Design and Implementation of Position Estimator Algorithm on Voice Coil Motor

Voice Coil Motors (VCMs) have been an inevitable element in the mechanisms that have been used for precise positioning in the applications like 3D printing., micro-stereolithography., etc. These voice coil motors translate in a linear direction and require a high accuracy position sensor that amounts for a major part in the budget. In this research work., an effort has been made to design and implement an algorithm that would predict the displacement of VCM and eliminate the need of high cost sensors. VCM was integrated with dSPACE DS1104 R&D controller via linear current amplifier (LCAM) which acts as a driver circuit for VCM. Sine input was given to VCM with various amplitude and frequency and the corresponding displacement is measured by using linear variable differential transformer (LVDT). The position estimator algorithm is also implemented at the same time on VCM and its output is compared with that of LVDT. It is observed that there is 97.8 % accuracy in between algorithm output and LVDT output. Further., PID controller is used in integration with the novel algorithm to minimize the error. The estimator algorithm is tested for various amplitudes and frequencies and it is found that it has a very good agreement of 99.2% with the actual displacement measured with the help of LVDT

A C3(H20) recycling pathway is a component of the intracellular complement system

An intracellular complement system (ICS) has recently been described in immune and nonimmune human cells. This system can be activated in a convertase-independent manner from intracellular stores of the complement component C3. The source of these stores has not been rigorously investigated. In the present study, Western blotting identified a band corresponding to C3 in freshly isolated human peripheral blood cells that was absent in corresponding cell lines. One difference between native cells and cell lines was the time absent from a fluid-phase complement source; therefore, we hypothesized that loading C3 from plasma was a route of establishing intracellular C3 stores. We found that many types of human cells specifically internalized C3(H(2)O), the hydrolytic product of C3, and not native C3, from the extracellular milieu. Uptake was rapid, saturable, and sensitive to competition with unlabeled C3(H(2)O), indicating a specific mechanism of loading. Under steady-state conditions, approximately 80% of incorporated C3(H(2)O) was returned to the extracellular space. These studies identify an ICS recycling pathway for C3(H(2)O). The loaded C3(H(2)O) represents a source of C3a, and its uptake altered the cytokine profile of activated CD4(+) T cells. Importantly, these results indicate that the impact of soluble plasma factors should be considered when performing in vitro studies assessing cellular immune function

Human surfactant protein D alters oxidative stress and HMGA1 expression to induce p53 apoptotic pathway in eosinophil leukemic cell line

This article is made available through the Brunel Open Access Publishing Fund. Copyright: © 2013 Mahajan et al. This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.Surfactant protein D (SP-D), an innate immune molecule, has an indispensable role in host defense and regulation of inflammation. Immune related functions regulated by SP-D include agglutination of pathogens, phagocytosis, oxidative burst, antigen presentation, T lymphocyte proliferation, cytokine secretion, induction of apoptosis and clearance of apoptotic cells. The present study unravels a novel ability of SP-D to reduce the viability of leukemic cells (eosinophilic leukemic cell line, AML14.3D10; acute myeloid leukemia cell line, THP-1; acute lymphoid leukemia cell lines, Jurkat, Raji; and human breast epithelial cell line, MCF-7), and explains the underlying mechanisms. SP-D and a recombinant fragment of human SP-D (rhSP-D) induced G2/M phase cell cycle arrest, and dose and timedependent apoptosis in the AML14.3D10 eosinophilic leukemia cell line. Levels of various apoptotic markers viz. activated p53, cleaved caspase-9 and PARP, along with G2/M checkpoints (p21 and Tyr15 phosphorylation of cdc2) showed significant increase in these cells. We further attempted to elucidate the underlying mechanisms of rhSP-D induced apoptosis using proteomic analysis. This approach identified large scale molecular changes initiated by SPD in a human cell for the first time. Among others, the proteomics analysis highlighted a decreased expression of survival related proteins such as HMGA1, overexpression of proteins to protect the cells from oxidative burst, while a drastic decrease in mitochondrial antioxidant defense system. rhSP-D mediated enhanced oxidative burst in AML14.3D10 cells was confirmed, while antioxidant, N-acetyl-L-cysteine, abrogated the rhSP-D induced apoptosis. The rhSP-D mediated reduced viability was specific to the cancer cell lines and viability of human PBMCs from healthy controls was not affected. The study suggests involvement of SP-D in host’s immunosurveillance and therapeutic potential of rhSP-D in the eosinophilic leukemia and cancers of other origins.Department of Biotechnology, Indi

