Boston University

About: Boston University is a education organization based out in Boston, Massachusetts, United States. It is known for research contribution in the topics: Population & Poison control. The organization has 48688 authors who have published 119622 publications receiving 6276020 citations. The organization is also known as: BU & Boston U.

Global forecasts of urban expansion to 2030 and direct impacts on biodiversity and carbon pools

Abstract: Urban land-cover change threatens biodiversity and affects ecosystem productivity through loss of habitat, biomass, and carbon storage. However, despite projections that world urban populations will increase to nearly 5 billion by 2030, little is known about future locations, magnitudes, and rates of urban expansion. Here we develop spatially explicit probabilistic forecasts of global urban land-cover change and explore the direct impacts on biodiversity hotspots and tropical carbon biomass. If current trends in population density continue and all areas with high probabilities of urban expansion undergo change, then by 2030, urban land cover will increase by 1.2 million km2, nearly tripling the global urban land area circa 2000. This increase would result in considerable loss of habitats in key biodiversity hotspots, with the highest rates of forecasted urban growth to take place in regions that were relatively undisturbed by urban development in 2000: the Eastern Afromontane, the Guinean Forests of West Africa, and the Western Ghats and Sri Lanka hotspots. Within the pan-tropics, loss in vegetation biomass from areas with high probability of urban expansion is estimated to be 1.38 PgC (0.05 PgC yr−1), equal to ∼5% of emissions from tropical deforestation and land-use change. Although urbanization is often considered a local issue, the aggregate global impacts of projected urban expansion will require significant policy changes to affect future growth trajectories to minimize global biodiversity and vegetation carbon losses.

Estimates of the prevalence of arthritis and selected musculoskeletal disorders in the United States

Abstract: Objective To provide a single source for the best available estimates of the national prevalence of arthritis in general and of selected musculoskeletal disorders (osteoarthritis, rheumatoid arthritis, juvenile rheumatoid arthritis, the spondylarthropathies, systemic lupus erythematosus, scleroderma, polymyalgia rheumatica/giant cell arteritis, gout, fibromyalgia, and low back pain). Methods The National Arthritis Data Workgroup reviewed data from available surveys, such as the National Health and Nutrition Examination Survey series. For overall national estimates, we used surveys based on representative samples. Because data based on national population samples are unavailable for most specific musculoskeletal conditions, we derived data from various smaller survey samples from defined populations. Prevalence estimates from these surveys were linked to 1990 US Bureau of the Census population data to calculate national estimates. We also estimated the expected frequency of arthritis in the year 2020. Results Current national estimates are provided, with important caveats regarding their interpretation, for self-reported arthritis and selected conditions. An estimated 15% (40 million) of Americans had some form or arthritis in 1995. By the year 2020, an estimated 18.2% (59.4 million) will be affected. Conclusion Given the limitations of the data on which they are based, this report provides the best available prevalence estimates for arthritis and other rheumatic conditions overall, and for selected musculoskeletal disorders, in the US population.

Fission and selective fusion govern mitochondrial segregation and elimination by autophagy

Abstract: Accumulation of depolarized mitochondria within β-cells has been associated with oxidative damage and development of diabetes. To determine the source and fate of depolarized mitochondria, individual mitochondria were photolabeled and tracked through fusion and fission. Mitochondria were found to go through frequent cycles of fusion and fission in a ‘kiss and run' pattern. Fission events often generated uneven daughter units: one daughter exhibited increased membrane potential (Δψm) and a high probability of subsequent fusion, while the other had decreased membrane potential and a reduced probability for a fusion event. Together, this pattern generated a subpopulation of non-fusing mitochondria that were found to have reduced Δψm and decreased levels of the fusion protein OPA1. Inhibition of the fission machinery through DRP1K38A or FIS1 RNAi decreased mitochondrial autophagy and resulted in the accumulation of oxidized mitochondrial proteins, reduced respiration and impaired insulin secretion. Pulse chase and arrest of autophagy at the pre-proteolysis stage reveal that before autophagy mitochondria lose Δψm and OPA1, and that overexpression of OPA1 decreases mitochondrial autophagy. Together, these findings suggest that fission followed by selective fusion segregates dysfunctional mitochondria and permits their removal by autophagy.