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Dive into the research topics where Tasha E. Fingerlin is active.

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Featured researches published by Tasha E. Fingerlin.


The New England Journal of Medicine | 2011

A common MUC5B promoter polymorphism and pulmonary fibrosis.

Max A. Seibold; Anastasia L. Wise; Marcy C. Speer; Mark P. Steele; Kevin K. Brown; James E. Loyd; Tasha E. Fingerlin; Weiming Zhang; Gunnar Gudmundsson; Steve D. Groshong; Christopher M. Evans; Stavros Garantziotis; Kenneth B. Adler; Burton F. Dickey; Roland M. du Bois; Ivana V. Yang; Aretha Herron; Dolly Kervitsky; Janet Talbert; Cheryl Markin; Joungjoa Park; Anne L. Crews; Susan Slifer; Scott S. Auerbach; Michelle G. Roy; Jia Lin; Corinne E. Hennessy; Marvin I. Schwarz; David A. Schwartz

BACKGROUND The mutations that have been implicated in pulmonary fibrosis account for only a small proportion of the population risk. METHODS Using a genomewide linkage scan, we detected linkage between idiopathic interstitial pneumonia and a 3.4-Mb region of chromosome 11p15 in 82 families. We then evaluated genetic variation in this region in gel-forming mucin genes expressed in the lung among 83 subjects with familial interstitial pneumonia, 492 subjects with idiopathic pulmonary fibrosis, and 322 controls. MUC5B expression was assessed in lung tissue. RESULTS Linkage and fine mapping were used to identify a region of interest on the p-terminus of chromosome 11 that included gel-forming mucin genes. The minor-allele of the single-nucleotide polymorphism (SNP) rs35705950, located 3 kb upstream of the MUC5B transcription start site, was present at a frequency of 34% among subjects with familial interstitial pneumonia, 38% among subjects with idiopathic pulmonary fibrosis, and 9% among controls (allelic association with familial interstitial pneumonia, P=1.2×10(-15); allelic association with idiopathic pulmonary fibrosis, P=2.5×10(-37)). The odds ratios for disease among subjects who were heterozygous and those who were homozygous for the minor allele of this SNP were 6.8 (95% confidence interval [CI], 3.9 to 12.0) and 20.8 (95% CI, 3.8 to 113.7), respectively, for familial interstitial pneumonia and 9.0 (95% CI, 6.2 to 13.1) and 21.8 (95% CI, 5.1 to 93.5), respectively, for idiopathic pulmonary fibrosis. MUC5B expression in the lung was 14.1 times as high in subjects who had idiopathic pulmonary fibrosis as in those who did not (P<0.001). The variant allele of rs35705950 was associated with up-regulation in MUC5B expression in the lung in unaffected subjects (expression was 37.4 times as high as in unaffected subjects homozygous for the wild-type allele, P<0.001). MUC5B protein was expressed in lesions of idiopathic pulmonary fibrosis. CONCLUSIONS A common polymorphism in the promoter of MUC5B is associated with familial interstitial pneumonia and idiopathic pulmonary fibrosis. Our findings suggest that dysregulated MUC5B expression in the lung may be involved in the pathogenesis of pulmonary fibrosis. (Funded by the National Heart, Lung, and Blood Institute and others.).


Nature Genetics | 2013

Genome-wide association study identifies multiple susceptibility loci for pulmonary fibrosis

Tasha E. Fingerlin; Elissa Murphy; Weiming Zhang; Anna L. Peljto; Kevin K. Brown; Mark P. Steele; James E. Loyd; Gregory P. Cosgrove; David A. Lynch; Steve D. Groshong; Harold R. Collard; Paul J. Wolters; Williamson Ziegler Bradford; Karl Kossen; Scott D. Seiwert; Roland M. du Bois; Christine Kim Garcia; Megan S. Devine; Gunnar Gudmundsson; Helgi J. Ísaksson; Naftali Kaminski; Yingze Zhang; Kevin F. Gibson; Lisa H. Lancaster; Joy D. Cogan; Wendi R. Mason; Toby M. Maher; Philip L. Molyneaux; Athol U. Wells; Miriam F. Moffatt