Ocean mass, sterodynamic effects, and vertical land motion largely explain US coast relative sea level rise

© The Author(s), 2021. This article is distributed under the terms of the Creative Commons Attribution License. The definitive version was published in Harvey, T., Hamlington, B. D., Frederikse, T., Nerem, R. S., Piecuch, C. G., Hammond, W. C., Blewitt, G., Thompson, P. R., Bekaert, D. P. S., Landerer, F. W., Reager, J. T., Kopp, R. E., Chandanpurkar, H., Fenty, I., Trossman, D. S., Walker, J. S., & Boening, C. W. Ocean mass, sterodynamic effects, and vertical land motion largely explain US coast relative sea level rise. Communications Earth & Environment, 2(1), (2021): 233, https://doi.org/10.1038/s43247-021-00300-w.Regional sea-level changes are caused by several physical processes that vary both in space and time. As a result of these processes, large regional departures from the long-term rate of global mean sea-level rise can occur. Identifying and understanding these processes at particular locations is the first step toward generating reliable projections and assisting in improved decision making. Here we quantify to what degree contemporary ocean mass change, sterodynamic effects, and vertical land motion influence sea-level rise observed by tide-gauge locations around the contiguous U.S. from 1993 to 2018. We are able to explain tide gauge-observed relative sea-level trends at 47 of 55 sampled locations. Locations where we cannot explain observed trends are potentially indicative of shortcomings in our coastal sea-level observational network or estimates of uncertainty.The research was carried out in part at the Jet Propulsion Laboratory, California Institute of Technology, under a contract with the National Aeronautics and Space Administration. C.G.P. was supported by NASA grant 80NSSC20K1241. B.D.H., T.C.H., and T.F. were supported by NASA JPL Task 105393.281945.02.25.04.59. R.E.K. and J.S.W. were supported by U.S. National Aeronautics and Space Administration (grants 80NSSC17K0698, 80NSSC20K1724 and JPL task 105393.509496.02.08.13.31) and U.S. National Science Foundation (grant ICER-1663807). P.R.T. acknowledges financial support from the NOAA Global Ocean Monitoring and Observing program in support of the University of Hawaii Sea Level Center (NA11NMF4320128). The ECCO project is funded by the NASA Physical Oceanography; Modeling, Analysis, and Prediction; and Cryosphere Programs

Local complement activation is associated with primary graft dysfunction after lung transplantation

BACKGROUNDThe complement system plays a key role in host defense but is activated by ischemia/reperfusion injury (IRI). Primary graft dysfunction (PGD) is a form of acute lung injury occurring predominantly due to IRI, which worsens survival after lung transplantation (LTx). Local complement activation is associated with acute lung injury, but whether it is more reflective of allograft injury compared with systemic activation remains unclear. We proposed that local complement activation would help identify those who develop PGD after LTx. We also aimed to identify which complement activation pathways are associated with PGD.METHODSWe performed a multicenter cohort study at the University of Pennsylvania and Washington University School of Medicine. Bronchoalveolar lavage (BAL) and plasma specimens were obtained from recipients within 24 hours after LTx. PGD was scored based on the consensus definition. Complement activation products and components of each arm of the complement cascade were measured using ELISA.RESULTSIn both cohorts, sC4d and sC5b-9 levels were increased in BAL of subjects with PGD compared with those without PGD. Subjects with PGD also had higher C1q, C2, C4, and C4b, compared with subjects without PGD, suggesting classical and lectin pathway involvement. Ba levels were higher in subjects with PGD, suggesting alternative pathway activation. Among lectin pathway-specific components, MBL and FCN-3 had a moderate-to-strong correlation with the terminal complement complex in the BAL but not in the plasma.CONCLUSIONComplement activation fragments are detected in the BAL within 24 hours after LTx. Components of all 3 pathways are locally increased in subjects with PGD. Our findings create a precedent for investigating complement-targeted therapeutics to mitigate PGD.FUNDINGThis research was supported by the NIH, American Lung Association, Children\u27s Discovery Institute, Robert Wood Johnson Foundation, Cystic Fibrosis Foundation, Barnes-Jewish Hospital Foundation, Danish Heart Foundation, Danish Research Foundation of Independent Research, Svend Andersen Research Foundation, and Novo Nordisk Research Foundation

