The effect of the support on the surface composition of PtCu alloy nanocatalysts: In situ XPS and HS-LEIS studies

Pt是一类高效、稳定的催化剂, 但Pt资源短缺且价格昂贵, 限制了其广泛商业化应用. 合金化可以使Pt的用量大为减少,; 且往往能显著提高其催化性能, 因而广泛应用于多相催化和电催化. 其中PtCu合金是一类很有前景的催化剂, Cu资源丰富、价格低廉,; 不仅降低了成本, 而且由于合金效应提高了催化剂的活性和稳定性. 由于合金的粒径、形状、组成及结构是影响其催化性能的重要因素,; 目前研究大多关注这些特征的可控合成.然而, 大多工业金属催化剂都是负载于氧化物上以提高催化性能,; 合金纳米粒子的形貌以及表面组成因与载体作用而发生改变, 也就是所谓的载体效应. 这体现在金属/氧化物界面处,; 能够促进金属粒子分散、改变其形貌甚至化学态、进而改变其催化性能, 其中最具代表性的金属-载体强相互作用. 因此,; 研究不同氧化物载体上合金催化剂的分散度、表面组成、化学态, 特别是不同气氛的影响, 对明确影响催化剂性能的关键控制因素非常重要.; 但是由于多相催化剂的复杂性, 且表面灵敏的测试手段很少, 目前相关报道还不多.; 近年发展起来的高灵敏度低能离子散射谱(HS-LEIS)是表面层灵敏的测试技术,; 可以测定最表面层的组成和含量.本文采用溶剂热共还原法成功制备了均一单相、粒径分布较窄的PtCu_x合金纳米颗粒,; 并运用浸渍法将其负载在TiO_2载体上, 以保证载体上纳米粒子组成的均一性.; 应用准原位X-射线光电子能谱(XPS)和高HS-LEIS对负载的PtCu合金纳米催化剂在不同条件处理后的表面组成和化学状态进行表征,; 发现催化剂的表面组成、分布、形貌和化学状态显著受到载体和处理条件的影响, 同时得到负载和未负载的催化剂表面组成与体相组成关系的相图. 结果表明,; PtCu_x/TiO_2催化剂在连续氧化过程中, Cu被氧化并较好在载体表面铺展, Pt-Cu合金状态被破坏,; Pt可能主要形成单一金属的纳米粒子, 并在界面处形成Ptd+. 在连续还原过程中, 部分被还原的Cu, 与Pt形成富Pt合金粒子.; 催化剂表面层主要是Cu, Pt很少, 与体相组成有很大差别, 说明载体对Cu的分散起到重要作用.Supported PtCu alloys have been broadly applied in heterogeneous catalysis and electrocatalysis owing to their excellent catalytic performance and high CO tolerance. It is important to analyze the outermost surface composition of the supported alloy nanoparticles to understand the nature of the catalytically active sites. In this paper, homogeneous face-centered cubic PtCu nanoparticles with a narrow particle size distribution were successfully fabricated and dispersed on a high-surface-area TiO2 powder support. The samples were oxidized and reduced in situ and then introduced into the ultrahigh vacuum chamber to measure the topmost surface composition by high-sensitivity low-energy ion scattering spectroscopy, and to determine the oxidation states of the elements by X-ray photoelectron spectroscopy. The surface composition and morphology, elemental distribution, and oxidation states of the components were found to be significantly affected by the support and treatment conditions. The PtCu is de-alloyed upon oxidation with CuO wetting on the TiO2 surface and re-alloyed upon reduction. Phase diagrams of the surface composition and the bulk composition were plotted and compared for the supported and unsupported materials. (C) 2017, Dalian Institute of Chemical Physics, Chinese Academy of Sciences. Published by Elsevier B.V. All rights reserved.National Basic Research Program of China (973 Program) [2013CB933102];; National Natural Science Foundation of China [21273178, 21573180,; 91545204]; Xiamen-Zhuoyue Biomass Energy Co. Ltd

Chronic Lymphocytic Leukemia: Insights from Lymph Nodes & Bone Marrow and Clinical Perspectives

