Patterns of dreissenid mussel invasions in western US lakes within an integrated gravity model framework.

Freshwater invasive species, such as the quagga mussel (Dreissena rostriformis bugensis), are causing over $1 billion USD annually in damages to water infrastructure, recreation, and the environment. Once established, quagga and other dreissenid mussels are extremely difficult to eradicate. Preventing the spread of these invasives is critical and of high management concern. Invasive dreissenid establishment is predicated upon both successful dispersal from a source and suitable habitat in the uninfested waterbody to which they are transported. Recreational boaters have become predominant dispersal vectors making it possible to forecast the risk of invasion of waterbodies for more targeted management and prevention. We developed an integrated mussel dispersal model that couples a constrained gravity model and habitat suitability model to forecast future invasions. The model simulates boater movement between lakes, the likelihood of boats transporting mussels, and the likelihood that those mussels survive in the environmental conditions of the new lake. Model output was most sensitive to changes in boater threshold, then buffer zones, while not as sensitive to changes in habitat suitability. From an initial infested source pool of 11 among 402 Western inland US lakes, we forecast additional lakes infested in several possible simulation scenarios. Constraining movement reduced connectivity between waterbodies with amplifying effects at different distance levels. This model can be used to determine waterbodies most at risk for dreissenid mussel invasion and to highlight the importance of multifactor integrated models in environmental management.

Earliest changes in the left ventricular transcriptome postmyocardial infarction.

We report a genome-wide survey of early responses of the mouse heart transcriptome to acute myocardial infarction (AMI). For three regions of the left ventricle (LV), namely, ischemic/infarcted tissue (IF), the surviving LV free wall (FW), and the interventricular septum (IVS), 36,899 transcripts were assayed at six time points from 15 min to 48 h post-AMI in both AMI and sham surgery mice. For each transcript, temporal expression patterns were systematically compared between AMI and sham groups, which identified 515 AMI-responsive genes in IF tissue, 35 in the FW, 7 in the IVS, with three genes induced in all three regions. Using the literature, we assigned functional annotations to all 519 nonredundant AMI-induced genes and present two testable models for central signaling pathways induced early post-AMI. First, the early induction of 15 genes involved in assembly and activation of the activator protein-1 (AP-1) family of transcription factors implicates AP-1 as a dominant regulator of earliest post-ischemic molecular events. Second, dramatic increases in transcripts for arginase 1 (ARG1), the enzymes of polyamine biosynthesis, and protein inhibitor of nitric oxide synthase (NOS) activity indicate that NO production may be regulated, in part, by inhibition of NOS and coordinate depletion of the NOS substrate, L: -arginine. ARG1: was the single-most highly induced transcript in the database (121-fold in IF region) and its induction in heart has not been previously reported.