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The simulated rough surface with desired parameters is widely used as an input for the numerical simulation of tribological behavior such as the asperity contact, lubrication, and wear. In this study, a simulation method for generating non-Gaussian rough surfaces with desired autocorrelation function (ACF) and spatial statistical parameters, including skewness (Ssk) and kurtosis (Sku), was developed by combining the fast Fourier transform (FFT), translation process theory, and Johnson translator system. The proposed method was verified by several numerical examples and proved to be faster and more accurate than the previous methods used for the simulation of non-Gaussian rough surfaces. It is convenient to simulate the non-Gaussian rough surfaces with various types of ACFs and large autocorrelation lengths. The significance of this study is to provide an efficient and accurate method of non-Gaussian rough surfaces generation to numerically simulate the tribological behavior with desired rough surface parameters.

Propofol, a widely used anesthetic, can cause addictive behaviors in both human and experimental animals. In the present study, we examined the involvement of glucocorticoid receptor (GR) signaling in the molecular process by which propofol may cause addiction. The propofol self-administration model was established by a fixed ratio 1 (FR1) schedule of reinforced dosing over successive 14days in rats. On day 15, the rats were treated with dexamethasone, a GR agonist (10-100μg/kg), or RU486, a GR antagonist (10-100μg/kg) at 1h prior to the last training. The animal behaviors were recorded automatically by the computer. The expression of dopamine D1 receptor in the nucleus accumbens (NAc) was examined by Western blot and the concentrations of plasma corticosterone were measured by enzyme-linked immunosorbent assay (ELISA). To further examine the specificity of GR in the process, mineralocorticoid receptor (MR) antagonist, spironolactone, and dexamethasone plus MR agonist, aldosterone, were also tested. Administration of dexamethasone (100μg/kg) or RU486 (⩾10mg/kg) significantly attenuated the rate of propofol maintained active nose-poke responses and infusions, which were accompanied by reductions in both plasma corticosterone level and the expression of D1 receptor in the NAc. Neither spironolactone alone nor dexamethasone combined with aldosterone affected the propofol-maintaining self-administrative behavior, indicating GR, but not MR, modulates the propofol reward in rats. In addition, neither the food-maintaining sucrose responses under FR1 schedule nor the locomotor activity was affected by any doses of dexamethasone or RU486 tested. These findings provide evidence that GR signaling may play an important role in propofol reward.

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