Adsorption and diffusion of selenite on Boda Claystone Formation

This study provides adsorption and diffusion data of selenite on Boda Claystone Formation (BCF) which is a potential host rock of a deep geological disposal of high-level radioactive waste. The experiments were performed on two diverse core samples: one albitic claystone sample characteristic for the entire BCF and one pyrite containing sample sparsely occurring in BCF. The experiments were carried out under atmospheric conditions. Batch experiments were carried out to study the kinetics of adsorption at a high initial concentration (1.2 × 10−3 M), the adsorption isotherms and reversibility were investigated in the 10−10–10−3 M concentration range. Adsorption onto petrographic thin sections was done to study the elemental distribution on the microscale and the oxidation state of selenium. The maximum of the distribution coefficient was found as Kd ≈ 200 L/kg and a decrease was experienced around 10−6–10−7 M equilibrium concentration, which showed similarities to other argillaceous rocks. Isotopic exchange experiments revealed reversibility of selenite adsorption. Diffusion was studied with through-diffusion and in-diffusion experiments. Using X-ray fluorescence, despite a low initial concentration of 2.3 × 10−5 M in the in-diffusion experiment, a meaningful diffusion profile of selenium could be obtained, from which the selenite apparent diffusion coefficient Dappselenite = (1.5–4.3) × 10−14 m2/s and the selenite rock capacity factor αselenite = 1.4–2.2 were determined. As selenium species are redox sensitive the oxidation state of adsorbed species was studied with X-ray absorption near edge structure spectroscopy on Se–K edge. Adsorbed selenium remained in +IV oxidation state, however reduction was experienced on the pyritic sample

Homeobox NKX2-3 promotes marginal-zone lymphomagenesis by activating B-cell receptor signalling and shaping lymphocyte dynamics.

NKX2 homeobox family proteins have a role in cancer development. Here we show that NKX2-3 is overexpressed in tumour cells from a subset of patients with marginal-zone lymphomas, but not with other B-cell malignancies. While Nkx2-3-deficient mice exhibit the absence of marginal-zone B cells, transgenic mice with expression of NKX2-3 in B cells show marginal-zone expansion that leads to the development of tumours, faithfully recapitulating the principal clinical and biological features of human marginal-zone lymphomas. NKX2-3 induces B-cell receptor signalling by phosphorylating Lyn/Syk kinases, which in turn activate multiple integrins (LFA-1, VLA-4), adhesion molecules (ICAM-1, MadCAM-1) and the chemokine receptor CXCR4. These molecules enhance migration, polarization and homing of B cells to splenic and extranodal tissues, eventually driving malignant transformation through triggering NF-κB and PI3K-AKT pathways. This study implicates oncogenic NKX2-3 in lymphomagenesis, and provides a valid experimental mouse model for studying the biology and therapy of human marginal-zone B-cell lymphomas.This work was supported by Grants from the Instituto de Salud Carlos III (ISCIII), Spanish Ministry of Economy and Competitiveness, FIS-PI12/00202 (to J.A.M.-C.), RTICC-RD12/0036/0063 (to J.A.M-C.), RTICC-RD12/0036/0068 (to M.J.C and F.P.), RTICC-RD12/0036/0022 (to J.L.F-L.), RTICC-RD12/0036/0070 (to J.C.), RTICC-RD12/0036/0010 (to B.B.), RTICC- RD12/0036/0044 (to M.J.B.) and RTICC-RD12/0036/0069 (to J.M.H.R. and M.G.); by Worldwide Cancer Research project grant 15-1322 (to J.A.M.-C., Y.R.C. and M.-Q.D.); by BFU2011-30097 (to Y.R.C); by MINECO SAF2013-45787-R and Marie Curie Programme FP7-PIIF-2012-328177 (to S.R.); by the French-Spanish CITTIL project (to F.P., X.A., J.A.M.-C., C.B. and P. Brousset); by SAF2012-32810, SAF2014-57791-REDC; PIE14/00066, BIO/SA32/14 and CSI001U14 (to I.S.G); by FIS-ISCIII projects PI13/00160 and PI14/00025, and Fundación Inocente Inocente (to C.C.); by Deutsche Krebshilfe, Molecular Mechanisms in Malignant Lymphomas Network Project (to R.S.); by the Institut Universitaire de France (to P. Brousset); by the Broad Medical Research Program of The Eli and Edythe Broad Foundation and the Hungarian Scientific Research Fund (OTKA K108429) (to P. Balogh); by pre- and post-doctoral fellowships from the Foundation for Applied Medical Research (to M.M.V. and E.F.R., respectively); and by a post-doctoral fellowship from the Basque Government (to I.M.-G.). All Spanish funding is co-sponsored by theEuropean Union FEDER progra