Field-free spin-orbit torque switching assisted by in-plane unconventional spin torque in ultrathin [Pt/Co]N.

Electrical manipulation of magnetization without an external magnetic field is critical for the development of advanced non-volatile magnetic-memory technology that can achieve high memory density and low energy consumption. Several recent studies have revealed efficient out-of-plane spin-orbit torques (SOTs) in a variety of materials for field-free type-z SOT switching. Here, we report on the corresponding type-x configuration, showing significant in-plane unconventional spin polarizations from sputtered ultrathin [Pt/Co]N, which are either highly textured on single crystalline MgO substrates or randomly textured on SiO2 coated Si substrates. The unconventional spin currents generated in the low-dimensional Co films result from the strong orbital magnetic moment, which has been observed by X-ray magnetic circular dichroism (XMCD) measurement. The x-polarized spin torque efficiency reaches up to -0.083 and favors complete field-free switching of CoFeB magnetized along the in-plane charge current direction. Micromagnetic simulations additionally demonstrate its lower switching current than type-y switching, especially in narrow current pulses. Our work provides additional pathways for electrical manipulation of spintronic devices in the pursuit of high-speed, high-density, and low-energy non-volatile memory.

The effect of mitochondria-targeted slow hydrogen sulfide releasing donor AP39-treatment on airway inflammation.

Mitochondrial dysfunction has been shown to contribute to the pathophysiology of airway diseases. Therefore, mitochondria are targeted in the development of new therapeutic approaches. Hydrogen sulfide (H2S) has been shown to be involved in the pathophysiological processes of airway inflammation. We aimed to evaluate the effect of mitochondria-targeted slow H2S releasing donor AP39 [(10-oxo-10-(4-(3-thioxo-3H-1,2-dithiol5yl)phenoxy)decyl)triphenylphosphoniumbromide)] on lipopolysaccharide (LPS)-induced airway inflammation in mice. LPS was applied to female Balb/c mice by intranasal (i.n.) route to induce airway inflammation and the subgroups of mice were treated with i.n. AP39 (250-1000 nmol/kg). 48 h after LPS administration airway reactivity was evaluated in vivo, then bronchoalveolar lavage (BAL) fluid and lungs were collected. LPS application led to bronchial hyperreactivity and neutrophil infiltration into the lung tissues along with increased TNF-α, IL-1ß and IL-6 levels in BAL fluid. LPS also induced an increase in the rate of glycolysis, glycogenolysis and Krebs-cycle. AP39 treatment prevented the LPS-induced bronchial hyperreactivity and reversed the increase in TNF-α and IL-6 levels in BAL fluid. The increase in neutrophil numbers in BAL fluid was also prevented by AP39 treatment at the highest dose. Our results indicate that AP39 can prevent bronchial hyperreactivity and decrease airway inflammation. Targeting H2S to the mitochondria may be a new therapeutic approach in airway inflammation.

Engineering Pt/Co/AlOxheterostructures to enhance the Dzyaloshinskii-Moriya interaction.

The study of interfacial Dzyaloshinskii-Moriya interaction (DMI) in perpendicularly magnetized structurally asymmetric heavy metal/ferromagnet multilayer systems is of high importance due to the formation of chiral magnetic textures in the presence of DMI. Here, we report the impact of cobalt oxidation at the Co/AlOxinterface in Pt/Co/AlOxtrilayer structures on the DMI by varying the post-growth annealing time, Al thickness and substrate. To quantify DMI we employed magneto-optical imaging of the asymmetric domain wall expansion, hysteresis loop shift, and spin-wave spectroscopy techniques. We further correlated the Co oxidation with low-temperature Hall effect measurements and x-ray photoelectron spectroscopy. Our results emphasize the importance of full characterization of the magnetic films that could be used for magnetic random access memory technologies when subjected to the semiconductor temperature processing conditions, as the magnetic interactions are critical for device performance and can be highly sensitive to oxidation and other effects.

Lorentz electron ptychography for imaging magnetic textures beyond the diffraction limit.