We performed a genome-wide association study of non-Hispanic, white individuals with fibrotic idiopathic interstitial pneumonias (IIPs; n = 1,616) and controls (n = 4,683), with follow-up replication analyses in 876 cases and 1,890 controls. We confirmed association with TERT at 5p15, MUC5B at 11p15 and the 3q26 region near TERC, and we identified seven newly associated loci (Pmeta = 2.4 × 10−8 to 1.1 × 10−19), including FAM13A (4q22), DSP (6p24), OBFC1 (10q24), ATP11A (13q34), DPP9 (19p13) and chromosomal regions 7q22 and 15q14-15. Our results suggest that genes involved in host defense, cell-cell adhesion and DNA repair contribute to risk of fibrotic IIPs.


American Journal of Human Genetics | 2000

The Finland-United States investigation of non-insulin-dependent diabetes mellitus genetics (FUSION) study. I. An autosomal genome scan for genes that predispose to type 2 diabetes

Soumitra Ghosh; Richard M. Watanabe; Timo T. Valle; Elizabeth R. Hauser; Victoria L. Magnuson; Carl D. Langefeld; Delphine S. Ally; Karen L. Mohlke; Kaisa Silander; Kimmo Kohtamäki; Peter S. Chines; James E. Balow; Gunther Birznieks; Jennie Chang; William Eldridge; Michael R. Erdos; Zarir E. Karanjawala; Julie I. Knapp; Kristina Kudelko; Colin Martin; Anabelle Morales-Mena; Anjene Musick; Tiffany Musick; Carrie Pfahl; Rachel Porter; Joseph B. Rayman; David Rha; Leonid Segal; Shane Shapiro; Ben Shurtleff

We performed a genome scan at an average resolution of 8 cM in 719 Finnish sib pairs with type 2 diabetes. Our strongest results are for chromosome 20, where we observe a weighted maximum LOD score (MLS) of 2.15 at map position 69.5 cM from pter and secondary weighted LOD-score peaks of 2.04 at 56.5 cM and 1.99 at 17.5 cM. Our next largest MLS is for chromosome 11 (MLS = 1.75 at 84.0 cM), followed by chromosomes 2 (MLS = 0.87 at 5.5 cM), 10 (MLS = 0.77 at 75.0 cM), and 6 (MLS = 0.61 at 112.5 cM), all under an additive model. When we condition on chromosome 2 at 8.5 cM, the MLS for chromosome 20 increases to 5.50 at 69.0 cM (P=.0014). An ordered-subsets analysis based on families with high or low diabetes-related quantitative traits yielded results that support the possible existence of disease-predisposing genes on chromosomes 6 and 10. Genomewide linkage-disequilibrium analysis using microsatellite marker data revealed strong evidence of association for D22S423 (P=.00007). Further analyses are being carried out to confirm and to refine the location of these putative diabetes-predisposing genes.


JAMA | 2013

Association Between the MUC5B Promoter Polymorphism and Survival in Patients With Idiopathic Pulmonary Fibrosis

Anna L. Peljto; Yingze Zhang; Tasha E. Fingerlin; Shwu-Fan Ma; Joe G. N. Garcia; Thomas J. Richards; Lori J. Silveira; Kathleen O. Lindell; Mark P. Steele; James E. Loyd; Kevin F. Gibson; Max A. Seibold; Kevin K. Brown; Janet Talbert; Cheryl Markin; Karl Kossen; Scott D. Seiwert; Elissa Murphy; Imre Noth; Marvin I. Schwarz; Naftali Kaminski; David A. Schwartz

