94 research outputs found

    Reduction of handover delay in WiMAX for high mobility

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    In emerging technologies, WiMAX is identified as a cheaper replacement to mobile and wireless technologies such as 3G, 4G or any other future generation technologies and can provide highspeed data transfer over long distances and at suitable Quality of Service (QoS) at high mobility. WiMAX requires support and capacity for high mobility to avoid the loss of quality of service. The goal of faster mobility can be achieved, but WiMAX needs the support of an effective handover mechanism to ensure continuous and without any interruption in data transfer. This thesis focusses to solve the handover problem in mobile WiMAX (IEEE 802.16e and IEEE802.16m) and to find and identify the factors which directly affect the handover process. There is a range of factors which can affect the mobility process in Mobile WiMAX. The acceptable handover delay is 50 ms as per IEEE WiMAX standards (Radio-Electronics.com, 2012). This study has identified that there is a total of 16 factors which have direct and indirect effect but after detailed simulation and analysis, it has been found out that only 7 factors could be used to improve handover delay in WiMAX and that’s why the initial RIVERBED simulations tried to identify the extent of these factors which directly affect the handover delay in WiMAX. The following parameters that are directly linked to the handover success are identified are as follows: a) Link goes down faster b) Scan iteration c) Interleaving Interval d) Timeout Parameter e) Frame Duration f) Client Timeout g) Scan Duration The simulation experiments on individual factors has identified that these factors result in a minimum handover delay at specific values which are called best performing values. When these best performing values of the 7 factors were applied to single WiMAX experiment, the improvement was identified, which showed that there have been better handover delay results due to the better-received signal strength, better average delay per Second and the throughput was drastically improved. There was further need to improve the handover decisions and therefor handover algorithm was used for this purpose. The handover algorithm used was a dual trigger algorithm which improved the handover delay, but resulted in packet loss and consequently resulted in retransmissions. To solve to problem of handover delay without downgrading the WiMAX signal, a new algorithm was suggested and tested which has shown results in lowering the handover delay and increasing the signal level. The handover improvement was done in stages and therefore there was a gradual improvement in handover delay in each individual stage. The overall problem has been divided into stages considering that the solution is dependent on many factors. The development of the WiMAX model is the main issue in this research. Different types of scenarios were adopted on RIVERBED simulations to produce significant data for analysis and validation

    DataSheet1_The Long-Term Efficacy of “Social Buffering” in Artificial Social Agents: Contextual Affective Perception Matters.ZIP

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    In dynamic (social) environments, an affective state of “stress” can be adaptive and promote agent wellbeing, but maladaptive if not appropriately regulated. The presence of (and interactions with) affect-based social support has been hypothesised to provide mechanisms to regulate stress (the “social buffering” hypothesis), though the precise, underlying mechanisms are still unclear. However, the hormone oxytocin has been implicated in mediating these effects in at least two ways: by improving social appraisals and reducing the short-term release of stress hormones (i.e., cortisol), and adapting an agent’s long-term stress tolerance. These effects likely facilitate an agent’s long-term adaptive ability by grounding their physiological and behavioural adaptation in the (affective) social environment, though these effects also appear to be context-dependent. In this paper, we investigate whether two of the hypothesised hormonal mechanisms that underpin the “social buffering” phenomenon affect the long-term wellbeing of (artificial) social agents who share affective social bonds, across numerous social and physical environmental contexts. Building on previous findings, we hypothesise that “social buffering” effects can improve the long-term wellbeing of agents who share affective social bonds in dynamic environments, through regular prosocial interactions with social bond partners. We model some of the effects associated with oxytocin and cortisol that underpin these hypothesised mechanisms in our biologically-inspired, socially-adaptive agent model, and conduct our investigation in a small society of artificial agents whose goal is to survive in challenging environments. Our results find that, while stress can be adaptive and regulated through affective social support, long-term behavioural and physiological adaptation is determined by the contextual perception of affective social bonds, which is influenced by early-stage interactions between affective social bond partners as well as the degree of the physical and social challenges. We also show how these low-level effects associated with oxytocin and cortisol can be used as “biomarkers” of social support and environmental stress. For socially-situated artificial agents, we suggest that these “social buffering” mechanisms can adapt the (adaptive) stress mechanisms, but that the long-term efficacy of this adaptation is related to the temporal dynamics of social interactions and the contextual perception of the affective social and physical environments.</p

