RNA interference in Lepidoptera: an overview of successful and unsuccessful studies and implications for experimental design

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Fault Detection based on MCSA for a 400Hz Asynchronous Motor for Airborne Applications

Future health monitoring concepts in different fields of engineering require reliable fault detection to avoid unscheduled machine downtime. Diagnosis of electrical induction machines for industrial applications is widely discussed in literature. In aviation industry, this topic is still only rarely discussed.A common approach to health monitoring for electrical induction machines is to use Motor Current Signature Analysis (MCSA) based on a Fast Fourier Transform (FFT). Research results on this topic are available for comparatively large motors, where the power supply is typically based on 50Hz alternating current, which is the general power supply frequency for industrial applications.In this paper, transferability to airborne applications, where the power supply is 400Hz, is assessed. Three phase asynchronous motors are used to analyse detectability of different motor faults. The possibility to transfer fault detection results from 50Hz to 400Hz induction machines is the main question answered in this research work. 400Hz power supply frequency requires adjusted motor design, causing increased motor speed compared to 50Hz supply frequency. The motor used for experiments in this work is a 800W motor with 200V phase to phase power supply, powering an avionic fan. The fault cases to be examined are a bearing fault, a rotor unbalance, a stator winding fault, a broken rotor bar and a static air gap eccentricity. These are the most common faults in electrical induction machines which can cause machine downtime. The focus of the research work is the feasibility of the application of MCSA for small scale, high speed motor design, using the Fourier spectra of the current signal.Detectability is given for all but the bearing fault, although rotor unbalance can only be detected in case of severe damage level. Results obtained in the experiments are interpreted with respect to the motor design. Physical interpretation are given in case the results differ from those found in literature for 50Hz electrical machines

Evolutionarily conserved partial gene duplication in the Triticeae tribe of grasses confers pathogen resistance

Abstract Background The large and highly repetitive genomes of the cultivated species Hordeum vulgare (barley), Triticum aestivum (wheat), and Secale cereale (rye) belonging to the Triticeae tribe of grasses appear to be particularly rich in gene-like sequences including partial duplicates. Most of them have been classified as putative pseudogenes. In this study we employ transient and stable gene silencing- and over-expression systems in barley to study the function of HvARM1 (for H. vulgare Armadillo 1), a partial gene duplicate of the U-box/armadillo-repeat E3 ligase HvPUB15 (for H. vulgare Plant U-Box 15). Results The partial ARM1 gene is derived from a gene-duplication event in a common ancestor of the Triticeae and contributes to quantitative host as well as nonhost resistance to the biotrophic powdery mildew fungus Blumeria graminis. In barley, allelic variants of HvARM1 but not of HvPUB15 are significantly associated with levels of powdery mildew infection. Both HvPUB15 and HvARM1 proteins interact in yeast and plant cells with the susceptibility-related, plastid-localized barley homologs of THF1 (for Thylakoid formation 1) and of ClpS1 (for Clp-protease adaptor S1) of Arabidopsis thaliana. A genome-wide scan for partial gene duplicates reveals further events in barley resulting in stress-regulated, potentially neo-functionalized, genes. Conclusion The results suggest neo-functionalization of the partial gene copy HvARM1 increases resistance against powdery mildew infection. It further links plastid function with susceptibility to biotrophic pathogen attack. These findings shed new light on a novel mechanism to employ partial duplication of protein-protein interaction domains to facilitate the expansion of immune signaling networks