Relevant bibliographies by topics / Ischaemia

Academic literature on the topic 'Ischaemia'

Author: Grafiati
Published: 4 June 2021
Last updated: 25 May 2024

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Journal articles on the topic "Ischaemia"

1

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 derivatives and advanced oxidized protein products (AOPPs) were evaluated. RESULTS: The size of brain infarction after ischaemic postconditioning was significantly smaller compared with the ischaemia group, and was concomitant with significant reduction in protein carbonyl derivatives and AOPPs. The activities of SOD, CAT and proteasomes were elevated by ischaemic postconditioning compared with the ischaemia group. CONCLUSIONS: Ischaemic post-conditioning is an effective way of reducing the size and effects of brain infarction caused by focal ischaemia/reperfusion, possibly due to a decrease in oxidized protein levels. Decreasing protein oxidization may, therefore, be a useful target for preventing cerebral injury.
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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 rats, and during a 1 min probe trial, only ischaemic rats were impaired. On the matching-to-position task, ibotenic rats showed greater impairment than ischaemic rats in terms of one-trial learning, whereas ischaemic rats were more impaired after Trial 2. Ischaemia and ibotenic acid lesions resulted in equivalent CA1 loss, but silver impregnation revealed additional extra-CA1 cell loss in ischaemic rats. Together with the greater behavioural deficits of ischaemic rats, these data indicate a role for extra-CA1 cell loss in ischaemia-induced memory impairments in both animals and humans.
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Saeid, Feyzizadeh, Javadi Aniseh, Badalzadeh Reza, and Vafaee S. Manouchehr. "Signaling mediators modulated by cardioprotective interventions in healthy and diabetic myocardium with ischaemia–reperfusion injury." European Journal of Preventive Cardiology 25, no. 14 (February 14, 2018): 1463–81. http://dx.doi.org/10.1177/2047487318756420.

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Ischaemic heart diseases are one of the major causes of death in the world. In most patients, ischaemic heart disease is coincident with other risk factors such as diabetes. Patients with diabetes are more prone to cardiac ischaemic dysfunctions including ischaemia–reperfusion injury. Ischaemic preconditioning, postconditioning and remote conditionings are reliable interventions to protect the myocardium against ischaemia–reperfusion injuries through activating various signaling pathways and intracellular mediators. Diabetes can disrupt the intracellular signaling cascades involved in these myocardial protections, and studies have revealed that cardioprotective effects of the conditioning interventions are diminished in the diabetic condition. The complex pathophysiology and poor prognosis of ischaemic heart disease among people with diabetes necessitate the investigation of the interaction of diabetes with ischaemia–reperfusion injury and cardioprotective mechanisms. Reducing the outcomes of ischaemia–reperfusion injury using targeted strategies would be particularly helpful in this population. In this study, we review the protective interventional signaling pathways and mediators which are activated by ischaemic conditioning strategies in healthy and diabetic myocardium with ischaemia–reperfusion injury.
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Dart, A. M., and R. A. Riemersma. "Origins of endogenous noradrenaline overflow during reperfusion of the ischaemic rat heart." Clinical Science 74, no. 3 (March 1, 1988): 269–74. http://dx.doi.org/10.1042/cs0740269.

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1. Reperfusion of the globally ischaemic isolated rat heart is associated with an enhanced overflow of endogenous noradrenaline (NA) after ischaemic periods of 20, 40 or 60 min but not of 10 min. 2. Reperfusion NA overflow, after 40 min of ischaemia, is suppressed by desipramine and increased when ischaemia follows a period of substrate deprivation. 3. Reperfusion after 40 min of ischaemia is associated with a significant rise in NA concentration despite a simultaneous 20-fold increase in flow. This increase in concentration is abolished by treatment with desipramine or if ischaemia follows a period of substrate deprivation. 4. Reperfusion NA overflow correlates with the reperfusion overflow of an extracellular space marker infused before the ischaemic episode. 5. These results suggest that ischaemia is heterogeneous and that NA is released into regions of particularly profound ischaemia from which it is subsequently eluted during reperfusion.
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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 leading to reduced post-ischaemic brain tissue inflammation. This article argues that the systemic balance of the immune system might explain the reduced neurodegeneration observed after stem cell treatment in cerebral ischaemia. Consequently, systemic immunoregulatory neuroprotection using stem and precursor cells should be considered an important therapeutic option to prevent post-ischaemic neurodegeneration in 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 damage (from 1,625 ± 384 mm3 of the cerebral hemisphere in vehicle-treated cats to 792 ± 385 mm3 in MK-801-treated cats). The demonstration of reduced ischaemic brain damage with MK-801, when the agent is administered after the induction of ischaemia, extends the therapeutic potential of such agents in the treatment of focal cerebral ischaemia in humans.
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Churchill, E. N., and D. Mochly-Rosen. "The roles of PKCδ and ϵ isoenzymes in the regulation of myocardial ischaemia/reperfusion injury." Biochemical Society Transactions 35, no. 5 (October 25, 2007): 1040–42. http://dx.doi.org/10.1042/bst0351040.

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Reperfusion of ischaemic cardiac tissue is associated with increased apoptosis and oncosis, resulting in diminished heart function. Short bouts of ischaemia before the prolonged ischaemic event (ischaemic preconditioning) protect the heart from injury mediated by reperfusion. The PKC (protein kinase C) family of serine/threonine kinases are involved in many different signalling processes. Two calcium-insensitive isoforms of the novel PKC subfamily, PKCδ and ϵ, play opposing roles in ischaemia/reperfusion injury. Activation of PKCδ during reperfusion induces cell death through the regulation of mitochondrial function and induction of apoptosis and oncosis. In contrast, activation of PKCϵ before ischaemia protects mitochondrial function and diminishes apoptosis and oncosis. How can two highly homologous PKC isoenzymes play such opposing roles through the regulation of mitochondrial function? This review will highlight what is known about PKCδ and ϵ function during ischaemia/reperfusion injury and will suggest a novel regulatory pathway which determines the fate of the cell following ischaemic stress.
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AL-QATTAN, M. M. "Ischaemia-Reperfusion Injury." Journal of Hand Surgery 23, no. 5 (October 1998): 570–73. http://dx.doi.org/10.1016/s0266-7681(98)80003-x.

