Superior removal of arsenic from water with zirconium metal-organic framework UiO-66

10.1038/srep16613Scientific Reports51661

A metal–organic framework/α-alumina composite with a novel geometry for enhanced adsorptive separation

The development of a metal–organic framework/α-alumina composite leads to a novel concept: efficient adsorption occurs within a plurality of radial micro-channels with no loss of the active adsorbents during the process. This composite can effectively remediate arsenic contaminated water producing potable water recovery, whereas the conventional fixed bed requires eight times the amount of active adsorbents to achieve a similar performance

Protein kinase A (PKA) phosphorylation of Shp2 inhibits its phosphatase activity and modulates ligand specificity.

Pathological cardiac hypertrophy (an increase in cardiac mass resulting from stress-induced cardiac myocyte growth) is a major factor underlying heart failure. Src homology 2 domain-containing phosphatase (Shp2) is critical for cardiac function as mutations resulting in loss of Shp2 catalytic activity are associated with congenital cardiac defects and hypertrophy. We have identified a novel mechanism of Shp2 inhibition that may promote cardiac hypertrophy. We demonstrate that Shp2 is a component of the A-kinase anchoring protein (AKAP)-Lbc complex. AKAP-Lbc facilitates protein kinase A (PKA) phosphorylation of Shp2, which inhibits Shp2 phosphatase activity. We have identified two key amino acids in Shp2 that are phosphorylated by PKA: Thr73 contributes a helix-cap to helix αB within the N-terminal SH2 domain of Shp2, whereas Ser189 occupies an equivalent position within the C-terminal SH2 domain. Utilizing double mutant PKA phospho-deficient (T73A/S189A) and phospho-mimetic (T73D/S189D) constructs, in vitro binding assays, and phosphatase activity assays, we demonstrate that phosphorylation of these residues disrupts Shp2 interaction with tyrosine-phosphorylated ligands and inhibits its protein tyrosine phosphatase activity. Overall, our data indicate that AKAP-Lbc integrates PKA and Shp2 signaling in the heart and that AKAP-Lbc-associated Shp2 activity is reduced in hypertrophic hearts in response to chronic β-adrenergic stimulation and PKA activation. Thus, while induction of cardiac hypertrophy is a multifaceted process, inhibition of Shp2 activity through AKAP-Lbc-anchored PKA is a previously unrecognized mechanism that may promote this compensatory response

Solution heat treatment, forming and in-die quenching of a commercial sheet magnesium alloy into a complex-shaped component: experimentation and FE analysis

Interest in lightweight materials, particularly magnesium alloys, has increased significantly with rising efficiency requirements in the automotive sector. Magnesium is the lightest available structural metal, with a density approximately 35% lower than that of aluminium. The potential is great for magnesium to become a primary material used in future low carbon vehicle structures; however, there are significant obstacles, namely low ductility and formability, particularly at room temperature. The aim of this work is to present the feasibility of using the solution Heat treatment, Forming, and in-die Quenching (HFQ) process to produce complex shapes from a sheet magnesium alloy, and to use the results to verify a simulation of the process developed using commercial FE software. Uniaxial tensile tests were initially conducted to establish the optimum parameters for forming the part. Stamping trials were then carried out using these parameters, and a simulation set up modelling the forming operation. It was shown that the HFQ process could be used to form a successful component from this alloy, and that a good match was achieved between the results of the forming experiments and the simulation.The authors gratefully acknowledge the support from the EPSRC (Grant Ref: EP/I038616/1) for TARF-LCV: Towards Affordable, Closed-Loop Recyclable Future Low Carbon Vehicle Structures

Interactions between landscape changes and host communities can regulate echinococcus multilocularis transmission

An area close to the Qinghai-Tibet plateau region and subject to intensive deforestation contains a large focus of human alveolar echinococcosis while sporadic human cases occur in the Doubs region of eastern France. The current review analyses and compares epidemiological and ecological results obtained in both regions. Analysis of rodent species assemblages within quantified rural landscapes in central China and eastern France shows a significant association between host species for the pathogenic helminth Echinococcus multilocularis, with prevalences of human alveolar echinococcosis and with land area under shrubland or grassland. This suggests that at the regional scale landscape can affect human disease distribution through interaction with small mammal communities and their population dynamics. Lidicker's ROMPA hypothesis helps to explain this association and provides a novel explanation of how landscape changes may result in increased risk of a rodent-borne zoonotic disease