Produktion und Qualitätssicherung von Pyrethrumpräparaten

In Kenia wird seit 1928 Pyrethrum-Anbau betrieben. Organisiert und gemanagt wird der Pyrethrum-Anbau der Kleinbauern in Kenia vom sog. „Pyrethrum Board of Kenia“. Bei dieser Institution handelt es sich um eine staatlich kontrollierte Genossenschaft, die alle notwendigen Aktivitäten organisiert und verwaltet. Anbaubedinungen sowie Aufbereitung oder Fertigung des Flüssigextraktes werden beschrieben

Spezifität und Nebenwirkungen auf Nutzorganismen von pyrethrinhaltigen Pflanzenschutzpräparaten

Spezifisch wirkt Pyrethrum nicht. Das liegt an seiner chemischen Zusammensetzung und dem zugrundeliegenden Wirkmechanismus. Das Pyrethrumkonzentrat, wie es in dem gereinigten Pale-Extrakt vorliegt, besteht aus sechs insektiziden, optisch aktiven Estern der Chrysanthemum- und Pyrethrinsäure. Diese aktiven Bestandteile des Pyrethrums werden auch Pyrethrine genannt. Die Hauptbestandteile jedes Pyrethrum Konzentrats sind Pyrethrin I und II. Die Pyrethrine beeinträchtigen die normale Funktion des zentralen Nervensystems der Insekten. In Freilandversuchen, in denen Photolyse und mikrobieller Abbau parallel erfolgen, war die ermittelte Halbwertzeit von Pyrethrin gering

Aiming for long-term, objective-driven science communication in the UK [Version 2]

Communicating science to wider lay audiences is an increasingly important part of a scientist's remit, and is something that many scientists are keen to embrace. However, based on surveys carried out amongst the UK public, as well as our own experiences in developing and delivering such activities, we believe that they are not always as effective at engaging members of the general public as they could be. In this opinion article we argue that in order to achieve more effective science communication, we need more objective-driven and long-term initiatives. As well as being implemented by the scientists themselves, funding organisations can play an important role in helping to drive such initiatives, and we suggest a list of actionable items that might allow for some of these ideas to be implemented

Science communication in the field of fundamental biomedical research (editorial)

The aim of this special issue on science communication is to inspire and help scientists who are taking part or want to take part in science communication and engage with the wider public, clinicians, other scientists or policy makers. For this, some articles provide concise and accessible advice to individual scientists, science networks, or learned societies on how to communicate effectively; others share rationales, objectives and aims, experiences, implementation strategies and resources derived from existing long-term science communication initiatives. Although this issue is primarily addressing scientists working in the field of biomedical research, much of it similarly applies to scientists from other disciplines. Furthermore, we hope that this issue will also be used as a helpful resource by academic science communicators and social scientists, as a collection that highlights some of the major communication challenges that the biomedical sciences face, and which provides interesting case studies of initiatives that use a breadth of strategies to address these challenges. In this editorial, we first discuss why we should communicate our science and contemplate some of the different approaches, aspirations and definitions of science communication. We then address the specific challenges that researchers in the biomedical sciences are faced with when engaging with wider audiences. Finally, we explain the rationales and contents of the different articles in this issue and the various science communication initiatives and strategies discussed in each of them, whilst also providing some information on the wide range of further science communication activities in the biomedical sciences that could not all be covered here

Periodic actin structures in neuronal axons are required to maintain microtubules

Axons are cable-like neuronal processes wiring the nervous system. They contain parallel bundles of microtubules as structural backbones, surrounded by regularly spaced actin rings termed the periodic membrane skeleton (PMS). Despite being an evolutionarily conserved, ubiquitous, highly ordered feature of axons, the function of PMS is unknown. Here we studied PMS abundance, organization, and function, combining versatile Drosophila genetics with superresolution microscopy and various functional readouts. Analyses with 11 actin regulators and three actin-targeting drugs suggest that PMS contains short actin filaments that are depolymerization resistant and sensitive to spectrin, adducin, and nucleator deficiency, consistent with microscopy-derived models proposing PMS as specialized cortical actin. Upon actin removal, we observed gaps in microtubule bundles, reduced microtubule polymerization, and reduced axon numbers, suggesting a role of PMS in microtubule organization. These effects become strongly enhanced when carried out in neurons lacking the microtubule-stabilizing protein Short stop (Shot). Combining the aforementioned actin manipulations with Shot deficiency revealed a close correlation between PMS abundance and microtubule regulation, consistent with a model in which PMS-dependent microtubule polymerization contributes to their maintenance in axons. We discuss potential implications of this novel PMS function along axon shafts for axon maintenance and regeneration

A conceptual view at microtubule plus end dynamics in neuronal axons

AbstractAxons are the cable-like protrusions of neurons which wire up the nervous system. Polar bundles of microtubules (MTs) constitute their structural backbones and are highways for life-sustaining transport between proximal cell bodies and distal synapses. Any morphogenetic changes of axons during development, plastic rearrangement, regeneration or degeneration depend on dynamic changes of these MT bundles. A key mechanism for implementing such changes is the coordinated polymerisation and depolymerisation at the plus ends of MTs within these bundles. To gain an understanding of how such regulation can be achieved at the cellular level, we provide here an integrated overview of the extensive knowledge we have about the molecular mechanisms regulating MT de/polymerisation. We first summarise insights gained from work in vitro, then describe the machinery which supplies the essential tubulin building blocks, the protein complexes associating with MT plus ends, and MT shaft-based mechanisms that influence plus end dynamics. We briefly summarise the contribution of MT plus end dynamics to important cellular functions in axons, and conclude by discussing the challenges and potential strategies of integrating the existing molecular knowledge into conceptual understanding at the level of axons

Determination of the rate limiting step during zearalenone hydrolysis by ZenA

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Dissecting Regulatory Networks of Filopodia Formation in a Drosophila Growth Cone Model

F-actin networks are important structural determinants of cell shape and morphogenesis. They are regulated through a number of actin-binding proteins. The function of many of these proteins is well understood, but very little is known about how they cooperate and integrate their activities in cellular contexts. Here, we have focussed on the cellular roles of actin regulators in controlling filopodial dynamics. Filopodia are needle-shaped, actin-driven cell protrusions with characteristic features that are well conserved amongst vertebrates and invertebrates. However, existing models of filopodia formation are still incomplete and controversial, pieced together from a wide range of different organisms and cell types. Therefore, we used embryonic Drosophila primary neurons as one consistent cellular model to study filopodia regulation. Our data for loss-of-function of capping proteins, enabled, different Arp2/3 complex components, the formin DAAM and profilin reveal characteristic changes in filopodia number and length, providing a promising starting point to study their functional relationships in the cellular context. Furthermore, the results are consistent with effects reported for the respective vertebrate homologues, demonstrating the conserved nature of our Drosophila model system. Using combinatorial genetics, we demonstrate that different classes of nucleators cooperate in filopodia formation. In the absence of Arp2/3 or DAAM filopodia numbers are reduced, in their combined absence filopodia are eliminated, and in genetic assays they display strong functional interactions with regard to filopodia formation. The two nucleators also genetically interact with enabled, but not with profilin. In contrast, enabled shows strong genetic interaction with profilin, although loss of profilin alone does not affect filopodia numbers. Our genetic data support a model in which Arp2/3 and DAAM cooperate in a common mechanism of filopodia formation that essentially depends on enabled, and is regulated through profilin activity at different steps