5 research outputs found
Effects of the Incorporation of Distinct Cations in Titanate Nanotubes on the Catalytic Activity in NOx Conversion
Effects of the incorporation of Cr, Ni, Co, Ag, Al, Ni and Pt cations in titanate nanotubes (NTs) were examined on the NOx conversion. The structural and morphological characterizations evidenced that the ion-exchange reaction of Cr, Co, Ni and Al ions with the NTs produced catalysts with metals included in the interlayer regions of the trititanate NTs whereas an assembly of Ag and Pt nanoparticles were either on the nanotubes surface or inner diameters through an impregnation process. Understanding the role of the different metal cations intercalated or supported on the nanotubes, the optimal selective catalytic reduction of NOx by CO reaction (SCR) conditions was investigated by carrying out variations in the reaction temperature, SO2 and H2O poisoning and long-term stability runs. Pt nanoparticles on the NTs exhibited superior activity compared to the Cr, Co and Al intercalated in the nanotubes and even to the Ag and Ni counterparts. Resistance against SO2 poisoning was low on NiNT due to the trititanate phase transformation into TiO2 and also to sulfur deposits on Ni sites. However, the interaction between Pt2+ from PtOx and Ti4+ in the NTs favored the adsorption of both NOx and CO enhancing the catalytic performance
Correction: Carmo et al. Effects of the Incorporation of Distinct Cations in Titanate Nanotubes on the Catalytic Activity in NOx Conversion. Materials 2021, 14, 2181
In the original publication, there was a mistake in Figure 1 as published [...
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Alzheimer and Parkinson diseases, frontotemporal lobar degeneration and amyotrophic lateral sclerosis overlapping neuropathology start in the first two decades of life in pollution exposed urbanites and brain ultrafine particulate matter and industrial nanoparticles, including Fe, Ti, Al, V, Ni, Hg, Co, Cu, Zn, Ag, Pt, Ce, La, Pr and W are key players. Metropolitan Mexico City health crisis is in progress
The neuropathological hallmarks of Alzheimer’s disease (AD), Parkinson’s disease (PD), frontotemporal lobar degeneration (FTLD), and amyotrophic lateral sclerosis (ALS) are present in urban children exposed to fine particulate matter (PM2.5), combustion and friction ultrafine PM (UFPM), and industrial nanoparticles (NPs). Metropolitan Mexico City (MMC) forensic autopsies strongly suggest that anthropogenic UFPM and industrial NPs reach the brain through the nasal/olfactory, lung, gastrointestinal tract, skin, and placental barriers. Diesel-heavy unregulated vehicles are a key UFPM source for 21.8 million MMC residents. We found that hyperphosphorylated tau, beta amyloid1-42, α-synuclein, and TAR DNA-binding protein-43 were associated with NPs in 186 forensic autopsies (mean age 27.45 ± 11.89 years). The neurovascular unit is an early NPs anatomical target, and the first two decades of life are critical: 100% of 57 children aged 14.8 ± 5.2 years had AD pathology; 25 (43.9%) AD+TDP-43; 11 (19.3%) AD + PD + TDP-43; and 2 (3.56%) AD +PD. Fe, Ti, Hg, Ni, Co, Cu, Zn, Cd, Al, Mg, Ag, Ce, La, Pr, W, Ca, Cl, K, Si, S, Na, and C NPs are seen in frontal and temporal lobes, olfactory bulb, caudate, substantia nigra, locus coeruleus, medulla, cerebellum, and/or motor cortical and spinal regions. Endothelial, neuronal, and glial damages are extensive, with NPs in mitochondria, rough endoplasmic reticulum, the Golgi apparatus, and lysosomes. Autophagy, cell and nuclear membrane damage, disruption of nuclear pores and heterochromatin, and cell death are present. Metals associated with abrasion and deterioration of automobile catalysts and electronic waste and rare earth elements, i.e., lanthanum, cerium, and praseodymium, are entering young brains. Exposure to environmental UFPM and industrial NPs in the first two decades of life are prime candidates for initiating the early stages of fatal neurodegenerative diseases. MMC children and young adults—surrogates for children in polluted areas around the world—exhibit early AD, PD, FTLD, and ALS neuropathological hallmarks forecasting serious health, social, economic, academic, and judicial societal detrimental impact. Neurodegeneration prevention should be a public health priority as the problem of human exposure to particle pollution is solvable. We are knowledgeable of the main emission sources and the technological options to control them. What are we waiting for? Copyright © 2024 CalderĂłn-Garcidueñas, Stommel, Torres-JardĂłn, Hernández-Luna, Aiello-Mora, González-Maciel, Reynoso-Robles, PĂ©rez-GuillĂ©, Silva-Pereyra, Tehuacanero-Cuapa, RodrĂguez-GĂłmez, Lachmann, Galaz-Montoya, Doty, Roy and Mukherjee.Open access journalThis item from the UA Faculty Publications collection is made available by the University of Arizona with support from the University of Arizona Libraries. If you have questions, please contact us at [email protected]