Bielefeld University

About: Bielefeld University is a education organization based out in Bielefeld, Nordrhein-Westfalen, Germany. It is known for research contribution in the topics: Population & Quantum chromodynamics. The organization has 10123 authors who have published 26576 publications receiving 728250 citations. The organization is also known as: University of Bielefeld & UNIVERSITAET BIELEFELD.

Peroxiredoxin Q of Arabidopsis thaliana is attached to the thylakoids and functions in context of photosynthesis.

Abstract: Peroxiredoxin Q (Prx Q) is one out of 10 peroxiredoxins encoded in the genome of Arabidopsis thaliana, and one out of four that are targeted to plastids. Peroxiredoxin Q functions as a monomeric protein and represents about 0.3% of chloroplast proteins. It attaches to the thylakoid membrane and is detected in preparations enriched in photosystem II complexes. Peroxiredoxin Q decomposes peroxides using thioredoxin as an electron donor with a substrate preference of H(2)O(2) > cumene hydroperoxide >> butyl hydroperoxide >> linoleoyl hydroperoxide and insignificant affinity towards complex phospholipid hydroperoxide. Plants with decreased levels of Prx Q did not have an apparently different phenotype from wildtype at the plant level. However, similar to antisense 2-cysteine (2-Cys) Prx plants [Baier, M. et al. (2000)Plant Physiol., 124, 823-832], Prx Q-deficient plants had a decreased sensitivity to oxidants in a leaf slice test as indicated by chlorophyll a fluorescence measurements. Increased fluorescence ratios of photosystem II to I at 77 K and modified transcript levels of plastid- and nuclear-encoded proteins show that regulatory mechanisms are at work to compensate for the lack of Prx Q. Apparently Prx Q attaches to photosystem II and has a specific function distinct from 2-Cys peroxiredoxin in protecting photosynthesis. Its absence causes metabolic changes that are sensed and trigger appropriate compensatory responses.

Large-Scale Neuromorphic Spiking Array Processors: A Quest to Mimic the Brain

Abstract: Neuromorphic engineering (NE) encompasses a diverse range of approaches to information processing that are inspired by neurobiological systems, and this feature distinguishes neuromorphic systems from conventional computing systems. The brain has evolved over billions of years to solve difficult engineering problems by using efficient, parallel, low-power computation. The goal of NE is to design systems capable of brain-like computation. Numerous large-scale neuromorphic projects have emerged recently. This interdisciplinary field was listed among the top 10 technology breakthroughs of 2014 by the MIT Technology Review and among the top 10 emerging technologies of 2015 by the World Economic Forum. NE has two-way goals: one, a scientific goal to understand the computational properties of biological neural systems by using models implemented in integrated circuits (ICs); second, an engineering goal to exploit the known properties of biological systems to design and implement efficient devices for engineering applications. Building hardware neural emulators can be extremely useful for simulating large-scale neural models to explain how intelligent behavior arises in the brain. The principal advantages of neuromorphic emulators are that they are highly energy efficient, parallel and distributed, and require a small silicon area. Thus, compared to conventional CPUs, these neuromorphic emulators are beneficial in many engineering applications such as for the porting of deep learning algorithms for various recognitions tasks. In this review article, we describe some of the most significant neuromorphic spiking emulators, compare the different architectures and approaches used by them, illustrate their advantages and drawbacks, and highlight the capabilities that each can deliver to neural modelers. This article focuses on the discussion of large-scale emulators and is a continuation of a previous review of various neural and synapse circuits (Indiveri et al., 2011). We also explore applications where these emulators have been used and discuss some of their promising future applications.

Adaptation of the photosynthetic electron transport chain in cyanobacteria to iron deficiency: The function of IdiA and IsiA.

Abstract: In this review we give an overview on the adaptational responses of photosystem (PS) II and PSI in cyanobacteria to iron starvation, mainly summarizing our results with the mesophilic Synechococcus elongatus PCC 7942. We also discuss this process with respect to the strong interrelationship between iron limitation and oxidative stress that exists in cyanobacteria as oxygenic photosynthetic organisms. The adaptation of the multiprotein complexes PSII and PSI to iron starvation is a sequential process, which is characterized by the enhanced expression of two major iron-regulated proteins, IdiA (iron deficiency induced protein A) and IsiA (iron stress induced protein A). Our results suggest that IdiA protects the acceptor side of PSII against oxidative stress under conditions of mild iron limitation in a currently unclear way, whereas prolonged iron deficiency leads to the synthesis of a chlorophyll a antenna around PSI-trimers consisting of IsiA molecules. The physiological consequences of these alterations under prolonged iron starvation, as shown by acridine yellow fluorescence measurements, are a reduction of linear electron transport activity through PSII and an increase of cyclic electron flow around PSI as well as an increase in respiratory activity. IdiA and IsiA expression are mediated by two distinct helix-turn-helix transcriptional regulators of the Crp/Fnr family. IdiB positively regulates expression of idiA under iron starvation, and Fur represses transcription of isiA under iron-sufficient conditions. Although both transcriptional regulators seem to operate independently of each other, our results indicate that a cross-talk between the signal transduction pathways exists. Moreover, IdiA as well as IsiA expression are affected by hydrogen peroxide. We suggest that due to the interdependence of iron limitation and the formation of reactive oxygen species, peroxide stress might be the superior trigger that leads to expression of these proteins under iron starvation. The modifications of PSII and PSI under iron starvation influence the redox state of redox-sensitive components of the electron transport chain, and thus the activity of metabolic pathways being regulated in dependence of the redox state of these components.