Environmental Particle Emissions due to Automated Drilling of Polypropylene Composites and Nanocomposites Reinforced with Talc, Montmorillonite and Wollastonite

In this study, the effect on nanoparticle emissions due to drilling on Polypropylene (PP) reinforced with 20% talc, 5% montmorillonite (MMT) and 5% Wollastonite (WO) is investigated. The study is the first to explore the nanoparticle release from WO and talc reinforced composites and compares the results to previously researched MMT. With 5% WO, equivalent tensile properties with a 10 % weight reduction were obtained relative to the reference 20% talc sample. The materials were fabricated through injection moulding. The nanorelease studies were undertaken using the controlled drilling methodology for nanoparticle exposure assessment developed within the European Commission funded SIRENA Life 11 ENV/ES/506 project. Measurements were taken using CPC and DMS50 equipment for real-time characterization and measurements. The particle number concentration (of particles <1000nm) and particle size distribution (4.87nm - 562.34nm) of the particles emitted during drilling were evaluated to investigate the effect of the silicate fillers on the particles released. The nano-filled samples exhibited a 33% decrease (MMT sample) or a 30% increase (WO sample) on the average particle number concentration released in comparison to the neat polypropylene sample. The size distribution data displayed a substantial percentage of the particles released from the PP, PP/WO and PP/MMT samples to be between 5-20nm, whereas the PP/talc sample emitted larger particle diameters.The work is funded by and part of the European Commission Life project named Simulation of the release of nanomaterials from consumer products for environmental exposure assessment (SIRENA, Pr. No. LIFE 11 ENV/ES/596). The access and use of the facilities at the Flemish Institute for Technological Research (VITO) was funded by QualityNano Project through Transnational Access (TA Application VITO-TAF-382 and VITO-TAF-500) under the European Commission, Grant Agreement No: INFRA-2010-262163. Kristof is also thankful for partial funding by the School of Engineering at Robert Gordon University for his studentship

Tensile and flexural properties of hybrid graphene oxide/epoxy carbon fibre reinforced composites.

In this study, nano-sized graphene oxide sheets were homogenously dispersed via sonication methods in epoxy followed by vacuum resin infusion for the fabrication of the epoxy, graphene oxide (GO) and micro-sized carbon fibre reinforced nanocomposites (EP/CF/GO). Graphene oxide concentrations ranging from 0.1 - 0.5 wt. % were studied to investigate the effect on tensile and flexural strength. It was observed that the tensile strength of the EP/CF decreased with the addition of GO but increased with GO weight concentration in the nanocomposites studied from 498MPa to 519 MPa for the inclusion of 0.1 to 0.5 wt.% GO respectively. The 0.5 wt. % EP/CF/GO recorded a 10% increase in Young's modulus compared to the classical epoxy / carbon fibre composites, and similar trend was observed for the flexural properties. However flexural strength of the GO samples did not surpass the control sample (epoxy /carbon fibre composites) with the 0.3 wt.% GO samples (EP/CF/GO) providing the greatest flexural strength of >580 MPa compared to the 0.1 wt.% and 0.5 wt.% GO samples

Ambient Oxygen Promotes Tumorigenesis

Oxygen serves as an essential factor for oxidative stress, and it has been shown to be a mutagen in bacteria. While it is well established that ambient oxygen can also cause genomic instability in cultured mammalian cells, its effect on de novo tumorigenesis at the organismal level is unclear. Herein, by decreasing ambient oxygen exposure, we report a ∼50% increase in the median tumor-free survival time of p53−/− mice. In the thymus, reducing oxygen exposure decreased the levels of oxidative DNA damage and RAG recombinase, both of which are known to promote lymphomagenesis in p53−/− mice. Oxygen is further shown to be associated with genomic instability in two additional cancer models involving the APC tumor suppressor gene and chemical carcinogenesis. Together, these observations represent the first report directly testing the effect of ambient oxygen on de novo tumorigenesis and provide important physiologic evidence demonstrating its critical role in increasing genomic instability in vivo

Accumulation of the inner nuclear envelope protein Sun1 is pathogenic in progeric and dystrophic laminopathies

10.1016/j.cell.2012.01.059Cell1493565-577CELL

Inflammatory cardiac valvulitis in TAX1BP1-deficient mice through selective NF-κB activation

Nuclear factor kappa B (NF-κB) is a key mediator of inflammation. Unchecked NF-κB signalling can engender autoimmune pathologies and cancers. Here, we show that Tax1-binding protein 1 (TAX1BP1) is a negative regulator of TNF-α- and IL-1β-induced NF-κB activation and that binding to mono- and polyubiquitin by a ubiquitin-binding Zn finger domain in TAX1BP1 is needed for TRAF6 association and NF-κB inhibition. Mice genetically knocked out for TAX1BP1 are born normal, but develop age-dependent inflammatory cardiac valvulitis, die prematurely, and are hypersensitive to low doses of TNF-α and IL-1β. TAX1BP1−/− cells are more highly activated for NF-κB than control cells when stimulated with TNF-α or IL-1β. Mechanistically, TAX1BP1 acts in NF-κB signalling as an essential adaptor between A20 and its targets

Alternate protein kinase A activity identifies a unique population of stromal cells in adult bone

A population of stromal cells that retains osteogenic capacity in adult bone (adult bone stromal cells or aBSCs) exists and is under intense investigation. Mice heterozygous for a null allele of prkar1a (Prkar1a+/−), the primary receptor for cyclic adenosine monophosphate (cAMP) and regulator of protein kinase A (PKA) activity, developed bone lesions that were derived from cAMP-responsive osteogenic cells and resembled fibrous dysplasia (FD). Prkar1a+/− mice were crossed with mice that were heterozygous for catalytic subunit Cα (Prkaca+/−), the main PKA activity-mediating molecule, to generate a mouse model with double heterozygosity for prkar1a and prkaca (Prkar1a+/−Prkaca+/−). Unexpectedly, Prkar1a+/−Prkaca+/− mice developed a greater number of osseous lesions starting at 3 months of age that varied from the rare chondromas in the long bones and the ubiquitous osteochondrodysplasia of vertebral bodies to the occasional sarcoma in older animals. Cells from these lesions originated from an area proximal to the growth plate, expressed osteogenic cell markers, and showed higher PKA activity that was mostly type II (PKA-II) mediated by an alternate pattern of catalytic subunit expression. Gene expression profiling confirmed a preosteoblastic nature for these cells but also showed a signature that was indicative of mesenchymal-to-epithelial transition and increased Wnt signaling. These studies show that a specific subpopulation of aBSCs can be stimulated in adult bone by alternate PKA and catalytic subunit activity; abnormal proliferation of these cells leads to skeletal lesions that have similarities to human FD and bone tumors