569 research outputs found

    Weak-Coupling Theory of Pair Density-Wave Instabilities in Transition Metal Dichalcogenides

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    The possibility of realizing pair density wave (PDW) phases, in which Cooper pairs have a finite momentum, presents an interesting challenge that has been studied in a wide variety of systems. In conventional superconductors, this is only possible when external fields lift the spin degeneracy of the Fermi surface, leading to pair formation at an incommensurate momentum. Here, we study a second possibility, potentially relevant to transition metal dichalcogenides, in which the Fermi surface consists of a pair of pockets centered at the ±K\pm K points of the Brillouin zone as well as a central pocket at the Γ\Gamma point. In the limit where these three pockets are identical, the pairing susceptibility has a logarithmic divergence at the non-zero wave-vectors ±K\pm \mathbf{K}, allowing for a weak-coupling analysis of the PDW instability. We find that repulsive electronic interactions combine to yield effective attractive interactions in the singlet and triplet PDW channels, as long as the Γ\Gamma pocket is present. Because these PDW channels decouple from the uniform superconducting channel, they can become the leading unconventional pairing instability of the system. Upon solving the linearized gap equations, we find that the PDW instability is robust against small trigonal warping of the ±K\pm K pockets and small detuning between the Γ\Gamma and ±K\pm K pockets, which affect the PDW transition in a similar way as the Zeeman magnetic field affects the uniform superconducting transition. We also derive the Ginzburg-Landau free energy for the PDW gaps with momenta ±K\pm \mathbf{K}, analyzing the conditions for and consequences of the emergence of FF-type and LO-type PDW ground states. Our classification of the induced orders in each ground state reveals unusual phases, including an odd-frequency charge-2e2e superconductor in the LO-type PDW.Comment: 24 pages, 11 figure

    Changes in J-SOAP-II and SAVRY Scores Over the Course of Residential, Cognitive-Behavioral Treatment for Adolescent Sexual Offending

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    Although the Juvenile Sex Offender Assessment Protocol-II (J-SOAP-II) and the Structured Assessment of Violence Risk in Youth (SAVRY) include an emphasis on dynamic, or modifiable factors, there has been little research on dynamic changes on these tools. To help address this gap, we compared admission and discharge scores of 163 adolescents who attended a residential, cognitive-behavioral treatment program for sexual offending. Based on reliable change indices, one-half of youth showed a reliable decrease on the J-SOAP-II Dynamic Risk Total Score and one-third of youth showed a reliable decrease on the SAVRY Dynamic Risk Total Score. Contrary to expectations, decreases in risk factors and increases in protective factors did not predict reduced sexual, violent nonsexual, or any reoffending. In addition, no associations were found between scores on the Psychopathy Checklist: Youth Version and levels of change. Overall, the J-SOAP-II and the SAVRY hold promise in measuring change, but further research is needed

    Effects of Smoking and Genotype on the PSR Index of Periodontal Disease in Adults Aged 18–49

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    Studies have found both genetic and environmental influences on chronic periodontitis. The purpose of this study was to examine the relationships among previously identified genetic variants, smoking status, and two periodontal disease-related phenotypes (PSR1 and PSR2) in 625 Caucasian adults (aged 18–49 years). The PSR Index was used to classify participants as affected or unaffected under the PSR1 and PSR2 phenotype definitions. Using logistic regression, we found that the form of the relationship varied by single nucleotide polymorphism (SNP): For rs10457525 and rs12630931, the effects of smoking and genotype on risk were additive; whereas for rs10457526 and rs733048, smoking was not independently associated with affected status once genotype was taken into consideration. In contrast, smoking moderated the relationships of rs3870371 and rs733048 with affected status such that former and never smokers with select genotypes were at increased genetic risk. Thus, for several groups, knowledge of genotype may refine the risk prediction over that which can be determined by knowledge of smoking status alone. Future studies should replicate these findings. These findings provide the foundation for the exploration of novel pathways by which periodontitis may occur

    Searching QTL by gene expression: analysis of diabesity

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    BACKGROUND: Recent developments in sequence databases provide the opportunity to relate the expression pattern of genes to their genomic position, thus creating a transcriptome map. Quantitative trait loci (QTL) are phenotypically-defined chromosomal regions that contribute to allelically variant biological traits, and by overlaying QTL on the transcriptome, the search for candidate genes becomes extremely focused. RESULTS: We used our novel data mining tool, ExQuest, to select genes within known diabesity QTL showing enriched expression in primary diabesity affected tissues. We then quantified transcripts in adipose, pancreas, and liver tissue from Tally Ho mice, a multigenic model for Type II diabetes (T2D), and from diabesity-resistant C57BL/6J controls. Analysis of the resulting quantitative PCR data using the Global Pattern Recognition analytical algorithm identified a number of genes whose expression is altered, and thus are novel candidates for diabesity QTL and/or pathways associated with diabesity. CONCLUSION: Transcription-based data mining of genes in QTL-limited intervals followed by efficient quantitative PCR methods is an effective strategy for identifying genes that may contribute to complex pathophysiological processes

