In ferromagnetic thin films, broken inversion symmetry and spin-orbit coupling give rise to interfacial Dzyaloshinskii-Moriya interactions. Analytic expressions for spin-wave properties show that the interfacial Dzyaloshinskii-Moriya interaction leads to non-reciprocal spin-wave propagation, i.e. different properties for spin waves propagating in opposite directions. In favorable situations, it can increase the spin-wave attenuation length. Comparing measured spin wave properties in ferromagnet|normal metal bilayers and other artificial layered structures with these calculations can provide a useful characterization of the interfacial Dzyaloshinskii-Moriya interactions.

Recent evidence shows that amniotic fluid (AF) contains multiple cell types derived from the developing fetus, and may represent a novel source of stem cells for cell therapy. In this study, we examined the paracrine factors released by human amniotic fluid-derived mesenchymal stem cells (AF-MSCs) and their ability to accelerate the wound-healing process by stimulating proliferation and migration of dermal fibroblasts. AF-MSCs expressed the typical MSC marker proteins CD13, CD29, and CD44 and differentiated into adipocytes, osteoblasts, and chondrocytes when exposed to the appropriate differentiation media. In addition, AF-MSC-conditioned media (AF-MSC-CM) significantly enhanced proliferation of dermal fibroblasts. Antibody-based protein array and enzyme-linked immunosorbent assay (ELISA) indicated that AF-MSC-CM contains various cytokines and chemokines that are known to be important in normal wound healing, including IL-8, IL-6, TGF-beta, TNFRI, VEGF, and EGF. Application of AF-MSC-CM significantly enhanced wound healing by dermal fibroblasts via the TGF-beta/SMAD2 pathway. Levels of p-SMAD2 were increased by AF-MSC-CM, and both the increase in p-SMAD2 and migration of dermal fibroblasts were blocked by inhibiting the TGF-beta/SMAD2 pathway. Moreover, in a mouse excisional wound model, AF-MSC-CM accelerated wound healing. These data provide the first evidence of the potential for AF-MSC-CM in the treatment of skin wounds.

In a previous study, we isolated human amniotic fluid (AF)-derived mesenchymal stem cells (AF-MSCs) and utilized normoxic conditioned medium (AF-MSC-norCM) which has been shown to accelerate cutaneous wound healing. Because hypoxia enhances the wound healing function of mesenchymal stem cell-conditioned medium (MSC-CM), it is interesting to explore the mechanism responsible for the enhancement of wound healing function. In this work, hypoxia not only increased the proliferation of AF-MSCs but also maintained their constitutive characteristics (surface marker expression and differentiation potentials). Notably, more paracrine factors, VEGF and TGF-β1, were secreted into hypoxic conditioned medium from AF-MSCs (AF-MSC-hypoCM) compared to AF-MSC-norCM. Moreover, AF-MSC-hypoCM enhanced the proliferation and migration of human dermal fibroblasts in vitro, and wound closure in a skin injury model, as compared to AF-MSC-norCM. However, the enhancement of migration of fibroblasts accelerated by AF-MSC-hypoCM was inhibited by SB505124 and LY294002, inhibitors of TGF-β/SMAD2 and PI3K/AKT, suggesting that AF-MSC-hypoCM-enhanced wound healing is mediated by the activation of TGF-β/SMAD2 and PI3K/AKT. Therefore, AF-MSC-hypoCM enhances wound healing through the increase of hypoxia-induced paracrine factors via activation of TGF-β/SMAD2 and PI3K/AKT pathways.