Nanoscale spin textures, especially magnetic skyrmions, have attracted intense interest as candidate high-density and power-efficient information carriers for spintronic devices1,2. Facilitating a deeper understanding of sub-hundred-nanometre to atomic-scale spin textures requires more advanced magnetic imaging techniques3-5. Here we demonstrate a Lorentz electron ptychography method that can enable high-resolution, high-sensitivity magnetic field imaging for widely available electron microscopes. The resolution of Lorentz electron ptychography is not limited by the usual diffraction limit of lens optics, but instead is determined by the maximum scattering angle at which a statistically meaningful dose can still be recorded-this can be an improvement of up to 2-6 times depending on the allowable dose. Using FeGe as the model system, we realize a more accurate magnetic field measurement of skyrmions with an improved spatial resolution and sensitivity by also correcting the probe-damping effect from the imaging optics via Lorentz electron ptychography. This allows us to directly resolve subtle internal structures of magnetic skyrmions near the skyrmion cores, boundaries and dislocations in an FeGe single crystal. Our study establishes a quantitative, high-resolution magnetic microscopy technique that can reveal nanoscale spin textures, especially magnetization discontinuities and topological defects in nanomagnets6. The technique's high-dose efficiency should also make it well suited for the exploration of magnetic textures in electron radiation-sensitive materials such as organic or molecular magnets7.

Endocannabinoid metabolism inhibition ameliorates ovalbumin-induced allergic airway inflammation and hyperreactivity in Guinea pigs.

AIMS: Endocannabinoids are biologically active cannabinoid-related substances endogenously synthesized in many mammalian tissues. Mainly two enzymes carry out their degradation; Fatty Acid Amide Hydrolase (FAAH) and Monoacylglycerol Lipase (MAGL). Endocannabinoids are shown to affect the modulation of inflammatory processes and airway responsiveness. In the present study, we investigated the effects of FAAH and MAGL inhibitor treatments in experimental allergic airway inflammation in guinea pigs. MATERIALS AND METHODS: Guinea pigs were sensitized and challenged by ovalbumin to induce an allergic asthma model. Then, the effects of FAAH inhibitor URB597, MAGL inhibitor JZL184, and dual (FAAH/MAGL) inhibitor JZL195 on airway inflammation and hyperreactivity were evaluated. KEY FINDINGS: Ovalbumin challenge increased airway reactivity, IgE in serum, IL-4, and IL-13, and the percentage of eosinophils in bronchoalveolar lavage (BAL). In addition, inhibition of FAAH or MAGL enzymes leads to an increase in endocannabinoid levels. The selective inhibition of the FAAH enzyme prevented inflammation indicators such as cytokine production and inflammatory cell infiltration but had a negligible effect on airway hyperreactivity. However, the inhibition of the MAGL enzyme or dual inhibition of both FAAH and MAGL enzymes tent to moderate both pulmonary inflammation and airway hyperreactivity. SIGNIFICANCE: We have previously demonstrated that modulation of endocannabinoid levels in the airways by FAAH or MAGL inhibition can be useful in preventing acute lung inflammation. The results of the present study further suggest that FAAH and MAGL inhibitor treatment can also be a promising strategy for bronchial hyperreactivity and airway inflammation in allergic asthma.

Hopfion dynamics in chiral magnets.

Resonant spin dynamics of topological spin textures are correlated with their topological nature, which can be employed to understand this nature. In this study, we present resonant spin dynamics of three-dimensional topological spin texture, i.e., Neel and Bloch hopfions. Using micromagnetic simulations, we stabilize Bloch and Neel hopfions with bulk and interfacial Dzyaloshinskii-Moriya interaction, respectively. We identify the ground state spin configuration of both hopfions, effects of anisotropies, geometric confinements, and demagnetizing fields. To confirm topological nature, Hopf number is calculated for each spin texture. Then, we calculate the resonance frequencies and spin-wave modes of spin precessions under multiple magnetic fields. Unique resonance frequencies and specific magnetic field dependence can help to guide experimental studies to identify the three-dimensional topological spin texture of hopfions in functioning chiral magnets when imaging is not possible.

