The functionalization of graphene and (8,0) single-walled carbon nanotubes (SWCNTs) with individual 3d transition metal (TM) atoms was modeled using density functional theory (DFT) calculations. The structural geometry, magnetism, and binding energies were analyzed in terms of the density of states (DOS), Bader charges, and organometallic M(η 6 -C 6 H 6 ) orbital molecular models. Trends in the binding energies were explained by a model, which included several contributions from the chemisorbed atoms: Coulomb interaction, 3d n 4s x f 3d n+x electronic promotion energy (EPE), and occupation of the 1e 2 (δ), 2e 1 (π), and 2a 1 (σ) metal orbitals. 4s occupation, which causes Pauli repulsion, explained the physisorption trends of Cr, Mn, and Cu. The model was successfully extrapolated to a convex surface, such as that of (8,0) SWCNTs. The potential energy surfaces for the adatoms adsorbed on graphene were determined to evaluate the diffusion energy barriers. We found that Sc, Ti, Fe, and Co metals could be isolated on the graphene surface, whereas all other 3d TM atoms diffused (with possible aggregate formation).

Uranyl-peroxide nanoclusters display different topologies based on square, pentagonal and hexagonal building blocks. Computed complexation energies of different cations (Li(+), Na(+), K(+), Rb(+), and Cs(+)) with [UO(2)(O(2))(H(2)O)](n) (n = 4, 5, and 6) macrocycles suggest a strong cation templating effect. The inherent bent structure of a U-O(2)-U model dimer is demonstrated and justified through the analysis of its electronic structure, as well as of the inherent curvature of the four-, five-, and six-uranyl macrocyles. The curvature is enhaced by cation coordination, which is suggested to be the driving force for the self-assembly of the nanocapsules.

Exposure of pancreatic β cells to long-chain saturated fatty acids (SFA) induces a so-called endoplasmic reticulum (ER) stress that can ultimately lead to cell death. This process is believed to participate in insulin deficiency associated with type 2 diabetes, via a decrease in β-cell mass. By contrast, some unsaturated fatty acid species appear less toxic to the cells and can even alleviate SFA-induced ER stress. In the present study, we took advantage of a simple yeast-based model, which brings together most of the trademarks of lipotoxicity in human cells, to screen fatty acids of various structures for their capacity to counter ER stress. Here we demonstrate that the tendency of a free fatty acid (FFA) to reduce SFA toxicity depends on a complex conjunction of parameters, including chain length, level of unsaturation, position of the double bonds and nature of the isomers (cis or trans). Interestingly, potent FFA act as building blocks for phospholipid synthesis and help to restore an optimal membrane organization, compatible with ER function and normal protein trafficking.