Kaikki aineistot
Lisää
Abstract A comprehensive record of research data provenance is essential for the successful curation, management, and reuse of data over time. However, creating such detailed metadata can be onerous, and there are few structured methods for doing so. In this case study of data curation in support of geobiology research conducted at Yellowstone National Park, we describe a method of “Research Process Modeling” for documenting noncomputational data provenance in a structured yet flexible way. The method combines systems analysis techniques to model research activities, the World Wide Web Consortium Provenance (PROV) ontology to illustrate relationships between data products, and simple inventory methods to account for research processes and data products. It also supports collaborative data curation between information professionals and researchers, and is therefore a significant step toward producing more useable and interpretable research data. We demonstrate how this method describes data provenance more robustly than “flat” metadata alone and fills a critical gap in the documentation of provenance for field‐based and noncomputational workflows. We discuss potential applications of this approach to other research domains.
Long and short sleep duration are associated with elevated blood pressure (BP), possibly through effects on molecular pathways that influence neuroendocrine and vascular systems. To gain new insights into the genetic basis of sleep-related BP variation, we performed genome-wide gene by short or long sleep duration interaction analyses on four BP traits (systolic BP, diastolic BP, mean arterial pressure, and pulse pressure) across five ancestry groups in two stages using 2 degree of freedom (df) joint test followed by 1df test of interaction effects. Primary multi-ancestry analysis in 62,969 individuals in stage 1 identified three novel gene by sleep interactions that were replicated in an additional 59,296 individuals in stage 2 (stage 1 + 2 Pjoint < 5 × 10−8), including rs7955964 (FIGNL2/ANKRD33) that increases BP among long sleepers, and rs73493041 (SNORA26/C9orf170) and rs10406644 (KCTD15/LSM14A) that increase BP among short sleepers (Pint < 5 × 10−8). Secondary ancestry-specific analysis identified another novel gene by long sleep interaction at rs111887471 (TRPC3/KIAA1109) in individuals of African ancestry (Pint = 2 × 10−6). Combined stage 1 and 2 analyses additionally identified significant gene by long sleep interactions at 10 loci including MKLN1 and RGL3/ELAVL3 previously associated with BP, and significant gene by short sleep interactions at 10 loci including C2orf43 previously associated with BP (Pint < 10−3). 2df test also identified novel loci for BP after modeling sleep that has known functions in sleep–wake regulation, nervous and cardiometabolic systems. This study indicates that sleep and primary mechanisms regulating BP may interact to elevate BP level, suggesting novel insights into sleep-related BP regulation.