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Purpose: To assess the relationship between combined serum lutein and zeaxanthin (L+Z) concentration and macular pigment optical density (MPOD), and to investigate the effect of L+Z+docosahexaenoic acid (DHA) dietary supplementation on the spatial distribution of MPOD. Methods: Twenty healthy fellow eyes with unilateral wet age-related macular degeneration or chronic central serous chorioretinopathy were included. All participants received a dietary supplement for 6 months that contained 20 mg L, 1 mg Z, and 200 mg DHA. The best-corrected visual acuity and contrast sensitivity (CS) were measured at baseline and at 1, 3, and 6 months. Serum L+Z concentrations were measured at baseline and at 3 months. MPOD was calculated at each time point using fundus autofluorescent images. Results: Serum L+Z concentration was correlated with MPOD at 1°-2° eccentricity at baseline (r=0.63, P=0.003) and 3 months (r=0.53, P=0.015). Serum L+Z concentration increased by a factor of 2.3±1.0 (P<0.0001). At 6 months, MPOD was significantly higher compared to the baseline level at 0°-0.25° (P=0.034) and 0.25°-0.5° (P=0.032) eccentricity. CS improved after 3 or 6 months of L+Z+DHA supplementation (P<0.05). Conclusion: Juxtafoveal MPOD was associated with serum L+Z concentration. Foveal MPOD was increased by L+Z+DHA dietary supplementation. [ABSTRACT FROM AUTHOR]

We report the effect of the rare earth metal Gd on current-induced spin-orbit torques (SOTs) in perpendicularly magnetized Pt/Co/Gd heterostructures, characterized using harmonic measurements and spin-torque ferromagnetic resonance (ST-FMR). By varying the Gd metal layer thickness from 0 nm to 8 nm, harmonic measurements reveal a significant enhancement of the effective fields generated from the Slonczewski-like and field-like torques. ST-FMR measurements confirm an enhanced effective spin Hall angle and show a corresponding increase in the magnetic damping constant with increasing Gd thickness. These results suggest that Gd plays an active role in generating SOTs in these heterostructures. Our finding may lead to spin-orbitronics device application such as non-volatile magnetic random access memory, based on rare earth metals. [ABSTRACT FROM AUTHOR]

We investigate the in-plane field dependence of current-induced magnetic domain wall motion in asymmetric Co/Ni nanowires. The application of an in-plane field changed the direction of domain wall motion. In a systematic study, by varying the magnetic layer thickness, we show that the in-plane field induces a crossover from spin Hall torque to adiabatic spin-transfer torque for the magnetic domain wall motion. Furthermore, the dependence of the threshold current density on the in-plane longitudinal field provides a way for determining the strength of the Dzyaloshinskii-Moriya interaction. [ABSTRACT FROM AUTHOR]

The temperature dependence of spin-orbit torques (SOTs) and spin-dependent transport parameters is measured in bilayer Ta/TbCo ferrimagnetic alloy films with bulk perpendicular magnetic anisotropy. We find that the dampinglike (DL)-SOT effective field diverges as temperature is swept through the magnetic compensation temperature (TM), where the net magnetization vanishes due to the opposing contributions from the Tb and Co sublattices. We show that DL-SOT scales with the inverse of the saturation magnetization (Ms), whereas the spin-torque efficiency is independent of the temperature-dependent Ms. Our findings provide insight into spin transport mechanisms in ferrimagnets and highlight low-Ms rare-earth/transition-metal alloys as promising candidates for SOT device applications. [ABSTRACT FROM AUTHOR]

Aging is associated with a high prevalence of hypertension due to elevated susceptibility of BP to dietary salt, but its mechanism is unknown. Serum levels of Klotho, an anti-aging factor, decline with age. We found that high salt (HS) increased BP in aged mice and young heterozygous Klotho-knockout mice and was associated with increased vascular expression of Wnt5a and p-MYPT1, which indicate RhoA activity. Not only the Wnt inhibitor LGK974 and the Wnt5a antagonist Box5 but Klotho supplementation inhibits HS-induced BP elevation, similarly to the Rho kinase inhibitor fasudil, associated with reduced p-MYPT1 expression in both groups of mice. In cultured vascular smooth muscle cells, Wnt5a and angiotensin II (Ang II) increased p-MYPT1 expression but knockdown of Wnt5a with siRNA abolished Ang II-induced upregulation of p-MYPT1, indicating that Wnt5a is indispensable for Ang II-induced Rho/ROCK activation. Notably, Klotho inhibited Wnt5a- and Ang II-induced upregulation of p-MYPT1. Consistently, Klotho supplementation ameliorated HS-induced augmentation of reduced renal blood flow (RBF) response to intra-arterial infusion of Ang II and the thromboxane A2 analog U46619, which activated RhoA in both groups of mice and were associated with the inhibition of BP elevation, suggesting that abnormal response of RBF to Ang II contributes to HS-induced BP elevation. Thus, Klotho deficiency underlies aging-associated salt-sensitive hypertension through vascular non-canonical Wnt5a/RhoA activation. [ABSTRACT FROM AUTHOR]

Epigenetic abnormalities have been suggested to mediate metabolic memory observed in diabetic complications. We have shown that epigenetic alterations may induce persistent phenotypic changes in the proximal tubules of the diabetic kidneys. In this study, we show that pregnane X receptor (PXR), a xenobiotic nuclear receptor, is epigenetically altered and upregulated and may have a possible function in the diabetic kidney. PXR has been shown to play a critical role in metabolic changes in obesity and diabetes; however, its distribution and function in the kidney are unknown. In the normal kidney, Pxr was selectively expressed in the proximal tubular cells with demethylation in the promoter DNA. In db/db mice, significant increases in Pxr mRNA, further demethylation of DNA, and stimulatory histone marks in the promoter were observed. Epigenetic changes are likely to play a causative role in PXR induction, since a DNA methyltransferase inhibitor increased PXR mRNA in cultured human proximal tubular cells. Administration of a PXR agonist increased mRNA levels of solute carrier organic anion transporter family member 2B1 (Slco2b1), a xenobiotic transporter; response gene to complement 32 (Rgc32), a molecule known to exert fibrotic effects in the kidney; and phosphoenolpyruvate carboxykinase 1 (Pck1), a gluconeogenic enzyme in the kidney. The expressions of these genes were inhibited by PXR small interfering RNA in cultured proximal tubular cells. Increased mRNA levels of Slco2b1, Rgc32, and Pck1 were also observed in the kidney of db/db mice. These data indicate that PXR is upregulated in the diabetic kidney with aberrant epigenetic modifications and may modulate the course of diabetic kidney disease through the activation of these genes. [ABSTRACT FROM AUTHOR]