Water sorption isotherms and hysteresis of cement paste at moderately high temperature, up to 80 °C

The constitutive models of concrete often consider water desorption isotherms to be near-equilibrium and significantly affected by moderately high temperature, 40–80◦C, typically through microstructural changes. However literature data suggest that adsorption, not desorption, is near-equilibrium and moderate temperatures do not cause microstructural changes. This work supports the latter theory, through dynamic vapor sorption experiments on cement paste at 20–80◦C. Samples were pre-conditioned at 60% relative humidity and 20◦C, and isotherms were measured for several humidity ranges and testing rates. The results, corroborated by classical DFT simulations, indicate that adsorption is near-equilibrium and mostly unaffected by temperature, whereas desorption is out-of-equilibrium due to the ink-bottle effect at high humidity, and interlayer water at low humidity. Starting from the second cycle, desorption at higher temperatures features a shift of the cavitation pressure and overall a smaller hysteresis. A conceptual model of pore-specific temperature-dependent hysteresis is proposed to qualitatively explain the results

Measurement of erythrocyte membrane mannoses to assess splenic function

ACKNOWLEDGEMENTS This work was funded by Aberdeen University Development Trust and Friends of Anchor. The University of Aberdeen is applying for a patent based on this work. Aberdeen University Development Trust (GrantNumber(s): DB10452-11) Friends of Anchor (GrantNumber(s): RS 2018 001)Peer reviewedPublisher PD

Chronic exposure to short chain fatty acids modulates transport and metabolism of microbiome-derived phenolics in human intestinal cells

Dietary fibre-derived short chain fatty acids (SCFA) and phenolics produced by the gut microbiome have multiple effects on health. We have tested the hypothesis that long term exposure to physiological concentrations of SCFA can affect the transport and metabolism of (poly)phenols by the intestinal epithelium using the Caco-2 cell model. Metabolites and conjugates of hesperetin (HT) and ferulic acid (FA), gut-derived from dietary hesperidin and chlorogenic acid respectively, were quantified by LC–MS with authentic standards following transport across differentiated cell monolayers. Changes in metabolite levels were correlated with effects on mRNA and protein expression of key enzymes and transporters. Propionate and butyrate increased both FA transport and rate of appearance of FA-glucuronide apically and basolaterally, linked to an induction of MCT1. Propionate was the only SCFA that augmented the rate of formation of basolateral FA-sulfate conjugates, possibly via basolateral transporter upregulation. In addition, propionate enhanced the formation of HT-glucuronide conjugates and increased HT-sulfate efflux towards the basolateral compartment. Acetate treatment amplified transepithelial transport of FA in the apical to basolateral direction, associated with lower levels of MCT1 protein expression. Metabolism and transport of both HT and FA were curtailed by the organic acid lactate owing to a reduction of UGT1A1 protein levels. Our data indicate a direct interaction between microbiota-derived metabolites of (poly)phenols and SCFA through modulation of transporters and conjugating enzymes, and increase our understanding of how dietary fibre, via the microbiome, may affect and enhance uptake of bioactive molecules

Study protocol: MyoFit46-the cardiac sub-study of the MRC National Survey of Health and Development

BACKGROUND: The life course accumulation of overt and subclinical myocardial dysfunction contributes to older age mortality, frailty, disability and loss of independence. The Medical Research Council National Survey of Health and Development (NSHD) is the world's longest running continued surveillance birth cohort providing a unique opportunity to understand life course determinants of myocardial dysfunction as part of MyoFit46-the cardiac sub-study of the NSHD. METHODS: We aim to recruit 550 NSHD participants of approximately 75 years+ to undertake high-density surface electrocardiographic imaging (ECGI) and stress perfusion cardiovascular magnetic resonance (CMR). Through comprehensive myocardial tissue characterization and 4-dimensional flow we hope to better understand the burden of clinical and subclinical cardiovascular disease. Supercomputers will be used to combine the multi-scale ECGI and CMR datasets per participant. Rarely available, prospectively collected whole-of-life data on exposures, traditional risk factors and multimorbidity will be studied to identify risk trajectories, critical change periods, mediators and cumulative impacts on the myocardium. DISCUSSION: By combining well curated, prospectively acquired longitudinal data of the NSHD with novel CMR-ECGI data and sharing these results and associated pipelines with the CMR community, MyoFit46 seeks to transform our understanding of how early, mid and later-life risk factor trajectories interact to determine the state of cardiovascular health in older age. TRIAL REGISTRATION: Prospectively registered on ClinicalTrials.gov with trial ID: 19/LO/1774 Multimorbidity Life-Course Approach to Myocardial Health- A Cardiac Sub-Study of the MCRC National Survey of Health and Development (NSHD)

