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• Blueprint: A human variation panel of genetic influences on epigenomes and transcriptomes in three immune cells, (ChIP-Seq_H3K27me3 for mature neutrophil, on genome GRCh37)

  ChIP-Seq_H3K27me3 data for 131 mature neutrophil sample(s). 321 run(s), 134 experiment(s), 134 analysis(s) on human genome GRCh37. Analysis documentation available at http://ftp.ebi.ac.uk/pub/databases/blueprint/blueprint_Epivar/protocols/README_chipseq_analysis_ebi_20160816

  Dataset EGAD00001002712

• Blueprint: A human variation panel of genetic influences on epigenomes and transcriptomes in three immune cells, (ChIP-Seq_H3K4me3 for mature neutrophil, on genome GRCh37)

  ChIP-Seq_H3K4me3 data for 133 mature neutrophil sample(s). 208 run(s), 136 experiment(s), 136 analysis(s) on human genome GRCh37. Analysis documentation available at http://ftp.ebi.ac.uk/pub/databases/blueprint/blueprint_Epivar/protocols/README_chipseq_analysis_ebi_20160816

  Dataset EGAD00001002711

• Metagenome for FINRISK2002

  The dataset contains data for n=7211 FINRISK 2002 participants who underwent fecal sampling. Demultiplexed shallow shotgun metagenomic sequences were quality filtered and adapter trimmed using Atropos (Didion et al., 2017), and human filtered using Bowtie2 (Langmead and Salzberg, 2012). The files are in FASTQ format.

  Dataset EGAD00001007035

• X Ten analysis of spiked placental tissue samples

  Metagenomics data of 80 placental tissue samples analyzed by X Ten for their possible microbial content. These 80 samples from pre-labor C-section deliveries, representing Cohort 1, were spiked with 1100 CFU Salmonella bongori. These same samples were also analyzed by 16S amplicon sequencing (search for ERP109246 in ENA).

  Dataset EGAD00001004198

• Coagulation and Fibrinolysis in a Pediatric Insulin Titration Trial

  Summary of the Design and Aims: The Coagulation and Fibrinolysis in a Pediatric Insulin Titration Trial (CAF-PINT) is an ancillary study to the HALF PINT (NCT01565941) randomized, controlled trial that was originally designed to study changes in inflammatory and thrombosis pathways in the setting of an interventional trial. The parent HALF PINT study was designed to study the impact of tight glycemic control (TGC) using an explicit insulin titration algorithm to safely achieve a normal glucose in target range of 80-110 mg/dL versus 150-180mg/dL on clinical outcomes among critically ill hyperglycemic children with Heart and Lung Failure. The CAF PINT study collected blood samples pre randomization and at 2 and 4 days after randomization. Blood samples collected in EDTA tubes were centrifuged at local sites to separate the plasma from cell pellets and frozen prior to shipment. In addition, 0.5 mL of whole blood collected in PAXgene tubes modified for use in pediatrics frozen 24 hours after collection prior to shipment.Population Information: Setting: Twenty-one academic children's hospitals (HALF-PINT) and 1 academic children's hospital (IIT-SBPP). Participants: Critically ill hyperglycemic children requiring mechanical ventilation/vasoactive support (n=293).Interventions and Exposures: Patients in HALF PINT were randomized to achieve a low target glucose (80-110 mg/dL) vs. a higher target (150-180 mg/dL). The primary trial was stopped early due to low likelihood of achieving a statistically significant difference in the primary outcomes. Molecular Technologies Employed: Plasma biomarkers were assayed on thawed plasma using a Luminex panel. RNA was extracted from PAXgene Blood RNA Kits modified for pediatric use. Extracted RNA was sequenced with the Novaseq S4 system (Illumina) to generate 2 x 150 base paired end reads to a target depth of 50 million read-pairs per sample.Principal Findings of the Study: We tested for heterogeneity of treatment effects according to baseline blood inflammatory proteins using logistic regression with individual biomarkers as interaction terms and Cox regression analysis using biomarker-derived latent classes. Children with higher inflammatory proteins including TNFR-1, IL-6, IL-8, and IL-10 had lower mortality when treated with insulin to a target glucose of 80-110 mg/dL as compared to 150-180 mg/dL (interaction p<0.05). Causal forest estimates ranged from a 40% mortality reduction to a 15% mortality increase with TGC, depending on each patient’s individual biomarker profile. Latent class categorization strongly interacted with TGC with respect to mortality (Cox regression interaction p=0.005). Specifically, patients with higher inflammation benefited from TGC (6% mortality with TGC vs. 48% mortality, p=0.004) whereas hypoinflamed patients showed a trend towards harm (14% mortality with TGC vs. 7% mortality, p=0.055).Data available through dbGaP: Transcriptomic (Gene Counts) and phenotype data

