The electrochemical properties of LiMn2O4 and LiMyMn2−yO4 false(M=normalTi,normalGe,normalFe,normalZn,normalor Nifalse) were studied for different conditions of sample preparation and different degrees of cation substitution false(yfalse) . In the voltage range 3.5–4.5 V, cells of either spinel LiMn2O4 or λ‐MnO2 (made by leaching the Li from LiMn2O4 ) reversibly insert 0.4 Li per Mn at an average voltage of 4.1 V, leading to an energy density of 480 Wh/kg of cathode. Cells cycled 50 times lost less than 10% of their initial capacity, suggesting that this material could be used instead of LiCoO2 or LiNiO2 as the cathode in the new generation of “rocking chair batteries.” Replacing Mn with cations of valence 2 (Ni, Zn) or 3 (Fe) reduces the amount of Mn+3 and correspondingly reduces the capacity of the cells at 4.1 V, but does not affect their cycling performance.

The Hall coefficient RH

Transforming growth factor (TGF)-b plays a dual role in tumorigenesis, switching from acting as a growth inhibitory tumor suppressor early in the process, to a tumor promoter in late-stage disease. Since TGF-b's prometastatic role may be linked to its ability to induce tumor cell epithelial-to-mesenchymal transition (EMT), we explored TGF-b's EMT-promoting pathways by analysing the transcriptome changes occurring in BRI-JM01 mammary tumor epithelial cells undergoing a TGF-b-induced EMT. We found the clusterin gene to be the most highly upregulated throughout most of the TGF-b time course, and showed that this results in an increase of the secreted form of clusterin. By monitoring several hallmark features of EMT, we demonstrated that antibodies targeting secreted clusterin inhibit the TGF-b-induced EMT of BRI-JM01 cells, as well as the invasive phenotype of several other breast and prostate tumor cell lines (4T1, NMuMG, MDA-MB231LM2 and PC3), without affecting the proliferation of these cells. These results indicate that secreted clusterin is a functionally important EMT mediator that lies downstream within TGF-b's EMTpromoting transcriptional cascade, but not within its growth-inhibitory pathways. To further investigate the role played by secreted clusterin in tumor metastasis, we assessed the effect of several anti-clusterin monoclonal antibodies in vivo using a 4T1 syngeneic mouse breast cancer model and found that these antibodies significantly reduce lung metastasis. Taken together, our results reveal a role for secreted clusterin as an important extracellular promoter of EMT, and suggest that antibodies targeting clusterin may inhibit tumor metastasis without reducing the beneficial growth inhibitory effects of TGF-b.