Engineering Crystal Facet of α‑MnO₂ Nanowire for Highly Efficient Catalytic Oxidation of Carcinogenic Airborne Formaldehyde

The activity of exposed crystal facets directly determines its physicochemical properties. Thus, acquiring a high percentage of reactive facets by crystal facet engineering is highly desirable for improving the catalytic reactivity. Herein, single-crystalline α-MnO₂ nanowires with major exposed high-index {310} facets were synthesized via a facile hydrothermal route with the assistance of a capping agent of oxalate ions. Comparing with two other low-index facets ({100} and {110}), the resulting α-MnO₂ nanowires with exposed {310} facets exhibited much better activity and stability for carcinogenic formaldehyde (HCHO) oxidation, making 100% of 100 ppm of HCHO mineralize into CO₂ at 60 °C, even better than some Ag supported catalysts. The density functional theory (DFT) calculations were used to investigate the difference in the catalytic activity of α-MnO₂ with exposed {100}, {110}, and {310} facets. The experimental characterization and theoretical calculations all confirm that the {310} facets with high surface energy can not only facilitate adsorption/activation of O₂ and H₂O but also be beneficial to the generation of oxygen vacancies, which result in significantly enhanced activity for HCHO oxidation. This is a valuable report on engineering surface facets in the preparation of α-MnO₂ as highly efficient oxidation catalysts. This study deepens the understanding of facet-dependent activity of α-MnO₂ and points out a strategy to improve their catalytic activity by crystal facet engineering

Large-Area Highly Conductive Transparent Two-Dimensional Ti₂CT_<i>x</i> Film

We report a simple and scalable method to fabricate homogeneous transparent conductive thin films (Ti₂CT_<i>x</i>, one of the MXene) by dip coating of an Al₂O₃ substrate in a colloidal solution of large-area Ti₂CT_<i>x</i> thin flakes. Scanning electron microscopy and atomic force microscopy images exhibit the wafer-scale homogeneous Ti₂CT_<i>x</i> thin film (∼5 nm) covering the whole substrate. The sheet resistance is as low as 70 Ω/sq at 86% transmittance, which corresponds to the high figure of merit (FOM) of 40.7. Furthermore, the thickness of the film is tuned by a SF₆+Ar plasma treatment, which etches Ti₂CT_<i>x</i> film layer by layer and removes the top oxidized layer without affecting the bottom layer of the Ti₂CT_<i>x</i> flake. The resistivity of plasma-treated Ti₂CT_<i>x</i> film is further decreased to 63 Ω/sq with an improved transmittance of 89% and FOM of 51.3, demonstrating the promise of Ti₂CT_<i>x</i> for future transparent conductive electrode application

Colourful cholesteric liquid crystal polymer network gratings prepared through nanoimprinting

Both the colourful cholesteric liquid crystal polymer network (CLCN) patterns and the gratings have attracted much attention for their applications as optical materials. Herein, the photochromic cholesteric liquid crystal (CLC) mixtures were prepared using a photoisomerizable chiral dopant. The structural colour of the CLC mixtures was tunable by changing the chiral dopant concentration and the intensity of the 365-nm irradiation light. The CLCN gratings with a structural colour were prepared using the UV nanoimprinting lithography method. The structural colours of the CLCN gratings originate from both the cholesteric and the grating structures. Moreover, a patterned CLCN grating was prepared using a photochromic CLC mixture, which could be applied for decoration and anti-counterfeiting.</p

Supplemental Material - Effect of Physiotherapy Interventions on Motor Symptoms in People With Parkinson’s Disease: A Systematic Review and Meta-Analysis

Supplemental Material for Effect of Physiotherapy Interventions on Motor Symptoms in People with Parkinson’s Disease: A Systematic Review and Meta-Analysis by Yajie Yang, Yang Wang, Tianzi Gao, Abudurousuli Reyila, Jiaxin Liu, Jiajia Liu, and Hongbin Han in Biological Research For Nursing</p

UCSC Genome Browser view of LANA binding on the KSHV genome.

<p>ChIP-seq was performed in BCBL-1, TIVE-LTC with or without SureSelect Target Enrichment System with LANA-specific antibody. Sequencing tags were mapped to viral genome and visualized in UCSC Genome Browser.</p

Genome-wide epigenome analysis of KSHV in BCBL-1 cells.

