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Обухова, Ольга Анатоліївна, Ольга Анатольевна Обухова, Olha Anatoliivna Obukhova, and K. M. Sheikh. "Candidate genes of ischemic stroke." Thesis, Сумський державний університет, 2013. http://essuir.sumdu.edu.ua/handle/123456789/32180.
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Stroke has long been recognized as a major problem for public health. Ischemic stroke (IS) ranks third (after myocardial infarction and cancer) as a cause of death around the world.
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Kostulas, Konstantinos. "Genetic analysis of ischemic stroke and predisposing carotid artery stenosis : a stroke carol /." Stockholm : Karolinska institutet, 2007. http://diss.kib.ki.se/2007/978-91-7357-395-5/.
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Chong, Boon Hor, and 鍾文一. "Risk of ischemic stroke and recurrent hemorrhagic stroke in Chinese population." Thesis, The University of Hong Kong (Pokfulam, Hong Kong), 2011. http://hub.hku.hk/bib/B47323450.
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Stroke is a devastating, neurological dysfunction due to brain blood supply disturbance. It is responsible for increasingly high rate of mortality and disability worldwide. This thesis comprises two original studies involving 868 patients at risk of ischemic stroke and/or hemorrhagic stroke.
The first study investigated aspirin’s effect among patients with intracranial hemorrhage. Unlike Caucasians which hemorrhagic strokes account for 10-15% of all strokes; in Chinese, intracranial hemorrhages strike up to 35%. After such, anti-platelet agent like aspirin is often avoided for fear of recurrent intracranial hemorrhages, despite compelling indications. However, clinical data is limited. In this single-centered observational study, we included 440 consecutive Chinese patients with a first spontaneous intracranial hemorrhage surviving the first month performed during 1996-2010. 56 patients (12.7%) of these 440 patients were prescribed aspirin after intracranial hemorrhage (312 patient-aspirin years). After a mean follow-up of 62.2 ± 1.8 months, 47 patients had recurrent intracranial hemorrhage(10.7%, 20.6 per 1,000 patient years). Patients prescribed aspirin did not have higher risk of recurrent intracranial hemorrhage compared with those without (22.7 per 1,000 patient-aspirin years vs. 22.4 per 1,000 patient years, p=0.70). Multivariate analysis identified age > 60 years and hypertension as independent predictors for recurrent intracranial hemorrhage. In a subgroup analysis: the incidence of combined vascular events including recurrent intracranial hemorrhage, ischemic stroke, and acute coronary syndrome was statistically lower in patients prescribed aspirin than without (52.4 per 1,000 patient-aspirin years, vs. 112.8 per 1,000 patient-years, p=0.04). Implications of the results: despite having a substantial risk for recurrent intracranial hemorrhage, post-intracranial hemorrhage ones are at risk for thrombotic vascular events and management goal should thus focus on ameliorating overall cardiovascular risk instead of preventing recurrent intracranial hemorrhage. Hence, thrombo-prophylaxis should still be considered.
The second study investigated the relation between premature atrial complexes and new-onset atrial fibrillation together with other cardiovascular events. Premature atrial complexes though taken as benign phenomenon, are common in patients with underlying conditions such as coronary heart disease, chronic rheumatic heart disease. While prompt management of atrial fibrillation may prevent ischemic stroke, atrial fibrillation is often unfound until ischemic stroke occurs. In this study, 428 patients without atrial fibrillation but complained of palpitations, dizziness or syncope were recruited. 107 patients with >100 premature atrial complexes/day were defined to have frequent premature atrial complexes. After a mean follow-up of 6.1 ±1.3 years, 31 patients (29%) with frequent premature atrial complexes developed atrial fibrillation compared with 29 patients (9%) with premature atrial complexes?100/day (p<0.01). Cox regression analysis revealed: frequent premature atrial complexes, age>75 years and coronary artery disease were independent predictors. In secondary endpoint (ischemic stroke, congestive heart failure, and death), patients with frequent premature atrial complexes were more at risk than those without (34.5% vs. 19.3%) (Hazard ratio: 1.95, 95% confidence interval: 1.37-3.50, p=0.001). Cox regression analysis showed: age> 75 years, coronary artery disease and frequent premature atrial complexes were independent predictors. These permit early identification of high risks patients of new atrial fibrillation and other events, thus promoting appropriate preventive treatment.published_or_final_version
Medicine
Master
Master of Philosophy
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裴中 and Zhong Pei. "Neuroprotection of melatonin in ischemic stroke models." Thesis, The University of Hong Kong (Pokfulam, Hong Kong), 2002. http://hub.hku.hk/bib/B31243526.
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McVerry, Ferghal. "Multimodal CT imaging in acute ischemic stroke." Thesis, University of Glasgow, 2014. http://theses.gla.ac.uk/4868/.