    Periodontal Status and Quality of Life: Impact of Fear of Pain and Dental Fear

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    Background. Oral health-related quality of life (OHRQoL) is impacted by periodontal disease and orofacial pain. There is a limited research examining the impact of avoidance of care or physiological arousal related to the fear of pain response on periodontal-related OHRQoL. Methods. Data are from the Center for Oral Health Research in Appalachia family-based study focusing on 1,339 adults. Measures included a modified Periodontal Screening and Recording Index across sextants of dentition, dental fear survey, Fear of Pain Questionnaire-9, and Oral Health Impact Profile-14. Structural equation modeling was used to estimate the effects of periodontal disease screening indicators on OHRQoL including the mediating role of dental fear while accounting for fear of pain. Results. A significant total effect was found for the mandibular anterior sextant, components of dental anxiety/fear, and indicators of OHRQoL (pain and discomfort, , ; psychosocial impact, , ). The maxillary anterior region was significantly associated with pain discomfort (, ) and functionality (, ). Conclusions. Findings provide a granular perspective of periodontal disease indicators and OHRQoL. Dental avoidance/anticipatory fear and physiological arousal mediate OHRQoL in individuals who have indicators of periodontal disease in sextants that may be visible and susceptible to higher pain and psychosocial impact

    Genome-Wide Association Study of Periodontal Health Measured by Probing Depth in Adults Ages 18−49 years

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    The etiology of chronic periodontitis clearly includes a heritable component. Our purpose was to perform a small exploratory genome-wide association study in adults ages 18–49 years to nominate genes associated with periodontal disease−related phenotypes for future consideration. Full-mouth periodontal pocket depth probing was performed on participants (N = 673), with affected status defined as two or more sextants with probing depths of 5.5 mm or greater. Two variations of this phenotype that differed in how missing teeth were treated were used in analysis. More than 1.2 million genetic markers across the genome were genotyped or imputed and tested for genetic association. We identified ten suggestive loci (p-value ≤ 1E-5), including genes/loci that have been previously implicated in chronic periodontitis: LAMA2, HAS2, CDH2, ESR1, and the genomic region on chromosome 14q21-22 between SOS2 and NIN. Moreover, we nominated novel loci not previously implicated in chronic periodontitis or related pathways, including the regions 3p22 near OSBPL10 (a lipid receptor implicated in hyperlipidemia), 4p15 near HSP90AB2P (a heat shock pseudogene), 11p15 near GVINP1 (a GTPase pseudogene), 14q31 near SEL1L (an intracellular transporter), and 18q12 in FHOD3 (an actin cytoskeleton regulator). Replication of these results in additional samples is needed. This is one of the first research efforts to identify genetic polymorphisms associated with chronic periodontitis-related phenotypes by the genome-wide association study approach. Though small, efforts such this are needed in order to nominate novel genes and generate new hypotheses for exploration and testing in future studies

    Novel caries loci in children and adults implicated by genome-wide analysis of families

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    Background: Dental caries is a common chronic disease among children and adults alike, posing a substantial health burden. Caries is affected by multiple genetic and environmental factors, and prior studies have found that a substantial proportion of caries susceptibility is genetically inherited. Methods: To identify such genetic factors, we conducted a genome-wide linkage scan in 464 extended families with 2616 individuals from Iowa, Pennsylvania and West Virginia for three dental caries phenotypes: (1) PRIM: dichotomized as zero versus one or more affected primary teeth, (2) QTOT1: age-adjusted quantitative caries measure for both primary and permanent dentitions including pre-cavitated lesions, and (3) QTOT2: age-adjusted quantitative caries excluding pre-cavitated lesions. Genotyping was conducted for approximately 600,000 SNPs on an Illumina platform, pruned to 127,511 uncorrelated SNPs for the analyses reported here. Results: Multipoint non-parametric linkage analyses generated peak LOD scores exceeding 2.0 for eight genomic regions, but no LOD scores above 3.0 were observed. The maximum LOD score for each of the three traits was 2.90 at 1q25.3 for PRIM, 2.38 at 6q25.3 for QTOT1, and 2.76 at 5q23.3 for QTOT2. Some overlap in linkage regions was observed among the phenotypes. Genes with a potential role in dental caries in the eight chromosomal regions include CACNA1E, LAMC2, ALMS1, STAMBP, GXYLT2, SLC12A2, MEGF10, TMEM181, ARID1B, and, as well as genes in several immune gene families. Our results are also concordant with previous findings from association analyses on chromosomes 11 and 19. Conclusions: These multipoint linkage results provide evidence in favor of novel chromosomal regions, while also supporting earlier association findings for these data. Understanding the genetic etiology of dental caries will allow designing personalized treatment plans based on an individual’s genetic risk of disease
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