Applying event-related potentials to measure consumer preferences for apparel products

By analyzing ERP waveforms generated by sensory and cognitive processing of external stimuli, the researchers attempted to observe how consumers respond emotionally to apparel products and to explain why they responded as they did. In this research, ERPs were applied to explore consumers\u27 subconscious, real-time emotional responses to apparel products. Overall, the favored shirts produced more enhanced ERP amplitude at the FZ, CA, and PZ site than the less favored shirts supporting the hypothesis. As this shows, the P3 and LPP components can be evoked by emotional visual stimuli. More positive-going ERP waves are associated with favorable and pleasant responses to the visual stimuli. Apparel companies would be able to utilize this ERP technique especially the P3 and LPP component to verify consumer preferences

What most Matters in Strengthening Educational Competitiveness?: An Application of FS/QCA Method

AbstractThis study was conducted in order to investigate the relationships between different factors affecting educational competitiveness, which is crucial to enhancing national competitiveness in every country, and to put forward policy implications whereby each country may raise the level of its educational competitiveness. PISA score was selected as an indicator representing the educational competitiveness of 22 OECD countries, and this included some independent variables, such as per capita GDP, total public expenditure on education as a percentage of GDP, and total per capita public expenditure on education (US dollars), affecting educational competitiveness. We employed the fuzzy set analysis method (FS/QCA) to analyze the complex causal relationships among the factors affecting educational competitiveness. The research results show that there are three significant combinations of variables affecting educational competitiveness (PISA score). Model 1 is a configuration of four variables (high total expenditure on education as a percentage of GDP, high total per capita expenditure on education, high ratio of private-source expenditure on education to GDP, and high GDP), and includes Netherlands, Finland, Australia, and Ireland. Model 2 is a configuration of five variables (low total expenditure on education, low total per capita expenditure on education, low ration of students to teaching staff, low private-source expenditure on education, and low GDP, and includes Poland. Model 3 is a configuration of five variables (low total expenditure on education, low total per capita expenditure on education, high private-source expenditure on education, high ratio of students to teaching staff, and high GDP), and includes Japan. Finally, the study suggests that each country should endeavour to enhance its own educational competitiveness, considering how the factors associated with this relate to each other

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

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

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

PPM1A Controls Diabetic Gene Programming through Directly Dephosphorylating PPAR?? at Ser273

Peroxisome proliferator-activated receptor gamma (PPAR gamma) is a master regulator of adipose tissue biology. In obesity, phosphorylation of PPAR gamma at Ser273 (pSer273) by cyclin-dependent kinase 5 (CDK5)/extracellular signal-regulated kinase (ERK) orchestrates diabetic gene reprogramming via dysregulation of specific gene expression. Although many recent studies have focused on the development of non-classical agonist drugs that inhibit the phosphorylation of PPAR gamma at Ser273, the molecular mechanism of PPAR gamma dephosphorylation at Ser273 is not well characterized. Here, we report that protein phosphatase Mg2+/Mn2+-dependent 1A (PPM1A) is a novel PPAR gamma phosphatase that directly dephosphorylates Ser273 and restores diabetic gene expression which is dysregulated by pSer273. The expression of PPM1A significantly decreases in two models of insulin resistance: diet-induced obese (DIO) mice and db/db mice, in which it negatively correlates with pSer273. Transcriptomic analysis using microarray and genotype-tissue expression (GTEx) data in humans shows positive correlations between PPM1A and most of the genes that are dysregulated by pSer273. These findings suggest that PPM1A dephosphorylates PPAR gamma at Ser273 and represents a potential target for the treatment of obesity-linked metabolic disorders

Prediction of the Chemical Composition and Fermentation Parameters of Fresh Coarse Italian Ryegrass Haylage Using Near Infrared Spectroscopy

Italian ryegrass (Lolium multiflorum) is an annual forage grass species which is widely cultivated in South Korea. It grows extensively in the southern part of the country and is an important component of winter forage for livestock. Each year, in Korea, over one million hectares of Italian ryegrass is converted to round bale haylage. Quality control is an important field in forage utilization research and marketing, and involves the estimation of forage nutrient content. Wet chemistry is the traditional method used to analyze the nutrient content of forage. However, this technique is often destructive, expensive, and time consuming, and it is not suitable for real-time feedstuff analysis. Near infrared spectroscopy (NIRS), on the other hand, is an alternative technique that has several major advantages over traditional methods. The analysis of silage nutrient content, using NIR, conventionally includes the drying and milling of samples. However, these processes can lead to reduction of volatile acids, which are important components of silage. NIRS can be affected by spectral regions, drying and grinding methods, particle size, packing density and the temperature of samples (Reeves and Blosser, 1991). In order to obtain accurate NIRS results, sample preparation, and the measurement conditions of the calibration set and predicted samples, need to match. The objectives of this study were to (1) assess the usefulness of NIRS in determining the nutritional composition and fermentative parameters of fresh coarse samples of Italian ryegrass haylage, (2) assess the predictive value of various NIRS calibration models, and (3) explore cost-effective and time saving methods for forage quality estimation, in field populations

Role of Neuronal NADPH Oxidase 1 in the Peri-Infarct Regions after Stroke

The molecular mechanism underlying the selective vulnerability of neurons to oxidative damage caused by ischemia-reperfusion (I/R) injury remains unknown. We sought to determine the role of NADPH oxidase 1 (Nox1) in cerebral I/R-induced brain injury and survival of newborn cells in the ischemic injured region. Male Wistar rats were subjected to 90 min middle cerebral artery occlusion (MCAO) followed by reperfusion. After reperfusion, infarction size, level of superoxide and 8-hydroxy-20-deoxyguanosine (8-oxo-2dG), and Nox1 immunoreactivity were determined. RNAi-mediated knockdown of Nox1 was used to investigate the role of Nox1 in I/R-induced oxidative damage, neuronal death, motor function recovery, and ischemic neurogenesis. After I/R, Nox1 expression and 8-oxo-2dG immunoreactivity was increased in cortical neurons of the peri-infarct regions. Both infarction size and neuronal death in I/R injury were significantly reduced by adeno-associated virus (AAV)-mediated transduction of Nox1 short hairpin RNA (shRNA). AAV-mediated Nox1 knockdown enhanced functional recovery after MCAO. The level of survival and differentiation of newborn cells in the peri-infarct regions were increased by Nox1 inhibition. Our data suggest that Nox-1 may be responsible for oxidative damage to DNA, subsequent cortical neuronal degeneration, functional recovery, and regulation of ischemic neurogenesis in the peri-infarct regions after stroke