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Relevant bibliographies by topics / Cerebral ischaemia

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Academic literature on the topic 'Cerebral ischaemia'

Author: Grafiati

Published: 4 June 2021

Last updated: 6 February 2022

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Journal articles on the topic "Cerebral ischaemia"

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Park, C. K., D. G. Nehls, D. I. Graham, G. M. Teasdale, and J. McCulloch. "Focal Cerebral Ischaemia in the Cat: Treatment with the Glutamate Antagonist MK-801 after Induction of Ischaemia." Journal of Cerebral Blood Flow & Metabolism 8, no. 5 (October 1988): 757–62. http://dx.doi.org/10.1038/jcbfm.1988.124.

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The effects of the glutamate N-methyl-D-aspartate receptor antagonist MK-801 in reducing ischaemic brain damage have been examined in anaesthetised cats, with drug treatment being initiated 2 h after the induction of cerebral ischaemia. Focal cerebral ischaemia was produced by permanent occlusion of one middle cerebral artery, and the animals were killed 6 h later. The amount of early irreversible ischaemic damage was assessed at 16 predetermined stereotactic planes. Treatment with MK-801 (5 mg/kg, i.v.) 2 h after middle cerebral artery occlusion reduced significantly the volume of ischaemic d

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2

Schwarting, Sönke, and Harald Neumann. "Immunoregulatory Neuroprotection of Cerebral Ischaemia by Haematopoietic Stem and Precursor Cells." European Neurological Review 4, no. 2 (2009): 42. http://dx.doi.org/10.17925/enr.2009.04.02.42.

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Cerebral ischaemia leads to early immune system activation followed by delayed immunosuppression. Post-ischaemic inflammation contributes to neurodegeneration. Although experimental approaches using adult stem or precursor cells have repeatedly demonstrated neuroprotective effects in cerebral ischaemia, the underlying mechanism of cell-mediated neuroprotection is still debated. It was suggested that stem or precursor cells invade ischaemic brain regions and act locally. However, recent data demonstrate that systemically transplanted stem or precursor cells have strong immunoregulatory effects

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Li, Zy, B. Liu, J. Yu, Fw Yang, Yn Luo, and Pf Ge. "Ischaemic Postconditioning Rescues Brain Injury Caused by Focal Ischaemia/Reperfusion via Attenuation of Protein Oxidization." Journal of International Medical Research 40, no. 3 (June 2012): 954–66. http://dx.doi.org/10.1177/147323001204000314.

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OBJECTIVE: To investigate the effects of ischaemic postconditioning on brain injury and protein oxidization in focal ischaemia/reperfusion. METHODS: Adult male Wistar rats ( n = 30) were randomly divided into sham-operated, ischaemia, and ischaemic postconditioning groups. Ischaemia was produced by middle cerebral artery occlusion and ischaemic postconditioning was performed using three cycles of 30-s/30-s reperfusion/reocclusion after 2 h of ischaemia. Brain infarction size, hydrogen peroxide concentration, superoxide dismutase (SOD), catalase (CAT) and proteasome activities, protein carbonyl

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O'Shaughnessy, C. T., N. J. Rothwell, and J. Shrewsbury-Gee. "Effects of an analogue of thyrotrophin-releasing hormone, RX77368, on infarct size and cerebral blood flow in focal cerebral ischaemia in the rat." Canadian Journal of Physiology and Pharmacology 67, no. 10 (October 1, 1989): 1345–50. http://dx.doi.org/10.1139/y89-214.

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Effects of a stable analogue of thyrotrophin-releasing hormone, RX77368, on cerebral blood flow and infarct size have been studied in an acute model of cerebral ischaemia in the rat. Two hours after electrocoagulation of the left middle cerebral artery (MCA), the mean area of ischaemia (± SEM), determined histochemically, was 11.5 ± 2.2% of a single hemisphere and blood flow, determined using radiolabeled microspheres, was reduced by 40% in the left forebrain (p < 0.001 compared with sham-operated animals). Administration of RX77368 (50 μg/kg, intracerebroventricularly) within 10 min of art

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Kendall, B. "Cerebral Ischaemia." Rivista di Neuroradiologia 3, no. 2_suppl (September 1990): 35–38. http://dx.doi.org/10.1177/19714009900030s208.

