Denitrification by sulfur-oxidizing bacteria in a eutrophic lake

Understanding the mechanistic controls of microbial denitrification is of central importance to both environmental microbiology and ecosystem ecology. Loss of nitrate (NO3 −) is often attributed to carbon-driven (heterotrophic) denitrification. However, denitrification can also be coupled to sulfur (S) oxidation by chemolithoautotrophic bacteria. In the present study, we used an in situ stable isotope (15NO3 −) tracer addition in combination with molecular approaches to understand the contribution of sulfur-oxidizing bacteria to the reduction of NO3 − in a eutrophic lake. Samples were incubated across a total dissolved sulfide (H2S) gradient (2 to 95 μM) between the lower epilimnion and the upper hypolimnion. Denitrification rates were low at the top of the chemocline (4.5 m) but increased in the deeper waters (5.0 and 5.5 m), where H2S was abundant. Concomitant with increased denitrification at depths with high sulfide was the production of sulfate (SO4 2−), suggesting that the added NO3 − was used to oxidize H2S to SO4 2−. Alternative nitrate removal pathways, including dissimilatory nitrate reduction to ammonium (DNRA) and anaerobic ammonium oxidation (anammox), did not systematically change with depth and accounted for 1 to 15% of the overall nitrate loss. Quantitative PCR revealed that bacteria of the Sulfurimonas genus that are known denitrifiers increased in abundance in response to NO3 − addition in the treatments with higher H2S. Stoichiometric estimates suggest that H2S oxidation accounted for more than half of the denitrification at the depth with the highest sulfide concentration. The present study provides evidence that microbial coupling of S and nitrogen (N) cycling is likely to be important in eutrophic freshwater ecosystems

An Inversion Method for Measuring Beta in Large Redshift Surveys

A precision method for determining the value of Beta= Omega_m^{0.6}/b, where b is the galaxy bias parameter, is presented. In contrast to other existing techniques that focus on estimating this quantity by measuring distortions in the redshift space galaxy-galaxy correlation function or power spectrum, this method removes the distortions by reconstructing the real space density field and determining the value of Beta that results in a symmetric signal. To remove the distortions, the method modifies the amplitudes of a Fourier plane-wave expansion of the survey data parameterized by Beta. This technique is not dependent on the small-angle/plane-parallel approximation and can make full use of large redshift survey data. It has been tested using simulations with four different cosmologies and returns the value of Beta to +/- 0.031, over a factor of two improvement over existing techniques.Comment: 16 pages including 6 figures Submitted to The Astrophysical Journa

IL-4 sensitivity shapes the peripheral CD8\u3csup\u3e+\u3c/sup\u3e T cell pool and response to infection

Previous studies have revealed that a population of innate memory CD8+ T cells is generated in response to IL-4, first appearing in the thymus and bearing high expression levels of Eomesodermin (Eomes) but not T-bet. However, the antigen specificity and functional properties of these cells is poorly defined. In this study, we show that IL-4 regulates not only the frequency and function of innate memory CD8+ T cells, but also regulates Eomes expression levels and functional reactivity of naive CD8+ T cells. Lack of IL-4 responsiveness attenuates the capacity of CD8+ T cells to mount a robust response to lymphocytic choriomeningitis virus infection, with both quantitative and qualitative effects on effector and memory antigen-specific CD8+ T cells. Unexpectedly, we found that, although numerically rare, memory phenotype CD8+ T cells in IL-4Rα–deficient mice exhibited enhanced reactivity after in vitro and in vivo stimulation. Importantly, our data revealed that these effects of IL-4 exposure occur before, not during, infection. Together, these data show that IL-4 influences the entire peripheral CD8+ T cell pool, influencing expression of T-box transcription factors, functional reactivity, and the capacity to respond to infection. These findings indicate that IL-4, a canonical Th2 cell cytokine, can sometimes promote rather than impair Th1 cell–type immune responses

Ara h 6 Complements Ara h 2 as an Important Marker for IgE Reactivity to Peanut

The similarities of two major peanut allergens, Ara h 2 and Ara h 6, in molecular size, amino acid sequence, and structure have made it difficult to obtain natural Ara h 6 free of Ara h 2. The objectives of this study were to purify natural Ara h 6 that is essentially free of Ara h 2 and to compare its IgE reactivity and potency in histamine release assays to Ara h 2. SDS-PAGE of the highly purified allergen (\u3c0.01% Ara h 2) revealed a single 14.5kD band and the identity of Ara h 6 was confirmed by LC-MS/MS. Ara h 6 showed a higher seroprevalence in chimeric-IgE ELISA (n=54), but a weaker biological activity in basophil histamine release assays than Ara h 2. Purified Ara h 6 will be useful for diagnostic IgE antibody assays, as well as molecular and cellular studies to investigate the immunological mechanisms of peanut allergy

Ara h 6 Complements Ara h 2 as an Important Marker for IgE Reactivity to Peanut

The similarities of two major peanut allergens, Ara h 2 and Ara h 6, in molecular size, amino acid sequence, and structure have made it difficult to obtain natural Ara h 6 free of Ara h 2. The objectives of this study were to purify natural Ara h 6 that is essentially free of Ara h 2 and to compare its IgE reactivity and potency in histamine release assays to Ara h 2. SDS-PAGE of the highly purified allergen (\u3c0.01% Ara h 2) revealed a single 14.5kD band and the identity of Ara h 6 was confirmed by LC-MS/MS. Ara h 6 showed a higher seroprevalence in chimeric-IgE ELISA (n=54), but a weaker biological activity in basophil histamine release assays than Ara h 2. Purified Ara h 6 will be useful for diagnostic IgE antibody assays, as well as molecular and cellular studies to investigate the immunological mechanisms of peanut allergy