Effects of increased pCO2 and temperature on the North Atlantic spring bloom. III. Dimethylsulfoniopropionate

The CLAW hypothesis argues that a negative feedback mechanism involving phytoplankton- derived dimethylsulfoniopropionate (DMSP) could mitigate increasing sea surface temperatures that result from global warming. DMSP is converted to the climatically active dimethylsulfide (DMS), which is transferred to the atmosphere and photochemically oxidized to sulfate aerosols, leading to increases in planetary albedo and cooling of the Earth’s atmosphere. A shipboard incubation experiment was conducted to investigate the effects of increased temperature and pCO2 on the algal community structure of the North Atlantic spring bloom and their subsequent impact on particulate and dissolved DMSP concentrations (DMSPp and DMSPd). Under ‘greenhouse’ conditions (elevated pCO2; 690 ppm) and elevated temperature (ambient + 4°C), coccolithophorid and pelagophyte abundances were significantly higher than under control conditions (390 ppm CO2 and ambient temperature). This shift in phytoplankton community structure also resulted in an increase in DMSPp concentrations and DMSPp:chl a ratios. There were also increases in DMSP-lyase activity and biomass-normalized DMSP-lyase activity under ‘greenhouse’ conditions. Concentrations of DMSPd decreased in the ‘greenhouse’ treatment relative to the control. This decline is thought to be partly due to changes in the microzooplankton community structure and decreased grazing pressure under ‘greenhouse’ conditions. The increases in DMSPp in the high temperature and greenhouse treatments support the CLAW hypothesis; the declines in DMSPd do not

Particulate iron dynamics during FeCycle in subantarctic waters southeast of New Zealand

The FeCycle experiment provided an SF6 labeled mesoscale patch of high-nitrate low-chlorophyll (HNLC) water in austral summer 2003. These labeled waters enabled a comparison of the inventory of particulate iron (PFe) in the 45-m-deep surface mixed layer with the concurrent downward export flux of PFe at depths of 80 and 120 m. The partitioning of PFe between four size fractions (0.2-2, 2-5, 5-20, and >20 μm) was assessed, and PFe was mainly found in the >20-μm size fraction throughout FeCycle. Estimates of the relative contribution of the biogenic and lithogenic components to PFe were based on an Al:Fe molar ratio (0.18) derived following analysis of dust/soil from the nearest source of aerosol Fe: the semi-arid regions of Australia. The lithogenic component dominated each of the four PFe size fractions, with medians ranging from 68 to 97% of PFe during the 10-day experiment. The Fe:C ratios for mixed-layer particles were ∼40 μmol/mol. PFe export was ∼300 nmol m-2 d-2 at 80 m depth representing a daily loss of ∼1% from the mixed-layer PFe inventory. There were pronounced increases in the Fe:C particulate ratios with depth, with a five-fold increase from the surface mixed layer to 80 m depth, consistent with scavenging of the remineralized Fe by sinking particles and concurrent solubilization and loss of particulate organic carbon. Significantly, the lithogenic fraction of the sinking PFe intercepted at both 80 in and 120 m was >40%; that is, there was an approximately twofold decrease in the proportion of lithogenic iron exported relative to that in the mixed-layer lithogenic iron inventory. This indicates that the transformation of lithogenic to biogenic PFe takes place in the mixed layer, prior to particles settling to depth. Moreover, the magnitude of lithogenic Fe supply from dust deposition into the waters southeast of New Zealand is comparable to that of the export of PFe from the mixed layer, suggesting that a large proportion of the deposited dust eventually exits the surface mixed layer as biogenic PFe in this HNLC region. Copyright 2006 by the American Geophysical Union.Peer Reviewe

Distribution of Pfiesteria piscicida cyst populations in sediments of the Delaware Inland Bays, USA

The toxic dinoflagellate, Pfiesteria piscicida, is a common constituent of the phytoplankton community in the Delaware Inland Bays, USA. In this study, molecular methods were used to investigate the distributions of benthic stages (cysts) of P. piscicida in sediment cores from the Delaware Inland Bays. Cores from 35 sites were partitioned into nephloid and anoxic layers and analyzed for P. piscicida by nested amplification of the 18S rDNA gene using P. piscicida-specific primers. The presence of inhibitory substances in the PCR reaction was evaluated by inclusion of an exogenous control DNA in the extraction buffer, thus eliminating samples that may yield false-negative results. Our results indicate a patchy distribution of P. piscicida in sediments of the Delaware Inland Bays, with distinct differences between each of the three bays. Overall, P. piscicida was found more frequently in sediments from Rehoboth Bay compared to Indian River and Little Assawoman Bays. These differences suggest (i) that populations of P. piscicida may be more widely distributed in Rehoboth Bay, (ii) that populations of P. piscicida may have been introduced to Rehoboth Bay at an earlier time, (iii) that past blooms of P. piscicida in Rehoboth Bay estuaries may have seeded the sediments with higher numbers of cysts, and/or (iv) that Rehoboth Bay sediments may be more resistant to clearing due to storm turbulence

Meteorological and Wave Measurements for Improving Meteorological and Air Quality Modeling

This is a report on the developed atmospheric boundary layer environmental observations program on offshore platforms in the Gulf of Mexico. The report provides information on the project objectives, deployment of instruments, data availability, data processing, data formats, preliminary data analyses, and recommendations

Amyotrophic lateral sclerosis-like superoxide dismutase 1 proteinopathy is associated with neuronal loss in Parkinson’s disease brain

Neuronal loss in numerous neurodegenerative disorders has been linked to protein aggregation and oxidative stress. Emerging data regarding overlapping proteinopathy in traditionally distinct neurodegenerative diseases suggest that disease-modifying treatments targeting these pathological features may exhibit efficacy across multiple disorders. Here, we describe proteinopathy distinct from classic synucleinopathy, predominantly comprised of the anti-oxidant enzyme superoxide dismutase-1 (SOD1), in the Parkinson’s disease brain. Significant expression of this pathology closely reflected the regional pattern of neuronal loss. The protein composition and non-amyloid macrostructure of these novel aggregates closely resembles that of neurotoxic SOD1 deposits in SOD1-associated familial amyotrophic lateral sclerosis (fALS). Consistent with the hypothesis that deposition of protein aggregates in neurodegenerative disorders reflects upstream dysfunction, we demonstrated that SOD1 in the Parkinson’s disease brain exhibits evidence of misfolding and metal deficiency, similar to that seen in mutant SOD1 in fALS. Our data suggest common mechanisms of toxic SOD1 aggregation in both disorders and a potential role for SOD1 dysfunction in neuronal loss in the Parkinson’s disease brain. This shared restricted proteinopathy highlights the potential translation of therapeutic approaches targeting SOD1 toxicity, already in clinical trials for ALS, into disease-modifying treatments for Parkinson’s disease