Manganese containing copper aluminate catalysts:Genesis of structures and active sites for hydrogenation of aldehydes

Copper aluminate spinel (CuO.CuAl2O4) is the favoured Cr-free substitute for the copper chromite catalyst (CuO.CuCr2O4) in the industrial hydrogenation of aldehydes. New insights in the catalytic mechanism were obtained by systematically studying the structure and activity of these catalysts including effects of manganese as a catalyst component. The hydrogenation of butyraldehyde to butanol was studied as a model reaction and the active structure was characterised using X-ray diffraction, temperature programmed reduction, N2O chemisorption, EXAFS and XANES, including in-situ investigations. The active catalyst is a reduced spinel lattice that is stabilised by protons, with copper metal nanoparticles grown upon its surface. Incorporation of Mn into the spinel lattice has a profound effect on the spinel structure. Mn stabilises the spinel towards reduction of CuII to Cu0 by occupation of tetrahedral sites with Mn cations, but also causes decreased catalytic activity. Structural data, combined with the effect on catalysis, indicate a predominantly interface-based reaction mechanism, involving both the spinel and copper nanoparticle surface in protonation and reduction of the aldehyde. The electron reservoir of the metallic copper particles is regenerated by the dissociative adsorption and oxidation of H2 on the metal surface. The generated protons are stored in the spinel phase, acting as proton reservoir. Cu(I) species located within the spinel and identified by XANES are probably not involved in the catalytic cycle

Rare tumors of the internal auditory canal

Dazert S, Aletsee C, Brors D, et al. Rare tumors of the internal auditory canal. European Archives of Oto-Rhino-Laryngology. 2005;262(7):550-554

Ras/MEK But Not p38 Signaling Mediates NT-3-Induced Neurite Extension from Spiral Ganglion Neurons

Neurotrophin (NT)-3 is expressed in the neuronal target tissue of the developing rat cochlea and has been shown to promote the survival and neurite outgrowth of spiral ganglion (SG) neurons, suggesting a role for this protein during the innervation of the organ of Corti. In other neurons, NT-3 can mediate neuritogenesis and survival via a number of intracellular signal pathways. To date, the intracellular transduction pathways involved in the mediation of NT-3 effects have not been investigated in SG neurons. To determine whether the activities of NT-3 on SG neurons are dependent on the activation of mitogen-activated protein kinase kinases (MEK)/extracellular-signal-regulated kinases (ERK), Ras, and/or p38, SG explants from postnatal-day 4 rats were cultured with NT-3 and increasing concentrations of the MEK inhibitor U0126, the Ras farnesyl-transferase inhibitor (FTI)-277, and the p38 inhibitor SB203580. After fixation and immunocytochemical labeling, neurite growth was evaluated. A dose-dependent decrease of the effects of NT-3 on length and number of processes was observed in the U0126- and FTI-277-treated SG neurons. In contrast, SB203580 had no significant effect on NT-3-mediated stimulation of neurite growth, in terms of either number or length. The results suggest that NT-3 effects on SG neurons are mediated primarily by the Ras/MEK/ERK signaling pathway

Role of p38 Mitogen-Activated Protein Kinase in Middle Ear Mucosa Hyperplasia during Bacterial Otitis Media

Hyperplasia of the middle ear mucosa contributes to the sequelae of acute otitis media. Understanding the signal transduction pathways that mediate hyperplasia could lead to the development of new therapeutic interventions for this disease and its sequelae. Endotoxin derived from bacteria involved in middle ear infection can contribute to the hyperplastic response. The p38 mitogen-activated protein kinase (MAPK) is known to be activated by endotoxin as well as cytokines and other inflammatory mediators that have been documented in otitis media. We assessed the activation of p38 in the middle ear mucosa of an in vivo rat bacterial otitis media model. Strong activity of p38 was observed 1 to 6 h after bacterial inoculation. Activity continued at a lower level for at least 7 days. The effects of p38 activation were assessed using an in vitro model of rat middle ear mucosal hyperplasia in which mucosal growth is stimulated by nontypeable Haemophilus influenzae during acute otitis media. Hyperplastic mucosal explants treated with the p38α and p38β inhibitor SB203580 demonstrated significant inhibition of otitis media-stimulated mucosal growth. The results of this study suggest that intracellular signaling via p38 MAPK influences the hyperplastic response of the middle ear mucosa during bacterial otitis media