13 research outputs found
West Florida Shelf: A Natural Laboratory for the Study of Ocean Acidification
Declining oceanic pH and carbonate-ion concentrations are well-known consequences of increased atmospheric and surface-ocean partial pressure of carbon dioxide (pCO2). The possible subject of shifts in seawater carbonate chemistry on biocalcification and survival rates of marine organisms provides questions amenable to both experimental and field study (Kleypas and Langdon, 2006). To date, limited quantitative data exist with which to formalize and test hypotheses regarding such impacts, particularly in continental-shelf settings. The continental shelves of Florida provide an ideal natural laboratory in which to test latitudinal (and temperature and depth) shifts in habitat ranges of calcifying organisms. Both the east and west Florida shelves extend from warm temperate to subtropical latitudes; additionally, the west Florida shelf has very little siliciclastic influx to mask the carbonate production.
This study utilizes the natural laboratory of the west and southwest Florida shelf (fig 1.1) to examine the transition from foramol (predominately foraminifera and molluscan) carbonate sediments, characteristic of the west-central Florida shelf, to chlorozoan (algal and coral) sediments characteristic of the southwest Florida shelf.
The west Florida shelf is a mixed siliciclastic carbonate ramp that to the south transitions to the carbonate-dominated southwest Florida shelf (Enos, 1977; Brooks and others, 2003). The west Florida shelf is a distally steepened carbonate ramp that is ~250 kilometers (km) wide (Read, 1985). It is covered by a veneer of unconsolidated sediment consisting of mainly biogenic carbonate and quartz in the near shore, with subordinate amounts of phosphate. The sediment-distribution pattern is largely a function of proximity to source, with physical processes playing a minor role in distribution. The carbonate sand-and-gravel fraction is produced by organisms within the depositional basin of the west Florida shelf (Brooks and others, 2003). The southwest Florida shelf is a rimmed carbonate margin where organisms produce virtually all of the substrate; it also exhibits a greater sediment thickness as compared to the west Florida shelf (Enos, 1977).
Temperature, which is usually associated with latitude, plays a major role in locations of foramol versus chlorozoan assemblages, but other factors beyond latitude influence temperature on the west and southwest Florida shelves. The potential of cooler, deep-water upwelling and transport over the bottom waters of the shelf may have a significant role in the species assemblage at the sediment/water interface and ultimately on location of foramol versus chlorozoan production. Deep water transported onto and over the shelf may also have environmental ramifications beyond temperature by bringing in water of different chemistry
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Formoterol, a β-adrenoreceptor agonist, induces mitochondrial biogenesis and promotes cognitive recovery after traumatic brain injury
Traumatic brain injury (TBI) leads to acute necrosis at the site of injury followed by a sequence of secondary events lasting from hours to weeks and often years. Targeting mitochondrial impairment following TBI has shown improvements in brain mitochondrial bioenergetics and neuronal function. Recently formoterol, a highly selective β2-adrenoreceptor agonist, was found to induce mitochondrial biogenesis (MB) via Gβγ-Akt-eNOS-sGC pathway. Activation of MB is a novel approach that has been shown to restore mitochondrial function in several disease and injury models. We hypothesized that activation of MB as a target of formoterol after TBI would mitigate mitochondrial dysfunction, enhance neuronal function and improve behavioral outcomes. TBI-injured C57BL/6 male mice were injected (i.p.) with vehicle (normal saline) or formoterol (0.3 mg/kg) at 15 min, 8 h, 16 h, 24 h and then daily after controlled cortical impact (CCI) until euthanasia. After CCI, mitochondrial copy number and bioenergetic function were decreased in the ipsilateral cortex of the CCI-vehicle group. Compared to CCI-vehicle, cortical and hippocampal mitochondrial respiration rates as well as cortical mitochondrial DNA copy number were increased in the CCI-formoterol group. Mitochondrial Ca2+ buffering capacity in the hippocampus was higher in the CCI-formoterol group compared to CCI-vehicle group. Both assessments of cognitive performance, novel object recognition (NOR) and Morris water maze (MWM), decreased following CCI and were restored in the CCI-formoterol group. Although no changes were seen in the amount of cortical tissue spared between CCI-formoterol and CCI-vehicle groups, elevated levels of hippocampal neurons and improved white matter sparing in the corpus callosum were observed in CCI-formoterol group. Collectively, these results indicate that formoterol-mediated MB activation may be a potential therapeutic target to restore mitochondrial bioenergetics and promote functional recovery after TBI.Open access articleThis item from the UA Faculty Publications collection is made available by the University of Arizona with support from the University of Arizona Libraries. If you have questions, please contact us at [email protected]