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This article examines the relationship between the level of tourism specialization (TS) and economic growth using a panel dataset covering 31 provinces in mainland China from 1995 to 2013. A quadratic function was introduced following the basic economic law of returns to overcome the weaknesses of constant returns to scale associated with the tourism-led economic growth hypothesis (TLGH). Using tourist arrivals as a percentage of host population (TA) and tourism receipts as a share of real GDP (TR) as the indicators of TS which represent respectively the level/size and the quality/structure dimension of TS, the system generalized method of moments (SYSGMM) regression results suggest that a meaningful inverted-U- or an N-shaped relationship exists between tourism specialization and economic growth. Based on the portfolio of TA and TR in destinations, the effects and characters of tourism on economic growth are discussed regarding the future direction of regional development.

Chronic infection of hepatitis B virus (HBV) is associated with an increased incidence of hepatocellular carcinoma (HCC). HBV encodes an oncoprotein, hepatitis B x protein (HBx), that is crucial for viral replication and interferes with multiple cellular activities including gene expression, histone modifications, and genomic stability. To date, it remains unclear how disruption of these activities contributes to hepatocarcinogenesis. Here, we report that HBV exhibits antiresection activity by disrupting DNA end resection, thus impairing the initial steps of homologous recombination (HR). This antiresection activity occurs in primary human hepatocytes undergoing a natural viral infection–replication cycle as well as in cells with integrated HBV genomes. Among the seven HBV‐encoded proteins, we identified HBx as the sole viral factor that inhibits resection. By disrupting an evolutionarily conserved Cullin4A–damage‐specific DNA binding protein 1–RING type of E3 ligase, CRL4 WDR70 , through its H‐box, we show that HBx inhibits H2B monoubiquitylation at lysine 120 at double‐strand breaks, thus reducing the efficiency of long‐range resection. We further show that directly impairing H2B monoubiquitylation elicited tumorigenesis upon engraftment of deficient cells in athymic mice, confirming that the impairment of CRL4 WDR70 function by HBx is sufficient to promote carcinogenesis. Finally, we demonstrate that lack of H2B monoubiquitylation is manifest in human HBV‐associated HCC when compared with HBV‐free HCC, implying corresponding defects of epigenetic regulation and end resection. Conclusion: The antiresection activity of HBx induces an HR defect and genomic instability and contributes to tumorigenesis of host hepatocytes.

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