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Introduction: Options for imaging in acute stroke are expanding with the potential to select therapy based on imaging targets, as well as providing additional diagnostic and prognostic information. Multimodal CT has been used to image the ischemic penumbra, infarct core, and to detect leptomeningeal collateral flow although the optimum way to image these variables is not clear. Methods: In addition to a systematic literature review of imaging for leptomeningeal collaterals, Data from observational studies of acute stroke which employed multimodal CT imaging on admission and follow up was used to evaluate feasibility of acute stroke imaging with CT and MRI, Perfusion thresholds for core and ischemic penumbra, methods to quantify leptomeningeal collateral flow and sensitivity of non contrast CT for detecting infarct core pixels. Results: Advanced imaging in acute stroke and at follow up was more feasible with CT compared to MRI with the possible suggestion that imaging with MRI alone could introduce a bias regarding age and clinical severity for patients entered into clinical studies Heterogeneity in grading and detecting collateral flow was found in the literature providing an opportunity to devise a novel assessment method. Well developed collaterals were associated with imaging and clinical markers for good outcome as well as some potential biomarkers including atrial fibrillation and blood fibrinogen level. Relative cerebral blood flow and delay time were found to be the best predictors on infarct core and ischemic penumbra after derivation of optimum perfusion thresholds and subsequent validation in independent patient groups. Pixel based comparison of infarct core on CT perfusion and non contrast CT highlighted the lack of sensitivity of CT for detecting infarct core based on Hounsfield unit value alone. Conclusion: Multimodal CT for acute stroke assessment offers the potential for measuring infarct core, ischemic penumbra and leptomeningeal collateral flow status rapidly according to novel grading scales and thresholds and provides information on tissue viability which cannot be detected on non-contrast CT. Further evaluation on the impact additional imaging should have in clinical practice is needed.
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Daubenspeck, April Arnold. "Proteomic Analysis of Ischemic Stroke Blood Biomarkers." Wright State University / OhioLINK, 2017. http://rave.ohiolink.edu/etdc/view?acc_num=wright1515748115902114.
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Vendrame, Martina. "Cord blood cell therapy for ischemic stroke." [Tampa, Fla.] : University of South Florida, 2004. http://purl.fcla.edu/fcla/etd/SFE0000462.
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Walsh, Kyle B. "Plasma Biomarkers for Ischemic and Hemorrhagic Stroke Diagnosis." University of Cincinnati / OhioLINK, 2017. http://rave.ohiolink.edu/etdc/view?acc_num=ucin1511859455574062.
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Abulafia, Denise P. "Inflammatory Mechanisms After Thromboembolic Ischemic Stroke in Mice." Scholarly Repository, 2008. http://scholarlyrepository.miami.edu/oa_dissertations/122.
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Stroke induces multiple pathological sequelae directly affecting neuronal survival and eliciting short and long-term deficits in behavioral outcome. Most of stroke models utilized to investigate these pathological consequences are based on pure cerebral ischemia models. However, human thromboembolic stroke is characterized by a complex multifactorial response that involves the activation of the cerebral microcirculation by the occluding thrombus. Here, we have characterized a novel mouse model of tromboembolic stroke that mimics most of the clinical aspects of the human pathology. The common carotid artery thrombosis (CCAT) model produces consistent and reproducible infarcts and triggers an inflammatory response comparable to other well established models of stroke. Several of the pathological consequences of cerebral ischemia are triggered by focal inflammatory processes that occur early after the ischemic event. Cerebral inflammation is initiated by an early release of pro-inflammatory cytokines. These active cytokines promote the recruitment of inflammatory cells from the blood cerebral circulation into the brain parenchyma and subsequent release of additional amounts of inflammatory cytokines. This exacerbated cytokine response result in further irreversible neuronal and histopathological damage. Cytokines interleukyne-1 beta (IL-1 beta) and interleukyne-18 (IL-18) maturation requires the presence of active caspase-1. Activation of caspase-1 in the peripheral immune response involves the recruitment of several caspase-1 molecules into a macromolecular complex termed the inflammasome. Cerebral ischemia triggers the synthesis and activation of caspase-1. However, the cellular mechanisms associated to the activation of caspase-1 in the ischemic brain remain to be elucidated. In this study, we demonstrate that the NLRP1-inflammasome composed by capase-1, ASC (apoptosis-associated speck-like protein containing a caspase-activating recruitment domain) and NLRP1 (NLR (nucleotide binding, leucine-rich repeat) is assembled following the ischemic event. Moreover, we have characterized the cellular distribution of the inflammasome proteins in the normal and the ischemic brain. Data from this investigation suggest that six to twenty four hours following CCAT the inflammasome complex is assembled in neurons while microglia, macrophages and astrocytes form this complex at 7 days following cerebral ischemia. On the basis of these findings we next investigated whether inhibition of the inflammasome complex reduces the inflammatory response after ischemia. Neutralization of NLRP1 utilizing a specific antibody, revealed decreased activation of caspase-1 and IL-1 beta and reduced histopathological damage within the ischemic brain. Thus, the inflammasome complex is a major contributor of the inflammatory response following cerebral ischemia and inhibition of this complex may be a novel therapeutic target for reducing the pathological consequences of stroke.
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Yadav, Sunaina. "Strategies towards understanding the genetics of ischemic stroke." Thesis, Imperial College London, 2013. http://hdl.handle.net/10044/1/24899.
