Volcanic ash ice nucleation activity is variably reduced by aging in water and sulfuric acid: the effects of leaching, dissolution, and precipitation

Volcanic ash nucleates ice when immersed in supercooled water droplets, giving it the potential to influence weather and climate from local to global scales. This ice nucleation activity (INA) is likely derived from a subset of the crystalline mineral phases in the ash. The INA of other mineral-based dusts can change when exposed to various gaseous and aqueous chemical species, many of which also interact with volcanic ash in the eruption plume and atmosphere. However, the effects of aqueous chemical aging on the INA of volcanic ash have not been explored. We show that the INA of two mineralogically distinct ash samples from Fuego and Astroni volcanoes is variably reduced following immersion in water or aqueous sulfuric acid for minutes to days. Aging in water decreases the INA of both ash samples by up to two orders of magnitude, possibly due to a reduction in surface crystallinity and cation availability accompanying leaching. Aging in sulfuric acid leads to minimal loss of INA for Fuego ash, which is proposed to reflect a quasi-equilibrium between leaching that removes ice-active sites and dissolution that reveals or creates new sites on the pyroxene phases present. Conversely, exposure to sulfuric acid reduces the INA of Astroni ash by one to two orders of magnitude, potentially through selective dissolution of ice-active sites associated with surface microtextures on some K-feldspar phases. Analysis of dissolved element concentrations in the aged ash leachates shows supersaturation of certain mineral species which could have precipitated and altered the INA of the ash. These results highlight the key role that leaching, dissolution, and precipitation likely play in the aqueous aging of volcanic ash with respect to its INA. Finally, we discuss the implications for understanding the nature and reactivity of ice-active sites on volcanic ash and its role in influencing cloud properties in the atmosphere

Study of Adenine and Guanine Oxidation Mechanism by Surface-Enhanced Raman Spectroelectrochemistry

Metal nanoparticles are systems largely employed in surface-enhanced Raman spectroscopy (SERS). In particular, gold nanoparticles are one of the best substrates used in this field. In this work, the optimal conditions for gold nanoparticles electrodeposition on single-walled carbon nanotubes electrodes have been established to obtain the best SERS response. Using this substrate and analyzing the changes of in situ Raman spectra obtained at different potentials, we have been able to explain simultaneously the oxidation mechanism of purine bases, differentiating the oxidation intermediates and their orientation during the different oxidation steps. Adenine orientation hardly changes during the whole oxidation; the molecule maintains a parallel configuration and only shows a slightly tilted orientation after the first oxidation step. On the other hand, guanine orientation changes completely during its oxidation. Initially, guanine is perpendicular respect to gold nanoparticles, changing its orientation after the first oxidation process when the molecule shows a slightly tilted orientation, and it finishes parallel respect to the electrode surface after the second oxidation step.Junta de Castilla y Leon (GR71, BU349-U13) and Ministerio de Economia y Competitividad (CTQ2010-17127) is gratefully acknowledged. D.I. thanks Ministerio de Economia y Competitividad for his predoctoral FPI fellowship. A.S. and M.K. acknowledge the support from MSMT ERC-CZ project: LL1301.This document is the Accepted Manuscript version of a Published Work that appeared in final form in Journal of Physical Chemistry C, copyright © American Chemical Society after peer review and technical editing by the publishe

TNF-α-induced up-regulation of pro-inflammatory cytokines is reduced by phosphatidylcholine in intestinal epithelial cells

<p>Abstract</p> <p>Background</p> <p>Phosphatidylcholine (PC) is a major lipid of the gastrointestinal mucus layer. We recently showed that mucus from patients suffering from ulcerative colitis has low levels of PC. Clinical studies reveal that the therapeutic addition of PC to the colonic mucus using slow release preparations is beneficial. The positive role of PC in this disease is still unclear; however, we have recently shown that PC has an intrinsic anti-inflammatory property. It could be demonstrated that the exogenous application of PC inhibits membrane-dependent actin assembly and TNF-α-induced nuclear NF-κB activation. We investigate here in more detail the hypothesis that the exogenous application of PC has anti-inflammatory properties.</p> <p>Methods</p> <p>PC species with different fatty acid side chains were applied to differentiated and non-differentiated Caco-2 cells treated with TNF-α to induce a pro-inflammatory response. We analysed TNF-α-induced NF-κB-activation via the transient expression of a NF-κB-luciferase reporter system. Pro-inflammatory gene transcription was detected with the help of a quantitative real time (RT)-PCR analysis. We assessed the binding of TNF-α to its receptor by FACS and analysed lipid rafts by isolating detergent resistant membranes (DRMs).</p> <p>Results</p> <p>The exogenous addition of all PC species tested significantly inhibited TNF-α-induced pro-inflammatory signalling. The expression levels of IL-8, ICAM-1, IP-10, MCP-1, TNF-α and MMP-1 were significantly reduced after PC pre-treatment for at least two hours. The effect was comparable to the inhibition of NF-kB by the NF-kB inhibitor SN 50 and was not due to a reduced binding of TNF-α to its receptor or a decreased surface expression of TNF-α receptors. PC was also effective when applied to the apical side of polarised Caco-2 cultures if cells were stimulated from the basolateral side. PC treatment changed the compartmentation of the TNF-α-receptors 1 and 2 to DRMs.</p> <p>Conclusion</p> <p>PC induces a prolonged inhibition of TNF-α-induced pro-inflammatory signalling. This inhibition may be caused by a shift of the TNF-α receptors at the surface to lipid rafts. Our results may offer a potential molecular explanation for the positive role of PC seen in clinical studies for the treatment of ulcerative colitis.</p