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Homojunctions between Bi2Se3 and its Mn-doped phase are investigated as a sample geometry to study the influence of spin degrees of freedom on topological insulator properties. n quintuple layers of Bi2Se3 are grown on top of Mn-doped Bi2Se3 by molecular beam epitaxy for 0 ≤ n ≤ 30QLs, allowing to unhamperedly monitor the development of electronic and topological properties by surface sensitive techniques like angle resolved photoemission spectroscopy. With increasing n, a Mninduced gap at the Dirac point is gradually filled in an "hourglass" fashion to reestablish a topological surface state at n ∼ 9QLs. Our results suggest a competition of upward and downward band bending effects due to the presence of an n-p type interface, which can be used to tailor topological and quantum well states independently. [ABSTRACT FROM AUTHOR]

The electronic structure of thin films of FeTe grown on Bi 2 Te 3 is investigated using angle-resolved photoemission spectroscopy, scanning tunneling microscopy and first principles calculations. As a comparison, data from cleaved bulk Fe 1.08 Te taken under the same experimental conditions is also presented. Due to the substrate and thin film symmetry, FeTe thin films grow on Bi 2 Te 3 in three domains, rotated by 0°, 120°, and 240°. This results in a superposition of photoemission intensity from the domains, complicating the analysis. However, by combining bulk and thin film data, it is possible to partly disentangle the contributions from three domains. We find a close similarity between thin film and bulk electronic structure and an overall good agreement with first principles calculations, assuming a p-doping shift of 65 meV for the bulk and a renormalization factor of around two. By tracking the change of substrate electronic structure upon film growth, we find indications of an electron transfer from the FeTe film to the substrate. No significant change of the film's electronic structure or doping is observed when alkali atoms are dosed onto the surface. This is ascribed to the film's high density of states at the Fermi energy. This behavior is also supported by the ab initio calculations.

We report scanning tunnelling microscopy and spectroscopy (STM/STS) studies on one and two unit cell (UC) high FeSe thin films grown on Bi 2 Se 3 (0 0 0 1). In our thin films, we find the tetragonal phase of FeSe and dumb-bell shaped defects oriented along Se-Se bond directions. In addition, we observe striped moiré patterns with a periodicity of (7.3  ±  0.1) nm generated by the mismatch between the FeSe lattice and the Bi 2 Se 3 lattice. We could not find any signature of a superconducting gap in the tunneling spectra measured on the surface of one and two UC thick islands of FeSe down to 6.5 K. The spectra rather show an asymmetric behavior across and a finite density of states at the Fermi level (E F ) resembling those taken in the normal state of bulk FeSe.

Objective: An overview of medical, cognitive, and affective changes experienced by geriatric long-term care residents during a migration from traditional healthcare delivery to a cottage-based model., Background: New architectural models hold great promise for improving health and social outcomes for residents. New studies must explore the resident, family, and staff outcomes across transformations, as well as the business case for change., Methods: A longitudinal, quasi-experimental design was employed, with an emphasis on regularly acquired institutional data, including the Minimum Data Set, as well as commonly available survey instruments including the MOSES, the 2005 NSWHN, and Castle's Job Satisfaction Questionnaire. Descriptive statistics, McNemar's Exact Test, repeated measures ANOVA, and t-tests were used as well as narratives from families, staff, and management., Results: Staff perceived enhanced institutional respect (t(72) = 2.38, p = 0.02) and work environment, and families perceived more staff cooperation and a better bond between staff and residents. No changes were discerned in a resident's prevalence of pain (odds ratio 0.43, p = .34, 95% CI [0.07, 1.88]), mobility (odds ratio 0.50, p =.19, 95% CI [0.17, 1.32]), range of motion(odds ratio 0.57, p = .55, 95% CI [0.12, 2.25]), or depression and anxiety (odds ratio 2.33, p =.11,95% CI [0.84, 7.41]). A modest decline in residents' systolic (t(101) = 3.74, p < .001) and diastolic (t(101) = 2.870, p < .01) blood pressures was demonstrated. The rate at which a resident's Activities of Daily Living score declined was attenuated (t(57) = 3.37, p < .001). Operational costs remained constant across the move., Conclusions: Cottage settings were aesthetically appealing to residents, family, and staff. Modest improvements in health outcomes were observed, and operational costs remained stable.