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Stroke is the second largest cause of death and disability in the world and 80% of all strokes are ischemic in nature. While most risk factors have been investigated in depth, others such as South Asian ethnicity, long term blood pressure variability and symptomatic carotid stenosis remain largely understudied. In order to understand the genetic etiology underlining ischemic stroke, it is important to study the genetic burden shouldered by these phenotypes as well. This thesis examined the genetics of ischemic stroke in the presence of the above risk factors using three independent lines of investigation: a) literature based meta-analysis, b) candidate gene based approach and c) genome-wide association study. Using a literature based meta-analysis comprising 2529 ischemic stroke cases and 2881 healthy controls, genetic risk variants associated with ischemic stroke in South Asians were investigated. Genes PDE4D SNP 83, ACE I/D and IL10 G1082A were associated with South Asian ischemic stroke risk, with no major differences in strength of association for the same susceptibility genes in other ethnic groups. A candidate gene study was conducted using 8295 ischemic stroke cases and 12722 controls of European ancestry to test the association of GWAS-derived blood pressure variability associated cluster of 17 NLGN1 intronic SNPs. The study did not confirm the risk association of NLGN1 with ischemic stroke. Finally, a genome-wide association study was conducted to identify novel gene variants associated with ≥ 50% carotid stenosis in ischemic stroke, using 1164 cases and 13,703 healthy controls from seven independent cohorts. Three genetic loci at LRIG1, ROBO1 and CAPN7 were found to be associated at genome-wide significance. The findings of this thesis provide new insights into the genetic mechanisms underpinning ischemic stroke, by examining genetic variants associated with unusual stroke related phenotypes. Future directions include replication of sentinel SNPs in larger study populations and a GWAS for South Asian ischemic stroke cases.
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Voetsch, Barbara. "Inherited thrombophilias among young patients with ischemic stroke." [s.n.], 2002. http://repositorio.unicamp.br/jspui/handle/REPOSIP/308456.
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Orientadores: Benito Pereira Damasceno, Valder Roberval ArrudaTese (doutorado) - Universidade Estadual de Campinas, Faculdade de Ciencias Medicas
Made available in DSpace on 2018-08-02T22:17:13Z (GMT). No. of bitstreams: 1 Voetsch_Barbara_D.pdf: 55176396 bytes, checksum: f274efe61664e0541b7ed17b893440eb (MD5) Previous issue date: 2002
Resumo: Introdução e Objetivo: A etiologia de acidentes vasculares cerebrais isquêmicos (AVCi) em pacientes jovens permanece desconhecida em um terço dos casos, justificando a procura por novos fatores de risco protrombóticos. Causas comuns de trombofilia hereditária incluem o fator V de Leiden, a mutação G20210A no gene da protrombina, e hiperhomocisteinemia moderada secundária à variante termolábil da metilenotetrahidrofolato redutase (MTHFR-T). A atividade da paroxonase (PON1), uma esterase associada a lipoproteínas de alta densidade (HDL) com propriedades antioxidantes e antiaterogênicas, é determinada pelos polimorfismos Q192R e L55M da região codificadora e pelas substituições C(-107)T e G(-824)A no promotor do seu gene. A correlação destes fatores genéticos com o risco de AVCi é controversa. Além disso, foi recentemente descrita em crianças com AVCi uma deficiência hereditária de glutationa peroxidase plasmática (GPx-3), uma enzima com função de inativar espécies reativas de oxigênio que limitam a biodisponibilidade e os efeitos antiplaquetários do óxido nítrico. Porém, a base molecular dessa alteração ainda não foi identificada. Métodos: Analisamos e 118 a 167 pacientes jovens (< 45 anos) com AVCi não-fatal de etiologia indeterminada e um número equivalente de controles pareados por sexo e idade quanto à presença de fatores de risco protrombóticos. O fator V de Leiden, a variante da protrombina, homozigose para MTHFR-T, e as substituições Q192R, L55M e G(-824)A no gene da PON1 foram determinados através de PCR e digestão com enzimas de restrição. O polimorfismo PON1 C(-1O7)T foi detectado através de análise por single-strand conformational polymorphism (SSCP). Rastreamento do gene da GPx-3 foi realizado através de análise por SSCP, seguido de seqüenciamento de fragmentos com shift eletroforético. Resultados: A prevalência do genótipo 192RR da PON1 foi significativamente mais elevada em pacientes jovens com AVCi que controles (P=0.006), sendo o fator de risco que demonstrou a associação mais forte com AVCi de todos os fatores genéticos estudados (OR=4.1, 95% CI, 1.14 to 14.73). A presença isolada do alelo de baixa expressão -107T causou um aumento modesto no risco de AVCi, porém demonstrou ação sinergística com o genótipo 192RR, elevando a estimativa de risco de AVCi em portadores de ambas as variantes para 17 (95% CI, 1.74 to 166.35; P=0.015). Através de rastreamento do gene da GPx-3 por SSCP, identificamos quatro polimorfismos novos, ligados, no promotor do gene, associados ao risco de AVCi: A(-68)T, A(-622)T, T(-688)C e A(-703)C. Portadores do haplótipo combinando os nucleotídeos -622T, -688C e -703C foram significativamente mais prevalentes entre pacientes que controles (27.6% vs. 15.4%; P=0.020) e tiveram um risco de AVCi duas vezes