B-cell chronic lymphocytic leukemia (B-CLL) is characterized by highly variable distribution of tumor mass between peripheral blood, bone marrow and lymphoid organs which is important for staging, classification and prognosis. These clinical findings with novel data about importance of B-cell receptor and its stimulation with the support of microenvironment indicate important role of tissues (lymphoid organs and bone marrow) in the pathogenesis of B-CLL. Here is presented the novel approach of simultaneous characterization of B-CLL cells form peripheral blood, bone marrow and lymph nodes by flow cytometry and immunocytochemistry, defining inter- and intraclonal diversity with respect to various molecules. These include adhesion molecules (integrins, immunoglobulins, selectins), chemokine receptors (including CXCR-4), signaling molecules and prognostic factors (CD38 and ZAP-70), proliferation and apoptosis markers (including Ki67, AgNORs with PK index, survivin, bcl-2) and therapeutic targets (CD20 and CD52) and residual hematopoietic stem cells. A number of interesting significant interactions have been discovered, pointing to the important role of neoplastic cell microenvironment. These may in addition to insights in pathogenesis and roles of different microenvironments add to diagnosis, prognosis and treatment of B-CLL patients

Effects of hyperbaric oxygen on the osteogenic differentiation of mesenchymal stem cells

BACKGROUND: Hyperbaric oxygenation was shown to increase bone healing in a rabbit model. However, little is known about the regulatory factors and molecular mechanism involved.We hypothesized that the effect of hyperbaric oxygen (HBO) on bone formation is mediated via increases in the osteogenic differentiation of mesenchymal stem cells (MSCs) which are regulated by Wnt signaling. METHODS: The phenotypic characterization of the MSCs was analyzed by flow cytometric analysis. To investigate the effects of HBO on Wnt signaling and osteogenic differentiation of MSCs, mRNA and protein levels of Wnt3a, beta-catenin, GSK-3beta, Runx 2, as well as alkaline phosphatase activity, calcium deposition, and the intensity of von Kossa staining were analyzed after HBO treatment. To investigate the effects of HBO on Wnt processing and secretion, the expression of Wntless and vacuolar ATPases were quantified after HBO treatment. RESULTS: Cells expressed MSC markers such as CD105, CD146, and STRO-1. The mRNA and protein levels of Wnt3a, β-catenin, and Runx 2 were up-regulated, while GSK-3β was down-regulated after HBO treatment. Western blot analysis showed an increased β-catenin translocation with a subsequent stimulation of the expression of target genes after HBO treatment. The above observation was confirmed by small interfering (si)RNA treatment. HBO significantly increased alkaline phosphatase activity, calcium deposition, and the intensity of von Kossa staining of osteogenically differentiated MSCs. We further showed that HBO treatment increased the expression of Wntless, a retromer trafficking protein, and vacuolar ATPases to stimulate Wnt processing and secretion, and the effect was confirmed by siRNA treatment. CONCLUSIONS: HBO treatment increased osteogenic differentiation of MSCs via regulating Wnt processing, secretion, and signaling

Morals and climate decision-making: insights from social and behavioural sciences

Decisions about climate change are inherently moral. They require making moral judgements about important values and the desired state of the present and future world. Hence there are potential benefits in explaining climate action by integrating well-established and emerging knowledge on the role of morality in decision-making. Insights from the social and behavioural sciences can help ground climate change decisions in empirical understandings of how moral values and worldviews manifest in people and societies. Here, we provide an overview of progress in research on morals in the behavioural and social sciences, with an emphasis on empirical research. We highlight the role morals play in motivating and framing climate decisions; outline work describing morals as relational, situated, and dynamic; and review how uneven power dynamics between people and groups with multiple moralities shape climate decision-making. Effective and fair climate decisions require practical understandings of how morality manifests to shape decisions and action. To this end, we aim to better connect insights from social and behavioural scholarship on morality with real-world climate change decision-making