  Study phs003016

• Prematurity and Respiratory Outcomes Program (PROP) Core Database Protocol (PROP-BioLINCC)

  Data Access NOTE: Please refer to the "Authorized Access" section below for information about how access to the data from this accession differs from many other dbGaP accessions. Objectives: The Prematurity and Respiratory Outcomes Program (PROP) was performed to identify suitable predictors of respiratory outcomes that may serve as surrogate endpoints in future trials of prevention and therapy of respiratory diseases in preterm infants.Background: Acute and chronic respiratory morbidities are common in premature births, and can pose significant risk to the infant's health, particularly during the first two years of life. One such condition is bronchopulmonary dysplasia (BPD) where infants require oxygen therapy due to abnormal repair and impaired lung development after acute lung injury. BPD poses a high mortality risk, even in infants that survive the initial hospitalization. Regardless of BPD diagnosis, preterm infants frequently return for medical care due to symptoms of post-prematurity respiratory disease (PRD), which includes intermittent or chronic wheezing, cough without cold, poor growth, apnea and cyanosis, and lower respiratory tract infections. Impaired lung function can persist into adulthood, contributing to chronic respiratory diseases including asthma and emphysema.However, at the time of the PROP study, there were no objective measures to predict which preterm infants would have persistent respiratory problems after discharge from the hospital. Furthermore, improved survival rates of premature infants and the high prevalence of lasting respiratory morbidities highlight the need for more comprehensive strategies to address both short-term and long-term respiratory complications. Thus, the Prematurity and Respiratory Outcomes Program (PROP) was formed to investigate multiple research hypotheses on the molecular mechanisms that contribute to respiratory disease risk of premature neonates over the first year of life. Specifically, PROP investigators hypothesized that in survivors of extreme prematurity to 36 weeks postmenstrual age (PMA), specific biologic, physiologic and clinical data obtained during the initial hospitalization will predict respiratory morbidity between discharge and 1 year corrected age. Participants: A total of 835 infants were enrolled.Design: PROP was a collaboratively developed multicenter prospective cohort study of very preterm infants from birth through the time of discharge from the NICU and up to one year corrected age.Clinical data included maternal and infant demographics, co-morbidities, and daily infant respiratory, nutritional, and medication data until discharge. These were prospectively collected from birth using medical record review and family interviews. After discharge, phone interviews were conducted with the infant's main caregiver at 3, 6, 9 and 12 months corrected age to assess domains of respiratory morbidity. At 6 and 12 months corrected age, a survey of environmental respiratory irritant exposures and an assessment for gastroesophageal reflux disease were also completed. A standardized physical exam was performed at 36-40 weeks PMA and again at one year corrected age. The exam focused on anthropometrics, vital signs, and respiratory system signs. At 34-41 weeks PMA and within one week of anticipated discharge based on physiologic stability, a set of non-invasive respiratory assessments were performed to assess physiologic biomarkers in infants that were not mechanically ventilated or receiving non-invasive positive pressure ventilation. Respiratory inductance plethysmography (RIP) was performed before and after inhaled albuterol to assess potential airway reactivity. During the RIP study, continuous pulse oximetry was performed during quiet sleep in order to analyze oxygen desaturations and apneas. Standardized oxygen requirement challenge tests were performed at about 36 weeks PMA, and at about 40 weeks PMA if the infant was still hospitalized and was not eligible for, or failed, the previous challenge. Failure was defined as SpO2 20 seconds at any point in the testing. Infants breathing ambient air or that passed the 36 week challenge test underwent a hypoxia challenge consisting of a 15-minute trial of FiO2 of 0.15. Failure was defined as SpO2 The primary outcome was respiratory morbidity, as measured by the presence or absence of substantial post-prematurity respiratory disease (PRD) up to one year corrected age. PRD was classified as a positive response in at least one of four morbidity domains during at least two separate parental interviews. The domains were respiratory medications, hospitalizations for cardiopulmonary cause, respiratory symptoms, and home technology dependence (oxygen, ventilator, or CPAP/BiPAP). Mortality from a respiratory cause was also incorporated.

