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.

Sensor networks for emergency response: challenges and opportunities

Abstract: Sensor networks, a new class of devices has the potential to revolutionize the capture, processing, and communication of critical data for use by first responders. CodeBlue integrates sensor nodes and other wireless devices into a disaster response setting and provides facilities for ad hoc network formation, resource naming and discovery, security, and in-network aggregation of sensor-produced data. We designed CodeBlue for rapidly changing, critical care environments. To test it, we developed two wireless vital sign monitors and a PDA-based triage application for first responders. Additionally, we developed MoteTrack, a robust radio frequency (RF)-based localization system, which lets rescuers determine their location within a building and track patients. Although much of our work on CodeBlue is preliminary, our initial experience with medical care sensor networks raised many exciting opportunities and challenges.

Soil fertility limits carbon sequestration by forest ecosystems in a CO 2 -enriched atmosphere

Abstract: Northern mid-latitude forests are a large terrestrial carbon sink. Ignoring nutrient limitations, large increases in carbon sequestration from carbon dioxide (CO2) fertilization are expected in these forests. Yet, forests are usually relegated to sites of moderate to poor fertility, where tree growth is often limited by nutrient supply, in particular nitrogen. Here we present evidence that estimates of increases in carbon sequestration of forests, which is expected to partially compensate for increasing CO2 in the atmosphere, are unduly optimistic. In two forest experiments on maturing pines exposed to elevated atmospheric CO2, the CO2-induced biomass carbon increment without added nutrients was undetectable at a nutritionally poor site, and the stimulation at a nutritionally moderate site was transient, stabilizing at a marginal gain after three years. However, a large synergistic gain from higher CO2 and nutrients was detected with nutrients added. This gain was even larger at the poor site (threefold higher than the expected additive effect) than at the moderate site (twofold higher). Thus, fertility can restrain the response of wood carbon sequestration to increased atmospheric CO2. Assessment of future carbon sequestration should consider the limitations imposed by soil fertility, as well as interactions with nitrogen deposition.

MYD88 L265P Somatic Mutation in Waldenström's Macroglobulinemia

Abstract: A b s t r ac t Background Waldenstrom’s macroglobulinemia is an incurable, IgM-secreting lymphoplasmacytic lymphoma (LPL). The underlying mutation in this disorder has not been delineated. Methods We performed whole-genome sequencing of bone marrow LPL cells in 30 patients with Waldenstrom’s macroglobulinemia, with paired normal-tissue and tumor-tissue sequencing in 10 patients. Sanger sequencing was used to validate the findings in samples from an expanded cohort of patients with LPL, those with other B-cell disorders that have some of the same features as LPL, and healthy donors. Results Among the patients with Waldenstrom’s macroglobulinemia, a somatic variant (T→C) in LPL cells was identified at position 38182641 at 3p22.2 in the samples from all 10 patients with paired tissue samples and in 17 of 20 samples from patients with unpaired samples. This variant predicted an amino acid change (L265P) in MYD88, a mutation that triggers IRAK-mediated NF-κB signaling. Sanger sequencing identified MYD88 L265P in tumor samples from 49 of 54 patients with Waldenstrom’s macroglobulinemia and in 3 of 3 patients with non–IgM-secreting LPL (91% of all patients with LPL). MYD88 L265P was absent in paired normal tissue samples from patients with Waldenstrom’s macroglobulinemia or non-IgM LPL and in B cells from healthy donors and was absent or rarely expressed in samples from patients with multiple myeloma, marginal-zone lymphoma, or IgM monoclonal gammopathy of unknown significance. Inhibition of MYD88 signaling reduced IκBα and NF-κB p65 phosphorylation, as well as NF-κB nuclear staining, in Waldenstrom’s macroglobulinemia cells expressing MYD88 L265P. Somatic variants in ARID1A in 5 of 30 patients (17%), leading to a premature stop or frameshift, were also identified and were associated with an increased disease burden. In addition, 2 of 3 patients with Waldenstrom’s macroglobulinemia who had wild-type MYD88 had somatic variants in MLL2. Conclusions MYD88 L265P is a commonly recurring mutation in patients with Waldenstrom’s macroglobulinemia that can be useful in differentiating Waldenstrom’s macroglobulinemia and non-IgM LPL from B-cell disorders that have some of the same features. (Funded by the Peter and Helen Bing Foundation and others.)