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Dissertations / Theses on the topic 'Cerebral ischaemia'

Author: Grafiati

Published: 4 June 2021

Last updated: 6 February 2022

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1

Rowe, Jeremy Geraint. "Cerebral ischaemia complicating subarachnoid haemorrage." Thesis, University of Oxford, 1996. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.320671.

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2

Peters, Elaine Elizabeth. "Inflammatory responses and cerebral ischaemia." Thesis, University of Glasgow, 1999. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.252469.

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3

Kelly, Stephen. "Neuroprotection and functional alterations in mice over-expressing heat shock protein 70i." Thesis, University of Glasgow, 2000. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.327580.

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4

Fitridge, Robert Alwyn. "Reperfusion injury in focal cerebral ischaemia /." Title page, table of contents and abstract only, 1995. http://web4.library.adelaide.edu.au/theses/09MS/09msf546.pdf.

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5

Yam, Philippa S. "Axonal injury following focal cerebral ischaemia." Thesis, University of Glasgow, 1998. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.298683.

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6

McCarter, Jennifer F. "Inflammatory mechanisms in focal cerebral ischaemia." Thesis, University of Edinburgh, 2001. http://hdl.handle.net/1842/28562.

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In this thesis, focal cerebral ischaemia was induced in three animal models in an attempt to investigate the contribution of the inflammatory response. The rat monofilament model of middle cerebral artery (MCA) occlusion, considered by some to be a pro-inflammatory model, was set up for the first time in Edinburgh and validated as suitable model for further investigation. Permanent and transient models were established to allow the evaluation of possible reperfusion injury. Both monofilament models were compared with the endothelin-1 model already established and routinely in use in the labora

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7

Dreier, Jens P. "Cortical spreading ischaemia and delayed ischaemic neurological deficits after subarachnoid haemorrhage." Doctoral thesis, [S.l.] : [s.n.], 2003. http://deposit.ddb.de/cgi-bin/dokserv?idn=970109342.

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8

McCaig, David. "Characterisation of Gadd34 response after cerebral ischaemia." Thesis, University of Glasgow, 2005. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.433083.

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9

Lee, Vee Meng. "Magnetic resonance imaging of cerebral ischaemia models." Thesis, University of Cambridge, 1995. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.242995.

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10

Mokhtarudin, Mohd Jamil Mohamed. "Mathematical modelling of cerebral ischaemia-reperfusion injury." Thesis, University of Oxford, 2016. http://ora.ox.ac.uk/objects/uuid:3f5dd7cf-e403-4cf0-b725-4ac235c1b37e.

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Restoring cerebral blood flow using reperfusion treatment is a common method in treating ischaemic stroke. Reperfusion treatment should be given within 4.5 hours from stroke onset. However, reperfusion beyond this time window poses the risk of reperfusion injuries such as intracranial haemorrhage and cerebral tissue swelling. The focus of this thesis is to study the effect of cerebral tissue swelling after reperfusion as it can occur in a few hours after the treatment. Cerebral tissue swelling may cause brain structure movement and cerebral microvessel compression; the latter may then lead to

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11

Murray, Katie. "Actions of interleukin-1 in cerebral ischaemia." Thesis, University of Manchester, 2014. https://www.research.manchester.ac.uk/portal/en/theses/actions-of-interleukin1-in-cerebral-ischaemia(76a8206b-4153-437d-9616-7d668a35db51).html.

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Cerebral ischaemia is characterised by an interruption in cerebral blood flow (CBF) leading to neuronal dysfunction and death. Pre-existing systemic inflammation is strongly associated with exaggerated brain injury following cerebral ischaemia with experimental studies showing that increased damage is mediated by interleukin (IL)-1 dependent pathways. The mechanisms through which systemic inflammation worsens stroke have yet to be elucidated, therefore in this thesis we sought to further determine how systemic inflammation affects outcome after acute cerebral ischaemia. The effects of acute pr

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12

Bowler, John Vaughan. "Cerebral infarction and '9'9Tc'm HMPAO SPECT." Thesis, King's College London (University of London), 1992. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.260983.

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13

Pathmanathan, Saidharshini. "Development of in vitro models of cerebral ischaemia." Thesis, University of Oxford, 2002. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.249162.

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14

Whitfield, Peter Cyril. "Gene expression after global and focal cerebral ischaemia." Thesis, University of Southampton, 1997. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.242632.

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15

McMahon, Catherine Jane. "Inflammation and delayed cerebral ischaemia induced byaneurysmal subarachnoid haemorrhage." Thesis, University of Manchester, 2008. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.491335.

