Reduction of large vessel traffic improves water quality and alters fish habitat-use throughout a large river.

Rivers are increasingly used as superhighways for the continental-scale transportation of freight goods, but the ecological impact of large vessel traffic on river ecosystems is difficult to study. Recently, the temporary maintenance closure of lock and dam systems on the Illinois Waterway (USA) brought commercial vessel traffic to a halt along the river's length, offering a rare opportunity to study the response of the ecosystem before, during, and after an extended pause of this persistent anthropogenic disturbance. We observed improvements in main- and side-channel water quality and a redistribution of fish habitat-use during a months-long, near-complete reduction of large vessel traffic. Over 3600 water quality and 1300 fish community samples indicate that large vessel traffic reduction coincided with a 33 % reduction in turbidity as well as increased use of sampling strata near vessel navigation corridors by sound-sensitive and rheophilic fishes. Gizzard shad (Dorosoma cepedianum), the most abundant species in the system, also expanded their use of these 'impact' areas. Though inland waterway transport is an economically- and climate-friendly alternative to trucking and rail for the shipment of freight, our data suggest that intense vessel traffic may have profound physical and biological impacts across a large river. Monitoring and mitigation of ecological impacts of the ongoing expansion of inland waterway transport around the world will be critical to balancing large rivers as both useful navigation corridors and functional ecosystems.

Can data from disparate long-term fish monitoring programs be used to increase our understanding of regional and continental trends in large river assemblages?

Understanding trends in the diverse resources provided by large rivers will help balance tradeoffs among stakeholders and inform strategies to mitigate the effects of landscape scale stressors such as climate change and invasive species. Absent a cohesive coordinated effort to assess trends in important large river resources, a logical starting point is to assess our ability to draw inferences from existing efforts. In this paper, we use a common analytical framework to analyze data from five disparate fish monitoring programs to better understand the nature of spatial and temporal trends in large river fish assemblages. We evaluated data from programs that monitor fishes in the Colorado, Columbia, Illinois, Mississippi, and Tallapoosa rivers using non-metric dimensional scaling ordinations and associated tests to evaluate trends in fish assemblage structure and native fish biodiversity. Our results indicate that fish assemblages exhibited significant spatial and temporal trends in all five of the rivers. We also document native species diversity trends that were variable within and between rivers and generally more evident in rivers with higher species richness and programs of longer duration. We discuss shared and basin-specific landscape level stressors. Having a basic understanding of the nature and extent of trends in fish assemblages is a necessary first step towards understanding factors affecting biodiversity and fisheries in large rivers.

Mice expressing BMPR2R899X transgene in smooth muscle develop pulmonary vascular lesions.

Familial pulmonary arterial hypertension (PAH) is associated with mutations in bone morphogenetic protein type II receptor (BMPR2). Many of these mutations occur in the BMPR2 tail domain, leaving the SMAD functions intact. To determine the in vivo consequences of BMPR2 tail domain mutation, we created a smooth muscle-specific doxycycline-inducible BMPR2 mutation with an arginine to termination mutation at amino acid 899. When these SM22-rtTA x TetO(7)-BMPR2(R899X) mice had transgene induced for 9 wk, starting at 4 wk of age, they universally developed pulmonary vascular pruning as assessed by fluorescent microangiography. Approximately one-third of the time, the induced animals developed elevated right ventricular systolic pressures (RVSP), associated with extensive pruning, muscularization of small pulmonary vessels, and development of large structural pulmonary vascular changes. These lesions included large numbers of macrophages and T cells in their adventitial compartment as well as CD133-positive cells in the lumen. Small vessels filled with CD45-positive and sometimes CD3-positive cells were a common feature in all SM22-rtTA x TetO(7)-BMPR2(R899X) mice. Gene array experiments show changes in stress response, muscle organization and function, proliferation, and apoptosis and developmental pathways before RVSP increases. Our results show that the primary phenotypic result of BMPR2 tail domain mutation in smooth muscle is pulmonary vascular pruning leading to elevated RVSP, associated with early dysregulation in multiple pathways with clear relevance to PAH. This model should be useful to the research community in examining early molecular and physical events in the development of PAH and as a platform to validate potential treatments.

Modification of heat shock protein 90 by 4-hydroxynonenal in a rat model of chronic alcoholic liver disease.

Lipid peroxidation during oxidative stress leads to increased concentrations of thiol-reactive alpha,beta-unsaturated aldehyde, including 4-hydroxy-2-nonenal (4-HNE) and 4-oxo-2-nonenal (4-ONE). These aldehydes have a documented ability to disrupt protein function following adduct formation with specific residues. Therefore, to identify 4-HNE-modified proteins in a model of ethanol-induced oxidative stress, a proteomic approach was applied to liver fractions prepared from rats fed a combination high-fat/ethanol diet. The results revealed that essential 90-kDa heat shock protein (Hsp90) was consistently modified by 4-HNE in the alcohol-treated animals. In vitro chaperoning experiments using firefly luciferase as a client protein were then performed to assess the functional effect of 4-HNE modification on purified recombinant human Hsp90, modified with concentrations of this aldehyde ranging from 23 to 450 microM. Modification of Hsp90 with 4-ONE also led to significant inhibition of the chaperone. Because 4-HNE and 4-ONE react selectively with Cys, a thiol-specific mechanism of inhibition was suggested by these data. Therefore, thiol sensitivity was confirmed following treatment of Hsp90 with the specific thiol modifier N-ethylmaleimide, which resulted in more than 99% inactivation of the chaperone by concentrations as low as 6 microM (1:1 M ratio). Finally, tryptic digest of 4-HNE-modified Hsp90 followed by liquid chromatography/tandem mass spectrometry peptide analysis identified Cys 572 as a site for 4-HNE modification. The results presented here thus establish that 4-HNE consistently modifies Hsp90 in a rat model of alcohol-induced oxidative stress and that the chaperoning activity of this protein is subject to dysregulation through thiol modification.