407 research outputs found

    Protection, Automation, and Frequency Stability Analysis of a Laboratory Microgrid System

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    Due to increasing changes in the power industry, Cal Poly San Luis Obispo\u27s electrical engineering department introduced a set of initiatives to adequately equip students with the skills and knowledge to interact with new technologies. Specifically, the department proposed a microgrid and power systems protection and automation laboratory to strengthen students\u27 knowledge of microprocessor-based relays. This paper outlines a microgrid laboratory system that fulfills the initiative\u27s goal and proposes a collection of laboratory experiments for inclusion in a new laboratory course at Cal Poly. The experiments provide students with practical experience using Schweitzer Engineering Laboratory (SEL) relays and teach fundamental concepts in semi-automated generator synchronization and power system data acquisition. The microgrid laboratory system utilizes SEL relays and a centralized SEL controller to automate frequency regulation through load shedding, power factor correction, generator and utility synchronization, and relay protection group switching

    Seasonal Nonstationarity and Near-Nonstationarity

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    This paper presents a detailed discussion of the characteristics of seasonal integrated and near integrated processes, as well as the asymptotic properties of seasonal unit root tests. More specifically, the characteristics of a seasonal random walk and a more general seasonal integrated ARMA process are analysed. Also the implications of modelling nonstationary stochastic season-ality as deterministic are highlighted. A further observation made includes the asymptotic distributions and power functions of several seasonal unit root tests. Dans cet article, nous étudions les propriétés des processsus avec racines unitaires saisonnières et avec racines quasi-unitaires. Nous traitons le cas des marchés aléatoires ainsi que les processus plus généraux et analysons les distributions des estimateurs et les fonctions de puissances de plusieurs tests.Deterministic/stochastic seasonality, seasonal unit roots, Saisonnalité déterministique et stochastique, racines unitaires saisonnières

    The Current Use of Stem Cells in Bladder Tissue Regeneration and Bioengineering.

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    Many pathological processes including neurogenic bladder and malignancy necessitate bladder reconstruction, which is currently performed using intestinal tissue. The use of intestinal tissue, however, subjects patients to metabolic abnormalities, bladder stones, and other long-term sequelae, raising the need for a source of safe and reliable bladder tissue. Advancements in stem cell biology have catapulted stem cells to the center of many current tissue regeneration and bioengineering strategies. This review presents the recent advancements in the use of stem cells in bladder tissue bioengineering

    Ultra-rapid well construction: sustainability of a semi-household level, post-emergency intervention

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    After cyclone Gafilo hit Madagascar in March 2004, an emergency relief project was implemented by an international NGO in the flood-hit region around the town of Maroantsetra. With wind speeds of over 300 kilometres per hour, whole villages had been destroyed, forests uprooted, bridges swept away and crops damaged. A deluge of rainfall caused massive flooding and most water sources became heavily contaminated with faecal matter. Immediately, several (household level) emergency actions were undertaken. To mitigate against future contamination of open water sources, a permanent solution was pioneered through the very rapid construction of more than 200 new wells equipped with hand pumps, making use of an innovative well jetting technique. Thanks to its potential to rapidly reach large numbers of people in an affordable manner, jetting is now being integrated in ongoing development project

    Actin remodeling in motile cells

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    Thesis (Ph. D.)--Harvard-MIT Division of Health Sciences and Technology, 2004.Includes bibliographical references.Non-muscle cell shape change and motility depend primarily on the dynamics and distributions of cytoplasmic actin. In cells, actin cycles between monomeric and polymeric phases tightly regulated by actin binding proteins that control cellular architecture and movement. Here, we characterize actin remodeling in shear stress stimulated endothelial cells and in actin networks reconstituted with purified proteins. Fluid shear stress stimulation induces endothelial cells to elongate and align in the direction of applied flow. Alignment requires 24 h of exposure to flow, but the cells respond within minutes to flow by diminishing their movements by 50%. Although movement slows, actin filament turnover times and the amount of polymerized actin in cells decreases, increasing actin filament remodeling in individual cells composing a confluent endothelial monolayer to levels used by disperse, non-confluent cells for rapid movement. Hours later, motility returns to pre-shear stress levels, but actin remodeling remains highly dynamic in many cells. We conclude that shear stress initiates a cytoplasmic actin remodeling response that is used to modify endothelial cell shape instead of bulk cell translocation. We determine the steady state dynamics of purified actin filament networks in the entangled state and after orthogonal cross-linking with filamins using a novel, non-perturbing fluorescence system. Human filamin A or Dictyosteliun discoidium filamin slow actin filament turnover by [approximately] 50% and recruit much of a significant population of actin oligomers that we measure are present in polymerized purified actin solutions into the immobile filament fraction. Surprisingly, these observations occur at very low stoichiometry to actin, approximately requiring only one(cont.) filamin molecule bound per actin filament, similar to the amount required for actin filament gelation in vitro. Networks formed with filamin truncates localize this activity to the actin binding domain and reveal that dimerization and orthogonal cross-linking are not required for dynamic stabilization. Re-expression of filamin A with or without the actin binding domain in human melanoma cells that naturally lack this protein support the findings in purified actin networks. These results indicate that filamin cross-linking stabilizes filament dynamics by, slowing filament subunit cycling rates and by either decreasing spontaneous filament fragmentation or promoting filament annealing.by Eric A. Osborn.Ph.D

