Kaimal spectrum based H2 optimization of tuned mass dampers for wind turbines

The closed-form analytical expression of the objective function of a single degree of freedom system with the tuned mass damper, subjected to Gaussian white noise and Kaimal forcing spectrum, is derived implementing the H2 optimization technique. To illustrate the procedure, a wind turbine tower with and without the tuned mass damper, subjected to wind load, has been presented. The Kaimal spectrum has been considered to model the effects of wind load. Usually, the parameters of the tuned mass damper is optimized by implementing the H2 optimization technique on Gaussian white noise even though the system is subject to any other forcing spectrum. Obtaining an analytical closed-form expression of the objective function for a tuned mass damper system considering a real spectrum is very challenging as a real spectrum may contain fractional order of the frequency. Therefore, either objective function can be obtained numerically or an analytical form can be obtained but only for Gaussian white noise as an input forcing spectrum. To address the above-mentioned issue, in this paper, the concept of near identity spectrum is introduced to idealize the Kaimal spectrum with high accuracy from which a closed-form expression of the objective function can be established. Further, histogram plots of the response reduction have been made to show a comparison between the tuned mass damper system optimized with Gaussian white noise and the Kaimal spectrum. The results showed that the displacement response of the tuned mass damper system subjected to the Kaimal spectrum yields better performance if it is optimized according to the Kaimal spectrum rather than Gaussian white noise and vice versa

ATP Synthase and Mitochondrial Bioenergetics Dysfunction in Alzheimer’s Disease

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