1,827 research outputs found

    The structural architecture of seismogenic faults, Sierra Nevada, California; implications for earthquake rupture processes

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    Earthquake ruptures along tectonically active faults nucleate predominantly at depths of 5 to 12km in the crust, so the portions of faults that slip in these events cannot be directly observed. The geometry and composition of seismogenic faults controls the nucleation, propagation and termination of the earthquake rupture process. This study aims to place constraints on the geometry and composition of seismogenic faults by examining ancient faults exhumed from the depths at which earthquakes are observed to nucleate. Faults exposed in the Sierra Nevada, California, show that the internal architecture of earthquake faults is heterogeneous at a variety of scales. Field and microstructural observations are used to describe in detail the architecture of two pseudotachylyte-bearing fault systems in the Granite Pass region of Sequoia and Kings Canyon National Park; the Granite Pass fault (GPF) and associated faults, and the Glacier Lakes fault (GLF) and faults that splay from the GLF. The GPF and sub-parallel faults are 1 to 6.7km long with left-lateral strike-slip displacements up to 80m. The GPF and GPF-parallel faults have architectures that are heterogeneous along strike. They are composed of one to four fault core strands containing cataclasites and ultracataclasites that cross-cut early localized crystal-plastic deformation. Slip surfaces developed at the edges of, within and between fault cores are defined by pseudotachylytes and cataclasites with thicknesses of ~0.01 to 20mm. Fault-related subsidiary structures are developed on either side of fault cores, and comprise damage zones with widths orthogonal to the fault of up to 30m. The GLF and splay faults have architectures that are more homogeneous along strike. These faults are composed of a tabular volume of heavily fractured and altered host rock between approximately planar fault core strands. The fault cores are centimetres wide and contain cataclasites and foliated cataclasites that are cross-cut by pseudotachylytes. Fault-related damage is limited in extent to several metres beyond the bounding fault cores. The GLF contains additional cataclasites, ultracataclasites and pseudotachylytes in a fault core strand within the tabular zone of fractured rock. Thermochronologic analyses of the host rock granodiorite, combined with previously published palaeogeobarometry and apatite fission track data, define the temperature and pressure changes associated with cooling and exhumation of the pluton. The P-T conditions prevalent during the deformation history of the GPF fault system are evaluated by relating recrystallisation mechanisms in quartz to temperature, showing that the early stages of deformation occurred at temperatures of 450 to 600ºC. Dating of pseudotachylytes by the K-Ar isotopic method suggests subsequent brittle deformation took place at temperatures <350ºC and pressures ≤150MPa. A model for the architecture of the GPF architecture therefore has well constrained environmental controls, and should be transferrable to faults with comparable deformation histories. Small faults (cumulative displacements <1m) in the Mount Abbot Quadrangle, 55km north of Granite Pass, have been examined to illustrate the processes associated with the earliest stages of slip in the Sierra Nevada faults. The faults have branched or straight fault traces. Pseudotachylytes in branching faults show that these faults accumulated displacement in high velocity slip events, rather than by quasi-static fault growth. Branching faults without pseudotachylytes contain chlorite breccias interpreted to have formed in response to slip along faults with elevated pore fluid pressure. Straight faults also likely underwent slip events, but contain cataclased chlorite and epidote, suggesting low fluid pressures during slip. The small faults show that fluid-rock interactions are critical to fault geometry, and that lateral structural heterogeneity is established after small finite displacements. Field and thin section observations of exhumed seismogenic faults show that fault architecture and fault rock assemblage are critical to the earthquake rupture process. The heterogeneous composition of slip surfaces in the GPF faults imply that melt lubrication cannot account for all of the dynamic slip weakening as there are no continuous pseudotachylyte generation surfaces through the fault zones. Multiple slip weakening mechanisms must have been active during single rupture events. Slip weakening mechanisms also change at a given point on the fault in response to continued deformation. Splay faults at the GLF termination suggest that structural complexity observed at the terminations of fault surface traces can also be expected at depth. The off-fault damage at the termination of the GLF will change the bulk elastic properties of the host rock and must be accounted for in models of rupture propagation beyond fault terminations, or across geometrical discontinuities. Additionally, aftershock distributions and focal mechanisms may be controlled by the geometry of structures present at fault terminations

