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The Mississippi River is one of the world's 10 largest rivers, with average freshwater discharge into the northern Gulf of Mexico (GOM) of 380km(3) year(-1). In the northern GOM, anthropogenic nitrogen is primarily derived from agricultural fertilizer and delivered via the Mississippi River. The general consensus is that hypoxia in the northern Gulf of Mexico is caused primarily by algal production stimulated by excess nitrogen delivered from the Mississippi-Atchafalaya River Basin and seasonal vertical stratification of incoming stream flow and Gulf waters, which restricts replenishment of oxygen from the atmosphere. In this paper, we review the controversial aspects of the largely nutrient-centric view of the hypoxic region, and introduce the role of non-riverine organic matter inputs as other oxygen-consuming mechanisms. Similarly, we discuss non-nutrient physically-controlled impacts of freshwater stratification as an alternative mechanism for controlling in part, the seasonality of hypoxia. We then explore why hypoxia in this dynamic river-dominated margin (RiOMar) is not comparable to many of the other traditional estuarine systems (e.g., Chesapeake Bay, Baltic Sea, and Long Island Sound). The presence of mobile muds and the proximity of the Mississippi Canyon are discussed as possible reasons for the amelioration of hypoxia (e.g., healthy fisheries) in this region. The most recent prediction of hypoxia area for 2009, using the current nutrient-centric models, failed due to the limited scope of these simple models and the complexity of this system. Predictive models should not be the main driver for management decisions. We postulate that a better management plan for this region can only be reached through a more comprehensive understanding of this RiOMar system-not just more information on river fluxes (e.g., nutrients) and coastal hypoxia monitoring programs.
Assuntos
Oxigênio/química , Água do Mar/química , EcossistemaRESUMO
Observations of neutral-current nu interactions on deuterium in the Sudbury Neutrino Observatory are reported. Using the neutral current (NC), elastic scattering, and charged current reactions and assuming the standard 8B shape, the nu(e) component of the 8B solar flux is phis(e) = 1.76(+0.05)(-0.05)(stat)(+0.09)(-0.09)(syst) x 10(6) cm(-2) s(-1) for a kinetic energy threshold of 5 MeV. The non-nu(e) component is phi(mu)(tau) = 3.41(+0.45)(-0.45)(stat)(+0.48)(-0.45)(syst) x 10(6) cm(-2) s(-1), 5.3sigma greater than zero, providing strong evidence for solar nu(e) flavor transformation. The total flux measured with the NC reaction is phi(NC) = 5.09(+0.44)(-0.43)(stat)(+0.46)(-0.43)(syst) x 10(6) cm(-2) s(-1), consistent with solar models.
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The Sudbury Neutrino Observatory (SNO) has measured day and night solar neutrino energy spectra and rates. For charged current events, assuming an undistorted 8B spectrum, the night minus day rate is 14.0%+/-6.3%(+1.5%)(-1.4%) of the average rate. If the total flux of active neutrinos is additionally constrained to have no asymmetry, the nu(e) asymmetry is found to be 7.0%+/-4.9%(+1.3%)(-1.2%). A global solar neutrino analysis in terms of matter-enhanced oscillations of two active flavors strongly favors the large mixing angle solution.
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Solar neutrinos from (8)B decay have been detected at the Sudbury Neutrino Observatory via the charged current (CC) reaction on deuterium and the elastic scattering (ES) of electrons. The flux of nu(e)'s is measured by the CC reaction rate to be straight phi(CC)(nu(e)) = 1.75 +/- 0.07(stat)(+0.12)(-0.11)(syst) +/- 0.05(theor) x 10(6) cm(-2) s(-1). Comparison of straight phi(CC)(nu(e)) to the Super-Kamiokande Collaboration's precision value of the flux inferred from the ES reaction yields a 3.3 sigma difference, assuming the systematic uncertainties are normally distributed, providing evidence of an active non- nu(e) component in the solar flux. The total flux of active 8B neutrinos is determined to be 5.44+/-0.99 x 10(6) cm(-2) s(-1).
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We report two group B Rho(D)-positive bone marrow transplant recipients who had sudden onset of massive intravascular hemolysis following the use of intravenous immunoglobulin (i.v. Ig). The first case developed chills and hypotension followed by hemoglobinuria with the first infusion of i.v. Ig. More severe symptoms occurred when infusion was reattempted. The second case developed hemoglobinuria without other symptomatology. In both patients, direct and indirect antiglobulin tests became positive following the use of i.v. Ig. Sera and eluates demonstrated IgG anti-B. Samples of i.v. Ig received by both patients contained both anti-B and anti-A and were incompatible with patients' red blood cells. These serologic findings indicate acute hemolysis secondary to the presence of IgG anti-B in i.v. Ig preparations.