Metal-insulator transition in a multilayer system with a strong magnetic field

We study the Anderson localization in a weakly coupled multilayer system with a strong magnetic field perpendicular to the layers. The phase diagram of 1/3 flux quanta per plaquette is obtained. The phase diagram shows that a three-dimensional quantum Hall effect phase exists for a weak on-site disorder. For intermediate disorder, the system has insulating and normal metallic phases separated by a mobility edge. At an even larger disorder, all states are localized and the system is an insulator. The critical exponent of the localization length is found to be $\nu=1.57\pm0.10$.Comment: Latex file, 3 figure

Universal scaling, beta function, and metal-insulator transitions

We demonstrate a universal scaling form of longitudinal resistance in the quantum critical region of metal-insulator transitions, based on numerical results of three-dimensional Anderson transitions (with and without magnetic field), two-dimensional quantum Hall plateau to insulator transition, as well as experimental data of the recently discovered two-dimensional metal-insulator transition. The associated reflection symmetry and a peculiar logarithmic form of the beta function exist over a wide range in which the resistance can change by more than one order of magnitude. Interesting implications for the two-dimensional metal-insulator transition are discussed.Comment: 4 pages, REVTEX, 4 embedded figures; minor corrections to figures and tex

Vibratool

Function used to apply delay modulation to an input wave for the purpose of creating a more natural vibrato akin to that created on a violin.Architecture & Allied Art

Personality Function Pairs and their Effect on 360-Feedback Reports

Personality Function Pairs and their effect on 360-Feedback Reports Cooper Drose, Keith Eigel, Ph.D, Sara Musgrove, Ph.D. Abstract For years, researchers in psychology have researched the impact of one’s personality type and what effects it has on their everyday lives; however, there has been a lack of research on each person’s personality function pair. The personality function pair is the middle two letters in someone’s four-letter personality code, (Golden, 1979) often labeled as their decision-making style (Sefcik, Prerost, Arbet, 2009). For this study, we compiled data from the past 8 years and have a total of 609 participants. We sought to discover a relationship between subjects’ function pairs using the Golden Personality Type Indicator and their score on The Leaders Lyceum 360-Feedback Report (Eigel & Musgrove, 2013). We hypothesized that the “Sensing Feeling” function pair would score highest on our 360-feedback report based on The Ohio State Leadership studies. These studies found that subjects listed the two most important qualities with regard to leaders and effective leadership as “consideration” and “initiating structure” (Hemphill, Coons, 1957). Because SF’s are both empathetic and detail oriented, we hypothesized they would be most likely to score higher than the other function pairs on our 360. In our results we found that SF’s scored significantly higher than ST’s and NT’s on 26 of the 40 questions which showed significant differences, but were only significantly higher than NF’s on 3 of the 40 questions. In future research it will be important that the 360 is constructed in a way that has different portions tailored to the strengths of each function pair as this will allow for the results to better illustrate where the strengths and weaknesses of the types of minds exist

The Epstein-Barr Virus G-Protein-Coupled Receptor Contributes to Immune Evasion by Targeting MHC Class I Molecules for Degradation

Epstein-Barr virus (EBV) is a human herpesvirus that persists as a largely subclinical infection in the vast majority of adults worldwide. Recent evidence indicates that an important component of the persistence strategy involves active interference with the MHC class I antigen processing pathway during the lytic replication cycle. We have now identified a novel role for the lytic cycle gene, BILF1, which encodes a glycoprotein with the properties of a constitutive signaling G-protein-coupled receptor (GPCR). BILF1 reduced the levels of MHC class I at the cell surface and inhibited CD8+ T cell recognition of endogenous target antigens. The underlying mechanism involves physical association of BILF1 with MHC class I molecules, an increased turnover from the cell surface, and enhanced degradation via lysosomal proteases. The BILF1 protein of the closely related CeHV15 c1-herpesvirus of the Rhesus Old World primate (80% amino acid sequence identity) downregulated surface MHC class I similarly to EBV BILF1. Amongst the human herpesviruses, the GPCR encoded by the ORF74 of the KSHV c2-herpesvirus is most closely related to EBV BILF1 (15% amino acid sequence identity) but did not affect levels of surface MHC class I. An engineered mutant of BILF1 that was unable to activate G protein signaling pathways retained the ability to downregulate MHC class I, indicating that the immune-modulating and GPCR-signaling properties are two distinct functions of BILF1. These findings extend our understanding of the normal biology of an important human pathogen. The discovery of a third EBV lytic cycle gene that cooperates to interfere with MHC class I antigen processing underscores the importance of the need for EBV to be able to evade CD8+ T cell responses during the lytic replication cycle, at a time when such a large number of potential viral targets are expressed