The human brain intrinsically operates with a large number of synapses, more than 10 15. Therefore, one of the most critical requirements for constructing artificial neural networks (ANNs) is to achieve extremely dense synaptic array devices, for which the crossbar architecture containing an artificial synaptic node at each cross is indispensable. However, crossbar arrays suffer from the undesired leakage of signals through neighboring cells, which is a major challenge for implementing ANNs. In this work, we show that this challenge can be overcome by using Pt/TaO y / nanoporous (NP) TaO x /Ta memristor synapses because of their self-rectifying behavior, which is capable of suppressing unwanted leakage pathways. Moreover, our synaptic device exhibits high non-linearity (up to 10 4), low synapse coupling (S.C, up to 4.00 × 10 −5), acceptable endurance (5000 cycles at 85°C), sweeping (1000 sweeps), retention stability and acceptable cell uniformity. We also demonstrated essential synaptic functions, such as long-term potentiation (LTP), long-term depression (LTD), and spiking-timing-dependent plasticity (STDP), and simulated the recognition accuracy depending on the S.C for MNIST handwritten digit images. Based on the average S.C (1.60 × 10 −4) in the fabricated crossbar array, we confirmed that our memristive synapse was able to achieve an 89.08% recognition accuracy after only 15 training epochs.

Solid electrolyte memories utilizing voltage‐induced resistance change display the capability of multilevel switching, but understanding of the microscopic switching mechanism has been left incomplete. Here, in situ TEM observation of voltage‐induced changes in the microstructure of a solid electrolyte memory is reported, revealing that the multilevel switching originates from the growth of multiple conducting filaments with nanometer‐sized diameter and spacing.

Keloids are benign skin tumors characterized by collagen accumulation and hyperproliferation of fibroblasts. To find an effective therapy for keloids, we explored the pharmacological potential of (-)-epigallocatechin-3-gallate (EGCG), a widely investigated tumor-preventive agent. When applied to normal and keloid fibroblasts (KFs) in vitro, proliferation and migration of KFs were more strongly suppressed by EGCG than normal fibroblast proliferation and migration (IC(50): 54.4 microM (keloid fibroblast (KF)) versus 63.0 microM (NF)). The level of Smad2/3, signal transducer and activator of transcription-3 (STAT3), and p38 phosphorylation is more enhanced in KFs, and EGCG inhibited phosphorylation of phosphatidylinositol-3-kinase (PI3K), extracellular signal-regulated protein kinase 1/2 (ERK1/2), and STAT3 (Tyr705 and Ser727). To evaluate the contribution of these pathways to keloid pathology, we treated KFs with specific inhibitors for PI3K, ERK1/2, or STAT3. Although a PI3K inhibitor significantly suppressed proliferation, PI3K and MEK/ERK inhibitors had a minor effect on migration and collagen production. However, a JAK2/STAT3 inhibitor and a STAT3 siRNA strongly suppressed proliferation, migration, and collagen production by KFs. We also found that treatment with EGCG suppressed growth and collagen production in the in vivo keloid model. This study demonstrates that EGCG suppresses the pathological characteristics of keloids through inhibition of the STAT3-signaling pathway. We propose that EGCG has potential in the treatment and prevention of keloids.

Photoelectrochemical hydrogen production from solar energy has been attracting much attention in the field of renewable energy technology. The realization of cost-effective hydrogen production by water splitting requires electrolysis or photoelectrochemical cells decorated with highly efficient co-catalysts. A critical requirement for catalysts in the photoelectrochemical cells is not only the ability to boost the 10 kinetics of a chemical reaction but also to exhibit durability against electrochemical and photoinduced degradation. In the race to replace previous noble-metal catalysts, the design of carbon-based catalysts represents an important research direction in the search for non-precious, environmentally benign, and corrosion-resistant catalysts. Herein, we suggest graphene quantum sheets as a catalyst for the solardriven hydrogen evolution reaction on Si nanowire photocathodes. The optimum nanostructures for the Si 15 photocathodes exhibit an enhanced photocurrent and a lower overpotential compared to those of a planar Si surface. This significant enhancement demonstrates how graphene quantum sheet catalysts can be used to produce Si nanowire photocathodes as hydrogen evolution reaction catalysts with high activity.

Somatic cells can be reprogrammed into induced pluripotent stem (iPS) cells by the transcription factors