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    A survey of eight successful enrichment programs.

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    Thesis (Ed.M.)--Boston Universit

    Laboratory and Well-Log Velocity and Density Measurements from the Ontong Java Plateau: New in-situ corrections to laboratory data for pelagic carbonates

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    During Ocean Drilling Program Leg 130, sonic velocity and bulk density/porosity well logs were measured in five separate holes drilled through the sequence of pelagic carbonate oozes, chalks, and limestones that comprise the thick, continuous sedimentary cover on the Ontong Java Plateau. An internally consistent and continuous suite of shipboard laboratory velocity and sediment physical properties measurements were made from the top of each hole down through the entire logged interval. Because of the high quality of the data, extensive overlap of 500 m or more between the log and laboratory measurements at each hole, and the homogeneous nature of the sediments, we have been able to compare laboratory and in-situ log measurements in detail and to evaluate factors that alter laboratory data from their in-situ values. For measurements of bulk density and porosity, differences between laboratory and in-situ log measurements are very small and remain constant over the entire range of depths studied. We have applied a simple hydraulic rebound correction to the laboratory data that compensates for pore fluid expansion after removal of a sediment sample from in-situ conditions. The small, correctable differences between the laboratory and log data imply that mechanical rebound is significantly less than previous estimates (maximum near 5%) of rebound in pelagic carbonates. Furthermore, porosity rebound cannot be used to correct laboratory sonic velocity measurements to in-situ values. Such a rebound correction implicitly requires that laboratory and in-situ data must occupy identical fields on velocity-porosity crossplots. This condition is not met for the Ontong Java Plateau results because laboratory and in-situ logging data occupy distinct trends with little overlap between the two types of measurement. Mechanical rebound in pelagic carbonates cannot be used to correct either laboratory porosity or velocity measurements to in-situ values. The complex porosity systematics of these carbonates resulting from varying abundances of hollow foraminifer grains precluded use of an empirical correction derived from the log porosity and velocity data. Laboratory sonic velocity measurements can be corrected to in-situ values at all of the Ontong Java Plateau sites using a depth-based function derived from downhole differences between log and laboratory velocities in Hole 807A. The applicability of the depth correction implies that the effect of overburden pressure reduction on sediment elastic moduli is the most significant factor affecting laboratory velocity measurements. The depth correction to laboratory velocity measurements appears to be generally applicable to pelagic carbonate oozes and chalks of the Ontong Java Plateau, regardless of depositional depth or sediment age

    Seismic stratigraphy of the Ontong Java Plateau

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    The Ontong Java Plateau, a large, deep-water carbonate plateau in the western equatorial Pacific, is an ideal location for studying responses of carbonate sedimentation to the effects of changing paleoceanographic conditions. These carbonate responses are often reflected in the physical properties of the sediment, which in turn control the appearance of seismic reflection profiles. Seismic stratigraphy analyses, correlating eight reflector horizons to each drill site, have been conducted in an attempt to map stratigraphic data. Accurate correlation of seismic stratigraphic data to drilling results requires conversion of traveltime to depth in meters. Synthetic seismogram models, using shipboard physical properties data, have been generated in an attempt to provide this correlation. Physical properties, including laboratory-measured and well-log data, were collected from sites drilled during Deep Sea Drilling Project Legs 30 and 89, and Ocean Drilling Program Leg 130, on the top and flank of the Ontong Java Plateau. Laboratory-measured density is corrected to in-situ conditions by accounting for porosity rebound resulting from removal of the sediment from its overburden. The correction of laboratory-measured compressional velocity to in situ appears to be largely a function of increases in elastic moduli (especially shear rigidity) with depth of burial, more than a function of changes in temperature, pressure, or density (porosity rebound). Well-log velocity and density data for the ooze intervals were found to be greatly affected by drilling disturbance; hence, they were disregarded and replaced by lab data for these intervals. Velocity and density data were used to produce synthetic seismograms. Correlation of seismic reflection data with synthetic data, and hence with depth below seafloor, at each drill site shows that a single velocity-depth function exists for sediments on the top and flank of the Ontong Java Plateau. A polynomial fit of this function provides an equation for domain conversion: Depth (mbsf) = 44.49 + 0.800(traveltime[ms]) + 3.308 × 10 4 (traveltime[ms]2 ) Traveltime (ms) = -35.18 + 1.118(depth[mbsf]) - 1.969 × KT* (depth[mbsf]2 ) Seismic reflection profiles down the flank of the plateau undergo three significant changes: (1) a drastic thinning of the sediment column with depth, (2) changes in the echo-character of the profile (development of seismic facies), and (3) loss of continuous, coherent reflections. Sediments on the plateau top were largely deposited by pelagic processes, with little significant postdepositional or syndepositional modification. Sediments on the flank of the plateau are also pelagic, but they have been modified by faulting, erosion, and mass movement. These processes result in disrupted and incoherent reflectors, development of seismic facies, and redistribution of sediment on the flank of the plateau. Seismic stratigraphic analyses have shown that the sediment section decreases in thickness by as much as 65% between water depths of 2000 m water depth (at the top of the plateau) and 4000 m (near the base of the plateau). Thinning is attributed to increasing carbonate dissolution with depth. If this assumption is correct, then changes in the relative thicknesses of seismostratigraphic units at each drill site are indicative of changes in the position of the lysocline and the dissolution gradient between the lysocline and the carbonate compensation depth. We think that a shallow lysocline in the early Miocene caused sediment thinning. A deepening of the lysocline in the late-early Miocene caused relative thickening at each site. Within the middle Miocene, a sharp rise in lysoclinal depth occurs, concurrent with a steepening of the dissolution gradient. These events result in sediment thinning at all four sites. The thicker sections in the late Miocene likely correspond to a deepening of the lysocline, and a subsequent rise in the lysocline again hinders accumulation of sediment in the very late Miocene and Pliocene

