ALBERT

Description: Boundary layer and turbulent characteristics (surface fluxes, turbulent kinetic energy – TKE, turbulent kinetic energy dissipation rate – ϵ), along with synoptic-scale changes in these properties over time, are examined using data collected from 18 research flights made with the CIRPAS Twin Otter Aircraft. Data were collected during the Variability of the American Monsoon Systems (VAMOS) Ocean–Cloud–Atmosphere–Land Study Regional Experiment (VOCALS-REx) at Point Alpha (20∘ S, 72∘ W) in October and November 2008 off the coast of South America. The average boundary layer depth is found to be 1148 m, with 28 % of the boundary layer profiles analyzed displaying decoupling. Analysis of correlation coefficients indicates that as atmospheric pressure decreases, the boundary layer height (zi) increases. As has been shown previously, the increase in zi is accompanied by a decrease in turbulence within the boundary layer. As zi increases, cooling near cloud top cannot sustain mixing over the entire depth of the boundary layer, resulting in less turbulence and boundary layer decoupling. As the latent heat flux (LHF) and sensible heat flux (SHF) increase, zi increases, along with the cloud thickness decreasing with increasing LHF. This suggests that an enhanced LHF results in enhanced entrainment, which acts to thin the cloud layer while deepening the boundary layer. A maximum in TKE on 1 November (both overall average and largest single value measured) is due to sub-cloud precipitation acting to destabilize the sub-cloud layer while acting to stabilize the cloud layer (through evaporation occurring away from the surface, primarily confined between a normalized boundary layer height, z/zi, of 0.40 to 0.60). Enhanced moisture above cloud top from a passing synoptic system also acts to reduce cloud-top cooling, reducing the potential for mixing of the cloud layer. This is observed in both the vertical profiles of the TKE and ϵ, in which it is found that the distributions of turbulence for the sub-cloud and in-cloud layer are completely offset from one another (i.e., the range of turbulent values measured have slight or no overlap for the in-cloud and sub-cloud regions), with the TKE in the sub-cloud layer maximizing for the analysis period, while the TKE in the in-cloud layer is below the average in-cloud value for the analysis period. Measures of vertical velocity variance, TKE, and the buoyancy flux averaged over all 18 flights display a maximum near cloud middle (between normalized in-cloud height, Z*, values of 0.25 and 0.75). A total of 10 of the 18 flights display two peaks in TKE within the cloud layer, one near cloud base and another near cloud top, signifying evaporative and radiational cooling near cloud top and latent heating near cloud base. Decoupled boundary layers tend to have a maximum in turbulence in the sub-cloud layer, with only a single peak in turbulence within the cloud layer.

Description: Alzheimer’s Disease (AD) is the most common neurodegenerative disorder in our society, as the population ages, its incidence is expected to increase in the coming decades. The etiopathology of this disease still remains largely unclear, probably because of the highly complex and multifactorial nature of AD. However, the presence of mitochondrial dysfunction has been broadly described in AD neurons and other cellular populations within the brain, in a wide variety of models and organisms, including post-mortem humans. Mitochondria are complex organelles that play a crucial role in a wide range of cellular processes, including bioenergetics. In fact, in mammals, including humans, the main source of cellular ATP is the oxidative phosphorylation (OXPHOS), a process that occurs in the mitochondrial electron transfer chain (ETC). The last enzyme of the ETC, and therefore the ulterior generator of ATP, is the ATP synthase. Interestingly, in mammalian cells, the ATP synthase can also degrade ATP under certain conditions (ATPase), which further illustrates the crucial role of this enzyme in the regulation of cellular bioenergetics and metabolism. In this collaborative review, we aim to summarize the knowledge of the presence of dysregulated ATP synthase, and of other components of mammalian mitochondrial bioenergetics, as an early event in AD. This dysregulation can act as a trigger of the dysfunction of the organelle, which is a clear component in the etiopathology of AD. Consequently, the pharmacological modulation of the ATP synthase could be a potential strategy to prevent mitochondrial dysfunction in AD.