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Bittencourt, P. R. M., S. Padilha, and S. Mazer. "Simple and safe heparin regimen for acute ischaemia." Arquivos de Neuro-Psiquiatria 44, no. 1 (March 1986): 32–37. http://dx.doi.org/10.1590/s0004-282x1986000100003.

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The risk/benefit ratio of acute anticoagulation in ischaemic cerebro-vascular disease is not clearly established. A simple and safe intermittent intravenous heparin regimen (20000 IU daily) was used prospectively in 50 patients of 57 ± 14 (m ± sd) years of age whose blood pressures ranged from normal to severe hypertension. Twenty-two patients had cardiogenic embolism and the remaining had recurrent severe transient ischaemic attacks of recent onset or progressive cerebral infarcts. Time of exposure to heparin was 6.4 ± 4 (m±sd) days. Two patients had recurrences of cerebral thromboembolism an

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7

Zhang, Pei-Lei, Hai-Tao Lu, Jun-Gong Zhao, and Ming-Hua Li. "Protective effect of dl-3n-butylphthalide preconditioning on focal cerebral ischaemia-reperfusion injury in rats." Acta Neuropsychiatrica 25, no. 1 (February 2013): 12–17. http://dx.doi.org/10.1111/j.1601-5215.2012.00649.x.

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ObjectiveTo investigate the effect of dl-3n-butylphthalide (NBP) on the protection of cerebral tissue and possible mechanism on ischaemia-reperfusion injury, and to find out whether NBP therapy can extend the reperfusion window in an experimental stroke model in rats.MethodsSeventy-two Sprague-Dawley rats were randomly divided into sham operation, ischaemia-reperfusion and ischaemia-reperfusion with NBP groups. Focal cerebral ischaemia was induced using the modified intraluminal thread method and maintained for 2, 3 or 4 h. The ischaemia-reperfusion group received reperfusion immediately after

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Tian, Lin, Yunqian Li, Wei Hua, Ying Jia, Min Zhou, Yunhe Gu, and Jiping Qi. "Expression of Urotensin II During Focal Cerebral Ischemic in Diabetic Rats." Canadian Journal of Neurological Sciences / Journal Canadien des Sciences Neurologiques 41, no. 4 (July 2014): 498–503. http://dx.doi.org/10.1017/s0317167100018552.

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Background:The objective of this study was to explore the expression of urotensin II (UII), its receptor (GPR14), and vascular endothelial growth factor (VEGF), as well as their associations in the ischaemic brains of rats with focal cerebral ischaemia, under normal and diabetic conditions.Methods:Diabetes mellitus (DM) was induced by injection of streptozotocin (STZ) into Sprague—Dawley rats. Focal cerebral ischaemia was induced by middle cerebral artery occlusion (MCAO) four weeks after DM onset by STZ. Rats (n=80) were divided into four groups: normal control, DM, MCAO, and DM/MCAO. Immunoh

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Tang, LL, K. Ye, XF Yang, and JS Zheng. "Apocynin Attenuates Cerebral Infarction after Transient Focal Ischaemia in Rats." Journal of International Medical Research 35, no. 4 (July 2007): 517–22. http://dx.doi.org/10.1177/147323000703500411.

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This study investigated whether inhibition of reduced nicotinamide adenine dinucleotide phosphate (NADPH) oxidase attenuates cerebral infarction after transient focal ischaemia in rats. Focal ischaemia (1.5 h) was produced in male Sprague-Dawley rats (250 − 280 g) by middle cerebral artery occlusion. Some rats also received treatment with 50 mg/kg apocynin, a NADPH oxidase inhibitor, by intraperitoneal injection 30 min prior to reperfusion. Two hours after reperfusion, brains were harvested to measure NADPH oxidase activity and superoxide levels. After 24 h, the remaining brains were harvested

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Nunn, J. A., J. A. Gray, and H. Hodges. "Neurotoxic Dorsal CA1 Lesions versus 4 VO Ischaemic Lesions: Behavioural Comparisons." Behavioural Neurology 11, no. 4 (1999): 217–26. http://dx.doi.org/10.1155/1999/603123.

