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1.
Sci Rep ; 8(1): 3826, 2018 Feb 28.
Article in English | MEDLINE | ID: mdl-29491458

ABSTRACT

Spin-orbit torque has attracted considerable attention as a means to overcome limits of devices based on spin-transfer torque. However, a small magnetic field that is collinear to the current flow must be applied to break symmetry and induce deterministic current-induced magnetization switching. Recently, a junction utilizing interlayer coupling mediated by a Ru spacer layer between two CoFe layers was designed for symmetry breaking and exhibited current-induced magnetization switching without a magnetic field. Here, we demonstrate zero-field current-induced switching of the perpendicular magnetization of a Co layer that is indirectly coupled with a CoFe layer via a Ta spacer. The weak interlayer coupling exhibited by Ta allows the layer thickness to be relatively small (≈0.5 nm), enabling appropriate interlayer coupling to induce spin-orbit torque for current-induced magnetic switching. External magnetic field effects on switching characteristics show that the current switching process is quite stable against external environments.

2.
Phys Rev Lett ; 87(15): 157202, 2001 Oct 08.
Article in English | MEDLINE | ID: mdl-11580722

ABSTRACT

We study interlayer exchange coupling in epitaxial Fe/Fe(0.56)Si(0.44)/Fe trilayers. Iron-silicide spacers with high structural and compositional homogeneity for thicknesses up to 34 A are grown by coevaporation from two electron-beam sources. The coupling strength oscillates with spacer thickness for temperatures from 20 to 300 K with two antiferromagnetic maxima at 12 and 26 A, and it clearly increases with decreasing temperature down to 80 K. We conclude that the coupling across ordered Fe(1-x)Si(x) ( x approximately 0.5) is described by the conventional theory of interlayer coupling across metallic spacers.

3.
J Infect Dis ; 178(4): 1209-12, 1998 Oct.
Article in English | MEDLINE | ID: mdl-9806063

ABSTRACT

Interleukin-12 (IL-12) is a key cytokine in the immune response to infection with Mycobacterium avium complex (MAC). Human immunodeficiency virus infection, a predisposing factor for disseminated MAC infection, causes a drop of bioactive IL-12(p70), mainly by decreasing the constitutive production of p35. IL-12(p40) and tumor necrosis factor-alpha (TNF-alpha) levels in supernatants of MAC-infected human monocyte-derived macrophages with intracellular growth rates were compared. Isolates from AIDS patients showed high growth rates and induced low TNF-alpha but high IL-12(p40) levels. In contrast, environmental isolates with fast growth rates induced only low levels of IL-12(p40) secretion. The increased IL-12(p40) stimulus seen with the clinical isolates could lead to a p40 surplus, which, alone or as the (p40)2 homodimer, has immunosuppressive properties. An immunosuppressive effect of MAC isolates may be an important advantage for their survival in vivo and may explain the contribution of MAC infection to the progression of AIDS.


Subject(s)
Acquired Immunodeficiency Syndrome/microbiology , Interleukin-12/metabolism , Macrophages/immunology , Monocytes/immunology , Mycobacterium avium Complex/immunology , Enzyme-Linked Immunosorbent Assay , Humans , Immune Tolerance , Macrophages/cytology , Macrophages/microbiology , Monocytes/cytology , Monocytes/microbiology , Phenotype , Tumor Necrosis Factor-alpha/metabolism
4.
Infect Immun ; 66(9): 4549-52, 1998 Sep.
Article in English | MEDLINE | ID: mdl-9712818

ABSTRACT

The capacity of 20 Mycobacterium avium complex isolates to multiply intracellularly in human monocyte-derived macrophages was assessed and correlated to the clinical relevance of each isolate and its reactivity with several candidate genetic virulence markers. The strongest correlation with a virulence phenotype was found for a conserved coding sequence of the macrophage-induced gene mig identified by a specific mig restriction fragment length polymorphism type.


Subject(s)
Genes, Bacterial , Macrophages/microbiology , Mycobacterium avium Complex/pathogenicity , Biomarkers , Humans , Mycobacterium avium Complex/genetics , Mycobacterium avium-intracellulare Infection/metabolism , Mycobacterium avium-intracellulare Infection/physiopathology , Virulence
14.
Int J Vitam Nutr Res ; 53(2): 210-7, 1983.
Article in German | MEDLINE | ID: mdl-6885278

ABSTRACT

In order to estimate the linoleic acid requirement of the rat, four groups of weanling male Wistar-Rats, 18 animals each, were fed isoenergetic semi-synthetic diets containing 14 cal% fat. The linoleic acid content (as linoleic acid methyl ester) amounted to 0; 0.5; 1.3 and 4.0% of total energy intake. The experiment lasted 14 weeks. The parameters analysed were the concentrations of total lipids (TL), free cholesterol (Ch), cholesterol esters (ChE), triglycerides (TG) and phospholipids (PL) in plasma and liver. - Clinical signs of linoleic acid deficiency were only found in the rats fed the linoleic acid free diet. With 0.5 cal% linoleic acid in the diet no deficiency symptoms were observed. - In plasma of the linoleic acid deficient animals the concentrations of TL, Ch, ChE and TG were decreased. Plasma PL contents were insignificantly altered. - While the contents of TL, TG and ChE in the liver of the deficient rats increased significantly, those of PL and Ch were hardly affected. The results show that a linoleic acid supply of 0.5 cal% prevents nearly all alterations of plasma and liver lipid concentrations noticed in linoleic acid deficiency. The effect of this dose was as good as that of 1.3 cal% linoleic acid. Therefore we assume that the minimum requirement of male young rats for linoleic acid is markedly less than 1,3% of total energy intake.


Subject(s)
Linoleic Acids/administration & dosage , Lipid Metabolism , Liver/metabolism , Animals , Energy Intake , Energy Metabolism , Linoleic Acids/deficiency , Linoleic Acids/pharmacology , Male , Nutritional Requirements , Rats , Rats, Inbred Strains
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