A preliminary assessment of water partitioning and ecohydrological coupling in northern headwaters using stable isotopes and conceptual runoff models

Funded by European Research Council ERC. Grant Number: GA 335910 VEWA Swedish Science Foundation (SITES) Future Forest Formas (ForWater) SKB the Kempe foundation Environment Canada the Garfield Weston Foundation the Natural Sciences and Engineering Research Council of Canada (NSERC) the Northwest Territories Cumulative Impacts Monitoring ProgramPeer reviewedPublisher PD

Technology Readiness Level Assessment Process as Applied to NASA Earth Science Missions

Technology assessments of fourteen science instruments were conducted within NASA using the NASA Technology Readiness Level (TRL) Metric. The instruments were part of three NASA Earth Science Decadal Survey missions in pre-formulation. The Earth Systematic Missions Program (ESMP) Systems Engineering Working Group (SEWG), composed of members of three NASA Centers, provided a newly modified electronic workbook to be completed, with instructions. Each instrument development team performed an internal assessment of its technology status, prepared an overview of its instrument, and completed the workbook with the results of its assessment. A team from the ESMP SEWG met with each instrument team and provided feedback. The instrument teams then reported through the Program Scientist for their respective missions to NASA's Earth Science Division (ESD) on technology readiness, taking the SEWG input into account. The instruments were found to have a range of TRL from 4 to 7. Lessons Learned are presented; however, due to the competition-sensitive nature of the assessments, the results for specific missions are not presented. The assessments were generally successful, and produced useful results for the agency. The SEWG team identified a number of potential improvements to the process. Particular focus was on ensuring traceability to guiding NASA documents, including the NASA Systems Engineering Handbook. The TRL Workbook has been substantially modified, and the revised workbook is described

The essential value of long-term experimental data for hydrology and water management

We would like to thank the European Research Council ERC for funding the VeWa project and most of Tetzlaff's time (project GA 335910 VeWa). No data were used in producing this manuscript.Peer reviewedPublisher PD

Inhibition of inducible nitric oxide synthase limits nitric oxide production and experimental aneurysm expansion

AbstractPurpose: Nitric oxide (NO), frequently cited for its protective role, can also generate toxic metabolites known to degrade elastin. Both abdominal aortic aneurysms (AAAs) and inducible nitric oxide synthase (iNOS) are associated with inflammatory states, yet the relationship between NO production by iNOS and AAA development is unknown. The current study examines iNOS expression, NO production, and the effects of selective inhibition of iNOS by aminoguanidine in experimental AAA. Methods: An intra-aortic elastase infusion model was used. Control rats received intra-aortic saline infusion and postoperative intraperitoneal saline injections (Group 1). In the remaining groups, intra-aortic elastase infusion was used to induce aneurysm formation. These rats were treated with intraperitoneal injections of saline postoperatively (Group 2), aminoguanidine postoperatively (Group 3), or aminoguanidine preoperatively and postoperatively (Group 4). Aortic diameter and plasma nitrite/nitrate levels were measured on the day of surgery and postoperative day 7. Aortas were harvested for biochemical and histologic analysis on postoperative day 7. Results: Infusion of elastase produced AAAs (P <.001) with significant production of iNOS (P <.05) and nitrite/nitrate (P <.003) compared with controls. Selective inhibition of iNOS with aminoguanidine in elastase-infused aortas significantly reduced aneurysm size (P <.01) compared with elastase infusion alone. Aminoguanidine-treated rats displayed suppression of iNOS expression and plasma nitrite/nitrate production not significantly different from the control group. Histologic evaluation revealed equivalent inflammatory infiltrates in elastase-infused groups. Conclusion: Expression of iNOS is induced and plasma nitrite/nitrate levels are increased in experimental AAA. Inhibition of iNOS limits NO production and iNOS expression, resulting in smaller aneurysm size. NO production by iNOS plays an important role with detrimental effects during experimental aneurysm development. (J Vasc Surg 2001;33:579-86.

Stable isotopes of water reveal differences in plant – soil water relationships across northern environments

Funding Information: We thank the European Research Council ERC for funding (VeWa project GA 335910). Contributions from CS were supported by the Leverhulme Trust through the ISO-LAND project (RPG 2018 375). Support for MJK and JPM were provided by the US National Science Foundation (EAR0842367) and Boise State University. We thank Dr. Samantha Evans for technical support. Thanks to the Dorset Environmental Science Centre for provision of meteorological data. The work conducted in Krycklan was partly financed by SITES (VR) and the KAW Branch-Point project. We would like to acknowledge Dr. Nadine Shatilla for collection of the Wolf Creek samples and the Global Water Futures program for financial support. We also would like to sincerely thank Jeff McDonnell for his support throughout the VeWa project and all participants in the different VeWa workshops esp. Tanya Doody and Marco Maneta for their invaluable input into the discussions.Peer reviewedPublisher PD

Simvastatin suppresses experimental aortic aneurysm expansion

ObjectiveAbdominal aortic aneurysm (AAA) formation is a result of inflammation and extracellular matrix (ECM) remodeling mediated by matrix metalloproteinases (MMPs). Hydroxymethylglutaryl-coenzyme A inhibitors (statins), although clinically used as lipid-lowering agents, have also been demonstrated to have anti-inflammatory effects. This study was designed to determine whether the hydroxymethylglutaryl-coenzyme A inhibitor simvastatin suppresses aneurysm formation in an elastase-induced rat AAA model.MethodsAneurysms were created in adult male Wistar rats by infusion of elastase into isolated infrarenal aortic segments. The rats were randomized to receive either simvastatin (n = 17) or placebo (n = 17) by gastric lavage daily starting the day before surgery. The rats were euthanized and the infrarenal aortas harvested on postoperative day 7. Aortic diameters were measured before infusion, immediately after infusion, and at the time of harvesting. Protein expression was measured by immunoblot analysis. Gene expression profiling using Affymetrix U34A rat genome chips was performed to identify changes in gene expression caused by simvastatin treatment.ResultsMean aneurysm diameter was significantly less in the simvastatin treatment group compared with controls (3.4 ± 0.08 mm vs 4.3 ± 0.19 mm; P = .0001). MMP-9 and nuclear factor-κB protein levels were decreased in the aortas of simvastatin-treated animals. Gene microarray analysis revealed 315 genes with statistically significant changes in expression (P < .05) in the simvastatin group. Genes related to inflammation, ECM remodeling, and oxidative stress function were downregulated. These included genes for interleukin 1, interleukin 4, inducible nitric oxide synthase, P-selectin, platelet-derived growth factor α, tumor necrosis factor, and several chemokines.ConclusionsSimvastatin significantly suppresses experimental aneurysm expansion and reduces protein levels of MMP-9 and nuclear factor-κB. Gene array analysis provides evidence that several mediators of inflammation, matrix remodeling, and oxidative stress are downregulated by simvastatin treatment. This suggests that simvastatin inhibits AAA formation by blocking the expression of certain proinflammatory genes. Simvastatin may be useful as an adjuvant therapy to suppress the growth of small aneurysms.Clinical RelevanceHuman aortic aneurysms are characterized histologically by an inflammatory infiltrate with severe proteolytic destruction. Statins, although used clinically as lipid-lowering agents, have been shown to have anti-inflammatory effects. Simvastatin reduced experimental aneurysm size in this study. It seems that this reduction is mediated by interfering with multiple pathways, including oxidative stress, inflammation, and ECM and matrix remodeling. Further study into the effect of statins in reducing the growth of AAAs in patients is warranted