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Thesis (D. Sc.)--University of Adelaide, 1988. / Collection of previously published articles. Includes Allozyme electrophoresis / B.J. Richardson, P.R. Baverstock and M. Adams (1986). Includes bibliographical references.

Cross-over electrophoresis, an immunological method for analyzing blood residues on archaeological artifacts, is tested. Artifacts from three sites were utilized in the testing of this methodology. The sites are the Dietz site in south-central Oregon (282 artifacts), Konemehu in northern California (48 artifacts tested for Winthrop Associates), and Chimney Shelter in southwestern Oregon (3 artifacts from the Umpqua National Forest).

Thesis (M.Sc.)--Memorial University of Newfoundland, 1987. / Typescript. Bibliography : leaves 91-103. Also available online.

Collection of previously published articles / Includes Allozyme electrophoresis / B.J. Richardson, P.R. Baverstock and M. Adams (1986) / Includes bibliographies / 2 v. : / Title page, contents and abstract only. The complete thesis in print form is available from the University Library. / Thesis (D. Sc.)--University of Adelaide, 1988

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Vitronectin (VTN) is a glycoprotein enriched in the blood and activates integrin receptors. VTN blood levels increase only in female mice 24 h after an ischemic stroke and exacerbate brain injury through IL-6-driven inflammation, but the VTN induction mechanism is unknown. Here, a 30 min middle cerebral artery occlusion (MCAO) in female mice induced VTN protein in the liver (normally the main source) in concert with plasma VTN. Male mice were excluded as VTN is not induced after stroke. MCAO also increased plasma VTN levels after de novo expression of VTN in the liver of VTN female mice, using a hepatocyte-specific (SERPINA1) promoter. MCAO did not affect SERPINA1 or VTN mRNA in the liver, brain, or several peripheral organs, or platelet VTN, compared to sham mice. Thus, hepatocytes are the source of stroke-induced increases in plasma VTN, which is independent of transcription. The cholinergic innervation by the parasympathetic vagus nerve is a potential source of brain-liver signaling after stroke. Right-sided vagotomy at the cervical level led to increased plasma VTN levels, suggesting that VTN release is inhibited by vagal tone. Co-culture of hepatocytes with cholinergic neurons or treatment with acetylcholine, but not noradrenaline (sympathetic transmitter), suppressed VTN expression. Hepatocytes have muscarinic receptors and the M1/M3 agonist bethanechol decreased VTN mRNA and protein release in vitro via M1 receptors. Finally, systemic bethanechol treatment blocked stroke-induced plasma VTN. Thus, VTN translation and release are inhibited by muscarinic signaling from the vagus nerve and presents a novel target for lessening detrimental VTN expression.