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    PARTISAN PREFERENCES REGARDING DISCLOSURE MECHANISMS IN HYDRAULIC FRACTURING LEGISLATION

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    Honors (Bachelor's)EnvironmentUniversity of Michiganhttp://deepblue.lib.umich.edu/bitstream/2027.42/113085/1/thesis 5-2-14 final.pdfDescription of thesis 5-2-14 final.pdf : Thesi

    The Ultrastructural Basis of Transcapillary Exchanges

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    A brief survey is given of current views correlating the ultrastructural and permeability characteristics of capillaries. Observations based on the use of peroxidase (mol wt 40,000), as an in vivo, and colloidal lanthanum, as an in vitro, ultrastructural tracer, are presented. In capillaries with "continuous" endothelium, the endothelial intercellular junctions are thought to be permeable to the tracers, and are regarded as maculae occludentes rather than zonulae occludentes, with a gap of about 40 A in width between the maculae. Some evidence for vesicular transport is also presented. It is inferred that the cell junctions are the morphological equivalent of the small-pore system, and the vesicles the equivalent of the large-pore system. Peroxidase does not apparently cross brain capillaries: the endothelial cell junctions are regarded as zonulae occludentes, and vesicles do not appear to transport across the endothelium. This is regarded as the morphological equivalent of the blood-brain barrier for relatively large molecules. The tracers appear to permeate the fenestrae of fenestrated capillaries, and the high permeability of these capillaries to large molecules is attributed to the fenestrae. Capillaries with discontinuous endothelium readily allow passage of the tracers through the intercellular gaps. A continuous basement membrane may act as a relatively coarse filter for large molecules. In general, the morphology of capillaries correlates well with physiological observations

    Growth regulation by heparin in the vascular wall

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    A Thesis Submitted to the Faculty of Medicine University of the Witwatersrand, Johannesburg in fulfillment of the requirements for the Degree of Doctor of Science in Medicine Boston, U.S.A. 1983Vascular smooth muscle proliferation follows upon endothelial injury, and is thought to be an early component in the pathogenesis of atherosclerosis, and a possible noxious consequence of vascular surgery. We have shown that heparin suppresses vascular smooth muscle proliferation iri vivo and in vitro. The inhibitory effect is specific for heparin, and not other anions, and is not related to the antithrombin III binding activity of heparin. It is dependent on the size of the molecule, (hexasaccharidees or smaller being ineffective), and O-sulfation, but not N-sulfationIT201
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