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Prolonged ischaemia sometimes occurs in replantation and free flap surgery. The re-establishment of circulatory flow to the ischaemic tissue leads to a cascade of events which augments tissue necrosis. This paper reviews the pathophysiology of this ischaemia-reperfusion injury and discusses different methods to modulate this injury.
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Simon, R., and Z. Xiong. "Acidotoxicity in brain ischaemia." Biochemical Society Transactions 34, no. 6 (October 25, 2006): 1356–61. http://dx.doi.org/10.1042/bst0341356.

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Intracellular calcium toxicity remains the central feature in the pathophysiology of ischaemic cell death in brain. Glutamate-gated channels have been thought to be the major sites of ischaemia-induced toxic calcium entry, but the failure of glutamate antagonists in clinical trials has suggested that glutamate-independent mechanisms of calcium entry during ischaemia must exist and may prove central to ischaemic injury. We have shown that ASICs (acid-sensing ion channels) in brain are glutamate-independent vehicles of calcium flux and transport calcium in greater measure in the setting of the two major neurochemical components of ischaemia: acidosis and substrate depletion. Pharmacological blockade of ASICs markedly attenuates stroke injury with a robust therapeutic time window of 5 h following stroke onset. Here, we describe this new mechanism of calcium toxicity in brain ischaemia and offer a potential new therapy for stroke.
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HILLIER, C., R. D. SAYERS, P. A. C. WATT, R. NAYLOR, P. R. F. BELL, and H. THURSTON. "Altered small artery morphology and reactivity in critical limb ischaemia." Clinical Science 96, no. 2 (February 1, 1999): 155–63. http://dx.doi.org/10.1042/cs0960155.

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Although the pathophysiology of critical limb ischaemia is poorly understood, there is evidence that the condition of the small arteries may determine the outcome of revascularization procedures. This study was designed to investigate the effects of critical limb ischaemia on the structure and function of the small arteries in the leg. Small arteries (< 500 μm) from proximal (non-ischaemic) and distal (ischaemic) sites were obtained from patients undergoing bypass surgery for critical limb ischaemia and mounted in a myograph. Reactivity and morphological measurements were carried out and compared with controls. Control vessels from the thigh and calf showed no difference in media to lumen ratio. However, a comparison of ischaemic and non-ischaemic vessels from the patients with critical limb ischaemia showed significant thinning of the ischaemic vessel wall. Contraction studies using noradrenaline and angiotensin II revealed a significant decrease in the response of ischaemic vessels compared with the non-ischaemic vessels from the same patient. Moreover, these differences in reactivity were still apparent after the responses were corrected for wall thickness. Endothelial function assessed using the endothelium-dependent agonists acetylcholine and bradykinin showed a significantly impaired relaxation response to acetylcholine but not to bradykinin in the ischaemic vessels, and acetylcholine-induced relaxation was not improved after incubation with indomethacin. There was no change in the response to the endothelium-independent cAMP-mediated vasodilator iloprost but a significant impairment to sodium nitroprusside which acts via cGMP. These results suggest that small arteries in critical limb ischaemia are altered in both structure and function, with vessel wall thinning and impaired responses to acetylcholine and sodium nitroprusside.
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Dissertations / Theses on the topic "Ischaemia"

1

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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Willems, Laura E., and n/a. "Adenosine and Ischaemia in Young To Aged Hearts." Griffith University. School of Medical Science, 2006. http://www4.gu.edu.au:8080/adt-root/public/adt-QGU20061011.163451.

