Computational fluid dynamics simulation as a tool for optimizing the hydrodynamic performance of membrane bioreactors.

The hydrodynamic properties and shear stresses experienced by a membrane bioreactor (MBR) are directly related to its rate of membrane fouling. In this study, computational fluid dynamic models have been combined with cold model PIV experimental studies to optimize the performance properties of MBRs. The effects of membrane module height, number of aeration tubes and membrane spacing on liquid phase flow rates, gas holdup and shear stresses at the membrane surface have been investigated. It has been found that optimal MBRs experience the greatest shear forces on their surfaces at a distance of 250 mm from the aeration tube, around the 7 aeration tubes used to introduce gas and at the 40 mm spacings between the membrane sheets. Use of an aeration intensity of between 0.02 and 0.47 m3 min-1 generated shear stresses that were 50-85% higher than the original MBR for the same aeration intensity, thus affording optimal membrane performance that minimizes membrane fouling.

Leaching process for recovering valuable metals from the LiNi1/3Co1/3Mn1/3O2 cathode of lithium-ion batteries.

In view of the importance of environmental protection and resource recovery, recycling of spent lithium-ion batteries (LIBs) and electrode scraps generated during manufacturing processes is quite necessary. An environmentally sound leaching process for the recovery of Li, Ni, Co, and Mn from spent LiNi1/3Co1/3Mn1/3O2-based LIBs and cathode scraps was investigated in this study. Eh-pH diagrams were used to determine suitable leaching conditions. Operating variables affecting the leaching efficiencies for Li, Ni, Co, and Mn from LiNi1/3Co1/3Mn1/3O2, such as the H2SO4 concentration, temperature, H2O2 concentration, stirring speed, and pulp density, were investigated to determine the most efficient conditions for leaching. The leaching efficiencies for Li, Ni, Co, and Mn reached 99.7% under the optimized conditions of 1M H2SO4, 1vol% H2O2, 400rpm stirring speed, 40g/L pulp density, and 60min leaching time at 40°C. The leaching kinetics of LiNi1/3Co1/3Mn1/3O2 were found to be significantly faster than those of LiCoO2. Based on the variation in the weight fraction of the metal in the residue, the "cubic rate law" was revised as follows: θ(1-f)1/3=(1-kt/r0ρ), which could characterize the leaching kinetics optimally. The activation energies were determined to be 64.98, 65.16, 66.12, and 66.04kJ/mol for Li, Ni, Co, and Mn, respectively, indicating that the leaching process was controlled by the rate of surface chemical reactions. Finally, a simple process was proposed for the recovery of valuable metals from spent LiNi1/3Co1/3Mn1/3O2-based LIBs and cathode scraps.

Recovery of cathode materials and Al from spent lithium-ion batteries by ultrasonic cleaning.

Cathode materials are difficult to separate from Al-foil substrates during the recycling of spent lithium-ion batteries (LIBs), because of the strong bonding force present. In this study, ultrasonic cleaning was used to separate and recycle these cathode materials. The mechanism of separation was ascribed to the dissolution of polyvinylidene fluoride (PVDF) and the cavitation caused by ultrasound. Based on this mechanism, the key parameters affecting the peel-off efficiency of cathode materials from Al foil was identified as solvent nature, temperature, ultrasonic power, and ultrasonic time. The peel-off efficiency of cathode materials achieved ∼ 99% under the optimized conditions of N-methyl-2-pyrrolidone (NMP) cleaning fluid, 70°C process temperature, 240 W ultrasonic power, and 90 min of ultrasonication. The cathode materials separated from Al foil displayed a low agglomeration degree, which is beneficial to the subsequent leaching process. Finally, a new, environmentally-sound process was proposed to efficiently recycle cathode materials and Al from spent LIBs, consisting of manual dismantling, ultrasonic cleaning, and picking.

[Inhibitory effect of Akt inhibitor deguelin on the growth of PC-3 prostate cancer cells].

OBJECTIVE: To study the inhibitory effect of Akt inhibitor deguelin on PC-3 human prostate cancer cell lines and its possible mechanism. METHODS: PC-3 human prostate cancer cells were cultured in deguelin at the concentrations of 10, 100, 500 and 1 000 nmol/L for 24, 48 and 72 hours, respectively. Then the inhibitory effect of deguelin on the proliferation of the PC-3 cells was determined by MTT assay and that on the cell cycle was detected by flow cytometry. The expression levels of MDM2 and GSK3beta mRNA were measured by RT-PCR and those of MDM2 and GSK3beta proteins by Western blot. RESULTS: At 24, 48 and 72 hours, the inhibition rates of deguelin on the proliferation of the PC-3 prostate cancer cells were (91.10 +/- 3.75), (86.39 +/- 1.16) and (79.51 +/- 2.63)% at 10 nmol/L, (82.46 +/- 3.65), (76.84 +/- 0.97) and (69.69 +/- 2.30) % at 100 nmol/L, (81.46 +/- 0.41), (75.56 +/- 1.12) and (54.07 +/- 3.21)% at 500 nmol/L, and (66.77 +/- 2.82), (58.22 +/- 0.35) and (39.34 +/- 2.40)% at 1000 nmol/L, all with statistically significant differences from the control group (P < 0.01). Deguelin at 10, 100, 500 and 1 000 nmol/L increased the cell cycles blocked in the G0/G1 phase ([62.4 +/- 2.2], [63.6 +/- 1.1 ], [65.0 +/- 0.3] and [66.5 +/- 1.9]%, P < 0.01) and reduced the percentage of the S-phase cells ([14.7 +/- 2.4], [11.1 +/- 5.2], [5.8 +/- 1.1] and [7.0 +/- 0.6]%, P < 0.01). RT-PCR and Western blot showed markedly up-regulated expressions of GSK3 P3 a3beta down-regulated expressions of MDM2 mRNA and proteins in the PC-3 cells treated with deguelin. CONCLUSION: Akt inhibitor deguelin can inhibit the proliferation of PC-3 human prostate cancer cells by affecting the down-stream signal molecules GSK3P3 and betaDM2 in the Akt pathway.

Rapamycin regulates Akt and ERK phosphorylation through mTORC1 and mTORC2 signaling pathways.

Numerous studies have shown that mammalian target of rapamycin (mTOR) inhibitor activates Akt signaling pathway via a negative feedback loop while inhibiting mTORC1 signaling. In this report, we focused on studying the role of mTORC1 and mTORC2 in rapamycin-mediated Akt and ERK phosphorylation, and the antitumor effect of rapamycin in cancer cells in combination with Akt and ERK inhibitors. Moreover, we analyzed the effect of mTORC1 and mTORC2 on regulating cell cycle progression. We found that low concentrations rapamycin increased Akt and ERK phosphorylation through a mTORC1-dependent mechanism because knockdowned raptor induced the activation of Akt and ERK, but higher doses of rapamycin inhibited Akt and ERK phosphorylation mainly via the mTORC2 signaling pathway because that the silencing of rictor led to the inhibition of Akt and ERK phosphorylation. We further showed that mTORC2 was tightly associated with the development of cell cycle through an Akt-dependent mechanism. Therefore, we combined PI3K and ERK inhibitors prevent rapamycin-induced Akt activation and enhanced antitumor effects of rapamycin. Collectively, we conclude that mTORC2 plays a much more important role than mTORC1 in rapamycin-mediated phosphorylation of Akt and ERK, and cotargeting AKT and ERK signaling may be a new strategy for enhancing the efficacy of rapamycin-based therapeutic approaches in cancer cells.