Srinivasa Rao R.,SVEC |
Journal of Computational Electronics | Year: 2012
Here we consider two popular techniques useful for time domain signature analysis of direct scattering problem i.e., given the incident waveform and the target geometry, find the scattered field. We present in this paper a comparison of two popular time domain numerical techniques, viz., the transmission line matrix (TLM) method and the finite-difference time-domain (FDTD) method for electromagnetic scattering problems. Even though there are many similarities between the two methods, the modeling philosophy is different. Whereas in FDTD Maxwell's equations are solved using a differencing scheme, in TLM a scattering approach akin to Huygens principle is implemented by replacing the space domain with a system of interconnected transmission-lines. The comparison is made via standard canonical shapes, a dielectric cube, and a dielectric sphere, to address the factors affecting accuracy, efficiency, and the required computer resources. © Springer Science+Business Media LLC 2012.
News Article | November 23, 2016
To address potential cross-regulation between phagocytes, we initially tested a panel of eleven soluble mediators that have been linked to tissue repair, inflammation dampening, and tissue morphogenesis11, for their ability to modulate engulfment by LR73 fibroblasts, a non-professional phagocytic cell line. Of the eleven factors tested, only insulin-like growth factor 1 (IGF-1) significantly dampened apoptotic cell uptake, at concentrations reported in mouse and human serum (100–600 ng ml–1)12 (Fig. 1a, b). Other factors such as EGF, FGF2, VEGF, PDGF-AA and PDGF-BB did not alter phagocytic activity over a range of concentrations (Extended Data Fig. 1a), although each elicited early downstream signalling events (Extended Data Fig. 1b–e). The engulfment-dampening effect of IGF-1 was also seen with airway epithelial cell lines BEAS-2B and 16HBE14o-, and the endothelial cell line SVEC-40 (Fig. 1c, Extended Data Fig. 1f, g). The IGF-1 effect was not due to masking phosphatidylserine (PtdSer) on the apoptotic cells (Fig. 1d). LR73 cells express the IGF-1 receptor (IGF-1R), and IGF-1 treatment elicited phosphorylation of Akt, a signalling molecule downstream of IGF-1R (Fig. 1b). In blood, IGF-1 is bound to IGF-binding proteins (IGFBPs) that stabilize and sequester IGF-1 (ref. 13). Addition of IGFBP3 with IGF-1 restored the phagocytic capability of LR73 cells (Fig. 1e), suggesting that binding of active IGF-1 to IGF-1R was necessary. A neutralizing antibody against the human IGF-1R reversed the engulfment-dampening effect of IGF-1 on BEAS-2B cells (Fig. 1f). Further, OSI-906 (a small molecule kinase inhibitor of IGF-1R currently tested in clinical trials) and the inhibitor NVP-AEW541 rescued the engulfment capacity of LR73 cells treated with IGF-1, with concomitant decrease in phosphorylation of IGF-1R and Erk (Fig. 1g, Extended Data Fig. 2a). IGF-II and insulin, which share structural similarity with IGF-1 but have lower affinities for IGF-1R13, could also reduce apoptotic cell uptake (Extended Data Fig. 2b, c), albeit at higher concentrations. Thus, productive signalling through the IGF-1R is necessary for IGF-1 to dampen apoptotic cell uptake. In contrast to the inhibitory effect on apoptotic cell uptake, IGF-1 enhanced the uptake of PtdSer-containing liposomes of 150–200 nm in size (Fig. 1h). This was not seen with EGF or VEGF. IGF-1 enhancement required IGF-1R signalling, as the inhibitor OSI-906 reduced the increased liposome uptake (Fig. 1i). Thus, IGF-1 can redirect phagocytosis by non-professional phagocytes, suppressing uptake of larger apoptotic cells and enhancing internalization of smaller particles. The IGF-1 effect was reversible, as washing phagocytes that were pre-treated with IGF-1 resulted in near-complete restoration of phagocytic activity (Fig. 1j). The effect of IGF-1 on phagocytes was also rapid, as adding IGF-1 simultaneously with apoptotic cells inhibited engulfment in a similar manner as that seen with the pre-treated cells (data not shown), which suggests IGF-1 interferes with early step(s) during phagocytosis. Blocking certain early signalling pathways downstream of IGF-1R, such as