Communication-Micro-Scale Columnar Architecture Composed of Copper Nano Sheets by Electrodeposition Technique

Micro-scale columnar architectures composed of copper sheets with nanometer thickness were fabricated by electrodeposition using a photolithography technique. A copper sulfate solution containing a polyacrylic acid was used as the plating bath, and the electrodeposition was conducted under galvanostatic conditions. Patterned electrodeposits with a cylindrical shape and composed of thin copper sheets were formed. Every copper deposit had openings on the top and side regions and also had a porous interior. This novel three-dimensional (3D) copper architecture should provide functional copper electrodes with large effective surface areas. (C) The Author(s) 2016. Published by ECS. All rights reserved.ArticleJOURNAL OF THE ELECTROCHEMICAL SOCIETY. 164(2):D72-D74 (2017)journal articl

Fabrication of Three-Dimensional (3D) Copper/Carbon Nanotube Composite Film by One-Step Electrodeposition

A three-dimensional (3D) composite film containing copper nanostructures and carbon nanotubes (3DC/CNT composite film) was fabricated by one-step electrodeposition. The 3DC/CNT composite film was formed under galvanostatic conditions using a copper sulfate bath containing CNTs and polyacrylic acid which acts as both a 3DC-forming and a CNT-dispersing agent. The composite film consists of thin copper sheets with thicknesses of ca. 70-80 nm and CNTs, with large interior spaces between sheets. The CNTs were homogeneously distributed inside the composite film and were fixed by the copper sheets where CNTs pierce the copper sheets. The CNT content in the composite films increased with the CNT concentration of the plating bath. The 3DC film without CNTs did not maintain its 3D spaces when the film thickness was increased due to insufficient structural strength, whereas the 3DC/CNT composite film maintained the 3D spaces despite an increase in film thickness, which suggests that the CNTs reinforce the film to maintain the 3D spaces. (C) The Author(s) 2016. Published by ECS. All rights reserved.ArticleJOURNAL OF THE ELECTROCHEMICAL SOCIETY. 163(14):D774-D779 (2016)journal articl

Renin-Angiotensin System Hyperactivation Can Induce Inflammation and Retinal Neural Dysfunction

The renin-angiotensin system (RAS) is a hormone system that has been classically known as a blood pressure regulator but is becoming well recognized as a proinflammatory mediator. In many diverse tissues, RAS pathway elements are also produced intrinsically, making it possible for tissues to respond more dynamically to systemic or local cues. While RAS is important for controlling normal inflammatory responses, hyperactivation of the pathway can cause neural dysfunction by inducing accelerated degradation of some neuronal proteins such as synaptophysin and by activating pathological glial responses. Chronic inflammation and oxidative stress are risk factors for high incidence vision-threatening diseases such as diabetic retinopathy (DR), age-related macular degeneration (AMD), and glaucoma. In fact, increasing evidence suggests that RAS inhibition may actually prevent progression of various ocular diseases including uveitis, DR, AMD, and glaucoma. Therefore, RAS inhibition may be a promising therapeutic approach to fine-tune inflammatory responses and to prevent or treat certain ocular and neurodegenerative diseases

Blockade of vascular adhesion protein-1 attenuates choroidal neovascularization

Purpose: Vascular adhesion protein (VAP)-1 is an adhesion molecule elucidated as a mediator of the leukocyte recruitment cascade. The purpose of this study was to investigate the role of VAP-1 in ocular inflammatory neovascularization using a mouse laser-induced choroidal neovascularization (CNV) model. Methods: CNV was induced with 532 nm laser irradiation in C57BL/6 mice, and production of VAP-1 protein in the retinal pigment epithelium (RPE) choroid during CNV formation was examined. CNV animals were treated with the specific VAP-1 inhibitor U-V002 or vehicle solution, and the volume of CNV tissue was evaluated with volumetric measurements. Macrophage infiltration into the CNV lesions was evaluated using two different techniques, flatmount staining and real-time polymerase chain reaction (PCR) for F4/80. The protein levels of intercellular adhesion molecule (ICAM)-1, monocyte chemoattractant protein (MCP)-1, P-selectin, and vascular endothelial growth factor (VEGF) in the RPE-choroid were measured with enzyme-linked immunosorbent assay (ELISA). Results: VAP-1 inhibition significantly suppressed CNV formation in a dose-dependent manner and reduced macrophage infiltration into CNV lesions. Furthermore, VAP-1 blockade decreased the expression of ICAM-1 and MCP-1, both of which play a pivotal role in macrophage recruitment. Conclusions: Our data suggest VAP-1 has an important role during ocular inflammatory neovascularization through leukocyte recruitment. VAP-1 inhibition may be a novel and potent therapeutic strategy in treating CNV formation

