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We present a graph neural network approach that fully automates the prediction of defect formation enthalpies for any crystallographic site from the ideal crystal structure, without the need to create defected atomic structure models as input. Here we used density functional theory reference data for vacancy defects in oxides, to train a defect graph neural network (dGNN) model that replaces the density functional theory supercell relaxations otherwise required for each symmetrically unique crystal site. Interfaced with thermodynamic calculations of reduction entropies and associated free energies, the dGNN model is applied to the screening of oxides in the Materials Project database, connecting the zero-kelvin defect enthalpies to high-temperature process conditions relevant for solar thermochemical hydrogen production and other energy applications. The dGNN approach is applicable to arbitrary structures with an accuracy limited principally by the amount and diversity of the training data, and it is generalizable to other defect types and advanced graph convolution architectures. It will help to tackle future materials discovery problems in clean energy and beyond., (© 2023. The Author(s), under exclusive licence to Springer Nature America, Inc.)

Understanding hydrogen incorporation into palladium requires detailed knowledge of surface and subsurface structure and atomic interactions as surface hydrogen is being embedded. Using density functional theory (DFT), we examine the energies of hydrogen layers of varying coverage adsorbed on Pd(111). We find that H-H and H-Pd interactions promote the formation of the well-known 3×3 phases but also favor an unreported (3 × 3) phase at high H coverages for which we present experimental evidence. We relate the stability of isolated H vacancies of the (3 × 3) phase to the need of H 2 molecules to access bare Pd before they can dissociate. Following higher hydrogen dosage, we observe initial steps of hydride formation, starting with small clusters of subsurface hydrogen. The interaction between H and Pd is complicated by the persistent presence of carbon at the surface. X-ray photoelectron spectroscopy experiments show that trace amounts of carbon, emerging from the Pd bulk despite many surface cleaning cycles, become mobile enough to repopulate the C-depleted surface at temperatures above 200 K. When exposed to hydrogen, these surface carbon atoms react to form benzene, as evidenced by scanning tunneling microscopy observations interpreted with DFT.

To fine map a mouse QTL for lean body mass (Burly1), we used information from intercross, backcross, consomic, and congenic mice derived from the C57BL/6ByJ (host) and 129P3/J (donor) strains. The results from these mapping populations were concordant and showed that Burly1 is located between 151.9 and 152.7 Mb (rs33197365 to rs3700604) on mouse chromosome 2. The congenic region harboring Burly1 contains 26 protein-coding genes, 11 noncoding RNA elements (e.g., lncRNA), and 4 pseudogenes, with 1949 predicted functional variants. Of the protein-coding genes, 7 have missense variants, including genes that may contribute to lean body weight, such as Angpt41, Slc52c3, and Rem1. Lean body mass was increased by the B6-derived variant relative to the 129-derived allele. Burly1 influenced lean body weight at all ages but not food intake or locomotor activity. However, congenic mice with the B6 allele produced more heat per kilogram of lean body weight than did controls, pointing to a genotype effect on lean mass metabolism. These results show the value of integrating information from several mapping populations to refine the map location of body composition QTLs and to identify a short list of candidate genes.

An average mouse in midlife weighs between 25 and 30 g, with about a gram of tissue in the largest adipose depot (gonadal), and the weight of this depot differs between inbred strains. Specifically, C57BL/6ByJ mice have heavier gonadal depots on average than do 129P3/J mice. To understand the genetic contributions to this trait, we mapped several quantitative trait loci (QTLs) for gonadal depot weight in an F2 intercross population. Our goal here was to fine-map one of these QTLs, Adip20 (formerly Adip5), on mouse chromosome 9. To that end, we analyzed the weight of the gonadal adipose depot from newly created congenic strains. Results from the sequential comparison method indicated at least four rather than one QTL; two of the QTLs were less than 0.5 Mb apart, with opposing directions of allelic effect. Different types of evidence (missense and regulatory genetic variation, human adiposity/body mass index orthologues, and differential gene expression) implicated numerous candidate genes from the four QTL regions. These results highlight the value of mouse congenic strains and the value of this sequential method to dissect challenging genetic architecture.