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Ischaemic heart disease is a major contributor to premature death and heart failure in the Westernised world. Ischaemic injury within the heart may be beneficially modulated by the nucleoside adenosine. Derived from catabolism of ATP, adenosine was initially known as a potent bradycardic and hypotensive agent. However, more recently the protective function of adenosine has been investigated. The protective effects of adenosine are mediated via activation of adenosine receptors: A1, A2A, A2B, and A3 receptors. Activation of these potentially protective (or retaliatory) adenosine receptors hinges upon accumulation of adenosine during ischaemia-reperfusion. This Thesis examines the role and mechanisms of adenosine mediated cardioprotection in young and aged hearts, exploring endogenous and exogenous adenosine receptor activation, genetic manipulation of A1 receptors and adenosine deaminase and pharmacological manipulation of adenosine metabolism. The effects of age on ischaemic responses and adenosine handling and protection are also assessed. The core approach to assess each of the above issues involved the Langendorff isolated mouse heart preparation. Experiments within Chapter 3 focuses on the contractile effects of adenosine receptors in normoxic hearts. This study indicates A2A receptors have no direct effect on contractility, while adenosine exerts positive inotropy independently of coronary flow and perfusion pressure (i.e. Independent of the Gregg phenomenon). In addition, investigations in genetically modified hearts hint at positive inotropy in response to A1 receptors. Since the latter is only evidenced in modified lines, it is possible A1-mediated inotropy may be abnormal or supraphysiological. In Chapter 4 the impact of genetic 'deletion' of A1ARs and/or adenosine deaminase (ADA) on intrinsic tolerance to ischaemia were studied. Data demonstrate that genetic deletion of A1 receptors significantly limits the ability of the mouse myocardium to withstand injury during ischaemic insult. Thus, providing strong support for a role of A1ARs in determining intrinsic tolerance to ischaemia-reperfusion. ADA KO mice confirm protection afforded by endogenous adenosine and the notion of adenosine metabolism modification as a protective strategy. Interestingly, effects of A1AR KO differ from A1AR overexpression or A1AR agonism in that the latter decrease contractile diastolic dysfunction while A1AR KO selectively increase systolic dysfunction and increase oncosis without altering diastolic injury. This challenges current dogma regarding the action of A1 adenosine receptors on ischaemic injury. In Chapter 5 the effects of adenosine metabolism inhibition (via adenosine deaminase (ADA) and adenosine kinase (AK) inhibitors) were studied. Inhibition of adenosine deaminase with the drug EHNA, and adenosine phosphorylation with iodotubercidin significantly protected mouse hearts from ischaemia-reperfusion, reducing contractile dysfunction and cardiac enzyme efflux. However, inhibitors failed to improve the outcome of the aged myocardium. 8-SPT and 5-HD reduced the protective effects of EHNA and iodotubercidin demonstrating thus; cardioprotection via ADA and AK appears to rely on adenosine receptor activation and involves a mitoK ATP dependent mechanism. Since aging is of considerable importance with regard to outcomes of ischaemic heart disease, experiments in Chapter 6 focused on effects of aging (and gender) on cardiovascular function and injury during ischaemia-reperfusion. In assessing post ischaemic outcomes in hearts from young adult (2-4 months), mature adult (8 months), middle aged (12 months), aged (18 months) and senescent (24-28 months) C57/BL/6J mice, data reveal a substantial age-related decline in ischaemic tolerance (which appears selective for myocardial vs. vascular injury). The decline in ischaemic tolerance is expressed primarily within the initial 12 months in both males and females with relatively little further decline with continued aging. There is evidence of a modest improvement in tolerance in senescence vs. aged hearts possibly reflecting selection of a protected phenotype in senescent populations. In addition, mature and middle-aged female hearts showed improved tolerance to ischaemia-reperfusion compared to males, supporting a role for hormonal changes. Effects of aging and purine metabolism were studied in Chapter 7. Data suggest impaired tolerance to ischaemia-reperfusion in older hearts may stem in part from shifts in myocardial purine catabolism. Data reveal reduced accumulation of salvageable and cardioprotective adenosine and enhanced accumulation of poorly salvaged (and potentially injurious) hypoxanthine and xanthine. These changes may potentially predispose the aged myocardium to ischaemic injury and radical generation via the xanthine oxidase reaction. The final data Chapter of this Thesis describes preliminary data regarding aging, signalling and adenosine mediated protection. It was found that protein kinase C (PKC) and A1 receptors mediate protection in young hearts and also that A1 receptors appear to mediate protection via a PKC LindependentLi signalling cascade. In addition, experiments in aged hearts (attempting to elucidate mechanisms behind impaired adenosinergic protection with age) suggest a PKC-independent A1-mediated protection path may be preserved with aging, since A1 receptors continue to offer some protection while PKC activation does not. It is possible the failure of exogenous adenosine to offer protection in aged hearts may result from a lesion at or downstream of PKC.
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Willems, Laura E. "Adenosine and Ischaemia in Young To Aged Hearts." Thesis, Griffith University, 2006. http://hdl.handle.net/10072/365196.

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Ischaemic heart disease is a major contributor to premature death and heart failure in the Westernised world. Ischaemic injury within the heart may be beneficially modulated by the nucleoside adenosine. Derived from catabolism of ATP, adenosine was initially known as a potent bradycardic and hypotensive agent. However, more recently the protective function of adenosine has been investigated. The protective effects of adenosine are mediated via activation of adenosine receptors: A1, A2A, A2B, and A3 receptors. Activation of these potentially protective (or retaliatory) adenosine receptors hinges upon accumulation of adenosine during ischaemia-reperfusion. This Thesis examines the role and mechanisms of adenosine mediated cardioprotection in young and aged hearts, exploring endogenous and exogenous adenosine receptor activation, genetic manipulation of A1 receptors and adenosine deaminase and pharmacological manipulation of adenosine metabolism. The effects of age on ischaemic responses and adenosine handling and protection are also assessed. The core approach to assess each of the above issues involved the Langendorff isolated mouse heart preparation. Experiments within Chapter 3 focuses on the contractile effects of adenosine receptors in normoxic hearts. This study indicates A2A receptors have no direct effect on contractility, while adenosine exerts positive inotropy independently of coronary flow and perfusion pressure (i.e. Independent of the Gregg phenomenon). In addition, investigations in genetically modified hearts hint at positive inotropy in response to A1 receptors. Since the latter is only evidenced in modified lines, it is possible A1-mediated inotropy may be abnormal or supraphysiological. In Chapter 4 the impact of genetic 'deletion' of A1ARs and/or adenosine deaminase (ADA) on intrinsic tolerance to ischaemia were studied. Data demonstrate that genetic deletion of A1 receptors significantly limits the ability of the mouse myocardium to withstand injury during ischaemic insult. Thus, providing strong support for a role of A1ARs in determining intrinsic tolerance to ischaemia-reperfusion. ADA KO mice confirm protection afforded by endogenous adenosine and the notion of adenosine metabolism modification as a protective strategy. Interestingly, effects of A1AR KO differ from A1AR overexpression or A1AR agonism in that the latter decrease contractile diastolic dysfunction while A1AR KO selectively increase systolic dysfunction and increase oncosis without altering diastolic injury. This challenges current dogma regarding the action of A1 adenosine receptors on ischaemic injury. In Chapter 5 the effects of adenosine metabolism inhibition (via adenosine deaminase (ADA) and adenosine kinase (AK) inhibitors) were studied. Inhibition of adenosine deaminase with the drug EHNA, and adenosine phosphorylation with iodotubercidin significantly protected mouse hearts from ischaemia-reperfusion, reducing contractile dysfunction and cardiac enzyme efflux. However, inhibitors failed to improve the outcome of the aged myocardium. 8-SPT and 5-HD reduced the protective effects of EHNA and iodotubercidin demonstrating thus; cardioprotection via ADA and AK appears to rely on adenosine receptor activation and involves a mitoK ATP dependent mechanism. Since aging is of considerable importance with regard to outcomes of ischaemic heart disease, experiments in Chapter 6 focused on effects of aging (and gender) on cardiovascular function and injury during ischaemia-reperfusion. In assessing post ischaemic outcomes in hearts from young adult (2-4 months), mature adult (8 months), middle aged (12 months), aged (18 months) and senescent (24-28 months) C57/BL/6J mice, data reveal a substantial age-related decline in ischaemic tolerance (which appears selective for myocardial vs. vascular injury). The decline in ischaemic tolerance is expressed primarily within the initial 12 months in both males and females with relatively little further decline with continued aging. There is evidence of a modest improvement in tolerance in senescence vs. aged hearts possibly reflecting selection of a protected phenotype in senescent populations. In addition, mature and middle-aged female hearts showed improved tolerance to ischaemia-reperfusion compared to males, supporting a role for hormonal changes. Effects of aging and purine metabolism were studied in Chapter 7. Data suggest impaired tolerance to ischaemia-reperfusion in older hearts may stem in part from shifts in myocardial purine catabolism. Data reveal reduced accumulation of salvageable and cardioprotective adenosine and enhanced accumulation of poorly salvaged (and potentially injurious) hypoxanthine and xanthine. These changes may potentially predispose the aged myocardium to ischaemic injury and radical generation via the xanthine oxidase reaction. The final data Chapter of this Thesis describes preliminary data regarding aging, signalling and adenosine mediated protection. It was found that protein kinase C (PKC) and A1 receptors mediate protection in young hearts and also that A1 receptors appear to mediate protection via a PKC LindependentLi signalling cascade. In addition, experiments in aged hearts (attempting to elucidate mechanisms behind impaired adenosinergic protection with age) suggest a PKC-independent A1-mediated protection path may be preserved with aging, since A1 receptors continue to offer some protection while PKC activation does not. It is possible the failure of exogenous adenosine to offer protection in aged hearts may result from a lesion at or downstream of PKC.
Thesis (PhD Doctorate)
Doctor of Philosophy (PhD)
School of Medical Science
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4

