4,122 research outputs found

    Defining Measures for Location Visiting Preference

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    AbstractFor better location based service or better analysis of human mobility pattern, measures for presenting frequently visiting locations are usually required. In this paper, we will establish related measures for specific meaningful locations. Location points as well as Location clusters are objects of the measurements. In order to represent the degree of a specific location visit, the degree of location visit called Position Frequency (PF), and Inverse Location Frequency (ILF) are defined. In order to represent the degree of location area (cluster) visit, Inverse Cluster Frequency (ICF) is established. Moreover, along with the frequency of location visit, the duration of location visit is also considered. Therefore Position Duration (PD), Inverse Location Duration (ILD), and Inverse Cluster Duration (ICD) are defined. Using R language, real positioning data set collected by volunteers are analyzed in order to demonstrate the usefulness of these measures. The definitions of measures and the application of measures will be presented

    The Effect of Touch Simulation in Virtual Reality Shopping

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    This study aims to explore the effect of touch simulation on virtual reality (VR) store satisfaction mediated by VR shopping self-efficacy and VR shopping pleasure. The moderation effects of the autotelic and instrumental need for touch between touch simulation and VR store satisfaction are also explored. Participants wear a head-mounted display VR device (Oculus Go) in a controlled laboratory environment, and their VR store experience is recorded as data. All participants’ responses (n = 58) are analyzed using SPSS 20.0 for descriptive statistics, reliability analysis, exploratory factor analysis, and the Process macro model analysis. The results show that touch simulation positively influences VR store satisfaction, which is mediated by the self-efficacy and by the dual path of the self-efficacy and the pleasure. Furthermore, the relation between touch simulation and pleasure is moderated by need for touch. For individuals with a high level of autotelic need for touch, the effect of touch simulation on the pleasure is heightened. However, instrumental need for touch does not moderate the path of touch simulation on the self-efficacy

    Matrix Metalloproteinase-3 Causes Dopaminergic Neuronal Death through Nox1-Regenerated Oxidative Stress

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    In the present study we investigated the interplay between matrix metalloproteinase 3 (MMP3) and NADPH oxidase 1 (Nox1) in the process of dopamine (DA) neuronal death. We found that MMP3 activation causes the induction of Nox1 via mitochondrial reactive oxygen species (ROS) production and subsequently Rac1 activation, eventually leading to Nox1-derived superoxide generation in a rat DA neuronal N27 cells exposed to 6-OHDA. While a MMP3 inhibitor, NNGH, largely attenuated mitochondrial ROS and subsequent Nox1 induction, both apocynin, a putative Nox inhibitor and GKT137831, a Nox1 selective inhibitor failed to reduce 6-OHDA-induced mitochondrial ROS. However, both inhibitors for MMP3 and Nox1 similarly attenuated 6-OHDA-induced N27 cell death. RNAi-mediated selective inhibition of MMP3 or Nox1 showed that knockdown of either MMP3 or Nox1 significantly reduced 6-OHDA-induced ROS generation in N27 cells. While 6-OHDA-induced Nox1 was abolished by MMP3 knockdown, Nox1 knockdown did not alter MMP3 expression. Direct overexpression of autoactivated MMP3 (actMMP3) in N27 cells or in rat substantia nigra (SN) increased expression of Nox1. Selective knockdown of Nox1 in the SN achieved by adeno-associated virus-mediated overexpression of Nox1-specific shRNA largely attenuated the actMMP3-mediated dopaminergic neuronal loss. Furthermore, Nox1 expression was significantly attenuated in Mmp3 null mice treated with N-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP). Together we established novel molecular mechanisms underlying oxidative stress-mediated dopaminergic neuronal death in which MMP3 activation is a key upstream event that leads to mitochondrial ROS, Nox1 induction and eventual dopaminergic neuronal death. Our findings may lead to the development of novel therapeutic approach

    Matrix Metalloproteinase-3 Causes Dopaminergic Neuronal Death through Nox1-Regenerated Oxidative Stress

    Get PDF
    In the present study we investigated the interplay between matrix metalloproteinase 3 (MMP3) and NADPH oxidase 1 (Nox1) in the process of dopamine (DA) neuronal death. We found that MMP3 activation causes the induction of Nox1 via mitochondrial reactive oxygen species (ROS) production and subsequently Rac1 activation, eventually leading to Nox1-derived superoxide generation in a rat DA neuronal N27 cells exposed to 6-OHDA. While a MMP3 inhibitor, NNGH, largely attenuated mitochondrial ROS and subsequent Nox1 induction, both apocynin, a putative Nox inhibitor and GKT137831, a Nox1 selective inhibitor failed to reduce 6-OHDA-induced mitochondrial ROS. However, both inhibitors for MMP3 and Nox1 similarly attenuated 6-OHDA-induced N27 cell death. RNAi-mediated selective inhibition of MMP3 or Nox1 showed that knockdown of either MMP3 or Nox1 significantly reduced 6-OHDA-induced ROS generation in N27 cells. While 6-OHDA-induced Nox1 was abolished by MMP3 knockdown, Nox1 knockdown did not alter MMP3 expression. Direct overexpression of autoactivated MMP3 (actMMP3) in N27 cells or in rat substantia nigra (SN) increased expression of Nox1. Selective knockdown of Nox1 in the SN achieved by adeno-associated virus-mediated overexpression of Nox1-specific shRNA largely attenuated the actMMP3-mediated dopaminergic neuronal loss. Furthermore, Nox1 expression was significantly attenuated in Mmp3 null mice treated with N-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP). Together we established novel molecular mechanisms underlying oxidative stress-mediated dopaminergic neuronal death in which MMP3 activation is a key upstream event that leads to mitochondrial ROS, Nox1 induction and eventual dopaminergic neuronal death. Our findings may lead to the development of novel therapeutic approach

    Cancer risk in Vietnam war veterans from the Korean Vietnam war veterans’ health study cohort

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    IntroductionDuring the Vietnam War, several unknown chemicals, such as Agent Orange, were used in Vietnam by the military. Therefore, there have been continuous health concerns among the Vietnamese population and veterans exposed to these hazardous chemicals. This study aimed to investigate the risk of all cancers and also organ-specific cancers among Korean veterans of the Vietnam War.MethodsThis study used a national representative cohort that included all Korean Vietnam War veterans as the interest group, with 1:4 age-sex-region-matched general Korean citizens as the reference group, from 2002 to 2018. Age-standardized incidence ratios (SIRs) and 95% confidence intervals (CIs) were calculated for all cancers and for 31 organ-specific cancer categories based on the medical facility visit data.ResultsAn increased SIR of 1.07 (95% CI, 1.06–1.08) was observed for all cancers among the veterans. There was a significantly increased risk of cancer among 22/31 organspecific cancers, with 18 cancer categories showing a significantly higher risk than all cancers. The highest risk was observed for “malignant neoplasms of other parts of the central nervous system” (SIR, 1.71; 95% CI, 1.51–1.92).DiscussionThis study evaluated the risk of cancer among Korean Vietnam War veterans. Further studies are warranted to investigate various health determinants in the veterans as well as the Vietnamese population
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