Dodecahedron-Shaped Porous Vanadium Oxide and Carbon Composite for High-Rate Lithium Ion Batteries

Carbon-based nanocomposites have been extensively studied in energy storage and conversion systems because of their superior electrochemical performance. However, the majority of metal oxides are grown on the surface of carbonaceous material. Herein, we report a different strategy of constructing V₂O₅ within the metal organic framework derived carbonaceous dodecahedrons. Vanadium precursor is absorbed into the porous dodecahedron-shaped carbon framework first and then <i>in situ</i> converted into V₂O₅ within the carbonaceous framework in the annealing process in air. As cathode materials for lithium ion batteries, the porous V₂O₅@C composites exhibit enhanced electrochemical performance, due to the synergistic effect of V₂O₅ and carbon composite

Relative expression of <i>duIFIT5</i> in liver (A) and spleen (B) after poly (I:C) injection.

<p>qRT-PCR was used to determine the relative expression of <i>duIFIT5</i> in liver and spleen tissues at 0, 4, 8, 12, 24, 36, 48, 72 and 96 h after infection with poly (I:C). The expression of <i>duIFIT5</i> was normalized to <i>GAPDH</i>. Different letter showed significant difference (p < 0.05).</p

The predicted conserved domains predicted from the amino acid sequence of <i>duIFIT5</i> and human <i>IFIT5</i>.

<p>Both <i>duIFIT5</i>and human <i>IFIT5</i> have eight TPR motifs and multi-domains TPR_11 and TPR_12.</p

Phylogenetic tree of <i>IFIT5</i> amino acid sequences generated with the neighbor-joining tree method.

<p>Numbers at each branch indicate the percent a node was supported in 1,000 bootstrap replicates.</p

Identification and Expression Analysis of the Interferon-Induced Protein with Tetratricopeptide Repeats 5 (<i>IFIT5</i>) Gene in Duck (<i>Anas platyrhynchos domesticus</i>)

<div><p>The interferon-induced proteins with tetratricopeptide repeats (IFITs) protein family mediates antiviral effects by inhibiting translation initiation, cell proliferation, and migration in the interferon (IFN) dependent innate immune system. Several members of this family, including <i>IFIT1</i>, <i>IFIT2</i>, <i>IFIT3</i> and <i>IFIT5</i>, have been heavily studied in mammals. Avian species contain only one family member, <i>IFIT5</i>, and little is known about the role of this protein in birds. In this study, duck <i>IFIT5</i> (<i>duIFIT5</i>) full-length mRNA was cloned by reverse transcription polymerase chain reaction (RT-PCR) and rapid amplification of the cDNA ends (RACE). Based on the sequence obtained, we performed a series of bioinformatics analyses, and found that <i>duIFIT5</i> was most similar to homologs in other avian species. Also, <i>duIFIT5</i> contained eight conserved TPR motifs and two conserved multi-domains (TPR_11 and TPR_12). Finally, we used duck hepatitis virus type 1 (DHV-1) and polyriboinosinicpolyribocytidylic acid (poly (I:C)) as a pathogen or a pathogen-associated molecular pattern induction to infect three-day-old domestic ducklings. The liver and spleen were collected to detect the change in <i>duIFIT5</i> transcript level upon infection by quantitative real-time PCR (qRT-PCR). <i>DuIFIT5</i> expression rapidly increased after DHV-1 infection and maintained a high level, while the transcripts of <i>duIFIT5</i> peaked at 8h after poly (I:C) infection and then returned to normal. Taken together, these results provide a greater understanding of avian <i>IFIT5</i>.</p></div

Relative expression levels of <i>duIFIT5</i> in the following tissues: heart, liver, spleen, lung, kidney, cerebrum, cerebellum, large intestine, small intestine, glandular stomach, muscular stomach, and muscle.

<p>The expression of <i>duIFIT5</i> was normalized to <i>GAPDH</i>. Different letter showed significant difference (p < 0.05).</p

Relative expression of <i>duIFIT5</i> in liver (A) and spleen (B) after DHV-1 injection.

