Anti-LIF (internal region) polyclonal antibody

X-ray photoelectron spectroscopy (XPS) is a widely used technique to study surface chemistry and ageing mechanisms of LiNxMnyCozO2 (NMC) based cathodes of lithium ion batteries. Analysis of the literature, however, reveals common problems in interpretation of their XPS spectra: (1) confusion of Ni2p spectra with Auger electron spectra (F-KLL) of fluorine from commonly used PVdF binder and from decomposition of the fluorinated electrolyte components, when the XPS spectra are acquired with Al K alpha X-ray source; (2) ambiguous fitting of the XPS spectral lines with several Lorentzian-Gaussian shapes leads to doubtful assignments of the oxidation states and questionable conclusions on the ageing mechanisms of the electrode materials. Revisiting the XPS data from aged NMC electrodes emphasizes the contribution of LiF and downplays the effect of nickel and manganese fluorides in the formation of cathode-electrolyte interface. To quantify Ni2+/Ni3+ ratio we introduce a novel method based on the ratio between Ni2p(3/2) main peak intensity and intensity of the shake-up satellite. Applying this approach for commercial NMC333, NMC532, NMC622 and NMC811 powder materials we find good correlation with theoretically predicted values for freshly made materials.

Bone tissues have trabecular bone with a high bone turnover and cortical bone with a low turnover. The mechanisms by which the turnover rate of these bone tissues is determined remain unclear. Osteocytes secrete sclerostin, a Wnt/beta -catenin signaling antagonist, and inhibit bone formation. We found that sclerostin expression in cortical bone is more marked than in trabecular bone in Sost reporter mice. Leukemia inhibitory factor (LIF) secreted from osteoclasts reportedly suppressed sclerostin expression and promoted bone formation. Here, we report that osteoclasts downregulate sclerostin expression in trabecular bone and promote bone turnover. Treatment of C57BL/6 mice with an anti-RANKL antibody eliminated the number of osteoclasts and LIF-positive cells in trabecular bone. The number of sclerostin-positive cells was increased in trabecular bone, while the number of beta -catenin-positive cells and bone formation were decreased in trabecular bone. Besides, Tnfsf11 heterozygous (Rankl(+/-)) mice exhibited a decreased number of LIF-positive cells and increased number of sclerostin-positive cells in trabecular bone. Rankl(+/-) mice exhibited a decreased number of beta -catenin-positive cells and reduced bone formation in trabecular bone. Furthermore, in cultured osteoclasts, RANKL stimulation increased Lif mRNA expression, suggesting that RANKL signal increased LIF expression. In conclusion, osteoclasts downregulate sclerostin expression and promote trabecular bone turnover.