The volumetric redox (chemical) capacitance of the surface of CeO2-δ films is quantified in situ to be 100-fold larger than the bulk values under catalytically relevant conditions. Sm addition slightly lowers the surface oxygen nonstoichiometry, but effects a 10-fold enhancement in surface chemical capacitance by mitigating defect interactions, highlighting the importance of differential nonstoichiometry for catalysis., (© 2016 WILEY-VCH Verlag GmbH & Co. KGaA, Weinheim.)

Genetic variation contributes to individual differences in obesity, but defining the exact relationships between naturally occurring genotypes and their effects on fatness remains elusive. As a step toward positional cloning of previously identified body composition quantitative trait loci (QTLs) from F2 crosses of mice from the C57BL/6ByJ and 129P3/J inbred strains, we sought to recapture them on a homogenous genetic background of consomic (chromosome substitution) strains. Male and female mice from reciprocal consomic strains originating from the C57BL/6ByJ and 129P3/J strains were bred and measured for body weight, length, and adiposity. Chromosomes 2, 7, and 9 were selected for substitution because previous F2 intercross studies revealed body composition QTLs on these chromosomes. We considered a QTL confirmed if one or both sexes of one or both reciprocal consomic strains differed significantly from the host strain in the expected direction after correction for multiple testing. Using these criteria, we confirmed two of two QTLs for body weight (Bwq5-6), three of three QTLs for body length (Bdln3-5), and three of three QTLs for adiposity (Adip20, Adip26 and Adip27). Overall, this study shows that despite the biological complexity of body size and composition, most QTLs for these traits are preserved when transferred to consomic strains; in addition, studying reciprocal consomic strains of both sexes is useful in assessing the robustness of a particular QTL.

Obesity is a heritable trait caused by complex interactions between genes and environment, including diet. Gene-by-diet interactions are difficult to study in humans because the human diet is hard to control. Here, we used mice to study dietary obesity genes, by four methods. First, we bred 213 F2 mice from strains that are susceptible [C57BL/6ByJ (B6)] or resistant [129P3/J (129)] to dietary obesity. Percent body fat was assessed after mice ate low-energy diet and again after the same mice ate high-energy diet for 8 weeks. Linkage analyses identified QTLs associated with dietary obesity. Three methods were used to filter candidate genes within the QTL regions: (a) association mapping was conducted using >40 strains; (b) differential gene expression and (c) comparison of genomic DNA sequence, using two strains closely related to the progenitor strains from Experiment 1. The QTL effects depended on whether the mice were male or female or which diet they were recently fed. After feeding a low-energy diet, percent body fat was linked to chr 7 (LOD=3.42). After feeding a high-energy diet, percent body fat was linked to chr 9 (Obq5; LOD=3.88), chr 12 (Obq34; LOD=3.88), and chr 17 (LOD=4.56). The Chr 7 and 12 QTLs were sex dependent and all QTL were diet-dependent. The combination of filtering methods highlighted seven candidate genes within the QTL locus boundaries: Crx, Dmpk, Ahr, Mrpl28, Glo1, Tubb5, and Mut. However, these filtering methods have limitations so gene identification will require alternative strategies, such as the construction of congenics with very small donor regions.

Nickel is the most commonly used anode for solid-oxide fuel cells (SOFC) due to its fast kinetics and low price. A leading cause of degradation in Ni electrodes is oxidation. Here we use operando ambient-pressure X-ray photoelectron spectroscopy (XPS) to chemically characterize the Ni electrode of a fuel cell anode during oxidation in a H2/H2O atmosphere. We find three different stages of Ni oxidation in the model SOFC. In the first two stages, the Ni exposed to the gas remains metallic but the Ni at the interface with the zirconia electrolyte is oxidized. In the third oxidation stage, we find that Ni transforms to NiOOH, a phase not previously considered in the SOFC literature. We show that the transformation between Ni and NiOOH is reversible and is initiated at the Ni/gas interface. In addition we find that NiOOH stores charge, as evidenced by the stable discharge plateau (voltage) measured as this oxyhydroxide phase reduces to metallic Ni.