The yeast Candida albicans possesses a gene family that encodes secreted aspartic proteases (Saps), which are important for the virulence of this human fungal pathogen. Inhibitors of the Saps could therefore be used as novel antimycotic agents for the treatment of C. albicans infections. In the present study, we established a bioassay which allows testing of the activity of potential protease inhibitors against specific Sap isoenzymes by their ability to inhibit protease-dependent growth of C. albicans. In a medium containing bovine serum albumin (BSA) as the sole source of nitrogen, C. albicans specifically expresses the Sap2p isoenzyme, which degrades the BSA and thereby enables the fungus to grow. As the other SAP genes are not significantly expressed under these conditions, mutants lacking SAP2 are unable to utilize BSA as a nitrogen source and cannot grow in such a medium. To investigate whether forced expression of SAP genes other than SAP2 would also allow growth on BSA, we constructed a set of strains expressing each of the 10 SAP genes from a tetracycline-inducible promoter in a sap2Delta mutant background. Expression of Sap1p, Sap2p, Sap3p, Sap4p, Sap5p, Sap6p, Sap8p, and a C-terminally truncated, secreted Sap9p restored the growth of the sap2Delta mutant with different efficiencies. This set of strains was then used to test the activities of various aspartic protease inhibitors against specific Sap isoenzymes by monitoring growth on BSA in the presence of the inhibitors. While pepstatin blocked the activity of all of the Saps tested, the human immunodeficiency virus protease inhibitors ritonavir and saquinavir inhibited growth of the strains expressing Sap1p to Sap3p and Sap1p, respectively, but not that of strains expressing other Saps. Therefore, the strain set can be used to test the activity of new protease inhibitors against individual C. albicans Sap isoenzymes by their ability to block the growth of the pathogen.

Constitutive overexpression of the MDR1 (multidrug resistance) gene, which encodes a multidrug efflux pump of the major facilitator superfamily, is a frequent cause of resistance to fluconazole and other toxic compounds in clinical Candida albicans strains, but the mechanism of MDR1 upregulation has not been resolved. By genome-wide gene expression analysis we have identified a zinc cluster transcription factor, designated as MRR1 (multidrug resistance regulator), that was coordinately upregulated with MDR1 in drug-resistant, clinical C. albicans isolates. Inactivation of MRR1 in two such drug-resistant isolates abolished both MDR1 expression and multidrug resistance. Sequence analysis of the MRR1 alleles of two matched drug-sensitive and drug-resistant C. albicans isolate pairs showed that the resistant isolates had become homozygous for MRR1 alleles that contained single nucleotide substitutions, resulting in a P683S exchange in one isolate and a G997V substitution in the other isolate. Introduction of these mutated alleles into a drug-susceptible C. albicans strain resulted in constitutive MDR1 overexpression and multidrug resistance. By comparing the transcriptional profiles of drug-resistant C. albicans isolates and mrr1Delta mutants derived from them and of C. albicans strains carrying wild-type and mutated MRR1 alleles, we defined the target genes that are controlled by Mrr1p. Many of the Mrr1p target genes encode oxidoreductases, whose upregulation in fluconazole-resistant isolates may help to prevent cell damage resulting from the generation of toxic molecules in the presence of fluconazole and thereby contribute to drug resistance. The identification of MRR1 as the central regulator of the MDR1 efflux pump and the elucidation of the mutations that have occurred in fluconazole-resistant, clinical C. albicans isolates and result in constitutive activity of this trancription factor provide detailed insights into the molecular basis of multidrug resistance in this important human fungal pathogen.