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Adaptive Regulation (adaptive + regulation)

Distribution by Scientific Domains

Engineering	50%

Selected Abstracts

Adaptive regulation of MIMO linear systems against unknown sinusoidal exogenous inputs

INTERNATIONAL JOURNAL OF ADAPTIVE CONTROL AND SIGNAL PROCESSING, Issue 6 2009
Maurizio Ficocelli
Abstract This paper deals with the adaptive regulation problem in linear multi-input multi-output systems subject to unknown sinusoidal exogenous inputs, where the frequencies, amplitudes, and phases of the sinusoids are unknown and where the number of sinusoids is assumed to be known. The design of an adaptive regulator for the system under consideration is performed within a set of Q -parameterized stabilizing controllers. To facilitate the design of the adaptive regulator, triangular decoupling is introduced in part of the closed-loop system dynamics. This is achieved through the proper selection of the controller state feedback gain and the structure of the Q parameter. Regulation conditions are then presented for the case where the sinusoidal exogenous input properties are known. For the case where the sinusoidal exogenous input properties are unknown, an adaptation algorithm is proposed to tune the Q parameter in the expression of the parameterized controller. The online tuning of the Q parameter allows the controller to converge to the desired regulator. Convergence results of the adaptation algorithm are presented. A simulation example involving a retinal imaging adaptive optics system is used to illustrate the performance of the proposed adaptive system. Copyright © 2008 John Wiley & Sons, Ltd. [source]

Adaptive regulation of cascade systems with nonlinear parameterization

INTERNATIONAL JOURNAL OF ROBUST AND NONLINEAR CONTROL, Issue 12 2002
Wei Lin
Abstract This article provides a solution to the problem of global adaptive regulation, for a class of nonlinearly parameterized cascade systems including feedback linearizable and minimum-phase systems with nonlinear parameterization. The solution is derived by using a novel parameter separation technique combined with a feedback domination design. We remove all the restrictive conditions previously imposed on the unknown parameters, such as linear parameterization or convex/concave parameterization conditions, which have been commonly assumed so far in the literature of nonlinear adaptive control. Copyright © 2002 John Wiley & Sons, Ltd. [source]

Regulation of glucose transporter 4 traffic by energy deprivation from mitochondrial compromise

ACTA PHYSIOLOGICA, Issue 1 2009
A. Klip
Abstract Skeletal muscle is the major store and consumer of fatty acids and glucose. Glucose enters muscle through glucose transporter 4 (GLUT4). Upon insufficient oxygen availability or energy compromise, aerobic metabolism of glucose and fatty aids cannot proceed, and muscle cells rely on anaerobic metabolism of glucose to restore cellular energy status. An increase in glucose uptake into muscle is a key response to stimuli requiring rapid energy supply. This chapter analyses the mechanisms of the adaptive regulation of glucose transport that rescue muscle cells from mitochondrial uncoupling. Under these conditions, the initial drop in ATP recovers rapidly, through a compensatory increase in glucose uptake. This adaptive response involves AMPK activation by the initial ATP drop, which elevates cell surface GLUT4 and glucose uptake. The gain in surface GLUT4 involves different signals and routes of intracellular traffic compared with those engaged by insulin. The hormone increases GLUT4 exocytosis through phosphatidylinositol 3-kinase and Akt, whereas energy stress retards GLUT4 endocytosis through AMPK and calcium inputs. Given that energy stress is a component of muscle contraction, and that contraction activates AMPK and raises cytosolic calcium, we hypothesize that the increase in glucose uptake during contraction may also involve a reduction in GLUT4 endocytosis. [source]

The taurine transporter: mechanisms of regulation

ACTA PHYSIOLOGICA, Issue 1-2 2006
X. Han
Abstract Taurine transport undergoes an adaptive response to changes in taurine availability. Unlike most amino acids, taurine is not metabolized or incorporated into protein but remains free in the intracellular water. Most amino acids are reabsorbed at rates of 98,99%, but reabsorption of taurine may range from 40% to 99.5%. Factors that influence taurine accumulation include ionic environment, electrochemical charge, and post-translational and transcriptional factors. Among these are protein kinase C (PKC) activation and transactivation or repression by proto-oncogenes such as WT1, c-Jun, c-Myb and p53. Renal adaptive regulation of the taurine transporter (TauT) was studied in vivo and in vitro. Site-directed mutagenesis and the oocyte expression system were used to study post-translational regulation of the TauT by PKC. Reporter genes and Northern and Western blots were used to study transcriptional regulation of the taurine transporter gene (TauT). We demonstrated that (i) the body pool of taurine is controlled through renal adaptive regulation of TauT in response to taurine availability; (ii) ionic environment, electrochemical charge, pH, and developmental ontogeny influence renal taurine accumulation; (iii) the fourth segment of TauT is involved in the gating of taurine across the cell membrane, which is controlled by PKC phosphorylation of serine 322 at the post-translational level; (iv) expression of TauT is repressed by the p53 tumour suppressor gene and is transactivated by proto-oncogenes such as WT1, c-Jun, and c-Myb; and (v) over-expression of TauT protects renal cells from cisplatin-induced nephrotoxicity. [source]

Free fatty acids as mediators of adaptive compensatory responses to insulin resistance in dexamethasone-treated rats

DIABETES/METABOLISM: RESEARCH AND REVIEWS, Issue 2 2008
Michela Novelli
Abstract Background Chronic low-dose dexamethasone (DEX) treatment in rats is associated to insulin resistance with compensatory hyperinsulinaemia and reduction in food intake. We tested the hypothesis that the elevation in circulating free fatty acids (FFAs) induced by DEX is the common mediator of both insulin resistance and insulin hyperproduction. Methods For this purpose, an anti-lipolytic agent was administered during DEX treatment to lower lipacidaemia for several hours prior to glucose and insulin tolerance tests. Leptin expression in adipose tissue (by Northern blot) and plasma leptin levels (by radioimmunoassay) were also investigated to verify whether a rise in circulating leptin could be responsible for the anorectic effect of DEX. Results Our data show that a transient pharmacological reduction of elevated plasma FFA levels abates the post-loading hyperinsulinaemia and counteracts the insulin resistance induced by DEX, supporting the hypothesis that the chronic elevation in FFAs is the common mediator of DEX-induced changes. Despite enhanced leptin expression in white adipose tissue, DEX-treated rats show no significant increase in plasma leptin levels. This suggests that the anorectic effect of DEX should be mediated, at least partially, by other factors, possibly related to the influence of concomitantly elevated plasma FFA and insulin levels on the hypothalamic centers regulating feeding. Conclusions Our results sustain the idea that a prolonged increase in plasma FFA levels plays an important role in the adaptive regulation of glucose and energy homeostasis, not only by potentiating insulin secretion but also by providing a signal of ,nutrient abundance' capable of restraining food intake. Copyright © 2007 John Wiley & Sons, Ltd. [source]