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An as-synthesized recyclable Al-NDC@GO composite exhibited remarkable adsorption capacity and high selectivity for pyridine, quinoline and indole.

For the development of supercapacitors, electrode materials with the advantages of simple synthesis and high specific capacitance are one of the very important factors. Herein, we synthesized g-C3N4 and NiCo2O4 by thermal polymerization method and hydrothermal method, respectively, and finally synthesized NiCo2O4/g-C3N4 nanomaterials by mixing, grinding, and calcining g-C3N4 and NiCo2O4. NiCo2O4/g-C3N4 nanomaterials are characterized by X-ray diffraction and X-ray photoelectron spectroscopy. The microscopic morphology, lattice structure, and element distribution of NiCo2O4/g-C3N4 nanomaterials were characterized by scanning electron microscopy (SEM), transmission electron microscopy, high resoultion transmission electron microscopy, and mapping methods. The electrochemical performance and cycle stability of NiCo2O4/g-C3N4 were tested in a 6 M KOH aqueous solution as electrolyte under a three-electrode system. Due to the physical mixing structure of g-C3N4 and NiCo2O4 nanomaterials, the electrochemical energy storage performance of NiCo2O4/g-C3N4 supercapacitor electrodes is better than that of NiCo2O4 supercapacitor electrodes. At a current density of 1 A/g, the capacitances of NiCo2O4 and NiCo2O4/g-C3N4 are 98.86 and 1,127.71 F/g, respectively. At a current density of 10 A/g, the capacitance of NiCo2O4/g-C3N4 supercapacitor electrode maintains 70.5% after 3,000 cycles. NiCo2O4/g-C3N4 electrode has excellent electrochemical performance, which may be due to the formation of physical mixing between NiCo2O4 and g-C3N4, which has broad application prospects. This research is of great importance for the development of materials in high-performance energy storage devices, catalysis, sensors, and other applications.

Specific mutations within the replication foci targeting sequence (RFTS) domain of human DNMT1 are causative of two types of adult-onset neurodegenerative diseases, HSAN1E and ADCA-DN, but the underlying mechanisms are largely unknown. We generated

ZnO nanotowers have potential advantages in field emissions, photocatalysis, self-cleaning devices, solar cells and chronic-disease diagnosis. In this paper tailored size and apex angles of the pencil-like ZnO nanotower arrays were obtained by the aqueous solution method via systematically controlling the ammonia volume. The relationship between the main Zn-containing species in the precursor solutions and the ammonia volume was analyzed by the X-ray powder diffraction and infrared spectra. The effects of different proportion of Zn-species on the characteristics of ZnO nanotower arrays were explained by chemical reaction kinetics.

In mammals it is unclear if UHRF1-mediated DNA maintenance methylation by DNMT1 is strictly dependent on histone H3K9 methylation. Here we have generated an Uhrf1 knockin (KI) mouse model that specifically abolishes the H3K9me2/3-binding activity of Uhrf1. The homozygous Uhrf1 KI mice are viable and fertile, and exhibit ∼10% reduction of DNA methylation in various tissues. The reduced DNA methylation occurs globally in the genome and does not restrict only to the H3K9me2/3 enriched repetitive sequences. In vitro UHRF1 binds with higher affinity to reconstituted nucleosome with hemi-methylated CpGs than that with H3K9me2/3, although it binds cooperatively to nucleosome with both modifications. We also show that the nucleosome positioning affects the binding of methylated DNA by UHRF1. Thus, while our study supports a role for H3K9 methylation in promoting DNA methylation, it demonstrates for the first time that DNA maintenance methylation in mammals is largely independent of H3K9 methylation., There is crosstalk between the maintenance of DNA methylation and histone methylation. Here, the authors create an Uhrf1 knockin mouse model that abolishes the H3K9me2/3-binding activity of Uhrf1, and show that DNA maintenance methylation in mammals is largely independent of H3K9 methylation.

UHRF2 has been implicated as a novel regulator for both DNA methylation (5mC) and hydroxymethylation (5hmC), but its physiological function and role in DNA methylation/hydroxymethylation are unknown. Here we show that in mice, UHRF2 is more abundantly expressed in the brain and a few other tissues. Uhrf2 knock-out mice are viable and fertile and exhibit no gross defect. Although there is no significant change of DNA methylation, the Uhrf2 null mice exhibit a reduction of 5hmC in the brain, including the cortex and hippocampus. Furthermore, the Uhrf2 null mice exhibit a partial impairment in spatial memory acquisition and retention. Consistent with the phenotype, gene expression profiling uncovers a role for UHRF2 in regulating neuron-related gene expression. Finally, we provide evidence that UHRF2 binds 5hmC in cells but does not appear to affect the TET1 enzymatic activity. Together, our study supports UHRF2 as a bona fide 5hmC reader and further demonstrates a role for 5hmC in neuronal function.

Postnatal growth of mammalian oocytes is accompanied by a progressive gain of DNA methylation, which is predominantly mediated by DNMT3A, a de novo DNA methyltransferase1,2. Unlike the genome of sperm and most somatic cells, the oocyte genome is hypomethylated in transcriptionally inert regions2-4. However, how such a unique feature of the oocyte methylome is determined and its contribution to the developmental competence of the early embryo remains largely unknown. Here we demonstrate the importance of Stella, a factor essential for female fertility5-7, in shaping the oocyte methylome in mice. Oocytes that lack Stella acquire excessive DNA methylation at the genome-wide level, including in the promoters of inactive genes. Such aberrant hypermethylation is partially inherited by two-cell-stage embryos and impairs zygotic genome activation. Mechanistically, the loss of Stella leads to ectopic nuclear accumulation of the DNA methylation regulator UHRF18,9, which results in the mislocalization of maintenance DNA methyltransferase DNMT1 in the nucleus. Genetic analysis confirmed the primary role of UHRF1 and DNMT1 in generating the aberrant DNA methylome in Stella-deficient oocytes. Stella therefore safeguards the unique oocyte epigenome by preventing aberrant de novo DNA methylation mediated by DNMT1 and UHRF1.

Achromatic spherical microlens array is fabricated successfully on gelatin film by combining the highly efficient techniques of one-step gray-tone photolithography and novel enzyme etched silver-halide-sensitized gelatin. The microlens array has spherically continuous surface relief profile, 100% fill factor and high energy efficiency, and is ready for UV-vis-NIR broadband applications. The gray-tone mask design, reflection-type projection photolithography setup, enzyme etching processing, and the characterization of fabricated 11x11 gelatin microlens array, are presented in this paper.