188 research outputs found

    First person – Shweta Yadav

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    ABSTRACT First Person is a series of interviews with the first authors of a selection of papers published in Journal of Cell Science, helping early-career researchers promote themselves alongside their papers. Shweta Yadav is the first author on ‘RDGBα localization and function at membrane contact sites is regulated by FFAT–VAP interactions’, published in Journal of Cell Science. Shweta is a post-doctoral associate in the laboratory of Prof. Juan Botas at Baylor College of Medicine, Texas, USA, investigating neurodegenerative diseases.</jats:p

    The social correlates of value consensus

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    This paper examines societal value consensus, or the extent to which individuals within a culture share similar values. This topic has been extensively theoretically discussed, but has received limited empirical attention. This paper explores the social variables of economic equality, religiosity and religious homogeneity and their relation to value consensus. Publicly available data from the latest wave of World Values Survey (N = 73,256), CIA world factbook and the World Bank World Development Indicators are used for analysis. Results reveal that value consensus is not correlated with religiosity, religious homogeneity or economic equality. Implications of these findings, with specific reference to economic developmental theories are discussed.M.A.Includes bibliographical referencesby Shweta A. Kulkarn

    Adaptive geolocation based interference control for hierarchical cellular network with femtocells

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    This thesis presents adaptive interference control methods to mitigate undesirable interference effects from femtocells to macrocell users in hierarchical cellular networks. The study in this thesis begins by quantifying the deterioration in performance experienced by macrocell users on the downlink in a simulated 3G/CDMA environment. Our baseline results show that the median deterioration in signal-to-interference plus noise ratio (SINR) observed for the macrocell users may be up to 10dB and the outage probability increases by large extend. In the next part of study, we propose interference mitigation schemes - ‘Proximity Based Iterative’ (PBI) scheme and ‘Adaptive Interference Scaling’ (AIS) scheme to adjust femtocell power to reduce femtocell interference effect on macrocell users. We show that previously studied mechanisms like the load-spillage, utility based power adaptation usually require relatively high system overhead due to over-the-air signalling for estimation of interference. Proposed PBI and AIS schemes avoid such over-the-air signalling and make use of geo-location information and backhaul signalling for the femtocell interference estimation. These schemes achieve power re-distribution by scaling power uniformly across femtocells, while allowing the network operators to set desired target data rates. Results from simulations show that the PBI and AIS schemes are able to increase the number of macrocell users achieving chosen target data rates by up to 158% when compared with the value when femtocell transmission power is at maximum. However, in case of the PBI scheme, results shows that 25% of femtocell users may receive rates below the target rate. The AIS scheme provides an improvement over the PBI scheme by adjusting femtocell power according to the interference contribution by each femtocell. Thus, AIS achieves better performance and only up to 12:2% of femtocell users receive rates below the target rate. This study concludes with parametric evaluation of system throughput as a function of both macrocell and femtocell user densities. Qualitative results are provided to support the conclusion.M.S.Includes bibliographical referencesby Shweta Sagar

    Roll-Call: an energy efficient radio frequency identification system.

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    In this thesis, we investigate two of the major challenges in pervasive systems: energy efficiency and co-existence of uncoordinated wireless messages by exploring the design of a Radio Frequency Identification (RFID) system intended to support the simultaneous and real time monitoring of thousands of entities. These entities, which may be individuals or inventory items, each carry a low-power transmit-only tag and are monitored by a collection of networked base-stations reporting to a central database. We have built a customized transmit-only tag with a small form-factor, and have implemented a real-time monitoring application intended to verify the presence of each tag in order to detect potential disappearance of a tag (perhaps due to item theft). Throughout the construction of our system, we have carefully engineered it for extended tag lifetime and reliable monitoring capabilities in the presence of packet collisions, while keeping the tags small and inexpensive. The major challenge in this architecture (called Roll-Call) is to supply the energy needed for long range continuous tracking for a year or more of reporting once a second while keeping the tags (called PIPs) small and inexpensive. We have used this as a model problem for optimizing cost, size and lifetime across the entire pervasive, persistent system from firmware to protocol.M.S.Includes bibliographical references (p. 46-48)

    Molecular Responses of Nicotiana glutinosa to Infection to Lettuce necrotic yellows virus

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    Lettuce necrotic yellows virus (LNYV), a cytorhabdovirus endemic to Australia and New Zealand, comprises two subgroups: subgroup I (SI) and subgroup II (SII). SI has seemingly become extinct in Australia, potentially outcompeted by SII. This research helps in understanding the host-virus interactions of the model species N. glutinosa with LNYV (Cytorhabdoviridae type species Cytorhabdovirus lactucanecante). This study investigates the molecular and metabolic responses of the model host to infection by each subgroup using one-step reverse transcriptase quantitative polymerase chain reaction (RT-qPCR) and gas chromatography mass spectrometry (GCMS). Gene expression analysis revealed that both LNYV subgroups induced increased accumulation of AOX1a, NPR3, and RDR1, with LNYV-SII causing weaker responses for AOX1a and RDR1. These results point to a salicylic acid-dependent response by the plant host to infection, implying that LNYV-SII may have evolved mechanisms to dampen the host’s defensive response, potentially contributing to its competitive advantage over SI. In contrast, RDR6 and CPK3 transcript levels were unaffected by LNYV infection. To support these findings, reference genes ACT, EF1α, and SAND were validated for use in LNYV-infected N. glutinosa. EF1α was found to be the most stable, followed by SAND and ACT. Metabolic profiling using GCMS demonstrated differential levels of amino acids and organic acids in LNYV-SI and LNYV-SII infected plants respectively compared to mock-inoculated plants. This increase in TCA cycle intermediates and activation of the TCA cycle pathway in SII-infected plants implies that these host plants may have low host resistance and hence require more energy to battle viral infection. Compared to SI, the host resistance to LNYV-SII seems to be limited. Higher viral loads are made possible by poor resistance, and this encourages quicker viral multiplication and more efficient vector transmission within plant populations. Common pathways affected by both subgroups included glyoxylate and dicarboxylate metabolism, the citrate cycle (TCA cycle), alanine, aspartate, and glutamate metabolism, and sulphur metabolism. However, SI infection uniquely impacted glutathione metabolism and the metabolism of glycine, histidine, serine, and threonine. Conversely, SII infection uniquely affected arginine biosynthesis and tyrosine metabolism. These combined molecular and metabolomic analyses provide a greater understanding of LNYV infection in N. glutinosa, highlighting the distinct and overlapping impacts of the two LNYV subgroups. The findings suggest that LNYV-SII’s ability to alter host defence responses and its unique metabolic impacts may explain its rapid spread and competitive displacement of LNYV-SI in Australia. This research represents a significant step towards understanding the molecular process underlying LNYV infection and offers insights into the mechanisms driving the dispersal and dominance of LNYV-SII
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