Nickel Poisoning of a Cracking Catalyst Unravelled by Single‐Particle X‐ray Fluorescence‐Diffraction‐Absorption Tomography

Ni contamination from crude oil in the fluid catalytic cracking (FCC) process is one of the primary sources of catalyst deactivation, thereby promoting dehydrogenation–hydrogenation and speeding up coke growth. Herein, single‐particle X‐ray fluorescence, diffraction and absorption (μXRF‐μXRD‐μXAS) tomography is used in combination with confocal fluorescence microscopy (CFM) after thiophene staining to spatially resolve Ni interaction with catalyst components and study zeolite degradation, including the processes of dealumination and Brønsted acid sites distribution changes. The comparison between a Ni‐lean particle, exposed to hydrotreated feedstock, and a Ni‐rich one, exposed to non‐hydrotreated feedstock, reveals a preferential interaction of Ni, found in co‐localization with Fe, with the γ‐Al₂O₃ matrix, leading to the formation of spinel‐type hotspots. Although both particles show similar surface zeolite degradation, the Ni‐rich particle displays higher dealumination and a clear Brønsted acidity drop.     

Nonparametric Empirical Bayes Estimation of the Matrix Parameter of the Wishart Distribution

We consider independent pairs (X₁, Σ₁), (X₂, Σ₂), …, (X_n, Σ_n), where eachΣ_iis distributed according to some unknown density functiong(Σ) and, givenΣ_i=Σ,X_ihas conditional density functionq(xΣ) of the Wishart type. In each pair the first component is observable but the second is not. After the (n+1)th observationX_n+1is obtained, the objective is to estimateΣ_n+1corresponding toX_n+1. This estimator is called the empirical Bayes (EB) estimator ofΣ. An EB estimator ofΣis constructed without any parametric assumptions ong(Σ). Its posterior mean square risk is examined, and the estimator is demonstrated to be pointwise asymptotically optimal.     

Understanding the Mechanism of Action of NAI-112, a Lanthipeptide with Potent Antinociceptive Activity

NAI-112, a glycosylated, labionine-containing lanthipeptide with weak antibacterial activity, has demonstrated analgesic activity in relevant mouse models of nociceptive and neuropathic pain. However, the mechanism(s) through which NAI-112 exerts its analgesic and antibacterial activities is not known. In this study, we analyzed changes in the spinal cord lipidome resulting from treatment with NAI-112 of naive and in-pain mice. Notably, NAI-112 led to an increase in phosphatidic acid levels in both no-pain and pain models and to a decrease in lysophosphatidic acid levels in the pain model only. We also showed that NAI-112 can form complexes with dipalmitoyl-phosphatidic acid and that Staphylococcus aureus can become resistant to NAI-112 through serial passages at sub-inhibitory concentrations of the compound. The resulting resistant mutants were phenotypically and genotypically related to vancomycin-insensitive S. aureus strains, suggesting that NAI-112 binds to the peptidoglycan intermediate lipid II. Altogether, our results suggest that NAI-112 binds to phosphate-containing lipids and blocks pain sensation by decreasing levels of lysophosphatidic acid in the TRPV1 pathway.     

Zn(II) Heteroleptic Halide Complexes with 2-Halopyridines: Features of Halogen Bonding in Solid State

Reactions between Zn(II) dihalides and 2-halogen-substituted pyridines 2-XPy result in a series of heteroleptic molecular complexes [(2-XPy)₂ZnY₂] (Y = Cl, X = Cl (1), Br (2), I (3); Y = Br, X = Cl (4), Br (5), I (6), Y = I, X = Cl (7), Br (8), and I (9)). Moreover, 1–7 are isostructural (triclinic), while 8 and 9 are monoclinic. In all cases, halogen bonding plays an important role in formation of crystal packing. Moreover, 1–9 demonstrate luminescence in asolid state; for the best emitting complexes, quantum yield (QY) exceeds 21%.     

Larvicidal Activity of Cinnamic Acid Derivatives: Investigating Alternative Products for Aedes aegypti L. Control

The mosquito Aedes aegypti transmits the virus that causes dengue, yellow fever, Zika and Chikungunya viruses, and in several regions of the planet represents a vector of great clinical importance. In terms of mortality and morbidity, infections caused by Ae. aegypti are among the most serious arthropod transmitted viral diseases. The present study investigated the larvicidal potential of seventeen cinnamic acid derivatives against fourth stage Ae. aegypti larvae. The larvicide assays were performed using larval mortality rates to determine lethal concentration (LC₅₀). Compounds containing the medium alkyl chains butyl cinnamate (7) and pentyl cinnamate (8) presented excellent larvicidal activity with LC₅₀ values of around 0.21–0.17 mM, respectively. While among the derivatives with aryl substituents, the best LC₅₀ result was 0.55 mM for benzyl cinnamate (13). The tested derivatives were natural compounds and in pharmacology and antiparasitic studies, many have been evaluated using biological models for environmental and toxicological safety. Molecular modeling analyses suggest that the larvicidal activity of these compounds might be due to a multi-target mechanism of action involving inhibition of a carbonic anhydrase (CA), a histone deacetylase (HDAC2), and two sodium-dependent cation-chloride co-transporters (CCC2 e CCC3).     

Harnessing polarisation transfer to indazole and imidazole through signal amplification by reversible exchange to improve their NMR detectability

The signal amplification by reversible exchange (SABRE) approach has been used to hyperpolarise the substrates indazole and imidazole in the presence of the co‐ligand acetonitrile through the action of the precataysts [IrCl(COD)(IMes)] and [IrCl(COD)(SIMes)]. ²H‐labelled forms of these catalysts were also examined. Our comparison of the two precatalysts [IrCl(COD)(IMes)] and [IrCl(COD)(SIMes)], coupled with ²H labelling of the N‐heterocyclic carbene and associated relaxation and polarisation field variation studies, demonstrates the critical and collective role these parameters play in controlling the efficiency of signal amplification by reversible exchange. Ultimately, with imidazole, a 700‐fold¹H signal gain per proton is produced at 400 MHz, whilst for indazole, a 90‐fold increase per proton is achieved. The co‐ligand acetonitrile proved to optimally exhibit a 190‐fold signal gain per proton in these measurements, with the associated studies revealing the importance the substrate plays in controlling this value. Copyright © 2017 The Authors. Magnetic Resonance in Chemistry published by John Wiley & Sons Ltd.