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Anterograde amnesia, a common consequence of transient cerebral ischaemia, has been attributed to cell loss in the hippocampal CA1 subfield. However, variable, widespread damage outside hippocampal CA1 can also occur following ischaemia. We compared the functional consequences of ischaemia and ibotenate acid CA1 lesions on 2 spatial memory tasks (water maze ‘place’ and ‘matching-to-position’) to address the possibility that extra-CA1 loss contributes to ischaemia-induced memory deficits in the rat. During place task acquisition, ischaemic rats showed deficits on more measures than ibotenic rat

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Dissertations / Theses on the topic "Cerebral ischaemia"

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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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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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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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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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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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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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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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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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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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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Books on the topic "Cerebral ischaemia"

1

Bories, Jacques, ed. Cerebral Ischaemia. Berlin, Heidelberg: Springer Berlin Heidelberg, 1985. http://dx.doi.org/10.1007/978-3-642-70943-2.

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2

Loddick, Sarah Ann. The role of interleukin-1 in cerebral ischaemia. Manchester: University of Manchester, 1996.

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3

Nelson, Rachael M. Cellular effects of cerebral ischaemia in vitro: Cerebroprotective actions of GABAmimetic agents. Leicester: De Montfort University, 2002.

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4

Smith, T. C. G. 1939-, ed. Ischaemia in head injury: 10th European Congress of Neurosurgery, Berlin 1995 ; proceedings of a special symposium. Berlin: Springer, 1996.

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5

Kramer, G., W. Hacke, H. J. Gelmers, and M. Hennerici. Cerebral Ischaemia. Springer-Verlag Berlin and Heidelberg GmbH & Co. K, 1991.

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6

Krieglstein, Josef. Pharmacology of Cerebral Ischaemia. Elsevier, 1986.

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7

Cerebral Ischaemia: A Neuroradiological Study. Springer, 2011.

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8

Jacques, Bories, and Aymard A, eds. Cerebral ischaemia: A neuroradiological study. Berlin: Springer-Verlag, 1985.

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9

Alarcón, Gonzalo, Marian Lazaro, and Antonio Valentín. Migraine, stroke, and cerebral ischaemia. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780199688395.003.0033.

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This chapter reviews the electroencephalographic changes associated with migraine, stroke and cerebral ischaemia, and their interpretation to aid in their differential diagnosis. The incidence of stroke and cerebral ischaemia is increasing with population aging. They are some of the most common problems faced in emergency medicine, and their diagnosis can be puzzling. This chapter describes and illustrates the patterns seen in such conditions, such as slowing, frontal intermittent delta activity (FIRDA), periodic lateralized epileptiform discharge (PLED), generalized periodic lateralized epile

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R, Caplan Louis, ed. Cerebrovascular ischaemia investigation and management. London: Med-Orion, 1996.

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Book chapters on the topic "Cerebral ischaemia"

1

Bories, J. "Cerebral ischaemia: A neuroradiological study." In Cerebral Ischaemia, 1. Berlin, Heidelberg: Springer Berlin Heidelberg, 1985. http://dx.doi.org/10.1007/978-3-642-70943-2_1.

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Thiebot, J., and E. Clavier. "The place of digital intravenous angiography in cerebral infarcts." In Cerebral Ischaemia, 89–93. Berlin, Heidelberg: Springer Berlin Heidelberg, 1985. http://dx.doi.org/10.1007/978-3-642-70943-2_10.

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Boespflug, O. J. M. "Ultrasonography of supra-aortic trunks." In Cerebral Ischaemia, 94–97. Berlin, Heidelberg: Springer Berlin Heidelberg, 1985. http://dx.doi.org/10.1007/978-3-642-70943-2_11.

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4

Natali, J., and C. Ruotolo. "Post-operative angiographic control." In Cerebral Ischaemia, 98–106. Berlin, Heidelberg: Springer Berlin Heidelberg, 1985. http://dx.doi.org/10.1007/978-3-642-70943-2_12.