<p>qRT-PCR was used to determine the relative expression of <i>duIFIT5</i> in liver and spleen tissues at 0, 4, 8, 12, 24, 36, 48, 72 and 96 h after infection with DHV-1. The expression of <i>duIFIT5</i> was normalized to <i>GAPDH</i>. Different letter showed significant difference (p < 0.05).</p

Ru-Substituted MnO₂ for Accelerated Water Oxidation: The Feedback of Strain-Induced and Polymorph-Dependent Structural Changes to the Catalytic Activity and Mechanism

Heteroatomic modulation of MnO2 is an effective way to introduce and tailor the catalytically active sites for electrochemical water oxidation. While great efforts have been devoted to parsing the configuration and coordination of dopants in dictating the catalytic activity, less is considered about the feedback from the structurally adapted MnO2 host to the intrinsic activity of catalytic sites. In this study, the topological effect on oxygen evolution reaction (OER) activity was systemically investigated for partially Ru-substituted MnO2 of various polymorphs. We show that MnO2 of different porosities responds differently to the Ru integration, thereby resulting in varied lattice strains and morphological changes. While the highly porous τ-MnO2 undergoes amorphization upon Ru substitution, the closely packed β-MnO2 suffers crystal splintering with drastically enhanced structural defects, which lends to a low OER overpotential of 278 mV at 10 mA cm–2 and a high turnover frequency of 2022.2 h–1 that is 19.6-fold higher than that of the commercial RuO2 benchmark. Therefore, the integration of Ru does not simply append active sites to the relatively inert metal oxides but simultaneously modifies the crystal structure of MnO2 to retroactively modulate the catalytic activity. We further show that OER on the Ru-substituted β-MnO2 follows a lattice oxygen mechanism as a result of the adapted oxide substrate. This study furnishes a fresh and systemic view on the dopant–substrate interplay for modulating the electrocatalytic activity of tunneled MnO2 structures

A Post-Developmental Genetic Screen for Zebrafish Models of Inherited Liver Disease

<div><p>Nonalcoholic fatty liver disease (NAFLD) is one of the most common causes of chronic liver disease such as simple steatosis, nonalcoholic steatohepatitis (NASH), cirrhosis and fibrosis. However, the molecular pathogenesis and genetic variations causing NAFLD are poorly understood. The high prevalence and incidence of NAFLD suggests that genetic variations on a large number of genes might be involved in NAFLD. To identify genetic variants causing inherited liver disease, we used zebrafish as a model system for a large-scale mutant screen, and adopted a whole genome sequencing approach for rapid identification of mutated genes found in our screen. Here, we report on a forward genetic screen of ENU mutagenized zebrafish. From 250 F2 lines of ENU mutagenized zebrafish during post-developmental stages (5 to 8 days post fertilization), we identified 19 unique mutant zebrafish lines displaying visual evidence of hepatomegaly and/or steatosis with no developmental defects. Histological analysis of mutants revealed several specific phenotypes, including common steatosis, micro/macrovesicular steatosis, hepatomegaly, ballooning, and acute hepatocellular necrosis. This work has identified multiple post-developmental mutants and establishes zebrafish as a novel animal model for post-developmental inherited liver disease.</p></div

Histological phenotypes.

<p>On the left panel, H & E (top), DAPI (middle) and oil red oil (ORO, bottom) stained zebrafish livers at 8 dpf are shown. Wild-type control (A,F,K), and mutants (B-E, G-J, L-O) are shown. (B) shows and example of microvesicles in hepatocytes, (C) depicts a liver with swollen hepatocytes, (D) shows a liver with accumulation of large vesicles, and prenecrotic hepatocytes (asterisk), while (E) shows hepatic lysis. The black arrow in (E) points to a nucleus with nuclear membrane and the red arrow points to a condensed nucleus without nuclear membrane. The yellow arrowheads in (J) indicate granulated nuclei. g = gut. Scale bar = 100 μm (A-E) and 50 μm (F-O). n = 9/9 per control and each mutant.</p