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Stroke is a sudden, unpredictable, often devastating neurological event. The commonest cause of morbidity and mortality associated with subarachnoid haemorrhage (SAH) is delayed cerebral ischaemia (DCI). Ischaemic and haemorrhagic strokes are recognised to induce a significant peripheral and central inflammatory response. These responses may be important in the exacerbation of ischaemic damage and in the development and exacerbation of DCI after SAH. A number of studies have examined the potential contribution of pro-inflammatory cytokines, such as interleukin-l (IL-l) and interleukin-6 (IL-6)

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16

Stock, Christopher John. "Inflammatory cytokines in repair and recovery after cerebral ischaemia." Thesis, University of Manchester, 2006. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.633022.

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The cytokines, a family of poly-peptides that are central to the coordination of the inflammatory response, exert significant influence on the progression of acute cerebral ischaemic injury, or 'stroke'. Evidence has accumulated for a similarly significant role for cytokines in physical repair and neurological recovery after stroke, via actions within the injured central nervous system and through mediation of peripheral inflammation. This thesis addresses the spatio-temporal expression profile of cytokines in response to cerebral ischaemia in the rat, and the influence of elevated peripheral

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17

Calamante, Fernando. "Diffusion and perfusion MRI and applications in cerebral ischaemia." Thesis, University College London (University of London), 2000. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.314345.

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18

Taylor, Deanna Lesley. "Alterations in interstitial acid-base homeostasis during cerebral ischaemia." Thesis, University College London (University of London), 1997. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.267025.

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19

Sibson, Nicola Ruth. "A magnetic resonance imaging study of experimental cerebral ischaemia." Thesis, University of Cambridge, 1994. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.360825.

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20

Greenhalgh, Andrew. "Actions of interleukin-1 receptor antagonist in cerebral ischaemia." Thesis, University of Manchester, 2011. https://www.research.manchester.ac.uk/portal/en/theses/actions-of-interleukin1-receptor-antagonist-in-cerebral-ischaemia(50aacd97-68c1-4f91-90b5-8f8deff5d21d).html.

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Cerebral ischaemia, or stroke, is a leading cause of death and disability worldwide. Ischaemic stroke, as a result of arterial occlusion, and subarachnoid haemorrhage (SAH), as a consequence of arterial rupture in the subarachnoid space, are major subtypes of stroke. Treatment options for both are limited, and many therapeutic strategies have failed. In ischaemic stroke, lack of evidence of brain penetration of treatments has been cited as a major weakness and contributing factor to failed clinical trials. In SAH, animal models do not always mimic key pathophysiological hallmarks of the diseas

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21

Critchley, Giles Roderic. "Cerebral ischaemia following subarachnoid haemorrhage : a laboratory and clinical investigation of the cerebral microcirculation." Thesis, St George's, University of London, 2002. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.268382.

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22

Pell, Gabriel Simon. "Perfusion and diffusion magnetic resonance imaging studies of cerebral ischaemia." Thesis, University College London (University of London), 1999. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.313382.

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23

Neuhaus, Ain. "The effects of cerebral ischaemia on pericytes and neurovascular function." Thesis, University of Oxford, 2016. https://ora.ox.ac.uk/objects/uuid:836ac5ca-3f05-4a40-a19c-aec4f9c257af.

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Acute ischaemic stroke is a major cause of morbidity and mortality in the developed world, yet the treatment options available are limited to therapies that restore vessel patency. Recanalisation of the occluded artery does not necessarily result in reperfusion of the downstream microvasculature, however, and the pathomechanisms involved in this are incompletely understood. One putative mediator of this is the capillary pericyte, a vascular mural cell type that may constrict under ischaemic conditions. The overarching aim of this thesis was to characterise vascular function following cerebral

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24

Aspey, Benjamin Stephen. "Cerebral artheroembolism : an experimental study to determine the mechanism of cerebral vascular occlusion and ischaemia." Thesis, Imperial College London, 1991. http://hdl.handle.net/10044/1/46653.

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25

Jones, Paul A. "Modulation of kainate-induced excitotoxicity in rats." Thesis, University of Glasgow, 1997. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.244361.

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26

Murdoch, Iain. "Presynaptic pathology after acute brain injury." Thesis, University of Glasgow, 1999. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.340811.

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27

Shrewsbury-Gee, Joanne. "An investigation of compounds of potential value in experimental cerebral ischaemia." Thesis, University of Manchester, 1988. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.329110.