    The recognition of atrophic gastritis

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    The historical aspects of atrophic gastritis have been reviewed as has the evidence for the various theories as to the aetiology of the condition. The association between atrophic gastritis and the anaemias, its relationship to gastric cancer, and its significance as a disease entity have been discussed, and a fourfold rationale for the importance of recognising the condition have been advanced in the light of these associations.Multiple gastric biopsy was carried out upon one hundred and eleven patients over the age of forty years who were under investigation for dyspeptic symptoms. The overall incidence of atrophic gastritis was 64 %, being highest in those with gastric cancer and lowest in those with duodenal ulceration. Intestinal metaplasia of the gastric mucosa was found only in those with atrophic gastritis but was not confined to those with severe atrophic changes. No aspects of the clinical history or findings pointed to specific diagnostic features, but a significantly high incidence of gastric cancer was found in the family history of those with atrophic gastritis.The intramuscular pentagastrin test was evaluated by comparison with other tests of gastric secretion, and when employed in the patients under study was found to discriminate between those with atrophic and those with normal mucosa with an accuracy of 81 %. The value of radiology, gastroscopy and blind gastric photography in the recognition of atrophic gastritis was studied. Discrimination between atrophic and normal gastric mucosa was accurate in 68% by barium meal examination, 65% by gastroscopy and 53% by gastric photography.The haematological status of the subjects was studied, and a significantly high incidence of anaemia, but not of iron deficiency, was found among those with atrophic gastritis. Low serum Vitamin B12 levels were found in 8 %, and parietal cell antibodies in 17% of those with atrophic gastritis, and in none with normal mucosa, while the incidence of thyroid antibodies was higher in those with atrophic changes, but not significantly so. An increase in the incidence of blood group A was found in those with atrophic gastritis when compared with those with normal mucosa and with a comparable contrast group.Gastric emptying rates were studied using a radioactive labelled meal and were found to be significantly slower in subjects with atrophic gastritis and with gastric cancer when compared with a healthy contrast group of subjects. The significance of this finding has been discussed.The value and reliability of the clinical and haematological investigations in the detection of atrophic gastritis have been discussed, and an overall diagnostic accuracy of 89% with a false - positive incidence of 3% found, when the combined results were analysed

    Non-equivalence of antibiotic generic drugs and risk for intensive care patients

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    Background: The underlying axiom in applying generic drugs is the equivalence of their active ingredient with the (usually more expensive) innovator product, an all-embracing statement with the insidious result that physicians assume that the generic products have been subjected to the same rigorous testing regimens as the brand-name products. The present paper presents novel experimental data on an investigator-blinded comparison between the innovator imipenem antibiotic, and a number of its generics. Methods: Particulate matter contamination of each group was visualized by means of a membrane filter method. Functional studies in an animal model–the dorsal skinfold chamber technique in mice-designed to simulate the state of microcirculatory dysfunction in intensive care patients was performed, in order to assess the influence of the particulate matter of each group on the functional capillary density of the striated skin muscle, after their intravenous injection. Results: The results showed massive particulate contamination of the generics, in a size range relevant for impacting the microcirculation. The particulate contamination contributed in some generic groups to a significant shutdown of tissue perfusion. Conclusion: The presented data underscore the need to raise the regulatory barriers for the entry of generics to the market, well beyond the simplistic proof of “bioequivalence”, which in no measure deals with the essential questions of quality and patient safety. If generics are used, they should be tested by a filter technique and optical microscopy, to ensure the absence especially of small particulate contaminants and their purity

    Charge mobility of discotic mesophases: A multiscale quantum/classical study

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    A correlation is established between the molecular structure and charge mobility of discotic mesophases of hexabenzocoronene derivatives by combining electronic structure calculations, Molecular Dynamics, and kinetic Monte Carlo simulations. It is demonstrated that this multiscale approach can provide an accurate ab-initio description of charge transport in organic materials

    Examination of exogenous estrogenic chemical exposure and altered fetal nutrition in the CD-1 mouse fetus

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    Title from PDF of title page (University of Missouri--Columbia, viewed on September 15, 2010).The entire thesis text is included in the research.pdf file; the official abstract appears in the short.pdf file; a non-technical public abstract appears in the public.pdf file.Dissertation advisor: Dr. Frederick vom Saal.Vita.Ph. D. University of Missouri--Columbia 2009.My dissertation examines two issues related to disruption of fetal growth: exposure to exogenous estrogenic chemicals and altered nutrition. My first set of studies was aimed at manipulating isoflavones in feed on serum estradiol levels in pregnant female CD-1 mice and their fetuses. Results were that fetal serum estradiol concentrations were elevated due to the absence of either isoflavones or soy protein in feed. Also, I show a difference in response to low doses of natural estrogens compared to manmade estrogens. I also show that isoflavones gave a nonmonotonic dose-response curve in that low levels of isoflavones elevated fetal estradiol levels and higher doses decreased fetal estradiol levels. The data show that the feed groups that had earlier onset of puberty in females were the same feed groups with higher estradiol during fetal life. These finding show that isoflavones have the potential to disrupt the fetal endocrine system. My last study involved examining placental transport in a crowded uterine horn. In the model used here, uterine crowding causes differential blood flow to fetuses. The fetuses with decreased blood flow relative to their siblings show decreased growth. I show here that the placenta does influence amino acid transport and that a reduced fetal growth is related to a reduced placental transport of nutrients. The importance of the crowded uterine model for the study of the effects of fetal nutrition on fetal growth is that this model incidence of IUGR in developed countries.Includes bibliographical reference
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