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The Community Environmental Monitoring Program in the 21st Century: The Evolution of a Monitoring Network
This paper focuses on the evolution of the various operational aspects of the Community Environmental Monitoring Program (CEMP) network following the transfer of program administration from the U.S. Environmental Protection Agency (EPA) to the Desert Research Institute (DRI) of the Nevada System of Higher Education in 1999-2000. The CEMP consists of a network of 29 fixed radiation and weather monitoring stations located in Nevada, Utah, and California. Its mission is to involve stakeholders directly in monitoring for airborne radiological releases to the off site environment as a result of past or ongoing activities on the Nevada Test Site (NTS) and to make data as transparent and accessible to the general public as feasible. At its inception in 1981, the CEMP was a cooperative project of the U.S. Department of Energy (DOE), DRI, and EPA. In 1999-2000, technical administration of the CEMP transitioned from EPA to DRI. Concurrent with and subsequent to this transition, station and program operations underwent significant enhancements that furthered the mission of the program. These enhancements included the addition of a full suite of meteorological instrumentation, state-of-the-art electronic data collectors, on-site displays, and communications hardware. A public website was developed. Finally, the DRI developed a mobile monitoring station that can be operated entirely on solar power in conjunction with a deep-cell battery, and includes all meteorological sensors and a pressurized ion chamber for detecting background gamma radiation. Final station configurations have resulted in the creation of a platform that is well suited for use as an in-field multi-environment test-bed for prototype environmental sensors and in interfacing with other scientific and educational programs. Recent and near-future collaborators have included federal, state, and local agencies in both the government and private sectors. The CEMP also serves as a model for other programs wishing to involve stakeholders with a meaningful role in the process of monitoring and data collection
Antiinflammatory therapy with canakinumab for atherosclerotic disease
BACKGROUND: Experimental and clinical data suggest that reducing inflammation without affecting lipid levels may reduce the risk of cardiovascular disease. Yet, the inflammatory hypothesis of atherothrombosis has remained unproved. METHODS: We conducted a randomized, double-blind trial of canakinumab, a therapeutic monoclonal antibody targeting interleukin-1β, involving 10,061 patients with previous myocardial infarction and a high-sensitivity C-reactive protein level of 2 mg or more per liter. The trial compared three doses of canakinumab (50 mg, 150 mg, and 300 mg, administered subcutaneously every 3 months) with placebo. The primary efficacy end point was nonfatal myocardial infarction, nonfatal stroke, or cardiovascular death. RESULTS: At 48 months, the median reduction from baseline in the high-sensitivity C-reactive protein level was 26 percentage points greater in the group that received the 50-mg dose of canakinumab, 37 percentage points greater in the 150-mg group, and 41 percentage points greater in the 300-mg group than in the placebo group. Canakinumab did not reduce lipid levels from baseline. At a median follow-up of 3.7 years, the incidence rate for the primary end point was 4.50 events per 100 person-years in the placebo group, 4.11 events per 100 person-years in the 50-mg group, 3.86 events per 100 person-years in the 150-mg group, and 3.90 events per 100 person-years in the 300-mg group. The hazard ratios as compared with placebo were as follows: in the 50-mg group, 0.93 (95% confidence interval [CI], 0.80 to 1.07; P=0.30); in the 150-mg group, 0.85 (95% CI, 0.74 to 0.98; P=0.021); and in the 300-mg group, 0.86 (95% CI, 0.75 to 0.99; P=0.031). The 150-mg dose, but not the other doses, met the prespecified multiplicity-adjusted threshold for statistical significance for the primary end point and the secondary end point that additionally included hospitalization for unstable angina that led to urgent revascularization (hazard ratio vs. placebo, 0.83; 95% CI, 0.73 to 0.95; P=0.005). Canakinumab was associated with a higher incidence of fatal infection than was placebo. There was no significant difference in all-cause mortality (hazard ratio for all canakinumab doses vs. placebo, 0.94; 95% CI, 0.83 to 1.06; P=0.31). CONCLUSIONS: Antiinflammatory therapy targeting the interleukin-1β innate immunity pathway with canakinumab at a dose of 150 mg every 3 months led to a significantly lower rate of recurrent cardiovascular events than placebo, independent of lipid-level lowering. Copyright © 2017 Massachusetts Medical Society