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James B. Brown

Researcher at Lawrence Berkeley National Laboratory

Publications -  112
Citations -  25042

James B. Brown is an academic researcher from Lawrence Berkeley National Laboratory. The author has contributed to research in topics: Gene & Genome. The author has an hindex of 39, co-authored 110 publications receiving 22484 citations. Previous affiliations of James B. Brown include University of California, Berkeley & University of Alberta.

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Exploiting regulatory heterogeneity to systematically identify enhancers with high accuracy

TL;DR: It is shown that two classes of enhancer are active during early Drosophila embryogenesis and that by focusing on a single, relatively homogeneous class of elements, over 98% prediction accuracy can be achieved in a balanced, completely held-out test set.
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*-DCC: A platform to collect, annotate, and explore a large variety of sequencing experiments.

TL;DR: An annotation structure that captures the overall experimental design as well as the relevant details of the steps from the biological sample to the library preparation, the sequencing procedure, and the sequencing and processed files is developed and implemented in a user-hosted web platform.
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The Time Machine framework: monitoring and prediction of biodiversity loss.

TL;DR: In this article, the authors propose a framework to identify the causes of ecosystem function loss and forecast the future of ecosystem services under different climate and pollution scenarios, and illustrate the framework by applying it to watersheds, and provide system-level approaches that enable natural capital restoration by associating multidecadal biodiversity changes to chemical pollution.
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Endothelial activation is associated with intestinal epithelial injury, systemic inflammation and treatment regimen in children living with vertically acquired HIV-1 infection

TL;DR: Premature development of cardiovascular disease in children living with HIV‐1 (CLWH) may be associated with compromised gut barrier function, microbial translocation, immune activation, systemic inflammation and endothelial activation, and markers of these pathways may provide insights into pathogenesis of atherosclerotic disease in CLWH.