The potential role of cattail-reinforced clay plaster in sustainable building

Sustainable development is a key goal in town and country planning, as well as in the building industry. The main aims are to avoid inefficient land use, to improve the energy efficiency of buildings and, thus, to move towards meeting the challenges of climate change. In this article we consider how the use of a traditional low-energy building material, namely clay, might contribute. Recent research has identified a promising connection between the reinforcement of clay for internal wall plastering with fibres from the wetland plant Typha latifolia (cattail) and the positive environmental effects of cultivating this species. If large quantities of Typha fibres were to be used in building, the need for cultivation of the plant would increase and create new possibilities for the renaturalisation of polluted or/and degraded peatlands. We explore the topic first on the basis of literature, considering the suitability of Typha for this application and possibilities for its sustainable cultivation, as well as implications for the life cycle analyses of buildings in which it is used. We then report (qualitatively) the results of testing different combinations of clay with natural plant (straw and cattail) fibres for their suitability as a universal plaster, which demonstrate clearly the superior properties of Typha fibres as a reinforcement material for clay plaster mortars

Correction: Interaction between somatostatin analogues and targeted therapies in neuroendocrine tumor cells.

[This corrects the article DOI: 10.1371/journal.pone.0218953.]

Interaction between somatostatin analogues and targeted therapies in neuroendocrine tumor cells.

Somatostatin analogues (SSA) represent the standard of care for symptom control in patients with functional gastro-entero-pancreatic neuroendocrine tumors (GEP-NET). In addition, SSA exert significant anti-proliferative effects in mid-gut and pancreatic NET (PanNET). In parallel, molecularly targeted therapies (MTT) have been shown to improve progression free survival (PFS) in patients with PanNET. However, due to either primary or acquired resistance to MTT, their impact on overall survival (OS) remains unclear. To date, various hypotheses exist to explain differences in patient responsiveness to SSA and MTT. However, data addressing one of the most pivotal questions, whether combining SSA with novel MTT will result in synergistic or additive efficacy compared to monotherapy, are lacking. The aim of this study is to characterize the interaction, optimal sequence and dosing of SSA-based and molecularly targeted therapies in PanNET. Somatostatin receptor subtypes 1-5 (SSTR) were evaluated in the neuroendocrine cell lines Bon1, QGP1 and Ins-1 via immunoblot and qRT-PCR. The impact of the SSA-analogue lanreotide alone or in combination with the MTT sunitinib, everolimus and regorafenib on intracellular signalling, hormone secretion and cell proliferation was determined in cell lysates and supernatants. In addition, synergistic effects of SSA and MTT in various sequential therapeutic approaches were investigated. SSTR were differently expressed in the examined neuroendocrine tumor cell lines. SSTR modulation via lanreotide moderately influenced proliferation, mainly via modulating AKT and ERK signalling, which was paralleled by decreased chromogranin A (CgA) expression and secretion. Interestingly, MTT treatment with regorafenib upregulated the expression of SSTR-2 and -5, while sunitinib and everolimus did not significantly alter SSTR expression. Cell viability was significantly reduced by all MTT, with regorafenib exerting the most significant effects. However, compared to the marked effects of MTT alone, synergistic effects of combined MTT and lanreotide treatment were only modest and time- and dose-dependent. SSTR are differentially expressed in various NEN cell lines. Their expression is influenced by MTT treatment. Various sequential or simultaneous combinations of lanreotide and MTT did not lead to significant synergistic effects

Towards consistent demarcation of enterprise design domains

This article supports the ideology that enterprise engineering (EE) could add more value if EE researchers focus on facilitating effective conversations within design teams to create a common understanding of the enterprise. One way of creating a common understanding is to define and demarcate enterprise design domains in a consistent way. Literature presents different conceptualisations for demarcating design domains, without using a systematic demarcation rationale. As an example, this article introduces Hoogervorst’s approach and associated enterprise design domains to highlight practical difficulties when emerging design principles are applied to four main design domains, as defined by Hoogervorst. Based on the suggestion to apply the basic system design process to demarcate the main enterprise design domains in a consistent way and addressing the need for additional design domains, we present four alternative enterprise design domains, developed via design science research. We also demonstrate the usefulness of the new design domains by presenting several examples of enterprise design cycles that occur during enterprise design.http://link.springer.combookseries/5582018-11-10hj2018Industrial and Systems Engineerin

Prolyl isomerase Pin1 and protein kinase HIPK2 cooperate to promote cortical neurogenesis by suppressing groucho/TLE:Hes1-mediated inhibition of neuronal differentiation

The Groucho/transducin-like Enhancer of split 1 (Gro/TLE1):Hes1 transcriptional repression complex acts in cerebral cortical neural progenitor cells to inhibit neuronal differentiation. The molecular mechanisms that regulate the anti-neurogenic function of the Gro/TLE1:Hes1 complex during cortical neurogenesis remain to be defined. Here we show that prolyl isomerase Pin1 (peptidyl-prolyl cis-trans isomerase NIMA-interacting 1) and homeodomain-interacting protein kinase 2 (HIPK2) are expressed in cortical neural progenitor cells and form a complex that interacts with the Gro/TLE1:Hes1 complex. This association depends on the enzymatic activities of both HIPK2 and Pin1, as well as on the association of Gro/TLE1 with Hes1, but is independent of the previously described Hes1-activated phosphorylation of Gro/TLE1. Interaction with the Pin1:HIPK2 complex results in Gro/TLE1 hyperphosphorylation and weakens both the transcriptional repression activity and the anti-neurogenic function of the Gro/TLE1:Hes1 complex. These results provide evidence that HIPK2 and Pin1 work together to promote cortical neurogenesis, at least in part, by suppressing Gro/TLE1:Hes1-mediated inhibition of neuronal differentiation