DFT-Assisted Microkinetic Study of Transfer Hydrogenation over Homogeneous and Immobilized Cp*Ir Complexes.

DFT calculations were done to investigate the kinetic mechanism of benzaldehyde transfer hydrogenation using [Cp*IrCl] complexes in isopropyl alcohol in the presence of potassium butoxide. Predicted energy barriers provide evidence that the inner-sphere (IS) mechanism (effective barrier 53.0 kJ/mol) is favored over the outer-sphere (OS) and Meerwein-Pondorf-Verley (MPV) mechanisms.

Savor the flavor: A randomized double-blind study assessing taste-enhanced placebo analgesia in healthy volunteers.

Placebo effects substantially contribute to analgesic treatment outcomes and might be leveraged to enhance gold-standard treatments. The taste of oral medications has been proposed to boost placebo effects. Here, we aimed at estimating how far the taste of an oral medication enhances placebo analgesia.

Reverse engineering the kidney: modelling calcium oxalate monohydrate crystallization in the nephron.

Crystallization of calcium oxalate monohydrate in a section of a single kidney nephron (distal convoluted tubule) is simulated using a model adapted from industrial crystallization. The nephron fluid dynamics is represented as a crystallizer/separator series with changing volume to allow for water removal along the tubule. The model integrates crystallization kinetics and crystal size distribution and allows the prediction of the calcium oxalate concentration profile and the nucleation and growth rates.

Bcl-2 overexpression prevents apoptosis induced by ceramidase inhibitors in malignant melanoma and HaCaT keratinocytes.

We examined the biological effects of the ceramide analogues (1S,2R)-2-N-myristoylamino-1-phenyl-1-propanol (D-e-MAPP) and (1R,2R)-2-N-myristoylamino-1-(4-nitrophenyl)-1,3-propandiol (D-NMAPPD) on human HaCaT keratinocytes and human melanoma cells. We could demonstrate that D-e-MAPP and D-NMAPPD are able to suppress acid ceramidase activity. The elevation of the endogenous level of ceramide is followed by induction of apoptosis and suppression of proliferation in HaCaT keratinocytes.