Effect of hyperbaric oxygen on mesenchymal stem cells for lumbar fusion in vivo

<p>Abstract</p> <p>Background</p> <p>Hyperbaric oxygen (HBO) therapy has been proved in improving bone healing, but its effects on mesenchymal stem cells (MSCs) <it>in vivo </it>is not clear. The aims of this study are to clarify whether the HBO therapy has the same enhancing effect on MSCs with regard to bone formation and maturation and to ascertain whether the transplanted MSCs survive in the grafted area and contribute to new bone formation.</p> <p>Methods</p> <p>Twenty-three adult rabbits underwent posterolateral fusion at L4-L5 level. The animals were divided into three groups according to the material implanted and subsequent treatment: (1) Alginate carrier (n = 6); (2) Alginate-MSCs composite (n = 11); and (3) Alginate-MSCs composite with HBO therapy (n = 6). After 12 weeks, spine fusion was examined using radiographic examination, manual testing, and histological examination. Using a PKH fluorescence labeling system, whether the transplanted MSCs survived and contributed to new bone formation in the grafted area after HBO therapy was also examined.</p> <p>Results</p> <p>The bilateral fusion areas in each animal were evaluated independently. By radiographic examination and manual palpation, union for the Alginate, Alginate-MSCs, and Alginate-MSCs-HBO groups was 0 of 12, 10 of 22, and 6 of 12 respectively. The difference between the Alginate-MSCs and Alginate-MSCs-HBO groups was not significant (P = 0.7997). The fluorescence microscopy histological analysis indicated that the transplanted PKH67-labeled MSCs survived and partly contributed to new bone formation in the grafted area.</p> <p>Conclusions</p> <p>This study demonstrated that the preconditioned MSCs could survive and yield bone formation in the grafted area. HBO therapy did not enhance the osteogenic ability of MSCs and improve the success of spine fusion in the rabbit model. Although there was no significant effect of HBO therapy on MSCs for spine fusion, the study encourages us to research a more basic approach for determining the optimal oxygen tension and pressure that are required to maintain and enhance the osteogenic ability of preconditioned MSCs. Further controlled <it>in vivo </it>and <it>in vitro </it>studies are required for achieving a better understanding of the effect of HBO treatment on MSCs.</p

A Missense Mutation in a Highly Conserved Alternate Exon of Dynamin-1 Causes Epilepsy in Fitful Mice

Dynamin-1 (Dnm1) encodes a large multimeric GTPase necessary for activity-dependent membrane recycling in neurons, including synaptic vesicle endocytosis. Mice heterozygous for a novel spontaneous Dnm1 mutation—fitful—experience recurrent seizures, and homozygotes have more debilitating, often lethal seizures in addition to severe ataxia and neurosensory deficits. Fitful is a missense mutation in an exon that defines the DNM1a isoform, leaving intact the alternatively spliced exon that encodes DNM1b. The expression of the corresponding alternate transcripts is developmentally regulated, with DNM1b expression highest during early neuronal development and DNM1a expression increasing postnatally with synaptic maturation. Mutant DNM1a does not efficiently self-assemble into higher order complexes known to be necessary for proper dynamin function, and it also interferes with endocytic recycling in cell culture. In mice, the mutation results in defective synaptic transmission characterized by a slower recovery from depression after trains of stimulation. The DNM1a and DNM1b isoform pair is highly conserved in vertebrate evolution, whereas invertebrates have only one isoform. We speculate that the emergence of more specialized forms of DNM1 may be important in organisms with complex neuronal function

Cold and heterogeneous T cell repertoire is associated with copy number aberrations and loss of immune genes in small-cell lung cancer

Small-cell lung cancer (SCLC) is speculated to harbor complex genomic intratumor heterogeneity (ITH) associated with high recurrence rate and suboptimal response to immunotherapy. Here, using multi-region whole exome/T cell receptor (TCR) sequencing as well as immunohistochemistry, we reveal a rather homogeneous mutational landscape but extremely cold and heterogeneous TCR repertoire in limited-stage SCLC tumors (LS-SCLCs). Compared to localized non-small cell lung cancers, LS-SCLCs have similar predicted neoantigen burden and genomic ITH, but significantly colder and more heterogeneous TCR repertoire associated with higher chromosomal copy number aberration (CNA) burden. Furthermore, copy number loss of IFN-γ pathway genes is frequently observed and positively correlates with CNA burden. Higher mutational burden, higher T cell infiltration and positive PD-L1 expression are associated with longer overall survival (OS), while higher CNA burden is associated with shorter OS in patients with LS-SCLC

Molecular characterization of hepatitis B virus X gene in chronic hepatitis B patients

