Reversal of anomalous Hall effect and octahedral tilting in SrRuO₃ thin films via hydrogen spillover

The perovskite SrRuO3 (SRO) is a strongly correlated oxide whose physical and structural properties are strongly intertwined. Notably, SRO is an itinerant ferromagnet that exhibits a large anomalous Hall effect (AHE) whose sign can be readily modified. Here, a hydrogen spillover method is used to tailor the properties of SRO thin films via hydrogen incorporation. It is found that the magnetization and Curie temperature of the films are strongly reduced and, at the same time, the structure evolves from an orthorhombic to a tetragonal phase as the hydrogen content is increased up to ≈0.9 H per SRO formula unit. The structural phase transition is shown, via in situ crystal truncation rod measurements, to be related to tilting of the RuO6 octahedral units. The significant changes observed in magnetization are shown, via density functional theory (DFT), to be a consequence of shifts in the Fermi level. The reported findings provide new insights into the physical properties of SRO via tailoring its lattice symmetry and emergent physical phenomena via the hydrogen spillover technique

Control of oxygen vacancy ordering in brownmillerite thin films via ionic liquid gating

Oxygen defects and their atomic arrangements play a significant role in the physical properties of many transition metal oxides. The exemplary perovskite SrCoO3-δ (P-SCO) is metallic and ferromagnetic. However, its daughter phase, the brownmillerite SrCoO2.5 (BM-SCO), is insulating and an antiferromagnet. Moreover, BM-SCO exhibits oxygen vacancy channels (OVCs) that in thin films can be oriented either horizontally (H-SCO) or vertically (V-SCO) to the film’s surface. To date, the orientation of these OVCs has been manipulated by control of the thin film deposition parameters or by using a substrate-induced strain. Here, we present a method to electrically control the OVC ordering in thin layers via ionic liquid gating (ILG). We show that H-SCO (antiferromagnetic insulator, AFI) can be converted to P-SCO (ferromagnetic metal, FM) and subsequently to V-SCO (AFI) by the insertion and subtraction of oxygen throughout thick films via ILG. Moreover, these processes are independent of substrate-induced strain which favors formation of H-SCO in the as-deposited film. The electric-field control of the OVC channels is a path toward the creation of oxitronic devices

Large-area synthesis of ferromagnetic Fe5−x_{5-x}GeTe2_{2}/graphene van der Waals heterostructures with Curie temperature above room temperature

Van der Waals (vdW) heterostructures combining layered ferromagnets and other two-dimensional (2D) crystals are promising building blocks for the realization of ultra-compact devices with integrated magnetic, electronic and optical functionalities. Their implementation in various technologies depends strongly on the development of a bottom-up scalable synthesis approach allowing to realize highly uniform heterostructures with well-defined interfaces between different 2D layered materials. It also requires that each material component of the heterostructure remains functional, which ideally includes ferromagnetic order above room temperature for 2D ferromagnets. Here, we demonstrate large-area growth of Fe$_{5-x}$GeTe$_{2}$/graphene heterostructures achieved by vdW epitaxy of Fe$_{5-x}$GeTe$_{2}$ on epitaxial graphene. Structural characterization confirmed the realization of a continuous vdW heterostructure film with a sharp interface between Fe$_{5-x}$GeTe$_{2}$ and graphene. Magnetic and transport studies revealed that the ferromagnetic order persists well above 300 K with a perpendicular magnetic anisotropy. In addition, epitaxial graphene on SiC(0001) continues to exhibit a high electronic quality. These results represent an important advance beyond non-scalable flake exfoliation and stacking methods, thus marking a crucial step toward the implementation of ferromagnetic 2D materials in practical applications

Predictors of positive health in disability pensioners: a population-based questionnaire study using Positive Odds Ratio

BACKGROUND: Determinants of ill-health have been studied far more than determinants of good and improving health. Health promotion measures are important even among individuals with chronic diseases. The aim of this study was to find predictors of positive subjective health among disability pensioners (DPs) with musculoskeletal disorders. METHODS: Two questionnaire surveys were performed among 352 DPs with musculoskeletal disorders. Two groups were defined: DPs with positive health and negative health, respectively. In consequence with the health perspective in this study the conception Positive Odds Ratio was defined and used in the logistic regression analyses instead of the commonly used odds ratio. RESULTS: Positive health was associated with age ≥ 55 years, not being an immigrant, not having fibromyalgia as the main diagnosis for granting an early retirement, no regular use of analgesics, a high ADL capacity, a positive subjective health preceding the study period, and good quality of life. CONCLUSION: Positive odds ratio is a concept well adapted to theories of health promotion. It can be used in relation to positive outcomes instead of risks. Suggested health promotion and secondary prevention efforts among individuals with musculoskeletal disorders are 1) to avoid a disability pension for individuals <55 years of age; if necessary, to make sure rehabilitation actions continue, 2) to increase efforts to support immigrants to adjust to circumstances connected to ill-health and retirement, 3) to pay special attention to individuals with fibromyalgia and other general pain disorders, and 4) to strengthen ADL activities to support an independent active life among disability pensioners

Mycobacterial trehalose dimycolate reprograms macrophage global gene expression and activates matrix metalloproteinases.