Reprogramming alveolar macrophage responses to TGF-β reveals CCR2+ monocyte activity that promotes bronchiolitis obliterans syndrome

Bronchiolitis obliterans syndrome (BOS) is a major impediment to lung transplant survival and is generally resistant to medical therapy. Extracorporeal photophoresis (ECP) is an immunomodulatory therapy that shows promise in stabilizing BOS patients, but its mechanisms of action are unclear. In a mouse lung transplant model, we show that ECP blunts alloimmune responses and inhibits BOS through lowering airway TGF-β bioavailability without altering its expression. Surprisingly, ECP-treated leukocytes were primarily engulfed by alveolar macrophages (AMs), which were reprogrammed to become less responsive to TGF-β and reduce TGF-β bioavailability through secretion of the TGF-β antagonist decorin. In untreated recipients, high airway TGF-β activity stimulated AMs to express CCL2, leading to CCR2+ monocyte-driven BOS development. Moreover, we found TGF-β receptor 2-dependent differentiation of CCR2+ monocytes was required for the generation of monocyte-derived AMs, which in turn promoted BOS by expanding tissue-resident memory CD8+ T cells that inflicted airway injury through Blimp-1-mediated granzyme B expression. Thus, through studying the effects of ECP, we have identified an AM functional plasticity that controls a TGF-β-dependent network that couples CCR2+ monocyte recruitment and differentiation to alloimmunity and BOS

Development and Optimization of an ELISA to Quantitate C3(H2O) as a Marker of Human Disease

Discovery of a C3(H2O) uptake pathway has led to renewed interest in this alternative pathway triggering form of C3 in human biospecimens. Previously, a quantifiable method to measure C3(H2O), not confounded by other complement activation products, was unavailable. Herein, we describe a sensitive and specific ELISA for C3(H2O). We initially utilized this assay to determine baseline C3(H2O) levels in healthy human fluids and to define optimal sample storage and handling conditions. We detected ~500 ng/ml of C3(H2O) in fresh serum and plasma, a value substantially lower than what was predicted based on previous studies with purified C3 preparations. After a single freeze-thaw cycle, the C3(H2O) concentration increased 3- to 4-fold (~2,000 ng/ml). Subsequent freeze-thaw cycles had a lesser impact on C3(H2O) generation. Further, we found that storage of human sera or plasma samples at 4°C for up to 22 h did not generate additional C3(H2O). To determine the potential use of C3(H2O) as a biomarker, we evaluated specimens from patients with inflammatory-driven diseases. C3(H2O) concentrations were moderately increased (1.5- to 2-fold) at baseline in sera from active systemic lupus erythematosus (SLE) and rheumatoid arthritis (RA) patients compared to healthy controls. In addition, upon challenge with multiple freeze-thaw cycles or incubation at 22 or 37°C, C3(H2O) generation was significantly enhanced in SLE and RA patients' sera. In bronchoalveolar lavage fluid from lung-transplant recipients, we noted a substantial increase in C3(H2O) within 3 months of acute antibody-mediated rejection. In conclusion, we have established an ELISA for assessing C3(H2O) as a diagnostic and prognostic biomarker in human diseases