Population model of the recent subtidal invasion of Sargassum muticum in southern Portugal

Dissertação de Mestrado, Biologia Marinha, Especialização em Ecologia e Conservação, Faculdade de Ciências do Mar e do Ambiente, Universidade do Algarve, 2007

Disparity energy model with keypoint disparity validation

A biological disparity energy model can estimate local depth information by using a population of V1 complex cells. Instead of applying an analytical model which explicitly involves cell parameters like spatial frequency, orientation, binocular phase and position difference, we developed a model which only involves the cells’ responses, such that disparity can be extracted from a population code, using only a set of previously trained cells with random-dot stereograms of uniform disparity. Despite good results in smooth regions, the model needs complementary processing, notably at depth transitions. We therefore introduce a new model to extract disparity at keypoints such as edge junctions, line endings and points with large curvature. Responses of end-stopped cells serve to detect keypoints, and those of simple cells are used to detect orientations of their underlying line and edge structures. Annotated keypoints are then used in the leftright matching process, with a hierarchical, multi-scale tree structure and a saliency map to segregate disparity. By combining both models we can (re)define depth transitions and regions where the disparity energy model is less accurate.

A disparity energy model improved by line, edge and keypoint correspondences

Disparity energy models (DEMs) estimate local depth information on the basis ofVl complex cells. Our recent DEM (Martins et al, 2011 ISSPlT261-266) employs a population code. Once the population's cells have been trained with randorn-dot stereograms, it is applied at all retinotopic positions in the visual field. Despite producing good results in textured regions, the model needs to be made more precise, especially at depth transitions.

Insights into molecular and cellular events involved in normal and pathological vertebral development and fusion using zebrafish as model organism

The vertebral column and its units, the vertebrae, are fundamental features, characteristic of all vertebrates. Developmental segregation of the vertebral bodies as articulated units is an intrinsic requirement to guarantee the proper function of the spine. Whenever these units become fused either during development or postsegmentation, movement is affected in a more or less severe manner, depending on the number of vertebrae affected. Nevertheless, fusion may occur as part of regular development and as a physiological requirement, like in the tetrapod sacrum or in fish posterior vertebrae forming the urostyle. In order to meet the main objective of this PhD project, which aimed to better understand the molecular and cellular events underlying vertebral fusion under physiological and pathological conditions, a detailed characterization of the vertebral fusion occurring in zebrafish caudal fin region was conducted. This showed that fusion in the caudal fin region comprised 5 vertebral bodies, from which, only fusion between [PU1++U1] and ural2 [U2+] was still traceable during development. This involved bone deposition around the notochord sheath while fusion within the remaining vertebral bodies occur at the level of the notochord sheath, as during the early establishment of the vertebral bodies. A comparison approach between the caudal fin vertebrae and the remaining vertebral column showed conserved features such as the presence of mineralization related proteins as Osteocalcin were identified throughout the vertebral column, independently on the mineralization patterns. This unexpected presence of Osteocalcin in notochord sheath, here identified as Oc1, suggested that this gene, opposing to Oc2, generally associated with bone formation and mature osteoblast activity, is potentially associated with early mineralization events including chordacentrum formation. Nevertheless, major differences between caudal fin region and anterior vertebral bodies considering arch histology and mineralization patterns, led us to use RA as an inductive factor for vertebral fusion, allowing a direct comparison of equivalent structures under normal and fusion events. This fusion phenotype was associated with notochord sheath ectopic mineralization instead of ectopic perichordal bone formation related with increased osteoblast activity, as suggested in previous reports. Additionally, alterations in ECM content, cell adhesion and blood coagulation were discussed as potentially related with the fusion phenotype. Finally, Matrix gla protein, upregulated upon RA treatment and shown to be associated with chordacentrum mineralization sites in regular development, was further described considering its potential function in vertebral formation and pathological fusion. Therefore with this work we propose zebrafish caudal fin vertebral fusion as a potential model to study both congenital and postsegmentation fusion and we present candidate factors and genes that may be further explored in order to clarify whether we can prevent vertebral fusion.