The intercalation pathway of lithium iron phosphate (LFP) in the positive electrode of a lithium-ion battery was probed at the ∼40 nm length scale using oxidation-state-sensitive X-ray microscopy. Combined with morphological observations of the same exact locations using transmission electron microscopy, we quantified the local state-of-charge of approximately 450 individual LFP particles over nearly the entire thickness of the porous electrode. With the electrode charged to 50% state-of-charge in 0.5 h, we observed that the overwhelming majority of particles were either almost completely delithiated or lithiated. Specifically, only ∼2% of individual particles were at an intermediate state-of-charge. From this small fraction of particles that were actively undergoing delithiation, we conclude that the time needed to charge a particle is ∼1/50 the time needed to charge the entire particle ensemble. Surprisingly, we observed a very weak correlation between the sequence of delithiation and the particle size, contrary to the common expectation that smaller particles delithiate before larger ones. Our quantitative results unambiguously confirm the mosaic (particle-by-particle) pathway of intercalation and suggest that the rate-limiting process of charging is initiating the phase transformation by, for example, a nucleation-like event. Therefore, strategies for further enhancing the performance of LFP electrodes should not focus on increasing the phase-boundary velocity but on the rate of phase-transformation initiation.

We use spatially resolved photoelectron spectroscopy performed in operando to identify the reaction intermediates of the hydrogen electro-oxidation reaction on yttria-stabilized zirconia (YSZ) electrolytes with Pt electrodes. We find that hydroxyl on the zirconia electrolyte is a reaction intermediate in the hydrogen oxidation reaction and that it participates in the rate-determining step. In contrast to the general wisdom, the limiting step does not involve the transfer of charge. These results allow us to propose the detailed reaction pathway, which provides direct insight into how to accelerate the kinetics.

Photoelectron spectroscopic measurements have the potential to provide detailed mechanistic insight by resolving chemical states, electrochemically active regions and local potentials or potential losses in operating solid oxide electrochemical cells (SOCs), such as fuel cells. However, high-vacuum requirements have limited X-ray photoelectron spectroscopy (XPS) analysis of electrochemical cells to ex situ investigations. Using a combination of ambient-pressure XPS and CeO(2-x)/YSZ/Pt single-chamber cells, we carry out in situ spectroscopy to probe oxidation states of all exposed surfaces in operational SOCs at 750 °C in 1 mbar reactant gases H(2) and H(2)O. Kinetic energy shifts of core-level photoelectron spectra provide a direct measure of the local surface potentials and a basis for calculating local overpotentials across exposed interfaces. The mixed ionic/electronic conducting CeO(2-x) electrodes undergo Ce(3+)/Ce(4+) oxidation-reduction changes with applied bias. The simultaneous measurements of local surface Ce oxidation states and electric potentials reveal the active ceria regions during H(2) electro-oxidation and H(2)O electrolysis. The active regions extend ~150 μm from the current collectors and are not limited by the three-phase-boundary interfaces associated with other SOC materials. The persistence of the Ce(3+)/Ce(4+) shifts in the ~150 μm active region suggests that the surface reaction kinetics and lateral electron transport on the thin ceria electrodes are co-limiting processes.

We use photo-electrons as a non-contact probe to measure local electrical potentials in a solid-oxide electrochemical cell. We characterize the cell in operando at near-ambient pressure using spatially-resolved X-ray photoemission spectroscopy. The overpotentials at the interfaces between the Ni and Pt electrodes and the yttria-stabilized zirconia (YSZ) electrolyte are directly measured. The method is validated using electrochemical impedance spectroscopy. Using the overpotentials, which characterize the cell's inefficiencies, we compare without ambiguity the electro-catalytic efficiencies of Ni and Pt, finding that on Ni H(2)O splitting proceeds more rapidly than H(2) oxidation, while on Pt, H(2) oxidation proceeds more rapidly than H(2)O splitting.

