Eocene calcareous nannofossils in DSDP Holes 95-612 and 95-613

Lower Eocene calcareous nannofossil limestone cored at DSDP Site 612 on the middle slope off New Jersey represents an almost complete biostratigraphic sequence; only the lowest biozone (CP9a; NP10*) was not recovered. The thickness of the strata (198 m), the good preservation of the nannofossils, and the lack of long hiatuses justify the acceptance of this section as a lower Eocene reference for the western North Atlantic margin. The widely recognized and very similar nannofossil zonations of Martini (NP zones) and Bukry-Okada (CP zones) are emended slightly to make their lower Eocene biozones coeval; in addition, five new subzones are erected that subdivide zones CP10 and CPU (NP12 and NP13). Established biozone names are retained as they are altered little in concept, but alphanumeric code systems are changed somewhat by appending an asterisk (*) to identify zones that are emended. Zone CP10* (NP12*) is divided into two parts, the Lophodolithus nascens Subzone (CP10*a; NP12*a) and the Helicosphaera seminulum Subzone (CP10*b; NP12*b). Zone CPU* (NP13*) is divided into three parts, the Helicosphaera lophota Subzone (CP11*a; NP13*a), the Cyclicargolithuspseudogammation Subzone (CP11*b; NP13*b), and the Rhabdosphaera tenuis Subzone (CP11*c; NP13*c). At Site 612, a time-depth curve based on nannofossil datums dated in previous studies reveals a smoothly declining sediment accumulation rate, from 4.9 cm/10**3yr in CP10* (NP12*) to 2.8 cm/103 yr. in CP12* (NP14*). The ages of first-occurrence datums not previously dated are approximated by projection onto this timedepth curve and are as follows: Helicosphaera seminulum, 55.0 Ma; Helicosphaera lophota, 54.5 Ma; Cyclicargolithus pseudogammation, 53.7 Ma; Rhabdosphaera tenuis, 52.6 Ma; and Rhabdosphaera inflata, 50.2 Ma. At nearby Site 613 on the upper rise, strata of similar age, 139 m thick, contain an unconformity representing Subzone CPll*b (NP13*b) and a hiatus of approximately 1.1 m.y. duration. The sediment accumulation rate in the lower part of this section (9.7 cm/10**3yr.) is twice that observed for equivalent strata at Site 612. The hiatus and the heightened sediment accumulation rate at Site 613 probably represent the effects of episodic mass wasting on the early Eocene continental slope and rise.

Distribution of biological, anthropogenic, and volcanic constituents in the San Francisco Bay Coastal System

Although conventional sediment parameters (mean grain size, sorting, and skewness) and provenance have typically been used to infer sediment transport pathways, most freshwater, brackish, and marine environments are also characterized by abundant sediment constituents of biological, and possibly anthropogenic and volcanic, origin that can provide additional insight into local sedimentary processes. The biota will be spatially distributed according to its response to environmental parameters such as water temperature, salinity, dissolved oxygen, organic carbon content, grain size, and intensity of currents and tidal flow, whereas the presence of anthropogenic and volcanic constituents will reflect proximity to source areas and whether they are fluvially- or aerially-transported. Because each of these constituents have a unique environmental signature, they are a more precise proxy for that source area than the conventional sedimentary process indicators. This San Francisco Bay Coastal System study demonstrates that by applying a multi-proxy approach, the primary sites of sediment transport can be identified. Many of these sites are far from where the constituents originated, showing that sediment transport is widespread in the region. Although not often used, identifying and interpreting the distribution of naturally-occurring and allochthonous biologic, anthropogenic, and volcanic sediment constituents is a powerful tool to aid in the investigation of sediment transport pathways in other coastal systems.

Genotypic data for nine microsatellite loci for the seagrass Zostera muelleri collections from Lake Macquarie, NSW, Australia

Seagrasses are ecosystem engineers that offer important habitat for a large number of species and provide a range of ecosystem services. Many seagrass ecosystems are dominated by a single species; with research showing that genotypic diversity at fine spatial scales plays an important role in maintaining a range of ecosystem functions. However, for most seagrass species, information on fine-scale patterns of genetic variation in natural populations is lacking. In this study we use a hierarchical sampling design to determine levels of genetic and genotypic diversity at different spatial scales (centimeters, meters, kilometers) in the Australian seagrass Zostera muelleri. Our analysis shows that at fine-spatial scales (< 1 m) levels of genotypic diversity are relatively low (R (Plots) = 0.37 ± 0.06 SE), although there is some intermingling of genotypes. At the site (10's m) and meadow location (km) scale we found higher levels of genotypic diversity (R (sites) = 0.79 ± 0.04 SE; R (Locations) = 0.78 ± 0.04 SE). We found some sharing of genotypes between sites within meadows, but no sharing of genotypes between meadow locations. We also detected a high level of genetic structuring between meadow locations (FST = 0.278). Taken together, our results indicate that both sexual and asexual reproduction are important in maintaining meadows of Z. muelleri. The dominant mechanism of asexual reproduction appears to occur via localised rhizome extension, although the sharing of a limited number of genotypes over the scale of 10's of metres could also result from the localised dispersal and recruitment of fragments. The large number of unique genotypes at the meadow scale indicates that sexual reproduction is important in maintaining these populations, while the high level of genetic structuring suggests little gene flow and connectivity between our study sites. These results imply that recovery from disturbances will occur through both sexual and asexual regeneration, but the limited connectivity at the landscape-scale implies that recovery at meadow-scale losses is likely to be limited.