Akt, mTOR, Erk or PI3-kinase14, did not rescue the IGF-1-mediated decrease in apoptotic cell uptake (Extended Data Fig. 3a–d). Although IGF-1 can activate RhoA, which is known to decrease apoptotic cell engulfment15, inhibition of RhoA-mediated signalling did not reverse the suppression of IGF-1-mediated engulfment (Extended Data Fig. 3e, f). Overexpressing activated Rac1 (which promotes apoptotic cell engulfment16, 17) bypassed attenuation of apoptotic cell uptake (Fig. 1k), suggesting that IGF-1R acts at or before a step regulated by active Rac1. As apoptotic cell uptake requires both Rac1-dependent actin polymerization and de-polymerization18, we explored actin regulation via IGF-1. Cytochalasin D (cytoD), which promotes actin depolymerization, potently inhibited phagocytosis of apoptotic cells3 (data not shown). Although cytoD did not affect the basal uptake of liposomes by LR73 cells, it blocked the IGF-1-induced increase in liposome uptake (Fig. 1l). Notably, cytoD-treated LR73 cells appeared morphologically normal for the duration of the assay. Latrunculin A, which promotes actin depolymerization through a different mechanism, also reversed IGF-1-mediated enhancement of liposome uptake, without affecting the basal uptake of liposomes (Fig. 1m). Additionally, Arp2/3 complex can regulate phagocytosis through the formation of branched actin networks; however, CK-666, a small molecule inhibitor of Arp2/3, had minimal effect on the IGF-1-mediated increase of liposome uptake (Extended Data Fig. 3g). Collectively, IGF-1-mediated modulation of phagocytosis involves rapid and reversible modification of F-actin/G-actin dynamics, but probably not Arp2/3-mediated functions. We next tested the effect of IGF-1 on professional phagocytes. Adding IGF-1 to the macrophage cell lines J774 or IC-21, or primary macrophages (bone-marrow-derived or resident peritoneal macrophages), did not affect apoptotic cell uptake, even with supra-physiological concentrations of IGF-1, at every time point analysed (Fig. 1n–p, Extended Data Fig. 4a, d). Peritoneal macrophages exposed to IGF-1 also had comparable liposome uptake as control-treated cells (Fig. 1q). Importantly, IGF-1R expression was confirmed in all macrophage cell types analysed (Extended Data Fig. 4c) and IGF-1 initiated early signalling in macrophages, as assessed by IGF-1R and Akt phosphorylation (Fig. 1n, Extended Data Fig. 4a). These data suggest that IGF-1-mediated modulation of phagocytosis does not extend to macrophages. High levels of serum IGF-1 is linked to IGF-1 production in the liver, but macrophages can also produce IGF-1 in response to the cytokine IL-4 (ref. 19), raising the possibility that within a tissue, IGF-1 release from macrophages could regulate nearby non-professional phagocytes. We first confirmed IGF-1 secretion by peritoneal macrophages treated with IL-4 (Fig. 2a). Furthermore, resident peritoneal macrophages exposed to apoptotic Jurkat cells (but not live cells) produced IGF-1 (Fig. 2a). IGF-1 protein induction appears to be from newly transcribed Igf1 mRNA (Extended Data Fig. 5a). Macrophage-produced IGF-1 could also suppress apoptotic cell uptake by LR73 cells, and this was reversed by addition of IGFBP3 (Fig. 2b). We chose to examine lung tissue to investigate in vivo communication between phagocytes, as alveolar macrophages and airway epithelial cells reside in close proximity, and both engulf apoptotic cells3. Alveolar macrophages, similar to resident peritoneal macrophages, are derived from fetal monocytes20, and are readily isolated through CD11c+Siglec F+ expression, whereas the airway epithelial cells can be isolated and tracked with available genetic tools3. IGF-1R expression was prominent in the airway epithelial cells (Extended Data Fig. 5b, c), but was also detectable at lower levels in alveolar macrophages. To test the effect of IGF-1 in vivo, we used mice in which airway epithelial cells are specifically marked by yellow fluorescence protein (YFP). When apoptotic cells or liposomes were administered intranasally with IGF-1 (Fig. 2c), YFP+ airway epithelial cells had decreased apoptotic cell engulfment, but enhanced liposome uptake (Fig. 2d, e). Importantly, lung macrophages from the same IGF-1-treated