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- 저자 : Mufida, Amila (검색결과 2 건)
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What Explains Smartwatch Adoption? A Compatrative Study of South Korea and Indonesia
Sekardhani, Mufida,Song, Sujin Korean Marketing Association 2022 ASIA MARKETING JOURNAL Vol.24 No.2
Identifying factors that influence consumers' intentions to adopt a smartwatch has become a major research interest in marketing literature, yet little is known about it in dissimilar cultural settings. The current research employs a comparative study of South Korea and Indonesia, which differ in location and cultural heritage, smartwatch penetration rate, geographic size, level of income, and developmental stage as a country. An extended model of TAM is proposed, and PLS-SEM is employed to test the model on data collected from 262 respondents. The findings indicate that complementary goods and healthtology have positive influences on perceived usefulness and visibility has a positive influence on social image; these, together with perceived price value, lead to the behavioral intention to adopt a smartwatch in both countries. Perceived cost was only significant for Indonesia. Theoretical contributions and practical implications are further discussed.
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주혜림,Pachhapure, Shailashree,Mufida, Amila,김아련,Elmaleh, David R.,최성운,장병철 계명대학교 의과대학 2022 계명의대학술지 Vol.41 No.2
Inflammation is a common link in the pathophysiology of many neurological illnesses, including Alzheimer’s disease. Activated glial cells contribute to neuroinflammation by producing pro-inflammatory mediators. Naproxen and ibuprofen are nonsteroidal anti-inflammatory drugs with 2-aryl(s) propionic acid as a common pharmacophore. Here we designed a small series of naproxen and ibuprofen amide dimers and tested their effects on the expression of inducible nitric oxide synthase (iNOS), a neuroinflammatory enzyme in lipopolysaccharide (LPS)-stimulated BV2 mouse microglial cells. Of note, treatment with CNU 019, 020, 021, 023, 024, and 027 at 10 M markedly inhibited the LPS-induced iNOS expression in BV2 cells. CNU 024 was tested further at different concentrations to regulate the LPS-induced iNOS expression in BV2 cells. Treatment with CNU 024 at 5, 10, or 20 M dose-dependently suppressed the LPS-induced iNOS protein and mRNA expression levels in BV2 cells, in which maximal inhibition was seen at 20 M. CNU 024 treatment at doses tested further led to a concentration-dependent inhibition of the LPS-induced phosphorylation (activation) of p38 mitogen-activated protein kinase (MAPK) without influencing its total protein expression in BV2 cells, but it did not affect the LPS-induced activation of c-jun N-terminal kinase-1/2 and extracellular signal-regulated kinases-1/2 in these cells. In summary, our results demonstrate that CNU 024 inhibits the LPS-induced iNOS expression in BV2 cells, partly mediated by the inhibition of p38 MAPK. This work shows that CNU 024 could be a valuable ligand for further development as a potential drug candidate for treating neuroinflammatory pathologies.
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