Catalytic hydrodechlorination as polishing step in drinking water treatment for the removal of chlorinated micropollutants

This Accepted Manuscript will be available for reuse under a CC BY-NC-ND license after 24 months of embargo periodThe presence of micropollutants in fresh waters represents an important challenge for drinking water treatment plants (DWTPs). In particular, the chlorinated ones are especially harmful given their high toxicity and strong bioaccumulation potential. The aim of this work is to evaluate the feasibility of catalytic hydrodechlorination (HDC) for the removal of a representative group of chlorinated micropollutants commonly found in the source waters of DWTPs: the antibiotic chloramphenicol (CAP), the anti-inflammatory diclofenac (DCF), the antibacterial agent triclosan (TCL) and the antidepressant sertraline (SRT). The complete degradation of the isolated micropollutants (3 mg L−1) was achieved in 1 h reaction time using a Pd/Al2O3 catalyst load of 0.25 g L−1 and a H2 flow rate of 50 N mL min−1. The experimental data were properly described by a pseudo-first order kinetic equation, obtaining degradation rate constants in the range of 0.32–1.56 L gcat−1 min−1 and activation energy values within 42–52 kJ mol−1. In all cases, the final reaction products were chlorine-free compounds and thus, HDC effluents were non-toxic (<0.1 TU). Remarkably, the catalyst showed a suitable stability upon five consecutive applications. The versatility of the process was demonstrated in the treatment of the micropollutants mixture in different aqueous matrices (mineral, surface and tap waters). Strikingly, the removal rate was not affected by the presence of co-existing substances, being the micropollutants completely removed in 15 min with 1 g L−1 catalyst concentration. Finally, the potential of HDC for the removal of trihalomethanes, by-products formed along the oxidation step by chlorination in DWTPs, was also demonstratedThis research has been supported by the Spanish MINECO thorough the project CTM2016-76454-R and by the CM through the project P2018/EMT-4341. J. Nieto-Sandoval thanks the Spanish MINECO for the FPI predoctoral grant (BES-2017- 081346). M. Munoz thanks the Spanish MINECO for the Ramón y Cajal postdoctoral contract (RYC-2016-20648

Langerin-Heparin Interaction: Two Binding Sites for Small and Large Ligands as revealed by a combination of NMR Spectroscopy and Cross-Linking Mapping Experiments

Langerin is a C-type lectin present on Langerhans cells that mediates capture of pathogens in a carbohydrate-dependent manner, leading to subsequent internalization and elimination in the cellular organelles called Birbeck granules. This mechanism mediated by langerin was shown to constitute a natural barrier for HIV-1 particle transmission. Besides interacting specifically with high mannose and fucosylated neutral carbohydrate structures, langerin has the ability to bind sulfated carbohydrate ligands as 6-sulfated galactosides in the Ca2+ dependent binding site. Very recently langerin was demonstrated to interact with sulfated glycosaminoglycans (GAGs), in a Ca2+ independent way, resulting in the proposal of a new binding site for GAGs. Based on those results, we have conducted a structural study of the interactions of small heparin (HEP) like oligosaccharides with langerin in solution. Heparin-bead cross-linking experiments, an approach specifically designed to identify HEP/HS binding sites in proteins were first carried out and experimentally validated the previously proposed model for the interaction of Lg ECD with 6 kDa HEP. High-resolution NMR studies of a set of 8 synthetic HEP-like trisaccharides harboring different sulfation patterns demonstrated that all of them bound to langerin in a Ca2+ dependent way. The binding epitopes were determined by STD NMR and the bound conformations by transferred NOESY experiments. These experimental data were combined with docking and molecular dynamics and resulted in the proposal of a binding mode characterized by the coordination of calcium by the two equatorial hydroxyl groups OH3 and OH4 at the non-reducing end. The binding also includes the carboxylate group at the adjacent iduronate residue. Such epitope is shared by all the 8 ligands, explaining the absence of any impact on binding from their differences in substitution pattern. Finally, in contrast to the small trisaccharides, we demonstrated that a longer HEP-like hexasaccharide, bearing an additional O-sulfate group at the non-reducing end, which precludes binding to the Ca2+ site, interacts with langerin in the previously identified Ca2+ independent binding site

Dual-Specificity Phosphatase 1 (DUSP1) Has a Central Role in Redox Homeostasis and Inflammation in the Mouse Cochlea.

