High resolution fossil fuel combustion CO2 emission fluxes for the United States.

Quantification of fossil fuel CO2 emissions at fine space and time resolution is emerging as a critical need in carbon cycle and climate change research. As atmospheric CO2 measurements expand with the advent of a dedicated remote sensing platform and denser in situ measurements, the ability to close the carbon budget at spatial scales of approximately 100 km2 and daily time scales requires fossil fuel CO2 inventories at commensurate resolution. Additionally, the growing interest in U.S. climate change policy measures are best served by emissions that are tied to the driving processes in space and time. Here we introduce a high resolution data product (the "Vulcan" inventory: www.purdue.edu/eas/carbon/vulcan/) that has quantified fossil fuel CO2 emissions for the contiguous U.S. at spatial scales less than 100 km2 and temporal scales as small as hours. This data product completed for the year 2002, includes detail on combustion technology and 48 fuel types through all sectors of the U.S. economy. The Vulcan inventory is built from the decades of local/regional air pollution monitoring and complements these data with census, traffic, and digital road data sets. The Vulcan inventory shows excellent agreement with national-level Department of Energy inventories, despite the different approach taken by the DOE to quantify U.S. fossil fuel CO2 emissions. Comparison to the global 1degree x 1 degree fossil fuel CO2 inventory, used widely by the carbon cycle and climate change community prior to the construction of the Vulcan inventory, highlights the space/time biases inherent in the population-based approach.

Treatment of chronic nonhealing leg ulceration with gaseous nitric oxide: a case study.

BACKGROUND: Despite the best clinical practice, chronic nonhealing ulcers of the lower extremities present a significant challenge. Nitric oxide (NO) has been shown to play a significant role in biological functions including wound healing and as an antimicrobial agent in nonspecific immune response. OBJECTIVE: Our goal was to study the effect of gaseous NO (gNO) administered directly to a two-year-old nonhealing chronic venous ulcer in a 55-year-old male presenting with a 30-year history of severe venous disease. METHODS: gNO (200 ppm) was applied to the lower extremity using a delivery system connected to a "single patient use" plastic boot, at 1.0 L/min. RESULTS: The patient received an average of 8.1-h treatments for 14 consecutive nights. On day 0 the wound was malodorous and covered by bacterial biofilm with little healthy granulation tissue present. Following 3 days of gNO treatment, healthy granulation tissue was noted with absence of malodorous odor. At day 14, the ulcer was significantly reduced in size (p = 0.014) and almost completely reepithelialized. Day 10 post-treatment did not reveal any deterioration in healing. Six weeks later, the wound was 90% healed. At 26 weeks post gNO discontinuation, the ulcer was completely healed. CONCLUSIONS: This single case study demonstrated that gNO as a topical agent was well tolerated by the patient without any report of discomfort or side effect. The result of wound healing was very promising and warrants future exploration.

The slow axonal transport of the microtubule-associated protein tau and the transport rates of different isoforms and mutants in cultured neurons.

We demonstrate that the microtubule-associated protein tau, in the form of enhanced green fluorescent protein (EGFP) tau, is transported along axons of neurons in culture in the slow component of axonal transport with a speed comparable with that previously measured in vivo. It was demonstrated that the EGFP tag has no effect on transport characteristics, and the methodology enables slow transport rates of individual tau isoforms and tau mutants to be measured. We also expressed EGFP-tagged tau isoforms containing either three or four C-terminal repeats and zero or two N-terminal inserts in cultured neurons. No significant differences were found in the average rate of slow transport of the wild-type tau isoforms, suggesting that the exon 10 C-terminal repeat or the N-terminal inserts do not contain regions that play a significant regulatory role in axonal transport. Similarly, we found that missense mutations in tau have no noticeable effect on the rate of transport; hence their ability to cause neurodegeneration is by another mechanism other than that affecting the overall slow axonal transport of tau.