Stabilization of structure-preserving power networks with market dynamics

This paper studies the problem of maximizing the social welfare while stabilizing both the physical power network as well as the market dynamics. For the physical power grid a third-order structure-preserving model is considered involving both frequency and voltage dynamics. By applying the primal-dual gradient method to the social welfare problem, a distributed dynamic pricing algorithm in port-Hamiltonian form is obtained. After interconnection with the physical system a closed-loop port-Hamiltonian system of differential-algebraic equations is obtained, whose properties are exploited to prove local asymptotic stability of the optimal points.Comment: IFAC World Congress 2017, accepted, 6 page

An energy-based analysis of reduced-order models of (networked) synchronous machines

Stability of power networks is an increasingly important topic because of the high penetration of renewable distributed generation units. This requires the development of advanced techniques for the analysis and controller design of power networks. Although there are widely accepted reduced-order models to describe the power network dynamics, they are commonly presented without details about the reduction procedure. The present article aims to provide a modular model derivation of multi-machine power networks. Starting from first-principle fundamental physics, we present detailed dynamical models of synchronous machines and clearly state the underlying assumptions which lead to some of the standard reduced-order multi-machine models. In addition, the energy functions for these models are derived, which allows to represent the multi-machine systems as port-Hamiltonian systems. Moreover, the systems are proven to be shifted passive, which permits for a power-preserving interconnection with other passive components. [GRAPHICS]

Molecular biology of the blood-brain and the blood-cerebrospinal fluid barriers: similarities and differences

Efficient processing of information by the central nervous system (CNS) represents an important evolutionary advantage. Thus, homeostatic mechanisms have developed that provide appropriate circumstances for neuronal signaling, including a highly controlled and stable microenvironment. To provide such a milieu for neurons, extracellular fluids of the CNS are separated from the changeable environment of blood at three major interfaces: at the brain capillaries by the blood-brain barrier (BBB), which is localized at the level of the endothelial cells and separates brain interstitial fluid (ISF) from blood; at the epithelial layer of four choroid plexuses, the blood-cerebrospinal fluid (CSF) barrier (BCSFB), which separates CSF from the CP ISF, and at the arachnoid barrier. The two barriers that represent the largest interface between blood and brain extracellular fluids, the BBB and the BCSFB, prevent the free paracellular diffusion of polar molecules by complex morphological features, including tight junctions (TJs) that interconnect the endothelial and epithelial cells, respectively. The first part of this review focuses on the molecular biology of TJs and adherens junctions in the brain capillary endothelial cells and in the CP epithelial cells. However, normal function of the CNS depends on a constant supply of essential molecules, like glucose and amino acids from the blood, exchange of electrolytes between brain extracellular fluids and blood, as well as on efficient removal of metabolic waste products and excess neurotransmitters from the brain ISF. Therefore, a number of specific transport proteins are expressed in brain capillary endothelial cells and CP epithelial cells that provide transport of nutrients and ions into the CNS and removal of waste products and ions from the CSF. The second part of this review concentrates on the molecular biology of various solute carrier (SLC) transport proteins at those two barriers and underlines differences in their expression between the two barriers. Also, many blood-borne molecules and xenobiotics can diffuse into brain ISF and then into neuronal membranes due to their physicochemical properties. Entry of these compounds could be detrimental for neural transmission and signalling. Thus, BBB and BCSFB express transport proteins that actively restrict entry of lipophilic and amphipathic substances from blood and/or remove those molecules from the brain extracellular fluids. The third part of this review concentrates on the molecular biology of ATP-binding cassette (ABC)-transporters and those SLC transporters that are involved in efflux transport of xenobiotics, their expression at the BBB and BCSFB and differences in expression in the two major blood-brain interfaces. In addition, transport and diffusion of ions by the BBB and CP epithelium are involved in the formation of fluid, the ISF and CSF, respectively, so the last part of this review discusses molecular biology of ion transporters/exchangers and ion channels in the brain endothelial and CP epithelial cells

Astym treatment vs. eccentric exercise for lateral elbow tendinopathy: a randomized controlled clinical trial

Introduction. Patients with chronic lateral elbow (LE) tendinopathy, commonly known as tennis elbow, often experience prolonged symptoms and frequent relapses. Astym treatment, evidenced in animal studies to promote the healing and regeneration of soft tissues, is hypothesized to improve outcomes in LE tendinopathy patients. This study had two objectives: (1) to compare the efficacy of Astym treatment to an evidence-based eccentric exercise program (EE) for patients with chronic LE tendinopathy, and (2) to quantify outcomes of subjects non-responsive to EE who were subsequently treated with Astym treatment.Study Design. Prospective, two group, parallel, randomized controlled trial completed at a large orthopedic center in Indiana. Inclusion criteria: age range of 18–65 years old, with clinical indications of LE tendinopathy greater than 12 weeks, with no recent corticosteriod injection or disease altering comorbidities.Methods. Subjects with chronic LE tendinopathy (107 subjects with 113 affected elbows) were randomly assigned using computer-generated random number tables to 4 weeks of Astym treatment (57 elbows) or EE treatment (56 elbows). Data collected at baseline, 4, 8, 12 weeks, 6 and 12 months. Primary outcome measure: DASH; secondary outcome measures: pain with activity, maximum grip strength and function. The treating physicians and the rater were blinded; subjects and treating clinicians could not be blinded due to the nature of the treatments.Results. Resolution response rates were 78.3% for the Astym group and 40.9% for the EE group. Astym subjects showed greater gains in DASH scores (p = 0.047) and in maximum grip strength (p = 0.008) than EE subjects. Astym therapy also resolved 20/21 (95.7%) of the EE non-responders, who showed improvements in DASH scores (p < 0.005), pain with activity (p = 0.002), and function (p = 0.004) following Astym treatment. Gains continued at 6 and 12 months. No adverse effects were reported.Conclusion. This study suggests Astym therapy is an effective treatment option for patients with LE tendinopathy, as an initial treatment, and after an eccentric exercise program has failed.Registration/Funding. Ball Memorial Hospital provided limited funding. Trial registration was not required by FDAAA 801.Known about the Subject. Under the new paradigm of degenerative tendinopathy, eccentric exercise (EE) is emerging as a first line conservative treatment for LE tendinopathy. EE and Astym treatment are among the few treatment options aiming to improve the degenerative pathophysiology of the tendon. In this trial, Astym therapy, which has shown success in the treatment of tendinopathy, is compared to EE, which has also shown success in the treatment of tendinopathy.Clinical Relevance. There is a need for more effective, conservative treatment options. Based on the current efficacy study, Astym therapy appears to be a promising, non-invasive treatment option