Rational or Emotional? An Examination of Customer Loyalty in B2B Packaged Food Retail Setting

This study aims to examine the contributing rational and emotional transactionspecific characteristics to customer loyalty dimensions, namely repurchase intention and positive words of mouth (WoM); as well as the mediation role of customer satisfaction among the buyers of packaged food retail outlets. A total of 221 responses were collected from the food retail businesses using purposive sampling method. The results demonstrated only four significant contributing factors to customer satisfaction, namely product quality, price perception, brand image and manufacturing country’s product image among the eight factors examined; with product quality and price perception played the most important roles. Proxys of a satisfied customers can be used to predict both behavioural and attitudinal loyalty. The study expands on existing literature by presenting the results of an empirical study addressing the uniqueness of the Malaysian packaged food retail market and how the transaction specific characteristics influence satisfaction and loyalty

ROS from menadione induces astrocytic damage: protective effects of apocynin

Abstract only availableOxidative stress is a core cause of neurodegenerative diseases such as Alzheimer's disease. When cells are under oxidative stress, they will produce a high amount of reactive oxygen species (ROS). ROS are small and highly reactive and include compounds such as oxygen ions, free radicals, and peroxides. Understanding what triggers oxidative stress and how to ameliorate its damaging effects is a crucial step in discovering a cure for Alzheimer's disease. Menadione, a vitamin precursor of K2, is an oxidative compound that is capable of delivering ROS to the cells. Apocynin, a natural organic compound that has been isolated from Picrorhiza curroa grown in the Himalayan Mountains, is an inhibitor of NADPH oxidase, an enzyme for ROS production in cells. In this experiment, we studied whether apocynin may neutralize the effects of menadione using an immortalized astrocyte cell line DITNC. Astrocytes are glial cells that play a crucial role in the brain by providing necessary nutrient to surrounding neurons. We had three sample groups and treated each group with different drugs. The first group was the control, the second group was treated with menadione, and the third group was treated with both menadione and apocynin. After treating the cells, we recorded morphological changes of the cells by taking pictures of each sample group at three different time intervals (30 min, 1 and 2 hours). In addition to the morphological evidence, we also did a MTT assay to assess cell viability and later a data analysis based on the result from the MTT test. MTT assay measures mitochondrial activity and thus indirectly measures cell viability. Both morphological data and MTT analysis showed menadione caused DITNC cell damage with decreased mitochondrial activity. When cells are treated with menadione, they formed processes, shrink, and then round up. We also found apocynin protects against the oxidative damage caused by menadione to a certain extent. Since apocynin is an inhibitor of NADPH oxidase, this also indicates oxidative stress is generated by NADPH oxidase, suggesting apocynin may be a potential means to treat Alzheimer's disease.Alzheimer disease program project grant 2P01 AG018357 to G. Su

Role of Aβ-RAGE interaction in oxidative stress and cPLA2 activation in astrocytes and cerebral endothelial cells

Blood–brain barrier (BBB) dysfunctions have been implicated in the progression of Alzheimer's disease. Cerebral endothelial cells (CECs) and astrocytes are the main cell components of the BBB. Although amyloid-β oligomers (Aβ42) have been reported to mediate oxidative damage to the CECs and astrocytes and trigger the downstream mitogen-activated protein kinase/extracellular signal-regulated kinase (MAPK/ERK) pathway, the cell surface binding site for Aβ42 and exact sequence of these events have yet to be elucidated. In this study, the receptor for advanced glycation endproducts (RAGE) was postulated to function as a signal transducing cell surface receptor for Aβ42 to induce reactive oxygen species (ROS) generation from NADPH oxidase and trigger downstream pathways for the phosphorylation of extracellular signal-regulated kinases (ERK1/2) and cytosolic phospholipase A2 (cPLA2). We found that Aβ42 competed with the anti-RAGE antibody (AbRAGE) to bind to RAGE on the surfaces of CECs and primary astrocytes. In addition, AbRAGE abrogate Aβ42-induced ROS production and the colocalization between the cytosolic (p47-phox) and membrane (gp91-phox) subunits of NADPH oxidase in both cell types. AbRAGE as well as NADPH oxidase inhibitor and ROS scavenger suppressed Aβ42-induced ERK1/2 and cPLA2 phosphorylation in CECs. At the same time, only AbRAGE, but neither NADPH oxidase inhibitor nor ROS scavenger, inhibited the ERK1/2 pathway and cPLA2 phosphorylation in primary astrocytes. Therefore, this study demonstrates that NADPH oxidase complex assembly and ROS production are not required for Aβ42 binding to RAGE at astrocytic surface leading to sequential phosphorylation of ERK1/2 and cPLA2, and suggests the presence of two different RAGE-dependent downstream pathways in the CECs and astrocytes

Role of Aβ-RAGE interaction in oxidative stress and cPLA2 activation in astrocytes and cerebral endothelial cells