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28

Lythgoe, Mark Francis. "Studies of experimental cerebral ischaemia using magnetic resonance imaging and autoradiography." Thesis, University College London (University of London), 1999. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.300464.

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29

Gill, Ramanjit. "Neuroprotective studies of excitatory amino acid antagonists in focal cerebral ischaemia." Thesis, Royal Veterinary College (University of London), 1992. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.522532.

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30

McCracken, Eileen. "White matter damage after acute brain injury." Thesis, University of Glasgow, 1999. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.340812.

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31

Ben-Yoseph, O. "Multinuclear magnetic resonance spectroscopy studies of perturbed cerebral metabolism in vitro." Thesis, University of Cambridge, 1991. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.240078.

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32

Chrysanthou, Elvina. "The lectin pathway of complement activation in cerebral ischaemia and reperfusion injury." Thesis, University of Leicester, 2013. http://hdl.handle.net/2381/28171.

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The complement system constitutes a critical component of the innate immune response. The lectin pathway is one of the three activation pathways of the complement activation cascade that can recognise and respond to structures on oxygen deprived cells and contribute to ischaemia and reperfusion injury (IRI). Cerebral IRI mediated inflammation is known to be responsible for secondary damage in the penumbra region surrounding the initial area of infarct and the prevention of IRI-mediated secondary damage provides an attractive target for therapeutic intervention. Mannose binding lectin associate

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33

McColl, Barry. "Pathophysiology of cerebral ischaemia : effects of APOE genotype on outcome and endocytosis." Thesis, University of Glasgow, 2004. http://theses.gla.ac.uk/4324/.

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Apolipoprotein E (apoE denotes protein: APOE denotes gene) is a lipid-transport protein abundantly expressed in the brain and strongly upregulated after acute brain injury. The APOE e4 allele is the major genetic risk factor for Alzheimer’s disease (AD) and has been associated with poorer outcome after various types of acute brain injury, including traumatic brain injury and subarachnoid haemorrhage. However, the role of APOE genotype in focal ischaemic stroke is less clear. The mechanism(s) by which APOE genotype may modulate outcome after acute brain injury are also unclear at present. Accor

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34

Smith, Sharon Lesley. "Production of markers of neurological damage induced by cerebral ischaemia or neurotoxins." Thesis, University of Nottingham, 1993. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.359770.

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35

Gregory, Lloyd James. "Monitoring the neuropathogenic processes following global cerebral ischaemia using magnetic resonance imaging." Thesis, King's College London (University of London), 1999. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.325067.

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36

Nelson, Rachael Mary. "Cellular effects of cerebral ischaemia in vitro : cerebroprotective actions of GABAmimetic agents." Thesis, De Montfort University, 2002. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.393498.

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37

Mullins, Paul Gerald Mark. "Magnetic resonance imaging in the study of animal models of cerebral ischaemia /." [St. Lucia, Qld.], 2001. http://www.library.uq.edu.au/pdfserve.php?image=thesisabs/absthe16186.pdf.

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38

Marquardt, Lars. "Large artery disease in patients with cerebral ischaemia : frequency, investigation and management." Thesis, University of Oxford, 2010. http://ora.ox.ac.uk/objects/uuid:70b598c5-97ca-4567-ac32-ed5092972a16.

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Stroke is the third leading cause of death in the developed world and is the leading neurological cause of disability with a massive impact on personal life and society. Large artery atherosclerosis is one of the main causes of ischaemic stroke. However, in several aspects of this condition there is still a significant amount of uncertainty about its prevalence, appropriate investigation and possible treatment. Reliable data on epidemiology are therefore necessary to provide clinicians and researchers with crucial information to guide diagnostic and therapeutic management as well as further re

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39

Price, Christopher John Simon. "Patterns of inflammation and their role in the pathophysiology of cerebral ischaemia." Thesis, University of Cambridge, 2007. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.612974.

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40

Smart, Sean Christopher. "NMR examinations of control and ischemic rodent brain tissue." Thesis, Queen Mary, University of London, 1995. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.309450.

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41

McKittrick, Craig Martin. "The role of mast cells in a mouse model of focal cerebral ischaemia." Thesis, University of Strathclyde, 2013. http://oleg.lib.strath.ac.uk:80/R/?func=dbin-jump-full&object_id=22406.