maior quando comparado a não-portadores (OR=2.09, 95% CI, 1.12 to 3.92). O risco de AVCi associado ao genótipo PON1 192RR e aos polimorfismos do promotor da GPx-3 foi potenciado em indivíduos simultaneamente expostos a fatores de risco vasculares convencionais. Nenhuma diferença significativa na prevalência de fator V de Leiden, da variante da protrombina, ou homozigose para MTHFR-T foi encontrada entre pacientes e controles, com exceção de uma freqüência elevada de MTHFR-T em um grupo pequeno de indivíduos de origem negróide (OR=5.9, 95% CI, 0.88 to 49.2). Conclusões: Estes dados demonstram que variantes genéticas em enzimas antioxidantes predispõem ao desenvolvimento precoce de AVCi e sugerem um novo mecanismo para trombose arterial que envolve a biodisponibilidade diminuída de óxido nítrico. Além disso, a interação dos fatores genéticos com fatores de risco convencionais concordam com o conceito atual de que as doenças aterotrombóticas, incluindo AVCi em jovens, têm etiologia multifatorial
Abstract: Background and Purpose: The etiology of arterial ischemic stroke (AIS) in the young remains unknown in up to one-third of patients, warranting the search for novel prothrombotic risk factors. Common causes of inherited thrombophilia inc1ude factor V Leiden, the prothrombin G20210A mutation, and mild hyperhomocysteinemia due to the thermolabile variant ofmethylenetetrahydrofolate reductase (MTHFR-T). Activity levels of paraoxonase (PON1), an antioxidant and antiatherogenic HDL-bound esterase, are determined by the Q192R and L55M coding region polymorphisms and the C(-107)T and G(-824)A substitutions in the gene promoter. The correlation of these genetic factors with the risk of AIS is controversial. In addition, a heritable deficiency of plasma glutathione peroxidase (GPx-3), a reactive oxygen species scavenger that protects the bioavailability and antiplatelet effects of nitric oxide (NO), was recently described in association with childhood stroke, yet a molecular basis for this defect has not been identified. Methods: We analyzed up to 167 young patients (< 45 years ofage) with non-fatal AIS of undetermined etiology and an equivalent number of age- and gender-matched controls for the presence of inherited prothrombotic risk factors. Factor V Leiden, the prothrombin variant, homozygosity for MTHFR-T, and the Q192R, L55M, and G(-824)A substitutions in the PON1 gene were determined by PCR amplification and restriction digestion. The PON1 C(-107)T polymorphism was detected by single-strand conformational polymorphism (SSCP) analysis. Screening ofthe GPx-3 gene for genetic abnormalities was performed by SSCP, followed by sequencing offtagments with electrophoretic shifts. Results: The prevalence of the PONl 192RR genotype was significantly higher among patients than controls (P=0.006),showing the strongest independent association with the risk of AIS among all the genetic risk factors studied (OR=4.1, 95% CI, 1.14 to 14.73). The presence of the low expressor PON1 -107T allele was only modest1yassociated with AIS when ana1yzed alone, yet further increased the risk conferred by the 192RR genotype, yielding an adjusted risk estimate of 17 in carriers ofboth variants (95% CI, 1.74 to 166.35; P=0.015). By SSCP screening of the GPx-3 gene we identified four novel linked polymorphisms in the promoter associated with the risk of AIS: A(-68)T, A(-622)T, T(-688)C, and A(-703)C. Carriers ofthe haplotype combining nucleotides -622T, -688C, and -703C were significantly more frequent among patients than controls (27.6% vs. 15.4%; P=0.020) and had twice the risk of AIS as compared to non-carriers (OR=2.09, 95% CI, 1.12 to 3.92). The risk associated with the PON1 192RR genotype and the GPx-3 promoter polymorphisms was potentiated in individuaIs simultaneously exposed to conventional vascular risk factors. No significant difference in the prevalence of factor V Leiden, the prothrombin variant, and homozygosity for MTHFR-T was found between patients and controls, with the exceptio~ of a higher frequency of MTHFR-T in a small group ofindividuals of African descent (OR=5.9, 95% CI, 0.88 to 49.2). Conclusions: These data indicate that genetic variants in antioxidant enzymes predispose to the early development of AIS and support a novel mechanism for arterial thrombosis that involves reduced bioavailablity ofNO. In addition, the interaction ofthese genetic markers with conventional vascular risk factors support the current concept that atherothrombotic disease is a complex trait and multifactorial in nature
Doutorado
Neurologia
Doutor em Ciências Médicas
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Rink, Cameron L. "Nutritional Intervention And Modeling Of Acute Ischemic Stroke." The Ohio State University, 2008. http://rave.ohiolink.edu/etdc/view?acc_num=osu1210957018.
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Hajek, Christine A. "Cognitive Outcomes Following Arterial Ischemic Stroke in Children." The Ohio State University, 2012. http://rave.ohiolink.edu/etdc/view?acc_num=osu1332881238.
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Eckerle, Bryan. "Prevalence of Echocardiographic Abnormalities in Acute Ischemic Stroke." University of Cincinnati / OhioLINK, 2016. http://rave.ohiolink.edu/etdc/view?acc_num=ucin1459528281.
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Minzer, Brandon. "Fast and Slow Recovery Following Acute Ischemic Stroke." Thesis, The University of Arizona, 2014. http://hdl.handle.net/10150/315904.
