SUBSTRATE AND DEFECT INFLUENCES ON THE POSITION-RESPONSE LINEARITY OF POSITION-SENSITIVE DETECTORS

The performance of position-sensitive detectors (PSD's) with an epilayer was investigated. Defects which are responsible for a great position-response nonlinearity in the p-type resistive layer were fond. The influence of the substrate potential, the photocurrent generation in the junction between the epilayer and the substrate, and the dependency of the resistive layer thickness on the local potential were analyzed. By connecting the substrate to the same potential as the p-type layer, distortions in the position-response grid are reduced to a certain degree. A simple method was used to discover this kind of defect in an early stage

Tryptophan-metabolizing gut microbes regulate adult neurogenesis via the aryl hydrocarbon receptor

While modulatory effects of gut microbes on neurological phenotypes have been reported, the mechanisms remain largely unknown. Here, we demonstrate that indole, a tryptophan metabolite produced by tryptophanase-expressing gut microbes, elicits neurogenic effects in the adult mouse hippocampus. Neurogenesis is reduced in germ-free (GF) mice and in GF mice monocolonized with a single-gene tnaA knockout (KO) mutant Escherichia coli unable to produce indole. External administration of systemic indole increases adult neurogenesis in the dentate gyrus in these mouse models and in specific pathogen-free (SPF) control mice. Indole-treated mice display elevated synaptic markers postsynaptic density protein 95 and synaptophysin, suggesting synaptic maturation effects in vivo. By contrast, neurogenesis is not induced by indole in aryl hydrocarbon receptor KO (AhR−/−) mice or in ex vivo neurospheres derived from them. Neural progenitor cells exposed to indole exit the cell cycle, terminally differentiate, and mature into neurons that display longer and more branched neurites. These effects are not observed with kynurenine, another AhR ligand. The indole-AhR–mediated signaling pathway elevated the expression of β-catenin, Neurog2, and VEGF-α genes, thus identifying a molecular pathway connecting gut microbiota composition and their metabolic function to neurogenesis in the adult hippocampus. Our data have implications for the understanding of mechanisms of brain aging and for potential next-generation therapeutic opportunities