Stress-activated protein kinases (SAPK) are associated with sensorineural hearing loss (SNHL) of multiple etiologies. Their activity is tightly regulated by dual-specificity phosphatase 1 (DUSP1), whose loss of function leads to sustained SAPK activation. Dusp1 gene knockout in mice accelerates SNHL progression and triggers inflammation, redox imbalance and hair cell (HC) death. To better understand the link between inflammation and redox imbalance, we analyzed the cochlear transcriptome in Dusp1-/- mice. RNA sequencing analysis (GSE176114) indicated that Dusp1-/- cochleae can be defined by a distinct profile of key cellular expression programs, including genes of the inflammatory response and glutathione (GSH) metabolism. To dissociate the two components, we treated Dusp1-/- mice with N-acetylcysteine, and hearing was followed-up longitudinally by auditory brainstem response recordings. A combination of immunofluorescence, Western blotting, enzymatic activity, GSH levels measurements and RT-qPCR techniques were used. N-acetylcysteine treatment delayed the onset of SNHL and mitigated cochlear damage, with fewer TUNEL+ HC and lower numbers of spiral ganglion neurons with p-H2AX foci. N-acetylcysteine not only improved the redox balance in Dusp1-/- mice but also inhibited cytokine production and reduced macrophage recruitment. Our data point to a critical role for DUSP1 in controlling the cross-talk between oxidative stress and inflammation

A Hybrid Parameterization Technique for Speaker Identification

Classical parameterization techniques for Speaker Identification use the codification of the power spectral density of raw speech, not discriminating between articulatory features produced by vocal tract dynamics (acoustic-phonetics) from glottal source biometry. Through the present paper a study is conducted to separate voicing fragments of speech into vocal and glottal components, dominated respectively by the vocal tract transfer function estimated adaptively to track the acoustic-phonetic sequence of the message, and by the glottal characteristics of the speaker and the phonation gesture. The separation methodology is based in Joint Process Estimation under the un-correlation hypothesis between vocal and glottal spectral distributions. Its application on voiced speech is presented in the time and frequency domains. The parameterization methodology is also described. Speaker Identification experiments conducted on 245 speakers are shown comparing different parameterization strategies. The results confirm the better performance of decoupled parameterization compared against approaches based on plain speech parameterization

Towards Modelling QFT in Real Metamaterials: Singular Potentials and Self-Adjoint Extensions

[EN] Solutions of the one-dimensional Schrödinger equation are found when point interactions of the type aδ(x − q) + bδ'(x − q) are placed either in a couple of points or in a regular lattice. The results obtained in the present study are a first step toward a rigorous mathematical model of real metamaterials is Solid State Physics

G6PD overexpression protects from oxidative stress and age-related hearing loss

Aging of the auditory system is associated with the incremental production of reactive oxygen species (ROS) and the accumulation of oxidative damage in macromolecules, which contributes to cellular malfunction, compromises cell viability, and, ultimately, leads to functional decline. Cellular detoxification relies in part on the production of NADPH, which is an important cofactor for major cellular antioxidant systems. NADPH is produced principally by the housekeeping enzyme glucose-6-phosphate dehydrogenase (G6PD), which catalyzes the rate-limiting step in the pentose phosphate pathway. We show here that G6PD transgenic mice (G6PD-Tg), which show enhanced constitutive G6PD activity and NADPH production along life, have lower auditory thresholds than wild-type mice during aging, together with preserved inner hair cell (IHC) and outer hair cell (OHC), OHC innervation, and a conserved number of synapses per IHC. Gene expression of antioxidant enzymes was higher in 3-month-old G6PD-Tg mice than in wild-type counterparts, whereas the levels of pro-apoptotic proteins were lower. Consequently, nitration of proteins, mitochondrial damage, and TUNEL apoptotic cells were all lower in 9-month-old G6PD-Tg than in wild-type counterparts. Unexpectedly, G6PD overexpression triggered low-grade inflammation that was effectively resolved in young mice, as shown by the absence of cochlear cellular damage and macrophage infiltration. Our results lead us to propose that NADPH overproduction from an early stage is an efficient mechanism to maintain the balance between the production of ROS and cellular detoxification power along aging and thus prevents hearing loss progression.Secretaría de Estado de Investigación, Desarrollo e Innovación, Grant/Award Number: MINECO/FEDER SAF2017-86107-R; Comunidad de Madrid, Grant/Award Number: FEDER/CM-B2017/BMD-368

Degradation of widespread cyanotoxins with high impact in drinking water (microcystins, cylindrospermopsin, anatoxin-a and saxitoxin) by CWPO

