Pt–Ni Subsurface Alloy Catalysts: An Improved Performance toward CH₄ Dissociation

Methane-dissociative chemisorption is the rate-determining step in the industrially important steam reforming and dry reforming reactions of methane. Widely used industrial catalysts containing Ni as the active metal face the problems of carbon deposition and deactivation, whereas Pt surfaces with lower barrier are expensive to be used in the industrial scale. Using density functional theory calculations, a series of surface and subsurface Ni–Pt bimetallic surfaces were studied to understand the synergistic catalytic activity of alloying elements toward facilitating methane dissociation and in resisting carbon formation. Addition of Ni to Pt(111) decreased activation energy barriers, whereas a linear increase in barrier was found when Pt is added to Ni(111) surface. The observed reactivity trends were explained using surface-based descriptors like work function, surface energy, and d-band center and also using energy-based descriptors, namely, Bronsted–Evans–Polanyi and transition-state scaling relationships. Changes in barrier heights and locations of the barrier with lattice atom motion were calculated to include the effect of surface temperature on dissociation probabilities. Dissociation probabilities thus calculated at different surface temperatures using semiclassical methods showed that reactivity increased with surface temperature on all surface alloys. Overall, two surfaces, viz., Ni9/Pt(111) and sub-Pt9/Ni(111), showed improved behavior toward CH₄ dissociation, irrespective of the composition of underlying layers. C₂ formation on these two alloys also showed higher barriers compared to pure Ni(111) surface. However, considering all aspects like energy barriers to CH₄ dissociation and CH dissociation, carbon adsorption energy, and cost, the subsurface alloy, sub-Pt9/Ni(111), showed an enhanced overall performance as a reforming catalyst

Estimation of σ‑Donation and π‑Backdonation of Cyclic Alkyl(amino) Carbene-Containing Compounds

Herein, we present a general method for a reliable estimation of the extent of π-backdonation (C_cAAC←E) of the bonded element (E) to the carbene carbon atom and C_cAAC→E σ-donation. The C_cAAC←E π-backdonation has a significant effect on the electronic environments of the ¹⁵N nucleus. The estimation of the π-backdonation has been achieved by recording the chemical shift values of the ¹⁵N nuclei via two-dimensional heteronuclear multiple-bond correlation spectroscopy. The chemical shift values of the ¹⁵N nuclei of several cAAC-containing compounds and/or complexes were recorded. The ¹⁵N nuclear magnetic resonance chemical shift values are in the range from −130 to −315 ppm. When the cAAC forms a coordinate σ-bond (C_cAAC→E), the chemical shift values of the ¹⁵N nuclei are around −160 ppm. In case the cAAC is bound to a cationic species, the numerical chemical shift value of the ¹⁵N nucleus is downfield-shifted (−130 to −148 ppm). The numerical values of the ¹⁵N nuclei fall in the range from −170 to −200 ppm when σ-donation (C_cAAC→E) of cAAC is stronger than C_cAAC←E π-backacceptance. The π-backacceptance of cAAC is stronger than σ-donation, when the chemical shift values of the ¹⁵N nuclei are observed below −220 ppm. Electron density and charge transfer between C_cAAC and E are quantified using natural bonding orbital analysis and charge decomposition analysis techniques. The experimental results have been correlated with the theoretical calculations. They are in good agreement

Nucleotide sequence variations and amino acid changes within the E1 ORF of intact HPV16 isolates among the samples (non-malignant samples and CaCx cases) analysed.

<p>Nucleotide sequence variations and amino acid changes within the E1 ORF of intact HPV16 isolates among the samples (non-malignant samples and CaCx cases) analysed.</p

miRNA binding sites and variant nucleotide position within NCR2 of E2 intact/episomal (episomal or concomitant) HPV16 European (E) variant isolate within CaCx cases.

<p>(<b>A</b>) Depicts the NCR2 (nucleotide positions 4139–4236) located within 5′ UTR of L2 gene, with a single nucleotide polymorphism (SNP) at position 4228 (T to C). (<b>B</b>) RegRNA software based identification of fourteen miRNA binding sites within NCR2 with loss of binding sites corresponding to nine miRNAs (_*) of the hsa-miR-548family due to the SNP (T4228C).</p

Box plots representing distribution of miR-548a-5p and miR-548d-5p expression (normalized with RNU6b expression as endogenous miRNA control) among different categories of cervical samples.