The effects of systemic and local fatty acid amide hydrolase and monoacylglycerol lipase inhibitor treatments on the metabolomic profile of lungs.

The contribution of the endocannabinoid system to both physiology and pathological processes in the respiratory system makes it a promising target for inflammatory airway diseases. Previously, we have shown that increasing the tissue endocannabinoid levels by fatty acid amide hydrolase (FAAH) and monoacylglycerol lipase (MAGL) inhibitors can prevent airway inflammation and hyperreactivity. In this study, the changes in the levels of major metabolites of endocannabinoids by systemic and local FAAH or MAGL inhibitor treatments were evaluated. Mice were treated with either the FAAH inhibitor URB597 or the MAGL inhibitor JZL184 by local (intranasal) or systemic (intraperitoneal) application. Bronchoalveolar lavage (BAL) fluids and lungs were isolated afterward in order to perform histopathological and metabolomic analyses. There were no significant histopathological changes in the lungs and neutrophil, and macrophage and lymphocyte numbers in BAL fluid were not altered after local and systemic treatments. However, GC-MS-based metabolomics profile allowed us to identify 102 metabolites in lung samples, among which levels of 75 metabolites were significantly different from the control. The metabolites whose levels were changed by treatments were mostly related to the endocannabinoid system and energy metabolism. Therefore, these changes may contribute to the anti-inflammatory effects of URB597 and JZL184 treatments in mice.

Investigation of the relationship between chronic montelukast treatment, asthma and depression-like behavior in mice.

In 2008, the Food and Drug Administration of the US issued a warning about the neuropsychiatric side effects of montelukast. Previous clinical studies on montelukast have reported conflicting results and, to the best of our knowledge, no experimental studies concerning these side effects had been conducted. In the current study, the effect of montelukast on depression-like behavior in an ovalbumin (OVA)-induced mouse model was investigated. A total of 3 OVA challenges were applied at 2 week intervals for the persistence of asthma. Depression-like behavior was assessed using forced swim tests following each challenge and locomotor activities were evaluated using open field tests. At the end of the current study, plasma montelukast concentrations were measured and the development of asthma and effect of montelukast treatment were histopathologically examined. Inflammation scores that were increased in the OVA mice following all challenges were indicated to be reduced by montelukast treatment. The immobility time of mice increased beginning with the first challenge and this was also reduced by montelukast treatment. Montelukast administration to the control mice did not alter immobility times. Moreover, motor activity of the OVA and montelukast-treated mice were not altered. The results indicated there was no association between chronic montelukast treatment and depression. Furthermore, the chronic administration of montelukast to non-asthmatic mice did not increase immobility. However, depressive behavior increased at all time points in the OVA mice. These results indicated that chronic montelukast treatment is not associated with depression-like behavior and confirmed the association between asthma and depression. Further studies are required to provide an improved understanding of the neuropsychiatric side effects of montelukast.

The effects of fatty acid amide hydrolase and monoacylglycerol lipase inhibitor treatments on lipopolysaccharide-induced airway inflammation in mice.

