3D magnetization profile and multi-axes exchange bias in Co antidot arrays

Cu/Co/Cu trilayers have been deposited on nanoporous alumina membranes. Magnetic properties of the resulting Co antidot arrays are investigated using SQUID magnetometry. Hysteresis loops of these arrays show two-step magnetization reversal. In addition, exchange bias is observed, whether the cooling field is applied within or perpendicular to the surface plane. In the former case, the exchange bias changes sign close to the blocking temperature, and becomes positive. We attribute these effects to the local, crescent shape of the Co films, induced by the surface morphology of the alumina membranes. This morphology leads to a three-dimensional magnetization distribution at the nanoscale.Comment: 3 pages, 3 figure

Reduction of magnetostatic interactions in self-organized arrays of nickel nanowires using atomic layer deposition

Ordered arrays of magnetic nanowires are commonly synthesized by electrodeposition in nanoporous alumina templates. Due to their dense packing, strong magnetostatic interactions prevent the manipulation of wires individually. Using atomic layer deposition we reduce the diameter of the pores prior to electrodeposition. This reduces magnetostatic interactions, yielding fully remanent hysteresis loops. This is a first step towards the use of such arrays for magnetic racetrack memories

Role of caspases, calpain and cdk5 in ammonia-induced cell death in developing brain cells.

Hyperammonemia in neonates and infants causes irreversible damages in the developing CNS due to brain cell loss. Elucidating the mechanisms triggering ammonia-induced cell death in CNS is necessary for the development of neuroprotective strategies. We used reaggregated developing brain cell cultures derived from fetal rat telencephalon exposed to ammonia as an experimental model. Ammonia induced neuronal and oligodendroglial death, triggered apoptosis and activated caspases and calpain. Probably due to calpain activation, ammonia caused the cleavage of the cyclin-dependent kinase 5 activator, p35, to p25, the cdk5/p25 complex being known to lead to neurodegeneration. Roscovitine, a cdk5 inhibitor, protected neurons from ammonia-induced cell death. However, roscovitine also impaired axonal growth, probably through inhibition of the remaining cdk5/p35 activity, which is involved in neurite outgrowth. Thus, cdk5 appears as a promising therapeutic target for treating hyperammonemic newborns and infants, especially if one develops specific cdk5/p25 inhibitors

Study of spacecraft transponder power amplifier Final report

Communications satellite wideband transponder feasibility study with direct RF to RF CONVERSION and TWT in re-entrant mod

Ordered arrays of magnetic nanowires investigated by polarized small-angle neutron scattering

Polarized small-angle neutron scattering (PSANS) experimental results obtained on arrays of ferromagnetic Co nanowires ($\phi\approx13$ nm) embedded in self-organized alumina (Al$_{2}$O$_{3}$) porous matrices are reported. The triangular array of aligned nanowires is investigated as a function of the external magnetic field with a view to determine experimentally the real space magnetization $\vec{M}(\vec{r})$ distribution inside the material during the magnetic hysteresis cycle. The observation of field-dependentSANSintensities allows us to characterize the influence of magnetostatic fields. The PSANS experimental data are compared to magnetostatic simulations. These results evidence that PSANS is a technique able to address real-space magnetization distributions in nanostructured magnetic systems. We show that beyond structural information (shape of the objects, two-dimensional organization) already accessible with nonpolarized SANS, using polarized neutrons as the incident beam provides information on the magnetic form factor and stray fields \textgreek{m}0Hd distribution in between nanowires.Comment: 13 pages, 10 figures, submitted to Phys. Rev.

