Carbon‐based nanomaterials accelerate arteriolar thrombus formation in the murine microcirculation independently of their shape

Although carbon‐based nanomaterials (CBNs) have been shown to exert prothrombotic effects in microvessels, it is poorly understood whether CBNs also have the potential to interfere with the process of leukocyte‐endothelial cell interactions and whether the shape of CBNs plays a role in these processes. Thus, the aim of this study was to compare the acute effects of two differently shaped CBNs, fiber‐shaped single‐walled carbon nanotubes (SWCNT) and spherical ultrafine carbon black (CB), on thrombus formation as well as on leukocyte‐endothelial cell interactions and leukocyte transmigration in the murine microcirculation upon systemic administration in vivo. Systemic administration of both SWCNT and CB accelerated arteriolar thrombus formation at a dose of 1 mg kg^–1 body weight, whereas SWCNT exerted a prothrombotic effect also at a lower dose (0.1 mg kg^–1 body weight). In vitro, both CBNs induced P‐selectin expression on human platelets and formation of platelet‐granulocyte complexes. In contrast, injection of fiber‐shaped SWCNT or of spherical CB did not induce leukocyte–endothelial cell interactions or leukocyte transmigration. In vitro, both CBNs slightly increased the expression of activation markers on human monocytes and granulocytes. These findings suggest that systemic administration of CBNs accelerates arteriolar thrombus formation independently of the CBNs' shape, but does not induce leukocyte–endothelial cell interactions or leukocyte transmigration. Copyright © 2014 John Wiley & Sons, Ltd.     

The Effect of Severe Shot Peening on Fatigue Life of Laser Powder Bed Fusion Manufactured 316L Stainless Steel

Severe shot peening (SSP) was used on additive manufactured 316L by laser powder bed fusion. The effect of the post processing on the surface features of the material was analyzed through residual stress measurements, tensile testing, hardness-depth profiles, and fatigue testing by flexural bending. The results showed that SSP can be utilized to form residual stresses up to −400 MPa 200 μm below the surface. At the same time, a clear improvement on the surface hardness was achieved from 275 HV to near 650 HV. These together resulted in a clear improvement on material strength which was recorded at 10% improvement in ultimate tensile strength. Most significantly, the fatigue limit of the material was tripled from 200 MPa to over 600 MPa and the overall fatigue strength raised similarly from a low to high cycle regime.     

Genotoxicity of nanomaterials: DNA damage and micronuclei induced by carbon nanotubes and graphite nanofibres in human bronchial epithelial cells in vitro

Despite the increasing industrial use of different nanomaterials, data on their genotoxicity are scant. In the present study, we examined the potential genotoxic effects of carbon nanotubes (CNTs; >50% single-walled, ∼40% other CNTs; 1.1 nm × 0.5–100 μm; Sigma–Aldrich) and graphite nanofibres (GNFs; 95%; outer diameter 80–200 nm, inner diameter 30–50 nm, length 5–20 μm; Sigma–Aldrich) in vitro. Genotoxicity was assessed by the single cell gel electrophoresis (comet) assay and the micronucleus assay (cytokinesis-block method) in human bronchial epithelial BEAS 2B cells cultured for 24 h, 48 h, or 72 h with various doses (1–100 μg/cm², corresponding to 3.8–380 μg/ml) of the carbon nanomaterials. In the comet assay, CNTs induced a dose-dependent increase in DNA damage at all treatment times, with a statistically significant effect starting at the lowest dose tested. GNFs increased DNA damage at all doses in the 24-h treatment, at two doses (40 and 100 μg/cm²) in the 48-h treatment (dose-dependent effect) and at four doses (lowest 10 μg/cm²) in the 72-h treatment. In the micronucleus assay, no increase in micronucleated cells was observed with either of the nanomaterials after the 24-h treatment or with CNTs after the 72-h treatment. The 48-h treatment caused a significant increase in micronucleated cells at three doses (lowest 10 μg/cm²) of CNTs and at two doses (5 and 10 μg/cm²) of GNFs. The 72-h treatment with GNFs increased micronucleated cells at four doses (lowest 10 μg/cm²). No dose-dependent effects were seen in the micronucleus assay. The presence of carbon nanomaterial on the microscopic slides disturbed the micronucleus analysis and made it impossible at levels higher than 20 μg/cm² of GNFs in the 24-h and 48-h treatments. In conclusion, our results suggest that both CNTs and GNFs are genotoxic in human bronchial epithelial BEAS 2B cells in vitro. This activity may be due to the fibrous nature of these carbon nanomaterials with a possible contribution by catalyst metals present in the materials—Co and Mo in CNTs (<5 wt.%) and Fe (<3 wt.%) in GNFs.     