    Low-energy QCD: Chiral coefficients and the quark-quark interaction

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    A detailed investigation of the low-energy chiral expansion is presented within a model truncation of QCD. The truncation allows for a phenomenological description of the quark-quark interaction in a framework which maintains the global symmetries of QCD and permits a 1/Nc1/N_c expansion. The model dependence of the chiral coefficients is tested for several forms of the quark-quark interaction by varying the form of the running coupling, α(q2)\alpha (q^2), in the infrared region. The pattern in the coefficients that arises at tree level is consistent with large NcN_c QCD, and is related to the model truncation.Comment: 28 pages, Latex, 6 postscript figures available on request to [email protected]

    Patients with Neovascular Age-Related Macular Degeneration Requiring Intensive Intravitreal Aflibercept Treatment: An ARIES Post Hoc Analysis.

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    INTRODUCTION The aim of this post hoc analysis of the ARIES study is to explore the requirement for intravitreal aflibercept (IVT-AFL) treatment intervals of < 8 weeks (w) in patients with neovascular age-related macular degeneration (nAMD), and to assess vision and anatomic outcomes in such patients who require more intensive treatment. METHODS ARIES was a multicenter, randomized, phase 3b/4 study that investigated the efficacy of two IVT-AFL proactive, individualized, treat-and-extend regimens over 2 years in treatment-naïve patients with nAMD. Patients were determined as injection-intensive if the study investigator identified that a treatment interval of < 8 w was needed and if they had ≥ 1 interval of < 8 w after three initial monthly doses. Treatment intervals could be extended subsequently if extension criteria were met. This is a post hoc analysis of patients enrolled in ARIES and statistical analysis is descriptive. RESULTS Of 269 patients in the combined treatment arms, 23.0% (n = 62) were injection-intensive (Year 1: 13.8% [n = 37]; Year 2: 9.3% [n = 25]). Time from IVT-AFL initiation to injection-intensive determination varied (range, 16-100 w; median: 43.2 w). Mean treatment interval was 8.4 w before and 6.1 w after injection-intensive determination. Overall, 59.7% achieved treatment intervals of ≥ 8 w following injection-intensive determination. Vision improvements from baseline to Week 104 were smaller for injection-intensive patients than non-injection-intensive patients (mean [SD] best-corrected visual acuity change: + 2.3 [15.6] vs.  + 5.9 [12.3] letters). Anatomic outcomes were similar between injection-intensive and non-injection-intensive patients (central retinal thickness change from baseline to Week 104: - 160 [154] vs.  - 167 [136] µm). CONCLUSIONS In ARIES, 23% of treatment-naïve patients with nAMD experienced at least one treatment interval of < 8 w. Injection-intensive patients showed improved vision and anatomic outcomes. For most, treatment intervals could be extended to ≥ 8 w following injection-intensive determination. CLINICALTRIALS gov Identifier: NCT02581891

    Loss of Melanoregulin (MREG) Enhances Cathepsin-D Secretion by the Retinal Pigment Epithelium

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    Cathepsin-D (Cat-D) is a major proteolytic enzyme in phagocytic cells. In the retinal pigment epithelium (RPE), it is responsible for the daily degradation of photoreceptor outer segments (POSs) to maintain retinal homeostasis. Melanoregulin (MREG)-mediated loss of phagocytic capacity has been linked to diminished intracellular Cat-D activity. Here, we demonstrate that loss of MREG enhances the secretion of intermediate Cat-D (48 kDa), resulting in a net enhancement of extracellular Cat-D activity. These results suggest that MREG is required to maintain Cat-D homeostasis in the RPE and likely plays a protective role in retinal health. In this regard, in the Mreg dsu/dsu mouse, we observe increased basal laminin. Loss of the Mreg dsu allele is not lethal and therefore leads to slow age-dependent changes in the RPE. Thus, we propose that this model will allow us to study potential dysregulatory functions of Cat-D in retinal disease

    Loss of Melanoregulin (MREG) Enhances Cathepsin-D Secretion by the Retinal Pigment Epithelium

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    Abstract Cathepsin-D (Cat-D) is a major proteolytic enzyme in phagocytic cells. In the retinal pigment epithelium (RPE), it is responsible for the daily degradation of photoreceptor outer segments (POSs) to maintain retinal homeostasis. Melanoregulin (MREG)-mediated loss of phagocytic capacity has been linked to diminished intracellular Cat-D activity. Here, we demonstrate that loss of MREG enhances the secretion of intermediate Cat-D (48 kDa), resulting in a net enhancement of extracellular Cat-D activity. These results suggest that MREG is required to maintain Cat-D homeostasis in the RPE and likely plays a protective role in retinal health. In this regard, in the Mreg dsu/dsu mouse, we observe increased basal laminin. Loss of the Mreg dsu allele is not lethal and therefore leads to slow age-dependent changes in the RPE. Thus, we propose that this model will allow us to study potential dysregulatory functions of Cat-D in retinal disease. Copyright © Cambridge University Press, 2013
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