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In this study, a static electrical pitting tester, SEM, and EDS are employed to investigate the effects of supply voltage, supply current, MoS2 concentration, and oil film thickness on the mechanism of electrical pitting for the lubricated surface of Babbitt alloy/bearing steel pair under ac electric field. The pitting regimes, consisting of pitting and no-pitting regimes, have been established in terms of the supply voltage, the oil film thickness, and MoS2 concentration at different supply currents. The area of pitting regime increases with increasing MoS2 concentration and supply current. It is seen from the pitted surfaces of the Babbitt alloy block that there exists an obvious concave crater with a few plateaus. According to the force measurement, the formation process of the metal column is proposed. The cross-sectional area of the plateau significantly increases with increasing oil film thickness and MoS2 concentration. Moreover, the ratio of pitting area to interface power (Ap/P) increases with increasing MoS2 concentration and oil film thickness at the oil film thickness less than 6 μm. When the oil film thickness increases from 6 to 10 μm, the value of Ap/P quickly increases to about 10 times, because MoS2 powders can sufficiently suspend on the oil across the gap. [Copyright &y& Elsevier]

Coenzyme Q 0 (CoQ 0 , 2,3-dimethoxy-5-methyl-1,4-benzoquinone) has been reported to exert anticancer properties against human breast/lung cancer cells. This study investigated the in vitro and in vivo anticancer properties of CoQ 0 on human ovarian carcinoma (SKOV-3) cells and xenografted nude mice, and revealed the underlying molecular mechanism. CoQ 0 induced G 2 /M arrest through downregulation of cyclin B1/A and CDK1/K2 expressions. CoQ 0 -induced autophagy as a survival mechanism was evidenced by increased accumulation of LC3-II, GFP-LC3 puncta, AVOs formation and Beclin-1/Bcl-2 dysregulation. Increased TUNEL-positive cells and Annexin-V/PI stained cells indicated CoQ 0 -induced late apoptosis. Both mitochondrial (caspase-3, PARP and Bax/Bcl-2 dysregulation) and ER stress (caspase-12 and Hsp70) signals are involved in execution of apoptosis. Interestingly, CoQ 0 -induced apoptosis/autophagy is associated with suppression of HER-2/neu and PI 3 K/AKT signalling cascades. CoQ 0 triggered intracellular ROS production, whereas antioxidant N-acetylcysteine prevented CoQ 0 -induced apoptosis, but not autophagy. Inhibition of apoptosis by Z-VAD-FMK suppressed CoQ 0 -induced autophagy (diminished LC3-II/AVOs), indicates CoQ 0 -induced apoptosis led to evoke autophagy. Contrary, inhibition of autophagy by 3-MA/CQ potentiated CoQ 0 -induced apoptosis (increased DNA fragmentation/PARP cleavage). Furthermore, CoQ 0 treatment to SKOV-3 xenografted nude mice reduced tumor incidence and burden. Histopathological analyses confirmed that CoQ 0 modulated xenografted tumor progression by apoptosis induction. Our findings emphasize that CoQ 0 triggered ROS-mediated apoptosis and cytoprotective autophagy.