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A Thesis submitted to The University of Arizona College of Medicine - Phoenix in partial fulfillment of the requirements for the Degree of Doctor of Medicine.OBJECTIVE: To investigate the variability in early recovery after hemiparetic stroke. BACKGROUND: Prior work suggests that most hemiparetic patients recover approximately 70% of their initial impairment by 3-months, but the speed of the recovery is unknown. METHODS: We assessed 30 patients with first-ever hemiparetic stroke using the Fugl-Meyer upper extremity score (max score=66) at 24-72 hours (FMInit), 1-week (FM1wk), and 3-months (FM3mo). Patients who did not demonstrate proportional recovery (0.70 x initial impairment) were excluded from analysis. The distribution of recovery at 7-days among the proportional recoverers was characterized and contrasted with recovery at 90-days using the Shapiro-Wilk test for normality and Sarle’s binomial coefficient. Cluster analysis was then used to assess the distribution of recovery rates at 7-days. Tests of differences and association were performed to assess if the early recovery-rate groups differed significantly in clinical and demographic characteristics. RESULTS: Twenty-six of the 30 initial patients were identified as proportional recovers, the other 4 were non-recoverers at 90-days. Among the proportional recoverers, there was a bimodal distribution of recovery at 7-days. Cluster analysis identified patients who achieved virtually all of their total recovery at 7-days (n=13, percent recovery=0.89±0.19; 95%CI:0.79-1.00) and patients who achieved virtually none their total recovery at 7-days (n=13, percent recovery=-0.23±0.77, 95%CI:-0.65-0.19), but went on to achieve the expected recovery at 90 days. Initial stroke severity was the only characteristic that showed a statistically significant correlation with early recovery group membership. SIGNIFICANCE: Patients who demonstrate proportional recovery over the first 3-months fall into 2 distinct early recovery groups, either achieving approximately 90% of their total recovery by 1-week or making little or no recovery early, and only later achieving their total expected recovery. Implications for treatment planning are profound.
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Huhtakangas, J. (Jaana). "Evolution of obstructive sleep apnea after ischemic stroke." Doctoral thesis, Oulun yliopisto, 2019. http://urn.fi/urn:isbn:9789526224343.
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Abstract In Finland, the costs of stroke are approximately 1.1 billion euros annually due to long disability and hospitalization episodes. Sleep apnea is a risk factor for stroke. The prevalence of sleep apnea among stroke patients is unknown because sleep recording is not usually performed on stroke patients. There are no previous studies investigating the association of thrombolysis on the prognosis of sleep apnea. The relation between sleep apnea and cardiovascular events is still unclear. In this prospective, observational study, I recruited voluntary, consecutive ischemic stroke patients over the age of 18 years who were or were not eligible for thrombolysis treatment. The investigators did not affect the treatment and patients were not randomized to thrombolysis. The final analysis included 204 patients; of these, 110 underwent thrombolysis therapy and 94 were treated without thrombolysis. Cardiorespiratory polygraphy was carried out with a portable three-channel device (ApneaLinkPlus™, Resmed, Sydney, Australia) at the ward within 48 hours after the onset of stroke symptoms. The cardiorespiratory polygraphy was repeated at home after a six-month follow-up. Both automatic scoring and manual scoring pointed out excellent agreement in arterial oxyhemoglobin decrease of > 4% (ODI4), lowest arterial oxyhemoglobin saturation (SaO2) or percentage of time spent below 90 percent saturation. The automated scoring underestimated the severity of sleep apnea, recognized poorly the type of event, and missed 18.6% of sleep apnea diagnoses. The total prevalence of sleep apnea in this study was 91.2% on admission to hospital. The stroke patients treated with thrombolysis had more, and more severe sleep apnea in the first sleep recording compared to those without thrombolysis therapy. After follow-up, the prevalence of sleep apnea still remained high, and sleep apnea was aggravated in two thirds of the stroke patients. The study patients without thrombolysis treatment had six-fold higher risk for incident sleep apnea after the follow-up. The stroke patients with thrombolysis therapy and visible stroke on CT had more nocturnal hypoxemia and higher obstructive apnea index than the patients without stroke lesion on follow-up CT 24 hours after thrombolysis treatment. The larger the ischemic stroke volume, the greater the time spent with saturation below 90%Tiivistelmä Aivoinfarkti on yleinen ja kansanterveydellisesti sekä taloudellisesti merkittävä sairaus, jonka aiheuttamat kustannukset Suomessa ovat noin 1.1 miljardia euroa pitkistä työkyvyttömyys- ja sairaalajaksoista johtuen. Uniapnea on aivoinfarktille altistava tekijä. Uniapnean esiintyvyys suomalaisilla aivoinfarktipotilailla ei ole arvioitavissa, koska