During the 1990s, a large number of new tidal atlases were developed, primarily to provide accurate tidal corrections for satellite altimetry applications. During this decade, the French tidal group (FTG), led by C. Le Provost, produced a series of finite element solutions (FES) tidal atlases, among which FES2004 is the latest release, computed from the tidal hydrodynamic equations and data assimilation. The aim of this paper is to review the state of the art of tidal modelling and the progress achieved during this past decade. The first sections summarise the general FTG approach to modelling the global tides. In the following sections, we introduce the FES2004 tidal atlas and validate the model against in situ and satellite data. We demonstrate the higher accuracy of the FES2004 release compared to earlier FES tidal atlases, and we recommend its use in tidal applications. The final section focuses on the new dissipation term added to the equations, which aims to account for the conversion of barotropic energy into internal tidal energy. There is a huge improvement in the hydrodynamic tidal solution and energy budget obtained when this term is taken into account.

The study of mitochondrial diseases has revealed dramatic variability in the phenotypic presentation of mitochondrial genetic defects. To attempt to understand this variability, different authors have studied energy metabolism in transmitochondrial cell lines carrying different proportions of various pathogenic mutations in their mitochondrial DNA. The same kinds of experiments have been performed on isolated mitochondria and on tissue biopsies taken from patients with mitochondrial diseases. The results have shown that, in most cases, phenotypic manifestation of the genetic defect occurs only when a threshold level is exceeded, and this phenomenon has been named the 'phenotypic threshold effect'. Subsequently, several authors showed that it was possible to inhibit considerably the activity of a respiratory chain complex, up to a critical value, without affecting the rate of mitochondrial respiration or ATP synthesis. This phenomenon was called the 'biochemical threshold effect'. More recently, quantitative analysis of the effects of various mutations in mitochondrial DNA on the rate of mitochondrial protein synthesis has revealed the existence of a 'translational threshold effect'. In this review these different mitochondrial threshold effects are discussed, along with their molecular bases and the roles that they play in the presentation of mitochondrial diseases.

Mitochondria form a dynamic network, and it remains unclear how the alternate configurations interact with bioenergetics properties. The metabolic signals that link mitochondrial structure to its functional states have not been fully characterized. In this report, we analyze the bidirectional relationships between mitochondrial morphology and function in living human cells. First, we determined the effect of mitochondrial fission on energy production by using small interfering RNA (siRNA) targeting DRP1, which revealed the importance of membrane fluidity on the control of bioenergetics. Second, we followed the effect of rotenone, a specific inhibitor of respiratory chain complex I, which causes large structural perturbations, once a threshold was reached. Last, we followed changes in the mitochondrial network configuration in human cells that had been treated with modulators of oxidative phosphorylation, and in fibroblasts from two patients with mitochondrial disease where the respiratory rate, ΔΨ and the generation of reactive oxygen species (ROS) were measured. Our data demonstrate that the relationship between mitochondrial network organization and bioenergetics is bidirectional, and we provide a model for analyzing the metabolic signals involved in this crosstalk.