Cannabinoids and the endocannabinoid system significantly contributes to the airway inflammation. Fatty acid amide hydrolase (FAAH) and monoacylglycerol lipase (MAGL) are two main enzymes responsible for the metabolism of the endocannabinoids anandamide (AEA) and 2-arachydonoyl glycerol (2-AG), respectively. In the present study, we aimed to investigate the effects of local and systemic FAAH and MAGL inhibitor treatments in experimental airway inflammation and tracheal hyperreactivity in mice. Airway inflammation was induced by intranasal (i.n.) lipopolysaccharide (LPS) application (60 µl; 0,1 mg/ml in PBS) to mice and the control group received PBS. Systemic (intraperitoneal (i.p.)) or local (i.n.) FAAH inhibitor URB597 and MAGL inhibitor JZL184 treatments were administered 1h before LPS/PBS application. Fourty 8 h after LPS/PBS application, tracheas were removed to assess airway reactivity, and the lungs and bronchoalveolar lavage (BAL) fluids were isolated for histopathological evaluation, cytokine and endocannabinoid measurements. LPS application lead to an increase in 5-hydroxytryptamine (5-HT) contractions in isolated tracheal rings while carbachol contractions remained unchanged. The increased 5-HT contractions were prevented by both systemic and local URB597 and JZL184 treatments. Systemic treatment with URB597 and JZL184, and local treatment with JZL184 reduced peribronchial and paranchymal inflammation in the LPS group while i.n. application of URB597 worsened the inflammation in the lungs. Systemic URB597 treatment increased lung AEA level whereas it had no effect on 2-AG level. However, JZL184 treatment increased 2-AG level by either systemic or local application, and also elevated AEA level. Inflammation-induced increase in neutrophil numbers was only prevented by systemic URB597 treatment. However, both URB597 and JZL184 treatments abolished the increased TNF-α level either they are administered systemically or locally. These results indicate that FAAH and MAGL inhibition may have a protective effect in airway inflammation and airway hyperreactivity, and therefore their therapeutic potential for airway diseases should be further investigated.

Endocannabinoid System in the Airways.

Cannabinoids and the mammalian endocannabinoid system is an important research area of interest and attracted many researchers because of their widespread biological effects. The significant immune-modulatory role of cannabinoids has suggested their therapeutic use in several inflammatory conditions. Airways are prone to environmental irritants and stimulants, and increased inflammation is an important process in most of the respiratory diseases. Therefore, the main strategies for treating airway diseases are suppression of inflammation and producing bronchodilation. The ability of cannabinoids to induce bronchodilation and modify inflammation indicates their importance for airway physiology and pathologies. In this review, the contribution of cannabinoids and the endocannabinoid system in the airways are discussed, and the existing data for their therapeutic use in airway diseases are presented.

Rho Kinase and Protein Kinase C Pathways are Responsible for Enhanced Carbachol Contraction in Permeabilized Detrusor in a Rat Model of Cystitis.

Interstitial cystitis is a syndrome characterized by detrusor overactivity and chronic inflammation of the bladder. The mechanisms responsible for the altered smooth muscle contractility remain poorly understood. The aim of the study was to investigate the role of intracellular signalling pathways in carbachol-induced detrusor contraction in a rat model of interstitial cystitis. Cyclophosphamide (150 mg/kg, dissolved in saline) was injected to rats (Sprague-Dawley, female, 200-250 g) intraperitoneally once a day on days 1, 4 and 7 to induce interstitial cystitis. Control groups were injected with saline (0.9% NaCl). Detrusor smooth muscle strips were mounted in 1-ml organ baths containing HEPES-buffered modified Krebs' solution and permeabilized with 40 µM ß-escin for 30 min. Carbachol-induced contractions were significantly increased from 21.2 ± 1.6% (saline-treated) to 44 ± 4.4% in cyclophosphamide-treated group. The Rho kinase inhibitor Y-27632 (8.8 ± 2%) and the protein kinase C inhibitor GF-109203X (11.7 ± 2.8%) inhibited the increased contractile response (44 ± 4.4%) in rats with cystitis. The increased carbachol-induced contraction (44 ± 4.4%) was also significantly inhibited by the sarcoplasmic reticulum ryanodine channel blocker ryanodine (25.8 ± 3.2%) and the sarcoplasmic reticulum IP3 receptor blocker heparin (17.2 ± 2.2%) in cystitis. RhoA protein levels in the bladder of cyclophosphamide-treated rats were significantly increased while pan-protein kinase C (α, ß and γ isoforms) protein expression was unaltered between experimental groups. Carbachol-induced calcium sensitization at constant and clamped calcium (pCa 6) was also increased in cystitis (from 15.8 ± 2.2% to 24.7 ± 2.8%). This increased response (24.7 ± 2.8%) was significantly inhibited by both Y-27632 (7.9 ± 0.7%) and GF-109203X (4.4 ± 1.5%). We conclude that interstitial cystitis is characterized by an enhanced carbachol contractile response as well as by calcium sensitization of the detrusor smooth muscle. Activation of Rho kinase and protein kinase C pathways may be the molecular culprits responsible for the augmented muscarinic response observed in cystitis.