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Carpena, J. H., J. Bories, and J. Chiras. "Post-operative angiographic control." In Cerebral Ischaemia, 107–16. Berlin, Heidelberg: Springer Berlin Heidelberg, 1985. http://dx.doi.org/10.1007/978-3-642-70943-2_13.

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Raybaud, C. A., Marie-Odile Livet, M. Jiddane, and Nicole Pinsard. "Radiology of ischemic strokes in children." In Cerebral Ischaemia, 117–28. Berlin, Heidelberg: Springer Berlin Heidelberg, 1985. http://dx.doi.org/10.1007/978-3-642-70943-2_14.

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Grosgogeat, Y. "Cerebral ischemic accidents of cardiac origin." In Cerebral Ischaemia, 129–32. Berlin, Heidelberg: Springer Berlin Heidelberg, 1985. http://dx.doi.org/10.1007/978-3-642-70943-2_15.

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Bousser, M. G., J. C. Baron, and J. Chiras. "Ischemic strokes and migraine." In Cerebral Ischaemia, 133–37. Berlin, Heidelberg: Springer Berlin Heidelberg, 1985. http://dx.doi.org/10.1007/978-3-642-70943-2_16.

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Godon-Hardy, S., J. F. Meder, A. Dilouya, V. Monsaingeon, and D. Fredy. "Ischemic strokes and oral contraception." In Cerebral Ischaemia, 138–42. Berlin, Heidelberg: Springer Berlin Heidelberg, 1985. http://dx.doi.org/10.1007/978-3-642-70943-2_17.

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Chiras, J., M. Dubs, and J. Bories. "Venous infarctions." In Cerebral Ischaemia, 143–50. Berlin, Heidelberg: Springer Berlin Heidelberg, 1985. http://dx.doi.org/10.1007/978-3-642-70943-2_18.

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Conference papers on the topic "Cerebral ischaemia"

1

Dormandy, J. "RHEOLOGY AND ISCHAEMIA." In XIth International Congress on Thrombosis and Haemostasis. Schattauer GmbH, 1987. http://dx.doi.org/10.1055/s-0038-1643989.

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While the previous presentations have dealt with the experimental evidence linking flow patterns and shear stress to thrombosis and atherogenesis, this presentation will concentrate on the clinical evidence linking Theological abnormalities to macro and micro-circulatory ischaemia. Whole blood viscosity undoubtedly influences blood flow along larger vessels as suggested by Poiseuille. The two important determinants of whole blood viscosity are the red cell concentration and plasma fibrinogen.There is overwhelming epidemiological evidence that the red cell concentration is a primary risk factor

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SLOTWINSKI, K., P. CALABRESE, R. PODEMSKI, and W. GEHLEN. "HEMISPHERIC LATERALIZATION OF FOCAL CEREBRAL ISCHAEMIA AS REFERRED TO MEMORY PROCESSES." In Proceedings of the International School of Biocybernetics. WORLD SCIENTIFIC, 2002. http://dx.doi.org/10.1142/9789812776563_0036.

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Farrell-Dillon, Keith, Paul Fraser, Giovanni Mann, and Sarah Chapple. "9 P62 deficiency protects against cerebral ischaemia in insulin resistant mice." In Abstracts from the Fellowship of Postgraduate Medicine Centenary Conference 2018: Transforming Health and Health Care. The Fellowship of Postgraduate Medicine, 2018. http://dx.doi.org/10.1136/postgradmedj-2018-fpm.20.

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Farrell-Dillon, Keith, Paul A Fraser, and Giovanni E Mann. "7 Dietary sulforaphane reduces peri-infarct constriction frequency in mouse brain following focal cerebral ischaemia via a Nrf2-independent mechanism." In Abstracts from the Fellowship of Postgraduate Medicine Centenary Conference 2018: Transforming Health and Health Care. The Fellowship of Postgraduate Medicine, 2018. http://dx.doi.org/10.1136/postgradmedj-2018-fpm.18.