aivoinfarktin sairastaneille ei yleensä tehdä unirekisteröintiä. Kannettavat yöpolygrafialaitteet saattaisivat olla vaihtoehto aivoinfarktipotilaiden uniapnean diagnosoinnille. Tutkittua tietoa liuotushoidon yhteydestä uniapnean ennusteeseen ei ole. Uniapnean sekä sydän- ja verisuonitapahtumien syy-yhteys on edelleen epäselvä. Rekrytoin prospektiiviseen tutkimukseeni vapaaehtoisia, peräkkäisiä yli 18-vuotiaita iskeemiseen aivoinfarktiin sairastuneita liuotushoidettuja ja liuotushoitoon soveltumattomia potilaita. Tutkimuksen lopullinen potilasmäärä oli 204, joista 110 sai liuotushoidon ja 94 hoidettiin ilman liuotusta. Kaikille potilaille tehtiin yöpolygrafia kannettavalla, kolmikanavaisella yöpolygrafialaitteella (Apnealink Plus, Resmed, Sydney, Australia) osastolla 48 tunnin kuluessa sairastumisesta. Yöpolygrafia toistettiin potilaan kotona kuuden kuukauden kuluttua. Sekä automaattitulos että manuaalisesti arvioitu unirekisteröintitulos olivat erittäin yhteneväisiä, kun arvion kohteena olivat happikyllästeisyyden neljän prosenttiyksikön suuruiset pudotukset tuntia kohti, matalin veren happikyllästeisyys tai alle 90 % happikyllästeisyyden osuus yöstä. Automaattianalyysi aliarvioi uniapnean vaikeuden, havaitsi huonosti hengityskatkosten tyypin eikä löytänyt 18,6 prosenttia uniapneadiagnooseista. Uniapnean esiintyvyys koko aineistossa oli sairaalaan tullessa 91,2 %. Liuotushoidetuilla potilailla todettiin ensimmäisessä rekisteröinnissä enemmän uniapneaa ja se oli vaikeampaa kuin ei-liuotushoidetuilla. Seurannassa uniapnean määrä pysyi edelleen korkeana ja uniapnea vaikeutui kahdella potilaalla kolmesta. Liuotushoitoon soveltumattomilla aivoinfarktipotilailla todettiin liuotushoidon saaneisiin verrattuna kuusinkertainen riski sairastua uniapneaan puolen vuoden aikana. Liuotushoidetuilla aivoinfarktipotilailla, joilla oli infarktimuutos kuvantamistutkimuksessa, oli yöllistä valtimoveren happikyllästeisyyden huononemista ja ylähengitysteiden ahtautumisesta johtuvia hengityskatkoksia enemmän kuin niillä potilailla, joilla ei todettu iskeemisiä muutoksia aivokuvantamisessa 24 tuntia liuotushoidon jälkeen. Mitä suurempi aivoinfarktin tilavuus, sitä suuremman osuuden yöstä veren happikyllästeisyys oli alle 90 %
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Benarab, Ammar. "Harnessing endothelial lipid signaling for ischemic stroke protection." Electronic Thesis or Diss., Université Paris Cité, 2021. http://www.theses.fr/2021UNIP5197.
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Justification : La fonction cérébrovasculaire est essentielle à la santé du cerveau, et les voies de protection vasculaire endogènes peuvent fournir des cibles thérapeutiques pour les troubles neurologiques. La signalisation S1P (sphingosine 1-phosphate) coordonne les fonctions vasculaires dans d'autres organes et les modulateurs S1P1 (récepteur S1P-1), y compris le fingolimod, sont prometteurs pour le traitement de l'AVC ischémique et hémorragique. Cependant, S1P1 coordonne également le trafic lymphocytaire, et les lymphocytes sont actuellement considérés comme la principale cible thérapeutique pour la modulation de S1P1 dans les accidents vasculaires cérébraux. Objectif : Aborder les rôles et les mécanismes d'engagement de la cellule endothéliale S1P1 dans le cerveau naïf et ischémique et son potentiel en tant que cible pour la thérapie cérébrovasculaire. Méthodes et résultats : En utilisant la modulation spatiale de la fourniture et de la signalisation S1P, nous démontrons un rôle protecteur vasculaire critique pour S1P1 endothélial dans le cerveau de souris. Avec un journaliste de signalisation S1P1, nous révélons que la polarisation abluminale protège S1P1 des ligands endogènes et synthétiques circulants après maturation de la barrière hémato-neurale, limitant la signalisation homéostatique à un sous-ensemble de cellules endothéliales artériolaires. La signalisation S1P1 maintient les fonctions endothéliales caractéristiques dans le cerveau naïf et se développe pendant l'ischémie par l'engagement de la fourniture S1P autonome des cellules. La perturbation de cette voie par une déficience sélective des cellules endothéliales dans la production, l'exportation ou le récepteur S1P1 de S1P exacerbe considérablement les lésions cérébrales dans les modèles permanents et transitoires d'AVC ischémique. En revanche, la lymphopénie profonde induite par la perte du lymphocyte S1P1 n'offre une protection modeste que dans le cadre d'une reperfusion. Dans le cerveau ischémique, la cellule endothéliale S1P1 soutient la fonction de barrière hémato-encéphalique, la perméabilité microvasculaire et le réacheminement du sang vers le tissu cérébral hypoperfusé par le biais d'anastomoses collatérales. Le renforcement de ces fonctions par un engagement pharmacologique supplémentaire du pool de récepteurs endothéliaux avec une barrière hémato-encéphalique pénétrant un agoniste sélectif de S1P1 peut réduire davantage l'expansion de l'infarctus cortical dans un délai thérapeutiquement pertinent et indépendamment de la reperfusion. Conclusions : Cette étude fournit des preuves génétiques pour soutenir un rôle central de l'endothélium dans le maintien de la perfusion et de la perméabilité microvasculaire dans la