Evaporated manganese films as a starting point for the preparation of thin-layer MnO x water-oxidation anodes

A novel method to prepare anodes for water electrolysis cells has been developed, which starts from layers of elemental manganese deposited by physical vapour deposition (PVD) on indium-doped tin oxide (ITO). Oxidation in dry air at 300 °C transforms this metallic Mn layer into a manganese(II)-rich MnOx coating (x = 1–1.3), which also contains a buried layer of an In–Sn alloy originating from reactions with the ITO support. The MnOx films are well connected to the underlying substrate and act as efficient catalysts for water-oxidation catalysis (WOC) at neutral pH. Detailed post-operando analyses using XRD, SEM, TEM and XAS revealed that the dense MnO/Mn3O4 film is virtually not affected by 2 h of electrochemical WOC at E ≈ +1.8 V vs. RHE, corresponding well to the observed good stability of catalytic currents, which is unusual for such thin layers of a MnOx catalyst. The current densities during electrolyses are so far low (i ≈ 50–100 μA cm−2 at pH 7), but optimization of the preparation process may allow for significant improvements. This new, rather easy, and adaptable preparation method for stable, thin-layer MnOx water-oxidation anodes could thus prove to be very useful for a variety of applications

Operation of Calcium-Birnessite Water-Oxidation Anodes: Interactions of the Catalyst with Phosphate Buffer Anions

Investigating the interfaces between electrolytes and electrocatalysts during electrochemical water oxidation is of tremendous importance for an understanding of the factors influencing catalytic activity and stability. Here, the interaction of a wellestablished, nanocrystalline and mesoporous Ca-birnessite catalyst material (initial composition K0.2Ca0.21MnO2.21·1.4 H2O, initial Mn-Oxidation state ~+3.8) with an aqueous potassium phosphate buffer electrolyte at pH 7 was studied by using various electron microscopy and spectroscopy techniques. In comparison to electrolyte solutions not containing phosphate, Ca-birnessite electrodes show especially high and stable oxygen evolution activity in phosphate buffer. During electrolysis, partial ion substitutions of Ca2+ by K + and OH- / O 2- by HnPO4 (3-n)- were observed, leading to the formation of a stable, partially disordered Ca-K-Mn-HnPO4-H2O layer on the outer and the pore surfaces of the electrocatalyst. In this surface layer, Mn(III) ions are stabilized, which are often assumed to be of key importance for oxygen evolution catalysis. Furthermore, evidence for the formation of [Ca/PO4/H2O]- complexes located between the [MnO6] layers of the birnessite was found using Ca 2p and Ca L-edge the soft X-ray synchrotron-based spectroscopy. A possible way to interpret the obviously very favorable, “special relationship” between (hydrogen)phosphates and Ca-birnessites in electrocatalytic water oxidation would be that HnPO4 (3-n)- anions are incorporated into the catalyst material where they act as stabilizing units for Mn3+ centers and also as “internal bases” for the protons released during the reaction

HLA-DP on epithelial cells enables tissue damage by NKp44+ natural killer cells in ulcerative colitis

BACKGROUND & AIMS: Ulcerative colitis (UC) is characterized by severe inflammation and destruction of the intestinal epithelium, and is associated with specific risk single nucleotide polymorphisms in HLA class II. Given the recently discovered interactions between subsets of HLA-DP molecules and the activating natural killer (NK) cell receptor NKp44, genetic as-sociations of UC and HLA-DP haplotypes and their functional implications were investigated. METHODS: HLA-DP haplotype and UC risk association analyses were performed (UC: n = 13,927; control: n = 26,764). Expression levels of HLA-DP on intestinal epithelial cells (IECs) in individuals with and without UC were quantified. Human intestinal 3-dimensional (3D) organoid cocultures with human NK cells were used to deter-mine functional consequences of interactions between HLA-DP and NKp44. RESULTS: These studies identified HLA-DPA1*01:03-DPB1*04:01 (HLA-DP401) as a risk haplotype and HLA-DPA1*01:03-DPB1*03:01 (HLA-DP301) as a protective haplotype for UC in European populations. HLA-DP expression was significantly higher on IECs of individuals with UC compared with controls. IECs in human intestinal 3D organoids derived from HLA-DP401pos individuals showed significantly stronger binding of NKp44 compared with HLA-DP301pos IECs. HLA-DP401pos IECs in organoids triggered increased degranu-lation and tumor necrosis factor production by NKp44+ NK cells in cocultures, resulting in enhanced epithelial cell death compared with HLA-DP301pos organoids. Blocking of HLA-DP401-NKp44 interactions (anti-NKp44) abrogated NK cell activity in cocultures. CONCLUSIONS: We identified an UC risk HLA-DP haplotype that engages NKp44 and activates NKp44+ NK cells, mediating damage to intestinal epithelial cells in an HLA-DP haplotype-dependent manner. The molecular interac-tion between NKp44 and HLA-DP401 in UC can be targeted by therapeutic interventions to reduce NKp44+ NK cell-mediated destruction of the intestinal epithelium in UC