We describe a fixture that allows electrochemical devices to be studied under electrical bias in the type of vacuum systems commonly used in surface science. Three spring-loaded probes provide independent contacts for device operation and the characterization in vacuum or under in situ conditions with reactive gases. We document the robustness of the electrical contacts over large temperature changes and their reliability for conventional electrochemical measurements such as impedance spectroscopy. The optical access provided to the device enables the analysis by many techniques, as we demonstrate using x-ray photoelectron spectroscopy to measure local electrical potentials on a solid-oxide electrolyte device operating at high temperature in near-ambient pressure.

Objective: Previous studies in mice have detected quantitative trait loci (QTLs) on chromosome 7 that affect body composition. As a step toward identifying the responsible genes, we compared a chromosome 7 substitution strain C57BL/6J-Chr7(129S1/SvImJ)/Na (CSS-7) to its host (C57BL/6J) strain., Methods and Procedures: Fourteen-week-old mice were measured for body size (weight, length), organ weight (brain, heart, liver, kidneys, and spleen), body and bone composition (fat and lean weight; bone area, mineral content, and density), and individual adipose depot weights (gonadal, retroperitoneal, mesenteric, inguinal, and subscapular). Differences between the CSS-7 strain and the host strain were interpreted as evidence for the presence of one or more QTLs on chromosome 7., Results: Using this criterion, we detected QTLs for body weight, bone area, bone mineral content, brain, and heart weight, most adipose depot weights and some indices of fatness. A few strain differences were more pronounced in males (e.g., most adiposity measures) and others were more pronounced in females (e.g., bone area). QTLs for body length, lean weight, bone mineral density, and kidney, spleen, and liver weight were not detected., Discussion: This study found several associations that suggest one or more QTLs specific to the weight of select tissues and organs exist on mouse chromosome 7. Because these loci are detectable on a fixed and uniform genetic background, they are reasonable targets for high-resolution mapping and gene identification using a congenic approach.

To understand how genotype influences fat patterning and obesity, we conducted an autosomal genome scan using male and female F(2) hybrids between the C57BL/6ByJ and 129P3/J parental mouse strains. Mice were studied in middle-adulthood and were fed a low-energy, low-fat diet during their lifetime. We measured the weight of the retroperitoneal adipose depot (near the kidney) and the gonadal adipose depot (near the epididymis in males and ovaries in females). An important feature of the analysis was the comparison of linkage results for absolute adipose depot weight and depot weight adjusted for body size, i.e., relative weight. We detected 67 suggestive linkages for six phenotypes, which fell into one of three categories: those specific to absolute but not relative depot weight (Chr 5, 11, and 14), those specific to relative but not absolute depot weight (Chr 9, 15, and 16), and those involving both (Chr 2 and 7). Some quantitative trait loci (QTLs) affected one adipose depot more than another: Retroperitoneal depot weight was linked to Chr 8, 11, 12, and 17, but the linkage effects for the gonadal depot were stronger for Chr 5, 7, and 9. Several linkages were specific to sex; for instance, the absolute weight of gonadal fat was linked to Chromosome 7 in male (LOD = 3.4) but not female mice (LOD = 0.2). Refining obesity as a phenotype may uncover clues about gene function that will assist in positional cloning efforts.