IMPORTANCE Current prediction models of mortality in idiopathic pulmonary fibrosis (IPF), which are based on clinical and physiological parameters, have modest value in predicting which patients will progress. In addition to the potential for improving prognostic models, identifying genetic and molecular features that are associated with IPF mortality may provide insight into the underlying mechanisms of disease and inform clinical trials. OBJECTIVE To determine whether the MUC5B promoter polymorphism (rs35705950), previously reported to be associated with the development of pulmonary fibrosis, is associated with survival in IPF. DESIGN, SETTING, AND PARTICIPANTS Retrospective study of survival in 2 independent cohorts of patients with IPF: the INSPIRE cohort, consisting of patients enrolled in the interferon-γ1b trial (n = 438; December 15, 2003-May 2, 2009; 81 centers in 7 European countries, the United States, and Canada), and the Chicago cohort, consisting of IPF participants recruited from the Interstitial Lung Disease Clinic at the University of Chicago (n = 148; 2007-2010). The INSPIRE cohort was used to model the association of the MUC5B genotype with survival, accounting for the effect of matrix metalloproteinase 7 (MMP-7) blood concentration and other demographic and clinical covariates. The Chicago cohort was used for replication of findings. MAIN OUTCOMES AND MEASURES The primary end point was all-cause mortality. RESULTS The numbers of patients in the GG, GT, and TT genotype groups were 148 (34%), 259 (59%), and 31 (7%), respectively, in the INSPIRE cohort and 41 (28%), 98 (66%), and 9 (6%), respectively, in the Chicago cohort. The median follow-up period was 1.6 years for INSPIRE and 2.1 years for Chicago. During follow-up, there were 73 deaths (36 GG, 35 GT, and 2 TT) among INSPIRE patients and 64 deaths (26 GG, 36 GT, and 2 TT) among Chicago patients. The unadjusted 2-year cumulative incidence of death was lower among patients carrying 1 or more copies of the IPF risk allele (T) in both the INSPIRE cohort (0.25 [95% CI, 0.17-0.32] for GG, 0.17 [95% CI, 0.11-0.23] for GT, and 0.03 [95% CI, 0.00-0.09] for TT) and the Chicago cohort (0.50 [95% CI, 0.31-0.63] for GG, 0.22 [95% CI, 0.13-0.31] for GT, and 0.11 [95% CI, 0.00-0.28] for TT). In the INSPIRE cohort, the TT and GT genotypes (risk for IPF) were associated with improved survival compared with GG (hazard ratios, 0.23 [95% CI, 0.10-0.52] and 0.48 [95% CI, 0.31-0.72], respectively; P < .001). This finding was replicated in the Chicago cohort (hazard ratios, 0.15 [95% CI, 0.05-0.49] and 0.39 [95% CI, 0.21-0.70], respectively; P < .002). The observed association of MUC5B with survival was independent of age, sex, forced vital capacity, diffusing capacity of carbon monoxide, MMP-7, and treatment status. The addition of the MUC5B genotype to the survival models significantly improved the predictive accuracy of the model in both the INSPIRE cohort (C = 0.71 [95% CI, 0.64-0.75] vs C = 0.68 [95% CI, 0.61-0.73]; P < .001) and the Chicago cohort (C = 0.73 [95% CI, 0.62-0.78] vs C = 0.69 [95% CI, 0.59-0.75]; P = .01). CONCLUSIONS AND RELEVANCE Among patients with IPF, a common risk polymorphism in MUC5B was significantly associated with improved survival. Further research is necessary to refine the risk estimates and to determine the clinical implications of these findings.


The Journal of Clinical Endocrinology and Metabolism | 2008

Genetic and Environmental Determinants of 25-Hydroxyvitamin D and 1,25-Dihydroxyvitamin D Levels in Hispanic and African Americans

Corinne D. Engelman; Tasha E. Fingerlin; Carl D. Langefeld; Pamela J. Hicks; Stephen S. Rich; Lynne E. Wagenknecht; Donald W. Bowden; Jill M. Norris