mice were unaffected in their ability to engulf these targets (Fig. 2d, e). Thus, IGF-1 can differentially affect engulfment by professional and non-professional phagocytes that reside nearby in the same tissue. We next examined IGF-1 release by alveolar macrophages in vivo. Intranasal administration of IL-4 or apoptotic Jurkat cells resulted in an increased level of IGF-1 in the bronchoalveolar lavage (BAL) fluid (Fig. 2f). When we tested IL-13 or IL-5 (cytokines linked to lung homeostasis and inflammation21), IL-13 (whose receptor shares a common subunit with the IL-4R), but not IL-5, induced IGF-1 production (Fig. 2f). As the source of IGF-1 is difficult to distinguish in these experiments, we generated LysM-Cre/Igf1fl/fl mice, which express Cre under the control of the endogenous LysM (also known as Lyz2) promoter, and target IGF-1 deletion in the myeloid lineage. LysM-Cre/Igf1fl/fl mice showed loss of Igf1 mRNA in alveolar macrophages (Extended Data Fig. 5d) and IGF-1 induction after treatment with IL-4, IL-13 or apoptotic cells (Fig. 2g). This suggested that the macrophage/myeloid population is the predominant source of inducible IGF-1 in the lung. To investigate IGF-1–IGF-1R signalling in inflammation, we used a model of airway inflammation induced by the allergen house dust mite (HDM)21, where apoptotic cell recognition by airway epithelial cells influences inflammation3. We administered HDM intranasally in the allergen sensitization and challenge stage, modelling the natural route of allergen encounter (Fig. 3a). When we first tested LysM-Cre/Igf1fl/fl mice, these mice proved unsuitable, as we continued to detect variable levels of IGF-1 in the BAL fluid after HDM administration (probably owing to leakage of serum IGF-1 during inflammation). Therefore, we targeted instead IGF-1R on the epithelial cells. We crossed Igf1rfl/fl mice with CCSP-rtTA/tetO-Cre transgenic mice (see Methods), the latter driving Cre under the Club cell secretory protein (CCSP; also known as Scgb1a1) promoter in the epithelial cells of the trachea, bronchi and bronchioles. This CCSP-rtTA/tetO-Cre strain allows for inducible Cre expression through doxycycline administration through drinking water, thereby allowing normal development and gene deletion just before allergen exposure. We observed near-complete loss of IGF-1R on epithelial cells of CCSP-Cre/Igf1rfl/fl mice after doxycycline treatment (Fig. 3b). After sensitization and challenge with low-endotoxin HDM, the CCSP-Cre/Igf1rfl/fl mice had greater airway inflammation based on several parameters. (1) There was marked increase in eosinophils and CD4+ T cells in the BAL fluid (Fig. 3c) and trending increase in inflammatory cells in the lungs (Extended Data Fig. 6a). (2) Lung-draining lymph nodes were larger and contained more CD4+ T cells (Fig. 3d). (3) Lung sections showed increased peribronchial and perivascular cellular infiltration (Fig. 3e, f) and greater mucus accumulation after HDM treatment (Fig. 3g, h). (4) HDM-treated CCSP-Cre/Igf1rfl/fl mice displayed increased airway reactivity after methacholine challenge, a measure of the bronchial hyper-responsiveness (Extended Data Fig. 6b). There were more apoptotic cells in lung sections (cleaved caspase 3 staining) in HDM-treated CCSP-Cre/Igf1rfl/fl mice, probably owing to greater inflammation (Extended Data Fig. 6c). These data suggested a requirement for IGF-1R in the airway epithelial cells in minimizing inflammation in this model. These observations were initially surprising, as we expected the loss of IGF-1R on airway epithelial cells to improve apoptotic cell clearance and thereby attenuate, rather than worsen, inflammation. This prompted us to examine the temporal requirement of IGF-1–IGF-1R signalling in epithelial cells during allergen exposure. To distinguish the requirement for IGF-1–IGF-1R signalling at the sensitization versus challenge phase, we administered doxycycline at different times: deleting IGF-1R expression before allergen sensitization (Fig. 4a), or after the initial allergen sensitization but before the challenge phase (Extended Data Fig. 7a). Mice with IGF-1R deletion before allergen sensitization showed a significant increase in inflammatory parameters (Fig. 