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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Khalid, Usman. "The role of microRNAs and ischaemic preconditioning in kidney ischaemia reperfusion injury." Thesis, Cardiff University, 2016. http://orca.cf.ac.uk/95843/.

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Successful kidney transplantation transforms outcome for patients with end stage kidney disease. Delayed graft function (DGF) following Ischaemia Reperfusion Injury (IRI) is a major problem, is hard to predict or monitor, and preventative or therapeutic strategies are lacking. Ischaemic Preconditioning (IPC) may limit IRI, but results are variable and potential mechanisms are not well defined. The aims of this thesis were to study the role of microRNAs, which are post-transcriptional regulators of gene expression vital in many physiological and pathophysiological processes, in the context of IRI, IPC and DGF. An in vivo model of IRI and IPC was developed, and histological, biochemical and mRNA kidney injury marker analyses were undertaken. MicroRNAs were then profiled using both Next Generation Sequencing (NGS) and hybridisation arrays, and changes in selected microRNAs confirmed by RTqPCR. Histology scores, serum creatinine and expression of kidney injury markers were significantly reduced in IPC compared with IRI. Microarray and NGS analysis identified a highly reproducible IRI signature, which was attenuated by IPC. Subsequently, microRNAs were profiled using Taqman Low Density Array (TLDA) and validated by RT-qPCR, from urine samples of kidney transplant patients with and without DGF. A DGF microRNA profile was uncovered, with overlap to the results from the IRI model. These data have identified a microRNA signature of IRI that was attenuated by IPC, which also improved outcome. Urinary microRNAs also showed a promising capability to predict DGF in human kidney transplantation. MicroRNAs thus show significant promise as biomarkers and potential therapeutic targets in this context.
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Banga, Neal Roop. "Effects of Ischaemia-Reperfusion Injury and Ischaemic Preconditioning on Human Liver Sinusoidal Endothelial Cells." Thesis, University of Leeds, 2009. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.515298.

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Mallick, Ismail Hameed. "Role of haem oxygenase in ischaemic preconditioning on the intestinal microcirculation following ischaemia reperfusion injury." Thesis, University College London (University of London), 2006. http://discovery.ucl.ac.uk/1444963/.

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Intestinal ischaemia reperfusion (IR) injury is associated with various clinical conditions such as hypovolemic shock, strangulation-obstruction, cardiovascular surgery, abdominal aortic surgery and small bowel transplantation. IR injury of the intestine is a systemic phenomenon resulting in bacterial translocation, endotoxaemia, acute respiratory distress syndrome and acute hepatic injury culminating in multiple organ failure. It has been hypothesised that ischaemic preconditioning may protect against IR injury of the intestine through haem oxygenase formation. This thesis (study) investigated the relationship of haem oxygenase metabolism with intestinal microvascular perfusion, tissue oxygenation and function with ischaemic preconditioning of the intestine in an experimental model of ischaemia reperfusion injury of the small intestine. Male Sprague Dawley rats (250-300 grams) were subjected to 30 mins of ischaemia by clamping of superior mesenteric artery followed by 2 hrs (early phase) or 24 hrs (late phase) of reperfusion. Ischaemic preconditioning was performed with 10 min ischaemia and 10 min reperfusion before the sustained ischaemia. Pyrrolidine dithiocarbamate (PDTC) or Zinc Protoporrphyrrin (ZnPP) were administered to stimulate or block heme oxygenase synthesis. The study demonstrated that ischaemic preconditioning resulted in significantly improvement in intestinal microvascular perfusion, tissue oxygenation as well as decreased leukocyte-endothelial interactions and intestinal and pulmonary injury following both early and late phases of IR injury. The preconditioning effect was associated with significantly increased haem oxygenase production suggested by intestinal tissue haeme oxygenase levels as demonstrated by haem oxygenase assays and western blotting. PDTC treatment reproduced the protective effect of ischaemic preconditioning. Haem oxygenase inhibition with ZnPP antagonized the protective effect of ischaemic preconditioning. This thesis has shown that the protective effect of intestinal ischaemic preconditioning against both early and late phases of IR injury is associated with increased haem oxygenase production. These data may have important implications in intestinal surgery and transplantation and may lead to the development of pharmacological strategies for protecting the intestine from ischaemic injury.
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Robertson, F. "The effect of remote ischaemic preconditioning on CD4 T cells following hepatic ischaemia reperfusion injury." Thesis, University College London (University of London), 2018. http://discovery.ucl.ac.uk/10047916/.

