antisera inhibits DENV infection in Aedes aegypti. This work identifies a novel mosquito gene target for controlling DENV infection in mosquitoes that may also be used to develop broad preventative and therapeutic measures for multiple flaviviruses

Grazoprevir plus elbasvir in treatment-naive and treatment-experienced patients with hepatitis C virus genotype 1 infection and stage 4-5 chronic kidney disease (the C-SURFER study): a combination phase 3 study

Cellular mechanisms in basic and clinical gastroenterology and hepatolog

The Epstein–Barr virus nuclear antigen-1 promotes telomere dysfunction via induction of oxidative stress

The Epstein–Barr virus (EBV) nuclear antigen (EBNA)-1 promotes the accumulation of chromosomal aberrations in malignant B cells by inducing oxidative stress. Here we report that this phenotype is associated with telomere dysfunction. Stable or conditional expression of EBNA1 induced telomere abnormalities including loss or gain of telomere signals, telomere fusion and heterogeneous length of telomeres. This was accompanied by the accumulation of extrachromosomal telomeres, telomere dysfunction-induced foci (TIFs) containing phosphorylated histone H2AX and the DNA damage response protein 53BP1, telomere-associated promyelocytic leukemia nuclear bodies (APBs), telomeric-sister chromatid exchanges and displacement of the shelterin protein TRF2. The induction of TIFs and APBs was inhibited by treatment with scavengers of reactive oxygen species (ROS) that also promoted the relocalization of TRF2 at telomeres. These findings highlight a novel mechanism by which EBNA1 may promote malignant transformation and tumor progression