    Image1_The Long-Term Efficacy of “Social Buffering” in Artificial Social Agents: Contextual Affective Perception Matters.PNG

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    In dynamic (social) environments, an affective state of “stress” can be adaptive and promote agent wellbeing, but maladaptive if not appropriately regulated. The presence of (and interactions with) affect-based social support has been hypothesised to provide mechanisms to regulate stress (the “social buffering” hypothesis), though the precise, underlying mechanisms are still unclear. However, the hormone oxytocin has been implicated in mediating these effects in at least two ways: by improving social appraisals and reducing the short-term release of stress hormones (i.e., cortisol), and adapting an agent’s long-term stress tolerance. These effects likely facilitate an agent’s long-term adaptive ability by grounding their physiological and behavioural adaptation in the (affective) social environment, though these effects also appear to be context-dependent. In this paper, we investigate whether two of the hypothesised hormonal mechanisms that underpin the “social buffering” phenomenon affect the long-term wellbeing of (artificial) social agents who share affective social bonds, across numerous social and physical environmental contexts. Building on previous findings, we hypothesise that “social buffering” effects can improve the long-term wellbeing of agents who share affective social bonds in dynamic environments, through regular prosocial interactions with social bond partners. We model some of the effects associated with oxytocin and cortisol that underpin these hypothesised mechanisms in our biologically-inspired, socially-adaptive agent model, and conduct our investigation in a small society of artificial agents whose goal is to survive in challenging environments. Our results find that, while stress can be adaptive and regulated through affective social support, long-term behavioural and physiological adaptation is determined by the contextual perception of affective social bonds, which is influenced by early-stage interactions between affective social bond partners as well as the degree of the physical and social challenges. We also show how these low-level effects associated with oxytocin and cortisol can be used as “biomarkers” of social support and environmental stress. For socially-situated artificial agents, we suggest that these “social buffering” mechanisms can adapt the (adaptive) stress mechanisms, but that the long-term efficacy of this adaptation is related to the temporal dynamics of social interactions and the contextual perception of the affective social and physical environments.</p

    Effect of the Alkyl Chain Length of the Cation on the Interactions between Water and Ammonium-Based Ionic Liquids: Experimental and COSMO-RS Studies

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    To improve the understanding of the molecular interactions of water with tetraalkyl ammonium-based ionic liquids (ILs) such as tetra­methyl­ammonium hydroxide, tetra­ethyl­ammonium hydroxide, tetra­propyl­ammonium hydroxide, and tetra­butyl­ammonium hydroxide, thermophysical properties such as density (ρ), speed of sound (<i>u</i>), viscosity (η) and refractive index (<i>n</i><sub>D</sub>) were measured and a computational study using COSMO-RS was performed. The derived properties such as excess volumes (<i>V</i><sup>E</sup>), deviation in isentropic compressibilities (Δκ<sub><i>s</i></sub>), deviation in viscosities (Δη), and deviation in refractive indices (Δ<i>n</i><sub>D</sub>) under the same experimental conditions for these systems were also estimated. The observed <i>V</i><sup>E</sup> and Δκ<sub>s</sub> values are negative over the entire composition of ILs at all investigated temperatures, whereas Δη and Δ<i>n</i><sub>D</sub> values are positive under the same experimental conditions. These results reveal that the ammonium-based ILs significantly affect the intermolecular interactions between the solvent molecules. The computational study allows a qualitative analysis of the results in terms of the ion–dipole interactions, ion-pair formation, and hydrogen bonding between ammonium-based ILs and water