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Ischaemia Reperfusion (IR) injury is a major cause of morbidity and mortality following orthotopic liver transplantation. Remote Ischaemic Preconditioning (RIPC) reduces IR injury in small animal models. The mechanism remains unclear. The aim of this thesis was to explore the mechanism of RIPC and its clinical relevance to liver transplant recipients. Following a literature review a study was performed on optimal end points for clinical studies modulating IR injury in liver transplantation. Day 3 AST level was strongly associated with early post operative morbidity and mortality. A pilot randomised controlled trial of limb RIPC (3 cycles 5 minutes) in 40 liver transplant recipients was performed. Recruitment was successful and the intervention found to be safe and well tolerated. There was no significant difference in day 3 AST. CD4+T cell IFNγ and TNFα production was found to be significantly upregulated in patients post-reperfusion but not affected by RIPC. IFNγ and IL-2 were produced by a CD3-ve HLADR+ve cell population. Monocyte chemoattractant protein-1 (MCP-1) levels were significantly elevated following reperfusion and correlated with clinical outcomes. The T cell response to RIPC was further investigated in a murine model of RIPC and warm liver IR injury. The model demonstrated a reduction in warm liver IR injury following RIPC. Intrahepatic CD4+ T cell TNFα production was significantly increased following reperfusion and reduced by RIPC. Monocytes were recruited to the post ischaemic liver as demonstrated in the human clinical trial. MCP-1 levels and monocyte recruitment were significantly reduced following RIPC in the mouse. In conclusion clinical benefit of RIPC in OLT recipients was not achieved in this pilot study. The RIPC stimulus may be sub-optimal. CD4+T cells and monocytes were shown to have a key role in both the human and animal studies and their manipulation may provide new opportunities for modulating liver IR injury.
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Hobbs, Catherine E., and n/a. "Perinatal hypoxia-ischaemia : neuroprotective strategies." University of Otago. Department of Anatomy & Structural Biology, 2005. http://adt.otago.ac.nz./public/adt-NZDU20070221.145910.

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Perinatal hypoxia-ischaemia is a major cause of disability, including cerebral palsy, yet a neuroprotectant which fully protects the brain remains elusive. Following a hypoxic-ischaemic insult, striatal medium-spiny neurons and hippocampal CA1 neurons are vulnerable to a complex cascade of neurotoxic events. This cascade includes energy failure, a massive release of glutamate, the formation of free radicals and caspase activation. The overall aim of this thesis was to assess the efficacy of three potential neuroprotective strategies that target this cascade from different directions. Short-term, and where appropriate, long-term, neuroprotection was investigated. The first treatment strategy aimed to suppress the generation of free radicals through treatment with the potent free radical spin trap, N-tertbutyl-(2-sulphophenyl)-nitrone (S-PBN). The second compound tested was the caspase-3 inhibitor, minocycline. Finally, the third treatment strategy combined a series of S-PBN injections with 6 hours of moderate hypothermia immediately after hypoxia-ischaemia. Hypothermia is suggested to slow the rate of the neurotoxic cascade, thus potentially allowing other neuroprotective agents greater efficacy. Using an adaptation of the Rice et al. (1981) model, hypoxia-ischaemia was induced on postnatal day (PN) 8 in the right cerebral hemisphere. For the short-term studies, the rats were perfused at 14 days-of-age. The brains were dissected out and embedded in Technovit. Forty [mu]m serial sections were cut through the right striatum and hippocampus. The total number of medium-spiny neurons in the striatum and where appropriate, the total number of neurons in the hippocampal CA1 pyramidal layer, were stereologically determined using the optical disector/Cavalieri method. For the long-term study, fine motor control was assessed in half of the animals through the staircase test from 9-11 weeks-of-age. Neuroprotection was assessed in the remaining animals. All animals were sacrificed at 12 weeks-of-age. The total number of striatal medium-spiny neurons was stereologically determined in the non-behavioural animals as described above. A series of seven injections of S-PBN (100mg/kg) did not offer statistically significant neuroprotection to the striatum at one week after perinatal hypoxia-ischaemia. Similarly, a single injection of minocycline (45mg/kg) immediately after the insult did not offer significant neuroprotection to the striatum nor the CA1 region of the hippocampus at this early time-point. In contrast, when the series of S-PBN injections was combined with 6 hours of moderate hypothermia post-hypoxia-ischaemia, sterelogical analysis revealed significant neuroprotection of the striatal medium-spiny neurons to normal levels at one week after the injury. No significant neuroprotection was seen in the CA1 region of the same animals. To assess whether this impressive striatal neuroprotection was long-lasting and whether it represented functional rescue, the final experiment in this thesis investigated rat pups at 12 weeks-of-age after exposure to hypoxia-ischaemia at PN8. Treatment with S-PBN/hypothermia offered persistent neuroprotection of striatal medium-spiny neurons and preservation of fine motor skills compared to diluent-normothermia-treated controls. The long-term behavioural outcomes were compared with normal, uninjured controls and the total number of medium-spiny neurons was compared with normal numbers from the literature. These comparisons revealed that the histological and functional integrity of the striatum was rescued to normal levels. This is the first study to identify a treatment strategy that offers complete and long-lasting preservation of striatal neuronal numbers, by accurate and unbiased stereological methods, paired with persistent preservation of fine motor control following perinatal hypoxia-ischaemia.
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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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Books on the topic "Ischaemia"

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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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Dormandy, John A., and Günter Stock, eds. Critical Leg Ischaemia. Berlin, Heidelberg: Springer Berlin Heidelberg, 1990. http://dx.doi.org/10.1007/978-3-642-75625-2.