Theory and practice of electron diffraction from single atoms and extended objects using an EMPAD.

What does the diffraction pattern from a single atom look like? How does it differ from the scattering from long-range potential? With the development of new high-dynamic range pixel array detectors to measure the complete momentum distribution, these questions have immediate relevance for designing and understanding momentum-resolved imaging modes. We explore the asymptotic limits of long-range and short-range potentials. We use a simple quantum mechanical model to explain the general and asymptotic limits for the probability distribution in both real and reciprocal space. Features in the scattering potential much larger than the probe size cause the bright field (BF) disk to deflect uniformly, while features much smaller than the probe size, instead of a deflection, cause a redistribution of intensity within the BF disk. Because long-range and short-range features are encoded differently in the diffraction pattern, it is possible to separate their contributions in differential phase-contrast (DPC) or center-of-mass (CoM) imaging. The shape profiles for atomic resolution CoM imaging are dominated by the shape of the probe gradient and not the highly singular atomic potentials or their local fields. Instead, only the peak height shows an atomic number sensitivity, whose precise dependence is determined by the convergence angle. At lower convergence angles, the contrast oscillates with increasing atomic number, similar to BF imaging. The range of collection angles impacts DPC and CoM imaging differently, with CoM being more sensitive to the upper cutoff limit, while DPC is more sensitive to the lower cutoff.

Effects of intranasal treatment with slow (GYY4137) and rapid (NaHS) donors of hydrogen sulfide in lipopolysaccharide-induced airway inflammation in mice.

We have investigated the effects of slow (GYY4137) and rapid (NaHS) hydrogen sulfide (H2S) releasing donors in lipopolysaccharide (LPS)-induced airway inflammation in mice. LPS (0.1 mg/ml) in 60 µl PBS was administered by the intranasal (i.n.) route and control group received vehicle, whereas the subgroups of mice were treated with i.n. GYY4137 or NaHS. The tracheal reactivity, inflammatory cell count in bronchoalveolar lavage (BAL) fluid and lung histopathology were evaluated in all groups 48 h after LPS/PBS applications. 5-Hydroxytryptamine (5-HT)-induced contraction response in isolated tracheas was enhanced after LPS treatment but carbachol response was not altered. Incubation with atropine (10-6 M), 5-HT2A receptor antagonist ketanserin (10-9-10-7 M) and 5-HT3 receptor antagonist alosetron (10-8 and 10-7 M) prevented 5-HT-induced hyperreactivity whereas 5-HT4 receptor antagonist GR113808 (10-7 M, 10-6 M) did not have any effect in LPS-treated group. Electrical field stimulation (EFS) of isolated tracheas elicited frequency-dependent contractile response, which was not altered by LPS treatment alone but was enhanced in the presence of 5-HT (10-9-10-4 M). This data indicated that 5-HT2A and 5-HT3 receptors, and acetylcholine released from cholinergic nerves were contributing to 5-HT-induced hyperreactivity in the present experiments. The increase in neutrophil count along with cytokine (IL-1ß, TNF-α) levels in bronchoalveolar lavage (BAL) fluid and histopathological changes like paranchymal inflammation and interalveolar thickening were determined in LPS-treated mice. H2S production in lung homogenates were determined by the methylene blue assay, and found to be similar in both LPS and control groups. The experiments conducted after i.n. treatment with H2S donors has shown that only GYY4137 (1 mg/kg) inhibited 5-HT-induced hyperreactivity, and both GYY4137 and NaHS (1 mg/kg) prevented the neutrophil increase in BAL fluid in LPS-induced airway inflammation. IL-1ß increase in BAL fluid was abolished by both GYY4137 and NaHS treatments whereas TNF-α levels remained unchanged. Furthermore, GYY4137 treatment did not have any effect in LPS-induced changes of lung pathology whereas NaHS prevented the paranchymal inflammation. The different H2S releasing pattern of these donors may explain the difference of their effects in this model. Compounds that provide stable H2S levels via local application may be a new therapeutic approach in airway inflammation.

