Atomic-Scale Interface Engineering of Majorana Edge Modes in a 2D Magnet-Superconductor Hybrid System

Topological superconductors are predicted to harbor exotic boundary states - Majorana zero-energy modes - whose non-Abelian braiding statistics present a new paradigm for the realization of topological quantum computing. Using low-temperature scanning tunneling spectroscopy (STS), we here report on the direct real-space visualization of chiral Majorana edge states in a monolayer topological superconductor, a prototypical magnet-superconductor hybrid system comprised of nano-scale Fe islands of monoatomic height on a Re(0001)-O(2$\times$1) surface. In particular, we demonstrate that interface engineering by an atomically thin oxide layer is crucial for driving the hybrid system into a topologically non-trivial state as confirmed by theoretical calculations of the topological invariant, the Chern number.Comment: 26 pages, 9 figure

Surface X-ray Diffraction Studies of Electrode/Vacuum and Electrode/Electrolyte Interfaces

This thesis presents in situ Surface X-ray Diffraction (SXRD) studies of surfaces and interfaces, in both Ultra High Vacuum (UHV) and an electrochemical environment. Primarily Crystal Truncation Rod (CTR) measurements are utilised to determine a model for the atomic structure at the interface. A SXRD characterisation of the clean Ag(110) and Ag(111) surfaces in UHV were determined as a reference for the rest of the work in this thesis. Following this the growth conditions and structures of a silicene layer on Ag(111) were investigated, by Low Energy Electron Diffraction (LEED) and preliminary SXRD study of the interface structure is presented. A comprehensive study of the Ag(hkl)/alkaline interface is presented. X-ray Voltammetry (XRV) measurements have been performed to determine the potential dependence of the system. CTR measurements have been used to determine the structure at both the electrode and electrolyte sides of the interface. The results reveal large structural changes on the electrolyte side of the interface, with the response of relaxation of the surface layers in the metal. The presence of specifically adsorbed OH on the surface stabilises cations in a compact double layer through non-covalent interactions. The studies were extended to determine the effects of saturating the electrolyte gases, CO and O2 on the double layer structure. The results indicate that double layer structure is subtly perturbed, and hints at a change in the nature of bonding at the interface. Time resolved SXRD measurements are utilised to determine the dynamics of the restructuring of the electrolyte layering at the Ag(111)/Alkaline interface. In order to gain a comprehensive picture of the structural dynamics, two other systems are studied; the Au(111) reconstruction to determine the timescale of the (1 x 1) ↔ (p ×√3) reconstruction, and the underpotential deposition of Ag on Au(111). The results indicate that the mass transport of ions through electrolyte is on a timescale comparable to the charge transfer, whereas the ordering of ions and surface metal atoms occurs on much longer timescales

Effects of Physical Fitness and Body Cathexis on Self-Concept Change in Women after Aerobic Conditioning

Applied Behavioral Studie

Multiple, Nutrient Sensing Kinases Converge to Phosphorylate an Element of cdc34 That Increases Saccharomyces Cerevisiae Lifespan

Indiana University-Purdue University Indianapolis (IUPUI)Growth and division are tightly coordinated with available nutrient conditions. Cells of the budding yeast, Saccharomyces cerevisiae, grow to a larger size prior to budding and DNA replication when preferred carbon sources such as glucose, as opposed to less preferred sources like ethanol and acetate, are available. A culture’s doubling time is also significantly reduced when the available carbon and nitrogen sources are more favorable. These physiological phenomena are well documented but the precise molecular mechanisms relaying nutrient conditions to the growth and division machinery are not well defined. I demonstrate here that Cdc34, the ubiquitin conjugating enzyme that promotes S phase entry, is phosphorylated upon a highly conserved serine residue which is part of a motif that defines the family of Cdc34/Ubc7 ubiquitin conjugating enzymes. This phosphorylation is regulated by multiple, nutrient sensing kinases including Protein Kinase A, Sch9 and TOR. Furthermore, this phosphorylation event is regulated through the cell cycle with the sole induction occurring in the G1 phase which is when nutrients are sensed and cells commit to another round of division. This phosphorylation likely activates Cdc34 and in turn propagates a signal to the cell division cycle machinery that nutrient conditions are favorable for commitment to a new round of division. This phosphorylation is critical for normal cell cycle progression but must be carefully controlled when cells are deprived of nutrients. Crippling the activity of Protein Kinase A, SCH9 or TOR increases the proportion of cells that survive stationary phase conditions, which because of the metabolic conditions that must be maintained and the similarity to post-mitotic mammalian cells, is referred to as a yeast culture’s chronological lifespan. Yeast cells expressing Cdc34 mutants that are no longer subject to this regulation by phosphorylation have a reduced chronological lifespan. A precise molecular mechanism describing the change in Cdc34 activity after phosphorylation of this serine residue is discussed

The V1-V3 region of a brain-derived HIV-1 envelope glycoprotein determines macrophage tropism, low CD4 dependence, increased fusogenicity and altered sensitivity to entry inhibitors

<p>Abstract</p> <p>Background</p> <p>HIV-1 infects macrophages and microglia in the brain and can cause neurological disorders in infected patients. We and others have shown that brain-derived envelope glycoproteins (Env) have lower CD4 dependence and higher avidity for CD4 than those from peripheral isolates, and we have also observed increased fusogenicity and reduced sensitivity to the fusion inhibitor T-1249. Due to the genetic differences between brain and spleen <it>env </it>from one individual throughout gp120 and in gp41's heptad repeat 2 (HR2), we investigated the viral determinants for the phenotypic differences by performing functional studies with chimeric and mutant Env.</p> <p>Results</p> <p>Chimeric Env showed that the V1/V2-C2-V3 region in brain's gp120 determines the low CD4 dependence and high avidity for CD4, as well as macrophage tropism and reduced sensitivity to the small molecule BMS-378806. Changes in brain gp41's HR2 region did not contribute to the increased fusogenicity or to the reduced sensitivity to T-1249, since a T-1249-based peptide containing residues found in brain's but not in spleen's HR2 had similar potency than T-1249 and interacted similarly with an immobilized heptad repeat 1-derived peptide in surface plasmon resonance analysis. However, the increased fusogenicity and reduced T-1249 sensitivity of brain and certain chimeric Env mostly correlated with the low CD4 dependence and high avidity for CD4 determined by brain's V1-V3 region. Remarkably, most but not all of these low CD4-dependent, macrophage tropic envelopes glycoproteins also had increased sensitivity to the novel allosteric entry inhibitor HNG-105. The gp120's C2 region asparagine 283 (N283) has been previously associated with macrophage tropism, brain infection, lower CD4 dependence and higher CD4 affinity. Therefore, we introduced the N283T mutation into an <it>env </it>clone from a brain-derived isolate and into a brain tissue-derived <it>env </it>clone, and the T283N change into a spleen-derived <it>env </it>from the same individual; however, we found that their phenotypes were not affected.</p> <p>Conclusion</p> <p>We have identified that the V1-V3 region of a brain-derived envelope glycoprotein seems to play a crucial role in determining not only the low CD4 dependence and increased macrophage tropism, but also the augmented fusogenicity and reduced sensitivity to T-1249 and BMS-378806. By contrast, increased sensitivity to HNG-105 mostly correlated with low CD4 dependence and macrophage tropism but was not determined by the presence of the brain's V1-V3 region, confirming that viral determinants of phenotypic changes in brain-derived envelope glycoproteins are likely complex and context-dependent.</p