Ecosystem effects of a tropical cyclone on a network of lakes in northeastern North America.

Here we document the regional effects of Tropical Cyclone Irene on thermal structure and ecosystem metabolism in nine lakes and reservoirs in northeastern North America using a network of high-frequency, in situ, automated sensors. Thermal stability declined within hours in all systems following passage of Irene, and the magnitude of change was related to the volume of water falling on the lake and catchment relative to lake volume. Across systems, temperature change predicted the change in primary production, but changes in mixed-layer thickness did not affect metabolism. Instead, respiration became a driver of ecosystem metabolism that was decoupled from in-lake primary production, likely due to addition of terrestrially derived carbon. Regionally, energetic disturbance of thermal structure was shorter-lived than disturbance from inflows of terrestrial materials. Given predicted regional increases in intense rain events with climate change, the magnitude and longevity of ecological impacts of these storms will be greater in systems with large catchments relative to lake volume, particularly when significant material is available for transport from the catchment. This case illustrates the power of automated sensor networks and associated human networks in assessing both system response and the characteristics that mediate physical and ecological responses to extreme events.

Acute Response of the Hippocampal Transcriptome Following Mild Traumatic Brain Injury After Controlled Cortical Impact in the Rat.

We have previously demonstrated that mild controlled cortical impact (mCCI) injury to rat cortex causes indirect, concussive injury to underlying hippocampus and other brain regions, providing a reproducible model for mild traumatic brain injury (mTBI) and its neurochemical, synaptic, and behavioral sequelae. Here, we extend a preliminary gene expression study of the hippocampus-specific events occurring after mCCI and identify 193 transcripts significantly upregulated, and 21 transcripts significantly downregulated, 24 h after mCCI. Fifty-three percent of genes altered by mCCI within 24 h of injury are predicted to be expressed only in the non-neuronal/glial cellular compartment, with only 13% predicted to be expressed only in neurons. The set of upregulated genes following mCCI was interrogated using Ingenuity Pathway Analysis (IPA) augmented with manual curation of the literature (190 transcripts accepted for analysis), revealing a core group of 15 first messengers, mostly inflammatory cytokines, predicted to account for >99% of the transcript upregulation occurring 24 h after mCCI. Convergent analysis of predicted transcription factors (TFs) regulating the mCCI target genes, carried out in IPA relative to the entire Affymetrix-curated transcriptome, revealed a high concordance with TFs regulated by the cohort of 15 cytokines/cytokine-like messengers independently accounting for upregulation of the mCCI transcript cohort. TFs predicted to regulate transcription of the 193-gene mCCI cohort also displayed a high degree of overlap with TFs predicted to regulate glia-, rather than neuron-specific genes in cortical tissue. We conclude that mCCI predominantly affects transcription of non-neuronal genes within the first 24 h after insult. This finding suggests that early non-neuronal events trigger later permanent neuronal changes after mTBI, and that early intervention after mTBI could potentially affect the neurochemical cascade leading to later reported synaptic and behavioral dysfunction.