Electrical switching of antiferromagnetic Mn2_2Au and the role of thermal activation

Electrical manipulation of antiferromagnets with specific symmetries offers the prospect of creating novel, antiferromagnetic spintronic devices. Such devices aim to make use of the insensitivity to external magnetic fields and the ultrafast dynamics at the picosecond timescale intrinsic to antiferromagnets. The possibility to electrically switch antiferromagnets was first predicted for Mn2Au and then experimentally observed in tetragonal CuMnAs. Here, we report on the electrical switching and detection of the Neel order in epitaxial films of Mn2Au. The exponential dependences of the switching amplitude on the current density and the temperature are explained by a macroscopic thermal activation model taking into account the effect of the Joule heating in Hall cross devices and we observe that the thermal activation plays a key role in the reorientation process of the Neel order. Our model analysis shows that the electrically set Neel-state is long-term stable at room temperature, paving the way for practical applications in memory devices.Comment: 8 pages, 6 figure

Giant perpendicular exchange bias with antiferromagnetic MnN

Zilske P, Graulich D, Dunz M, Meinert M. Giant perpendicular exchange bias with antiferromagnetic MnN. Applied Physics Letters. 2017;110(19): 192402.We investigated an out-of-plane exchange bias system that is based on the antiferromagnet MnN. Polycrystalline, highly textured film stacks of Ta/MnN/CoFeB/MgO/Ta were grown on SiOx by (reactive) magnetron sputtering and studied by x-ray diffraction and Kerr magnetometry. Nontrivial modifications of the exchange bias and the perpendicular magnetic anisotropy were observed as functions of both film thicknesses and field cooling temperatures. In optimized film stacks, a giant perpendicular exchange bias of 3600Oe and a coercive field of 350 Oe were observed at room temperature. The effective interfacial exchange energy is estimated to be J(eff) = 0.24 mJ/m(2) and the effective uniaxial anisotropy constant of the antiferromagnet is K-eff = 24 kJ/m(3). The maximum effective perpendicular anisotropy field of the CoFeB layer is H-ani = 3400 Oe. These values are larger than any previously reported values. These results possibly open a route to magnetically stable, exchange biased perpendicularly magnetized spin valves. Published by AIP Publishing

Large exchange bias in polycrystalline MnN/CoFe bilayers at room temperature

Meinert M, Bueker B, Graulich D, Dunz M. Large exchange bias in polycrystalline MnN/CoFe bilayers at room temperature. Physical Review B. 2015;92(14): 144408.We report on the new polycrystalline exchange bias system MnN/CoFe, which shows exchange bias of up to 1800 Oe at room temperature with a coercive field around 600 Oe. The room-temperature values of the interfacial exchange energy and the effective uniaxial anisotropy are estimated to be J(eff) = 0.41 mJ/m(2) and K-eff = 37 kJ/m(3). The thermal stability was found to be tunable by controlling the nitrogen content of MnN. The maximum blocking temperature exceeds 325 degrees C, however the median blocking temperature in the limit of thick MnN is 160 degrees C. Good oxidation stability through self-passivation was observed, enabling the use of MnN in lithographically defined microstructures. As a proof of principle we demonstrate a simple giant magnetoresistance stack exchange biased with MnN, which shows clear separation between parallel and antiparallel magnetic states. These properties come along with a surprisingly simple manufacturing process for the MnN films

High Brain Tissue Oxygen Tension during Ventilation with 100% Oxygen after Fetal Asphyxia in Newborn Sheep.

The optimal FiO2 for newborn resuscitation is still not settled. We hypothesized that short-lasting oxygen ventilation after intrauterine asphyxia would not cause arterial or cerebral hyperoxia, and therefore be innocuous. The umbilical cord of fetal sheep was clamped and 10 min later, after delivery, ventilation with air (n=7) or with 100% oxygen for 3 (n=6) or 30 min (n=5), followed by air, was started. Among the eleven lambs given 100% O2, oxygen tension (PO2) was 10.7 (1.8 - 56) kPa [median (range)] in arterial samples taken after 2.5 min of ventilation. In those ventilated with 100% oxygen for 30 min, brain tissue PO2 (PbtO2) increased from less than 0.1 kPa in each lamb to individual maxima of 56 (30-61) kPa, while in those given oxygenfor just 3 min, PbtO2peaked at 4.2 (2.9 - 46) kPa. The maximal PbtO2 in air-ventilated lambs was 2.9 (0.8-5.4) kPa. Heart rate and blood pressure increased equally fast in the three groups. Thus, prolonged ventilation with 100% oxygen caused an increase in PbtO2of a magnitude previously only reported under hyperbaric conditions. Reducing the time of 100% oxygen ventilation to 3 min did not consistently avert systemic hyperoxia

Cerebral Inflammatory Response after Fetal Asphyxia and Hyperoxic Resuscitation in Newborn Sheep.

Resuscitation with pure oxygen at birth after fetal asphyxia may aggravate brain damage by inducing pro-inflammation. The toll-like receptors (TLRs) may serve a pro-inflammatory role in hyperoxemia during ischemia-reperfusion. Sixteen near-term fetal sheep (132-136 d) were subjected to 10 min of cord occlusion, delivery and mechanical ventilation with 100% O-2 (n = 8), or 21% O-2 (n = 8) for 30 min followed by normoxemia for 90 min. Eight sheep fetuses were delivered immediately with inspired O-2 targeted at normoxemia for 120 min (controls). Levels and distributions of mRNAs for IL-1 beta, TNF-alpha, IL-12p40, IL-18, IL-6, IL-10, IFN-gamma, TLR-2. -3 and -4 in cerebral tissue at 2 h after birth were evaluated with real-time polymerase chain reaction (PCR) and in situ hybridization. Expressions of IL-1 beta, IL-12p40, TLR-2, and TLR-4 were increased in cortex/subcortex after resuscitation with 100% 02 compared with 21% O-2 (all p < 0.05) and to controls (all p < 0.05). Increased cellular expression of IL-1 beta was localized to sub-meningeal cortical layers and to sub-cortical white matter. Hyperoxic resuscitation at birth following fetal asphyxia induces a cerebral pro-inflammatory response with an up-regulation of TLR-2 and -4. These may be early events leading to increased tissue damage after exposure to hyperoxemia at birth

Deregulation of tumor angiogenesis and blockade of tumor growth in PPARβ-deficient mice

The peroxisome proliferator-activated receptor-β (PPARβ) has been implicated in tumorigenesis, but its precise role remains unclear. Here, we show that the growth of syngeneic Pparb wild-type tumors is impaired in Pparb−/− mice, concomitant with a diminished blood flow and an abundance of hyperplastic microvascular structures. Matrigel plugs containing pro-angiogenic growth factors harbor increased numbers of morphologically immature, proliferating endothelial cells in Pparb−/− mice, and retroviral transduction of Pparb triggers microvessel maturation. We have identified the Cdkn1c gene encoding the cell cycle inhibitor p57Kip2 as a PPARβ target gene and a mediator of the PPARβ-mediated inhibition of cell proliferation, which provides a possible mechanistic explanation for the observed tumor endothelial hyperplasia and deregulation of tumor angiogenesis in Pparb−/− mice. Our data point to an unexpected essential role for PPARβ in constraining tumor endothelial cell proliferation to allow for the formation of functional tumor microvessels