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Treatments for ischaemic stroke are limited and have low efficacy despite many years of promising research uncovering many potential therapeutic targets. As a result, stroke ranks as the third leading cause of death and the leading cause of disability worldwide. Mast cells have been identified as contributors to ischaemic stroke pathology, and are therefore a novel candidate for targeted stroke therapy. Indeed, genetic mast cell deficiency prior to onset of transient middle cerebral artery occlusion (tMCAo) in rats resulted in a significant reduction in blood brain barrier (BBB) permeability,

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42

Thomas, David Lee. "Magnetic resonance imaging of diffusion and perfusion : techniques and applications to cerebral ischaemia." Thesis, University College London (University of London), 1999. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.391829.

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43

Henshall, David C. "The development of a novel model of focal cerebral ischaemia using endothelin isopeptides." Thesis, University of Edinburgh, 1997. http://hdl.handle.net/1842/21300.

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Several animal models of focal cerebral ischaemia have been developed to gain insight into the pathophysiology and possible therapeutic treatment of stroke. This thesis aimed to optimise & characterise a model of focal cerebral ischaemia that utilises perivascular microinjection of endothelin-1 (ET-1) to occlude the middle cerebral artery (MCA) of the rat, and to develop a novel model of endothelin-induced MCA occlusion with controlled reperfusion. The MCA of the anaesthetised rat was occluded by the intracerebral microinjection of ET-1 into the outer layers of cortex adjacent to the MCA. Elis

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44

Tseng, Ming-Yuan. "Maintenance of cerebral autoregulation and enhancement of blood flow as a therapeutic strategy against cerebral ischaemia following aneurysmal subarachnoid haemorrhage." Thesis, University of Cambridge, 2007. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.612923.

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45

Johnston, Andrew. "An investigation of free radical involvement in cell death in a cell culture model of ischaemia." Thesis, University of Warwick, 1999. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.343128.

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46

Sutherland, Brad Alexander, and n/a. "Heme oxygenase and the use of tin protoporphyrin in hypoxia-ischaemia-induced brain damage : mechanisms of action." University of Otago. Department of Pharmacology & Toxicology, 2009. http://adt.otago.ac.nz./public/adt-NZDU20090119.150318.

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Stroke is the third largest cause of death, and the leading cause of disability worldwide. Treatments are sought to reduce mortality, and increase survival time following an ischaemic stroke. Hypoxia-ischaemia (HI) is the combination of cerebral ischaemia and global hypoxia that can lead to neuronal damage, particularly perinatally. The complex neurodegenerative cascade following ischaemic stroke and HI activates many stress pathways, including heme oxygenase (HO). HO metabolises free heme to release iron, carbon monoxide, and biliverdin, which is subsequently metabolised to bilirubin. This th

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47

Kenny, Barry. "Differentiation between calcium antagonists in vitro and their effects in models of cerebral ischaemia." Thesis, University of Leicester, 1991. http://hdl.handle.net/2381/33589.

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Different classes of calcium antagonist were defined in vitro using radioligand binding studies and the efficacy of the classes as neuroprotective agents was assessed in vivo using a novel model of cerebral ischaemia. Radioligand binding studies indicated that the interactions of both class I (dihydropyridines) and class II (verapamil and diltiazem) calcium antagonists was temperature-, ligand- and tissue-dependent. Specific binding sites for class III antagonists (flunarizine, fluspirilene, etc.), labelled by [3H] fluspirilene in skeletal muscle, were not identified in brain membranes, althou

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48

Clarkson, Andrew N., and n/a. "Lasting neuroprotection with clomethiazole following hypoxia-ischaemia-induced neurodegeneration : a mechanistic study." University of Otago. Department of Pharmacology & Toxicology, 2005. http://adt.otago.ac.nz./public/adt-NZDU20070424.120005.

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Subsequent to an hypoxic-ischaemic (HI)-insult a multi-faceted complex cascade of events occurs that ultimately results in cellular and neurological impairments within cortical and sub-cortical central nervous system (CNS) regions. In the present studies a modified �Levine� rat-pup model of HI (left carotid artery ligation + 1 hour global hypoxia on post-natal day (PND) 26) was employed to assess the neuroprotective properties of clomethiazole (CMZ; a γ-aminobutyric acid (GABA)A receptor agonist). In this study, histological and electrophysiological paradigms were used to assess the long-term

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49

Gordon, Kirsty. "Investigation of the effects of oestrogen in rodent models of cerebral ischaemia and brain injury." Thesis, University of Glasgow, 2005. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.433066.

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50

Ekelund, Anders. "Detection and haemodilutive treatment of cerebral arterial vasospasm and delayed ischaemia after aneurysmal subarachnoid haemorrhage." Lund : Lund University, 1999. http://catalog.hathitrust.org/api/volumes/oclc/68945106.html.

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