Reduced energies for thin ferromagnetic films with perpendicular anisotropy

We derive four reduced two-dimensional models that describe, at different spatial scales, the micromagnetics of ultrathin ferromagnetic materials of finite spatial extent featuring perpendicular magnetic anisotropy and interfacial Dzyaloshinskii-Moriya interaction. Starting with a microscopic model that regularizes the stray field near the material's lateral edges, we carry out an asymptotic analysis of the energy by means of $\Gamma$-convergence. Depending on the scaling assumptions on the size of the material domain vs. the strength of dipolar interaction, we obtain a hierarchy of the limit energies that exhibit progressively stronger stray field effects of the material edges. These limit energies feature, respectively, a renormalization of the out-of-plane anisotropy, an additional local boundary penalty term forcing out-of-plane alignment of the magnetization at the edge, a pinned magnetization at the edge, and, finally, a pinned magnetization and an additional field-like term that blows up at the edge, as the sample's lateral size is increased. The pinning of the magnetization at the edge restores the topological protection and enables the existence of magnetic skyrmions in bounded samples.Comment: 29 pages, 1 figur

The Mass-Lumped Midpoint Scheme for Computational Micromagnetics: Newton Linearization and Application to Magnetic Skyrmion Dynamics

We discuss a mass-lumped midpoint scheme for the numerical approximation of the Landau-Lifshitz-Gilbert equation, which models the dynamics of the magnetization in ferromagnetic materials. In addition to the classical micromagnetic field contributions, our setting covers the non-standard Dzyaloshinskii-Moriya interaction, which is the essential ingredient for the enucleation and stabilization of magnetic skyrmions. Our analysis also includes the inexact solution of the arising nonlinear systems, for which we discuss both a constraint-preserving fixed-point solver from the literature and a novel approach based on the Newton method. We numerically compare the two linearization techniques and show that the Newton solver leads to a considerably lower number of nonlinear iterations. Moreover, in a numerical study on magnetic skyrmions, we demonstrate that, for magnetization dynamics that are very sensitive to energy perturbations, the midpoint scheme, due to its conservation properties, is superior to the dissipative tangent plane schemes from the literature

Anaplastic Lymphoma Kinase Receptor: Possible Involvement in Anorexia Nervosa

The pathophysiology of Anorexia Nervosa (AN) has not been fully elucidated. Anaplastic lymphoma kinase (ALK) receptor is a protein-tyrosine kinase mainly known as a key oncogenic driver. Recently, a genetic deletion of ALK in mice has been found to increase energy expenditure and confers resistance to obesity in these animals, suggesting its role in the regulation of thinness. Here, we investigated the expression of ALK and the downstream intracellular pathways in female rats subjected to the activity-based anorexia (ABA) model, which reproduces important features of human AN. In the hypothalamic lysates of ABA rats, we found a reduction in ALK receptor expression, a downregulation of Akt phosphorylation, and no change in the extracellular signal-regulated protein kinases 1 and 2 (ERK1/2) phosphorylation. After the recovery from body weight loss, ALK receptor expression returned to the control baseline values, while it was again suppressed during a second cycle of ABA induction. Overall, this evidence suggests a possible involvement of the ALK receptor in the pathophysiology of AN, that may be implicated in its stabilization, resistance, and/or its exacerbation

EZETIMIBE PROTECTS THP-1 CELLS FROM ISCHEMIA-REPERFUSION INJURY REDUCING OXIDATIVE STRESS AND UP-REGULATING NRF2/ ARE GENE EXPRESSION