CONTEXT Vitamin D deficiency is associated with many adverse health outcomes, yet little is known about the genetic epidemiology of vitamin D or its metabolites. OBJECTIVE Our objective was to examine the relationship among three vitamin D-related genes and levels of 25-hydroxyvitamin D [25(OH)D] and 1,25-dihydroxyvitamin D [1,25(OH)2D] in Hispanics (HAs) and African Americans (AAs). DESIGN AND SETTING The cross-sectional Insulin Resistance Atherosclerosis Family Study recruited and examined subjects in: Los Angeles, California (AAs; 513 individuals from 42 families); San Luis Valley (SLV), Colorado (HAs; 513 individuals from 30 families); and San Antonio (SA), Texas (HAs; 504 individuals from 58 families). MAIN OUTCOME MEASURES Plasma levels of 25(OH)D and 1,25(OH)2D were measured. RESULTS Levels of 25(OH)D were highest in SLV-HAs [18.3 +/- 7.7 ng/ml (45.7 +/- 19.2 nmol/liter)], lower in SA-HAs [14.6 +/- 6.4 ng/ml (36.4 +/- 16.0 nmol/liter)], and lowest in AAs [11.0 +/- 5.4 ng/ml (27.5 +/- 13.5 nmol/liter)]. Levels of 1,25(OH)2D were similar in AAs [43.5 +/- 13.9 pg/ml (113.1 +/- 36.1 pmol/liter)] and SLV-HAs [43.2 +/- 13.3 pg/ml (112.3 +/- 34.6 pmol/liter)], but higher in SA-HAs [48.6 +/- 17.0 pg/ml (126.4 +/- 44.2 pmol/liter)]. After adjusting for gender and age within the site, two single nucleotide polymorphisms (SNPs) in the vitamin D binding protein gene (DBP), rs4588 and rs7041, were associated with 25(OH)D, and one SNP in the DBP, rs4588, was associated with 1,25(OH)2D at all three study centers. CONCLUSIONS SNPs in the DBP are associated with levels of 25(OH)D and 1,25(OH)2D in HA and AA participants in the Insulin Resistance Atherosclerosis Family Study.


American Journal of Human Genetics | 2000

The Finland-United States investigation of non-insulin-dependent diabetes mellitus genetics (FUSION) study. II. An autosomal genome scan for diabetes-related quantitative-trait loci

Richard M. Watanabe; Soumitra Ghosh; Carl D. Langefeld; Timo T. Valle; Elizabeth R. Hauser; Victoria L. Magnuson; Karen L. Mohlke; Kaisa Silander; Delphine S. Ally; Peter S. Chines; Jillian Blaschak-Harvan; Julie A. Douglas; William L. Duren; Michael P. Epstein; Tasha E. Fingerlin; Hong Shi Kaleta; Ethan M. Lange; Chun Li; Richard C. McEachin; Heather M. Stringham; Edward H. Trager; Peggy P. White; James E. Balow; Gunther Birznieks; Jennie Chang; William Eldridge; Michael R. Erdos; Zarir E. Karanjawala; Julie I. Knapp; Kristina Kudelko

Type 2 diabetes mellitus is a complex disorder encompassing multiple metabolic defects. We report results from an autosomal genome scan for type 2 diabetes-related quantitative traits in 580 Finnish families ascertained for an affected sibling pair and analyzed by the variance components-based quantitative-trait locus (QTL) linkage approach. We analyzed diabetic and nondiabetic subjects separately, because of the possible impact of disease on the traits of interest. In diabetic individuals, our strongest results were observed on chromosomes 3 (fasting C-peptide/glucose: maximum LOD score [MLS] = 3.13 at 53.0 cM) and 13 (body-mass index: MLS = 3.28 at 5.0 cM). In nondiabetic individuals, the strongest results were observed on chromosomes 10 (acute insulin response: MLS = 3.11 at 21.0 cM), 13 (2-h insulin: MLS = 2.86 at 65.5 cM), and 17 (fasting insulin/glucose ratio: MLS = 3.20 at 9.0 cM). In several cases, there was evidence for overlapping signals between diabetic and nondiabetic individuals; therefore we performed joint analyses. In these joint analyses, we observed strong signals for chromosomes 3 (body-mass index: MLS = 3.43 at 59.5 cM), 17 (empirical insulin-resistance index: MLS = 3.61 at 0.0 cM), and 19 (empirical insulin-resistance index: MLS = 2.80 at 74.5 cM). Integrating genome-scan results from the companion article by Ghosh et al., we identify several regions that may harbor susceptibility genes for type 2 diabetes in the Finnish population.