Trehalose 6,6′-dimycolate (TDM) is a cell wall glycolipid and an important virulence factor of mycobacteria. In order to study the role of TDM in the innate immune response to Mycobacterium tuberculosis, microarray analysis was used to examine gene regulation in murine bone marrow-derived macrophages in response to 90-μm-diameter polystyrene microspheres coated with TDM. A large number of genes, particularly those involved in the immune response and macrophage function, were up- or downregulated in response to these TDM-coated beads compared to control beads. Genes involved in the immune response were specifically upregulated in a myeloid differentiation primary response gene 88 (MyD88)-dependent manner. The complexity of the transcriptional response also increased greatly between 2 and 24 h. Matrix metalloproteinases (MMPs) were significantly upregulated at both time points, and this was confirmed by quantitative real-time reverse transcription-PCR (RT-PCR). Using an in vivo Matrigel granuloma model, the presence and activity of MMP-9 were examined by immunohistochemistry and in situ zymography (ISZ), respectively. We found that TDM-coated beads induced MMP-9 expression and activity in Matrigel granulomas. Macrophages were primarily responsible for MMP-9 expression, as granulomas from neutrophil-depleted mice showed staining patterns similar to that for wild-type mice. The relevance of these observations to human disease is supported by the similar induction of MMP-9 in human caseous tuberculosis (TB) granulomas. Given that MMPs likely play an important role in both the construction and breakdown of tuberculous granulomas, our results suggest that TDM may drive MMP expression during TB pathogenesis

Genome-Wide Screen for Mycobacterium tuberculosis Genes That Regulate Host Immunity

In spite of its highly immunogenic properties, Mycobacterium tuberculosis (Mtb) establishes persistent infection in otherwise healthy individuals, making it one of the most widespread and deadly human pathogens. Mtb's prolonged survival may reflect production of microbial factors that prevent even more vigorous immunity (quantitative effect) or that divert the immune response to a non-sterilizing mode (qualitative effect). Disruption of Mtb genes has produced a list of several dozen candidate immunomodulatory factors. Here we used robotic fluorescence microscopy to screen 10,100 loss-of-function transposon mutants of Mtb for their impact on the expression of promoter-reporter constructs for 12 host immune response genes in a mouse macrophage cell line. The screen identified 364 candidate immunoregulatory genes. To illustrate the utility of the candidate list, we confirmed the impact of 35 Mtb mutant strains on expression of endogenous immune response genes in primary macrophages. Detailed analysis focused on a strain of Mtb in which a transposon disrupts Rv0431, a gene encoding a conserved protein of unknown function. This mutant elicited much more macrophage TNFα, IL-12p40 and IL-6 in vitro than wild type Mtb, and was attenuated in the mouse. The mutant list provides a platform for exploring the immunobiology of tuberculosis, for example, by combining immunoregulatory mutations in a candidate vaccine strain

Nuclear Factor-Kappa B Family Member RelB Inhibits Human Immunodeficiency Virus-1 Tat-Induced Tumor Necrosis Factor-Alpha Production

Human Immunodeficiency Virus-1 (HIV-1)-associated neurocognitive disorder (HAND) is likely neuroinflammatory in origin, believed to be triggered by inflammatory and oxidative stress responses to cytokines and HIV protein gene products such as the HIV transactivator of transcription (Tat). Here we demonstrate increased messenger RNA for nuclear factor-kappa B (NF-κB) family member, transcription factor RelB, in the brain of doxycycline-induced Tat transgenic mice, and increased RelB synthesis in Tat-exposed microglial cells. Since genetic ablation of RelB in mice leads to multi-organ inflammation, we hypothesized that Tat-induced, newly synthesized RelB inhibits cytokine production by microglial cells, possibly through the formation of transcriptionally inactive RelB/RelA complexes. Indeed, tumor necrosis factor-alpha (TNFα) production in monocytes isolated from RelB deficient mice was significantly higher than in monocytes isolated from RelB expressing controls. Moreover, RelB overexpression in microglial cells inhibited Tat-induced TNFα synthesis in a manner that involved transcriptional repression of the TNFα promoter, and increased phosphorylation of RelA at serine 276, a prerequisite for increased RelB/RelA protein interactions. The Rel-homology-domain within RelB was necessary for this interaction. Overexpression of RelA itself, in turn, significantly increased TNFα promoter activity, an effect that was completely blocked by RelB overexpression. We conclude that RelB regulates TNFα cytokine synthesis by competitive interference binding with RelA, which leads to downregulation of TNFα production. Moreover, because Tat activates both RelB and TNFα in microglia, and because Tat induces inflammatory TNFα synthesis via NF-κB, we posit that RelB serves as a cryoprotective, anti-inflammatory, counter-regulatory mechanism for pathogenic NF-κB activation. These findings identify a novel regulatory pathway for controlling HIV-induced microglial activation and cytokine production that may have important therapeutic implications for the management of HAND