Electronic structure and magnetic properties of the graphene/Fe/Ni(111) intercalation-like system

The electronic structure and magnetic properties of the graphene/Fe/Ni(111) system were investigated via combination of the density functional theory calculations and electron-spectroscopy methods. This system was prepared via intercalation of thin Fe layer (1 ML) underneath graphene on Ni(111) and its inert properties were verified by means of photoelectron spectroscopy. Intercalation of iron in the space between graphene and Ni(111) changes drastically the magnetic response from the graphene layer that is explained by the formation of the highly spin-polarized $3d_{z^2}$ quantum-well state in the thin iron layer.Comment: Manuscript and supplementary material

Disturbance of deep-sea environments induced by the M9.0 Tohoku Earthquake

The impacts of the M9.0 Tohoku Earthquake on deep-sea environment were investigated 36 and 98 days after the event. The light transmission anomaly in the deep-sea water after 36 days became atypically greater (∼35%) and more extensive (thickness ∼1500 m) near the trench axis owing to the turbulent diffusion of fresh seafloor sediment, coordinated with potential seafloor displacement. In addition to the chemical influx associated with sediment diffusion, an influx of 13C-enriched methane from the deep sub-seafloor reservoirs was estimated. This isotopically unusual methane influx was possibly triggered by the earthquake and its aftershocks that subsequently induced changes in the sub-seafloor hydrogeologic structures. The whole prokaryotic biomass and the development of specific phylotypes in the deep-sea microbial communities could rise and fall at 36 and 98 days, respectively, after the event. We may capture the snap shots of post-earthquake disturbance in deep-sea chemistry and microbial community responses

Limits to sustained energy intake XXIV : impact of suckling behaviour on the body temperatures of lactating female mice

We would like to thank the animal house staff and all members of the Energetics group for their invaluable help at various stages throughout the project. This work was supported by Natural Environment Research Council grant (NERC, NE/C004159/1). YG was supported by a scholarship from the rotary foundation. LV was supported by a Rubicon grant from the Netherlands Scientific Organisation (NWO).Peer reviewedPublisher PD

Oxidation resistance of graphene-coated Cu and Cu/Ni alloy

The ability to protect refined metals from reactive environments is vital to many industrial and academic applications. Current solutions, however, typically introduce several negative effects, including increased thickness and changes in the metal physical properties. In this paper, we demonstrate for the first time the ability of graphene films grown by chemical vapor deposition to protect the surface of the metallic growth substrates of Cu and Cu/Ni alloy from air oxidation. SEM, Raman spectroscopy, and XPS studies show that the metal surface is well protected from oxidation even after heating at 200 \degree C in air for up to 4 hours. Our work further shows that graphene provides effective resistance against hydrogen peroxide. This protection method offers significant advantages and can be used on any metal that catalyzes graphene growth

Identification of Collateral Sensitivity to Dihydroorotate Dehydrogenase Inhibitors in Plasmodium falciparum

Drug resistance has been reported for every antimalarial in use highlighting the need for new strategies to protect the efficacy of therapeutics in development. We have previously shown that resistance can be suppressed with a population biology trap: by identifying situations where resistance to one compound confers hypersensitivity to another (collateral sensitivity), we can design combination therapies that not only kill the parasite but also guide its evolution away from resistance. We applied this concept to the Plasmodium falciparum dihydroorotate dehydrogenase (PfDHODH) enzyme, a well validated antimalarial target with inhibitors in the development pipeline. Here, we report a high-throughput screen to identify compounds specifically active against PfDHODH resistant mutants. We additionally perform extensive cross-resistance profiling allowing us to identify compound pairs demonstrating the potential for mutually incompatible resistance. These combinations represent promising starting points for exploiting collateral sensitivity to extend the useful lifespan of new antimalarial therapeutics

Involvement of promoter methylation in the regulation of Pregnane X receptor in colon cancer cells

<p>Abstract</p> <p>Background</p> <p>Pregnane X receptor (PXR) is a key transcription factor that regulates drug metabolizing enzymes such as cytochrome P450 (CYP) 3A4, and plays important roles in intestinal first-pass metabolism. Although there is a large inter-individual heterogeneity with intestinal CYP3A4 expression and activity, the mechanism driving these differences is not sufficiently explained by genetic variability of PXR or CYP3A4. We examined whether epigenetic mechanisms are involved in the regulation of PXR/CYP3A4 pathways in colon cancer cells.</p> <p>Methods</p> <p>mRNA levels of PXR, CYP3A4 and vitamin D receptor (VDR) were evaluated by quantitative real-time PCR on 6 colon cancer cell lines (Caco-2, HT29, HCT116, SW48, LS180, and LoVo). DNA methylation status was also examined by bisulfite sequencing of the 6 cell lines and 18 colorectal cancer tissue samples. DNA methylation was reversed by the treatment of these cell lines with 5-aza-2'-deoxycytidine (5-aza-dC).</p> <p>Results</p> <p>The 6 colon cancer cell lines were classified into two groups (high or low expression cells) based on the basal level of PXR/CYP3A4 mRNA. DNA methylation of the CpG-rich sequence of the <it>PXR </it>promoter was more densely detected in the low expression cells (Caco-2, HT29, HCT116, and SW48) than in the high expression cells (LS180 and LoVo). This methylation was reversed by treatment with 5-aza-dC, in association with re-expression of PXR and CYP3A4 mRNA, but not VDR mRNA. Therefore, PXR transcription was silenced by promoter methylation in the low expression cells, which most likely led to downregulation of CYP3A4 transactivation. Moreover, a lower level of <it>PXR </it>promoter methylation was observed in colorectal cancer tissues compared with adjacent normal mucosa, suggesting upregulation of the PXR/CYP3A4 mRNAs during carcinogenesis.</p> <p>Conclusions</p> <p><it>PXR </it>promoter methylation is involved in the regulation of intestinal PXR and CYP3A4 mRNA expression and might be associated with the inter-individual variability of the drug responses of colon cancer cells.</p