Mitigation of CO poisoning on functionalized Pt-TiN surfaces.

It has been previously reported that the system of single Pt atoms embedded in N-vacancy (V(N)) sites on the TiN(100) surface (Pt-TiN) could be a promising catalyst for proton exchange membrane fuel cells (PEM FCs). The adsorption of molecules on Pt-TiN is an important step, when it is incorporated as the anode or cathode of PEM FCs. Utilizing first principles calculations based on density functional theory, systematic investigations are performed on the adsorption of several atomic and molecular species on the Pt-TiN system, as well as the co-adsorption of them. The favorable binding sites and adsorption energies of several molecular species, namely carbon dioxide (CO2), carbon monoxide (CO), oxygen (O2), hydrogen (H2), hydroxyl (OH), an oxygen atom (O), and a hydrogen atom (H), are explored. For each, the adsorption energy and preferred binding site are identified and the vibrational frequencies calculated. It is found that CO2, CO and H prefer the Pt top site while OH and O favorably adsorb on the Ti top site. When CO and OH are co-adsorbed on the Pt-TiN(100) surface, OH weakens the adsorption of CO. The weakening effect is enhanced by increasing the coverage of OH. A similar behavior occurs for H and OH co-adsorption on the Pt-TiN(100) surface. Because co-adsorption with OH and H species weakens the adsorption of CO on Pt-TiN, it is expected that the acid and base conditions in PEM FCs could mitigate CO poisoning on functionalized Pt-TiN surfaces.

Oxidation of step edges on Si(001)-c(4x2).

The initial oxidation process of the ultraclean Si(001)-c(4x2) surface is studied using scanning tunneling microscopy at low temperature. At the early stage of oxygen adsorption, reactions with Si atoms at SB steps are dominant over those at terraces by more than 2 orders of magnitude, and they proceed in two distinct stages to high oxidation states. Guided by the ab initio calculations, the oxidation structures at each stage are proposed. The extreme reactivity of the step edge is due to the presence of rebonded adatoms with dangling bonds and weak rebonds, and their proximity allows the formation of -Si-O- chain structures along the step edge, unlike those on the Si(111) surface.

Spontaneous N incorporation onto a Si(100) surface.

Initial nitridation of the Si(100) surface is investigated using photoemission, ion-scattering and ab initio calculations. After dissociation of NO or NH3, nitrogen atoms are found to spontaneously form a stable, highly coordinated N[triple bond]Si(3) species even at room temperature. The majority of the N species is incorporated into the subsurface Si layers occupying an interstitial site, whose atomic structure and unique bonding mechanism is clarified through ab initio calculations. This unusual adsorption behavior elucidates the atomistic mechanism of initial silicon nitride formation on the surface and has important implication on the N-rich layer formation at the SiO(x)N(y)/Si interface.

Novel pathway to the growth of diamond on cubic beta-SiC(001).

By carrying out first-principles calculations on diamond-forming processes, we predict a method for the heteroepitaxial growth of diamond on cubic beta-SiC(001). In the method, we used two processes: (i) the preformation of an sp(3)-like surface configuration of beta-SiC(001) by the adsorption of group-V surfactants; (ii) the successive growth of diamond by the segregation of the surfactants onto a surface and the desorption of surface hydrogen. Analyzing the segregation energies, we found that the atomic size effect plays a crucial role in the surfactant-mediated growth of diamond on beta-SiC(001).

Formation of an icosahedral structure during the freezing of gold nanoclusters: surface-induced mechanism.

The freezing behavior of gold nanoclusters was studied by employing molecular dynamics simulations based on the semiempirical embedded-atom method. Investigations of the gold nanoclusters revealed that, just after freezing, ordered nanosurfaces with a fivefold symmetry were formed with interior atoms remaining in the disordered state. Further lowering of temperatures induced nanocrystallization of the interior atoms that proceeded from the surface towards the core region, finally leading to an icosahedral structure. These dynamic processes explain why the icosahedral cluster structure is dominantly formed in spite of its energetic metastability.

Mammalian Trithorax and polycomb-group homologues are antagonistic regulators of homeotic development.

