1,503 research outputs found
Exploring Consumers’ Coping Behaviors in Online Double Deviation Scenarios: From Power Perspective
Service recovery is a critical moment of truth in retaining customers and reinforcing customer relationships, and has been considered as an “Achilles\u27 heel” in online marketplaces. Poor service recoveries exacerbate the negative effects of the failure, producing a “double deviation” effect. The double deviation effect may arise from the seller’s power misuse and then dissolve the buyer-seller relationship (e.g., violate consumer psychological contract), elicit consumer negative emotions which lead to customer coping behaviors. This study links the theories of psychological contract violation (PCV), emotion, and coping from the power perspective to investigate the double deviation scenario in online auction marketplaces. Two moderators (perceived power and perceived consumer empowerment) are considered in our proposed model. Data collected from 181 consumers of one auction website provide support for the proposed model. The results shed light on what constitutes the determinants of consumer judgments while facing double deviation scenario and how consumers react to and cope with it in online marketplaces. Implications and limitations are discussed
Molecular Adaptation of Borrelia burgdorferi in the Murine Host
An analysis of expression of 137 lipoprotein genes on the course of murine infection revealed a two-step molecular adaptation by Borrelia burgdorferi, the Lyme disease spirochete. For the first step, regardless whether the initial inocula of B. burgdorferi expressed either all (cultured spirochetes) or less than 40 (host-adapted spirochetes) of the 137 lipoprotein genes, the spirochetes were modulated to transcribe 116 of the genes within 10 d after being introduced to the murine host. This step of adaptation was induced by the microenvironment of the host tissue. During the second step, which was forced by host immune selection pressure and occurred between 17 and 30 d after infection, B. burgdorferi down-regulated most of the lipoprotein genes and expressed less than 40 of the 137 genes. This novel adaptation mechanism could be a critical step for B. burgdorferi to proceed to chronic infection, as the pathogen would be cleared at the early stage of infection if the spirochetes failed to undergo this process
Erratum to: On the existence of mild solutions to the Cauchy problem for a class of fractional evolution equation
Production of FMDV virus-like particles by a SUMO fusion protein approach in Escherichia coli
Virus-like particles (VLPs) are formed by the self-assembly of envelope and/or capsid proteins from many viruses. Some VLPs have been proven successful as vaccines, and others have recently found applications as carriers for foreign antigens or as scaffolds in nanoparticle biotechnology. However, production of VLP was usually impeded due to low water-solubility of recombinant virus capsid proteins. Previous studies revealed that virus capsid and envelope proteins were often posttranslationally modified by SUMO in vivo, leading into a hypothesis that SUMO modification might be a common mechanism for virus proteins to retain water-solubility or prevent improper self-aggregation before virus assembly. We then propose a simple approach to produce VLPs of viruses, e.g., foot-and-mouth disease virus (FMDV). An improved SUMO fusion protein system we developed recently was applied to the simultaneous expression of three capsid proteins of FMDV in E. coli. The three SUMO fusion proteins formed a stable heterotrimeric complex. Proteolytic removal of SUMO moieties from the ternary complexes resulted in VLPs with size and shape resembling the authentic FMDV. The method described here can also apply to produce capsid/envelope protein complexes or VLPs of other disease-causing viruses
An Immune Evasion Mechanism for Spirochetal Persistence in Lyme Borreliosis
Borrelia burgdorferi, the Lyme disease spirochete, persistently infects mammalian hosts despite the development of strong humoral responses directed against the pathogen. Here we describe a novel mechanism of immune evasion by B. burgdorferi. In immunocompetent mice, spirochetes that did not express ospC (the outer-surface protein C gene) were selected within 17 d after inoculation, concomitantly with the emergence of anti-OspC antibody. Spirochetes with no detectable OspC transcript that were isolated from immunocompetent mice reexpressed ospC after they were either cultured in vitro or transplanted to naive immunocompetent mice, but not in OspC-immunized mice. B. burgdorferi persistently expressed ospC in severe combined immune-deficient (SCID) mice. Passive immunization of B. burgdorferi–infected SCID mice with an anti-OspC monoclonal antibody selectively eliminated ospC-expressing spirochetes but did not clear the infection. OspC-expressing spirochetes reappeared in SCID mice after the anti-OspC antibody was eliminated. We submit that selection of surface-antigen nonexpressers is an immune evasion mechanism that contributes to spirochetal persistence
Comparative transcriptome profiling of the fertile and sterile flower buds of a dominant genic male sterile line in sesame (Sesamum indicum L.)
Expressions and annotations of the 1502 differentially expressed unigenes in sesame. (XLSX 338 kb
Anticancer potentials of sinomenine from Sinomenium acutum: A mini-review
Sinomenine, an important isoquinoline from Sinomenium acutum (Menispermaceae), is currently considered as a reliable drug for treating various malignant cancers including breast cancer, colon cancer, lung cancer, liver cancer, gastric cancer, osteosarcoma cervical cancer, and esophageal cancer. The pharmacological mechanisms are probably related to induction of apoptosis and cell cycle arrest. This paper was aimed at reviewing the anticancer potential of sinomenine, which is expected to be beneficial in developing this compound as a candidate drug for cancer therapy.Keywords: Sinomenine, Anticancer, Sinomenium acutum, Traditional Chinese Medicin
Apigenin Retards Atherogenesis by Promoting ABCA1-Mediated Cholesterol Efflux and Suppressing Inflammation
Background/Aims: The development of atherosclerosis is accompanied by escalating inflammation and lipid accumulation within blood vessel walls. ABCA1 plays a crucial role in mediating cholesterol efflux from macrophages, which protects against atherogenesis. This research was designed to explore the effects and underlying mechanisms of apigenin (4’, 5, 7-trihydroxyflavone) on ABCA1-mediated cellular cholesterol efflux and LPS-stimulated inflammation in RAW264.7 macrophages and apoE-/- mice. Methods: Expression of genes or proteins was examined by RT-PCR or western blot analysis. Liquid scintillation counting was used to detect percent cholesterol efflux. Cellular cholesterol content was measured using HPLC assay. The secretion levels of pro-inflammatory cytokines were quantified by ELISA assay. Atherosclerotic lesion sizes were determined with Oil Red O staining. The contents of macrophages and smooth muscle cells in atherosclerotic lesion were evaluated using immunohistochemistry. Plasma TC, TG, HDL-C and LDL-C levels in apoE-/- mice were evaluated using commercial test kits. Results: Apigenin potently increased ABCA1 expression through miR-33 repression in a dose- and time-dependent manner. Treatment with apigenin significantly increased ABCA1-mediated cholesterol efflux, and reduced TC, FC and CE levels in macrophage-derived foam cells. In LPS-treated macrophages, the expression levels of TLR-4, MyD88 and p-IκB-α as well as nuclear NF-κB p65 were decreased by the addition of apigenin. Moreover, apigenin markedly decreased secretion levels of several pro-inflammatory cytokines. Lastly, in LPS-challenged apoE-/- mice, apigenin administration augmented ABCA1 expression, decreased the contents of macrophages and smooth muscle cells in atherosclerotic lesion, reduced miR-33, TLR-4, and NF-κB p65 levels, improved plasma lipid profile and relieved inflammation, which results in less atherosclerotic lesion size. Conclusions: Taken together, these results suggest that apigenin may attenuate atherogenesis through up-regulating ABCA1-mediated cholesterol efflux and inhibiting inflammation
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