MeCP2 binds to nucleosome free (linker DNA) regions and to H3K9/H3K27 methylated nucleosomes in the brain

Methyl-CpG-binding protein 2 (MeCP2) is a chromatin-binding protein that mediates transcriptional regulation, and is highly abundant in brain. The nature of its binding to reconstituted templates has been well characterized in vitro. However, its interactions with native chromatin are less understood. Here we show that MeCP2 displays a distinct distribution within fractionated chromatin from various tissues and cell types. Artificially induced global changes in DNA methylation by 3-aminobenzamide or 5-aza-2′-deoxycytidine, do not significantly affect the distribution or amount of MeCP2 in HeLa S3 or 3T3 cells. Most MeCP2 in brain is chromatin-bound and localized within highly nuclease-accessible regions. We also show that, while in most tissues and cell lines, MeCP2 forms stable complexes with nucleosome, in brain, a fraction of it is loosely bound to chromatin, likely to nucleosome-depleted regions. Finally, we provide evidence for novel associations of MeCP2 with mononucleosomes containing histone H2A.X, H3K9me2 and H3K27me3 in different chromatin fractions from brain cortex and in vitro. We postulate that the functional compartmentalization and tissue-specific distribution of MeCP2 within different chromatin types may be directed by its association with nucleosomes containing specific histone variants, and post-translational modifications

The yeast Cyc8-Tup1 complex cooperates with Hda1p and Rpd3p histone deacetylases to robustly repress transcription of the subtelomeric FLO1 gene

AbstractWe demonstrate that the yeast flocculation gene, FLO1, is representative of a distinct subset of subtelomeric genes that are robustly repressed by the Cyc8–Tup1 complex. We have examined Cyc8–Tup1 localisation, histone acetylation and long-range chromatin remodelling within the extensive FLO1 upstream region. We show that Cyc8–Tup1 is localised in a DNase I hypersensitive site within an ordered array of strongly positioned nucleosomes around −700 base pairs upstream of the transcription start site. In cyc8 deletion mutant strains, Tup1p localisation is absent, with concomitant histone hyperacetylation of adjacent regions at the FLO1 promoter. This is accompanied by extensive histone depletion across the upstream region and gene activation. The yeast histone deacetylases, Hda1p and Rpd3p, occupy the repressed FLO1 promoter region in a Cyc8–Tup1 dependent manner and coordinate histone deacetylation, nucleosome stabilisation and gene repression. Moreover, we show that the ATP-dependent chromatin remodelling complex Swi–Snf occupies the site vacated by Cyc8–Tup1 in a cyc8 mutant. These data suggest that distinctly bound Cyc8–Tup1 cooperates with Hda1p and Rpd3p to establish or maintain an extensive array of strongly positioned, deacetylated nucleosomes over the FLO1 promoter and upstream region which inhibit histone acetylation, block Swi–Snf binding and prevent transcription

Synthesis and catalysis of chemically reduced metal–metalloid amorphous alloys

This is the published version. Copyright 2012 Royal Society of ChemistryAmorphous alloys structurally deviate from crystalline materials in that they possess unique short-range ordered and long-range disordered atomic arrangement. They are important catalytic materials due to their unique chemical and structural properties including broadly adjustable composition, structural homogeneity, and high concentration of coordinatively unsaturated sites. As chemically reduced metal–metalloid amorphous alloys exhibit excellent catalytic performance in applications such as efficient chemical production, energy conversion, and environmental remediation, there is an intense surge in interest in using them as catalytic materials. This critical review summarizes the progress in the study of the metal–metalloid amorphous alloy catalysts, mainly in recent decades, with special focus on their synthetic strategies and catalytic applications in petrochemical, fine chemical, energy, and environmental relevant reactions. The review is intended to be a valuable resource to researchers interested in these exciting catalytic materials. We concluded the review with some perspectives on the challenges and opportunities about the future developments of metal–metalloid amorphous alloy catalysts