BACKGROUND: HBV-X protein is associated with the pathogenesis of HBV related diseases, specially in hepatocellular carcinomas of chronic patients. Genetic variability of the X gene includes genotypic specific variations and mutations emerging during chronic infection. Its coding sequence overlaps important regions for virus replication, including the basal core promoter. Differences in the X gene may have implications in biological functions of the protein and thus, affect the evolution of the disease. There are controversial results about the consequences of mutations in this region and their relationship with pathogenesis. The purpose of this work was to describe the diversity of HBV-X gene in chronic hepatitis patients infected with different genotypes, according to liver disease. METHODS: HBV-X gene was sequenced from chronic hepatitis B patient samples, analyzed by phylogeny and genotyped. Nucleotide and aminoacid diversity was determined calculating intragenetic distances. Mutations at 127, 130 and 131 aminoacids were considered in relation to liver disease. RESULTS: The most prevalent genotype detected in this cohort was F (F1 and F4), followed by D and A. Most of the samples corresponding to genotypes A and F1 were HBeAg(+) and for genotypes D and F4, HBeAg(−) samples were represented in a higher percentage. Intragenetic distance values were higher in HBeAg(−) than in positive samples for all genotypes, and lower in overlapped regions, compared to single codification ones. Nucleotide and aminoacid diversities were higher in HBeAg(−), than in HBeAg(+) samples. CONCLUSIONS: Independently of the infecting genotypes, mutations at any of 127, 130 and/or 131 aminoacid positions and HBeAg(−) status were associated with mild liver disease in this cohort

SlimPLS: A Method for Feature Selection in Gene Expression-Based Disease Classification

A major challenge in biomedical studies in recent years has been the classification of gene expression profiles into categories, such as cases and controls. This is done by first training a classifier by using a labeled training set containing labeled samples from the two populations, and then using that classifier to predict the labels of new samples. Such predictions have recently been shown to improve the diagnosis and treatment selection practices for several diseases. This procedure is complicated, however, by the high dimensionality if the data. While microarrays can measure the levels of thousands of genes per sample, case-control microarray studies usually involve no more than several dozen samples. Standard classifiers do not work well in these situations where the number of features (gene expression levels measured in these microarrays) far exceeds the number of samples. Selecting only the features that are most relevant for discriminating between the two categories can help construct better classifiers, in terms of both accuracy and efficiency. In this work we developed a novel method for multivariate feature selection based on the Partial Least Squares algorithm. We compared the method's variants with common feature selection techniques across a large number of real case-control datasets, using several classifiers. We demonstrate the advantages of the method and the preferable combinations of classifier and feature selection technique

Transcriptional Activation of TINF2, a Gene Encoding the Telomere-Associated Protein TIN2, by Sp1 and NF-κB Factors

The expression of the telomere-associated protein TIN2 has been shown to be essential for early embryonic development in mice and for development of a variety of human malignancies. Recently, germ-line mutations in TINF2, which encodes for the TIN2 protein, have been identified in a number of patients with bone-marrow failure syndromes. Yet, the molecular mechanisms that regulate TINF2 expression are largely unknown. To elucidate the mechanisms involved in human TINF2 regulation, we cloned a 2.7 kb genomic DNA fragment containing the putative promoter region and, through deletion analysis, identified a 406 bp region that functions as a minimal promoter. This promoter proximal region is predicted to contain several putative Sp1 and NF-κB binding sites based on bioinformatic analysis. Direct binding of the Sp1 and NF-κB transcription factors to the TIN2 promoter sequence was demonstrated by electrophoretic mobility shift assay (EMSA) and/or chromatin immunoprecipitation (ChIP) assays. Transfection of a plasmid carrying the Sp1 transcription factor into Sp-deficient SL2 cells strongly activated TIN2 promoter-driven luciferase reporter expression. Similarly, the NF-κB molecules p50 and p65 were found to strongly activate luciferase expression in NF-κB knockout MEFs. Mutating the predicted transcription factor binding sites effectively reduced TIN2 promoter activity. Various known chemical inhibitors of Sp1 and NF-κB could also strongly inhibit TIN2 transcriptional activity. Collectively, our results demonstrate the important roles that Sp1 and NF-κB play in regulating the expression of the human telomere-binding protein TIN2, which can shed important light on its possible role in causing various forms of human diseases and cancers