A Versatile Coating Strategy to Highly Improve the Electrochemical Properties of Layered Oxide LiMO₂ (M = Ni_0.5Mn_0.5 and Ni_1/3Mn_1/3Co_1/3)

This work provides a convenient, effective and highly versatile coating strategy for the layered oxide LiMO₂ (M = Ni_0.5Mn_0.5 and Ni_1/3Mn_1/3Co_1/3). Here, layered oxide LiMO₂ (M = Ni_0.5Mn_0.5 and Ni_1/3Mn_1/3Co_1/3) has been successfully coated with ion conductor of Li₂SiO₃ by in situ hydrolysis of tetraethyl orthosilicate (TEOS) followed by the lithiation process. The discharge capacity, cycle stability, rate capability, and some other electrochemical performances of layered cathode materials LiMO₂ can be highly enhanced through surface-modification by coating appropriate content of Li₂SiO₃. Particularly, the 3 mol % Li₂SiO₃ coated LiNi_1/3Mn_1/3Co_1/3O₂ exhibits approximately a discharge capacity of 111 mAh/g after 300 cycles at the current density of 800 mA/g (5 C). Potentiostatic intermittent titration technique (PITT) test was carried out to investigate the mechanism of the improvement in the electrochemical properties. The diffusion coefficient of Li⁺-ion (D_Li) of Li₂SiO₃ coated layered oxide materials has been greatly increased. We believe our methodology provides a convenient, effective and highly versatile coating strategy, which can be expected to open the way to ameliorate the electrochemical properties of electrode materials for lithium ion batteries

Structure, Phase Transition, and Controllable Thermal Expansion Behaviors of Sc_2–<i>x</i>Fe_<i>x</i>Mo₃O₁₂

The crystal structures, phase transition, and thermal expansion behaviors of solid solutions of Sc_2–<i>x</i>Fe_<i>x</i>Mo₃O₁₂ (0 ≤ <i>x</i> ≤ 2) have been examined using X-ray diffraction (XRD), neutron powder diffraction (NPD), and differential scanning calorimetry (DSC). At room temperature, samples crystallize in a single orthorhombic structure for the compositions of <i>x</i> < 0.6 and monoclinic for <i>x</i> ≥ 0.6, respectively. DSC results indicate that the phase transition temperature from monoclinic to orthorhombic structure is enhanced by increasing the Fe³⁺ content. High-temperature XRD and NPD results show that Sc_1.3Fe_0.7Mo₃O₁₂ exhibits near zero thermal expansion, and the volumetric coefficients of thermal expansion derived from XRD and NPD are 0.28 × 10^–6 °C^–1 (250–800 °C) and 0.65 × 10^–6 °C^–1 (227–427 °C), respectively. NPD results of Sc₂Mo₃O₁₂ (<i>x</i> = 0) and Sc_1.3Fe_0.7Mo₃O₁₂ (<i>x</i> = 0.7) indicate that Fe substitution for Sc induces reduction of the mean Sc­(Fe)–Mo nonbond distance and the different thermal variations of Sc­(Fe)–O5–Mo2 and Sc­(Fe)–O3–Mo2 bond angles. The correlation between the displacements of oxygen atoms and the variation of unit cell parameters was investigated in detail for Sc₂Mo₃O₁₂

Additional file 1: of Sarcandra glabra (Caoshanhu) protects mesenchymal stem cells from oxidative stress: a bioevaluation and mechanistic chemistry

Experimental protocols for mechanistic chemistry. (DOCX 24 kb

MOESM2 of Two phenolic antioxidants in Suoyang enhance viability of •OH-damaged mesenchymal stem cells: comparison and mechanistic chemistry

Additional file 2. The dose response curves of PTIO, FRAP, DPPH, and ABTS assays

Additional file 1: of Lyophilized aqueous extracts of Mori Fructus and Mori Ramulus protect Mesenchymal stem cells from •OH–treated damage: bioassay and antioxidant mechanism

The dose response curves. (PNG 233 kb

The Expression Pattern of the Pre-B Cell Receptor Components Correlates with Cellular Stage and Clinical Outcome in Acute Lymphoblastic Leukemia

<div><p>Precursor-B cell receptor (pre-BCR) signaling represents a crucial checkpoint at the pre-B cell stage. Aberrant pre-BCR signaling is considered as a key factor for B-cell precursor acute lymphoblastic leukemia (BCP-ALL) development. BCP-ALL are believed to be arrested at the pre-BCR checkpoint independent of pre-BCR expression. However, the cellular stage at which BCP-ALL are arrested and whether this relates to expression of the pre-BCR components (<i>IGHM</i>, <i>IGLL1</i> and <i>VPREB1)</i> is still unclear. Here, we show differential protein expression and copy number variation (CNV) patterns of the pre-BCR components in pediatric BCP-ALL. Moreover, analyzing six BCP-ALL data sets (n = 733), we demonstrate that <i>TCF3-PBX1</i> ALL express high levels of <i>IGHM</i>, <i>IGLL1</i> and <i>VPREB1</i>, and are arrested at the pre-B stage. By contrast, <i>ETV6-RUNX1</i> ALL express low levels of <i>IGHM</i> or <i>VPREB1</i>, and are arrested at the pro-B stage. Irrespective of subtype, ALL with high levels of <i>IGHM</i>, <i>IGLL1</i> and <i>VPREB1</i> are arrested at the pre-B stage and correlate with good prognosis in high-risk pediatric BCP-ALL (n = 207). Our findings suggest that BCP-ALL are arrested at different cellular stages, which relates to the expression pattern of the pre-BCR components that could serve as prognostic markers for high-risk pediatric BCP-ALL patients.</p></div

GSEA reveals molecular signature similarities between the <i>IGHM</i>⁺<i>IGLL1</i>⁺<i>VPREB1</i>⁺ BCP-ALL and normal pre-B cells.