Vanadia–Zirconia and Vanadia–Hafnia Catalysts for Utilization of Volatile Organic Compound Emissions

Utilization is a sustainable and interesting alternative for the destructive treatment of volatile organic compounds due to avoided CO₂ emission. This work concentrates on the development of active and sulfur-tolerant catalysts for the utilization of contaminated methanol. Impregnated and sol–gel prepared vanadia–zirconia and vanadia–hafnia catalysts were thoroughly characterized by N₂ sorption, analytical (S)TEM, elemental analysis, XRD and Raman spectroscopy, and their performances were evaluated in formaldehyde production from methanol and methanethiol mixture. The results showed higher activity of the sol–gel prepared catalysts due to formation of mono- and polymeric vanadia species. Unfortunately, the most active vanadia sites were deactivated more easily than the metal-mixed oxide HfV₂O₇ and ZrV₂O₇ phases, as well as crystalline V₂O₅ observed in the impregnated catalysts. Metal-mixed oxide phases were formed in impregnated catalysts through formation of defects in HfO₂ and ZrO₂ structure during calcination at 600 °C, which was evidenced by Raman spectroscopy. The sol–gel prepared vanadia–zirconia and vanadia–hafnia catalysts were able to produce formaldehyde from contaminated methanol with high selectivity at temperature around 400 °C, while impregnated catalysts required 50–100 °C higher temperatures.     

Genotoxicity of polyvinylpyrrolidone-coated silver nanoparticles in BEAS 2B cells

Silver nanoparticles (AgNPs) are widely utilized in various consumer products and medical devices, especially due to their antimicrobial properties. However, several studies have associated these particles with toxic effects, such as inflammation and oxidative stress in vivo and cytotoxic and genotoxic effects in vitro. Here, we assessed the genotoxic effects of AgNPs coated with polyvinylpyrrolidone (PVP) (average diameter 42.5 ± 14.5 nm) on human bronchial epithelial BEAS 2B cells in vitro. AgNPs were dispersed in bronchial epithelial growth medium (BEGM) with 0.6 mg/ml bovine serum albumin (BSA). The AgNP were partially well-dispersed in the medium and only limited amounts (ca. 0.02 μg Ag⁺ ion/l) could be dissolved after 24 h. The zeta-potential of the AgNPs was found to be highly negative in pure water but was at least partially neutralized in BEGM with 0.6 mg BSA/ml. Cytotoxicity was measured by cell number count utilizing Trypan Blue exclusion and by an ATP-based luminescence cell viability assay. Genotoxicity was assessed by the alkaline single cell gel electrophoresis (comet) assay, the cytokinesis-block micronucleus (MN) assay, and the chromosomal aberration (CA) assay. The cells were exposed to various doses (0.5–48 μg/cm² corresponding to 2.5–240 μg/ml) of AgNPs for 4 and 24 h in the comet assay, for 48 h in the MN assay, and for 24 and 48 h in the CA assay. DNA damage measured by the percent of DNA in comet tail was induced in a dose-dependent manner after both the 4-h and the 24-h exposures to AgNPs, with a statistically significant increase starting at 16 μg/cm² (corresponding to 60.8 μg/ml) and doubling of the percentage of DNA in tail at 48 μg/cm². However, no induction of MN or CAs was observed at any of the doses or time points. The lack of induction of chromosome damage by the PVP-coated AgNPs is possibly due to the coating which may protect the cells from direct interaction with the AgNPs, either by reducing ion leaching from the particles or by causing extensive agglomeration of the nanoparticles, with a possible reduction of the cellular uptake.     

Sol-gel derived aluminosilicate coatings on alumina as substrate for osteoblasts

Rat bone marrow stromal cell differentiation on aluminosilicate 3Al₂O₃–2SiO₂ coatings was investigated. Thin ceramic coatings were prepared on -alumina substrates by the sol–gel process and calcined in order to establish an amorphous aluminosilicate ceramic phase with and without nanosized transitional mullite crystals. In addition, coatings of thermally sprayed aluminosilicate and diphasic γ-alumina–silica nanosized colloids were prepared. Cell culture testing by rat osteoblasts showed good biocompatibility for aluminosilicates with sustained normal osteoblast functions. Despite mutual disparities in physical and chemical nanostructures, the culture findings suggested fairly similar osteoblast response to all tested coatings. The results suggest that topographical frequency parameters and chemical uniformity are important parameters in determining the best conditions for osteoblasts on sol–gel derived aluminosilicate materials.     

Genetic modifiers of degeneration in the cathepsin D deficient Drosophila model for neuronal ceroid lipofuscinosis

Neuronal ceroid lipofuscinoses (NCLs) are pediatric, neurodegenerative, lysosomal storage disorders. Mutations in cathepsin D result in the most severe, congenital form of NCLs. We have previously generated a cathepsin D deficient Drosophila model, which exhibits the key features of NCLs: progressive intracellular accumulation of autofluorescent storage material and modest neurodegeneration in the brain areas related to visual functions. Here we extend the phenotypic characterization of cathepsin D deficient Drosophila and report that modest degenerative changes are also present in their retinae. Furthermore, by utilizing this phenotype, we examined the possible effect of 17 candidate modifiers, selected based on the results from other cathepsin D deficiency models. We found enhancers of this phenotype that support the involvement of endocytosis-, lipid metabolism- and oxidation-related factors in the cathepsin D deficiency induced degeneration. Our results warrant further investigation of these mechanisms in the pathogenesis of cathepsin D deficiency.