To obtain osmotic coefficients, a classic static–view apparatus was used to measure the difference between the vapor pressure of a solvent and that of its salt solution at 25 °C. Vapor–pressure lowering was measured for solutions containing a lithium salt (LiCl, LiBr, LiNO3, LiPF6 and LITFSI) dissolved in a non–aqueous solvent (dimethyl carbonate, dimethyl sulfoxide and acetonitrile) that may be used in a lithium–ion battery. The osmotic–coefficient data are represented by Archer's extended Pitzer equation. Mean ionic activity coefficients for the salts are calculated from the osmotic–coefficient data.

Solubilities were measured from 25 to 45 °C for six lithium salts (LiF, LiCl, LiBr, LiNO3, LiTFSI and LiPF6) in five pure non–aqueous solvents (ethanol, acetonitrile, dimethyl carbonate, dimethyl sulfoxide and propylene carbonate) and in a few of their binary mixtures (ethanol + DMSO, DMC + DMSO and DMC + PC). The experimental method uses a Varian inductively–coupled plasma–optical–emission spectrometer (ICP–OES). Solubilities increase with rising temperature. At a given temperature, LiNO3 shows the highest solubility in all solvents. Salt solubilities follow the order LiNO3 > LiTFSI > LiBr > LiCl > LiPF6 > LiF. The dissolving abilities of the solvents are in the order ethanol > DMSO > acetonitrile > PC > DMC. Coupled with the salt's melting temperature and enthalpy of fusion, liquid–phase activity coefficients for salts were obtained from the solubility data.

The mitochondrial unfolded protein response (UPR^mt) can be triggered in a cell-non-autonomous fashion across multiple tissues in response to mitochondrial dysfunction. The ability to communicate information about the presence of mitochondrial stress enables a global response that can ultimately better protect an organism from local mitochondrial challenges. We find that animals use retromer-dependent Wnt signaling to propagate mitochondrial stress signals from the nervous system to peripheral tissues. Specifically, the polyQ40-triggered activation of mitochondrial stress or reduction of cco-1 (complex IV subunit) in neurons of C. elegans results in the Wnt-dependent induction of cell-non-autonomous UPR^mt in peripheral cells. Loss-of-function mutations of retromer complex components that are responsible for recycling the Wnt secretion-factor/MIG-14 prevent Wnt secretion and thereby suppress cell-non-autonomous UPR^mt. Neuronal expression of the Wnt ligand/EGL-20 is sufficient to induce cell-non-autonomous UPR^mt in a retromer complex-, Wnt signaling-, and serotonin-dependent manner, clearly implicating Wnt signaling as a strong candidate for the "mitokine" signal.