<p>Box plots representing distribution of miR-548a-5p and miR-548d-5p expression (normalized with RNU6b expression as endogenous miRNA control) among different categories of cervical samples.</p

Differential Expression of HPV16 L2 Gene in Cervical Cancers Harboring Episomal HPV16 Genomes: Influence of Synonymous and Non-Coding Region Variations

<div><p>We tested the hypothesis that (i) synonymous variations within the coding regions, and (ii) variations within the non-coding regions of HPV, influence cervical cancer (CaCx) pathogenesis under the impact of intact HPV16 genomes. Whole genome sequence analysis of HPV16 isolates within 70 CaCx cases and 25 non-malignant samples revealed that synonymous variations were significantly higher within the E6 (p = 0.014), E5 (p = 0.001) and L2 (p = 0.0002) genes of HPV16 isolates within cases, compared to isolates within non-malignant samples. All of the 25 (100%) humanized codons identified within L2 ORF of the samples analyzed, were harbored by CaCx cases, while 8 out of 25 (32%) were harbored by HPV16 positive non-malignant samples (p = 3.87105E-07). L2 (mRNA and protein) expression was evident only among cases with episomal viral genomes and L2 mRNA expression correlated significantly with E2 gene copy numbers suggesting expression from all episomal genomes. Among such cases, Asian American (AA) isolates portrayed all of the humanized codons (100%; 4–6/sample) recorded within L2, which was significantly higher (p = 2.02E-7) compared to the European (E) isolates (22.8%; none or 1–2/sample). Additionally, majority of E variant isolates within cases (54/57; 94.7%) portrayed a variation (T4228C) within the short non-coding region (NCR2) between E5 and L2 genes, which portrays a weak promoter activity specific for L2 mRNA expression. This resulted in loss of 9 out of 14 miRNA binding sites (hsa-miR-548 family), despite the significant overexpression of miR548a-5p and miR548d-5p among such cases (28.64 and 36.25 folds, respectively), in comparison to HPV negative control samples. The findings exemplify the biological relevance of sequence variations in HPV16 genomes and highlight that episomal HPV16 in CaCx cases employ multiple mechanisms to sustain L2 expression, thereby justifying the potential role of L2 in such cancers, as opposed to those harboring viral integration.</p></div

Densitometric analysis of L2 protein expression (normalized with ACTB expression), among HPV16 positive E2 intact/episomal (episomal or concomitant) CaCx cases harboring Asian American and European variants.

<p>Densitometric analysis of L2 protein expression (normalized with ACTB expression), among HPV16 positive E2 intact/episomal (episomal or concomitant) CaCx cases harboring Asian American and European variants.</p

Relative quantification of L2 mRNA expression.

<p>(<b>A</b>) Amplification plot based on quantitative real time PCR of HPV16 L2 expression. L2 is transcribed in E2 intact/episomal (episomal or concomitant) but in E2 disrupted/integrated cases. (<b>B</b>) Dissociation curve depicting the first-derivative melting curve for the reaction characterizing the expression of L2 (Tm of 80.5°C). (<b>C</b>) Amplification plot based on quantitative real time PCR of ACTB expression. ACTB is expressed by both episomal and integrated HPV16 positive cases. (<b>D</b>) Dissociation curve depicting the first-derivative melting curve for the reaction characterizing the expression of ACTB (Tm of 81.0°C).</p

Distribution of synonymous variations between non-malignant samples and CaCx cases across the coding regions of the HPV16 intact isolates.

<p>The percentage of synonymous variations was estimated on the basis of total number of synonymous variations out of total number of nucleotides (normalized with the size of the ORFs) in cases or non-malignant samples within the respective ORFs; e.g. For E4: % within cases = [58/(287×70)]×100 and % within non-malignant samples = [12/(287×25)]×100.</p><p><b><i>Bold emphasis indicates statistically significant p-values.</i></b></p

Representative Immunoblot analysis of L2 and ACTB protein expression.

<p>Upper panel depicts L2 expression. Lanes 1 and 2: HPV16 positive E2 disrupted/integrated CaCx case samples (D1 and D2); Lanes 3, 5, and 7: HPV16 positive E2 intact/episomal (episomal or concomitant) European variants (EV1, EV2, EV3, respectively); Lanes 4, 6, and 8: HPV16 positive E2 intact/episomal (episomal or concomitant) Asian American variants (AAV3, AAV2, AAV1, respectively). Lower panel depicts ACTB expression among all the samples analysed. Sample details are illustrated in <a href="http://www.plosone.org/article/info:doi/10.1371/journal.pone.0065647#pone-0065647-t005" target="_blank">Table 5</a>.</p