15 research outputs found
Precession-torque-driven domain-wall motion in out-of-plane materials
Domain-wall (DW) motion in magnetic nanostrips is intensively studied, in
particular because of the possible applications in data storage. In this work,
we will investigate a novel method of DW motion using magnetic field pulses,
with the precession torque as the driving mechanism. We use a one dimensional
(1D) model to show that it is possible to drive DWs in out-of-plane materials
using the precession torque, and we identify the key parameters that influence
this motion. Because the DW moves back to its initial position at the end of
the field pulse, thereby severely complicating direct detection of the DW
motion, depinning experiments are used to indirectly observe the effect of the
precession torque. The 1D model is extended to include an energy landscape in
order to predict the influence of the precession torque in the depinning
experiments. Although preliminary experiments did not yet show an effect of the
precession torque, our calculations indicate that depinning experiments can be
used to demonstrate this novel method of DW motion in out-of-plane materials,
which even allows for coherent motion of multiple domains when the
Dzyaloshinskii-Moriya interaction is taken into account
Magnetic domain wall curvature induced by wire edge pinning
open14In this study, we report on the analysis of the magnetic domain wall (DW) curvature due to magnetic field induced motion in Ta/CoFeB/MgO and Pt/Co/Pt wires with perpendicular magnetic anisotropy. In wires of 20 mu m and 25 mu m, a large edge pinning potential produces the anchoring of the DW ends to the wire edges, which is evidenced as a significant curvature of the DW front as it propagates. As the driving magnetic field is increased, the curvature reduces as a result of the system moving away from the creep regime of DW motion, which implies a weaker dependence of the DW dynamics on the interaction between the DW and the wire edge defects. A simple model is derived to describe the dependence of the DW curvature on the driving magnetic field and allows us to extract the parameter sigma (E), which accounts for the strength of the edge pinning potential. The model describes well the systems with both weak and strong bulk pinning potentials like Ta/CoFeB/MgO and Pt/Co/Pt, respectively. This provides a means to quantify the effect of edge pinning induced DW curvature on magnetic DW dynamics.embargoed_20210815Herrera Diez, L.; Ummelen, F.; Jeudy, V.; Durin, G.; Lopez-Diaz, L.; Diaz-Pardo, R.; Casiraghi, A.; Agnus, G.; Bouville, D.; Langer, J.; Ocker, B.; Lavrijsen, R.; Swagten, H. J. M.; Ravelosona, D.Herrera Diez, L.; Ummelen, F.; Jeudy, V.; Durin, G.; Lopez-Diaz, L.; Diaz-Pardo, R.; Casiraghi, A.; Agnus, G.; Bouville, D.; Langer, J.; Ocker, B.; Lavrijsen, R.; Swagten, H. J. M.; Ravelosona, D
Controlling the canted state in antiferromagnetically coupled magnetic bilayers close to the spin reorientation transition
Canted magnetization is obtained in ultrathin, antiferromagnetically coupled magnetic bilayers with thicknesses around the spin reorientation transition. The canting angle is controlled by both the magnetic layer thickness and interlayer coupling strength, which are tuned independently. Hysteresis loops are obtained, where magnetization components parallel and transverse to the applied field are measured, and analyzed by comparison to micromagnetic simulations. This enables the canting angle to be extracted and the behavior of the individual layers to be distinguished. Two types of canted systems are obtained with either single-layer reversal or complex, coupled two-layer reversal, under moderate external magnetic fields. Controlling the magnetization canting and reversal behavior of ultra-thin layers is relevant for the development of magnetoresistive random-access memory and spin-torque oscillator devices.This research was funded by the FP7 ERC 3SPIN Advanced Grant and by a European Erasmus Mobility program. This work is part of the research programme of the Foundation for Fundamental Research on Matter (FOM), which is part of the Netherlands Organisation for Scientific Research (NWO). A. Fernández-Pacheco acknowledges support from an EPSRC Early Career Fellowship EP/M008517/1, and from the Winton Foundation
Proliferation and aneusomy predict survival of young patients with astrocytoma grade II
The clinical course of astrocytoma grade II (AII) is highly variable and not reflected by histological characteristics. As one of the best prognostic factors, higher age identifies rapid progressive A II. For patients over 35 years of age, an aggressive treatment is normally propagated. For patients under 35 years, there is no clear guidance for treatment choices, and therefore also the necessity of histopathological diagnosis is often questioned. We studied the additional prognostic value of the proliferation index and the detection of genetic aberrations for patients with A II. The tumour samples were obtained by stereotactic biopsy or tumour resection and divided into two age groups, that is 18–34 years (n=19) and 35 years (n=28). Factors tested included the proliferation (Ki-67) index, and numerical aberrations for chromosomes 1, 7, and 10, as detected by in situ hybridisation (ISH). The results show that age is a prognostic indicator when studied in the total patient group, with patients above 35 years showing a relatively poor prognosis. Increased proliferation index in the presence of aneusomy appears to identify a subgroup of patients with poor prognosis more accurately than predicted by proliferation index alone. We conclude that histologically classified cases of A II comprise a heterogeneous group of tumours with different biological and genetic constitution, which exhibit a highly variable clinical course. Immunostaining for Ki-67 in combination with the detection of aneusomy by ISH allows the identification of a subgroup of patients with rapidly progressive A II. This is an extra argument not to defer stereotactic biopsy in young patients with radiological suspicion of A II