    A bioactive cycloartane triterpene from <i>Garcinia hombroniana</i>

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    <p>The dichloromethane bark extract of <i>Garcinia hombroniana</i> yielded one new cycloartane triterpene; (22<i>Z</i>,24<i>E</i>)-3<i>β</i>-hydroxycycloart-14,22,24-trien-26-oic acid (<b>1</b>) together with five known compounds: garcihombronane G (<b>2</b>), garcihombronane J (<b>3</b>), 3<i>β</i> acetoxy-9<i>α</i>-hydroxy-17,14-friedolanostan-14,24-dien-26-oic acid (<b>4</b>), (22<i>Z</i>, 24<i>E</i>)-3<i>β</i>, 9<i>α</i>-dihydroxy-17,14-friedolanostan-14,22,24-trien-26-oic acid (<b>5</b>) and 3<i>β</i>, 23<i>α</i>-dihydroxy-17,14-friedolanostan-8,14,24-trien-26-oic acid (<b>6</b>). Their structures were established by the spectral techniques of NMR and ESI-MS. These compounds together with some previously isolated compounds; garcihombronane B (<b>7</b>), garcihombronane D (<b>8</b>) 2,3’,4,5’-tetrahydroxy-6-methoxybenzophenone (<b>9</b>), volkensiflavone (<b>10</b>), 4’’-<i>O</i>-methyll-volkensiflavone (<b>11</b>), volkensiflavone-7-<i>O</i>-glucopyranoside (<b>12</b>), volkensiflavone-7-<i>O</i>-rhamnopyranoside (<b>13</b>), Morelloflavone (<b>14</b>), 3’’-<i>O</i>-methyl-morelloflavone (<b>15</b>) and morelloflavone-7-<i>O</i>-glucopyranoside (<b>16</b>) were evaluated for cholinesterase enzymes inhibitory activities using acetylcholinesterase and butyrylcholinesterase. In these activities, compounds <b>1–9</b> showed good dual inhibition on both the enzymes while compounds <b>10–16</b> did not reasonably contribute to both the cholinesterases inhibitory effects.</p

    MODELIMG CROP PATTEN SYSTEM USING LINEAR PROGRAMMING

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    <p>In agricultural situations, farmers usually faced with the problem of how to allocate their<br>limited production resources among cropping and livestock activities. Farmer's planners can offer<br>effective techniques, such as linear programming (lp) to address the problem and produce optimal<br>solution. In this paper we have demonstrated that how a farmer who has limited resources such as farmers<br>availability ,storage capacity and availability of land can be formulated as a linear programming having<br>linear objective function with three constraints</p> <p> </p

    Activation of TGF-β Pathway by Areca Nut Constituents: A Possible Cause of Oral Submucous Fibrosis

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    <div><p>Oral submucous fibrosis (OSF) is a chronic inflammatory disease characterized by the accumulation of excess collagen, and areca nut chewing has been proposed as an important etiological factor for disease manifestation. Activation of transforming growth factor-β signaling has been postulated as the main causative event for increased collagen production in OSF. Oral epithelium plays important roles in OSF, and arecoline has been shown to induce TGF-β in epithelial cells. In an attempt to understand the role of areca nut constituents in the manifestation of OSF, we studied the global gene expression profile in epithelial cells (HaCaT) following treatment with areca nut water extract or TGF-β. Interestingly, 64% of the differentially regulated genes by areca nut water extract matches with the TGF-β induced gene expression profile. Out of these, expression of 57% of genes was compromised in the presence of ALK5 (TβRI) inhibitor and 7% were independently induced by areca nut, highlighting the importance of TGF-β in areca nut actions. Areca nut water extract treatment induced p-SMAD2 and TGF-β downstream targets in HaCaT cells but not in human gingival fibroblast cells (hGF), suggesting epithelial cells could be the source of TGF-β in promoting OSF. Water extract of areca nut consists of polyphenols and alkaloids. Both polyphenol and alkaloid fractions of areca nut were able to induce TGF-β signaling and its downstream targets. Also, SMAD-2 was phosphorylated following treatment of HaCaT cells by Catechin, Tannin and alkaloids namely Arecoline, Arecaidine and Guvacine. Moreover, both polyphenols and alkaloids induced TGF-β2 and THBS1 (activator of latent TGF-β) in HaCaT cells suggesting areca nut mediated activation of p-SMAD2 involves up-regulation and activation of TGF-β. These data suggest a major causative role for TGF-β that is induced by areca nut in OSF progression.</p> </div

    Diagrammatic representation of proposed model of OSF pathogenesis by areca nut and its constituents.

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    <p>Areca nut first comes in contact with epithelial cells where it's both the constituent, alkaloids and polyphenols acts on the epithelial cells and induces TGF-β signaling. This induced TGF-β signaling in the epithelial cells could be source of inflammation and can also diffuse into the connective tissue where it suppresses anti-fibrogenic cytokines like BMP7. In the connective tissue, areca nut acts on fibroblast cells along with TGF-β produced from the epithelium and potentiates its action in activating fibroblast cells responsible for inducing fibrosis.</p
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