  Study phs004117

• Gut microbiome profiles according to sex, body mass index and dietary fiber intake

  Findings from recent studies suggest that the community of microbes residing in the human body is important in disease etiology; however, it remains unclear whether personal factors modulate human microbial composition. Studies based on animal models indicate that differences in composition might be attributed to sex-mediated effects. We analyzed the relationship of sex, adiposity, and dietary fiber intake with gut microbial composition using fecal samples from human subjects. We explored the associations of these factors with metrics of community composition and specific taxon abundances. We found that men and women had significantly different microbial community composition and that women had reduced abundance of a major phylum. Adiposity was associated with gut microbiome composition and specifically in women but not in men. Fiber from fruits and vegetables and fiber from beans were each associated with increased abundance of specific bacterial taxa. These findings provide initial indications that sex, adiposity, and dietary fiber might play important roles in influencing the human gut microbiome. Better understanding of these factors may have significant implications for gastrointestinal health and disease prevention.

  Study phs000884

• National Heart, Lung, and Blood Institute (NHLBI) Heart Healthy Lenoir (HHL) Genomics Study

  The HHL genomics study uses a systems approach to develop models integrating clinical and genomic data. Previously we developed and tested an approach known as the SAMARA (Supporting A Multidisciplinary Approach to Research in Atherosclerosis) project that applied recent advances in biomedical and computational sciences at The University of North Carolina at Chapel Hill to develop a deeper understanding of human cardiovascular disease (CVD). The Heart-Healthy Lenoir Project expands these studies into the community, using this methodology to: 1) determine the prevalence of genomic risk signatures in high-risk community populations using genome-wide Single Nucleotide Polymorphism (SNP) analysis; 2) develop novel genomic models incorporating high-risk features in this population; and 3) determine whether genomic signatures can be used to predict responsiveness to interventions that underlie CVD disparities. DNA was obtained from participants enrolled in two of the HHL clinical trials, 1) Improving Care for Patients With High Blood Pressure (NCT01425515) or 2) Heart-Healthy Lenoir Lifestyle Study (NCT01433484). Participants could enroll in both trials concurrently.

  Study phs001471

• TGF-β signaling mediates microglial resilience to spatiotemporally restricted myelin degeneration

  Microglia survey and regulate central nervous system myelination during embryonic development and adult homeostasis. However, whether microglia-myelin interactions are spatiotemporally regulated remains unexplored. By examining spinal cord white matter tracts, we found that myelin degeneration was particularly prominent in the dorsal column (DC) during normal aging. This was accompanied by molecular and functional changes in DC microglia as well as an upregulation of TGF-β signaling. Disrupting TGF-β signaling in microglia led to unchecked microglial responses and myelin loss in the DC, accompanied by neurological deficits exacerbated with aging. snRNA-seq revealed the emergence of a TGF-β signaling-sensitive microglial subset and a disease-associated oligodendrocyte subset, both spatially restricted to the DC. We further discovered that microglia rely on a TGFβ autocrine mechanism to prevent damage of myelin in the DC. These findings demonstrate that TGF-β signaling is indispensable for maintaining microglial resilience to myelin degeneration in the DC during the aging process. This highlights a previously unresolved checkpoint mechanism of TGF-β signaling with regional specificity and spatially restricted microglia-oligodendrocyte interactions.

  Study EGAS50000001413

• Multi-focal genomic dissection of synchronous primary and metastatic tissue from de novo metastatic prostate cancer

  De novo metastatic prostate cancer is highly aggressive, but the paucity of routinely-collected tissue in this setting has hindered genomic stratification and jeopardizes precision oncology efforts. Here, we leveraged a rare study of surgical intervention in 43 de novo metastatic prostate cancers to assess somatic genotype across 607 synchronous primary and metastatic tissue foci plus circulating tumor DNA. Intra-prostate heterogeneity was pervasive and impacted clinically-relevant genes, resulting in frequent discordance between select primary-restricted foci and synchronous metastases. Additional complexity was driven in several instances by polyclonal metastatic seeding from the reservoir of phylogenetically-related primary populations. When simulating standard clinical practice relying on a single tissue focus, genomic heterogeneity plus highly variable per-sample tumor fraction caused false genotyping of dominant disease. However, in silico modeling demonstrated that analysis of multiple biopsy cores can rescue misassigned somatic genotypes. Our results define the relationship between synchronous treatment-naive primary and metastatic lesions in de novo metastatic prostate cancer and provide a framework for implementing genomics-guided patient management.

  Study EGAS00001006466