The eBird enterprise : an integrated approach to development and application of citizen science

Citizen-science projects engage volunteers to gather or process data to address scientific questions. But citizen-science projects vary in their ability to contribute usefully for science, conservation, or public policy. eBird has evolved from a basic citizen-science project into a collective enterprise, taking a novel approach to citizen science by developing cooperative partnerships among experts in a wide range of fields: population and distributions, conservation biologists, quantitative ecologists, statisticians, computer scientists, GIS and informatics specialists, application developers, and data administrators. The goal is to increase data quantity through participant recruitment and engagement, but also to quantify and control for data quality issues such as observer variability, imperfect detection of species, and both spatial and temporal bias in data collection. Advances at the interface among ecology, statistics, and computer science allow us to create new species distribution models that provide accurate estimates across broad spatial and temporal scales with extremely detailed resolution. eBird data are openly available and used by a broad spectrum of students, teachers, scientists, NGOs, government agencies, land managers, and policy makers. Feedback from this broad data use community helps identify development priorities. As a result, eBird has become a major source of biodiversity data, increasing our knowledge of the dynamics of species distributions, and having a direct impact on the conservation of birds and their habitats

Epithelial adhesion molecules can inhibit HIV-1–specific CD8+ T-cell functions

Under persistent antigenic stimulation, virus-specific CD8+ T cells become increasingly dysfunctional and up-regulate several inhibitory molecules such as killer lectin-like receptor G1 (KLRG1). Here, we demonstrate that HIV-1 antigen-specific T cells from subjects with chronic-progressive HIV-1 infection have significantly elevated KLRG1 expression (P < .001); show abnormal distribution of E-cadherin, the natural ligand of KLRG1, in the intestinal mucosa; and have elevated levels of systemic soluble E-cadherin (sE-cadherin) that significantly correlate with HIV-1 viral load (R = 0.7, P = .004). We furthermore demonstrate that in the presence of sE-cadherin, KLRG1hi HIV-1–specific CD8+ T cells are impaired in their ability to respond by cytokine secretion on antigenic stimulation (P = .002) and to inhibit viral replication (P = .03) in vitro. Thus, these data suggest a critical mechanism by which the disruption of the intestinal epithelium associated with HIV-1 leads to increased systemic levels of sE-cadherin, which inhibits the effector functions of KLRG1hi-expressing HIV-1–specific CD8+ T cells systemically