Person: White, Steve
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White
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White, Steve
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Publication Electronic quasiparticles in the quantum dimer model: Density matrix renormalization group results(American Physical Society (APS), 2016) Lee, Junhyun; Sachdev, Subir; White, SteveWe study a recently proposed quantum dimer model for the pseudogap metal state of the cuprates. The model contains bosonic dimers, representing a spin-singlet valence bond between a pair of electrons, and fermionic dimers, representing a quasiparticle with spin-1/2 and charge +e. By density matrix renormalization group calculations on a long but finite cylinder, we obtain the ground state density distribution of the fermionic dimers for a number of di↵erent total densities. From the Friedel oscillations at open boundaries, we deduce that the Fermi surface consists of small hole pockets near (⇡/2, ⇡/2), and this feature persists up to doping density 1/16. We also compute the entanglement entropy and find that it closely matches the sum of the entanglement entropies of a critical boson and a low density of free fermions. Our results support the existence of a fractionalized Fermi liquid (FL*) in this model.Publication Genome-Wide Interrogation of Longitudinal FEV 1 in Children With Asthma(American Thoracic Society, 2014) Wu, Kehua; Gamazon, Eric R.; Im, Hae Kyung; Geeleher, Paul; White, Steve; Solway, Julian; Clemmer, George L.; Weiss, Scott; Tantisira, Kelan; Cox, Nancy J.; Ratain, Mark J.; Huang, R. StephanieRationale: Most genomic studies of lung function have used phenotypic data derived from a single time-point (e.g., presence/absence of disease) without considering the dynamic progression of a chronic disease. Objectives: To characterize lung function change over time in subjects with asthma and identify genetic contributors to a longitudinal phenotype. Methods: We present a method that models longitudinal FEV1 data, collected from 1,041 children with asthma who participated in the Childhood Asthma Management Program. This longitudinal progression model was built using population-based nonlinear mixed-effects modeling with an exponential structure and the determinants of age and height. Measurements and Main Results: We found ethnicity was a key covariate for FEV1 level. Budesonide-treated children with asthma had a slight but significant effect on FEV1 when compared with those treated with placebo or nedocromil (P < 0.001). A genome-wide association study identified seven single-nucleotide polymorphisms nominally associated with longitudinal lung function phenotypes in 581 white Childhood Asthma Management Program subjects (P < 10−4 in the placebo [“discovery”] and P < 0.05 in the nedocromil treatment [“replication”] group). Using ChIP-seq and RNA-seq data, we found that some of the associated variants were in strong enhancer regions in human lung fibroblasts and may affect gene expression in human lung tissue. Genetic mapping restricted to genome-wide enhancer single-nucleotide polymorphisms in lung fibroblasts revealed a highly significant variant (rs6763931; P = 4 × 10−6; false discovery rate < 0.05). Conclusions: This study offers a strategy to explore the genetic determinants of longitudinal phenotypes, provide a comprehensive picture of disease pathophysiology, and suggest potential treatment targetsPublication A genome-wide survey of CD4+ lymphocyte regulatory genetic variants identifies novel asthma genes(Elsevier BV, 2014) Sharma, Sunita; Zhou, Xiaobo; Thibault, Derek M.; Himes, Blanca; Liu, Andy; Szefler, Stanley J.; Strunk, Robert; Castro, Mario; Hansel, Nadia N.; Diette, Gregory B.; Vonakis, Becky M.; Adkinson, N. Franklin; Avila, Lydiana; Soto-Quiros, Manuel; Barraza-Villareal, Albino; Lemanske, Robert F.; Solway, Julian; Krishnan, Jerry; White, Steve; Cheadle, Chris; Berger, Alan E.; Fan, Jinshui; Boorgula, Meher Preethi; Nicolae, Dan; Gilliland, Frank; Barnes, Kathleen; London, Stephanie J.; Martinez, Fernando; Ober, Carole; Celedón, Juan C.; Carey, Vincent; Weiss, Scott; Raby, BenjaminBackground: Genome-wide association studies have yet to identify the majority of genetic variants involved in asthma. We hypothesized that expression quantitative trait locus (eQTL) mapping can identify novel asthma genes by enabling prioritization of putative functional variants for association testing. Objective: We evaluated 6,706 cis-acting expression-associated variants (eSNP) identified through a genome-wide eQTL survey of CD4+ lymphocytes for association with asthma. Methods: eSNP were tested for association with asthma in 359 asthma cases and 846 controls from the Childhood Asthma Management Program, with verification using family-based testing. Significant associations were tested for replication in 579 parent-child trios with asthma from Costa Rica. Further functional validation was performed by Formaldehyde Assisted Isolation of Regulatory Elements (FAIRE)-qPCR and Chromatin-Immunoprecipitation (ChIP)-PCR in lung derived epithelial cell lines (Beas-2B and A549) and Jurkat cells, a leukemia cell line derived from T lymphocytes. Results: Cis-acting eSNP demonstrated associations with asthma in both cohorts. We confirmed the previously-reported association of ORMDL3/GSDMB variants with asthma (combined p=2.9 × 108). Reproducible associations were also observed for eSNP in three additional genes: FADS2 (p=0.002), NAGA (p=0.0002), and F13A1 (p=0.0001). We subsequently demonstrated that FADS2 mRNA is increased in CD4+ lymphocytes in asthmatics, and that the associated eSNPs reside within DNA segments with histone modifications that denote open chromatin status and confer enhancer activity. Conclusions: Our results demonstrate the utility of eQTL mapping in the identification of novel asthma genes, and provide evidence for the importance of FADS2, NAGA, and F13A1 in the pathogenesis of asthma.