538 research outputs found
Determination of the spin Hall angle, spin mixing conductance and spin diffusion length in Ir/CoFeB for spin-orbitronic devices
Iridium is a very promising material for spintronic applications due to its
interesting magnetic properties such as large RKKY exchange coupling as well as
its large spin-orbit coupling value. Ir is for instance used as a spacer layer
for perpendicular synthetic antiferromagnetic or ferrimagnet systems. However,
only a few studies of the spintronic parameters of this material have been
reported. In this paper, we present inverse spin Hall effect - spin pumping
ferromagnetic resonance measurements on CoFeB/Ir based bilayers to estimate the
values of the effective spin Hall angle, the spin diffusion length within
iridium, and the spin mixing conductance in the CoFeB/Ir bilayer. In order to
have reliable results, we performed the same experiments on CoFeB/Pt bilayers,
which behavior is well known due to numerous reported studies. Our experimental
results show that the spin diffusion length within iridium is 1.3 nm for
resistivity of 250 n.m, the spin mixing conductance of the CoFeB/Ir interface is 30 nm, and the spin Hall angle
of iridium has the same sign than the one of platinum and is evaluated at 26%
of the one of platinum. The value of the spin Hall angle found is 7.7% for Pt
and 2% for Ir. These relevant parameters shall be useful to consider Ir in new
concepts and devices combining spin-orbit torque and spin-transfer torque.Comment: 8 pages, 4 figure
A novel in ovo model to study cancer metastasis using chicken embryos and GFP expressing cancer cells.
Cancer metastasis is the leading cause of cancer-related mortality worldwide. To date, several in vitro methodologies have been developed to understand the mechanisms of cancer metastasis and to screen various therapeutic agents against it. Nevertheless, mimicking an in vivo microenvironment in vitro is not possible; while in vivo experiments are complex, expensive and bound with several regulatory requirements. Herein, we report a novel in ovo model that relies on chicken embryo to investigate cancer cell invasion and metastasis to various organs of the body. In this model, we directly inject green fluorescent protein (GFP) expressing cancer cells to the heart of chicken embryo at 3 days of incubation, then monitor cell migration to various organs. To this end, we used a simple tissue processing technique to achieve rapid imaging and quantification of invasive cells. We were able to clearly observe the migration of GFP expressing cancer cells into various organs of chicken embryo. Organ specific variation in cell migration was also observed. Our new slide pressing based tissue processing technique improved the detectability of migrated cells. We herein demonstrate that the use of GFP expressing cancer cells allows easy detection and quantification of migrated cancer cells in the chicken embryo model, which minimizes the time and effort required in this types of studies compared to conventional histopathological analysis. In conclusion, our investigation provides a new cancer metastasis model that can be further improved to include more complex aspects, such as the use of multiple cell lines and anti-metastatic agents, thus opening new horizons in cancer biology and pharmaceutical research
The promoters of human cell cycle genes integrate signals from two tumor suppressive pathways during cellular transformation
Deciphering regulatory events that drive malignant transformation represents
a major challenge for systems biology. Here we analyzed genome-wide
transcription profiling of an in-vitro transformation process. We focused on a
cluster of genes whose expression levels increased as a function of p53 and
p16INK4A tumor suppressors inactivation. This cluster predominantly consists of
cell cycle genes and constitutes a signature of a diversity of cancers. By
linking expression profiles of the genes in the cluster with the dynamic
behavior of p53 and p16INK4A, we identified a promoter architecture that
integrates signals from the two tumor suppressive channels and that maps their
activity onto distinct levels of expression of the cell cycle genes, which in
turn, correspond to different cellular proliferation rates. Taking components
of the mitotic spindle as an example, we experimentally verified our
predictions that p53-mediated transcriptional repression of several of these
novel targets is dependent on the activities of p21, NFY and E2F. Our study