To identify the gene or genes on mouse Chromosome 9 that contribute to strain differences in fatness, we conducted an expanded mapping analysis to better define the region where suggestive linkage was found, using the F(2 )generation of an intercross between the C57BL/6ByJ and 129P3/J mouse strains. Six traits were studied: the summed weight of two adipose depots, the weight of each depot, analyzed individually (the gonadal and retroperitoneal depot), and the weight of each depot (summed and individual) relative to body size. We found significant linkage (LOD = 4.6) that accounted for the relative weight of the summed adipose depots, and another for the relative weight of the gonadal (LOD = 5.3) but not retroperitoneal (LOD = 0.9) adipose depot. This linkage is near marker rs30280752 (61.1 Mb, Build 34) and probably is equivalent to the quantitative trait locus (QTL) Adip5. Because the causal gene is unknown, we identified and evaluated several candidates within the confidence interval with functional significance to the body fatness phenotype (Il18, Acat1, Cyp19a1, Crabp1, Man2c1, Neil1, Mpi1, Csk, Lsm16, Adpgk, Bbs4, Hexa, Thsd4, Dpp8, Anxa2, and Lipc). We conclude that the Adip5 locus is specific to the gonadal adipose depot and that a gene or genes near the linkage peak may account for this QTL.

Humans will eat almost anything, from caribou livers to rutabagas, but there are some types of foods, and their associated taste qualities, that are preferred by large groups of people regardless of culture or experience. When many choices are available, humans chose foods that taste good, that is, create pleasing sensations in the mouth. The concept of good taste for most people encompasses both flavor and texture of food, and these sensations merge with taste proper to form the concept of goodness. Although we acknowledge the universality of the goodness (sweet) or badness (bitter) of basic taste qualities, we also find that people differ, sometimes extremely so, in their ability to perceive and enjoy these qualities and, by extension, food and drink. The reasons for these differences among people are not clear but are probably due to a combination of experience beginning at an early age, perhaps in utero; learning, for example, as with conditioned taste aversions; sex and maturity; and perceptual differences that arise from genetic variation. In this review, we focus on individual variations that arise from genetic differences and review two domains of science: recent developments in the molecular biology of taste transduction, with a focus on the genes involved and second, studies that examine biological relatives to determine the heritability of taste perception. Because the receptors for sweet, savory (umami), and bitter have recently been discovered, we summarize what is known about their function by reviewing the effect of naturally occurring and man-made alleles of these receptors, their shape and function based on receptor modeling techniques, and how they differ across animal species that vary in their ability to taste certain qualities. We discuss this literature in the context of how taste genes may differ among people and give rise to individuated taste experience, and what is currently known about the genetic effects on taste perception in humans.

Humans love the taste of sugar and the word "sweet" is used to describe not only this basic taste quality but also something that is desirable or pleasurable, e.g., la dolce vita. Although sugar or sweetened foods are generally among the most preferred choices, not everyone likes sugar, especially at high concentrations. The focus of my group's research is to understand why some people have a sweet tooth and others do not. We have used genetic and molecular techniques in humans, rats, mice, cats and primates to understand the origins of sweet taste perception. Our studies demonstrate that there are two sweet receptor genes (TAS1R2 and TAS1R3), and alleles of one of the two genes predict the avidity with which some mammals drink sweet solutions. We also find a relationship between sweet and bitter perception. Children who are genetically more sensitive to bitter compounds report that very sweet solutions are more pleasant and they prefer sweet carbonated beverages more than milk, relative to less bitter-sensitive peers. Overall, people differ in their ability to perceive the basic tastes, and particular constellations of genes and experience may drive some people, but not others, toward a caries-inducing sweet diet. Future studies will be designed to understand how a genetic preference for sweet food and drink might contribute to the development of dental caries.