Blood–brain barrier (BBB) dysfunctions have been implicated in the progression of Alzheimer's disease. Cerebral endothelial cells (CECs) and astrocytes are the main cell components of the BBB. Although amyloid-β oligomers (Aβ42) have been reported to mediate oxidative damage to the CECs and astrocytes and trigger the downstream mitogen-activated protein kinase/extracellular signal-regulated kinase (MAPK/ERK) pathway, the cell surface binding site for Aβ42 and exact sequence of these events have yet to be elucidated. In this study, the receptor for advanced glycation endproducts (RAGE) was postulated to function as a signal transducing cell surface receptor for Aβ42 to induce reactive oxygen species (ROS) generation from NADPH oxidase and trigger downstream pathways for the phosphorylation of extracellular signal-regulated kinases (ERK1/2) and cytosolic phospholipase A2 (cPLA2). We found that Aβ42 competed with the anti-RAGE antibody (AbRAGE) to bind to RAGE on the surfaces of CECs and primary astrocytes. In addition, AbRAGE abrogate Aβ42-induced ROS production and the colocalization between the cytosolic (p47-phox) and membrane (gp91-phox) subunits of NADPH oxidase in both cell types. AbRAGE as well as NADPH oxidase inhibitor and ROS scavenger suppressed Aβ42-induced ERK1/2 and cPLA2 phosphorylation in CECs. At the same time, only AbRAGE, but neither NADPH oxidase inhibitor nor ROS scavenger, inhibited the ERK1/2 pathway and cPLA2 phosphorylation in primary astrocytes. Therefore, this study demonstrates that NADPH oxidase complex assembly and ROS production are not required for Aβ42 binding to RAGE at astrocytic surface leading to sequential phosphorylation of ERK1/2 and cPLA2, and suggests the presence of two different RAGE-dependent downstream pathways in the CECs and astrocytes

Downramp-assisted underdense photocathode electron bunch generation in plasma wakefield accelerators

It is shown that the requirements for high quality electron bunch generation and trapping from an underdense photocathode in plasma wakefield accelerators can be substantially relaxed through localizing it on a plasma density downramp. This depresses the phase velocity of the accelerating electric field until the generated electrons are in phase, allowing for trapping in shallow trapping potentials. As a consequence the underdense photocathode technique is applicable by a much larger number of accelerator facilities. Furthermore, dark current generation is effectively suppressed.Comment: 4 pages, 3 figure

A Sm(II)-mediated cascade approach to Dibenzoindolo[3,2-b]carbazoles:synthesis and evaluation

Previously unstudied dibenzoindolo[3,2-b]carbazoles have been prepared by two-directional, phase tag-assisted synthesis utilizing a connective-Pummerer cyclization and a SmI2-mediated tag cleavage-cyclization cascade. The use of a phase tag allows us to exploit unstable intermediates that would otherwise need to be avoided. The novel materials were characterized by X-ray, cyclic voltammetry, UV-vis spectroscopy, TGA, and DSC. Preliminary studies on the performance of OFET devices are also described

Low energy laser light (632.8 nm) suppresses amyloid-β peptide-induced oxidative and inflammatory responses in astrocytes

Oxidative stress and inflammation are important processes in the progression of Alzheimer's disease (AD). Recent studies have implicated the role of amyloid β-peptides (Aβ) in mediating these processes. In astrocytes, oligomeric Aβ induces the assembly of NADPH oxidase complexes resulting in its activation to produce anionic superoxide. Aβ also promotes production of pro-inflammatory factors in astrocytes. Since low energy laser has previously been reported to attenuate oxidative stress and inflammation in biological systems, the objective of this study was to examine whether this type of laser light was able to abrogate the oxidative and inflammatory responses induced by Aβ. Primary rat astrocytes were exposed to Helium-Neon laser (λ=632.8 nm), followed by the treatment with oligomeric Aβ. Primary rat astrocytes were used to measure Aβ-induced production of superoxide anions using fluorescence microscopy of dihydroethidium (DHE), assembly of NADPH oxidase subunits by the colocalization between the cytosolic p47phox subunit and the membrane gp91phox subunit using fluorescent confocal microscopy, phosphorylation of cytosolic phospholipase A2 (cPLA2), and expressions of pro-inflammatory factors including interleukin-1β (IL-1β) and inducible nitric-oxide synthase (iNOS) using Western blot Analysis. Our data showed that laser light at 632.8 nm suppressed Aβ-induced superoxide production, colocalization between NADPH oxidase gp91phox and p47phox subunits, phosphorylation of cPLA2, and the expressions of IL-1β and iNOS in primary astrocytes. We demonstrated for the first time that 632.8 nm laser was capable of suppressing cellular pathways of oxidative stress and inflammatory responses critical in the pathogenesis in AD. This study should prove to provide the groundwork for further investigations for the potential use of laser therapy as a treatment for AD