Halide-Induced Band Gap Enhancement from Ba₂SnSe₄ to KBa₂SnSe₄Cl

A new mixed-anion chalcohalide, KBa2SnSe4Cl, was synthesized by a conventional high-temperature solid state method. The introduction of KCl provides a significant increase in the band gap from Ba2SnSe4 (1.79 eV) to KBa2SnSe4Cl (2.37 eV). The theoretical analysis identifies the source of the band gap increase and gives the birefringence value (Δn = 0.042@2090 nm) of KBa2SnSe4Cl. The successful synthesis of KBa2SnSe4Cl enriches the database of chalcogenides and provides a new train of thought for regulating the band gap of crystals

Expression profile of MSK1 and p-MSK1 (Thr-581 and Ser-360) following LPS intracerebral injection.

<p><b>A</b>. Protein levels of t-MSK1, p-MSK1 Thr-581, p-MSK1 Ser-360 were detected before (control) and after injury. GAPDH was also detected by Western blotting. <b>B</b>. Quantification graphs (relative optical density) of the intensity of staining of p-MSK1 (Thr-581) and total MSK1 to GAPDH at each time point. GAPDH was used to confirm that equal amounts of protein were run on the gel. <b>C–H</b>. Immunofluorescence staining of MSK1 and p-MSk1 (Thr581) was performed to assess the staining changes for MSK1 and p-MSK1 immunoreactivity in the cortex at day 1 after LPS-injection. <b>I</b>. Negative control. * and ^# indicate significant differences at P<0.05, compared with normal brain cortex. Scale bars: 40 µm (C–F), 20 µm (G–J).</p

Immunolocalization of MSK1 and p-MSK1 (Thr-581) with different cellular markers in cerebral cortex by double immunofluorescence staining.

<p>In the adult rat brain cortex, within 5(red, <b>A</b> and <b>E</b>) and p-MSK1 (Thr581) (red, <b>I</b> and <b>M</b>) and different cell markers (green, <b>B, F, J, N</b>), such as a neuronal marker (NeuN) and an astrocyte marker (GFAP). The yellow color in the merged images represents colocalization of MSK1 or p-MSK1 (Thr581) with different phenotype-specific markers (<b>C, G, K, O</b>). Colocalization of MSK1 and p-MSK1 (Thr581) with different phenotype-specific markers in the normal group are shown in the brain cortex (<b>D, H, L, P</b>). Quantitative analysis of different phenotype-specific marker-positive cells expressing MSK1 (<b>Q</b>) and p-MSK1 (<b>R</b>) (%) in the unit area (mm²) in the normal group and 1 day after injury. *indicates significant difference at P<0.05, compared with the normal group. Error bars indicate SEM. Scale bars: 20 µm (<b>A–P</b>).</p

Effects of MSK1 gene silencing and Thr-581 mutation on cytokine production in LPS-treated astrocytes.

<p><b>A</b>. Effects of siRNA for MSK1 and non-specific siRNA on LPS-induced expression of MSK1, p-MSK1 (Thr581) and iNOS were detected by Western blotting. <b>B</b>. The bar chart shows the ratio of total MSK1 and p-MSK1 to β-actin. <b>C–E</b>. ELISA showed that MSK1 gene silencing by siRNA further promoted the LPS-mediated upregulation of inflammatory cytokines. <b>F</b>. Western blot analysis showed the effect of mutation of Thr-581 to an alanine residue on LPS-induced expression of p-MSK1 Thr-581, p-MSK1 Ser-360, and total MSK1. <b>G</b>. The bar chart shows the ratio of p-MSK1 Thr-581 and p-MSK1 Ser-360 to total MSK1. <b>H–J</b>. ELISA showed the effect of mutation of Thr-581 on LPS-induced TNFα, IL-6, and IL1-β production in activated astrocytes.</p

MOESM1 of High expression of ETS2 predicts poor prognosis in acute myeloid leukemia and may guide treatment decisions

Additional file 1. The hierarchical differentiation tree of relationship between ETS2 expression level and hematopoietic cell differentiation