    The dynamics and regulation of actin filaments in vascular endothelial cells and in a reconstituted purified protein system

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    Thesis (S.M.)--Massachusetts Institute of Technology, Dept. of Mechanical Engineering, 2001.Includes bibliographical references.This electronic version was submitted by the student author. The certified thesis is available in the Institute Archives and Special Collections.Cell motility and shape change are complex processes that depend primarily on the cytoplasmic dynamics and distribution of actin monomer and polymer. Proteins that regulate actin cycling control cellular architecture and movement. One method to measure parameters that characterize actin dynamics is photo activation of fluorescence (PAF), which can simultaneously estimate the fraction of total actin polymerized (PF) and the lifetime of actin filaments (t). By deciphering the relationships between actin dynamics and regulatory proteins, the complicated motions of cells and biological consequences of these movements can be better understood. In purified actin solutions at steady-state, actin filament dynamics can be analyzed with PAF at long times following photoactivation. By increasing the width of the photoactivated band, actin filament turnover (t ~ 8 hours) can be distinguished from actin filament diffusion. Proteins believed to stabilize actin filaments against depolymerization markedly slow actin filament turnover in wide photoactivated bands (t ~ 65 hours). Decreasing the band width causes photoactivated fluorescence to decay more rapidly (t ~ 3 hours) due to a combination of actin filament diffusion and turnover. Addition of actin binding protein forms crosslinked actin gels that hinder filament diffusion and slow filament turnover (t ~ 12 hours) in narrow photoactivated bands. Endothelial cells decrease t and PF in order to accelerate their migration speed, consistent with mechanisms attributed to ADF/cofilin in vitro. Removal of gelsolin in fibroblasts produces a similar correlation between motility, t, and PF. Consistent with increased actin filament severing, fast-moving endothelial cells have an increased number of short actin filaments and more uncapped barbed ends, but paradoxically bind less cofilin. A mechanism of increasing endothelial cell motility is proposed that relies on actin filament severing to create uncapped pointed ends for ADF/cofilin-mediated depolymerization.by Eric A. Osborn.S.M

    High temperature QCD with three flavors of improved staggered quarks

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    We present an update of our study of high temperature QCD with three flavors of quarks, using a Symanzik improved gauge action and the Asqtad staggered quark action. Simulations are being carried out on lattices with Nt=4, 6 and 8 for the case of three degenerate quarks with masses less than or equal to the strange quark mass, msm_s, and on lattices with Nt=6 and 8 for degenerate up and down quarks with masses in the range 0.2 m_s \leq m_{u,d} \leq 0.6 m_s, and the strange quark fixed near its physical value. We also report on first computations of quark number susceptibilities with the Asqtad action. These susceptibilities are of interest because they can be related to event-by-event fluctuations in heavy ion collision experiments. Use of the improved quark action leads to a substantial reduction in lattice artifacts. This can be seen already for free fermions and carries over into our results for QCD.Comment: Lattice2002(Non-zero temperature and density

    Dual modality intravascular optical coherence tomography (OCT) and near-infrared fluorescence (NIRF) imaging: a fully automated algorithm for the distance-calibration of NIRF signal intensity for quantitative molecular imaging

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    Intravascular optical coherence tomography (IVOCT) is a well-established method for the high-resolution investigation of atherosclerosis in vivo. Intravascular near-infrared fluorescence (NIRF) imaging is a novel technique for the assessment of molecular processes associated with coronary artery disease. Integration of NIRF and IVOCT technology in a single catheter provides the capability to simultaneously obtain co-localized anatomical and molecular information from the artery wall. Since NIRF signal intensity attenuates as a function of imaging catheter distance to the vessel wall, the generation of quantitative NIRF data requires an accurate measurement of the vessel wall in IVOCT images. Given that dual modality, intravascular OCT–NIRF systems acquire data at a very high frame-rate (>100 frames/s), a high number of images per pullback need to be analyzed, making manual processing of OCT–NIRF data extremely time consuming. To overcome this limitation, we developed an algorithm for the automatic distance-correction of dual-modality OCT–NIRF images. We validated this method by comparing automatic to manual segmentation results in 180 in vivo images from six New Zealand White rabbit atherosclerotic after indocyanine-green injection. A high Dice similarity coefficient was found (0.97 ± 0.03) together with an average individual A-line error of 22 µm (i.e., approximately twice the axial resolution of IVOCT) and a processing time of 44 ms per image. In a similar manner, the algorithm was validated using 120 IVOCT clinical images from eight different in vivo pullbacks in human coronary arteries. The results suggest that the proposed algorithm enables fully automatic visualization of dual modality OCT–NIRF pullbacks, and provides an accurate and efficient calibration of NIRF data for quantification of the molecular agent in the atherosclerotic vessel wall.National Institutes of Health (U.S.) (NIH R01HL093717)Merck & Co., Inc
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