Metal-to-glass ratio and the Magneto-Impedance of glass-covered CoFeBSi microwires at high frequencies

High frequency [1-500 MHz] measurements of the Magneto-Impedance (MI) of glass-covered Co$_{69.4}$Fe$_{3.7}$B$_{15.9}$Si$_{11}$ microwires are carried out with various metal-to-wire diameter ratios. A twin-peak, anhysteretic behaviour is observed as a function of magnetic field. A maximum in $\Delta Z/Z$ appears at different values of the frequency $f$, 125, 140 and 85 MHz with the corresponding diameter ratio $p$ = 0.80, 0.55 and 0.32. We describe the measurement technique and interpret our results with a thermodynamic model that leads to a clearer view of the effects of $p$ on the maximum value of MI and the anisotropy field.Comment: 5 pages and 6 figure

A Novel Broadband Measurement Method for the Magnetoimpedance of Ribbons and Thin Films

A novel broad-band measurement method of the MI in thin films and ribbons is presented. It is based on the automated measurement of the reflection coefficient of a cell loaded with the sample. Illustrative results obtained with a permalloy multilayer thin film are presented and discussed.Comment: Paper submitted to International Conference on Magnetism (Rome 2003

Geometric signature of reversal modes in ferromagnetic nanowires

Magnetic nanowires are a good platform to study fundamental processes in Magnetism and have many attractive applications in recording such as perpendicular storage and in spintronics such as non-volatile magnetic memory devices (MRAM) and magnetic logic devices. In this work, nanowires are used to study magnetization reversal processes through a novel geometric approach. Reversal modes imprint a definite signature on a parametric curve representing the locus of the critical switching field. We show how the different modes affect the geometry of this curve depending on the nature of the anisotropy (uniaxial or cubic anisotropy), demagnetization and exchange effects. The samples we use are electrochemically grown Nickel and Cobalt nanowires.Comment: 11 pages, 21 figures to submit to Europhysics Letter

Giant magnetoimpedance in Vitrovac amorphous ribbons over [0.3-400 MHz] frequency range

Giant magneto impedance (GMI) effect for as-cast Vitrovac$^{\textrm{\scriptsize\textregistered}}$ amorphous ribbons (Vacuumschmelze, Germany) in two configurations (parallel and normal to the ribbon axis) is studied over the frequency range [0.3-400 MHz] and under static magnetic fields -160 Oe $< H_{dc} <$+160 Oe. A variety of peak features and GMI ratio values, falling within a small field range, are observed and discussed.Comment: Paper submitted to International Conference on Magnetism 2003 (ICM Rome 2003

Nmrk2 gene is upregulated in dilated cardiomyopathy and required for cardiac function and nad levels during aging

Dilated cardiomyopathy (DCM) is a disease of multifactorial etiologies, the risk of which is increased by male sex and age. There are few therapeutic options for patients with DCM who would benefit from identification of common targetable pathways. We used bioinformatics to identify the Nmrk2 gene involved in nicotinamide adenine dinucleotde (NAD) coenzyme biosynthesis as activated in different mouse models and in hearts of human patients with DCM while the Nampt gene controlling a parallel pathway is repressed. A short NMRK2 protein isoform is also known as muscle integrin binding protein (MIBP) binding the α7β1 integrin complex. We investigated the cardiac phenotype of Nmrk2-KO mice to establish its role in cardiac remodeling and function. Young Nmrk2-KO mice developed an eccentric type of cardiac hypertrophy in response to pressure overload rather than the concentric hypertrophy observed in controls. Nmrk2-KO mice developed a progressive DCM-like phenotype with aging, associating eccentric remodeling of the left ventricle and a decline in ejection fraction and showed a reduction in myocardial NAD levels at 24 months. In agreement with involvement of NMRK2 in integrin signaling, we observed a defect in laminin deposition in the basal lamina of cardiomyocytes leading to increased fibrosis at middle age. The α7 integrin was repressed at both transcript and protein level at 24 months. Nmrk2 gene is required to preserve cardiac structure and function, and becomes an important component of the NAD biosynthetic pathways during aging. Molecular characterization of compounds modulating this pathway may have therapeutic potential

Identification of ALDH1A3 as a Viable Therapeutic Target in Breast Cancer Metastasis-Initiating Cells

The development of efficacious therapies targeting metastatic spread of breast cancer to the brain represents an unmet clinical need. Accordingly, an improved understanding of the molecular underpinnings of central nervous system spread and progression of breast cancer brain metastases (BCBM) is required. In this study, the clinical burden of disease in BCBM was investigated, as well as the role of aldehyde dehydrogenase 1A3 (ALDH1A3) in the metastatic cascade leading to BCBM development. Initial analysis of clinical survival trends for breast cancer and BCBM determined improvement of breast cancer survival rates; however, this has failed to positively affect the prognostic milestones of triple-negative breast cancer (TNBC) brain metastases (BM). ALDH1A3 and a representative epithelial-mesenchymal transition (EMT) gene signature (mesenchymal markers, CD44 or Vimentin) were compared in tumors derived from BM, lung metastases (LM), or bone metastases (BoM) of patients as well as mice after injection of TNBC cells. Selective elevation of the EMT signature and ALDH1A3 were observed in BM, unlike LM and BoM, especially in the tumor edge. Furthermore, ALDH1A3 was determined to play a role in BCBM establishment via regulation of circulating tumor cell adhesion and migration phases in the BCBM cascade. Validation through genetic and pharmacologic inhibition of ALDH1A3 via lentiviral shRNA knockdown and a novel small-molecule inhibitor demonstrated selective inhibition of BCBM formation with prolonged survival of tumor-bearing mice. Given the survival benefits via targeting ALDH1A3, it may prove an effective therapeutic strategy for BCBM prevention and/or treatment