4b), whereas deletion of IGF-1R after the sensitization phase had minimal effect on disease severity (Extended Data Fig. 7b, c). Airway epithelial cells that encounter allergens can produce cytokines, such as TSLP and CSF-2/GM-CSF (that affect dendritic cell maturation), as well as IL-33 and IL-25 that drive type-2 innate lymphoid cells (ILC2s) to proliferate and produce IL-13 (ref. 21). Human bronchial epithelial cells from individuals with asthma produce elevated levels of IL-6, IL-8, and CSF-2 (ref. 22), and TSLP released from airway epithelial cells (mice and human) can exacerbate airway inflammation23. When we assessed the cytokine profile in the BAL fluid of CCSP-Cre/Igf1rfl/fl mice sensitized with HDM, levels of TSLP and IL-6 were greater (Fig. 4d, e). We did not find increased levels of IL-33, as seen with Rac1 deletion in airway epithelial cells3, but this may be due to differences in inflammatory pathways regulated by the loss of IGF-1R rather than Rac1. These results suggest that IGF-1R in airway epithelial cells limits inflammatory cytokines during the initial antigen exposure/sensitization phase. Regarding trigger(s) for IGF-1 release from the alveolar macrophages in the sensitization phase, although IL-4 is often considered a classic T 2 cytokine from the adaptive immune response21, both IL-4 (refs 24, 25) and IL-13 (ref. 21) can be produced during the allergen sensitization phase by resident mast cells, basophils, and/or ILC2s. In fact, IL-4 was enhanced (along with IL-5 and eotaxin-1) in the BAL fluid of CCSP-Cre/Igf1rfl/fl mice sensitized with HDM (Fig. 4c). Thus, IL-4 and/or apoptotic cells present during the initial allergen exposure could elicit IGF-1 production from alveolar macrophages. Alveolar macrophages are reported to release microvesicles containing anti-inflammatory mediators during smoking-induced lung injury26. As IGF-1 enhances liposome uptake by airway epithelial cells, we tested whether microvesicles from alveolar macrophages may affect airway epithelial cell response to HDM. Using differential centrifugation and filtration, we isolated and characterized microvesicles from alveolar macrophages (Fig. 4f). Negative stain and cryo-electron microscopy revealed membrane-bound spherical structures >100 nm in diameter (Fig. 4g, h). Through ImagestreamX analysis, we determined that the particles from an alveolar macrophage cell line or primary mouse alveolar macrophages carried markers of lung macrophage origin, CD11c or Siglec F, with variable Annexin V staining (Fig. 4i). Tunable resistive pulse sensing analysis of microvesicles revealed a mean particle size of 357 ± 148.5 nm (Fig. 4j), within the reported 100–1,000 nm range for microvesicles27. Further, IL-4 treatment of macrophages increased microvesicles secretion (Extended Data Fig. 8a). In addition, uptake of these microvesicles by BEAS-2B airway epithelial cells was enhanced by IGF-1 (Fig. 4k). Notably, adding alveolar macrophage-derived microvesicles to HDM-treated BEAS-2B cells resulted in significantly lower TSLP, CSF2, IL6, and IL8 induction (Fig. 4l). To further explore this, we performed RNA-seq of BEAS-2B cells treated with HDM ± microvesicles. Whereas HDM treatment increased several known genes associated with asthma in humans28, 29, 30, such as FGF2, KLF4, IFIT2, and PTX3, adding microvesicles from alveolar macrophages suppressed transcription of these genes in the epithelial cells (Fig. 4m, Extended Data Fig. 8b). Thus, microvesicles released from alveolar macrophages acting on airway epithelial cells exposed to allergen could dampen airway inflammation. The data presented here provide several insights into phagocytosis and tissue inflammation. It has long been known that professional and non-professional phagocytes reside in proximity and can engulf dying cells and debris, yet communication between these phagocytes was not understood. The data presented here identifies a rapid, transient, and reversible regulation, wherein soluble IGF-1 from macrophages influences the type of particle taken up by epithelial cells. This transient effect might allow the macrophages to temporarily ‘redirect’ the non-professional phagocytes towards other function(s). Such a possible hierarchy in cell