Maximizing the Closed Loop Asymptotic Decay Rate for the Two-Mass-Spring Control Problem

We consider the following problem: find a fixed-order linear controller that maximizes the closed-loop asymptotic decay rate for the classical two-mass-spring system. This can be formulated as the problem of minimizing the abscissa (maximum of the real parts of the roots) of a polynomial whose coefficients depend linearly on the controller parameters. We show that the only order for which there is a non-trivial solution is 2. In this case, we derive a controller that we prove locally maximizes the asymptotic decay rate, using recently developed techniques from nonsmooth analysis

Multiobjective Robust Control with HIFOO 2.0

Multiobjective control design is known to be a difficult problem both in theory and practice. Our approach is to search for locally optimal solutions of a nonsmooth optimization problem that is built to incorporate minimization objectives and constraints for multiple plants. We report on the success of this approach using our public-domain Matlab toolbox HIFOO 2.0, comparing our results with benchmarks in the literature

Optimisation of movement detection and artifact removal during laser speckle contrast imaging

Introduction Laser speckle contrast imaging (LSCI) allows an easy non-contact monitoring of the cutaneous blood flow (CBF), but is highly sensitive to movement artifacts (ARTm). Subtraction of a signal recorded on an adhesive opaque surface (AOS) close to the area of interest was reported as a mean of reducing noise from the raw skin LSCI (LSCIsk) signal, provided an individual calibration was performed. Assuming that AOS = a · CBF + b · ARTm, an ideal patch should completely block the light reflection due to CBF and thus be insensitive to skin blood flow changes (“a” ~ 0), while keeping a reflection signal amplitude similar to the one from the skin in case of artifact (“b” ~ 1). This ideal AOS has not been determined and may discriminate flow from movements during LSCI recordings. Materials and methods We tested different AOSs to determine their “a” and “b” parameters in 35 and 34 healthy volunteers, respectively. The AOS surface providing results as close as possible to an ideal AOS, was used for a point-by-point de-noising of post occlusive reactive hyperemia (PORH) on two different days in 15 new subjects. Correlation of raw, smoothed (average smoothing over 1 s intervals) and denoised signals was tested through a cross-correlation analysis of the two POHR tests. Results The optimal “a” and “b” values were obtained with a homemade bilayer adhesive patch (a = 0.06 ± 0.05 and b = 1.03 ± 0.17) whereas other tested AOS had “a” values ranging from 0.05 to 0.23 and “b” values ranging from 2.69 to 3.82. Using the bilayer adhesive patch the cross-correlation between the two tests of POHR increased from 0.330 ± 0.128 for raw, to 0.461 ± 0.168 for smoothed and 0.649 ± 0.128 for denoised signals respectively (p < 0.05 from raw coefficients). Conclusion The home-made bilayer adhesive seems the optimal AOS for the removal of ARTm from the LSCIsk signal while respecting CBF signal. This specific AOS allows for an efficient de-noising of LSCI measurements without the need for individual calibration

Cyclooxygenase-2 preserves flow-mediated remodelling in old obese Zucker rat mesenteric arteries

AIMS: Resistance arteries have a key role in the control of local blood flow and pressure, and chronic increases in blood flow induce endothelium-dependent outward hypertrophic remodelling. The incidence of metabolic syndrome increases with age, and the combination of these two risk factors impairs endothelium integrity, in part through an inflammatory process. We hypothesized that cyclooxygenase-2 (COX2) would affect remodelling in 12-month-old obese rats compared with young rats. METHODS AND RESULTS: Mesenteric arteries of obese and lean Zucker rats were alternatively ligated to generate high flow (HF) in the median artery. After 21 days, arteries were isolated for in vitro analysis. After 21 days, outward hypertrophic remodelling occurred in HF arteries in obese (498 +/- 20 vs. 443 +/- 18 mum intraluminal diameter in normal flow (NF) arteries, P < 0.01), but not in lean rats (454 +/- 17 vs. 432 +/- 14, NS; n = 12 per group). Endothelium-dependent (acetylcholine)-mediated relaxation (AMR) was lower in obese than in lean rats. AMR was reduced by NO-synthase blockade in all groups, and eNOS expression was higher in HF than in NF arteries without difference between lean and obese rats. Indomethacin further reduced AMR in HF arteries from obese rats only. Obesity increased COX2 immunostaining in mesenteric arteries. Acute COX2 inhibition (NS398) significantly reduced AMR in HF arteries from obese rats only, suggesting production of vasodilator prostanoid(s). In obese rats chronically treated with the COX2 inhibitor celecoxib, outward remodelling did not occur in HF arteries and AMR was improved without reaching the level found in lean rats. CONCLUSION: COX2 preserved in part flow-mediated arterial remodelling in old obese rats. Nevertheless, this effect was not sufficient to keep endothelium-dependent relaxation to the level obtained in lean rats

The vascular phenotype in Pseudoxanthoma elasticum and related disorders: contribution of a genetic disease to the understanding of vascular calcification

