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The surface properties of fused silica (FS) change after H2O2 treatment, but the surface and subsurface damage behaviors and their mechanisms under various physical contact conditions have not been elucidated yet. This work investigated the effect of H2O2 treatment on mechanical and mechanochemical properties of FS surface. The results show that the hydrophilicity and adsorbed water film thickness of the FS surface increase with the concentration of H2O2 solution. The surface damage, nanowear, and subsurface deformation of FS caused by indentation increase with the concentration of H2O2 solution, while the nanohardness and reduced modulus decrease. Further analysis revealed that the water activity on the FS surface plays a critical role in reducing the mechanical and mechanochemical properties. In addition, the treatment with H2O2 solution on the FS surface shows a weakly corrosive effect, which implies the H2O2 treatment can be an alternative method to remove the surface defects on FS optics. [ABSTRACT FROM AUTHOR]

Metastasis remains the primary cause of prostate cancer (CaP)-related death. Using a genome wide shRNA screen, we identified GABARAPL1 as a potential CaP metastasis suppressor. GABARAPL1 mRNA levels inversely correlate with the invasive potential of a panel of human CaP cell lines. Lower mRNA levels correlate with higher Gleason scores in clinical CaP tumor samples. Moreover, Kaplan-Meier curves analysis showed that GABARAPL1 down-regulation in cancer tissues is associated with decreased disease-free survival in CaP patients. Knockdown of GABARAPL1 in human LNCaP cells results in increased invasion in vitro and lymph node metastasis in vivo. Vice versa, ectopic expression of GABARAPL1 decreases the invasiveness of CWR22Rv1 cells. Our previous in vitro shRNA screening identified FOXO4, a PI3K/Akt-inactivating downstream target, as a potential CaP metastasis suppressor. We show here that silencing FOXOs leads to reduced GABARAPL1 expression and enhanced invasion in LNCaP cells. Transfection of constitutively-activated Akt (myr-Akt) increased the invasion of LNCaP cells, which is associated with the inactivation of FOXOs and decreased GABARAPL1 expression. Indeed, forced expression of GABARAPL1 reversed the increased invasiveness of LNCaP/myr-Akt cells. Finally, immunohistochemistry analysis shows that Akt phosphorylation is negatively correlated with GABARAPL1 expression in human CaP tissues. Taken together, our data indicate that the suppression of FOXOs-GABARAPL1 signaling by Akt is an important mechanism for CaP progression and metastasis.