Fusion of Wild-Type Mesoangioblasts with Myotubes of mtDNA Mutation Carriers Leads to a Proportional Reduction in mtDNA Mutation Load
In 25% of patients with mitochondrial myopathies, pathogenic mitochondrial DNA (mtDNA) mutation are the cause. For heteroplasmic mtDNA mutations, symptoms manifest when the mutation load exceeds a tissue-specific threshold. Therefore, lowering the mutation load is expected to ameliorate disease manifestations. This can be achieved by fusing wild-type mesoangioblasts with mtDNA mutant myotubes. We have tested this in vitro for female carriers of the m.3271T>C or m.3291T>C mutation (mutation load >90%) using wild-type male mesoangioblasts. Individual fused myotubes were collected by a newly-developed laser capture microdissection (LCM) protocol, visualized by immunostaining using an anti-myosin antibody. Fusion rates were determined based on male-female nuclei ratios by fluorescently labelling the Y-chromosome. Using combined ‘wet’ and ‘air dried’ LCM imaging improved fluorescence imaging quality and cell yield. Wild-type mesoangioblasts fused in different ratios with myotubes containing either the m.3271T>C or the m.3291T>C mutation. This resulted in the reduction of the mtDNA mutation load proportional to the number of fused wild-type mesoangioblasts for both mtDNA mutations. The proportional reduction in mtDNA mutation load in vitro after fusion is promising in the context of muscle stem cell therapy for mtDNA mutation carriers in vivo, in which we propose the same strategy using autologous wild-type mesoangioblasts
Transition of high-grade cervical intraepithelial neoplasia to micro-invasive carcinoma is characterized by integration of HPV 16/18 and numerical chromosome abnormalities.
Item does not contain fulltextCervical intraepithelial neoplasia (CIN I, II, and III) and cases of CIN III associated with micro-invasive cervical carcinoma (CIN III & mCA) were analysed for evidence of episomal or integrated human papillomavirus (HPV) 16/18 DNA by fluorescence in situ hybridization (FISH). In parallel, numerical aberrations of chromosomes 1, 17, and X were determined in these lesions as indicators of genomic instability. HPV 16/18 DNA was present in 2 of 12 CIN I, 19 of 23 CIN II/III, and 10 of 12 CIN III & mCA. None of the CIN I and only two of the 19 HPV 16/18-positive solitary CIN II/III showed an integrated HPV pattern. However, all ten cases of HPV-positive CIN III & mCA showed this pattern. Transition of CIN II/III to CIN III & mCA therefore correlates strongly with viral integration (p<0.001). Chromosomal aberrations were detected in 23 of 31 HPV 16/18-positive lesions (14 solitary CIN I-III and nine CIN III & mCA) and 5 of 16 HPV-negative lesions. Nine of 21 HPV 16/18-positive solitary CIN I-III showed tetrasomy for all chromosomes tested, while trisomies for a single chromosome were seen in a further five of these HPV-positive lesions. In eight of ten HPV-positive CIN III & mCA, predominantly aneusomies and/or polysomies were detected. A significant correlation (p<0.02) was found between the chromosome copy number and the physical status of HPV, indicating that in its episomal form HPV induces genomic changes such as tetrasomies and single trisomies, while HPV integration correlates with aneusomies and polysomies, predominantly detected in CIN III & mCA. These data indicate that integration of HPV 16/18 DNA is a pivotal step in the transition of CIN to micro-invasive carcinoma
Controlling the canted state in antiferromagnetically coupled magnetic bilayers close to the spin reorientation transition
Gain of Chromosomal Region 3q26 as a Prognostic Biomarker for High-Grade Cervical Intraepithelial Neoplasia: Literature Overview and Pilot Study
Human papillomavirus typing by single tube multiplex amplification in real time (SMART): The Papilloma Finder (R) SMART 20 assay
Background: High-risk (hr) human papillomavirus (HPV) infections play a causal role in the development of cervical cancer. The detection of hrHPV is, therefore, advocated in cervical cancer screening programs. Objectives: The aim of this study was to determine the performance of a novel HPV typing assay, PapillomaFinder SMART 20. This is a one-tube-per-sample method, to be performed on standard real-time PCR platforms, using melting curve analysis to distinguish targets. The assay detects all 14 hrHPV types, of which 16, 18, 31, 33, 35, 39, 45, 52, 56 and 58 individually. HrHPV types 51, 59, 66 and 68 are detected in an hrHPV pool, and low-risk (lr) HPV types 6, 11, 40, 42, 43 and 44 in an IrHPV pool. Study design: The method was tested on HPV plasmid models, WHO and QCMD proficiency panels and a series of clinical cytological samples (n = 45), the latter in comparison with a clinically validated real-time quantitative PCR. Results: Type-specificity of the test was 100% using plasmids, the WHO and QCMD panels. Sensitivity for hrHPV in single infections was 100% using the WHO and QCMD panels and cytological samples, with an analytical sensitivity of 10-25 copies per reaction for all HPV types tested. Of the 34 HPV types present in the 8 multiple infections in the WHO panel, 30 were detected. In all cytological samples at least one hrHPV type was found, in concordance with the clinically validated method. Only when the viral load of the dominant HPV types in multiple infections greatly exceeded that of the other types in the infection, those other types were not always detected. Conclusions: PapillomaFinder SMART 20 is a rapid, easy to perform, single tube HPV typing assay. The assay detects the 14 hrHPV types, and the 6 most important IrHPV types with a high sensitivity and type-specificity