Vascular calcification is a complex and dynamic process occurring in various physiological conditions such as aging and exercise or in acquired metabolic disorders like diabetes or chronic renal insufficiency. Arterial calcifications are also observed in several genetic diseases revealing the important role of unbalanced or defective anti- or pro-calcifying factors. Pseudoxanthoma elasticum (PXE) is an inherited disease (OMIM 264800) characterized by elastic fiber fragmentation and calcification in various soft conjunctive tissues including the skin, eyes, and arterial media. The PXE disease results from mutations in the ABCC6 gene, encoding an ATP-binding cassette transporter primarily expressed in the liver, kidneys suggesting that it is a prototypic metabolic soft-tissue calcifying disease of genetic origin. The clinical expression of the PXE arterial disease is characterized by an increased risk for coronary (myocardial infarction), cerebral (aneurysm and stroke), and lower limb peripheral artery disease. However, the structural and functional changes in the arterial wall induced by PXE are still unexplained. The use of a recombinant mouse model inactivated for the Abcc6 gene is an important tool for the understanding of the PXE pathophysiology although the vascular impact in this model remains limited to date. Overlapping of the PXE phenotype with other inherited calcifying diseases could bring important informations to our comprehension of the PXE disease

Author's personal copy Discrete Optimization A model for dynamic chance constraints in hydro power reservoir management

a b s t r a c t In this paper, a model for (joint) dynamic chance constraints is proposed and applied to an optimization problem in water reservoir management. The model relies on discretization of the decision variables but keeps the probability distribution continuous. Our approach relies on calculating probabilities of rectangles which is particularly useful in the presence of independent random variables but works equally well in the case of correlated variables. Numerical results are provided for two and three stages

Exploiting symmetries in SDP-relaxations for polynomial optimization

In this paper we study various approaches for exploiting symmetries in polynomial optimization problems within the framework of semi definite programming relaxations. Our special focus is on constrained problems especially when the symmetric group is acting on the variables. In particular, we investigate the concept of block decomposition within the framework of constrained polynomial optimization problems, show how the degree principle for the symmetric group can be computationally exploited and also propose some methods to efficiently compute in the geometric quotient.Comment: (v3) Minor revision. To appear in Math. of Operations Researc

Computation with Polynomial Equations and Inequalities arising in Combinatorial Optimization

The purpose of this note is to survey a methodology to solve systems of polynomial equations and inequalities. The techniques we discuss use the algebra of multivariate polynomials with coefficients over a field to create large-scale linear algebra or semidefinite programming relaxations of many kinds of feasibility or optimization questions. We are particularly interested in problems arising in combinatorial optimization.Comment: 28 pages, survey pape

Exposure to Maternal Diabetes Is Associated With Early Abnormal Vascular Structure in Offspring

Aim/hypothesis: In utero exposure to maternal diabetes increases the risk of developing hypertension and cardiovascular disorders during adulthood. We have previously shown that this is associated with changes in vascular tone in favor of a vasoconstrictor profile, which is involved in the development of hypertension. This excessive constrictor tone has also a strong impact on vascular structure. Our objective was to study the impact of in utero exposure to maternal diabetes on vascular structure and remodeling induced by chronic changes in hemodynamic parameters. Methods and Results: We used an animal model of rats exposed in utero to maternal hyperglycemia (DMO), which developed hypertension at 6 months of age. At a pre-hypertensive stage (3 months of age), we observed deep structural modifications of the vascular wall without any hemodynamic perturbations. Indeed, in basal conditions, resistance arteries of DMO rats are smaller than those of control mother offspring (CMO) rats; in addition, large arteries like thoracic aorta of DMO rats have an increase of smooth muscle cell attachments to elastic lamellae. In an isolated perfused kidney, we also observed a leftward shift of the flow/pressure relationship, suggesting a rise in renal peripheral vascular resistance in DMO compared to CMO rats. In this context, we studied vascular remodeling in response to reduced blood flow by in vivo mesenteric arteries ligation. In DMO rats, inward remodeling induced by a chronic reduction in blood flow (1 or 3 weeks after ligation) did not occur by contrast to CMO rats in which arterial diameter decreased from 428 ± 17 μm to 331 ± 20 μm (at 125 mmHg, p = 0.001). In these animals, the transglutaminase 2 (TG2) pathway, essential for inward remodeling development in case of flow perturbations, was not activated in low-flow (LF) mesenteric arteries. Finally, in old hypertensive DMO rats (18 months of age), we were not able to detect a pressure-induced remodeling in thoracic aorta. Conclusions: Our results demonstrate for the first time that in utero exposure to maternal diabetes induces deep changes in the vascular structure. Indeed, the early narrowing of the microvasculature and the structural modifications of conductance arteries could be a pre-emptive adaptation to fetal programming of hypertension

The endothelial mineralocorticoid receptor regulates vasoconstrictor tone and blood pressure

Pathophysiological aldosterone (aldo)/mineralocorticoid receptor (MR) signaling has significant effects on the cardiovascular system, resulting in hypertension and cardiovascular remodeling; however, the specific contribution of the vascular MR to blood pressure regulation remains to be established. To address this question, we generated a mouse model with conditional overexpression of the MR in endothelial cells (MR-EC). In basal conditions, MR-EC mice developed moderate hypertension that could be reversed by canrenoate, a pharmacological MR antagonist. MR-EC mice presented increased contractile response of resistance arteries to vasoconstrictors (phenylephrine, thromboxane A(2) analog, angiotensin II, and endothelin 1) in the absence of vascular morphological alterations. The acute blood pressure response to angiotensin II or endothelin 1 infusion was increased in MR-EC mice compared with that in littermate controls. These observations demonstrate that enhanced MR activation in the endothelium generates an increase in blood pressure, independent of stimulation of renal tubular Na(+) transport by aldo/MR or direct activation of smooth muscle MR and establish one mechanism by which endothelial MR activation per se may contribute to impaired vascular reactivity