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DESTINATION BRAND COOLNESS: CONCEPTUALIZATION AND SCALE DEVELOPMENT
Hsiu-Yu Teng,Cheng-Hsien Tsai,Chia-Wen Hung,Hui-Chen Hung 글로벌지식마케팅경영학회 2023 Global Marketing Conference Vol.2023 No.07
Destination branding has become an important trend in modern tourism. The development of destination brands has become a strategic tool worldwide because of the growing competition between destinations. In recent years, many tourist destinations have combined unique, creative, and attractive elements to transform themselves into “cool” tourist destinations. Destination brand coolness refers to tourists’ subjective and positive perception of tourist destinations and their beliefs that the destination brand offer distinctive, novel characteristics and attributes that the visitors are attracted to. Creating destination brand coolness can help tourist destinations differentiate themselves from their competitive counterparts, thereby attracting tourists. However, no study has conceptualized the construct of destination brand coolness, let alone developing scales that measure destination brand coolness.
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Chiu Ya-Jen,Teng Yu-Shan,Chen Chiung-Mei,Sun Ying-Chieh,Hsieh-Li Hsiu Mei,Chang Kuo-Hsuan,Lee-Chen Guey-Jen 한국응용약물학회 2023 Biomolecules & Therapeutics(구 응용약물학회지) Vol.31 No.3
Alzheimer’s disease (AD) is a neurodegenerative disease with progressive memory loss and the cognitive decline. AD is mainly caused by abnormal accumulation of misfolded amyloid β (Aβ), which leads to neurodegeneration via a number of possible mechanisms such as down-regulation of brain-derived neurotrophic factor-tropomyosin-related kinase B (BDNF-TRKB) signaling pathway. 7,8-Dihydroxyflavone (7,8-DHF), a TRKB agonist, has demonstrated potential to enhance BDNF-TRKB pathway in various neurodegenerative diseases. To expand the capacity of flavones as TRKB agonists, two natural flavones quercetin and apigenin, were evaluated. With tryptophan fluorescence quenching assay, we illustrated the direct interaction between quercetin/ apigenin and TRKB extracellular domain. Employing Aβ folding reporter SH-SY5Y cells, we showed that quercetin and apigenin reduced Aβ-aggregation, oxidative stress, caspase-1 and acetylcholinesterase activities, as well as improved the neurite outgrowth. Treatments with quercetin and apigenin increased TRKB Tyr516 and Tyr817 and downstream cAMP-response-element binding protein (CREB) Ser133 to activate transcription of BDNF and BCL2 apoptosis regulator (BCL2), as well as reduced the expression of pro-apoptotic BCL2 associated X protein (BAX). Knockdown of TRKB counteracted the improvement of neurite outgrowth by quercetin and apigenin. Our results demonstrate that quercetin and apigenin are to work likely as a direct agonist on TRKB for their neuroprotective action, strengthening the therapeutic potential of quercetin and apigenin in treating AD.
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