Background and Aims: We demonstrated that physical training, characterized by repeated ischemia-reperfusion (I-R) episodes (ischemic conditioning, IC), protects circulating cells from peripheral artery disease (PAD) patients against ischemic harms by reducing oxidative stress (OS) and by up-regulating nuclear factor erythroid 2-related factor 2 (Nrf2)/antioxidant response element (ARE) pathway expression. Ezetimibe (Eze) has been shown to alleviate OS enhancing Nrf2 nuclear translocation in an AMPK/p62-dependent manner. In a cellular I-R and IC model, we aimed to investigate: 1) the effect of Eze on OS and Nrf2/ARE gene expression 2) whether Eze could have a synergistic effect on IC. Methods: THP-1 cells were treated with or without Eze (50mM) overnight, then subjected to 1 or 6 repetitive I-R cycles using EVOS FL Auto Imaging System. Reactive oxygen species (ROS) formation was evaluated with DCF in cytofluorimetry. Nrf2/ARE and p62 gene expression were evaluated by RT-PCR and western blotting. Results: When THP-1 cells were exposed to 1 I-R cycle, the preincubation with Eze significantly reduced ROS formation (p<0.01) and up-regulated Nrf2/ARE pathway expression and p62 phosphorylation (p<0.001). Multiple I-R cycles, acting as IC, significantly reduced ROS formation and upregulated Nrf2/ARE gene expression (p<0.001); in these conditions, Eze preincubation was able not only to almost abolish ROS formation (p<0.01) but also further up-regulate Nrf2/ARE expression. Conclusions: In our I-R model, Eze not only restores I-R-induced oxidative damages through Nrf2/ARE signaling up-regulation but also has a synergistic effect on IC. This new \u201cpleiotropic\u201d effect, if confirmed in vivo, may strengthen the use of Eze in PAD patien

A note on boundedness of operators in Grand Grand Morrey spaces

In this note we introduce grand grand Morrey spaces, in the spirit of the grand Lebesgue spaces. We prove a kind of \textit{reduction lemma} which is applicable to a variety of operators to reduce their boundedness in grand grand Morrey spaces to the corresponding boundedness in Morrey spaces. As a result of this application, we obtain the boundedness of the Hardy-Littlewood maximal operator and Calder\'on-Zygmund operators in the framework of grand grand Morrey spaces.Comment: 8 page

Spectroscopic follow-up of a subset of the Gaia/IPHAS catalogue of Hα-excess sources

State-of-the-art techniques to identify Hα emission-line sources in narrow-band photometric surveys consist of searching for  Hα excess with reference to nearby objects in the sky (position-based selection). However, while this approach usually yields very few spurious detections, it may fail to select intrinsically faint and/or rare Hα-excess sources. In order to obtain a more complete representation of the heterogeneous emission-line populations, we recently developed a technique to find outliers relative to nearby objects in the colour–magnitude diagram (CMD-based selection). By combining position-based and CMD-based selections, we built an updated catalogue of Hα-excess candidates in the Northern Galactic Plane. Here, we present spectroscopic follow-up observations and classification of 114 objects from this catalogue that enables us to test our novel selection method. Out of the 70 spectroscopically confirmed Hα-emitters in our sample, 15 were identified only by the CMD-based selection, and would have been thus missed by the classic position-based technique. In addition, we explore the distribution of our spectroscopically confirmed emitters in the Gaia CMD. This information can support the classification of emission-line sources in large surveys such as the upcoming WEAVE and 4-m Multi-Object Spectroscopic Telescope, especially if augmented with the introduction of other colours

Enhanced Levels of Oxidized Low-Density Lipoprotein Prime Monocytes to Cytokine Overproduction via Upregulation of CD14 and Toll-Like Receptor 4 in Unstable Angina

Objectives— The purpose of this study was to establish whether oxidized low-density lipoprotein (oxLDL) contributes to cytokine overproduction via upregulation of CD14 and toll-like receptor-4 (TLR-4) expression on circulating monocytes of unstable angina (UA) patients. Methods and Results— Expression of CD14 and TLR-4 on circulating monocytes, and the concentration of plasma oxLDL, (interleukin [IL])-6, IL-1 beta, IL-8, tumor necrosis factor (TNF)-alpha, monocyte chemoattractant protein-1 (MCP-1) were measured in 27 control (C) subjects, 29 patients with stable angina (SA), and 27 with UA. CD14 and TLR-4 expression on monocytes and circulating IL-6, IL-1 beta, and oxLDL were higher in UA than in SA and C subjects ( P <0.001). In in vitro experiments, oxLDL increased CD14 and TLR-4 expression ( P <0.001) in control monocytes as well as IL-6, IL-1 beta, and at a lower extent TNF-α and MCP-1 levels in the supernatant ( P from <0.05 to <0.001). The preincubation of sera derived from UA patients but with control monocytes also induced a significant increase of CD14 and TLR-4 expression ( P <0.001) and of IL-6 and IL-1 beta production ( P <0.001) in the supernatant. Conclusions— In UA patients oxLDL may contribute to monocyte overproduction of some cytokines by upregulating CD14 and TLR-4 expression

