Theoretical insights into the methane catalytic decomposition on graphene nanoribbons edges.

Catalytic methane decomposition (CMD) is receiving much attention as a promising application for hydrogen production. Due to the high energy required for breaking the C-H bonds of methane, the choice of catalyst is crucial to the viability of this process. However, atomistic insights for the CMD mechanism on carbon-based materials are still limited. Here, we investigate the viability of CMD under reaction conditions on the zigzag (12-ZGNR) and armchair (AGRN) edges of graphene nanoribbons employing dispersion-corrected density functional theory (DFT). First, we investigated the desorption of H and H2 at 1200 K on the passivated 12-ZGNR and 12-AGNR edges. The diffusion of hydrogen atom on the passivated edges is the rate determinant step for the most favourable H2 desorption pathway, with a activation free energy of 4.17 eV and 3.45 eV on 12-ZGNR and 12-AGNR, respectively. The most favourable H2 desorption occurs on the 12-AGNR edges with a free energy barrier of 1.56 eV, reflecting the availability of bare carbon active sites on the catalytic application. The direct dissociative chemisorption of CH4 is the preferred pathway on the non-passivated 12-ZGNR edges, with an activation free energy of 0.56 eV. We also present the reaction steps for the complete catalytic dehydrogenation of methane on 12-ZGNR and 12-AGNR edges, proposing a mechanism in which the solid carbon formed on the edges act as new active sites. The active sites on the 12-AGNR edges show more propensity to be regenerated due lower free energy barrier of 2.71 eV for the H2 desorption from the newly grown active site. Comparison is made between the results obtained here and experimental and computational data available in the literature. We provide fundamental insights for the engineering of carbon-based catalysts for the CMD, showing that the bare carbon edges of graphene nanoribbons have performance comparable to commonly used metallic and bi-metallic catalysts for methane decomposition.

Dehydrogenation of ammonia on free-standing and epitaxial hexagonal boron nitride.

We report a thermodynamically feasible mechanism for producing H2 from NH3 using hBN as a catalyst. 2D catalysts have exceptional surface areas with unique thermal and electronic properties suited for catalysis. Metal-free, 2D catalysts, are highly desirable materials that can be more sustainable than the ubiquitously employed precious and transition metal-based catalysts. Here, using density functional theory (DFT) calculations, we demonstrate that metal-free hexagonal boron nitride (hBN) is a valid alternative to precious metal catalysts for producing H2via reaction of ammonia with a boron and nitrogen divacancy (VBN). Our results show that the decomposition of ammonia proceeds on monolayer hBN with an activation energy barrier of 0.52 eV. Furthermore, the reaction of ammonia with epitaxially grown hBN on a Ru(0001) substrate was investigated, and we observed similar NH3 decomposition energy barriers (0.61 eV), but a much more facile H2 associative desorption barrier (0.69 eV vs 5.89 eV). H2 generation from the free-standing monolayer would instead occur through a diffusion process with an energy barrier of 3.36 eV. A detailed analysis of the electron density and charge distribution along the reaction pathways was carried out to rationalise the substrate effects on the catalytic reaction.

Loss of ZnT8 function protects against diabetes by enhanced insulin secretion.

A rare loss-of-function allele p.Arg138* in SLC30A8 encoding the zinc transporter 8 (ZnT8), which is enriched in Western Finland, protects against type 2 diabetes (T2D). We recruited relatives of the identified carriers and showed that protection was associated with better insulin secretion due to enhanced glucose responsiveness and proinsulin conversion, particularly when compared with individuals matched for the genotype of a common T2D-risk allele in SLC30A8, p.Arg325. In genome-edited human induced pluripotent stem cell (iPSC)-derived ß-like cells, we establish that the p.Arg138* allele results in reduced SLC30A8 expression due to haploinsufficiency. In human ß cells, loss of SLC30A8 leads to increased glucose responsiveness and reduced KATP channel function similar to isolated islets from carriers of the T2D-protective allele p.Trp325. These data position ZnT8 as an appealing target for treatment aimed at maintaining insulin secretion capacity in T2D.

Fine-mapping type 2 diabetes loci to single-variant resolution using high-density imputation and islet-specific epigenome maps.

We expanded GWAS discovery for type 2 diabetes (T2D) by combining data from 898,130 European-descent individuals (9% cases), after imputation to high-density reference panels. With these data, we (i) extend the inventory of T2D-risk variants (243 loci, 135 newly implicated in T2D predisposition, comprising 403 distinct association signals); (ii) enrich discovery of lower-frequency risk alleles (80 index variants with minor allele frequency <5%, 14 with estimated allelic odds ratio >2); (iii) substantially improve fine-mapping of causal variants (at 51 signals, one variant accounted for >80% posterior probability of association (PPA)); (iv) extend fine-mapping through integration of tissue-specific epigenomic information (islet regulatory annotations extend the number of variants with PPA >80% to 73); (v) highlight validated therapeutic targets (18 genes with associations attributable to coding variants); and (vi) demonstrate enhanced potential for clinical translation (genome-wide chip heritability explains 18% of T2D risk; individuals in the extremes of a T2D polygenic risk score differ more than ninefold in prevalence).

Type 2 diabetes risk alleles in PAM impact insulin release from human pancreatic ß-cells.

The molecular mechanisms underpinning susceptibility loci for type 2 diabetes (T2D) remain poorly understood. Coding variants in peptidylglycine α-amidating monooxygenase (PAM) are associated with both T2D risk and insulinogenic index. Here, we demonstrate that the T2D risk alleles impact negatively on overall PAM activity via defects in expression and catalytic function. PAM deficiency results in reduced insulin content and altered dynamics of insulin secretion in a human ß-cell model and primary islets from cadaveric donors. Thus, our results demonstrate a role for PAM in ß-cell function, and establish molecular mechanisms for T2D risk alleles at this locus.

Regional transport, source apportionment and health impact of PM10 bound polycyclic aromatic hydrocarbons in Singapore's atmosphere.

A study of 16 United States Environmental Protection Agency (USEPA) priority listed PAHs associated with particulate matter ≤ 10 µm (PM10) was conducted in Singapore during the period 29th May 2015 to 28th May 2016. The sampling period coincided with an extensive, regional smoke haze episode (5th September to 25th October) that occurred as a result of forest and peat fires in neighboring Indonesia. Throughout this study, 54 atmospheric PM10 samples were collected in 24 h periods using a high volume sampler (HVS) and quarts fiber filters (QFF) as the collection medium. Hysplit software for computing 3-D backward air mass trajectories, diagnostic ratio analysis and ring number distribution calculations were used to examine the sources of PAHs in the atmosphere in Singapore. Under normal conditions the total PAH concentrations were in a range from 0.68 ng m-3 to 3.07 ng m-3, while for the high haze period the results showed approximately double the concentrations with a maximum value of 5.97 ng m-3. Diagnostic ratio (DR) and principal component analysis (PCA) were conducted and indicated the contribution of the traffic as a dominant pyrogenic source of PAHs during normal periods, while results from the haze dataset showed relatively strong influence of smoke from peat and forest fires in Indonesia. Environmental and health risk from PAHs were assessed for both regular and hazy days.