Hyperammonemia-induced toxicity for the developing central nervous system

In pediatric patients, hyperammonemia can be caused by various acquired or inherited disorders such as urea cycle deficiencies or organic acidemias. The brain is much more susceptible to the deleterious effects of ammonium during development than in adulthood. Hyperammonemia can provoke irreversible damages to the developing central nervous system that lead to cortical atrophy, ventricular enlargement and demyelination, responsible for cognitive impairment, seizures and cerebral palsy. Until recently, the mechanisms leading to these irreversible cerebral damages were poorly understood. Using experimental models allowing the analysis of the neurotoxic effects of ammonium on the developing brain, these last years have seen the emergence of new clues showing that ammonium exposure alters several amino acid pathways and neurotransmitter systems, as well as cerebral energy metabolism, nitric oxide synthesis, oxidative stress, mitochondrial permeability transition and signal transduction pathways. Those alterations may explain neuronal loss and impairment of axonal and dendritic growth observed in the different models of congenital hyperammonemia. Some neuroprotective strategies such as the potential use of NMDA receptor antagonists, nitric oxide inhibitors, creatine and acetyl-l-carnitine have been suggested to counteract these toxic effects. Unraveling the molecular mechanisms involved in the chain of events leading to neuronal dysfunction under hyperammonemia may be useful to develop new potential strategies for neuroprotection

CNTF protects oligodendrocytes from ammonia toxicity: intracellular signaling pathways involved.

In pediatric patients, hyperammonemia can provoke irreversible damages to developing CNS like cortical atrophy, ventricular enlargement, demyelination or gray and white matter hypodensities which are concordant with alterations of neurons and oligodendrocytes. Cerebral injury triggers endogenous protective mechanisms that can prevent or limit brain damage. Understanding these mechanisms may lead to new therapeutic strategies. We investigated whether ciliary neurotrophic factor (CNTF), a cytokine-like protein expressed by astrocytes and described as an injury-associated survival factor, was up-regulated by ammonia in developing reaggregated 3D brain cell cultures. We showed that CNTF is up-regulated by ammonia exposure, through mediation of p38 MAPK activation in astrocytes. We also observed that SAPK/JNK and Erk1/2 activations in oligodendrocytes and neurons, respectively, also play indirect roles in CNTF synthesis by astrocytes. Co-treatment with exogenous CNTF demonstrated strong protective effects on oligodendrocytes, but not on neurons, against ammonia toxicity. These protective effects involved JAK/STAT, SAPK/JNK and c-jun proteins

Observation of Bloch-point domain walls in cylindrical magnetic nanowires

Topological protection is an elegant way of warranting the integrity of quantum and nanosized systems. In magnetism one example is the Bloch-point, a peculiar object implying the local vanishing of magnetization within a ferromagnet. Its existence had been postulated and described theoretically since several decades, however it has never been observed. We con rm experimentally the existence of Bloch points, imaged within domain walls in cylindrical magnetic nanowires, combining surface and transmission XMCD-PEEM magnetic microscopy. This opens the way to the experimental search for peculiar phenomena predicted during the motion of Bloch-point-based domain walls

Variation of oxygenation conditions on a hydrocarbonoclastic microbial community reveals Alcanivorax and Cycloclasticus ecotypes

Deciphering the ecology of marine obligate hydrocarbonoclastic bacteria (MOHCB) is of crucial importance for understanding their success in occupying distinct niches in hydrocarbon-contaminated marine environments after oil spills. In marine coastal sediments, MOHCB are particularly subjected to extreme fluctuating conditions due to redox oscillations several times a day as a result of mechanical (tide, waves and currents) and biological (bioturbation) reworking of the sediment. The adaptation of MOHCB to the redox oscillations was investigated by an experimental ecology approach, subjecting a hydrocarbon-degrading microbial community to contrasting oxygenation regimes including permanent anoxic conditions, anoxic/oxic oscillations and permanent oxic conditions. The most ubiquitous MOHCB, Alcanivorax and Cycloclasticus, showed different behaviors, especially under anoxic/oxic oscillation conditions, which were more favorable for Alcanivorax than for Cycloclasticus. The micro-diversity of 16S rRNA gene transcripts from these genera revealed specific ecotypes for different oxygenation conditions and their dynamics. It is likely that such ecotypes allow the colonization of distinct ecological niches that may explain the success of Alcanivorax and Cycloclasticus in hydrocarbon-contaminated coastal sediments during oil-spills