Participatory Design of Multi-Use Platforms at Sea

European oceans are subject to rapid development. New activities such as aquaculture and ocean energy have gained importance. This triggers interest in “multi-use platforms at sea” (MUPS), i.e., areas at sea in which different activities are combined. MUPS are complex features with regards to technology, governance, and financial, socioeconomic, and environmental aspects. To identify realistic and sustainable solutions and designs for MUPS, the MERMAID project applied a participatory design process (PDP) involving a range of stakeholders representing companies, authorities, researchers, and NGOs. This paper evaluates if and how the participatory design process contributed to the design of multi-use platforms. It is based on interviews with the managers of the case study sites and a questionnaire administered to all stakeholders participating in the PDP workshops. Analyzing the four case studies, we conclude that the participatory design process has had a valuable contribution to the development of the four different designs of MUPS, even though the preconditions for carrying out a participatory design process differed between sites. In all four cases, the process has been beneficial in generating new and shared knowledge. It brought new design issues to the table and increased knowledge and understanding among the different stakeholders

Gas Natural Fenosa: LNG in the spotlight

A Work Project, presented as part of the requirements for the Award of a Masters Degree in Finance from the NOVA – School of Business and Economic

Behavioral phenotyping of Parkin-deficient mice: looking for early preclinical features of Parkinson's disease.

There is considerable evidence showing that the neurodegenerative processes that lead to sporadic Parkinson's disease (PD) begin many years before the appearance of the characteristic motor symptoms. Neuropsychiatric, sensorial and cognitive deficits are recognized as early non-motor manifestations of PD, and are not attenuated by the current anti-parkinsonian therapy. Although loss-of-function mutations in the parkin gene cause early-onset familial PD, Parkin-deficient mice do not display spontaneous degeneration of the nigrostriatal pathway or enhanced vulnerability to dopaminergic neurotoxins such as 6-OHDA and MPTP. Here, we employed adult homozygous C57BL/6 mice with parkin gene deletion on exon 3 (parkin-/-) to further investigate the relevance of Parkin in the regulation of non-motor features, namely olfactory, emotional, cognitive and hippocampal synaptic plasticity. Parkin-/- mice displayed normal performance on behavioral tests evaluating olfaction (olfactory discrimination), anxiety (elevated plus-maze), depressive-like behavior (forced swimming and tail suspension) and motor function (rotarod, grasping strength and pole). However, parkin-/- mice displayed a poor performance in the open field habituation, object location and modified Y-maze tasks suggestive of procedural and short-term spatial memory deficits. These behavioral impairments were accompanied by impaired hippocampal long-term potentiation (LTP). These findings indicate that the genetic deletion of parkin causes deficiencies in hippocampal synaptic plasticity, resulting in memory deficits with no major olfactory, emotional or motor impairments. Therefore, parkin-/- mice may represent a promising animal model to study the early stages of PD and for testing new therapeutic strategies to restore learning and memory and synaptic plasticity impairments in PD

Effects of <i>parkin</i> genetic deletion on locomotor activity and habituation.

<p>(A) total distance traveled by wild-type and <i>parkin</i>^−/− mice at days 1 and 2 of analysis in an open field arena. <i>*P</i><0.05 compared to day 1, <i>^#P</i><0.05 compared to day 2 of wild-type group using a Newman-Keuls post-hoc test. (B) Pattern of locomotion at day 1 (divided in blocks of 5 min) of wild-type and <i>parkin</i>^−/− mice. (C) Pattern of locomotion at day 2 (divided in blocks of 5 min) of wild-type and <i>parkin</i>^−/− mice. Data are mean ± s.e.m. of n = 9–10 per group.</p

Summary of the performance of wild-type and <i>parkin</i> knockout (<i>parkin</i>^−/−) mice on behavioral tests evaluating olfactory, emotional and motor functions.

<p>Data are expressed as mean ± s.e.m. of 9–11 animals per group. Statistical analysis revealed absence of significant differences between wild-type and <i>parkin</i>^−/− mice in the performance of such behavioral test.</p><p>Summary of the performance of wild-type and <i>parkin</i> knockout (<i>parkin</i>^−/−) mice on behavioral tests evaluating olfactory, emotional and motor functions.</p

Effects of <i>parkin</i> genetic deletion on spatial recognition memory performance.

<p>(A and D) Total number of entries during the training and the test sessions (respectively) by wild-type and <i>parkin</i>^−/− mice. (B and E) Percentage of arms' entries during the training and test sessions (respectively); <i>*P</i><0.05 compared to the hypothetical value of 33% (random entries). (C and F) Percentage of time spent in each arm during the training and test sessions (respectively) by wild-type and <i>parkin</i>^−/− mice; <i>*P</i><0.05 compared to the hypothetical value of 33% (random time). Data are mean ± s.e.m. of n = 9–10 per group.</p

Effects of <i>parkin</i> genetic deletion on hippocampal synaptic transmission and plasticity processes.

<p>(A) Input-output curve of field excitatory post-synaptic potentials (fEPSP, measured as their slope) recorded in Schaffer fibers-CA1 pyramid synapses of hippocampal slices from wild-type and <i>parkin</i>^−/− mice. (B) Paired pulse facilitation (PPF), measured as the ratio of fEPSPs' slope ratio between the second and first paired stimuli (P2/P1 ratio) with different interpulse intervals (25, 50, 100, 200 and 400 ms) recorded in hippocampal slices from wild-type and <i>parkin</i>^−/− mice. (C) Modification of fEPSPs' slope, presented as % of baseline, before and after θ-burst stimulation in slices from wild-type and <i>parkin</i>^−/− mice. (D) Potentiation of fEPSPs' slope after the θ-burst stimulation, presentage as % increase of baseline fEPSPs' slope, in slices from wild-type and <i>parkin</i>^−/− mice <i>*P</i><0.05 compared to wild-type control group. Data are mean ± s.e.m. of n = 4 per group.</p

Effects of <i>parkin</i> genetic deletion on the spatial memory performance.

<p>(A) total investigation time by wild-type and <i>parkin</i>^−/− mice during the training session. (B) Recognition index of wild-type and <i>parkin</i>^−/− mice during the test session. <i>*P</i><0.05 compared to the hypothetical 50% (random investigation). <i>^#P</i><0.05 compared to the wild-type control group. Data are mean ± s.e.m. of n = 9–10 per group.</p

Basal rather than stimulated [³H]dopamine release is increased in striatal synaptosomes of parkin^−/−<i>versus</i> wild-type mice, whereas [¹⁴C]glutamate release is unchanged.

<p>Time course of the averaged time course of [³H]dopamine release (A) and [¹⁴C]glutamate release (D) from wild-type and parkin^−/− mice. S1, S2: stimulation for 1 min with 20 and 75 mM KCl. Ca²⁺-dependence of the resting and stimulated release of [³H]dopamine (B) and [¹⁴C]glutamate (E). Low-calcium experiments were carried out in the presence of 100 nM CaCl₂ and 10 mM MgCl₂. Release and uptake parameters of [³H]dopamine (C) and [¹⁴C]glutamate (F) from parkin^−/− mice normalized to the wild-type mice in the pairwise experiments. ***p<0.001, calculated with paired t-test (B,E) and one-sample t-test (C). Data are mean ± s.e.m. of n≥7 per group with each experiment performed in quadruplicate.</p