University of Patras

About: University of Patras is a education organization based out in Pátrai, Greece. It is known for research contribution in the topics: Population & Catalysis. The organization has 13372 authors who have published 31263 publications receiving 677159 citations. The organization is also known as: Panepistímio Patrón.

A Genetic Algorithm-Based Low Voltage Ride-Through Control Strategy for Grid Connected Doubly Fed Induction Wind Generators

Abstract: This paper proposes a new computational intelligence-based control strategy, to enhance the low voltage ride-through capability of grid-connected wind turbines (WTs) with doubly fed induction generators (DFIGs). Grid codes world-wide require that WTs should supply reactive power to the grid during and after the fault, in order to support the grid voltage. The conventional crowbar-based systems that were initially applied in order to protect the rotor-side converter at the occurrence of grid faults, do not fulfill this requirement, as during the connection of the crowbar, the DFIG behaves as a squirrel cage machine, absorbing reactive power from the grid. This drawback led to the design of control systems that eliminate or even avoid the use of the crowbar. In order to conform to the above-mentioned requirement, this paper proposes a coordinated control strategy of the DFIG converters during a grid fault, managing to ride-through the fault without the use of any auxiliary hardware. The coordination of the two controllers is achieved via a fuzzy controller which is properly tuned using genetic algorithms. To validate the proposed control strategy, a case study of a 1.5-MW DFIG supplying a relatively weak electrical system is carried out by simulation.

Intrauterine growth restriction as a potential risk factor for disease onset in adulthood.

Abstract: Intrauterine growth restriction (IUGR) is a risk factor for cardiovascular disease, type 2 diabetes mellitus, and obesity in adulthood. Several studies on diverse geographic and ethnic cohorts have provided evidence that being born small for gestational age (SGA) increases adult disease risk through various pathways of metabolic dysregulation. Unfavorable influences in the fetal environment may program metabolic homeostasis in later life affecting blood pressure, glucose tolerance and lipid regulation. Fetal restricted protein supply may impair the development of the kidney and reduce the nephron number, which is involved in blood pressure regulation. Moreover, children exposed to IUGR may exhibit postnatal rapid catch-up growth, altered body composition, increased visceral adiposity and low adiponectin levels which predispose to cardiovascular disease and type 2 diabetes mellitus in adulthood. Impairment in fetal pancreatic development and subsequent insulin signalling deficits due to IUGR may also be involved in the pathogenesis of these conditions. This review summarizes some of the hypotheses that have been put forward to explain the association between fetal growth restriction and subsequent metabolic dysregulation that may increase adult disease risk.

Regulation of mitochondrial bioenergetic function by hydrogen sulfide. Part II. Pathophysiological and therapeutic aspects

Abstract: Emerging work demonstrates the dual regulation of mitochondrial function by hydrogen sulfide (H2S), including, at lower concentrations, a stimulatory effect as an electron donor, and, at higher concentrations, an inhibitory effect on cytochrome C oxidase. In the current article, we overview the pathophysiological and therapeutic aspects of these processes. During cellular hypoxia/acidosis, the inhibitory effect of H2S on complex IV is enhanced, which may shift the balance of H2S from protective to deleterious. Several pathophysiological conditions are associated with an overproduction of H2S (e.g. sepsis), while in other disease states H2S levels and H2S bioavailability are reduced and its therapeutic replacement is warranted (e.g. diabetic vascular complications). Moreover, recent studies demonstrate that colorectal cancer cells up-regulate the H2S-producing enzyme cystathionine β-synthase (CBS), and utilize its product, H2S, as a metabolic fuel and tumour-cell survival factor; pharmacological CBS inhibition or genetic CBS silencing suppresses cancer cell bioenergetics and suppresses cell proliferation and cell chemotaxis. In the last chapter of the current article, we overview the field of H2S-induced therapeutic ‘suspended animation’, a concept in which a temporary pharmacological reduction in cell metabolism is achieved, producing a decreased oxygen demand for the experimental therapy of critical illness and/or organ transplantation. Linked Articles This article is part of a themed issue on Mitochondrial Pharmacology: Energy, Injury & Beyond. To view the other articles in this issue visit http://dx.doi.org/10.1111/bph.2014.171.issue-8