clearance could provide temporal and spatial cross-communication within a given tissue9. Our data identifies a two-part regulation of epithelial cells by macrophages that affects airway inflammation, that is, the secretion of IGF-1 redirects particle uptake, and the release of microvesicles dampens inflammatory cytokine production by epithelial cells (Extended Data Fig. 9). IGF-1 is a growth factor widely linked to growth, cellular proliferation, and ageing. Global IGF-1 deletion in mice results in dwarfism and perinatal lethality, and IGF-1 mutations are linked to human diseases13. This work identifies a previously unappreciated biological function for the IGF-1–IGF-1R signalling axis as a modulator of airway hyper-responsiveness to allergens with potential therapeutic relevance.
Dhanalakshmi P.,Computer Science and Engineering |
Ramani K.,SVEC |
Proceedings - 6th International Advanced Computing Conference, IACC 2016 | Year: 2016
The increased on-line applications are leading to exponential growth of the web content. Most of the business organizations are interested to know the web user behavior to enhance their business. In this context, users navigation in static and dynamic web applications plays an important role in understanding user's interests. The static mining techniques may not be suitable as it is for dynamic web log files and decision making. Traditional web log preprocessing approaches and weblog usage patterns have limitations to analyze the content relationship with the browsing history This paper, focuses on various static web log preprocessing and mining techniques and their applicable limitations for dynamic web mining. © 2016 IEEE.
Rupesh B.,SVEC |
Sunil Kumar M.,SVEC
International Journal of Applied Engineering Research | Year: 2015
Keyword queries based on database gives an solution to data. Even though it suffers due to low ranking quality. So, a database provides best alternatives to such type of hard queries. The characteristics of hard keyword queries over Relational Databases are analyzed for the novel composition to evaluate the amount of problems, and content of the Relational Databases is proposed and then hard keyword query prediction is evaluated against INEX and SemSearch benchmarks. In this work the hard keyword queries over Relational Databases is predicted by using Structured Robustness algorithm with Skyline Sweeping Algorithm and Joined Tuple Tree Technique. © Research India Publications
Deepika S.,SVEC |
International Journal of Applied Engineering Research | Year: 2015
Geo-social applications are most commonly used in which different communities integrate together with their surrounding environment through their friends and their recommendations. Such systems can be misused easily through various attacks. Hence providing privacy to the geo-social applications became main issue. The existed system, LocX, that provides significant improving location privacy by not adding uncertainty into the query results or rely on strong assumptions about security of the server. Here user send message to other user is of bigger size, so that the expense of the server database increases on existing system. Therefore compression algorithm is proposed to compress the message by that the message retrieval time reduces than the existed system. This method provides privacy and improves the performance of geo-social applications. © Research India Publications.
Vijayarekha K.,SVEC |
Madhusudana Rao C.,SVEC
International Journal of Applied Engineering Research | Year: 2015
In IEEE 802.11n an aggregate medium access control (MAC) service data unit (A_MSDU) contains multiple sub frames with a single sequence number. It has a major drawback in environment with high error rate because if any sub frames are corrupted then the entire A_MSDU will be lost, which results decrease in throughput. In AFR (aggregation frame retransmission) scheme retransmission is done only for packets which are erroneous but retransmission delay is not measured.In this paper retransmission delay is minimized which in turn reduces the end-end delay. A performance evaluation is made by calculating the retransmission delay which improves performance of IEEE 802.11. © Research India Publications.