pénombre ischémique qui est coordonnée par la signalisation S1P et peut être exploitée pour la neuroprotection avec des agonistes S1P1 pénétrant la barrière hémato-encéphaliqueRationale: Cerebrovascular function is critical for brain health, and endogenous vascular protective pathways may provide therapeutic targets for neurological disorders. S1P (Sphingosine 1-phosphate) signaling coordinates vascular functions in other organs and S1P1 (S1P receptor-1) modulators including fingolimod show promise for the treatment of ischemic and hemorrhagic stroke. However, S1P1 also coordinates lymphocyte trafficking, and lymphocytes are currently viewed as the principal therapeutic target for S1P1 modulation in stroke. Objective: To address roles and mechanisms of engagement of endothelial cell S1P1 in the naive and ischemic brain and its potential as a target for cerebrovascular therapy. Methods and results: Using spatial modulation of S1P provision and signaling, we demonstrate a critical vascular protective role for endothelial S1P1 in the mouse brain. With an S1P1 signaling reporter, we reveal that abluminal polarization shields S1P1 from circulating endogenous and synthetic ligands after maturation of the blood-neural barrier, restricting homeostatic signaling to a subset of arteriolar endothelial cells. S1P1 signaling sustains hallmark endothelial functions in the naive brain and expands during ischemia by engagement of cell-autonomous S1P provision. Disrupting this pathway by an endothelial cell-selective deficiency in S1P production, export, or the S1P1 receptor substantially exacerbates brain injury in permanent and transient models of ischemic stroke. By contrast, profound lymphopenia induced by loss of lymphocyte S1P1 provides modest protection only in the context of reperfusion. In the ischemic brain, endothelial cell S1P1 supports blood-brain barrier function, microvascular patency, and the rerouting of blood to hypoperfused brain tissue through collateral anastomoses. Boosting these functions by supplemental pharmacological engagement of the endothelial receptor pool with a blood-brain barrier penetrating S1P1-selective agonist can further reduce cortical infarct expansion in a therapeutically relevant time frame and independent of reperfusion. Conclusions: This study provides genetic evidence to support a pivotal role for the endothelium in maintaining perfusion and microvascular patency in the ischemic penumbra that is coordinated by S1P signaling and can be harnessed for neuroprotection with blood-brain barrier-penetrating S1P1 agonists
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Filipets, O. O. "Endocrine comorbidity and ischemic stroke: the impact on stroke severity and case fatality." Thesis, БДМУ, 2021. http://dspace.bsmu.edu.ua:8080/xmlui/handle/123456789/18741.
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BONCORAGLIO, GIORGIO BATTISTA. "Role of Ryanodine Receptor type 3 (RyR3) in ischemic stroke." Doctoral thesis, Università degli Studi di Milano-Bicocca, 2021. http://hdl.handle.net/10281/317052.
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L'ictus è una delle principali cause di mortalità e disabilità acquisita in tutto il mondo. Il primo studio di associazione genome-wide in pazienti con ictus ischemico italiano ha trovato un'associazione significativa con il polimorfismo missenso a singolo nucleotide (SNP) rs4780144 nel gene del recettore della rianodina di tipo 3 (RyR3), che porta a una potenziale perdita di funzione. Molteplici evidenze hanno suggerito che una ridotta funzione di RyR3 potrebbe migliorare l'esito dell'ictus.
Con questo studio abbiamo mirato a indagare il ruolo di RyR3 nell'ictus ischemico a livello funzionale, genomico e cellulare.
Le cellule staminali mesenchimali di derivazione adiposa (Ad-MSC) esprimono RyR3 ma non gli altri recettori della rianodina (RyR1 e RyR2). Abbiamo valutato l'effetto del genotipo rs4780144 sull'omeostasi del calcio intracellulare nelle linee Ad-MSC. I nostri risultati hanno confermato la riduzione della funzione RyR3 (ridotto rilascio di ioni calcio nel citoplasma) nelle cellule con alleli mutati, che era statisticamente significativa nel donatore omozigote.
Una seconda coorte di 319 pazienti italiani con ictus ischemico con buon esito clinico è stata genotipizzata con Illumina Human-24 720. I genotipi dei casi (sia la prima che la seconda coorte) e i controlli sono stati imputati utilizzando il pannello di riferimento TOPMed degli aplotipi umani. Questo secondo GWAS ha replicato l'associazione con rs4780144 e altri SNP nel gene RyR3.
Infine, il danno ischemico indotto dalla deprivazione di ossigeno-glucosio (OGD) è stato valutato in fette di cervello organotipiche da topi wild-type e RyR3-knockout. Il knockout di RyR3 ha mostrato una ridotta suscettibilità al danno ischemico rispetto alle sezioni wild-type come indicato dalla ridotta incorporazione di ioduro di propidio e dal rilascio di LDH a 48 e 72 ore dopo OGD. RyR3- fette knockout hanno mostrato anche un gonfiore ridotto dopo OGD, indicando una riduzione dell'edema citotossico. Tuttavia, ad oggi non sono state trovate differenze significative nell'analisi dell'espressione genica eseguita su geni correlati allo stress ossidativo e neuronale.