Enigmatic presence of mitochondrial complex I in Trypanosoma brucei bloodstream forms

The presence of mitochondrial respiratory complex I in the pathogenic bloodstream stages of Trypanosoma brucei has been vigorously debated: increased expression of mitochondrially encoded functional complex I mRNAs is countered by low levels of enzymatic activity that show marginal inhibition by the specific inhibitor rotenone. We now show that epitope-tagged versions of multiple complex I subunits assemble into α and β subcomplexes in the bloodstream stage and that these subcomplexes require the mitochondrial genome for their assembly. Despite the presence of these large (740- and 855-kDa) multisubunit complexes, the electron transport activity of complex I is not essential under experimental conditions since null mutants of two core genes (NUBM and NUKM) showed no growth defect in vitro or in mouse infection. Furthermore, the null mutants showed no decrease in NADH:ubiquinone oxidoreductase activity, suggesting that the observed activity is not contributed by complex I. This work conclusively shows that despite the synthesis and assembly of subunit proteins, the enzymatic function of the largest respiratory complex is neither significant nor important in the bloodstream stage. This situation appears to be in striking contrast to that for the other respiratory complexes in this parasite, where physical presence in a life-cycle stage always indicates functional significance

First Record of the Dolichoderine Ant Genus Gracilidris Wild & Cuezzo (Hymenoptera: Formicidae) from Southern Brazil

ABSTRACT - The dolichoderine ant species Gracilidris pombero, sole representative of the genus, is recorded for the first time in southern Brazil. Until now, the species was known only for the open fields of the South American dry diagonal and for a single locality in the Colombian Amazon. The specimens reported here were collected with pitfall traps in grasslands of the Pampa biome, Rio Grande do Sul state, Brazil. This record represents the southernmost occurrence for the genus, extending its distribution in approximately 450 km to the south in the Neotropics and in almost 1,150 km to the south in Brazil

Therapeutic effects of the mitochondrial ROS-redox modulator KH176 in a mammalian model of Leigh Disease

Leigh Disease is a progressive neurometabolic disorder for which a clinical effective treatment is currently still lacking. Here, we report on the therapeutic efficacy of KH176, a new chemical entity derivative of Trolox, in Ndufs4 (-/-) mice, a mammalian model for Leigh Disease. Using in vivo brain diffusion tensor imaging, we show a loss of brain microstructural coherence in Ndufs4 (-/-) mice in the cerebral cortex, external capsule and cerebral peduncle. These findings are in line with the white matter diffusivity changes described in mitochondrial disease patients. Long-term KH176 treatment retained brain microstructural coherence in the external capsule in Ndufs4 (-/-) mice and normalized the increased lipid peroxidation in this area and the cerebral cortex. Furthermore, KH176 treatment was able to significantly improve rotarod and gait performance and reduced the degeneration of retinal ganglion cells in Ndufs4 (-/-) mice. These in vivo findings show that further development of KH176 as a potential treatment for mitochondrial disorders is worthwhile to pursue. Clinical trial studies to explore the potency, safety and efficacy of KH176 are ongoing

Complexity of the microglial activation pathways that drive innate host responses during lethal alphavirus encephalitis in mice

Microglia express multiple TLRs (Toll-like receptors) and provide important host defence against viruses that invade the CNS (central nervous system). Although prior studies show these cells become activated during experimental alphavirus encephalitis in mice to generate cytokines and chemokines that influence virus replication, tissue inflammation and neuronal survival, the specific PRRs (pattern recognition receptors) and signalling intermediates controlling microglial activation in this setting remain unknown. To investigate these questions directly in vivo, mice ablated of specific TLR signalling molecules were challenged with NSV (neuroadapted Sindbis virus) and CNS viral titres, inflammatory responses and clinical outcomes followed over time. To approach this problem specifically in microglia, the effects of NSV on primary cells derived from the brains of wild-type and mutant animals were characterized in vitro. From the standpoint of the virus, microglial activation required viral uncoating and an intact viral genome; inactivated virus particles did not elicit measurable microglial responses. At the level of the target cell, NSV triggered multiple PRRs in microglia to produce a broad range of inflammatory mediators via non-overlapping signalling pathways. In vivo, disease survival was surprisingly independent of TLR-driven responses, but still required production of type-I IFN (interferon) to control CNS virus replication. Interestingly, the ER (endoplasmic reticulum) protein UNC93b1 facilitated host survival independent of its known effects on endosomal TLR signalling. Taken together, these data show that alphaviruses activate microglia via multiple PRRs, highlighting the complexity of the signalling networks by which CNS host responses are elicited by these infections