2,232 research outputs found

    Electrical Control of Magnetization in Charge-ordered Multiferroic LuFe2O4

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    LuFe2O4 exhibits multiferroicity due to charge order on a frustrated triangular lattice. We find that the magnetization of LuFe2O4 in the multiferroic state can be electrically controlled by applying voltage pulses. Depending on with or without magnetic fields, the magnetization can be electrically switched up or down. We have excluded thermal heating effect and attributed this electrical control of magnetization to an intrinsic magnetoelectric coupling in response to the electrical breakdown of charge ordering. Our findings open up a new route toward electrical control of magnetization.Comment: 14 pages, 5 figure

    Pole-skipping points in 2D gravity and SYK model

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    We represent the first investigation of pole-skipping on both the gravity and field theory sides. In contrast to the higher dimensional models, there is no momentum degree of freedom in (1+1)(1+1)-dimensional bulk theory. Thus, we then consider a scalar field mass as our degree of freedom for the pole-skipping phenomenon instead of momentum. The pole-skipping frequencies of the scalar field in 2D gravity are the same as higher dimensional cases: ω=i2πTn\omega=-i2\pi Tn for positive integer nn. At each of these frequencies, there is a corresponding pole-skipping mass, so the pole-skipping points exist in the (ω,m)(\omega,m) space. We also compute the pole-skipping points of the SYK model in (ω,h)(\omega, h) space where hh is the dimension of the bilinear primary operator. We find that there is a one-to-one correspondence of the pole-skipping points between the JT gravity and the SYK model. To obtain the pole-skipping points, we need to consider the parameter ϵ\epsilon related to chemical potential on the horizon of charged JT gravity and the particle-hole asymmetric parameter E\mathcal{E} of the complex SYK model as shift parameters. This highlights the ϵE\epsilon-\mathcal{E} correspondence in relation to pole-skipping

    Inhibition of c-Jun NH(2)-terminal kinase or extracellular signal-regulated kinase improves lung injury

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    BACKGROUND: Although in vitro studies have determined that the activation of mitogen-activated protein (MAP) kinases is crucial to the activation of transcription factors and regulation of the production of proinflammatory mediators, the roles of c-Jun NH(2)-terminal kinase (JNK) and extracellular signal-regulated kinase (ERK) in acute lung injury have not been elucidated. METHODS: Saline or lipopolysaccharide (LPS, 6 mg/kg of body weight) was administered intratracheally with a 1-hour pretreatment with SP600125 (a JNK inhibitor; 30 mg/kg, IO), or PD98059 (an MEK/ERK inhibitor; 30 mg/kg, IO). Rats were sacrificed 4 hours after LPS treatment. RESULTS: SP600125 or PD98059 inhibited LPS-induced phosphorylation of JNK and ERK, total protein and LDH activity in BAL fluid, and neutrophil influx into the lungs. In addition, these MAP kinase inhibitors substantially reduced LPS-induced production of inflammatory mediators, such as CINC, MMP-9, and nitric oxide. Inhibition of JNK correlated with suppression of NF-κB activation through downregulation of phosphorylation and degradation of IκB-α, while ERK inhibition only slightly influenced the NF-κB pathway. CONCLUSION: JNK and ERK play pivotal roles in LPS-induced acute lung injury. Therefore, inhibition of JNK or ERK activity has potential as an effective therapeutic strategy in interventions of inflammatory cascade-associated lung injury

    Visualizing Alzheimer's Disease Mouse Brain with Multispectral Optoacoustic Tomography using a Fluorescent probe, CDnir7

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    Alzheimer's disease (AD) is now clinically considered as a chronic inflammation-based neurodegenerative disease. The CDnir7 probe was previously developed as an optical imaging probe to target macrophages in order to image mouse inflammation using in vivo optical imaging modalities such as In Vivo imaging system (IVIS) and fluorescent molecular tomography (FMT). Here, we demonstrate the application of CDnir7 in AD mouse brain imaging via multispectral optoacoustic tomography (MSOT). Longitudinal MSOT imaging of CDnir7 showed higher CDnir7 localization in AD mouse cerebral cortex compared to that of normal mice. MSOT signals of CDnir7 localization in mouse brain were verified by ex vivo near-infrared (NIR) imaging and immunohistochemistry. Histological evaluation showed strong CDnir7 staining in AD cerebral cortex, hippocampus, basal ganglia and thalamus area. Based on the supporting evidence, CDnir7 has great potential as a molecular imaging probe for AD brain imaging.11Ysciescopu
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