Fabrication of Antireflective Compound Eyes by Imprinting

In this article, we demonstrate a simple and cost-effective approach to fabricate antireflective polymer coatings. The antireflective surfaces have 3D structures that mimick moth compound eyes. The fabrication is easily performed via a one-step imprinting process. The 3D arrays exhibit better antireflective performance than 2D arrays over most wavelengths from 400 to 2400 nm. The reflectivity of the 3D arrays is lower than 5.7% over the all of the wavelengths, and the minimum reflectivity is 0.27% at a wavelength of around 1000 nm

N‑Doped Ordered Mesoporous Carbon Originated from a Green Biological Dye for Electrochemical Sensing and High-Pressure CO₂ Storage

Herein, a series of nitrogen-doped ordered mesoporous carbons (NOMCs) with tunable porous structure were synthesized via a hard-template method with a green biological dye as precursor, under various carbonization temperatures (700–1100 °C). Compared with the ordered mesoporous silica-modified and unmodified electrodes, the use of electrodes coated by NOMCs (NOMC-700–NOMC-1100) resulted in enhanced signals and well-resolved oxidation peaks in electrocatalytic sensing of catechol and hydroquinone isomers, attributable to NOMCs’ open porous structures and increased edge-plane defect sites on the N-doped carbon skeleton. Electrochemical sensors using NOMC-1000-modified electrode were fabricated and proved feasible in tap water sample analyses. The NOMCs were also used as sorbents for high-pressure CO₂ storage. The NOMC with the highest N content exhibits the best CO₂ absorption capacities of 800.8 and 387.6 mg/g at 273 and 298 K (30 bar), respectively, which is better than those of other NOMC materials and some recently reported CO₂ sorbents with well-ordered 3D porous structures. Moreover, this NOMC shows higher affinity for CO₂ than for N₂, a benefit of its higher nitrogen content in the porous carbon framework

Conservation analysis of the COL2A1 p.Gly207 amino acid residue.

<p>Conservation analysis of the COL2A1 p.Gly207 amino acid residue.</p

Heterozygous c.620G>A (p.Gly207Glu) mutation in the <i>COL2A1</i> gene.

<p>Heterozygous c.620G>A (p.Gly207Glu) mutation in the <i>COL2A1</i> gene.</p

Pedigree and sequence analysis of an ARNSHL family.

<p>(A) Pedigree of the ARNSHL family. N, normal; M, the <i>MYO15A</i> c.9316dupC variant. (B) The homozygous <i>MYO15A</i> c.9316dupC variant of the affected individual (IV:2). (C) The heterozygous <i>MYO15A</i> c.9316dupC variant of the unaffected individual (III:1). (D) The <i>MYO15A</i> gene sequence of a normal control. ARNSHL, autosomal recessive nonsyndromic hearing loss; <i>MYO15A</i>, the myosin XVa gene.</p

The schematic structure and the mutations of the human myosin XVa.

<p>The myosin XVa consists of 3530 amino acids, including an N-terminal extension domain and Motor domain, two light chain binding IQ motifs, two myosin-tail homology 4 (MyTH4) domains and band 4.1/ezrin/radixin/moesin (FERM) domains, a Src-homology-3 (SH3) domain and a C-terminal class I PDZ-ligand domain. The novel <i>MYO15A</i> mutation in this study is showed with red box at the bottom of the figure, and previously reported mutations are displayed at the top of the figure. <i>MYO15A</i>, the myosin XVa gene.</p

The Proton-Sensing G-Protein Coupled Receptor GPR4 Promotes Angiogenesis in Head and Neck Cancer

<div><p>Squamous cell carcinoma of the head and neck (SCCHN) is an aggressive disease with poor survival and is the sixth most common cancer worldwide. Gastroesophageal reflux is a common event in SCCHN patients. GPR4 is a proton-sensing G-protein coupled receptor, which can be activated by acidosis. The objective of this study was to explore the role of GPR4 in acid exposure and tumor angiogenesis in SCCHN. In this study, we confirmed that overexpressing GPR4 in SCCHN cells could increase the expression and secretion of IL6, IL8 and VEGFA at pH 5.9. This effect could be inhibited by SB203580 (a p38 inhibitor). Western blot analysis indicated that phosphorylation of p38 increased in GPR4 infected cells at pH 5.9, which could be inhibited by SB203580. In tube formation assay, HMEC-1 cells were incubated with conditioned medium (CM, pH 5.9, 6.5, 7.4) derived from control and GPR4 infected SCCHN cells. Tube length was significantly increased in HMEC-1 cells incubated with CM from GPR4 infected cells compared with control cells at pH5.9, which indicated the pro-angiogenic effect of GPR4 in acidic pH. The neutralizing antibodies of IL6, IL8 and VEGFA could inhibit tube formation of HMEC-1 cells. In vivo, the effect of GPR4 on angiogenesis was investigated with the chick chorioallantoic membrane (CAM) model. Control and GPR4 infected SCCHN cells were seeded onto the upper CAM surface (n = 5 in each group) and 5 μL DMEM/F12 (pH 5.9, 6.5, 7.4) was added to the surface of the cell every 24 h. Four days later, the upper CAM were harvested and the ratio of the vascular area to the CAM area was quantified using Image-Pro Plus 6.0 software. GPR4 infected cells could recruit more vascular than control cells at pH5.9. In conclusion, we suggested that GPR4 induces angiogenesis via GPR4-induced p38-mediated IL6, IL8 and VEGFA secretion at acidic extracellular pH in SCCHN.</p></div

SB203580 reduces cytokine secretion by inhibiting p38 phosphorylation.

<p><b>(A)</b> In Ad-GPR4-FaDu cells, SB203580 reduced the expression of IL6, IL8 and VEGFA at pH 5.9. <b>(B)</b> SB203580 reduced secretion of IL6, IL8 and VEGFA. <b>(C)</b> GPR4 increased p38 phosphorylation at pH5.9. <b>(D)</b> SB203580 inhibit phosphorylation of p38 in GPR4 overexpressed cells. Similar results were observed in Tca8113 cells (<a href="http://www.plosone.org/article/info:doi/10.1371/journal.pone.0152789#pone.0152789.s002" target="_blank">S2 Fig</a>).</p

Tube formation assay.

<p><b>(A)</b> The tube length (arrows) of HMEC-1 cells was increased in CM derived from Ad-GPR4-FaDu cells compared with Ad-null-FaDu cells at pH 5.9. <b>(B)</b> The neutralizing antibodies of IL6, IL8 and VEGFA inhibited tube formation in HMEC-1 cells. Isotype IgG antibody was used as a control in neutralizing antibody test. <b>(C)</b> VEGFA (1 ng/mL) was used as a positive control and DMEM served as a negative control in tube formation assay. Tube lengths (pixels) were quantified from 6 representative fields using Image-Pro Plus 6.0 software. <b>(D)</b> GPR4 increased VEGFR2 phosphorylation in HMEC-1 cells at pH 5.9. Similar results were observed in Tca8113 cells (<a href="http://www.plosone.org/article/info:doi/10.1371/journal.pone.0152789#pone.0152789.s004" target="_blank">S4 Fig</a>).</p

Clinical and genetic data of 7 patients with <i>FBN2</i> c.3769T>C (p.C1257R) mutation.

<p>Clinical and genetic data of 7 patients with <i>FBN2</i> c.3769T>C (p.C1257R) mutation.</p