Control of cell identity during development is specified in large part by the unique expression patterns of multiple homeobox-containing (Hox) genes in specific segments of an embryo. Trithorax and Polycomb-group (Trx-G and Pc-G) proteins in Drosophila maintain Hox expression or repression, respectively. Mixed lineage leukemia (MLL) is frequently involved in chromosomal translocations associated with acute leukemia and is the one established mammalian homologue of Trx. Bmi-1 was first identified as a collaborator in c-myc-induced murine lymphomagenesis and is homologous to the Drosophila Pc-G member Posterior sex combs. Here, we note the axial-skeletal transformations and altered Hox expression patterns of Mll-deficient and Bmi-1-deficient mice were normalized when both Mll and Bmi-1 were deleted, demonstrating their antagonistic role in determining segmental identity. Embryonic fibroblasts from Mll-deficient compared with Bmi-1-deficient mice demonstrate reciprocal regulation of Hox genes as well as an integrated Hoxc8-lacZ reporter construct. Reexpression of MLL was able to overcome repression, rescuing expression of Hoxc8-lacZ in Mll-deficient cells. Consistent with this, MLL and BMI-I display discrete subnuclear colocalization. Although Drosophila Pc-G and Trx-G members have been shown to maintain a previously established transcriptional pattern, we demonstrate that MLL can also dynamically regulate a target Hox gene.

MLL, a mammalian trithorax-group gene, functions as a transcriptional maintenance factor in morphogenesis.

Determinative events in vertebrate embryogenesis appear to require the continuous expression of spatial regulators such as the clustered homeobox genes. The mechanisms that govern long-term patterns of gene expression are not well understood. In Drosophila, active and silent states of developmentally regulated loci are maintained by trithorax and Polycomb group. We have examined the developmental role of a mammalian homolog of trx and putative oncogene, Mll. Knockout mice reveal that Mll is required for maintenance of gene expression early in embryogenesis. Downstream targets of Mll including Hoxa7 are activated appropriately in the absence of Mll but require Mll for sustaining their expression. The Mll-/- phenotype manifests later in development and is characterized by branchial arch dysplasia and aberrant segmental boundaries of spinal ganglia and somites. Thus, Mll represents an essential mechanism of transcriptional maintenance in mammalian development, which functions in multiple morphogenetic processes.

Defects in yolk sac hematopoiesis in Mll-null embryos.

Translocations involving the mixed lineage leukemia gene (MLL), the human homolog of the Drosophila gene trithorax, are one of the most common genetic alterations in human acute leukemias. Each translocation involving MLL results in loss of one functional copy of MLL and the generation of a chimeric fusion protein with potential dominant negative or neomorphic activity. Mll is a positive regulator of Hox genes, which have been implicated in both axial skeleton patterning and hematopoietic development. Previous studies indicated that Hox gene expression is altered in Mll heterozygous (+/-) and homozygous (-/-) deficient mice. To study the role of Mll in hematopoiesis and to obtain insights into leukemogenesis, we have examined the effects of haplo-insufficiency or absence of Mll by in vitro differentiation of Mll +/+, +/-, and -/- yolk sac progenitor cells. Mll -/- colonies were fewer in number, took longer to develop, and contained fewer cells than their wild-type and heterozygous counterparts. Formation of colony-forming unit-granulocyte, erythroid, macrophage, megakaryocyte (CFU-GEMM), colony-forming unit-macrophage (CFU-M), and burst-forming unit-erythroid (BFU-E) was markedly decreased in Mll -/- cultures, while numbers of colony-forming unit-erythroid (CFU-E), colony-forming unit-granulocyte (CFU-G), and colony-forming unit-granulocyte macrophage (CFU-GM) were essentially unaffected. Despite the decreased numbers of colonies present, Mll -/- cultures showed all cell types without morphologic evidence of maturation arrest. These studies indicate that Mll is required for normal numbers of hematopoietic progenitors and their proper differentiation, especially along the myeloid and macrophage pathways.

Altered Hox expression and segmental identity in Mll-mutant mice.

The mixed-lineage leukaemia gene (MLL/HRX/ALL-1) is disrupted by chromosomal translocation in human acute leukaemias that often display mixed lymphoid-myeloid phenotypes and present in infancy. MLL possesses a highly conserved SET domain also found in Drosophila trithorax (trx) and Polycomb group (Pc-G) genes, which are known to regulate homeotic genes (HOM-C) in a positive or negative fashion, respectively. Mll was targeted in mice by homologous recombination in embryonic stem (ES) cells to assess its role in pattern development. Mll heterozygous (+/-) mice had retarded growth, displayed haematopoietic abnormalities, and demonstrated bidirectional homeotic transformations of the axial skeleton as well as sternal malformations. Mll deficiency (-/-) was embryonic lethal. Anterior boundaries of Hoxa-7 and Hoxc-9 expression were shifted posteriorly in Mll +/- embryos, but their expression was abolished in Mll -/- embryos. Thus Mll is required for proper segment identity in mammals, displays haplo-insufficiency, and positively regulates Hox gene expression.