Halogen-Induced Corrosion of Platinum

The interaction of Cl with Pt(110) was studied in UHV by scanning tunneling microscopy, low-energy electron diffraction, temperature- programmed desorption, and DFT calculations. Up to half a monolayer (ML) of Cl forms an adsorbate structure. Compression to higher local coverages leads to erosion of Pt atoms from the top layer and formation of PtCl(4) pentamers. Anneating results in heating of the Pt defects and formation of a long- range-ordered PtCl(4)/Cl/Pt(110) adlayer that is remarkably simitar to the adtayer structure found after deposition of [PtCl(4)](2-) from an electrolyte onto Au(100). Coadsorption of 0.5 ML of Cl with CO initiates PtCl(4) formation, but no volatile compounds are formed under these conditions. In similar experiments with Br, the original Pt surface is left intact, even if Br is compressed to local coverages of 0.75 ML, in agreement with the expected tower corrosion activity of Br

Structure of the c(2x2)-Br/Pt(110) surface

We present a detailed investigation of the c(2x2)-Br/Pt(110) adlayer structure supplemented by the analysis of the (1x2) missing-row (MR) structure of the clean Pt(110) surface. Quantitative low energy electron diffraction analyses and first-principles calculations are in impressive agreement in both cases. The clean surface reconstruction is determined with unprecedented accuracy. For the adsorbate, the analysis retrieves a simple Br-adlayer structure with the Br atoms residing in every second short bridge position on the close-packed Pt rows with the MR reconstruction lifted. The Br-Pt bond length L=2.47 Angstrom is almost equal to the sum of the atomic radii. The substrate below the adsorbate exhibits a contraction of the first layer spacing which amounts to half of that calculated for an unreconstructed clean surface

(3x1)-Br/Pt(110) structure and the charge-density-wave-assisted c(2x2) to (3x1) phase transition

After our recent report on the formation of a (3x1) charge-density-wave phase in the quasi-one-dimensional system Br/Pt(110) we present a detailed investigation of the c(2x2)-->(3x1) transition in the Br/Pt(110) adsorption system. This includes the atomic structure of the (3x1) phase as determined by quantitative low-energy electron diffraction (LEED) and density functional theory calculations. While in the parent c(2x2) phase with coverage Theta=1/2 ML the Br atoms occupy every second short-bridge site on the unreconstructed (1x1)-Pt(110) surface, the adatoms in the (3x1) phase at coverage Theta=2/3 ML reside in every third short-bridge and long-bridge sites. Charge densities and vertical relaxations of the Pt atoms forming the short- and long-bridge sites are different, thus yielding a modulation of both, the charge and the position of the outermost Pt atoms with a period of three nearest-neighbor spacings. For 1/2 M

Sodium/hydrogen exchanger NHA2 is critical for insulin secretion in β-cells.

NHA2 is a sodium/hydrogen exchanger with unknown physiological function. Here we show that NHA2 is present in rodent and human β-cells, as well as β-cell lines. In vivo, two different strains of NHA2-deficient mice displayed a pathological glucose tolerance with impaired insulin secretion but normal peripheral insulin sensitivity. In vitro, islets of NHA2-deficient and heterozygous mice, NHA2-depleted Min6 cells, or islets treated with an NHA2 inhibitor exhibited reduced sulfonylurea- and secretagogue-induced insulin secretion. The secretory deficit could be rescued by overexpression of a wild-type, but not a functionally dead, NHA2 transporter. NHA2 deficiency did not affect insulin synthesis or maturation and had no impact on basal or glucose-induced intracellular Ca(2+) homeostasis in islets. Subcellular fractionation and imaging studies demonstrated that NHA2 resides in transferrin-positive endosomes and synaptic-like microvesicles but not in insulin-containing large dense core vesicles in β-cells. Loss of NHA2 inhibited clathrin-dependent, but not clathrin-independent, endocytosis in Min6 and primary β-cells, suggesting defective endo-exocytosis coupling as the underlying mechanism for the secretory deficit. Collectively, our in vitro and in vivo studies reveal the sodium/proton exchanger NHA2 as a critical player for insulin secretion in the β-cell. In addition, our study sheds light on the biological function of a member of this recently cloned family of transporters

Electronically driven phase transitions in a quasi-one-dimensional adsorbate system

A quasi-1D system is prepared using the Pt(110) surface as a template. The electronic surface resonance structure is studied by angle-resolved photoemission spectroscopy for the clean surface as well as for different Bromine coverages. A Fermi surface mapping reveals saddle points at the Fermi level in the interior of the surface Brillouin zone. Correspondingly, a maximum in the static response function chi(q, 0) at the connecting vector q is expected. With 1/2G(x) < q < 2/3G(x) one observes indeed a 3-fold periodicity around defects and a 2-fold periodicity at low temperature for I similar to(Br) = 0.5 ML. Cooling of a defect-free c(2x2)-Br/Pt(110) preparation counter-intuitively results in a loss of long-range order. Motivated by DFT calculations this is attributed to an anomalous order-order phase transition into the (2x1) phase accompanied by intense, strongly anisotropic fluctuations within a temperature range of similar to 200 K. The peculiar behaviour is rationalised in terms of a competition between inter-adsorbate repulsion and an adsorbate triggered 2k(F) interaction in the substrate