Rashba Effect in Functional Spintronic Devices.

Exploiting spin transport increases the functionality of electronic devices and enables such devices to overcome physical limitations related to speed and power. Utilizing the Rashba effect at the interface of heterostructures provides promising opportunities toward the development of high-performance devices because it enables electrical control of the spin information. Herein, the focus is mainly on progress related to the two most compelling devices that exploit the Rashba effect: spin transistors and spin-orbit torque devices.

Interface morphology effect on the spin mixing conductance of Pt/FeO bilayers.

Non-magnetic (NM) metals with strong spin-orbit coupling have been recently explored as a probe of interface magnetism on ferromagnetic insulators (FMI) by means of the spin Hall magnetoresistance (SMR) effect. In NM/FMI heterostructures, increasing the spin mixing conductance (SMC) at the interface comes as an important step towards devices with maximized SMR. Here we report on the study of SMR in Pt/FeO bilayers at cryogenic temperature, and identify a strong dependence of the determined real part of the complex SMC on the interface roughness.

Field-free switching of perpendicular magnetization through spin-orbit torque in antiferromagnet/ferromagnet/oxide structures.

Spin-orbit torques arising from the spin-orbit coupling of non-magnetic heavy metals allow electrical switching of perpendicular magnetization. However, the switching is not purely electrical in laterally homogeneous structures. An extra in-plane magnetic field is indeed required to achieve deterministic switching, and this is detrimental for device applications.

Glutathione prevented dopamine-induced apoptosis of melanocytes and its signaling.

Background: Dopamine (DA), a monoamine neurotransmitter, is a well-known neurotoxin and plays an etiologic role in neurodegenerative disorders such as Parkinson's disease. DA exerts its toxic effect by generation of reactive oxygen species and quinone product. Vitiligo, a depigmentary disorder of the skin and hair characterized by selective destruction of melanocytes, has been reported to show increased levels of DA with onset and progression of the disease.

Sphingosylphosphorylcholine-induced ERK activation inhibits melanin synthesis in human melanocytes.

Sphingosylphosphorylcholine (SPC) is emerging as a potent signaling-lipid mediator. In this study, we investigated the effects of SPC on melanogenesis using cultured human melanocytes. Our results show that SPC significantly inhibits melanin synthesis in a concentration-dependent manner, and further that it reduces the activity of tyrosinase, the rate-limiting melanogenic enzyme.

Cytoprotective effect of green tea extract and quercetin against hydrogen peroxide-induced oxidative stress.

In this study, we evaluated the cytoprotective effects of antioxidative substances in hydrogen peroxide (H2O2) treated Mel-Ab melanocytes. Tested substances include selenium, quercetin, green tea (GT) extract, and several vitamins (ascorbic acid, Trolox, and folic acid). Of these, both quercetin and GT extract were found to have strong cytoprotective effects on H2O2-induced cell death.

Protective effects of EGCG on UVB-induced damage in living skin equivalents.

In this study, we evaluate the effects of (-)-epigallocatechin-3-gallate (EGCG) on ultraviolet B (UVB)-irradiated living skin equivalents (LSEs). Histologically, UVB irradiation induced thinning of the LSE epidermis, whereas EGCG treatment led to thickening of the epidermis. Moreover, EGCG treatment protected LSEs against damage and breakdown caused by UVB exposure.

Heat treatment decreases melanin synthesis via protein phosphatase 2A inactivation.

In the present study, we investigated the effects of heat treatment on melanogenesis in a mouse melanocyte cell line (Mel-Ab). It has been reported that activated extracellular signal-regulated kinase (ERK) is responsible for microphthalmia-associated transcription factor (MITF) degradation, which leads to a reduction in tyrosinase protein production and melanin synthesis. Here we demonstrate that heat treatment induces sustained ERK activation, which may inhibit melanogenesis.

Lysophosphatidic acid inhibits melanocyte proliferation via cell cycle arrest.

Lysophosphatidic acid (LPA) is a well-known mitogen in various cell types. However, we found that LPA inhibits melanocyte proliferation. Thus, we further investigated the possible signaling pathways involved in melanocyte growth inhibition.