This Accepted Manuscript will be available for reuse under a CC BY-NC-ND license after 24 months of embargo periodThe occurrence of harmful cyanobacterial blooms has unabated increased over the last few decades, posing a significant risk for public health. In this work, we investigate the feasibility of catalytic wet peroxide oxidation (CWPO) promoted by modified natural magnetite (Fe3O4-R400/H2O2), as an inexpensive, simple-operation and environmentally-friendly process for the removal of the cyanotoxins that show the major impact on drinking water: microcystins (MC-LR and MC-RR), cylindrospermopsin (CYN), anatoxin-a (ATX) and saxitoxin (STX). The performance of the system was evaluated under ambient conditions and circumneutral pH (pH0 = 5) using relevant cyanotoxin concentrations (100–500 μg L−1). The nature of the cyanotoxins determined their reactivity towards CWPO, which decreased in the following order: MC-RR > CYN > MC-LR ≫ ATX > STX. In this sense, microcystins and CYN were completely removed in short reaction times (1–1.5 h) with a low catalyst concentration (0.2 g L−1) and the stoichiometric amount of H2O2 (2–2.6 mg L−1), while only 60–80% conversion was achieved with ATX and STX in 5 h. In these cases, an intensification of the operating conditions (1 g L−1 catalyst and up to 30 mg H2O2 L−1) was required to remove both toxins in 1 h. The impact of the main components of freshwaters i.e. natural organic matter (NOM) and several inorganic ions (HCO3−, HPO42-, SO42-) on the performance of the process was also investigated. Although the former led to a partial inhibition of the reaction due to HO· scavenging and catalyst coating, the latter did not show any remarkably effect, and the versatility of the process was finally confirmed in a real surface water. To further demonstrate the effectiveness of the catalytic system, the toxicity of both the initial cyanotoxins and the resulting CWPO effluents was measured with the brine shrimp Artemia salina. Remarkably, all CWPO effluents were non-toxic at the end of the treatment.This research has been supported by the Spanish MINECO through the project CTM-2016-76454-R and by the CM through the project P2018/EMT-4341. M. Munoz thanks the Spanish MINECO for the Ramón y Cajal postdoctoral contract (RYC-2016-20648). J. Nieto-Sandoval thanks the Spanish MINECO for the FPI predoctoral grant (BES-2017-081346

Insights on the removal of the azole pesticides included in the EU Watch List by Catalytic Wet Peroxide Oxidation

The aim of this work is to evaluate the feasibility of the Catalytic Wet Peroxide Oxidation (CWPO) process using the inexpensive and environmentally friendly Fe3O4-R400 catalyst for the removal from water of a representative group of azole pesticides recently listed in the European Union (EU) Watch Lists (penconazole (PEN), prochloraz (PCZ), tebuconazole (TEB), tetraconazole (TET), metconazole (MET)). The complete removal of these pollutants (1000 μg L−1) was achieved in <1 h reaction time under ambient conditions using a catalyst concentration of 0.5 g L−1 and the stoichiometric dose of H2O2 (3 – 5 mg L−1) at a slightly acidic pH (pH0 = 5.0). To further demonstrate the effectiveness of the process, the ecotoxicity abatement was also considered. The initial toxicity of the pesticides and the CWPO effluents were evaluated with the brine shrimp Artemia salina and the bacterium Vibrio fischeri. Remarkably, the effluents were non-toxic for V. fischeri and a decrease of more than 80% in mortality was achieved for A. salina. Furthermore, the versatility of the system was proved in real water matrices (surface water and WWTP effluent), although a slight decrease on the oxidation rate was found due to the occurrence of organic matter and inorganic salts. The reactivity of the azole pesticides was finally compared with the achieved for other groups of pollutants included in the EU Watch Lists (pharmaceuticals, hormones, and neonicotinoid pesticides). Clearly, azole compounds showed the least reactivity to oxidation, suggesting that they can be used as general indicators of the overall efficiency of the proposed catalytic system for the removal of EU Watch Lists micropollutantsThis research has been supported by the Spanish AEI through the project PID2019-105079RB-100 and by the CM, Spain through the project P2018/EMT-4341. M. Munoz, N. Lopez-Arago and J. Nieto-Sandoval thanks the Spanish AEI for the Ramón y Cajal postdoctoral contract (RYC-2016-20648), the FPI predoctoral, Spain grant (PRE2020-09452) and the FPI postdoctoral, Spain grant (BES-2017-081346), respectivel