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A, Myers Kenneth, Nicolaides Andrew N, and Sumner David S, eds. Lower-limb ischaemia. London: Med-Orion, 1997.

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K, Widmer L., and Schering Health Care, eds. Critical limb ischaemia. Burgess Hill: Schering Health Care, 1991.

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Anderson, Robert H. The heart: Ischaemia. London: Gower, 1993.

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A, Grace P., and Mathie Robert T, eds. Ischaemia reperfusion injury. Oxford: Blackwell Science, 1999.

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O, Lowe Gordon D., and Schering Health Care, eds. Critical limb ischaemia. Burgess Hill: Schering Health Care, 1993.

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Alain, Branchereau, Fagrell Bengt, and Schering Health Care, eds. Critical limb ischaemia. Burgess Hill: Schering Health Care, 1992.

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S, Marber Michael, Yellon Derek M, and University College, London. Department of Molecular Pathology., eds. Ischaemia: Preconditioning and adaptation. Oxford: BIOS Scientific Publishers, 1996.

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Smith, Thomas C. G., ed. Ischaemia in Head Injury. Berlin, Heidelberg: Springer Berlin Heidelberg, 1996. http://dx.doi.org/10.1007/978-3-642-80172-3.

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Book chapters on the topic "Ischaemia"

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Piscioneri, Francesco. "Mesenteric Ischaemia and Ischaemic Colitis." In Hot Topics in Acute Care Surgery and Trauma, 115–20. Cham: Springer International Publishing, 2021. http://dx.doi.org/10.1007/978-3-030-68099-2_16.

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Cold, Georg E., and Bent L. Dahl. "Ischaemia." In Topics in Neuroanaesthesia and Neurointensive Care, 337–403. Berlin, Heidelberg: Springer Berlin Heidelberg, 2002. http://dx.doi.org/10.1007/978-3-662-04845-0_12.

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Cold, Georg Emil. "Ischaemic Thresholds and Development of Ischaemia." In Cerebral Blood Flow in Acute Head Injury, 14–15. Vienna: Springer Vienna, 1990. http://dx.doi.org/10.1007/978-3-7091-9101-9_3.

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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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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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Conference papers on the topic "Ischaemia"

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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 for the development of essential hypertension, myocardial, cerebral and leg ischaemia. It is also a secondary risk factor in patients who already had a clinical episode of ischaemia in any of these territories. There is similar evidence in relation to a high plasma fibrinogen.Furthermore therapeutic haemodilution or defibrinogenation are increasingly used in the prevention and treatment of ischaemia.Haemorheological factors in the microcirculation are probably equally important but more difficult to assess clinically. The concept of a 'vicious viscous spiral' in ischaemic tissue is gaining increasing support. Whatever the initial cause of the ischaemia, important secondary haemorheological changes occur which can perpetuate or aggravate the ischaemia. Most of the changes known to occur locally in ischaemic tissues such as hypoxia, acidosis, release of serotonin and platelet activation have been shown to impair the deformability of blood cells. This will be particularly important if the perfusion pressure is also decreased and may result in capillary plugging and uneven distribution of flow in the microcirculation. Abnormal blood cell filtrability, just as whole blood viscosity, has been shown to be associated with acute as well as chronic ischaemia in most territories. Furthermore there is a correlation between the magnitude of the haemorheological changes measured and the subsequent clinical course of the patient following an ischaemic injury.The newest aspect of haemorheology to attract clinical attention is the role of the white cell in ischaemia. Epidemiological as well as recent experimental and clinical studies suggest that the Theologically activated white cell may be the most dangerous component of blood in terms of perpetuating and extending tissue ischaemia.The assessment of the Theological properties of blood should form an integral part of studies looking at the causes and possible therapy of all forms of acute and chronic ischaemia.
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McGill, D., J. McGuiness, and N. Ardlie. "PLATELET FUNCTION ASSOCIATED WITH EXERCISE INDUCED MYOCARDIAL ISCHAEMIA: MODIFICATION BY COMBINED BETA-BL0CKER AND CALCIUM ENTRY BLOCKER THERAPY." In XIth International Congress on Thrombosis and Haemostasis. Schattauer GmbH, 1987. http://dx.doi.org/10.1055/s-0038-1643011.

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The relationship between platelet activation and exercise induced myocardial ischaemia is controversial, and the presence of measurable effects of anti-anginal drugs on platelet function requires further clarification. This study addresses these questions in patients with coronary artery disease (CAD), treated with metoprolol and nifedipine. Twenty seven clinically stable males aged 35 to 69 years (mean 53) with proven CAD, ceased all medications for 5 days, were maximally exercised on a treadmill, and then commenced treatment for 4 weeks. They were exercised to the same workload on treatment and again without drugs one week later. Blood samples were collected immediately before and after exercise in each of the three tests, to measure serum thromboxane B2 (TXB2). Myocardial ischaemia was assessed by ST segment depression. Statistical analysis was performed on paired and grouped data using the appropriate T-test. Baseline TXB2 levels were significantly lower in patients with exercise induced ischaemia, and this group had a significant increase in TXB2 production after exercise (Table). This increase was inhibited by therapy. .Those with a negative test had higher baseline TXB2 levels which not increase with exercise.It is concluded that myocardial ischaemia is associated with a lower potential for TXB2 production. It is also associated with an exercise induced increase in TXB2 which is prevented by anti-ischaemic drugs. It is suggested that continuous platelet activation may occur in CAD patients with ischaemia, depleting the potential for TXB2 production.
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Bashaeb, Khalid Omar, Marawan El Farargy, and George Antoniou. "Endovascular Treatment for Acute Mesenteric Ischaemia." In PAIRS Annual Meeting. Thieme Medical and Scientific Publishers Pvt. Ltd., 2017. http://dx.doi.org/10.1055/s-0041-1729783.

