This study developed a Smartphone Addiction Proneness Scale (SAPS) based on the existing internet and cellular phone addiction scales. For the development of this scale, 29 items (1.5 times the final number of items) were initially selected as preliminary items, based on the previous studies on internet/phone addiction as well as the clinical experience of involved experts. The preliminary scale was administered to a nationally representative sample of 795 students in elementary, middle, and high schools across South Korea. Then, final 15 items were selected according to the reliability test results. The final scale consisted of four subdomains: (1) disturbance of adaptive functions, (2) virtual life orientation, (3) withdrawal, and (4) tolerance. The final scale indicated a high reliability with Cronbach's α of .880. Support for the scale's criterion validity has been demonstrated by its relationship to the internet addiction scale, KS-II (r  =  .49). For the analysis of construct validity, we tested the Structural Equation Model. The results showed the four-factor structure to be valid (NFI  =  .943, TLI  =  .902, CFI  =  .902, RMSEA  =  .034). Smartphone addiction is gaining a greater spotlight as possibly a new form of addiction along with internet addiction. The SAPS appears to be a reliable and valid diagnostic scale for screening adolescents who may be at risk of smartphone addiction. Further implications and limitations are discussed.

We studied the role of the matrix metalloproteinase gelatinase B (gelB; MMP-9) in epithelial regeneration using the gelB-deficient mouse. We report the novel finding that, in contrast to other MMPs expressed at the front of the advancing epithelial sheet in wounds of cornea, skin, or trachea, gelB acts to inhibit the rate of wound closure. We determined this to be due to control of cell replication, a novel capacity for MMPs not previously described. We also found that gelB delays the inflammatory response. Acceleration of these processes in gelB-deficient mice is correlated with a delay in signal transduction through Smad2, a transcription factor that inhibits cell proliferation, and in accumulation of epithelial-associated interleukin-1␣, a cytokine that inhibits Smad2 signaling and promotes the inflammatory response. GelB-deficient mice also reveal defects in remodeling of extracellular matrix at the epithelial basement membrane zone, in particular, failure to effectively remove the fibrin(ogen) provisional matrix. We conclude that gelB coordinates and effects multiple events involved in the process of epithelial regeneration.

Natural killer (NK) cells play important roles in immune surveillance. However, the tumor microenvironment suppresses NK cell function and allows cancer cells to evade immune detection. In this study, we investigated whether the thyroid cancer cell microenvironment has this effect on NK cells. We found that prostaglandin (PG) E2 produced by thyroid cancer cells suppressed the cytolytic activity of NK cells by inhibiting the expression of the natural cytotoxicity receptors NKp44 and NKp30 and the death receptor tumor necrosis factor-related apoptosis-inducing ligand. PGE2 and cyclooxygenase-2 were highly expressed in thyroid cancer cells; moreover, anaplastic thyroid cancer cells released higher amounts of PGE2 than the papillary subtype, which was associated with suppression of NK cell-inducing nuclear factor-κB and mitogen-activated protein kinase/extracellular signal-regulated kinase pathways via PGE2 receptor (EP) 2 and EP4 expressed on the NK cell surface. In addition, PGE2 inhibited the functional maturation of NK cells and reduced their cytotoxicity against target cells. These results indicate that PGE2 promotes thyroid cancer progression by inhibiting NK cell maturation and cytotoxicity. Thus, therapeutic strategies that target PGE2 in thyroid cancer could potentiate the immune response and improve patient prognosis.

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