CZT-Based Harmonic Analysis in Smart Grid Using Low-Cost Electronic Measurement Boards

This paper validates the use of a harmonic analysis algorithm on a microcontroller to perform measurements of non-stationary signals in the context of smart grids. The increasing presence of electronic devices such as inverters of distributed generators (DG), power converters of charging stations for electric vehicles, etc. can drain non-stationary currents during their operation. A classical fast Fourier transform (FFT) algorithm may not have sufficient spectral resolution for the evaluation of harmonics and inter-harmonics. Thus, in this paper, the implementation of a chirp-Z transform (CZT) algorithm is suggested, which has a spectral resolution independent from the observation window. The CZT is implemented on a low-cost commercial microcontroller, and the absolute error is evaluated with respect to the same algorithm implemented in the LabVIEW environment. The results of the tests show that the CZT implementation on a low-cost microcontroller allows for accurate measurement results, demonstrating the feasibility of reliable harmonic analysis measurements even in non-stationary conditions on smart grids

Durand et al 2012 Supplemental figures

Objective. Our objective was to compare the osteoclastogenic capacity of peripheral blood mononuclear cells (PBMCs) from patients with osteoarthritis (OA) to that of PBMCs from self-reported normal individuals. Methods. PBMCs from 140 patients with OA and 45 healthy donors were assayed for CD14+ expression and induced to differentiate into osteoclasts (OCs) over 3 weeks in vitro. We assessed the number of the OCs, their resorptive activity, OC apoptosis, and expression of the following cytokine receptors: receptor activator of nuclear factor κB (RANK), interleukin-1 receptor type I (IL-1R1) and IL-1R2. A ridge logistic regression classifier was developed to discriminate OA patients from controls. Results. PBMCs from OA patients gave rise to more OCs that resorbed more bone surface than did PBMCs from controls. The number of CD14+ precursors was comparable in both groups, but there was less apoptosis in OCs obtained from OA patients. Although no correlation was found between osteoclastogenic capacity and clinical or radiologic scores, levels of IL-1R1 were significantly lower in cultures from patients with OA compared to controls. OC apoptosis and expression levels of IL-1R1 and IL-1R2 were used to build a multivariate predictive model for OA. Conclusion. During 3 weeks of culture under identical conditions, monocytes from patients with OA display enhanced capacity to generate OCs compared to cells from controls. Enhanced osteoclastogenesis is accompanied by increased resorptive activity, reduced OC apoptosis and diminished IL-1R1 expression. These findings support the possibility that generalized changes in bone metabolism affecting OCs participate in the pathophysiology of OA

Examining Novel Factors that Influence Contact-dependent Osteoblast and Osteoclast Differentiation

A dynamic equilibrium between bone destruction by osteoclasts and bone formation by osteoblasts is responsible for the maintenance of bone integrity, mineral homeostasis and protection from bone-related disease. As such, the focus of this work was to examine novel factors contributing to the contact-dependent differentiation of osteoblasts and osteoclasts. Osteoblast differentiation and maturation is stimulated by multiple external factors, two of which are ascorbic acid (AA) and bone morphogenetic protein-2 (BMP-2). Utilizing MC3T3-E1 cells and primary murine osteoblasts, we identified a novel role for EB1, a microtubule plus-end binding protein, during osteoblast differentiation. AA-stimulation strongly induced EB1 expression and EB1 knockdown significantly impaired the osteoblast differentiation program in both AA- and BMP-2-induced osteoblasts. Furthermore, we identified that EB1 function was important for the global stability of -catenin, a major signaling molecule in osteoblasts. Lastly, the influence of E-cadherin, a cell-cell adhesion and recognition molecule, was investigated in AA-stimulated osteoblasts. Up-regulation of Cdh1 (E-cadherin) paralleled that of Catnb (beta-catenin), and E-cadherin blocking antibody treatment dampened osteoblast-specific gene expression. E-cadherin is also expressed in monocyte/macrophage cells, which are precursors to osteoclasts. Receptor activator of nuclear factor-ÎşB ligand (RANKL)-stimulated osteoclast differentiation involves a period of precursor expansion followed by multiple fusion events to generate a multinucleated osteoclast. Interestingly, our results indicated that E-cadherin participated in early precursor interaction/recognition rather than during periods of osteoclast fusion. In both RAW 264.7 cells and primary murine macrophages, E-cadherin expression and surface localization was highest during early osteoclast differentiation. Utilizing E-cadherin blocking antibodies prior to the onset of fusion delayed osteoclast-specific gene expression and significantly impaired multinucleated osteoclast formation. Long-term imaging revealed that blocking E-cadherin function prolonged the proliferative phase of the precursor population while concomitantly decreasing the proportion of migrating precursors; the lamellipodium and polarized membrane extensions were identified as principal sites of fusion, establishing migration as a requirement for osteoclast differentiation. This work characterizes EB1 and E-cadherin function during osteoblast differentiation and the E-cadherin-mediated transition from proliferative to migratory activities during osteoclast differentiation. Taken together, both studies highlight the value of exploring the early intra- and intercellular events that direct osteoblast and osteoclast differentiation.Ph.D