10Be data for sediments from DSDP Leg 56 and ODP Leg 170

Sediment accretion and subduction at convergent margins play an important role in the nature of hazardous interplate seismicity (the seismogenic zone) and the subduction recycling of volatiles and continentally derived materials to the Earth's mantle. Identifying and quantifying sediment accretion, essential for a complete mass balance across the margin, can be difficult. Seismic images do not define the processes by which a prism was built, and cored sediments may show disturbed magnetostratigraphy and sparse biostratigraphy. This contribution reports the first use of cosmogenic 10Be depth profiles to define the origin and structural evolution of forearc sedimentary prisms. Biostratigraphy and 10Be model ages generally are in good agreement for sediments drilled at Deep Sea Drilling Project Site 434 in the Japan forearc, and support an origin by imbricate thrusting for the upper section. Forearc sediments from Ocean Drilling Program Site 1040 in Costa Rica lack good fossil or paleomagnetic age control above the decollement. Low and homogeneous 10Be concentrations show that the prism sediments are older than 3-4 Ma, and that the prism is either a paleoaccretionary prism or it formed largely from slump deposits of apron sediments. Low 10Be in Costa Rican lavas and the absence of frontal accretion imply deeper sediment underplating or subduction erosion.

[Missale]

Copia digital: Biblioteca valenciana, 2010

Plasminogen deficiency accelerates vessel wall disease in mice predisposed to atherosclerosis

A critical link between hemostatic factors and atherosclerosis has been inferred from a variety of indirect observations, including the expression of procoagulant and fibrinolytic factors within atherosclerotic vessels, the presence of fibrin in intimal lesions, and the cellular infiltration of mural thrombi leading to their incorporation into developing plaques. To directly examine the role of the key fibrinolytic factor, plasminogen, in atherogenesis, plasminogen-deficient mice were crossed to hypercholesterolemic, apolipoprotein E-deficient mice predisposed to atherosclerosis. We report that the loss of plasminogen greatly accelerates the formation of intimal lesions in apolipoprotein E-deficient animals, whereas plasminogen deficiency alone does not cause appreciable atherosclerosis. These studies provide direct evidence that circulating hemostatic factors strongly influence vessel wall disease in the context of a disorder in lipid metabolism.

Elevated free nitrotyrosine levels, but not protein-bound nitrotyrosine or hydroxyl radicals, throughout amyotrophic lateral sclerosis (ALS)-like disease implicate tyrosine nitration as an aberrant in vivo property of one familial ALS-linked superoxide dismutase 1 mutant

Mutations in superoxide dismutase 1 (SOD1; EC 1.15.1.1) are responsible for a proportion of familial amyotrophic lateral sclerosis (ALS) through acquisition of an as-yet-unidentified toxic property or properties. Two proposed possibilities are that toxicity may arise from imperfectly folded mutant SOD1 catalyzing the nitration of tyrosines [Beckman, J. S., Carson, M., Smith, C. D. & Koppenol, W. H. (1993) Nature (London) 364, 584] through use of peroxynitrite or from peroxidation arising from elevated production of hydroxyl radicals through use of hydrogen peroxide as a substrate [Wiedau-Pazos, M., Goto, J. J., Rabizadeh, S., Gralla, E. D., Roe, J. A., Valentine, J. S. & Bredesen, D. E. (1996) Science 271, 515–518]. To test these possibilities, levels of nitrotyrosine and markers for hydroxyl radical formation were measured in two lines of transgenic mice that develop progressive motor neuron disease from expressing human familial ALS-linked SOD1 mutation G37R. Relative to normal mice or mice expressing high levels of wild-type human SOD1, 3-nitrotyrosine levels were elevated by 2- to 3-fold in spinal cords coincident with the earliest pathological abnormalities and remained elevated in spinal cord throughout progression of disease. However, no increases in protein-bound nitrotyrosine were found during any stage of SOD1-mutant-mediated disease in mice or at end stage of sporadic or SOD1-mediated familial human ALS. When salicylate trapping of hydroxyl radicals and measurement of levels of malondialdehyde were used, there was no evidence throughout disease progression in mice for enhanced production of hydroxyl radicals or lipid peroxidation, respectively. The presence of elevated nitrotyrosine levels beginning at the earliest stages of cellular pathology and continuing throughout progression of disease demonstrates that tyrosine nitration is one in vivo aberrant property of this ALS-linked SOD1 mutant.

Inactivating mutations in an SH2 domain-encoding gene in X-linked lymphoproliferative syndrome

X-linked lymphoproliferative syndrome (XLP) is an inherited immunodeficiency characterized by increased susceptibility to Epstein–Barr virus (EBV). In affected males, primary EBV infection leads to the uncontrolled proliferation of virus-containing B cells and reactive cytotoxic T cells, often culminating in the development of high-grade lymphoma. The XLP gene has been mapped to chromosome band Xq25 through linkage analysis and the discovery of patients harboring large constitutional genomic deletions. We describe here the presence of small deletions and intragenic mutations that specifically disrupt a gene named DSHP in 6 of 10 unrelated patients with XLP. This gene encodes a predicted protein of 128 amino acids composing a single SH2 domain with extensive homology to the SH2 domain of SHIP, an inositol polyphosphate 5-phosphatase that functions as a negative regulator of lymphocyte activation. DSHP is expressed in transformed T cell lines and is induced following in vitro activation of peripheral blood T lymphocytes. Expression of DSHP is restricted in vivo to lymphoid tissues, and RNA in situ hybridization demonstrates DSHP expression in activated T and B cell regions of reactive lymph nodes and in both T and B cell neoplasms. These observations confirm the identity of DSHP as the gene responsible for XLP, and suggest a role in the regulation of lymphocyte activation and proliferation. Induction of DSHP may sustain the immune response by interfering with SHIP-mediated inhibition of lymphocyte activation, while its inactivation in XLP patients results in a selective immunodeficiency to EBV.