153 resultados para Schlafly, Phyllis


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Oxygen minimum zones are expanding globally, and at present account for around 20-40% of oceanic nitrogen loss. Heterotrophic denitrification and anammox-anaerobic ammonium oxidation with nitrite-are responsible for most nitrogen loss in these low-oxygen waters. Anammox is particularly significant in the eastern tropical South Pacific, one of the largest oxygen minimum zones globally. However, the factors that regulate anammox-driven nitrogen loss have remained unclear. Here, we present a comprehensive nitrogen budget for the eastern tropical South Pacific oxygen minimum zone, using measurements of nutrient concentrations, experimentally determined rates of nitrogen transformation and a numerical model of export production. Anammox was the dominant mode of nitrogen loss at the time of sampling. Rates of anammox, and related nitrogen transformations, were greatest in the productive shelf waters, and tailed off with distance from the coast. Within the shelf region, anammox activity peaked in both upper and bottom waters. Overall, rates of nitrogen transformation, including anammox, were strongly correlated with the export of organic matter. We suggest that the sinking of organic matter, and thus the release of ammonium into the water column, together with benthic ammonium release, fuel nitrogen loss from oxygen minimum zones.

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The ability to identify, isolate, and transplant progenitor cells from solid tissues would greatly facilitate the treatment of diseases currently requiring whole organ transplantation. In this study, cell fractions enriched in candidate epithelial progenitor cells from the rat pancreas were isolated and transplanted into the liver of an inbred strain of Fischer rats. Using a dipeptidyl dipeptidase IV genetic marker system to follow the fate of transplanted cells in conjunction with albumin gene expression, we provide conclusive evidence that, after transplantation to the liver, epithelial progenitor cells from the pancreas differentiate into hepatocytes, express liver-specific proteins, and become fully integrated into the liver parenchymal structure. These studies demonstrate the presence of multipotent progenitor cells in the adult pancreas and establish a role for the liver microenvironment in the terminal differentiation of epithelial cells of foregut origin. They further suggest that such progenitor cells might be useful in studies of organ repopulation following acute or chronic liver injury.

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Estradiol protects against brain injury, neurodegeneration, and cognitive decline. Our previous work demonstrates that physiological levels of estradiol protect against stroke injury and that this protection may be mediated through receptor-dependent alterations of gene expression. In this report, we tested the hypothesis that estrogen receptors play a pivotal role in mediating neuroprotective actions of estradiol and dissected the potential biological roles of each estrogen receptor (ER) subtype, ERα and ERβ, in the injured brain. To investigate and delineate these mechanisms, we used ERα-knockout (ERαKO) and ERβ-knockout (ERβKO) mice in an animal model of stroke. We performed our studies by using a controlled endocrine paradigm, because endogenous levels of estradiol differ dramatically among ERαKO, ERβKO, and wild-type mice. We ovariectomized ERαKO, ERβKO, and the respective wild-type mice and implanted them with capsules filled with oil (vehicle) or a dose of 17β-estradiol that produces physiological hormone levels in serum. One week later, mice underwent ischemia. Our results demonstrate that deletion of ERα completely abolishes the protective actions of estradiol in all regions of the brain; whereas the ability of estradiol to protect against brain injury is totally preserved in the absence of ERβ. Thus, our results clearly establish that the ERα subtype is a critical mechanistic link in mediating the protective effects of physiological levels of estradiol in brain injury. Our discovery that ERα mediates protection of the brain carries far-reaching implications for the selective targeting of ERs in the treatment and prevention of neural dysfunction associated with normal aging or brain injury.

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Insect damage on fossil leaves from the Central Rocky Mountains, United States, documents the response of herbivores to changing regional climates and vegetation during the late Paleocene (humid, warm temperate to subtropical, predominantly deciduous), early Eocene (humid subtropical, mixed deciduous and evergreen), and middle Eocene (seasonally dry, subtropical, mixed deciduous and thick-leaved evergreen). During all three time periods, greater herbivory occurred on taxa considered to have short rather than long leaf life spans, consistent with studies in living forests that demonstrate the insect resistance of long-lived, thick leaves. Variance in herbivory frequency and diversity was highest during the middle Eocene, indicating the increased representation of two distinct herbivory syndromes: one for taxa with deciduous, palatable foliage, and the other for hosts with evergreen, thick-textured, small leaves characterized by elevated insect resistance. Leaf galling, which is negatively correlated with moisture today, apparently increased during the middle Eocene, whereas leaf mining decreased.

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The cores described in this report were taken on AMPHITRITE Expedition in Decenber 1963 - February 1964 by Scripps Institution of Oceanography from, the R/V Argo. A total of 148 cores were recovered and are available at Scripps for sampling and study. The coring sites, all in the tropical central Pacific. The AMPHITRITE cores are here briefly described to identify visually distinct units based on lithology, color, texture, or other characteristic unique to an interval of sediment. For determination of lithology, the slides prepared from samples of the cores were examined microscopically in conjuction with the visual examination.

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Vertical distributions of benthic denitrification and anammox rates within the sediment were estimated from slurry incubation experiments. Rates were used to calculate the contribution of anammox and denitrification to the total N-loss. Briefly, MUC sediment cores were sliced in 2 cm intervals and the sediment was diluted and incubated with degassed bottom water in a gas tight bag. After pre-incubating the bags for 2 h, 15N-labeled substrates were injected into the bags and the slurries were thoroughly mixed. Incubations were performed in the dark at in situ temperatures. The N2 isotope ratio (28N2, 29N2, and 30N2) was determined by gas chromatography-isotopic ratio mass spectrometry (VG Optima, Micromass) and calculated according to Kuypers et al. (2005) and Holtappels et al. (2011), respectively.Furthermore, total organic carbon and nitrogen concentrations were measured of core sediment layers corresponding to those used for rate measurements. Concentrations of organic carbon and nitrogen were determined by combustion/gas chromatography (Carlo Erba NA-1500 CNS analyzer) of dried sediment samples after acidification. The same sediment layer were also used to extract nucleic acids. The concentrations of the DNA in the samples were measured spectrophotometrically with a NanoDrop instrument (Thermo Fisher Scientific Inc.). The biomarker functional gene nirS, encoding the cd1-containing nitrite reductase, for both denitrifiers and marine anammox bacteria were quantified with real-time PCR, using the primers cd3aF/R3cd (5'-GTSAACGTSAAGGARACSGG-3' (Michotey et al., 2000)/5'-GASTTCGGRTGSGTCTTGA-3'; Throback et al., 2004) and Scnir372F/Scnir845R (5'-TGTAGCCAGCATTGTAGCGT-3'/5'-TCAAGCCAGACCCATTTGCT-3'; Lam et al., 2009).