780 research outputs found
Magnetization relaxation in (Ga,Mn)As ferromagnetic semiconductors
We describe a theory of Mn local-moment magnetization relaxation due to p-d
kinetic-exchange coupling with the itinerant-spin subsystem in the
ferromagnetic semiconductor (Ga,Mn)As alloy. The theoretical Gilbert damping
coefficient implied by this mechanism is calculated as a function of Mn moment
density, hole concentration, and quasiparticle lifetime. Comparison with
experimental ferromagnetic resonance data suggests that in annealed strongly
metallic samples, p-d coupling contributes significantly to the damping rate of
the magnetization precession at low temperatures. By combining the theoretical
Gilbert coefficient with the values of the magnetic anisotropy energy, we
estimate that the typical critical current for spin-transfer magnetization
switching in all-semiconductor trilayer devices can be as low as .Comment: 4 pages, 2 figures, submitted to Rapid Communication
Embryonic exposure to the fungicide vinclozolin causes virilization of females and alteration of progesterone receptor expression in vivo: an experimental study in mice
BACKGROUND: Vinclozolin is a fungicide that has been reported to have anti-androgenic effects in rats. We have found that in utero exposure to natural or synthetic progesterones can induce hypospadias in mice, and that the synthetic progesterone medroxyprogesterone acetate (MPA) feminizes male and virilizes female genital tubercles. In the current work, we selected a relatively low dose of vinclozolin to examine its in utero effects on the development of the genital tubercle, both at the morphological and molecular levels. METHODS: We gave pregnant dams vinclozolin by oral gavage from gestational days 13 through 17. We assessed the fetal genital tubercles from exposed fetuses at E19 to determine location of the urethral opening. After determination of gonadal sex, either genital tubercles were harvested for mRNA quantitation, or urethras were injected with a plastic resin for casting. We analyzed quantified mRNA levels between treated and untreated animals for mRNA levels of estrogen receptors α and β, progesterone receptor, and androgen receptor using nonparametric tests or ANOVA. To determine effects on urethral length (males have long urethras compared to females), we measured the lengths of the casts and performed ANOVA analysis on these data. RESULTS: Our morphological results indicated that vinclozolin has morphological effects similar to those of MPA, feminizing males (hypospadias) and masculinizing females (longer urethras). Because these results reflected our MPA results, we investigated the effects of in utero vinclozolin exposure on the mRNA expression levels of androgen, estrogen α and β, and progesterone receptors. At the molecular level, vinclozolin down-regulated estrogen receptor α mRNA in females and up-regulated progesterone receptor mRNA. Vinclozolin-exposed males exhibited up-regulated estrogen receptor α and progesterone receptor mRNA, effects we have also seen with exposure to the synthetic estrogen, ethinyl estradiol. CONCLUSION: The results suggest that vinclozolin virilizes females and directly or indirectly affects progesterone receptor expression. It also affects estrogen receptor expression in a sex-based manner. We found no in vivo effect of vinclozolin on androgen receptor expression. We propose that vinclozolin, which has been designated an anti-androgen, may also exert its effects by involving additional steroid-signaling pathways
Imaging Oxygen Defects and their Motion at a Manganite Surface
Manganites are technologically important materials, used widely as solid
oxide fuel cell cathodes: they have also been shown to exhibit
electroresistance. Oxygen bulk diffusion and surface exchange processes are
critical for catalytic action, and numerous studies of manganites have linked
electroresistance to electrochemical oxygen migration. Direct imaging of
individual oxygen defects is needed to underpin understanding of these
important processes. It is not currently possible to collect the required
images in the bulk, but scanning tunnelling microscopy could provide such data
for surfaces. Here we show the first atomic resolution images of oxygen defects
at a manganite surface. Our experiments also reveal defect dynamics, including
oxygen adatom migration, vacancy-adatom recombination and adatom bistability.
Beyond providing an experimental basis for testing models describing the
microscopics of oxygen migration at transition metal oxide interfaces, our work
resolves the long-standing puzzle of why scanning tunnelling microscopy is more
challenging for layered manganites than for cuprates.Comment: 7 figure
Downregulation of the CCL2/CCR2 and CXCL10/CXCR3 axes contributes to antitumor effects in a mouse model of malignant glioma
Glioblastoma multiforme involves glioma stem cells (GSCs) that are resistant to various therapeutic approaches. Here, we studied the importance of paracrine signaling in the glioma microenvironment by focusing on the celecoxib-mediated role of chemokines C–C motif ligand 2 (CCL2), C-X-C ligand 10 (CXCL10), and their receptors, CCR2 and CXCR3, in GSCs and a GSC-bearing malignant glioma model. C57BL/6 mice were injected with orthotopic GSCs intracranially and divided into groups administered either 10 or 30 mg/kg celecoxib, or saline to examine the antitumor effects associated with chemokine expression. In GSCs, we analyzed cell viability and expression of chemokines and their receptors in the presence/absence of celecoxib. In the malignant glioma model, celecoxib exhibited antitumor effects in a dose dependent manner and decreased protein and mRNA levels of Ccl2 and CxcL10 and Cxcr3 but not of Ccr2. CCL2 and CXCL10 co-localized with Nestin+ stem cells, CD16+ or CD163+ macrophages and Iba-1+ microglia. In GSCs, celecoxib inhibited Ccl2 and Cxcr3 expression in a nuclear factor-kappa B-dependent manner but not Ccr2 and CxcL10. Moreover, Ccl2 silencing resulted in decreased GSC viability. These results suggest that celecoxib-mediated regulation of the CCL2/CCR2 and CXCL10/ CXCR3 axes may partially contribute to glioma-specific antitumor effects
Abnormal expansion of naïve B lymphocytes after unrelated cord blood transplantation – a case report
A 33-year-old woman underwent unrelated cord blood transplantation (U-CBT) for myelodysplastic syndrome (MDS)-related secondary AML. She showed impressive increases in the number of CD19(+) B cells in bone marrow and CD19(+)27(−)IgD(+) B cells in peripheral blood from about 1 month to 3 months after U-CBT. The serum level of IL-6 temporarily increased after transplantation, and this increase seemed to be correlated with the expansion of CD19(+) B cells. Although, compared with BMT, little is known about the kinetics of hematological and immunological reconstitution in U-CBT, there was initial B-cell recovery after CBT as some described. This B cell recovery may be associated with a high number of B-cell precursors present in cord blood (CB). The phenomenon of naïve B lymphocyte expansion that we found might be associated with a high number of B-cell precursors present in CB
Saturated Ferromagnetism and Magnetization Deficit in Optimally Annealed (Ga,Mn)As Epilayers
We examine the Mn concentration dependence of the electronic and magnetic
properties of optimally annealed Ga1-xMnxAs epilayers for 1.35% < x < 8.3%. The
Curie temperature (Tc), conductivity, and exchange energy increase with Mn
concentration up to x ~ 0.05, but are almost constant for larger x, with Tc ~
110 K. The ferromagnetic moment per Mn ion decreases monotonically with
increasing x, implying that an increasing fraction of the Mn spins do not
participate in the ferromagnetism. By contrast, the derived domain wall
thickness, an important parameter for device design, remains surprisingly
constant.Comment: 8 pages, 4 figures, submitted for Rapid Communication in Phys Rev
Serum macrophage migration inhibitory factor (MIF) levels after allogeneic hematopoietic stem cell transplantation
Peer Reviewedhttp://deepblue.lib.umich.edu/bitstream/2027.42/72178/1/j.1751-553X.2007.01016.x.pd
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