Mudadla D.,SVEC |
Sandeep N.,National Institute of Technology Karnataka |
4th IEEE Sponsored International Conference on Computation of Power, Energy, Information and Communication, ICCPEIC 2015 | Year: 2015
The performance of multilevel inverter is high compared to the classical two level inverters owing to their reduced total harmonic distortion, and lower electromagnetic interference. However the setbacks of multilevel inverter are increased number of power devices, complex PWM and gating circuitry. In this paper, a new multilevel inverter topology, capable of generating large number of levels with fewer number of power switches, gating circuits and power diodes is proposed. In contrast to classical multilevel topologies, the presented topology consequences in reduction of the number of power devices and conduction losses. The proposed topology is asymmetrical, employing isolated dc sources of voltage ratio 421 (Binary fashion). Staircase control PWM at fundamental frequency is employed for the gating of power switches makes it suitable in applications like flexible alternative current transmission systems (FACTS), renewable energy sources, drives control and vehicle propulsion system. The structure of the proposed inverter is modular and thus best suited for PV applications. Detailed simulation is carried out using MATLAB/SIMULINK platform and simulation results are presented. © 2015 IEEE.
Babu K.D.,SVEC |
Kumar D.G.,SVEC |
Proceedings of the 12th ACM International Conference on Computing Frontiers, CF 2015 | Year: 2015
Optimal resource utilization is one of the biggest challenges for executing tasks within the cloud. The resource provider is responsible for providing the resources by creating virtual machines for executing task over a cloud. To utilize the resources optimally, the resource provider has to take care of the process of allocating resources to Virtual Machine Manager (VMM). In this paper, an efficient way to utilize the resources, within the cloud, has been proposed consid-ering remaining resources should be maximum at a single machine but not distributed. As a framework to virtual re-source mapping, a Simple Genetic Algorithm is applied to solve the heuristic of allocating problem. We may also use conversion of multiple parameters into single equivalent pa-rameter so that number of inputs and comparisons will be reduced. © Copyright 2015 ACM.
Kartheek D.N.,SVEC |
Amarnath G.,SVEC |
Venkateswarlu Reddy P.,SVEC
Proceedings - 2013 IEEE International Multi Conference on Automation, Computing, Control, Communication and Compressed Sensing, iMac4s 2013 | Year: 2013
Most cryptographic mechanisms such as symmetric and asymmetric cryptography, often involve the use of cryptographic keys. However, all cryptographic techniques will be ineffective if the key distribution mechanism is weak. Quantum Key Distribution or Quantum Cryptography is attracting much attention as a solution of the problem of Key Distribution; QKD offers unconditionally secure communication based on quantum mechanics. This work presents quantum key distribution protocols (QKDP) to safeguard security i n large networks, ushering in new directions in classical cryptography and quantum cryptography. © 2013 IEEE.
Narendra Kumar Rao B.,SVEC |
Ramamohan Reddy A.,SVEC
2012 3rd International Conference on Computing, Communication and Networking Technologies, ICCCNT 2012 | Year: 2012
Case-based reasoning is an approach to problem solving and learning that has got a lot of attention over the last few years. This paper provides an overview of the foundational issues related to case-based reasoning, describing some of the leading methodological approaches within the field, and exemplifying the current state through pointers to some systems. The framework influences the recent methodologies for knowledge level descriptions of intelligent systems. The methods for case retrieval reuse, solution testing, and learning are summarized, and realization is discussed with few example systems that represent different CBR approaches. Regression testing occurs during the maintenance stage of the software life cycle, however, it requires large amounts of test cases to assure the attainment of a certain degree of quality. So, test suite sizes may grow significantly. This paper focuses primarily on application of CBR to test suite optimization. © 2012 IEEE.