Nano-Photocatalytic Materials: Possibilities and Challenges

Photocatalysis is one of the most promising processes within catalysis, due to its increasing potential and the possibility of its being combined with renewable solar energy [...

Nano-Photocatalytic Materials: Possibilities and Challenges.

Photocatalysis is one of the most promising processes within catalysis, due to its increasing potential and the possibility of its being combined with renewable solar energy [...]

Degradation of diphenhydramine pharmaceutical in aqueous solutions by using two highly active TiO2 photocatalysts: operating parameters and photocatalytic mechanism

In the present work the efficiency of a new TiO2 catalyst (ECT), synthesized by means of an optimized sol–gel method, is studied for degradation of an important pharmaceutical water pollutant, diphenhydramine (DP). Its activity is compared to P25, the benchmark catalyst, produced by Evonik Degussa Corporation, under different catalyst loadings (up to 2.00 g L−1) and initial solution pH (3.0–11.0). The results show that DP is very stable under non-catalytic conditions but complete degradation and considerable mineralization (ca. 60–70%) under near UV to visible irradiation (∼50 mW cm−2) can be achieved in 60 min by selecting the appropriate TiO2 loading. ECT is significantly more active than the benchmark catalyst for loadings higher than 1.00 g L−1 while the pseudo-first order rate constant increased with the initial solution pH from 3.0 to 11.0. The highest rate constant was obtained with ECT at pH 11 (173 × 10−3 min−1 against 116 × 10−3 min−1 for P25). Scavenger agents were used as a diagnostic tool for the analysis of the photocatalytic mechanism and it was possible to prove that holes were crucial active species participating in the photocatalytic mechanism as well as that ECT has a higher availability than P25 to generate reactive radicals, such as hydroxyl (HO•) and hydroperoxyl (HOO•) radicals.Financial support for this work was in provided by the European Commission (Clean Water – Grant Agreement no. 227017) and partially by project PEst-C/EQB/LA0020/2011, financed by FEDER through COMPETE – Programa Operacional Factores de Competitividade and by FCT – Fundação para a Ciência e a Tecnologia. Clean Water is a Collaborative Project co-funded by the Research DG of the European Commission within the joint RTD activities of the Environment and NMP Thematic Priorities. AMTS acknowledges financial support from POCI/N010/2006

NO photooxidation with TiO2 photocatalysts modified with gold and platinum

In this study, a comparative analysis is made of TiO modified with Pt or Au in NO photoxidation under different radiation and humidity conditions. The metals were deposited on the TiO surface using two methods, photodeposition and chemical reduction. All catalysts were supported on borosilicate 3.3 plates using a dip-coating technique. These modified photocatalysts were characterized by X-ray diffraction analysis (XRD), UV–vis diffuse reflectance spectra (DRS), Brunauer-Emmett-Teller measurements (BET), transmission electron microscopy (TEM) and X-ray photoelectron spectrum analysis (XPS). It was found from the XPS results that Pt and oxidized Pt species coexist on the samples obtained by photodeposition and chemical reduction. In the case of Au, though other oxidation states were also detected the dominant oxidation state for both catalysts is Au. TEM results showed most Au-C particles are below 5 nm, whereas for Au-P the nanoparticles are slightly bigger. With UV irradiation, the Pt modified catalysts do not show any significant improvement in NO photocatalytic oxidation in comparison with the unmodified P25. For Au, both modified photocatalysts (Au-P and Au-C) exceed the photocatalytic efficiency of the unmodified P25, with Au-C giving slightly better results. The incorporation of metals on the TiO increases its activity in the visible region.We are grateful for the financial support of the Spanish Ministry of Economy and Competitiveness through the project IPT-2012-0927-420000 (HORMIFOT) and thank the Spanish Ministry of Science and Innovation for the UNLP10-3E-726 infrastructure co-financed with ERDF funds. Part of this work was supported by research funding from Project Ref. CTQ2015-64664-C2-2-P (MINECO/FEDER, EU). XPS and other research services of SITIUS University of Seville are also acknowledged. M.J. Hernández Rodríguez and E. Pulido Melián would also like to thank the University of Las Palmas de Gran Canaria for, respectively, their research training grant and postdoctoral contract

Variants of CEP68 Gene Are Associated with Acute Urticaria/Angioedema Induced by Multiple Non-Steroidal Anti-Inflammatory Drugs

<div><p>Non-steroidal anti-inflammatory drugs (NSAIDs) are the most consumed drugs worldwide because of their efficacy and utility in the treatment of pain and inflammatory diseases. However, they are also responsible for an important number of adverse effects including hypersensitivity reactions. The most important group of these reactions is triggered by non-immunological, pharmacological mechanisms catalogued under the denomination of cross-intolerance (CRI), with acute urticaria/angioedema induced by multiple NSAIDs (MNSAID-UA) the most frequently associated clinical entity. A recent genome-wide association study identified the gene encoding the centrosomal protein of 68 KDa (<i>CEP68</i>) as the major locus associated with aspirin intolerance susceptibility in asthmatics. In this study, we aimed to assess the role of this locus in susceptibility to CRI to NSAIDs by examining 53 common gene variants in a total of 635 patients that were classified as MNSAID-UA (n = 399), airway exacerbations (n = 110) or blended pattern (n = 126), and 425 controls. We found in the MNSAID-UA group a number of variants (17) associated (lowest <i>p</i>-value = 1.13×10⁻⁶), including the non-synonymous Gly74Ser variant (rs7572857) previously associated with aspirin intolerance susceptibility in asthmatics. Although not being significant in the context of multiple testing, eight of these variants were also associated with exacerbated respiratory disease or blended reactions. Our results suggest that <i>CEP68</i> gene variants may play an important role in MNSAID-UA susceptibility and, despite the different regulatory mechanisms involved depending on the specific affected organ, in the development of hypersensitivity reactions to NSAIDs.</p></div

Demographic and clinical data of patients and controls.

<p><b>Abbreviations</b>: <b>AERD</b>, aspirin-exacerbated respiratory disease; <b>CI</b>, confidence intervals; <b>MNSAID-UA</b>, multiple NSAIDs-induced urticaria/angioedema; <b>NSAIDs</b>, non-steroidal anti-inflammatory drugs; <b>SD</b>, standard deviation.</p

Association results and the predicted function for the 17 <i>CEP68</i> SNPs surviving the correction for multiple comparisons.

<p><b>Abbreviations</b>: <b>miRNABS</b>, micro RNA binding site; <b>nsSNP</b>, non-synonymous single nucleotipe polymorphism; <b>TFBS</b>, transcription factor binding site.</p><p>* According to NCBI build 37.</p