Mind Your Writing: How to be a Professional Academic Writer

The author presents ten of the fundamental questions that every academic writer should be able to answer. He focuses on some questions which may appear trivial at first glance but will likely prove to have more impact on the writer's efficiency and success than initially expected. The author's main argument is that writers who become better acquainted with themselves become more productive and happier writers. By knowing their own skills and the specific challenges of academic writing, writing will become a task they can master. Because of its focus on these fundamental questions, the book differs from usual guide books on academic writing. It addresses writers irrespective of their disciplinary background.Um erfolgreich schreiben und publizieren zu können, müssen wissenschaftlich Schreibende sich über ihre Kompetenzen und ihre Rolle als Schreibende im Klaren sein. Sie müssen Grundsatzfragen über ihr Schreiben beantworten können, damit sie bewusste und strategische Entscheidungen treffen können. Nur so werden sie zu Schreibprofis, die ihren Beruf erfolgreich ausüben

Mind Your Writing

In order to write and publish successfully, academic writers must be aware of their skills and their role as writers. They need to be able to answer fundamental questions about their writing, enabling them to make conscious and strategic decisions. Only in that way they will become writing professionals who successfully carry out their profession

Targeting PI3Kδ and PI3Kγ signalling disrupts human AML survival and bone marrow stromal cell mediated protection

Phosphoinositide-3-kinase (PI3K) is an enzyme group, known to regulate key survival pathways in acute myeloid leukaemia (AML). It generates phosphatidylinositol-3,4,5-triphosphate, which provides a membrane docking site for protein kinaseB activation. PI3K catalytic p110 subunits are divided into 4 isoforms; α,β,δ and γ. The PI3Kδ isoform is always expressed in AML cells, whereas the frequency of PI3Kγ expression is highly variable. The functions of these individual catalytic enzymes have not been fully resolved in AML, therefore using the PI3K p110δ and p110γ-targeted inhibitor IPI-145 (duvelisib) and specific p110δ and p110γ shRNA, we analysed the role of these two p110 subunits in human AML blast survival. The results show that PI3Kδ and PI3Kγ inhibition with IPI-145 has anti-proliferative activity in primary AML cells by inhibiting the activity of AKT and MAPK. Pre-treatment of AML cells with IPI-145 inhibits both adhesion and migration of AML blasts to bone marrow stromal cells. Using shRNA targeted to the individual isoforms we demonstrated that p110δ-knockdown had a more significant anti-proliferative effect on AML cells, whereas targeting p110γ-knockdown significantly inhibited AML migration. The results demonstrate that targeting both PI3Kδ and PI3Kγ to inhibit AML-BMSC interactions provides a biologic rationale for the pre-clinical evaluation of IPI-145 in AML

Lack of genetic structure suggests high connectivity of Parnassius phoebus between nearby valleys in the Alps

The spatial scale of intraspecific genetic connectivity and population structure are important aspects of conservation genetics. However, for many species these properties are unknown. Here we used genomic data to assess the genetic structure of the small Apollo butterfly (Parnassius phoebus Fabricius, 1793; Lepidoptera: Papilionidae) across three nearby valleys in the Central Swiss Alps. One of the valleys is currently used for hydropower production with future plans to raise the existing dam wall further. We found no significant genetic structure, suggesting a currently high connectivity of this species in our studied region

Employability 4.0. Arbeitsmarktfähigkeit in einer sich wandelnden Arbeitswelt

Megatrends führen zu einem fundamentalen Wandel in der Arbeitswelt und stellen Unternehmen vor große Herausforderungen. Die Arbeitsmarktfähigkeit von Mitarbeitenden kann dabei zum wichtigen Erfolgsfaktor für die langfristige Wettbewerbsfähigkeit werden. Gleichzeitig führen die Arbeitsweltveränderungen auch zu neuen Anforderungen an die individuelle Arbeitsmarktfähigkeit der Mitarbeitenden. Anhand eines qualitativen Forschungsdesigns wurde für Schweizer Tochterunternehmen eines Industriekonzerns untersucht, welche Entwicklungen in der Schweizer Arbeitswelt zu erwarten sind, wie sich diese auf die Arbeitsmarktfähigkeit von Mitarbeitenden auswirken und wie das Human Resource Management (HRM) zur Arbeitsmarktfähigkeit der Mitarbeitenden beitragen kann. Die Ergebnisse zeigen, dass die Digitalisierung als relevantester Megatrend in der Arbeitswelt wahrgenommen wird und dass Anpassungsfähigkeit sowie lebenslanges Lernen der Mitarbeitenden essenziell für die Erhaltung und Förderung ihrer Arbeitsmarktfähigkeit sind

Loss of phosphatase activity in myotubularin-related protein 2 is associated with Charcot-Marie-Tooth disease type 4B1

Mutations in the gene encoding myotubularin-related protein 2 (MTMR2) are responsible for autosomal recessive Charcot-Marie-Tooth disease type 4B1 (CMT4B1), a severe hereditary motor and sensory neuropathy characterized by focally folded myelin sheaths and demyelination. MTMR2 belongs to the myotubularin family, which is characterized by the presence of a phosphatase domain. Myotubularin (MTM), the archetype member of this family, is mutated in X-linked myotubular myopathy. Although MTMR2 and MTM are closely related, they are likely to have different functions. Recent studies revealed that MTM dephosphorylates specifically phosphatidylinositol 3-phosphate. Here we analyze the biochemical properties of the mouse Mtmr2 protein, which shares 97% amino acid identity with human MTMR2. We show that phosphatidylinositol-3-phosphate is also a substrate for Mtmr2, but, unlike myotubularin, Mtmr2 dephosphorylates phosphatidylinositol 3,5-bisphosphate with high efficiency and peak activity at neutral pH. We demonstrate that the known disease-associated MTMR2 mutations lead to dramatically reduced phosphatase activity, suggesting that the MTMR2 phosphatase activity is crucial for the proper function of peripheral nerves in CMT4B1. Expression analysis of Mtmr2 suggests particularly high levels in neurons. Thus, the demyelinating neuropathy CMT4B1 might be triggered by the malfunction of neural membrane recycling, membrane trafficking, and/or endocytic or exocytotic processes, combined with altered axon-Schwann cell interactions. Furthermore, the different biochemical properties of MTM and MTMR2 offer a potential explanation for the different human diseases caused by mutations in their respective gene