Shape Transition in the Epitaxial Growth of Gold Silicide in Au Thin Films on Si(111)

Growth of epitaxial gold silicide islands on bromine-passivated Si(111) substrates has been studied by optical and electron microscopy, electron probe micro analysis and helium ion backscattering. The islands grow in the shape of equilateral triangles up to a critical size beyond which the symmetry of the structure is broken, resulting in a shape transition from triangle to trapezoid. The island edges are aligned along $Si[110]$ directions. We have observed elongated islands with aspect ratios as large as 8:1. These islands, instead of growing along three equivalent [110] directions on the Si(111) substrate, grow only along one preferential direction. This has been attributed to the vicinality of the substrate surface.Comment: revtex version 3.0, 11 pages 4 figures available on request from [email protected] - IP/BBSR/93-6

Structure determination of the (1×2) and (1×3) reconstructions of Pt(110) by low-energy electron diffraction

The atomic geometry of the (1×2) and (1×3) structures of the Pt(100) surface has been determined from a low-energy electron-diffraction intensity analysis. Both structures are found to be of the missing-row type, consisting of (111) microfacets, and with similar relaxations in the subsurface layers. In both reconstructions the top-layer spacing is contracted by approximately 20% together with a buckling of about 0.17 Å in the third layer and a small lateral shift of about 0.04 Å in the second layer. Further relaxations down to the fourth layer were detectable. The surface relaxations correspond to a variation of interatomic distances, ranging from -7% to +4%, where in general a contraction of approximately 3% for the distances parallel to the surface occurs. The Pendry and Zanazzi-Jona R factors were used in the analysis, resulting in a minimum value of RP=0.36 and RZJ=0.26 for 12 beams at normal incidence for the (1×2) structure, and similar agreement for 19 beams of the (1×3) structure. The (1×3) structure has been reproducibly obtained after heating the crystal in an oxygen atmosphere of 5×10-6 mbar at 1200 K for about 30 min and could be removed by annealing at 1800 K for 45 min after which the (1×2) structure appeared again. Both reconstructed surfaces are clean within the detection limits of the Auger spectrometer. CO adsorption lifts the reconstruction in both structures. After desorption at 500 K the initial structures appear again, indicating that at least one of the reconstructions does not represent the equilibrium structure of the clean surface and may be stabilized by impurities

Pro-autophagic signal induction by bacterial pore-forming toxins

Pore-forming toxins (PFT) comprise a large, structurally heterogeneous group of bacterial protein toxins. Nucleated target cells mount complex responses which allow them to survive moderate membrane damage by PFT. Autophagy has recently been implicated in responses to various PFT, but how this process is triggered is not known, and the significance of the phenomenon is not understood. Here, we show that S. aureus α-toxin, Vibrio cholerae cytolysin, streptolysin O and E. coli haemolysin activate two pathways leading to autophagy. The first pathway is triggered via AMP-activated protein kinase (AMPK). AMPK is a major energy sensor which induces autophagy by inhibiting the target of rapamycin complex 1 (TORC1) in response to a drop of the cellular ATP/AMP-ratio, as is also observed in response to membrane perforation. The second pathway is activated by the conserved eIF2α-kinase GCN2, which causes global translational arrest and promotes autophagy in response to starvation. The latter could be accounted for by impaired amino acid transport into target cells. Notably, PKR, an eIF2α-kinase which has been implicated in autophagy induction during viral infection, was also activated upon membrane perforation, and evidence was obtained that phosphorylation of eIF2α is required for the accumulation of autophagosomes in α-toxin-treated cells. Treatment with 3-methyl-adenine inhibited autophagy and disrupted the ability of cells to recover from sublethal attack by S. aureus α-toxin. We propose that PFT induce pro-autophagic signals through membrane perforation–dependent nutrient and energy depletion, and that an important function of autophagy in this context is to maintain metabolic homoeostasis

Underground coal gasification with CCS: A pathway to decarbonising industry

Underground coal gasification (UCG) opens up the prospect of accessing trillions of tonnes of otherwise unmineable coal. When combined with carbon capture and storage (CCS), UCG offers some attractive new low-carbon solutions on a vast scale. This paper has several aims: to review key developments in technologies for UCG, CCS and CO2 storage in coal seam voids; to quantify the scale of the opportunity that these technologies open up; to examine the scope for linking these developments to other more familiar plans for decarbonising the fossil fuel power generation industry and other carbon-intensive industries; to identify the main hurdles to be overcome in taking forward any large-scale UCG–CCS proposition; and to propose a basis on which UCG-CCS can sit at the heart of plans to decarbonise present day industry in a way that dove-tails with longer-term ambitions for an economy based on renewable energy

Oncolytic Activity of Vesicular Stomatitis Virus Is Effective against Tumors Exhibiting Aberrant p53, Ras, or Myc Function and Involves the Induction of Apoptosis

We have recently shown that vesicular stomatitis virus (VSV) exhibits potent oncolytic activity both in vitro and in vivo (S. Balachandran and G. N. Barber, IUBMB Life 50:135–138, 2000). In this study, we further demonstrated, in vivo, the efficacy of VSV antitumor action by showing that tumors that are defective in p53 function or transformed with myc or activated ras are also susceptible to viral cytolysis. The mechanism of viral oncolytic activity involved the induction of multiple caspase-dependent apoptotic pathways was effective in the absence of any significant cytotoxic T-lymphocyte response, and occurred despite normal PKR activity and eIF2α phosphorylation. In addition, VSV caused significant inhibition of tumor growth when administered intravenously in immunocompetent hosts. Our data indicate that VSV shows significant promise as an effective oncolytic agent against a wide variety of malignant diseases that harbor a diversity of genetic defects