The New England Journal of Medicine | 2013

MUC5B Promoter Polymorphism and Interstitial Lung Abnormalities

Gary M. Hunninghake; Hiroto Hatabu; Yuka Okajima; Wei Gao; Dupuis J; Jeanne C. Latourelle; Mizuki Nishino; Tetsuro Araki; Oscar E. Zazueta; Sila Kurugol; James C. Ross; San José Estépar R; Elissa Murphy; Mark P. Steele; James E. Loyd; Marvin I. Schwarz; Tasha E. Fingerlin; Ivan O. Rosas; George R. Washko; George T. O'Connor; David A. Schwartz

BACKGROUND A common promoter polymorphism (rs35705950) in MUC5B, the gene encoding mucin 5B, is associated with idiopathic pulmonary fibrosis. It is not known whether this polymorphism is associated with interstitial lung disease in the general population. METHODS We performed a blinded assessment of interstitial lung abnormalities detected in 2633 participants in the Framingham Heart Study by means of volumetric chest computed tomography (CT). We evaluated the relationship between the abnormalities and the genotype at the rs35705950 locus. RESULTS Of the 2633 chest CT scans that were evaluated, interstitial lung abnormalities were present in 177 (7%). Participants with such abnormalities were more likely to have shortness of breath and chronic cough and reduced measures of total lung and diffusion capacity, as compared with participants without such abnormalities. After adjustment for covariates, for each copy of the minor rs35705950 allele, the odds of interstitial lung abnormalities were 2.8 times greater (95% confidence interval [CI], 2.0 to 3.9; P<0.001), and the odds of definite CT evidence of pulmonary fibrosis were 6.3 times greater (95% CI, 3.1 to 12.7; P<0.001). Although the evidence of an association between the MUC5B genotype and interstitial lung abnormalities was greater among participants who were older than 50 years of age, a history of cigarette smoking did not appear to influence the association. CONCLUSIONS The MUC5B promoter polymorphism was found to be associated with interstitial lung disease in the general population. Although this association was more apparent in older persons, it did not appear to be influenced by cigarette smoking. (Funded by the National Institutes of Health and others; ClinicalTrials.gov number, NCT00005121.).


Proceedings of the National Academy of Sciences of the United States of America | 2002

High-throughput screening for evidence of association by using mass spectrometry genotyping on DNA pools.

Karen L. Mohlke; Michael R. Erdos; Laura J. Scott; Tasha E. Fingerlin; Anne U. Jackson; Kaisa Silander; Pablo Hollstein; Michael Boehnke; Francis S. Collins

To facilitate positional cloning of complex trait susceptibility loci, we are investigating methods to reduce the effort required to identify trait-associated alleles. We examined primer extension analysis by matrix-assisted laser desorption/ionization time-of-flight mass spectrometry to screen single-nucleotide polymorphisms (SNPs) for association by using DNA pools. We tested whether this method can accurately estimate allele frequency differences between pools while maintaining the high-throughput nature of assay design, sample handling, and scoring. We follow up interesting allele frequency differences in pools by genotyping individuals. We tested DNA pools of 182, 228, and 499 individuals using 16 SNPs with minor allele frequencies 0.026–0.486 and allele frequency differences 0.001–0.108 that we had genotyped previously on individuals and 381 SNPs that we had not. Precision, as measured by the average standard deviation among 16 semidependent replicates, was 0.021 ± 0.011 for the 16 SNPs and 0.018 ± 0.008 for the 291/381 SNPs used in further analysis. For the 16 SNPs, the average absolute error in predicting allele frequency differences between pools was 0.009; the largest errors were 0.031, 0.028, and 0.027. We determined that compensating for unequal peak heights in heterozygotes improved precision of allele frequency estimates but had only a very minor effect on accuracy of allele frequency differences between pools. Based on these data and assuming pools of 500 individuals, we conclude that at significance level 0.05 we would have 95% (82%) power to detect population allele frequency differences of 0.07 for control allele frequencies of 0.10 (0.50).


American Journal of Respiratory and Critical Care Medicine | 2015

RARE VARIANTS IN RTEL1 ARE ASSOCIATED WITH FAMILIAL INTERSTITIAL PNEUMONIA

Joy D. Cogan; Jonathan A. Kropski; Min Zhao; Daphne B. Mitchell; Lynette Rives; Cheryl Markin; Errine T. Garnett; Keri H. Montgomery; Wendi R. Mason; David F. McKean; Julia Powers; Elissa Murphy; Lana M. Olson; Leena Choi; Dong-Sheng Cheng; Elizabeth Blue; Lisa R. Young; Lisa H. Lancaster; Mark P. Steele; Kevin K. Brown; Marvin I. Schwarz; Tasha E. Fingerlin; David A. Schwartz; William Lawson; James E. Loyd; Zhongming Zhao; John A. Phillips; Timothy S. Blackwell