Modulation of Osteoclastogenesis with Macrophage M1- and M2-Inducing Stimuli

<div><p>Macrophages are generated through the differentiation of monocytes in tissues and they have important functions in innate and adaptive immunity. In addition to their roles as phagocytes, macrophages can be further differentiated, in the presence of receptor activator of nuclear factor kappa-B ligand (RANKL) and macrophage colony-stimulating factor (M-CSF), into osteoclasts (multinucleated giant cells that are responsible for bone resorption). In this work, we set out to characterize whether various inflammatory stimuli, known to induce macrophage polarization, can alter the type of multinucleated giant cell obtained from RANKL differentiation. Following a four-day differentiation protocol, along with lipopolysaccharide (LPS)/interferon gamma (IFNγ) as one stimulus, and interleukin-4 (IL-4) as the other, three types of multinucleated cells were generated. Using various microscopy techniques (bright field, epifluorescence and scanning electron), functional assays, and western blotting for osteoclast markers, we found that, as expected, RANKL treatment alone resulted in osteoclasts, whereas the addition of LPS/IFNγ to RANKL pre-treated macrophages generated Langhans-type giant cells, while IL-4 led to giant cells resembling foreign body giant cells with osteoclast-like characteristics. Finally, to gain insight into the modulation of osteoclastogenesis, we characterized the formation and morphology of RANKL and LPS/IFNγ-induced multinucleated giant cells.</p></div

Characterization of the ultrastructural differences of the various MGCs.

<p>Representative scanning electron microscopy images of the generated day 4 MGCs. Scale bars represent 50(middle-top and middle-bottom, respectively).</p

Resorption ability of generated MGCs.

<p>RAW 264.7 macrophages were plated and differentiated on Osteo Assay Surface plates. At the end of the assay, the MGCs were assessed on their ability to resorb the substrate throughout the protocol. (A) Two representative images of resorption pits by the various treated MGCs. (B) Quantification of resorption area (mean ± standard deviation of 3 independent assays) as determined by percentage resorbed versus total area. * indicates <i>p</i><0.001, ** indicates <i>p</i><0.01, and *** indicates <i>p</i><0.05 (<i>ANOVA</i>).</p

Golgi and stable microtubules are found at the periphery of RANKL+ LPS/IFNγ induced MGCs.

<p>(A) Representative images of day 4 MGCs treated with LPS/IFNγ and stained for GM130, a Golgi marker (green), α-tubulin (red), and nuclei (blue). (B) Representative images of day 4 MGCs treated with LPS/IFNγ stained for acetylated α-tubulin (green), α-tubulin (red), and DNA (blue). Images shown are representative of three independent experiments. Scale bars represent 50 microns.</p

Functional assays of generated MGCs.

<p>Day 4 MGCs were assessed on their ability to undergo phagocytosis of IgG-opsonized sheep red blood cells (IgG-sRBCs) and on their ability to produce TRAP. (A) Representative images of cells after phagocytosis assay (see <a href="http://www.plosone.org/article/info:doi/10.1371/journal.pone.0104498#s2" target="_blank">Methods</a>). IgG-sRBCs are in red, F-actin in green, and DNA in blue. (B) Quantification of internalized IgG-sRBCs per 100 MGCs (mean ± standard deviation). Quantification was done on three independent experiments, with between 100–150 MGCs counted per experiment. * indicates <i>p</i><0.001 (<i>ANOVA</i>). (C) Representative images of day 4 MGCs stained for TRAP. Top panel: RAW 264.7 macrophages on glass substrate. Bottom panel: RAW 264.7 macrophages on Osteo Assay Surface. Scale bars represent 50 microns.</p

Microtubule-organizing centre movement during the differentiation of RANKL+ LPS/IFNγ-treated cells.

<p>Representative images of cells treated with RANKL and LPS/IFNγ from early Day 3 of the differentiation protocol until the end of experimentation (day 4). Cells were stained with tubulin (red) and DNA (DAPI). Images shown are representative of three independent experiments. Scale bars represent 50 microns.</p

The effects of actin cytoskeleton, microtubule network, and myosin II disruption on the morphology of LPS/IFNγ induced MGCs.

<p>Day 4 LPS/IFNγ-induced MGCs were incubated with Nocodazole (5 µM), Cytochalasin D (1 µM), Wiscostatin (10 µM), or Blebbistatin (50 µM), for 4 hours. Cells were then stained for F-actin (green), α-tubulin (red), and DNA (blue). Images shown are representative of three independent experiments. Scale bars represent 50 microns.</p