How to make complexity look simple? Conveying ecosystems restoration complexity for socio-economic research and public engagement

Ecosystems degradation represents one of the major global challenges at the present time, threating people’s livelihoods and well-being worldwide. Ecosystem restoration therefore seems no longer an option, but an imperative. Restoration challenges are such that a dialogue has begun on the need to re-shape restoration as a science. A critical aspect of that reshaping process is the acceptance that restoration science and practice needs to be coupled with socio-economic research and public engagement. This inescapably means conveying complex ecosystem’s information in a way that is accessible to the wider public. In this paper we take up this challenge with the ultimate aim of contributing to making a step change in science’s contribution to ecosystems restoration practice. Using peatlands as a paradigmatically complex ecosystem, we put in place a transdisciplinary process to articulate a description of the processes and outcomes of restoration that can be understood widely by the public. We provide evidence of the usefulness of the process and tools in addressing four key challenges relevant to restoration of any complex ecosystem: (1) how to represent restoration outcomes; (2) how to establish a restoration reference; (3) how to cope with varying restoration time-lags and (4) how to define spatial units for restoration. This evidence includes the way the process resulted in the creation of materials that are now being used by restoration practitioners for communication with the public and in other research contexts. Our main contribution is of an epistemological nature: while ecosystem services-based approaches have enhanced the integration of academic disciplines and non-specialist knowledge, this has so far only followed one direction (from the biophysical underpinning to the description of ecosystem services and their appreciation by the public). We propose that it is the mix of approaches and epistemological directions (including from the public to the biophysical parameters) what will make a definitive contribution to restoration practice

Implication of the phosphatidylinositol-3 kinase/protein kinase b signaling pathway in the neuroprotective effect of estradiol in the striatum of 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine mice

The present experiments sought to determine the implication of estrogen receptors (ERα and ERβ) and their interaction with insulin-like growth factor receptor (IGF-IR) signaling pathways in neuroprotection by estradiol against 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP) toxicity. C57BL/6 male mice were pretreated for 5 days with 17β-estradiol, an estrogen receptor α(ERα) agonist, 4,4′,4″-(4-propyl-[1H] -pyrazole-1,3,5-triyl)tris-phenol (PPT), or an estrogen receptor β (ERβ) agonist, 5-androsten-3β, 17β-diol (Δ5-diol). On day 5, mice received MPTP (9 mg/kg) or saline injections, and estrogenic treatments were continued for 5 more days. MPTP decreased striatal dopamine, measured by high-performance liquid chromatography, to 59% of control values; 17β-estradiol and PPT but not δ5-diol protected against this depletion. MPTP increased IGF-IR measured by Western blot, which was prevented by PPT. The phosphorylation of protein kinase B (Akt) (at serine 473), an essential mediator of IGF-I neuroprotective actions, increased after 17β-estradiol and tended to increase with PPT but not with δ5-diol treatments in MPTP mice. Glycogen synthase kinase 3β (GSK3β) phosphorylation (at serine 9) was greatly reduced in MPTP mice; this was completely prevented by PPT, whereas 17β-estradiol and Δ5-diol treatments were less effective. The ratio between the levels of striatal Bcl-2 and BAD proteins, two apoptotic regulators, decreased after MPTP treatment. This effect was effectively prevented only in the animals treated with PPT. In nonlesioned mice, 17β-estradiol and PPT increased phosphorylation of striatal Akt and GSK3β, whereas the other markers measured remained unchanged. Δ5-Diol increased GSK3β phosphorylation less than the PPT treatment. These results suggest that a pretreatment with estradiol promoted dopamine neuron survival by activating ERα and increasing Akt and GSK3β phosphorylation. Copyright © 2006 The American Society for Pharmacology and Experimental Therapeutics.Peer Reviewe

Contribution of estrogen receptors alpha and beta to the effects of estradiol in the brain

Clinical and experimental studies show a modulatory role of estrogens in the brain and suggest their beneficial action in mental and neurodegenerative diseases. The estrogen receptors ERα and ERβ are present in the brain and their targeting could bring selectivity and reduced risk of cancer. Implication of ERs in the effect of estradiol on dopamine, opiate and glutamate neurotransmission is reviewed. The ERα agonist, PPT, is shown as estradiol to modulate hippocampal NMDA receptors and AMPA receptors in cortex and striatum of ovariectomized rats whereas the ERβ agonist DPN is inactive. Striatal DPN activity suggests implication of ERβ in estradiol modulation of D2 receptors and transporters in ovariectomized rats and is supported by the lack of effect of estradiol in ERβ knockout (ERKOβ) mice. Both ERα and ERβ agonists modulate striatal preproenkephalin (PPE) gene expression in ovariectomized rats. In male mice PPT protects against MPTP toxicity to striatal dopamine; this implicates Akt/GSK3β signaling and the apoptotic regulators Bcl2 and Bad. This suggests a role for ERα in striatal dopamine neuroprotection. ERKOα mice are more susceptible to MPTP toxicity and not protected by estradiol; differences in ERKOβ mice are subtler. These results suggest therapeutic potential for the brain of ER specific agonists. © 2007 Elsevier Ltd. All rights reserved.Peer Reviewe

Consumer perceptions of monetary and non-monetary introductory promotions for new products

Little research has examined how consumers respond to sales promotions in new product categories. This article fills this gap by integrating research on reference prices with literature on sales promotions for new product categories. Existing research suggests that consumers respond more favourably to non-monetary promotions (e.g. extra free promotions) than monetary promotions (e.g. price discounts) because non-monetary promotions are framed as segregated gains rather than reduced losses. However, both kinds of promotions are widely used in practice, suggesting the importance of other contributory factors. With a consumer experiment on a national panel of consumers, this research demonstrates that extra free product promotions are most preferred for existing products, and introductory low-price promotions are preferred for innovative products. The moderating effect of a product's innovativeness is explained via a new relationship in the marketing literature, whereby perceived risk mediates the relationship between perceived innovativeness and a consumer's tendency to stockpile