RATIONALE Up to 20% of cases of idiopathic interstitial pneumonia cluster in families, comprising the syndrome of familial interstitial pneumonia (FIP); however, the genetic basis of FIP remains uncertain in most families. OBJECTIVES To determine if new disease-causing rare genetic variants could be identified using whole-exome sequencing of affected members from FIP families, providing additional insights into disease pathogenesis. METHODS Affected subjects from 25 kindreds were selected from an ongoing FIP registry for whole-exome sequencing from genomic DNA. Candidate rare variants were confirmed by Sanger sequencing, and cosegregation analysis was performed in families, followed by additional sequencing of affected individuals from another 163 kindreds. MEASUREMENTS AND MAIN RESULTS We identified a potentially damaging rare variant in the gene encoding for regulator of telomere elongation helicase 1 (RTEL1) that segregated with disease and was associated with very short telomeres in peripheral blood mononuclear cells in 1 of 25 families in our original whole-exome sequencing cohort. Evaluation of affected individuals in 163 additional kindreds revealed another eight families (4.7%) with heterozygous rare variants in RTEL1 that segregated with clinical FIP. Probands and unaffected carriers of these rare variants had short telomeres (<10% for age) in peripheral blood mononuclear cells and increased T-circle formation, suggesting impaired RTEL1 function. CONCLUSIONS Rare loss-of-function variants in RTEL1 represent a newly defined genetic predisposition for FIP, supporting the importance of telomere-related pathways in pulmonary fibrosis.


Thorax | 2013

Expression of cilium-associated genes defines novel molecular subtypes of idiopathic pulmonary fibrosis

Yang; Christopher D. Coldren; Sonia M. Leach; Max A. Seibold; Elissa Murphy; Jia Lin; Rosen R; Neidermyer Aj; David F. McKean; Steve D. Groshong; Carlyne D. Cool; Gregory P. Cosgrove; David A. Lynch; Kevin K. Brown; Marvin I. Schwarz; Tasha E. Fingerlin; David A. Schwartz

Background Idiopathic pulmonary fibrosis (IPF) is an untreatable lung disease with a median survival of only 3–5 years that is diagnosed using a combination of clinical, radiographic and pathologic criteria. Histologically, IPF is characterised by usual interstitial pneumonia (UIP), a fibrosing interstitial pneumonia with a pattern of heterogeneous, subpleural regions of fibrotic and remodelled lung. We hypothesised that gene expression profiles of lung tissue may identify molecular subtypes of disease that could classify subtypes of IPF/UIP that have clinical implications. Methods and findings We collected transcriptional profiles on lung tissue from 119 patients with IPF/UIP and 50 non-diseased controls. Differential expression of individual transcripts was identified using an analysis of covariance (ANCOVA) model incorporating the clinical diagnosis of each patient as well as age, gender and smoking status. Validation was performed in an independent cohort of 111 IPF/UIP and 39 non-diseased controls. Our analysis identified two subtypes of IPF/UIP based on a strong molecular signature associated with expression of genes previously associated with fibrosis (matrix metalloproteinases, osteopontin, keratins), cilium genes and genes with unknown function. We demonstrate that elevated expression of cilium genes is associated with more extensive microscopic honeycombing and higher expression of both the airway mucin gene MUC5B and the metalloproteinase MMP7, a gene recently implicated in attenuating ciliated cell differentiation during wound repair. Conclusions Expression of cilium genes appears to identify two unique molecular phenotypes of IPF/UIP. The different molecular profiles may be relevant to therapeutic responsiveness in patients with IPF/UIP.

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David A. Schwartz

University of Colorado Denver

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Marvin I. Schwarz

University of Colorado Denver

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Jill M. Norris

Colorado School of Public Health

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Kevin K. Brown

University of Colorado Denver

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Lisa A. Maier

University of Colorado Denver

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Ivana V. Yang

University of Colorado Denver

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Elissa Murphy

University of Colorado Denver

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Lori J. Silveira

University of Colorado Denver

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