demonstrates how a well-controlled transformation process allows linking
between gene expression, promoter architecture and activity of upstream
signaling molecules.Comment: To appear in Molecular Systems Biolog
Tracking preleukemic cells in vivo to reveal the sequence of molecular events in radiation leukemogenesis
Epidemiological studies have demonstrated an increased leukemia incidence following ionizing radiation exposure, but to date, the target cells and underlying mechanisms of radiation leukemogenesis remain largely unidentified. We engineered a mouse model carrying a different fluorescent marker on each chromosome 2, located inside the minimum deleted region occurring after radiation exposure and recognized as the first leukemogenic event. Using this tailored model, we report that following radiation exposure, more than half of asymptomatic CBA Sfpi1GFP/mCh mice presented with expanding clones of preleukemic hematopoietic cells harboring a hemizygous interstitial deletion of chromosome 2. Moreover, following isolation of preleukemic hematopoietic stem and progenitor cells irradiated in their native microenvironment, we identified the presence of Sfpi1 point mutations within a subpopulation of these preleukemic cells expanding rapidly (increasing from 6% to 55% in 21 days in peripheral blood in one case), hence identifying for the first time the presence of such cells within a living animal. Importantly, we also report a previously undescribed gender difference in the phenotype of the preleukemic cells and leukemia, suggesting a gender imbalance in the radiation-induced leukemic target cell. In conclusion, we provide novel insights into the sequence of molecular events occurring during the (radiation-induced) leukemic clonal evolution
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Meeting Report of the 16th International Congress of Radiation Research and the 12th International Symposium on Chromosomal Aberrations
Meeting Report on ICRR2019, the 16th International Congress on Radiation Research
This is an Accepted Manuscript of an article published by Taylor & Francis in International Journal of Radiation Biology on 13 Nov 2019, available online: https://www.tandfonline.com/doi/full/10.1080/09553002.2020.1688886. Uploaded in accordance with the publisher's self-archiving policy.NIHR Manchester Biomedical Research Centr
Electrocardiographic imaging demonstrates electrical synchrony improvement by dynamic atrioventricular delays in patients with left bundle branch block and preserved atrioventricular conduction
Aims:
Cardiac resynchronization therapy programmed to dynamically fuse pacing with intrinsic conduction using atrioventricular (AV) timing algorithms (e.g. SyncAV) has shown promise; however, mechanistic data are lacking. This study assessed the impact of SyncAV on electrical dyssynchrony across various pacing modalities using non-invasive epicardial electrocardiographic imaging (ECGi).
Methods and results:
Twenty-five patients with left bundle-branch block (median QRS duration (QRSd) 162.7ā
ms) and intact AV conduction (PR interval 174.0ā
ms) were prospectively enrolled. ECGi was performed acutely during biventricular pacing with fixed nominal AV delays (BiV) and using SyncAV (optimized for the narrowest QRSd) during: BiV + SyncAV, LV-only single-site (LVSS + SyncAV), MultiPoint pacing (MPP + SyncAV), and LV-only MPP (LVMPP + SyncAV). Dyssynchrony was quantified via ECGi (LV activation time, LVAT; RV activation time, RVAT; LV electrical dispersion index, LVEDi; ventricular electrical uncoupling index, VEU; and biventricular total activation time, VVtat). Intrinsic conduction LVAT (124ā
ms) was significantly reduced by BiV pacing (109ā
ms) (P = 0.001) and further reduced by LVSS + SyncAV (103ā
ms), BiV + SyncAV (103ā
ms), LVMPP + SyncAV (95ā
ms), and MPP + SyncAV (90ā
ms). Intrinsic RVAT (93ā
ms), VVtat (130ā
ms), LVEDi (36ā
ms), VEU (50ā
ms), and QRSd (163ā
ms) were reduced by SyncAV across all pacing modes. More patients exhibited minimal LVAT, VVtat, LVEDi, and QRSd with MPP + SyncAV than any other modality.
Conclusion:
Dynamic AV delay programming targeting fusion with intrinsic conduction significantly reduced dyssynchrony, as quantified by ECGi and QRSd for all evaluated pacing modes. MPP + SyncAV achieved the greatest synchrony overall but not for all patients, highlighting the value of pacing mode individualization during fusion optimization
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