KOREA OUTBOUND TOURISM TO SEVEN COUNTRIES: VAR MODEL AND GRANGER CAUSALITY TEST

This paper investigates the causal relationship among Korean outbound tourism demand for seven countries such as United States, China, Hong Kong, Japan, Philippines, Singapore, and Thailand. Since there are no long-run relationships among Korean outbound tourism demand for those international destinations the vector autoregressive (VAR) model is used for testing such causality. From the causality results, we found United States is leading country for Korean outbound tourism demand. When Korean tourism demands for United States increase, those for the other countries get a raise. Also, tourism demand for Thailand is influenced by tourism demands for three countries such as Hong Kong, Singapore and United States. Our results imply that government and managerial implications are recognized based on the empirical findings

Interrelationships Among Korean Outbound Tourism Demand:Granger Causality Analysis

This study investigated Korean outbound tourism demand and its determinants using the Granger causality (GC) analysis. In contrast to previous studies, which dealt only with internal factors, such as exchange rate and income, this study examined the effects of interactions among countries and, therefore, more complete and relevant results were found. Korean outbound tourism to the USA is causally related to Korean outbound tourism to the other six countries in this present study. These results can be applicable for the purpose of tourism marketing and strategies for industries and governments to allocate tourism resources more efficiently.This paper is forthcoming in Tourism Economics

Quantile Elasticity of International Tourism Demand for South Korea using Quantile Autoregressive Distributed Lag Model

This paper investigates international inbound tourism demand for South Korea and its determinants using quantile autoregressive model. In contrast to previous studies which dealt with only conditional mean, we examine effects of covariates at various conditional quantile levels; and therefore, more complete and interesting results are found. For inbound tourism demand, U.S. and Japanese tourism  demand are considered. For U.S. tourism demand, costs of living in Korea and competing destinations have moderate significant negative effects only at very high and low quantiles, while income does not have any significant effect to tourism demand. On the other hand, for Japanese tourism demand, income has significantly positive effects at lower quantiles, and living costs in Korea and competing destinations have significant negative effects at higher quantiles. These results address the heterogeneity in the tourism demand analysis.This paper has been accepted for publication to Tourism Economics

The Seven Deadly Sins of Communication Research

Peer Reviewedhttp://deepblue.lib.umich.edu/bitstream/2027.42/74955/1/j.1460-2466.2008.00382.x.pd

Cocoa polyphenols suppress TNF-α-induced vascular endothelial growth factor expression by inhibiting phosphoinositide 3-kinase (PI3K) and mitogen-activated protein kinase kinase-1 (MEK1) activities in mouse epidermal cells

Cocoa polyphenols have antioxidant and anti-inflammatory effects. TNF-α is a pro-inflammatory cytokine that has a vital role in the pathogenesis of inflammatory diseases such as cancer and psoriasis. Vascular endothelial growth factor (VEGF) expression is associated with tumorigenesis, CVD, rheumatoid arthritis and psoriasis. We tested whether cocoa polyphenol extract (CPE) inhibited TNF-α-induced VEGF expression in promotion-sensitive JB6 mouse epidermal cells. CPE significantly inhibited TNF-α-induced up-regulation of VEGF via reducing TNF-α-induced activation of the nuclear transcription factors activator protein-1 (AP-1) and NF-κB, which are key regulators of VEGF expression. CPE also inhibited TNF-α-induced phosphorylation of protein kinase B (Akt) and extracellular signal-regulated kinase. CPE blocked activation of their downstream kinases, p70 kDa ribosomal protein S6 kinase and p90 kDa ribosomal protein S6 kinase. CPE suppressed phosphoinositide 3-kinase (PI3K) activity via binding PI3K directly. CPE did not affect TNF-α-induced phosphorylation of mitogen-activated protein kinase kinase-1 (MEK1) but suppressed TNF-α-induced MEK1 activity. Collectively, these results indicate that CPE reduced TNF-α-induced up-regulation of VEGF by directly inhibiting PI3K and MEK1 activities, which may contribute to its chemopreventive potentia