Nondestructive Measurement of the Evolution of Layer-Specific Mechanical Properties in Sub-10 nm Bilayer Films.

We use short wavelength extreme ultraviolet light to independently measure the mechanical properties of disparate layers within a bilayer film for the first time, with single-monolayer sensitivity. We show that in Ni/Ta nanostructured systems, while their density ratio is not meaningfully changed from that expected in bulk, their elastic properties are significantly modified, where nickel softens while tantalum stiffens, relative to their bulk counterparts. In particular, the presence or absence of the Ta capping layer influences the mechanical properties of the Ni film. This nondestructive nanomechanical measurement technique represents the first approach to date able to distinguish the properties of composite materials well below 100 nm in thickness. This capability is critical for understanding and optimizing the strength, flexibility and reliability of materials in a host of nanostructured electronic, photovoltaic, and thermoelectric devices.

The effect of cannabinoids on dinitrofluorobenzene-induced experimental asthma in mice.

Cannabinoids have anti-inflammatory effects and can produce bronchodilation in the airways. We have investigated the effects of cannabinoids on tracheal hyperreactivity and airway inflammation in dinitrofluorobenzene (DNFB)-induced experimental non-atopic asthma in mice. 5-hydroxytryptamine (5-HT)-induced contraction response was enhanced while carbachol- and electrical field stimulation-induced contractions, and isoprenaline-induced relaxation responses were remained unchanged in DNFB group. The increased 5-HT-induced contractions were inhibited by incubation with either atropine or tetrodotoxin. DNFB application resulted in increased macrophage number in the bronchoalveolar lavage fluid (BALF). In vivo ACEA (CB1 agonist) treatment prevented the increase in 5-HT contractions, while JWH133 (CB2 agonist) had no effect. However, neither ACEA nor JWH133 prevented the increase in macrophage number in BALF. In vitro ACEA incubation also inhibited the increase in 5-HT contraction in DNFB group. These results show that cannabinoid CB1 receptor agonist can prevent tracheal hyperreactivity to 5-HT in DNFB-induced non-atopic asthma in mice.

Stimulation of cannabinoid CB1 receptors prevents nerve-mediated airway hyperreactivity in NGF-induced inflammation in mouse airways.

Cannabinoids are known to inhibit neuronal activity and have significant immunomodulatory effects which suggest a role in inflammatory airway diseases. In the present study, we tested the hypothesis that cannabinoids have both acute and chronic modulatory effects on nerve-mediated contractions in NGF-induced airway inflammation. Contractions induced by electrical field stimulation (EFS) were examined in tracheal segments isolated from male BALB/c mice. Tissues were both used fresh or after four days of culture with NGF to induce airway inflammation, and further exposed to cannabinoid receptor agonists. In order to evaluate nerve density, tracheal segments were also examined by immunohistochemistry after in vitro treatments. The CB1 receptor agonists ACEA and ACPA inhibited the constant train EFS-induced contractions in both fresh and NGF-exposed tracheas, an effect that could be blocked by the CB1 receptor antagonist AM251. Culturing the tissues with NGF up-regulated the frequency-dependent EFS-contractions in isolated tracheas. This up-regulation could be inhibited by concomitant treatment with ACEA or ACPA. The treatment with NGF and/or ACEA did not affect the potency or the maximum response to carbachol. In histological sections, it was recognized that the enhanced effect induced by NGF was associated with an increase in nerve density, which, similarly, could be prevented by ACEA treatment. This study shows that stimulation of cannabinoid CB1 receptors modifies the increase of neuronal activity and density in NGF-induced airway inflammation and directly inhibits cholinergic contractions in the airways by a presynaptic mechanism. These findings indicate a protective role of CB1 receptors in airway inflammation.