The Gaia/IPHAS and Gaia/KIS value-added catalogues

We present a sub-arcsecond crossmatch of Gaia DR2 against the INT Photometric H α Survey of the Northern Galactic Plane Data Release 2 (IPHAS DR2) and the Kepler-INT Survey (KIS). The resulting value-added catalogues (VACs) provide additional precise photometry to the Gaia photometry (r, i, and H α for IPHAS, with additional U and g for KIS). In building the catalogue, proper motions given in Gaia DR2 are wound back to match the epochs of IPHAS DR2, thus ensuring high proper motion objects are appropriately crossmatched. The catalogues contain 7927 224 and 791 071 sources for IPHAS and KIS, respectively. The requirement of >5σ parallax detection for every included source means that distances out to 1–1.5 kpc are well covered. We define two additional parameters for each catalogued object: (i) fc, a magnitude-dependent tracer of the quality of the Gaia astrometric fit; (ii) fFP, the false-positive rate for parallax measurements determined from astrometric fits of a given quality at a given magnitude. Selection cuts based on these parameters can be used to clean colour–magnitude and colour–colour diagrams in a controlled and justified manner. We provide both full and light versions of the VAC, with VAC-light containing only objects that represent our recommended trade-off between purity and completeness. Uses of the catalogues include the identification of new variable stars in the matched data sets, and more complete identification of H α-excess emission objects due to separation of high-luminosity stars from the main sequence

Risk of Post-Traumatic Stress Disorder in 111 survivors the 2009 Viareggio (Italy) Rail Crash: The role of mood spectrum comorbidity

Objectives: To explore the presence of PTSD and the potential correlations between the risk of developing PTSD and the lifetime mood spectrum signs and symptoms, as assessed with the Mood Spectrum Questionnaire Lifetime Version (MOODS-SR), in a sample of survivors of a liquid gas train crash in Italy, in 2009. Methods: One hundred eleven subjects were assessed with the Structured Clinical Interview for Axis I Disorder (SCID-I), the Mood Spectrum Questionnaire (MOODS-SR) Lifetime version, the Impact of Event Scale-Revised (IES-R), and the Trauma and Loss Spectrum Questionnaire (TALS-SR). Results: Sixty-six subjects, of the 111 who completed the SCID-I (59.5%), met criteria for PTSD. PTSD patients showed higher comorbidity rates for Generalized Anxiety Disorder (GAD) (p < 0.001), and lifetime and current Major Depressive Disorder (MDD) (p < 0.001) than subjects who did not develop PTSD. Lifetime MOODS-SR 'Sociability/Extraversion' factor and the prevalence of lifetime MDD differentiated subjects with from those without PTSD, when a multiple logistic regression analysis was performed. Conclusions: Although further research is needed, our results show a significant correlation between the risk of developing PTSD and the mood spectrum comorbidity

Editorial: Epigenetic insights into diagnostic and therapeutic applications

Studies of the heredity and variation in DNA sequence that directs normal development of all living organisms has fundamentally reshaped our understanding of human disease. However, a greater focus on an additional layer of information that does not depend on the underlying DNA sequence referred to as “epigenetics”, has emerged. Epigenetic processes have been recognized as critical for refining DNA-encoded instructions that direct cellular function, and there is increasing evidence that epigenetic dysregulation plays a central role in human disease. In contrast to irreversible genetic mutations, alterations to epigenetic pathways are dynamic, making them attractive therapeutic targets