<p>(A) The BCP-ALL in data set GSE11877, including 207 high-risk patient samples, were classified into four clusters according the expression levels of <i>IGHM</i>, <i>IGLL1</i> and <i>VPREB1</i>: <i>IGHM+IGLL1+VPREB1+</i> (Cluster 1), <i>IGHM+IGLL1+/-VPREB1+/-</i> (not including <i>IGHM+IGLL1+VPREB1+</i>) (Cluster 2), <i>IGHM-IGLL1+/-VPREB1+/-</i> (not including <i>IGHM-IGLL1-VPREB1-</i>) (Cluster 3) and <i>IGHM-IGLL1-VPREB1-</i> (Cluster 4). (B) Genes highly expressed in pre-B cells are enriched in Cluster 1. Left: The pre-B signature was identified using supervised comparison in data set GSE45460. Middle: Heat map of the pre-B signature in Cluster 1 and the remaining ALL. Right: Enrichment plot shows the enrichment of pre-B signature in the Cluster 1. (C) Genes highly expressed in Cluster 1 are enriched in pre-B cells. Left: The top 400 genes highly expressed in Cluster 1 (Cluster 1 signature) were identified using supervised comparison. Middle: Heat map of the Cluster 1 signature in healthy pre-B cells. Right: Enrichment plot shows the enrichment of Cluster 1 signature in healthy pre-B cells. (D) Pie-chart shows the distribution of genetic subtypes in clusters 1–4. (E) Genes highly expressed in pre-B cells are enriched in the <i>TCF3-PBX1</i> ALL from Cluster 1 but not that from other clusters. Left: Heat map of the pre-B signature in the <i>TCF3-PBX1</i> ALL from Cluster1. Right: Enrichment plot shows the enrichment of pre-B signature in the <i>TCF3-PBX1</i> ALL from Cluster 1. (F) Genes highly expressed in pre-B cells are enriched in Cluster 1 without <i>TCF3-PBX1</i>. Left: Heat map of the pre-B signature in the Cluster1 without <i>TCF3-PBX1</i>. Right: Enrichment plot shows the enrichment of pre-B signature in Cluster 1 without the <i>TCF3-PBX1</i> ALL.</p

The pre-BCR components show differential protein expression and copy number variation patterns in BCP-ALL patients.

<p>(A) Histograms show the differential expression patterns of IGHM, VPREB1 and IGLL1 in CD19⁺-blasts from two patients (#12 and #15). Bone marrow samples were stained with antibodies against μ heavy chain (IGHM), CD179a (VPREB1) and CD179b (IGLL1), and then analyzed by flow cytometry. (B) Copy number variation (CNV) analysis shows the genetic aberration frequencies of the pre-BCR in 123 patients. The pre-BCR is defined as aberrant when one or more of the pre-BCR components showed CNVs. (C) CNV analyses show the percentage of amplifications and/or deletions of <i>IGHM</i>, <i>VPREB1</i> and <i>IGLL1</i>. HH, High Hyperdiploid.</p

The expression pattern of pre-BCR components associates with the clinical outcomes in high-risk patient group.

<p>(A) The percentage of MRD 29 positive patients was compared among clusters 1–4 using Fisher's exact test. MRD 29: minimal residual disease at day 29. (B-E) The Kaplan-Meier Log rank Survival analysis was performed to compare event free survival (B and C) and overall survival (D and E) of the 207 high-risk patients. Survival probabilities between patients within different clusters (1–4) are shown.</p

GSEA reveals molecular signature similarities between the <i>ETV6-RUNX1</i> BCP-ALL and normal pro-B cells.

<p>(A) Genes highly expressed in pro-B cells are enriched in the <i>ETV6-RUNX1</i>. Left: The top 400 genes highly expressed in pro-B cells (pro-B signature) were identified using supervised comparison in data set GSE45460. Middle: Heat map of the pro-B signature in the <i>ETV6-RUNX1</i> and the remaining ALL in data set GSE12995. Right: Enrichment plot show the enrichment of pro-B signature in the <i>ETV6-RUNX1</i> (B) Genes highly expressed in the <i>ETV6-RUNX1</i> are enriched in pro-B cells. Left: The top 400 genes highly expressed in the <i>ETV6-RUNX1</i> (<i>ETV6-RUNX1</i> signature) were identified using supervised comparison. Middle: Heat map of the <i>ETV6-RUNX1</i> signature in healthy pro-B cells. Right: Enrichment plot showing the enrichment of the <i>ETV6-RUNX1</i> signature in healthy pro-B cells.</p