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Gomez, D. Vazquez, M. Marques Cami, F. Vilardell Villellas, N. Zaragoza Velasco, I. Miguel Salas, D. C. Bayas Pástor, I. Pascual, L. Verges Aleix, F. González-Huix Lladó, and M. Planella De Rubinat. "COVID-19 vaccination-related intestinal ischaemia." In ESGE Days 2023. Georg Thieme Verlag KG, 2023. http://dx.doi.org/10.1055/s-0043-1765105.

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Johnston, Peter. "A Model of Anatomically Opposed Ischaemia: Revisited." In 2019 Computing in Cardiology Conference. Computing in Cardiology, 2019. http://dx.doi.org/10.22489/cinc.2019.228.

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Lowe, G. D. O., G. Thomson, S. E. Lennie, J. Anderson, S. M. Cobbe, and C. D. Forbes. "COMPARISON OF BLOOD, RED CELL AND WHITE CELL RHEOLOGY IN UNSTABLE ANGINA AND ACUTE MYOCARDIAL INFARCTION." In XIth International Congress on Thrombosis and Haemostasis. Schattauer GmbH, 1987. http://dx.doi.org/10.1055/s-0038-1642844.

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In acute coronary artery thrombosis, the flow properties of blood might conceivably influence progression to (a) complete thrombotic occlusion and transmural myocardial infarction, or (b) resolution of ischaemia without infarction (unstable angina). To test this hypothesis, several rheological variables were measured in the following groups of patients, matched for age, sex and smoking habit: (1) acute transmural myocardial infarction (n=15); (2) unstable angina (ischaemic pain and ECG but no significant enzyme rise, (n=16); (3) non-cardiac acute chest pain (n=9); and (4) healthy controls (n=20). Patients with infarction had significantly elevated levels of blood viscosity at high and low shear rates (94 and 0.94 s™1, Contraves LS30) compared to all other groups, associated with significantly higher levels of haematocrit, fibrinogen, plasma viscosity and fibrinogen: white cell count was also significantly higher. These abnormalities could therefore predispose to complete thrombotic occlusion and infarction. Patients with unstable angina also had significant increases in fibrinogen, plasma viscosity and white cell count, intermediate between infarct patients and controls: however blood viscosity increase was prevented by a lower haematocrit, which may predispose to resolution of thrombosis and ischaemia. Red cell deformability (Contraves visconeter and St. George's Filtrometer with 5 μm Nuclepore filters) was normal in infarction and m unstable angina, but significantly decreased in non-cardiac chest pain. Polymorph leucocyte filtration in a positive-pressure system (Nuclepore 5 μm filters) was normal in infarction and unstable angina, and mononuclear leucocyte filtration was only slightly reduced in both groups. Hence the major rheological changes in myocardial infarction and unstable angina are increases m fibrinogen and cell counts, rather than altered cell deformability.
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Antón-Munárriz, Cristina, Rafael Pastor-Vargas, Juan M. Haut, Antonio Robles-Gómez, Mercedes E. Paoletti, and José Alberto Benítez-Andrades. "Detection of cerebral ischaemia using transfer learning techniques." In 2023 IEEE 36th International Symposium on Computer-Based Medical Systems (CBMS). IEEE, 2023. http://dx.doi.org/10.1109/cbms58004.2023.00284.

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Panico, Karine, Giovanni Weber, Marcela S. Carneiro-Ramos, and Jo�o Salinet. "Electrophysiological Effects on Renal Ischaemia/Reperfusion-Induced Cardiac Hypertrophy." In 2017 Computing in Cardiology Conference. Computing in Cardiology, 2017. http://dx.doi.org/10.22489/cinc.2017.301-394.

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Chan, Kai Man. "27 Lower limb ischaemia in patients undergoing VA ECMO." In 2nd Asia Pacific Advanced Heart Failure Forum (APAHFF 2018), 16th November 2018, Hong Kong. BMJ Publishing Group Ltd, British Cardiovascular Society and Asia Pacific Heart Association, 2019. http://dx.doi.org/10.1136/heartasia-2019-apahff.27.

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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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Reports on the topic "Ischaemia"

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Issa, Allaudin, Christian D. Fankhauser, and Arie Stewart Parnham. What are ischaemic and non-ischaemic priapism and their underlying causes? BJUI Knowledge, March 2022. http://dx.doi.org/10.18591/bjuik.0750.

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Yang, Ying, Xiangting Huang, Yuge Wang, and Lan Chen. The impact of Triglyceride-Glucose Index on Ischemic Stroke: a systematic review and meta-analysis. INPLASY - International Platform of Registered Systematic Review and Meta-analysis Protocols, November 2022. http://dx.doi.org/10.37766/inplasy2022.11.0145.

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Review question / Objective: This Systematic review, describes two issues. 1. in the general population, a high TyG index predicts the risk of ischaemic stroke (IS) P: the general population without ischaemic stroke. I: higher TyG index. C: lower TyG index. O: first ischaemic stroke occurrence. S: Observational study. 2.In the ischaemic stroke(IS) population, a high tyg index predicts poor prognostic outcome. P: ischaemic stroke patient population. I: higher TyG index. C: lower TyG index O: death, stroke recurrence, poor functional outcome, deterioration in neurological function. S: Observational study. Information sources: We searched the Cochrane Library, Embase, MEDLINE, Web of Science, PubMed, and other relevant English databases and related websites. In addition, we reviewed the references for inclusion for literature that we may not have retrieved.
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Basu, Sayani. Nanoparticle-Based Therapeutics for the Treatment of Stroke. Nature Library Ltd, November 2020. http://dx.doi.org/10.47496/nl.blog.13.