<p>ChIP assays were performed in BCBL-1 cells with control IgG, H3K4me3, H3K27me3, and Pol II antibody. The resulting ChIP DNA was used for library construction followed by Illumina sequencing. Sequencing tags mapped to viral genome were visualized in UCSC Genome Browser. The number of sequence tags is indicated for each track (y-axis), which represents the number of times each region was recovered by the ChIP-seq. The highest coverage for H3K4me3 is 6,660 within the terminal repeat which was not shown in order to visualize the lower peaks.</p

Positions of LANA peaks to the transcription start sites of known genes in BCBL-1 and TIVE-LTC cells.

<p>LANA peaks within the +/−2 kb region of known genes are calculated and plotted for distance from center of the peaks to the transcription start sites in BCBL-1 cells (A) and TIVE-LTC cells (B).</p

LANA Binds to Multiple Active Viral and Cellular Promoters and Associates with the H3K4Methyltransferase hSET1 Complex

<div><p>Kaposi's sarcoma-associated herpesvirus (KSHV) is a γ-herpesvirus associated with KS and two lymphoproliferative diseases. Recent studies characterized epigenetic modification of KSHV episomes during latency and determined that latency-associated genes are associated with H3K4me3 while most lytic genes are associated with the silencing mark H3K27me3. Since the latency-associated nuclear antigen (LANA) (i) is expressed very early after <i>de novo</i> infection, (ii) interacts with transcriptional regulators and chromatin remodelers, and (iii) regulates the LANA and RTA promoters, we hypothesized that LANA may contribute to the establishment of latency through epigenetic control. We performed a detailed ChIP-seq analysis in cells of lymphoid and endothelial origin and compared H3K4me3, H3K27me3, polII, and LANA occupancy. On viral episomes LANA binding was detected at numerous lytic and latent promoters, which were transactivated by LANA using reporter assays. LANA binding was highly enriched at H3K4me3 peaks and this co-occupancy was also detected on many host gene promoters. Bioinformatic analysis of enriched LANA binding sites in combination with biochemical binding studies revealed three distinct binding patterns. A small subset of LANA binding sites showed sequence homology to the characterized LBS1/2 sequence in the viral terminal repeat. A large number of sites contained a novel LANA binding motif (TCCAT)₃ which was confirmed by gel shift analysis. Third, some viral and cellular promoters did not contain LANA binding sites and are likely enriched through protein/protein interaction. LANA was associated with H3K4me3 marks and in PEL cells 86% of all LANA bound promoters were transcriptionally active, leading to the hypothesis that LANA interacts with the machinery that methylates H3K4. Co-immunoprecipitation demonstrated LANA association with endogenous hSET1 complexes in both lymphoid and endothelial cells suggesting that LANA may contribute to the epigenetic profile of KSHV episomes.</p></div

LANA and H3K4me3 but not H3K27 overlap at many regions of the KSHV and human genome in BCBL-1 cells.

<p>(<b>A</b>) ChIP-seq was performed in BCBL-1, with LANA-, H3K4me3-, H3K27me3-specific antibodies. Sequencing tags were mapped to viral genome and visualized in UCSC Genome Browser. Cluster analysis (seqMINER) using sequence regions (plus/minus 5 kbp around TSSs) that were enriched by LANA ChIP-seq upstream of 1295 annotated transcripts in BCBL-1 cells (<a href="http://www.plospathogens.org/article/info:doi/10.1371/journal.ppat.1004240#ppat-1004240-t002" target="_blank">Table 2</a> and <a href="http://www.plospathogens.org/article/info:doi/10.1371/journal.ppat.1004240#ppat.1004240.s006" target="_blank">Table S1</a>). (B) Heterogeneous LANA binding patterns relative to TSSs; (C) H3K4me3 distribution at LANA-enriched sites and (D) H3K27me3 distribution at LANA-enriched sites.</p

LANA forms complex with H3K4me3 methyltransferase hSET1 <i>in vivo</i>.

<p>Nuclear extract was harvested from BCBL-1 cells (A) or BC-3 cells (B) and LTC-TIVE (C). The nuclear extract was immunoprecipitated with control IgG or monoclonal rat antibody against LANA. The immunoprecipitated complex was separated in 8% SDS-PAGE gel and immunoblotted with RbBP5, ASH2L, and hSET1, or MLL-1 antibody.</p