Nearly all mammalian species like sweet-tasting foods and drinks, but there are differences in the degree of 'sweet tooth' both between species and among individuals of the same species. Some individual differences can be explained by genetic variability. Polymorphisms in a sweet taste receptor (Tas1r3) account for a large fraction of the differences in consumption of sweet solutions among inbred mouse strains. We wondered whether mice and rats share the same Tas1r3 alleles, and whether this gene might explain the large difference in saccharin preference among rats. We conducted three experiments to test this. We examined DNA sequence differences in the Tas1r3 gene among rats that differed in their consumption of saccharin in two-bottle choice tests. The animals tested were from an outbred strain (Sprague-Dawley; experiment 1), selectively bred to be high- or low-saccharin consumers (HiS and LoS; experiment 2), or from inbred strains with established differences in saccharin preference (FH/Wjd and ACI; experiment 3). Although there was considerable variation in saccharin preference among the rats there was no variation in the protein-coding regions of the Tas1r3 gene. DNA variants in intronic regions were detected in 1 (of 12) outbred rat with lower-than-average saccharin preference and in the ACI inbred strain, which also has a lower saccharin preference than the FH/Wjd inbred partner strain. Possible effects of these intronic nucleotide variants on Tas1r3 gene expression or the presence of T1R3 protein in taste papillae were evaluated in the ACI and FH/Wjd strains. Based upon the results of these studies, we conclude that polymorphisms in the protein-coding regions of the sweet receptor gene Tas1r3 are uncommon and do not account for individual differences in saccharin preference for these strains of rats. DNA variants in intron 4 and 5 are more common but appear to be innocuous.

Mice have proved to be a powerful model organism for understanding obesity in humans. Single gene mutants and genetically modified mice have been used to identify obesity genes, and the discovery of loci for polygenic forms of obesity in the mouse is an important next step. To pursue this goal, the inbred mouse strains 129P3/J (129) and C57BL/6ByJ (B6), which differ in body weight, body length, and adiposity, were used in an F2 cross to identify loci affecting these phenotypes. Linkages were determined in a two-phase process. In the first phase, 169 randomly selected F2 mice were genotyped for 134 markers that covered all autosomes and the X Chromosome (Chr). Significant linkages were found for body weight and body length on Chr 2. In addition, we detected several suggestive linkages on Chr 2 (adiposity), 9 (body weight, body length, and adiposity), and 16 (adiposity), as well as two suggestive sex-dependent linkages for body length on Chrs 4 and 9. In the second phase, 288 additional F2 mice were genotyped for markers near these regions of linkage. In the combined set of 457 F2 mice, six significant linkages were found: Chr 2 (Bwq5, body weight and Bdln3, body length), Chr 4 (Bdln6, body length, males only), Chr 9 (Bwq6, body weight and Adip5, adiposity), and Chr 16 (Adip9, adiposity), as well as several suggestive linkages (Adip2, adiposity on Chr 2, Bdln4 and Bdln5, body length on Chr 9). In addition, there was a suggestive linkage to body length in males on Chr 9 (Bdln4). For adiposity, there was evidence for epistatic interactions between loci on Chr 9 (Adip5) and 16 (Adip9). These results reinforce the concept that obesity is a complex trait. Genetic loci and their interactions, in conjunction with sex, age, and diet, determine body size and adiposity in mice.

We examined the extent to which maintenance diet influences the taste preferences of mice. C57BL/6J (B6) and 129X1/SvJ (129) mice were fed one of three standard cereal-based diets (Teklad 8604, Zeigler NIH-07, Purina 5001), a cereal-based diet formulated for breeding (Purina 5015), or two purified diets (AIN-76A or AIN-93G). The mice were given 48-h two-bottle choice tests between water and the following seven taste solutions: 2 mmol/L saccharin, 5 mmol/L citric acid, 50 mmol/L citric acid, 30 micro mol/L quinine hydrochloride (QHCl), 300 micro mol/L QHCl, 75 mmol/L NaCl, and 10% ethanol. There were very few differences in taste solution preference scores among mice of the same strain fed the three different versions of standard cereal-based diet. There were also very few differences in taste solution preference scores between mice of the same strain fed the two purified diets. However, the mice fed standard cereal-based diets generally drank more water and total fluid than did mice fed purified diets. There were larger differences between the B6 and 129 strains in saccharin and ethanol preference scores with mice fed standard cereal-based diets than purified diets. Conversely, there were larger differences between the B6 and 129 strains in citric acid and NaCl preference scores with mice fed purified diets than standard cereal-based diets. These results show that maintenance diet composition can have strain-dependent effects on taste solution preference. They illustrate that attention must be paid to the effects of diet on phenotype in screens of mutagenized mice and other genetic studies.