Service Quality of Online Shopping Platforms: A Case-Based Empirical and Analytical Study

Customer service is crucially important for online shopping platforms (OSPs) such as eBay and Taobao. Based on the well-established service quality instruments and the scenario of the specific case on Taobao, this paper focuses on exploring the service quality of an OSP with an aim of revealing customer perceptions of the service quality associated with the provided functions and investigating their impacts on customer loyalty. By an empirical study, this paper finds that the “fulfillment and responsiveness” function is significantly related to the customer loyalty. Further analytical study is conducted to reveal that the optimal service level on the “fulfillment and responsiveness” function for the risk averse OSP uniquely exists. Moreover, the analytical results prove that (i) if the customer loyalty is more positively correlated to the service level, it will lead to a larger optimal service level, and (ii) the optimal service level is independent of the profit target, the source of uncertainty, and the risk preference of the OSP

Anesthetic Propofol Reduces Endotoxic Inflammation by Inhibiting Reactive Oxygen Species-regulated Akt/IKKβ/NF-κB Signaling

BACKGROUND: Anesthetic propofol has immunomodulatory effects, particularly in the area of anti-inflammation. Bacterial endotoxin lipopolysaccharide (LPS) induces inflammation through toll-like receptor (TLR) 4 signaling. We investigated the molecular actions of propofol against LPS/TLR4-induced inflammatory activation in murine RAW264.7 macrophages. METHODOLOGY/PRINCIPAL FINDINGS: Non-cytotoxic levels of propofol reduced LPS-induced inducible nitric oxide synthase (iNOS) and NO as determined by western blotting and the Griess reaction, respectively. Propofol also reduced the production of tumor necrosis factor-α (TNF-α), interleukin (IL)-6, and IL-10 as detected by enzyme-linked immunosorbent assays. Western blot analysis showed propofol inhibited LPS-induced activation and phosphorylation of IKKβ (Ser180) and nuclear factor (NF)-κB (Ser536); the subsequent nuclear translocation of NF-κB p65 was also reduced. Additionally, propofol inhibited LPS-induced Akt activation and phosphorylation (Ser473) partly by reducing reactive oxygen species (ROS) generation; inter-regulation that ROS regulated Akt followed by NF-κB activation was found to be crucial for LPS-induced inflammatory responses in macrophages. An in vivo study using C57BL/6 mice also demonstrated the anti-inflammatory properties against LPS in peritoneal macrophages. CONCLUSIONS/SIGNIFICANCE: These results suggest that propofol reduces LPS-induced inflammatory responses in macrophages by inhibiting the interconnected ROS/Akt/IKKβ/NF-κB signaling pathways

Glycogen synthase kinase-3 ss is critical for Interferon-a-induced serotonin uptake in human Jurkat T cells

Dysregulation of glycogen synthase kinase (GSK)-3 beta contributes to the pathophysiology of mood disorders. However, how its regulation is responsible for the functioning of serotonin (5-HT) requires further investigation. Although enhancement of T-cell function may present an alternative strategy to treat depression, the precise mechanisms have yet to be established. Our previous studies have found that interferon-alpha (IFN-a) up-regulates serotonin transporter (5-HTT) expression and induces 5-HT uptake in T cells. The present study is to examine GSK-3 beta regulation on IFN-a-induced 5-HTT functions. GSK-3 beta short hairpin RNAs (shRNAs) or GSK-3 beta inhibitors decreased IFN-a-induced 5-HT uptake and 5-HTT expression. Src activation and calcium/calcium-activated calmodulin kinase II (CaMKII) were involved in IFN-a-induced phosphorylation of proline-rich tyrosine kinase 2 (Pyk2) (Tyr402) and GSK-3 beta (Tyr216), which regulated 5-HT uptake. GSK-3 beta knockdown blocked the IFN-a-induced phosphorylation of extracellular signal-regulated kinase (ERK) 1/2 (Thr202/Tyr204) and signal transducer and transactivator (STAT) 1. In addition to inhibiting ERK, a selective 5-HTT inhibitor fluoxetine blocked IFN-a-induced activations of Src, CaMKII-regulated Pyk2/GSK-3 beta cascade, as well as STAT1 activation and translocation. These results indicated that calcium/CaMKII- and Src-regulated Pyk2 participated in IFN-a-induced GSK-3 beta activation and GSK-3 beta-regulated 5-HT uptake. GSK-3 beta signaling facilitated IFN-a-activated STAT1 by regulating ERK1/2, which controlled 5-HT uptake. Fluoxetine interfered with the Pyk2/GSK-3 beta cascade, thereby inhibiting IFN-a-induced 5-HT uptake. J. Cell. Physiol. 227: 25562566, 2012. (c) 2011 Wiley Periodicals, Inc

Macrophage migration inhibitory factor regulates interleukin-6 production by facilitating nuclear factor-kappa B activation during <it>Vibrio vulnificus </it>infection

Abstract Background Patients infected with Vibrio vulnificus (V. vulnificus) show severe inflammatory responses characterised by the upregulation of proinflammatory cytokines. Macrophage migration inhibitory factor (MIF), an upstream proinflammatory regulator, increases the inflammation caused by sepsis. Whether MIF regulates responses to V. vulnificus infection and the actual mechanism by which V. vulnificus initiates these MIF-modulated proinflammatory cytokines remain unclear. Results MIF increased inflammation during V. vulnificus infection in vivo. In V. vulnificus-infected mice, MIF was produced earlier than tumour necrosis factor (TNF)-α and interleukin (IL)-6 and was expressed in a time-dependent manner. ISO-1 ((S, R)-3-(4-hydroxyphenyl)-4,5-dihydro-5-isoxazole acetic acid methyl ester), a small-molecule inhibitor of MIF, significantly decreased IL-6, IL-8, and TNF-α production in a time- and dose-dependent manner in human peripheral blood cells infected with V. vulnificus. The induction of IL-6, IL-8, and TNF-α production by V. vulnificus infection was mediated via the NF-κB- and p38 MAPK-regulated pathways but not via the Akt pathway. ISO-1-treated human peripheral blood cells showed lower V. vulnificus-induced NF-κB activation, IL-6 mRNA expression, and IκB phosphorylation, but they did not show lower p38 MAPK activation. Conclusions We conclude that MIF regulates V. vulnificus-induced IL-6 production via NF-κB activation and that p38 MAPK activation in V. vulnificus infection is not MIF dependent.</p

Surface-Modified Wooden-Tip Electrospray Ionization Mass Spectrometry for Enhanced Detection of Analytes in Complex Samples

Replacement of capillary with solid substrates for sample loading and ionization has created many new possibilities for electrospray ionization mass spectrometry (ESI-MS). Surface modification is an attractive strategy to enhance the analytical capability of solid-substrate ESI-MS and allow understanding the relationship between surface activity of solid substrates and analytical properties. In this study, we performed surface modification of wooden tips with hydrophobic (−C₁₈), basic (−NH₂), and acidic (−SO₃H) functional groups and applied various sampling methods, i.e., extractive sampling and direct loading, to comprehensively investigate the analytical properties of solid-substrate ESI-MS. Our results showed that, for the direct loading method, analytes with weak interactions with solid-substrate surface could be readily sprayed out for detection. While for the extractive sampling method, analytes strongly retained on solid-substrate surface could be selectively enriched and detected, and a washing step after sample loading could effectively remove unbound components for reducing interference. Overall, the insights on the effects of surface–analyte interactions on the analytical features obtained in this study could aid the development of surface-modified strategies for enhancing the analytical capability of solid-substrate ESI-MS