High Dynamic Range Pixel Array Detector for Scanning Transmission Electron Microscopy.

We describe a hybrid pixel array detector (electron microscope pixel array detector, or EMPAD) adapted for use in electron microscope applications, especially as a universal detector for scanning transmission electron microscopy. The 128×128 pixel detector consists of a 500 µm thick silicon diode array bump-bonded pixel-by-pixel to an application-specific integrated circuit. The in-pixel circuitry provides a 1,000,000:1 dynamic range within a single frame, allowing the direct electron beam to be imaged while still maintaining single electron sensitivity. A 1.1 kHz framing rate enables rapid data collection and minimizes sample drift distortions while scanning. By capturing the entire unsaturated diffraction pattern in scanning mode, one can simultaneously capture bright field, dark field, and phase contrast information, as well as being able to analyze the full scattering distribution, allowing true center of mass imaging. The scattering is recorded on an absolute scale, so that information such as local sample thickness can be directly determined. This paper describes the detector architecture, data acquisition system, and preliminary results from experiments with 80-200 keV electron beams.

Controlling the competition between optically induced ultrafast spin-flip scattering and spin transport in magnetic multilayers.

The study of ultrafast dynamics in magnetic materials provides rich opportunities for greater fundamental understanding of correlated phenomena in solid-state matter, because many of the basic microscopic mechanisms involved are as-yet unclear and are still being uncovered. Recently, two different possible mechanisms have been proposed to explain ultrafast laser induced magnetization dynamics: spin currents and spin-flip scattering. In this work, we use multilayers of Fe and Ni with different metals and insulators as the spacer material to conclusively show that spin currents can have a significant contribution to optically induced magnetization dynamics, in addition to spin-flip scattering processes. Moreover, we can control the competition between these two processes, and in some cases completely suppress interlayer spin currents as a sample undergoes rapid demagnetization. Finally, by reversing the order of the Fe/Ni layers, we experimentally show that spin currents are directional in our samples, predominantly flowing from the top to the bottom layer.

Ultrafast magnetization enhancement in metallic multilayers driven by superdiffusive spin current.

Uncovering the physical mechanisms that govern ultrafast charge and spin dynamics is crucial for understanding correlated matter as well as the fundamental limits of ultrafast spin-based electronics. Spin dynamics in magnetic materials can be driven by ultrashort light pulses, resulting in a transient drop in magnetization within a few hundred femtoseconds. However, a full understanding of femtosecond spin dynamics remains elusive. Here we spatially separate the spin dynamics using Ni/Ru/Fe magnetic trilayers, where the Ni and Fe layers can be ferro- or antiferromagnetically coupled. By exciting the layers with a laser pulse and probing the magnetization response simultaneously but separately in Ni and Fe, we surprisingly find that optically induced demagnetization of the Ni layer transiently enhances the magnetization of the Fe layer when the two layer magnetizations are initially aligned parallel. Our observations are explained by a laser-generated superdiffusive spin current between the layers.

Probing the timescale of the exchange interaction in a ferromagnetic alloy.

The underlying physics of all ferromagnetic behavior is the cooperative interaction between individual atomic magnetic moments that results in a macroscopic magnetization. In this work, we use extreme ultraviolet pulses from high-harmonic generation as an element-specific probe of ultrafast, optically driven, demagnetization in a ferromagnetic Fe-Ni alloy (permalloy). We show that for times shorter than the characteristic timescale for exchange coupling, the magnetization of Fe quenches more strongly than that of Ni. Then as the Fe moments start to randomize, the strong ferromagnetic exchange interaction induces further demagnetization in Ni, with a characteristic delay determined by the strength of the exchange interaction. We can further enhance this delay by lowering the exchange energy by diluting the permalloy with Cu. This measurement probes how the fundamental quantum mechanical exchange coupling between Fe and Ni in magnetic materials influences magnetic switching dynamics in ferromagnetic materials relevant to next-generation data storage technologies.