ZIF-67-Derived CoFe₂O₄/NiCo₂O₄@NC/CC with Oxygen-Enriched Vacancy for High-Performance Electrocatalyst toward Oxygen Evolution Reaction

Oxygen evolution reaction (OER) impedes the electrochemical water splitting for H2 production, ascribing to the depressed kinetics of the four proton-coupled transfer process. Transition metal oxides, especially bimetallic oxides, have been proven to be promising OER electrocatalysts due to their part unoccupied d-band characteristics. More interestingly, oxygen vacancies (Ov) easily constructed in transition metal oxides can modulate the electron structures and thereby boost the OER performance. However, most synthesized processes involving oxygen vacancy engineering, such as atom dopant, chemical/electrochemical reduction, and H2/Ar-dependent calcination, are energy-intensive and time-consuming, largely hampering their commercial applications. Herein, we suggest a simple and facile strategy for fabricating double spinel oxides with abundant oxygen vacancies by calcinating Ni/Fe@ZIF-67/CC precursor under a nonoxidation condition. The obtained Ov-CF1N2O@NC/CC-550 with vast oxygen vacancies exhibits excellent OER performance, representing a lower overpotential of 185 mV at 10 mA cm–2, smaller Tafel slope of 47.3 mV dec–1, as well as faster interface reaction kinetics (Rct = 0.7336). Theoretical calculations further confirm that the excellent electrochemical activity strongly corresponds to the lower d-band center of active sites on the Ov-CoFe2O4 (311) model and decreased reaction Gibbs energy barrier. The work might shed light on oxygen vacancy engineering via a simple and facile strategy and inspire a smart design of multimetallic oxide electrocatalysts with high OER performance

Decreased expression of <i>TLR4</i>, <i>TLR21</i> and <i>TLR2-1</i> genes in susceptible chickens.

<p>The relative expression of <i>TLR4</i>, <i>TLR21</i>, <i>TLR2-1</i> and <i>TLR2-2</i> in leukocytes of susceptible (□ ---- □) and resistant (⧫——⧫) chickens at 8 h, 16 h, 24 h, 3 d, and 12 d after infection with <i>S.enteritidis</i> is shown. Relative values, normalized using <i>β-actin</i> mRNA levels and the average expression levels in both groups at 0 h, are shown. The data are means (SD shown by the vertical bars) of 6 birds (*P<0.05; **P<0.01). TPI is time post-infection.</p

Kinetics of <i>Salmonella Enteritidis</i> loads in inoculated SPF chickens determined by qPCR across all the times.

<p>Data are presented as the mean bacterial loads and is expressed as log₁₀ of the bacterial genome copy number per ml of blood (± SD) obtained from susceptible (S) and resistant (R) chickens.</p

Enhanced expression of <i>TOLLIP</i> and <i>ZNF493</i> genes in susceptible chickens.

<p>The relative expression of <i>TOLLIP</i>, <i>PI3K</i>, <i>SOCS1</i> and <i>ZNF493</i> genes in susceptible (open bars) and resistant (filled bars) chickens at 8 h and 16 h after infection with <i>S. enteritidis</i> is shown. Data are means (n = 6), normalized to <i>β-actin</i> mRNA and the average expression at 0 h (**P<0.01). The vertical bar is the SD from the error mean square of the ANOVA. HPI is hours post-infection.</p

Methylation of 15 CpG motifs in the predicted promoter region of the <i>TLR4</i> gene.

<p>(A) The distribution of the 15 CpG dinucleotides from −2443 to −1361 in the upstream region of the <i>TLR4</i> gene relative to the translation start site (+1). (B) Genomic DNA from peripheral blood leukocytes of uninfected chickens at 0 h (⁃), susceptible (□) and resistant (⧫) chickens at 16 h TPI was modified with sodium bisulfite, amplified by PCR, cloned, and 12–16 independent clones were sequenced. The frequency of methylated CpGs in each CpG site (data are means of 12 birds for uninfected chicken and 6 birds for susceptible and resistant chickens, respectively) are shown and comparisons were made between susceptible and resistant chickens. The average of % methylation at each CpG site within all 15 CpGs in peripheral blood leukocytes of uncharged chickens (0 h, filled grey bars), susceptible (S, open bars) and resistant (R, filled black bars) chickens at 16 h after infection with <i>S. enteritidis</i> are presented. The vertical bar is the SD from the error mean square of the ANOVA, * indicates P<0.05, ** indicates P<0.01.</p

qPCR primers used in this study.

<p>qPCR primers used in this study.</p

Primers for methylation detection.

<p>Primers for methylation detection.</p

Methylation of 18 CpG motifs in the exon and 10 CpG motifs in the predicted promoter region of <i>TLR2-1</i> gene.

<p>(A) the distribution of the 18 CpG dinucleotides from 1785 to 2283 in the exon region and 10 CpG dinucleotides from −4800 to −4367 in the predicted promoter region of the <i>TLR2-1</i> gene relative to the translation start site (+1). (B) Genomic DNA from peripheral blood leukocytes of uninfected chickens at 0 h (⁃), susceptible (□) and resistant (⧫) chickens at 16 h TPI was modified with sodium bisulfite, amplified by PCR, cloned, and 12–16 independent clones were sequenced. The frequency of methylated CpGs in each CpG site (data are means of 12 birds for uninfected chicken and 6 birds for susceptible and resistant chickens, respectively) are shown and comparisons were made between susceptible and resistant chickens. The average of % methylation at each CpG site within all 18 CpGs in peripheral blood leukocytes of uncharged chickens (0 h, filled grey bars), susceptible (S, open bars) and resistant (R, filled black bars) chickens at 16 h after infection with <i>S. enteritidis</i> are presented. The vertical bar is the SD from the error mean square of the ANOVA, * indicates P<0.05.</p

Methylation of 15 CpG motifs in the predicted promoter region of <i>TLR21</i> gene.

<p>(A) The distribution of the 15 CpG dinucleotides from −1531 to −9 in the upstream region of the <i>TLR21</i> gene relative to the translation start site (+1). (B) Genomic DNA from peripheral blood leukocytes of uninfected chickens at 0 h (⁃), susceptible (□) and resistant (⧫) chickens at 16 h TPI was modified with sodium bisulfite, amplified by PCR, cloned, and 12–16 independent clones were sequenced. The frequency of methylated CpGs in each CpG site (data are means of 12 birds for uninfected chicken and 6 birds for susceptible and resistant chickens, respectively) are shown and comparisons were made between susceptible and resistant chickens. The average of % methylation at each CpG site within all 15 CpGs in peripheral blood leukocytes of uncharged chickens (0 h, filled grey bars), susceptible (S, open bars) and resistant (R, filled black bars) chickens at 16 h after infection with <i>S. enteritidis</i> are presented. The vertical bar is the SD from the error mean square of the ANOVA, * indicates P<0.05, ** indicates P<0.01.</p

DNA methyltransferase inhibitor 5-Aza-dc and/or the histone deacetylase inhibitor TSA increased <i>TLR4</i>, <i>TLR21</i> and <i>TLR2-1</i> expression.

<p>Peripheral blood mononuclear cells were inoculated with <i>S. enteritidis</i> without additions (controls) or in the presence of 5-Aza-dc, TSA or TSA plus 5-Aza-dc. Relative abundances of <i>TLR4</i>, <i>TLR21</i> and <i>TLR2-1</i> mRNA were analyzed by qPCR and normalized to <i>β-actin</i> mRNA. Data are means (n = 3) and comparisons were made to expression in the controls (-,-). The vertical bar is the SD from the error mean square of the ANOVA, * indicates P<0.05.</p