Assessing spatio-temporal changes in marine communities along the Portuguese continental shelf and upper slope based on 25 years of bottom trawl surveys.

The Portuguese continental coast is influenced by several oceanographic processes and is located near the confluence of three biogeographic realms (from the North Atlantic, South Atlantic and Mediterranean). Given these features, the topography of the Portuguese coast, possible variations in fishing effort and reported increasing sea surface temperature in the last decades, we hypothesized that changes in marine communities in space and time occurred since 1990. In this study, research survey data collected yearly along the Portuguese continental slope (20-500 m deep) from 1990 to 2016 were analysed with the objective of identifying spatio-temporal changes.

The MOVE.TE Falls Prevention and Management Program: lessons learnt in the Portuguese context.

MOVE.TE is a non-profit participatory physiotherapy platform that aims at translating knowledge in the field of physiotherapy and developing freely available evidence-based physiotherapy programmes targeting the primary care services of the Portuguese National Health service. A group of volunteer academics and clinicians collaborated at different stages and time points to create the first ever falls prevention and management programme and guidance for Physiotherapy in primary care, in Portugal.

Molecular mechanisms of disease for mutations at Gly-90 in rhodopsin.

Two different mutations at Gly-90 in the second transmembrane helix of the photoreceptor protein rhodopsin have been proposed to lead to different phenotypes. G90D has been classically associated with congenital night blindness, whereas the newly reported G90V substitution was linked to a retinitis pigmentosa phenotype. Here, we used Val/Asp replacements of the native Gly at position 90 to unravel the structure/function divergences caused by these mutations and the potential molecular mechanisms of inherited retinal disease.

Pharmacological manipulation of rhodopsin retinitis pigmentosa.

Mutations in rhodopsin cause autosomal dominant retinitis pigmentosa. The majority of these mutations (class II) lead to protein misfolding. The misfolded protein is retained in the ER then retrotranslocated into the cytoplasm for degradation by the proteasome.

Pharmacological manipulation of gain-of-function and dominant-negative mechanisms in rhodopsin retinitis pigmentosa.

Mutations in the dim light photoreceptor protein rod opsin cause autosomal dominant retinitis pigmentosa. The majority of these mutations (class II) lead to protein misfolding. For example, the common class II rod opsin mutation P23H misfolds and is retained in the ER, prior to retrotranslocation and degradation by the proteasome.

Mechanisms of cell death in rhodopsin retinitis pigmentosa: implications for therapy.

Retinitis pigmentosa (RP) is a group of retinal degenerative diseases that are characterised primarily by the loss of rod photoreceptor cells. Mutations in rhodopsin are the most common cause of autosomal-dominant RP (ADRP). Here, we propose a new classification for rhodopsin mutations based on their biochemical and cellular properties.