Trialling water treatment residuals in the remediation of former mine site soils: investigating improvements achieved for plants, earthworms and soil solution.

During clarification processes of raw water a vast amount of by-product known as drinking water treatment residuals (WTRs) are produced, being principally composed of hydroxides of the Al or Fe salts added during water treatment plus the impurities they remove. Aluminium-based (Al-WTR) and iron-based (Fe-WTR) materials were applied at 10% w/w to degraded, bare (un-vegetated) soils from a restored coal mining site in central England (pH <3.9) to study their potential amelioration effects on earthworm mortality, biomass yield of seedling plants and element concentrations in plant tissues, earthworm tissues and in soil solutions. A separate treatment with agricultural lime was also conducted for comparison to evaluate whether any observed improvements were attributable to the liming capacity of the WTRs. After completion of the trials all samples were subjected to a wet-dry cycle and the experiments were repeated (i.e. simulating longer-term effects in the field). Both types of WTRs significantly increased biomass of plants and, in some treatments, survival of earthworms was also enhanced compared to non-amended soils. Excess plant tissue element concentrations and element concentrations in soil solutions were reduced in amended soils. The implications are that adding WTRs to mining impacted soils is a potentially viable, sustainable and low cost remediation method that could be used globally to improve the soil condition. This article is protected by copyright. All rights reserved

Active Chromatin Marks Are Retained on X Chromosomes Lacking Gene or Repeat Silencing Despite XIST/Xist Expression in Somatic Cell Hybrids

X-chromosome inactivation occurs early in mammalian development and results in the inactive X chromosome acquiring numerous hallmarks of heterochromatin. While XIST is a key player in the inactivation process, the method of action of this ncRNA is yet to be determined.To assess which features of heterochromatin may be directly recruited by the expression and localization of the XIST RNA we have analyzed a mouse/human somatic cell hybrid in which expression of human and mouse XIST/Xist has been induced from the active X by demethylation. Such hybrids had previously been demonstrated to disconnect XIST/Xist expression from gene silencing and we confirm maintenance of X-linked gene expression, even close to the Xist locus, despite the localized expression of mouse Xist.Loss of the active chromatin marks H3 acetylation and H3 lysine 4 methylation was not observed upon XIST/Xist expression, nor was there a gain of DNA methylation; thus these marks of facultative heterochromatin are not solely dependent upon Xist expression. Cot-1 holes, regions of depleted RNA hybridization with a Cot-1 probe, were observed upon Xist expression; however, these were at reduced frequency and intensity in these somatic cells. Domains of human Cot-1 transcription were observed corresponding to the human chromosomes in the somatic cell hybrids. The Cot-1 domain of the X was not reduced with the expression of XIST, which fails to localize to the human X chromosome in a mouse somatic cell background. The human inactive X in a mouse/human hybrid cell also shows delocalized XIST expression and an ongoing Cot-1 domain, despite X-linked gene silencing. These results are consistent with recent reports separating Cot-1 silencing from genic silencing, but also demonstrate repetitive element expression from an otherwise silent X chromosome in these hybrid cells

Visualizing early splenic memory CD8+ T cells reactivation against intracellular bacteria in the mouse

International audienceMemory CD8(+) T cells represent an important effector arm of the immune response in maintaining long-lived protective immunity against viruses and some intracellular bacteria such as Listeria monocytogenes (L.m). Memory CD8(+) T cells are endowed with enhanced antimicrobial effector functions that perfectly tail them to rapidly eradicate invading pathogens. It is largely accepted that these functions are sufficient to explain how memory CD8(+) T cells can mediate rapid protection. However, it is important to point out that such improved functional features would be useless if memory cells were unable to rapidly find the pathogen loaded/infected cells within the infected organ. Growing evidences suggest that the anatomy of secondary lymphoid organs (SLOs) fosters the cellular interactions required to initiate naive adaptive immune responses. However, very little is known on how the SLOs structures regulate memory immune responses. Using Listeria monocytogenes (L.m) as a murine infection model and imaging techniques, we have investigated if and how the architecture of the spleen plays a role in the reactivation of memory CD8(+) T cells and the subsequent control of L.m growth. We observed that in the mouse, memory CD8(+) T cells start to control L.m burden 6 hours after the challenge infection. At this very early time point, L.m-specific and non-specific memory CD8(+) T cells localize in the splenic red pulp and form clusters around L.m infected cells while naïve CD8(+) T cells remain in the white pulp. Within these clusters that only last few hours, memory CD8(+) T produce inflammatory cytokines such as IFN-gamma and CCL3 nearby infected myeloid cells known to be crucial for L.m killing. Altogether, we describe how memory CD8(+) T cells trafficking properties and the splenic micro-anatomy conjugate to create a spatio-temporal window during which memory CD8(+) T cells provide a local response by secreting effector molecules around infected cells

A synopsis of history. General history, from B.C. 800 to A.D. 1876, outlined in diagrams and tables; with index and genealogies. For general reference, and for schools and colleges.

Mode of access: Internet

Substrate-Dependent Exciton Diffusion and Annihilation in Chemically Treated MoS2and WS2

Atomically thin semiconductors such as monolayer MoS2 and WS2 exhibit nonlinear exciton-exciton annihilation at notably low excitation densities (below ∼10 excitons/μm2 in exfoliated MoS2). Here, we show that the density threshold at which annihilation occurs can be tuned by changing the underlying substrate. When the supporting substrate is changed from SiO2 to Al2O3 or SrTiO3, the rate constant for second-order exciton-exciton annihilation, kXX [cm2/s], is reduced by 1 or 2 orders of magnitude, respectively. Using transient photoluminescence microscopy, we measure the effective room-temperature exciton diffusion coefficient in bis(trifluoromethane)sulfonimide-treated MoS2 to be in the range D = 0.03-0.06 cm2/s, corresponding to a diffusion length of LD = 350 nm for an exciton lifetime of τ = 18 ns, which does not depend strongly on the substrate. We discuss possible mechanisms for the observed behavior, including substrate permittivity, long-range exciton-exciton or exciton-charge interactions, defect-mediated Auger recombination, and spatially inhomogeneous exciton populations arising from substrate-induced disorder. Exciton annihilation limits the overall efficiency of 2D semiconductor devices operating at high exciton densities; the ability to tune these interactions via the underlying substrate is an important step toward more efficient optoelectronic technologies featuring atomically thin materials