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Tang, Yanbing, Zilan Wang, Haiying Teng, Huiru Chen, Jiaye Lu, Zhouqing Chen, and Zhong Wang. Bone marrow mononuclear cell transplantation in patients with ischaemic stroke: protocol for a meta-analysis. INPLASY - International Platform of Registered Systematic Review and Meta-analysis Protocols, April 2023. http://dx.doi.org/10.37766/inplasy2023.4.0061.

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Chen, Chen, Xiao Li Yang, Yun Zhi Shen, Hui Weng Jiang, and Yan Hua Yin. A Systematic Review and Meta-analysis of Perioperative Ischaemic Stroke in Non-Cardiac Surgical Patients with Patent Foramen Ovale. INPLASY - International Platform of Registered Systematic Review and Meta-analysis Protocols, July 2023. http://dx.doi.org/10.37766/inplasy2023.7.0113.

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Zhou, Zhuo, Guixing Xu, Liuyang Huang, Hao Tian, Fengyuan Huang, Yilin Liu, Mingsheng Sun, and Fanrong Liang. Effectiveness and Safety of Electroacupuncture for Depression: a systematic review and meta-analysis. INPLASY - International Platform of Registered Systematic Review and Meta-analysis Protocols, January 2022. http://dx.doi.org/10.37766/inplasy2022.1.0068.

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Review question / Objective: Is electroacupuncture a safe therapy for the treatment of depression? Is electroacupuncture effective for the treatment of depression, as compared with sham control, or conventional drugs？ Condition being studied: Depression is a mood disorder that causes sufferers to feel sadness, decreased interest, guilt, self-blame, loss of energy, and experience sleep disorders such as insomnia. People suffering from depression even feel they have no way out and have suicidal thoughts. In the United States, the prevalence of a major depressive disorder is 16.2%1-3. The 2010 Global Burden of Disease Study identified major depression as the second leading cause of disability worldwide and a leading cause of the burden of suicide and ischaemic heart disease. At present, depression patients are mainly treated with antidepressants, but the efficacy is extremely unstable. Studies have shown that acupuncture can help improve symptoms in patients with depression, but these clinical studies have not been systematically evaluated, and further confirmation is needed to confirm the efficacy of electroacupuncture in treating depression.
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LI, Zhendong, Chengcheng Zhang, Hangjian Qiu, Xiaoqian Wang, and Yuejuan Zhang. Different Acupuncture Intervention Time-points for Rehabilitation of Post-Stroke Cognitive Impairment：Protocol For a Network Meta-analysis of Randomized Controlled Trials. INPLASY - International Platform of Registered Systematic Review and Meta-analysis Protocols, May 2022. http://dx.doi.org/10.37766/inplasy2022.5.0043.

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Review question / Objective: This study will provide evidence-based references for the efficacy of different acupuncture interventions time-point in the treatment of post-stroke cognitive impairment(PSCI). 1. Types of studies. Only randomized controlled trials (RCTs) of acupuncture for PSCI will be recruited. Additionally, Studies should be available in full papers as well as peer-reviewed and the original data should be clear and adequate. 2. Types of participants. All adults with a recent or previous history of ischaemic or hemorrhagic stroke and diagnosed according to clearly defined or internationally recognized diagnostic criteria, regardless of nationality, race, sex, age, or educational background. 3. Types of interventions and controls. The control group takes non-acupuncture treatment, including conventional rehabilitation or in combination with symptomatic support therapy. The experimental group should be treated with acupuncture on basis of the control group. 4. Types of outcomes. The primary outcomes are measured with The Mini-Mental State Examination (MMSE) and/or The Montreal Cognitive Assessment Scale (MoCA), which have been widely used to evaluate cognitive abilities.
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LI, Zhendong, Hangjian Qiu, xiaoqian Wang, chengcheng Zhang, and Yuejuan Zhang. Comparative Efficacy of 5 non-pharmaceutical Therapies For Adults With Post-stroke Cognitive Impairment: Protocol For A Bayesian Network Analysis Based on 55 Randomized Controlled Trials. INPLASY - International Platform of Registered Systematic Review and Meta-analysis Protocols, June 2022. http://dx.doi.org/10.37766/inplasy2022.6.0036.

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Review question / Objective: This study will provide evidence-based references for the efficacy of 5 different non-pharmaceutical therapies in the treatment of post-stroke cognitive impairment(PSCI). 1. Types of studies. Only randomized controlled trials (RCTs) of Transcranial Magnetic Stimulation(TMS), Transcranial Direct Current Stimulation(tDCS), Acupuncture, Virtual Reality Exposure Therapy(VR) and Computer-assisted cognitive rehabilitation(CA) for PSCI will be recruited. Additionally, Studies should be available in full papers as well as peer reviewed and the original data should be clear and adequate. 2. Types of participants. All adults with a recent or previous history of ischaemic or hemorrhagic stroke and diagnosed according to clearly defined or internationally recognized diagnostic criteria, regardless of nationality, race, sex, age, or educational background. 3.Types of interventions and controls. The control group takes non-acupuncture treatment, including conventional rehabilitation or in combination with symptomatic support therapy. The experimental group should be treated with acupuncture on basis of the control group. 4.The interventions of the experimental groups were Transcranial Magnetic Stimulation(TMS), Transcranial Direct Current Stimulation(tDCS), Acupuncture, Virtual Reality Exposure Therapy(VR) or Computer-assisted cognitive rehabilitation(CA), and the interventions of the control group takes routine rehabilitation and cognition training or other therapies mentioned above that were different from the intervention group. 5.Types of outcomes. The primary outcomes are measured with The Mini-Mental State Examination (MMSE) and/or The Montreal Cognitive Assessment Scale (MoCA), which have been widely used to evaluate the cognitive abilities. The secondary outcome indicator was the Barthel Index (BI) to assess independence in activities of daily living (ADLs).
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Transient ischaemic attacks may have greater long-term impact than previously thought. National Institute for Health Research, February 2017. http://dx.doi.org/10.3310/signal-000376.

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