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Nechipurenko, N., L. Vasilevskaya, J. Musienko, and G. Maslova. "THE INFLUENCE OF INTRAVENOUS LASER IRRADIATION OF BLOOD ON SOME METABOLIC AND FUNCTIONAL PARAMATERS IN INTACT RABBITS AND EXPERIMENTAL CEREBRAL ISCHAEMIA." In European Conference on Biomedical Optics. Washington, D.C.: OSA, 2007. http://dx.doi.org/10.1364/ecbo.2007.6632_55.

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Nechipurenko, N., L. Vasilevskaya, J. Musienko, and G. Maslova. "The influence of intravenous laser irradiation of blood on some metabolic and functional parameters in intact rabbits and experimental cerebral ischaemia." In European Conference on Biomedical Optics, edited by Alfred Vogel. SPIE, 2007. http://dx.doi.org/10.1117/12.728721.

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Alessandri, C., F. Violi, M. Rasura, C. Caliendo, and P. Pelaia. "BEHAVIOUR OF ADREN0CHR0ME PATHWAY IN PATIENTS WITH CEREBROVASCULAR DISEASES." In XIth International Congress on Thrombosis and Haemostasis. Schattauer GmbH, 1987. http://dx.doi.org/10.1055/s-0038-1643169.

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Histopathological studies in segments of cerebral ischaemia show local inflammation with leucocytes infiltration.This event has been confirmed in vivo by means of radiolabelled leucocytes. This inflammatory response could be of detriment to cerebral tissue since leucocytes release toxic substances such as oxygen free radicals.A free radical mechanism,in fact,has been supposed as an event worsening the evolution of ischemia.Evidence of neutrophil activation in stroke patients was shown by us in previous reports, where we have described that the plasma of these patients contained an excess of a

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Zhou, Mingchao, Shanshan Ling, Hongxia Chen, and Ruihuan Pan. "Inhibition of notch signaling pathways contribute to neuroprotection effect by the combination of astragalus membranaceus and ligustrazine in rat model after thrombolysis of cerebral ischaemia." In 2017 IEEE International Conference on Bioinformatics and Biomedicine (BIBM). IEEE, 2017. http://dx.doi.org/10.1109/bibm.2017.8218051.

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Prins, M. H., G. J. H. den Ottolander, R. Gelsema, T. C. M. van Woerkom, A. K. Sing, and I. Heller. "DEEP VENOUS THROMBOSIS PR0FYLAXIS WITH A LMW HEPARIN (KABI 2165) IN STROKE PATIENTS." In XIth International Congress on Thrombosis and Haemostasis. Schattauer GmbH, 1987. http://dx.doi.org/10.1055/s-0038-1643217.

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In a group of 60 patients entering our hospital for completed stroke, within 72 hours after onset of symptoms, treatment with Kabi 2165 2x 2500 anti-Xa U s.c. was compared to placebo 2x s.c. in a double blind trial to test the assumption that Kabi 2165 could prevent DVT, without causing cerebral bleeding in the ischaemic area. The diagnosis of stroke was made on clinical grounds. A.CT-scan of the head was performed before entering the trial to exclude cerebral bleeding or tumor. Follow-up during a trial period of 14 days included a Fibrinogen scan - if positive followed by flebografy. After th

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Montecchio, G. P., P. Custodi, S. Carbone, C. Bendotti, and F. Piovella. "TICLOPIDINE AND INDOBUFEN: EFFECTS ON HAEMOSTATIC FUNCTIONS." In XIth International Congress on Thrombosis and Haemostasis. Schattauer GmbH, 1987. http://dx.doi.org/10.1055/s-0038-1643418.

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Many different mechanisms are involved in thrombus formation. We compared the effects on haemostatic function of two drugs having different mechanism of action, the one interfering with arachidonic acid metabolic cascade (Indobufen) and the other (Ticlopidine) independent from it. 18 adult patients of both sexes suffering from cerebral Transient Ischaemic Attack (T.I.A.) or Reversible Ischaemic Neurologic Disability (R.I.N.D.) have been treated with Indobufen (400 mg daily) or Ticlopidine (500 mg daily) for three weeks. The effects on various haemostatic parameters including bleeding time, pla

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