Purpose – This paper aims to analyze the influence of innovation-based orientation on hotel performance, how the management’s perception of market turbulence moderates this relationship and the effect of an atmosphere of crisis. Design/methodology/approach – The research carried out used an on-line survey among four-star hotel managers in 52 Spanish cities. Findings – The results obtained indicate that the tendency of a hotel to innovate does not contribute directly and positively on short-term performance. However, it does confirm its importance when improving hotel performance in the medium- and long-term. This work discusses how the perception of technological turbulence influences the willingness to innovate, together with the effect that an economic-crisis-related-pessimistic management view has on marketing performance and long-term results. Originality/value – Reliable and valid scales, applicable to the hotel sector and useful both for researchers and managers, are provided to measure the tendency to innovate, perceived technological turbulence and company performance. Knowledge regarding innovation is expanded, including a critical factor to increase business profits and competitiveness in uncertain environments. The model proposed is tested in a sector where there is little empirical evidence about the effect of innovation on performance.
BackgroundNeuroprotection with cannabinoids in Parkinson’s disease (PD) has been afforded predominantly with antioxidant or anti-inflammatory cannabinoids. In the present study, we investigated the anti-inflammatory and neuroprotective properties of VCE-003.2, a quinone derivative of the non-psychotrophic phytocannabinoid cannabigerol (CBG), which may derive its activity at the peroxisome proliferator-activated receptor-γ (PPARγ). The compound is also an antioxidant.MethodsWe evaluated VCE-003.2 in an in vivo [mice subjected to unilateral intrastriatal injections of lipopolysaccharide (LPS)] model of PD, as well as in in vitro (LPS-exposed BV2 cells and M-213 cells treated with conditioned media generated from LPS-exposed BV2 cells) cellular models. The type of interaction of VCE-003.2 at the PPARγ receptor was furtherly investigated in bone marrow-derived human mesenchymal stem cells (MSCs) and sustained with transcriptional assays and in silico docking studies.ResultsVCE-003.2 has no activity at the cannabinoid receptors, a fact that we confirmed in this study using competition studies. The administration of VCE-003.2 to LPS-lesioned mice attenuated the loss of tyrosine hydroxylase (TH)-containing nigrostriatal neurons and, in particular, the intense microgliosis provoked by LPS in the substantia nigra, measured by Iba-1/Cd68 immunostaining. The analysis by qPCR of proinflammatory mediators such as tumor necrosis factor-α (TNF-α), interleukin-1β (IL-1β), and inducible nitric oxide synthase (iNOS) in the striatum showed they were markedly elevated by the LPS lesion and strongly reduced by the treatment with VCE-003.2. The effects of VCE-003.2 in LPS-lesioned mice implied the activation of PPARγ receptors, as they were attenuated when VCE-003.2 was co-administered with the PPARγ inhibitor T0070907. We then moved to some in vitro approaches, first to confirm the anti-inflammatory profile of VCE-003.2 in cultured BV2 cells exposed to LPS. VCE-003.2 was able to attenuate the synthesis and release of TNF-α and IL-1β, as well as the induction of iNOS and cyclooxygenase-2 (COX-2) elicited by LPS in these cells. However, we found such effects were not reversed by GW9662, another classic PPARγ antagonist. Next, we investigated the neuroprotective effects of VCE-003.2 in cultured M-213 neuronal cells exposed to conditioned media generated from LPS-exposed cultured BV2 cells. VCE-003.2 reduced M-213 cell death, but again, such effects were not reversed by T0070907. Using docking analysis, we detected that VCE-003.2 binds both the canonical and the alternative binding sites in the PPARγ ligand-binding pocket (LBP). Functional assays further showed that T0070907 almost abolished PPARγ transcriptional activity induced by rosiglitazone (RGZ), but it did not affect the activity of VCE-003.2 in a Gal4-Luc system. However, T0070907 inhibited the effects of RGZ and VCE-003.2 on the expression of PPARγ-dependent genes upregulated in MSCs.ConclusionsWe have demonstrated that VCE-003.2 is neuroprotective against inflammation-driven n...
This paper examines tourists' knowledge sharing behavior in social media. Based on social capital theory, we aim to examine the effects of three dimensions of social capital—structural (social interaction ties), cognitive (shared vision) and relational (trust)—for two different types of social media: Facebook and TripAdvisor. We propose a structural model that connects an antecedent (homophily) and a consequence (knowledge sharing through posting) of these main dimensions of social capital. An online survey is conducted with 1200 Spanish consumers. Based on the full sample, our structural equation modeling supports most of the hypothesized paths, while trust does not affect either social interaction ties or knowledge sharing. Examining the difference between Facebook and TripAdvisor, our multigroup analysis finds that neither trust nor shared vision drives knowledge sharing on TripAdvisor, while shared vision affects knowledge sharing in Facebook. In both media, social interaction ties play an important role in motivating users to post comments. The effects of homophily on social interaction ties and on shared vision were statistically greater in TripAdvisor than in Facebook. Homophily did not affect trust in either media. In closing, both theoretical and managerial implications are discussed, important limitations are recognized and future research directions are suggested. Copyright © 2016 John Wiley & Sons, Ltd.
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