An endogenous factor enhances ferulic acid decarboxylation catalyzed by phenolic acid decarboxylase from Candida guilliermondii

Resource subsidies in the form of allochthonous primary production drive secondary production in many ecosystems, often sustaining diversity and overall productivity. Despite their importance in structuring marine communities, there is little understanding of how subsidies move through juxtaposed habitats and into recipient communities. We investigated the transport of detritus from kelp forests to a deep Arctic fjord (northern Norway). We quantified the seasonal abundance and size structure of kelp detritus in shallow subtidal (0‒12 m), deep subtidal (12‒85 m), and deep fjord (400‒450 m) habitats using a combination of camera surveys, dive observations, and detritus collections over 1 year. Detritus formed dense accumulations in habitats adjacent to kelp forests, and the timing of depositions coincided with the discrete loss of whole kelp blades during spring. We tracked these blades through the deep subtidal and into the deep fjord, and showed they act as a short-term resource pulse transported over several weeks. In deep subtidal regions, detritus consisted mostly of fragments and its depth distribution was similar across seasons (50% of total observations). Tagged pieces of detritus moved slowly out of kelp forests (displaced 4‒50 m (mean 11.8 m ± 8.5 SD) in 11‒17 days, based on minimum estimates from recovered pieces), and most (75%) variability in the rate of export was related to wave exposure and substrate. Tight resource coupling between kelp forests and deep fjords indicate that changes in kelp abundance would propagate through to deep fjord ecosystems, with likely consequences for the ecosystem functioning and services they provide

Neuroprotective response after photodynamic therapy: Role of vascular endothelial growth factor

Background: Anti-vascular endothelial growth factor (VEGF) drugs and/or photodynamic therapy (PDT) constitute current treatments targeting pathological vascular tissues in tumors and age-related macular degeneration. Concern that PDT might induce VEGF and exacerbate the disease has led us to current practice of using anti-VEGF drugs with PDT simultaneously. However, the underlying molecular mechanisms of these therapies are not well understood. Methods: We assessed VEGF levels after PDT of normal mouse retinal tissue, using a laser duration that did not cause obvious tissue damage. To determine the role of PDT-induced VEGF and its downstream signaling, we intravitreally injected a VEGF inhibitor, VEGFR1 Fc, or a PI3K/Akt inhibitor, LY294002, immediately after PDT. Then, histological and biochemical changes of the retinal tissue were analyzed by immunohistochemistry and immunoblot analyses, respectively. Results: At both the mRNA and protein levels, VEGF was upregulated immediately and transiently after PDT. VEGF suppression after PDT resulted in apoptotic destruction of the photoreceptor cell layer in only the irradiated area during PDT. Under these conditions, activation of the anti-apoptotic molecule Akt was suppressed in the irradiated area, and levels of the pro-apoptotic protein BAX were increased. Intravitreal injection of a PI3K/Akt inhibitor immediately after PDT increased BAX levels and photoreceptor cell apoptosis. Conclusion: Cytotoxic stress caused by PDT, at levels that do not cause overt tissue damage, induces VEGF and activates Akt to rescue the neural tissue, suppressing BAX. Thus, the immediate and transient induction of VEGF after PDT is neuroprotective

Transcriptional factors associated with epithelial-mesenchymal transition in choroidal neovascularization

Purpose: To investigate the transcriptional factors associated with epithelial-mesenchymal transition (EMT) in choroidal neovascularization (CNV) secondary to age-related macular degeneration (AMD). Methods: Paraffin sections of CNV obtained from patients with AMD (n=12) were stained for transcriptional factors related to EMT, i.e., Snail, Slug, SIP1, and Twist. As a control, postmortem sections of ocular normal tissue were used. Furthermore, using a human retinal pigment epithelial (RPE) cell line (ARPE-19), reverse transcription–polymerase chain reaction (RT–PCR) and immunofluorescence microscopy were performed to explore the cellular localization and expression levels of EMT-associated transcriptional factors upon cytokine stimulation. Results: Of 12 specimens, 11 CNV tissues (91.6%) showed staining for Snail localized in cellular nuclei, particularly in those of RPE cells. Snail was strongly co-localized with α-smooth muscle antigen (SMA) in RPE cells. In contrast, postmortem human retina showed no Snail staining in RPE cells. Other transcriptional factors, Slug, Twist and SIP1 were not detected in CNV or normal human retina. In ARPE-19 cells, RT–PCR and immunofluorescence microscopy showed that Snail mRNA was upregulated by transforming growth factor (TGF)-β and VEGF stimulation. Furthermore, TGF-β induced relocalization of Snail to the nucleus in RPE cells. Conclusions: The current data indicate that Snail is a major transcriptional factor for EMT changes of RPE cells in human CNV