Ectopic expression of metabotropic glutamate receptor subtype 1 (mGluR1) in mouse melanocytes induces melanoma formation. Although requirement of mGluR1 for development of melanoma in the initial stage has been demonstrated, its role in melanoma growth in vivo remains unclear. In this study, we developed novel transgenic mice that conditionally express mGluR1 in melanocytes, using a tetracycline regulatory system. Pigmented lesions on the ears and tails of the transgenic mice began to appear 29 weeks after activation of the mGluR1 transgene, and the transgenic mice produced melanomas at a frequency of 100% 52 weeks after transgene activation. Subsequent inactivation of the mGluR1 transgene in melanomabearing mice inhibited melanoma growth with reduction of immunoreactivity to phosphorylated ERK1/2, whereas mice with persistent expression of mGluR1 developed larger melanoma burdens. mGluR1 expression is thus required not only for melanoma development but also for melanoma growth in vivo. These findings suggest that growth of melanoma can be inhibited in vivo by eliminating only one of the multiple genetic anomalies involved in tumorigenesis.

A large-scale coherent structure responsible for the enhancement of stagnation-point heat transfer was successfully determined using a statistical analysis with conditional sampling in an impinging round jet. It was found that the optimal nozzle-to-plate spacing for maximal stagnation-point heat transfer is identical with the jet development length for a strong turbulent stream carrying large-scale energy-containing eddies. Aphysical model of heat transfer enhancementwas experimentally derived from the viewpoint of turbulent surface-renewal induced by large-scale eddies impinging on the stagnation-point boundary layer. It was found that the effect of heat transfer enhancementis a function of the proposed surface-renewal parameter consisting of the characteristic turbulence intensity and frequency of the large-scale eddies.

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