I risultati di questo lavoro confermano che RyR3 può svolgere un ruolo nell'ictus ischemico. In particolare, l'inibizione di RyR3 potrebbe modulare positivamente il danno ischemico, determinando una nuova e promettente strategia neuroprotettiva nei pazienti con ictus ischemico acuto. Tuttavia, sono necessari ulteriori studi per chiarire i meccanismi che potrebbero eventualmente essere alla base della neuroprotezione osservata.Stroke is a leading cause of mortality and acquired disability worldwide. The first genome-wide association study in Italian ischemic stroke patients found a significant association with the missense single nucleotide polymorphism (SNP) rs4780144 in the ryanodine receptor type 3 (RyR3) gene, which leads to a potential loss of function. Multiple evidences suggested that a reduced function of RyR3 could improve stroke outcome. With this study we aimed at investigating the role of RyR3 in ischemic stroke at functional, genomic, and cellular level. Adipose-derived mesenchymal stem cells (Ad-MSCs) express RyR3 but not the other ryanodine receptors (RyR1 and RyR2). We assessed the effect of the rs4780144 genotype on intracellular calcium homeostasis in Ad-MSC lines. Our results confirmed the reduction of the RyR3 function (reduced release of calcium ions into the cytoplasm) in cells with the mutated alleles, which was statistically significant in homozygous donor. A second cohort of 319 Italian ischemic stroke patients with good clinical outcome was genotyped with Illumina Human-24 720. Genotypes of cases (both first and second cohorts) and controls were imputed using the TOPMed reference panel of human haplotypes. This second GWAS replicated the association with rs4780144 and other SNPs in the RyR3 gene. Finally, ischemic injury induced by oxygen-glucose deprivation (OGD) was evaluated in organotypic brain slices from wild-type and RyR3-knockout mice. RyR3- knockout showed a decreased susceptibility to ischemic damage compared to wild-type slices as indicated by the reduced propidium iodide incorporation and LDH release at 48 and 72 h after OGD. RyR3- knockout slices showed also a reduced swelling after OGD, indicating reduction of cytotoxic edema. However, to date no significant differences were found in gene expression analysis performed on neuronal and oxidative stress related genes. The results of this work confirm that RyR3 may play a role in ischemic stroke. In particular, the inhibition of RyR3 could positively modulate ischemic damage, resulting in a new and promising neuroprotective strategy in patients with acute ischemic stroke. However, further studies are needed to clarify the mechanisms that could possibly underlie the observed neuroprotection.
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Ström, Jakob. "The dose-dependent effects of estrogens on ischemic stroke." Doctoral thesis, Linköpings universitet, Klinisk kemi, 2012. http://urn.kb.se/resolve?urn=urn:nbn:se:liu:diva-77193.
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Estrogens are a group of female sex hormones that in addition to central roles in reproductive functions also have profound impact on for example brain development, blood vessels, bone tissue, metabolism and the immune system. The dominant endogenous production sites for estrogens in females are the ovaries and adipose tissue, while exogenous sources include combined contraceptive hormone treatments and menopausal hormone therapy. A few decades ago, the observation that females in comparison to men seemed to be protected against cerebral ischemia, and that this benefit was partially lost during menopause, sparked the hypothesis that estrogens protect against stroke. This was later confirmed by epidemiological studies and a large number of experimental animal studies, which motivated extensive clinical trials in which estrogens and/or progestagens were administered with the intent to prevent degenerative conditions rather than to ameliorate menopausal symptoms. However, the results were generally disappointing. The largest study, the Women’s Health Initiative (WHI), was discontinued due to the observation of an increased risk of breast cancer, cardiovascular disease and stroke. In parallel, a small number of animal studies in which estrogens were shown to increase damage from cerebral ischemia were published, one of these originating from our laboratory. This was, despite the WHI outcome, a surprising result, since the vast majority of previous animal studies had demonstrated protective effects. Therefore, in an attempt to explain the discordant results, Paper 1, and later Paper 4, of the current thesis were planned, in which four 17β-estradiol administration methods were tested. Substantial differences in serum hormone concentrations resulted from the different methods. Most importantly, the commercially available slow-release pellets used in our earlier experiments resulted in extremely high serum concentrations of 17β-estradiol. In Paper 2, 66 published studies that had investigated the effects of estrogens on stroke were meta-analyzed to pin-point the methodological reasons for the result dichotomy. Strikingly, in all six studies in which estrogens had produced damaging effects, the same type of slow-release pellets had been used, although these were used in a minority of the total number of studies. Paper 3 substantially strengthened the hypothesis that administration methods were crucial by showing that repeating the earlier experiment from our laboratory in which pellets had been used, but using a low-dose regimen instead, switched the estrogen effects from neurodamaging to neuroprotective. In Paper 5, an effort was made to challenge the assumption that the dose, and not the administration method per se, was the key factor, however this failed due to large intra-group infarct size variability. The current thesis adds evidence to the notion that differences in administration methods and their resulting serum concentrations of 17β-estradiol constitute a major factor responsible for the dichotomous results in studies investigating estrogens’ effects on cerebral ischemia. Even though results from animal studies are difficult to extrapolate to humans, this has a bearing on the menopausal hormone therapy debate, indicating that the risk of stroke could be reduced if serum concentrations of estrogens are minimized.
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Grohs, Gillian. "THE EFFECTS OF EXERCISE PRECONDITIONING ON FOCAL ISCHEMIC STROKE." UKnowledge, 2017. http://uknowledge.uky.edu/medsci_etds/8.
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Cleaved fragments of the extracellular matrix protein perlecan have been shown to promote neuroprotection and repair after ischemic stroke. The cysteine proteases cathepsin B and L as well as the metalloprotease bone morphogenic protein 1 (BMP-1) are capable of releasing the biologically active C-terminal laminin-like globular domain (LG3) of perlecan. Exercise, a known method of reducing stroke risk and severity, has been shown to increase the expression of some proteases associated with perlecan processing. Using a transient distal middle cerebral artery occlusion (MCAo) model for focal ischemic stroke we show that while 7 days of running only slightly decreased infarct volume, BMP1 and perlecan (HSPG2) RNA expression in skeletal muscle was significantly increased in 3-month-old male wild type C57/BL6 mice. Moreover, elevated levels of BMP1 RNA were still detectable after 3 days of detraining, suggesting a prolonged effect of exercise on BMP1 expression. Levels of LG3 in the blood were below the limit of detection in the current study, however it is likely that a more sensitive method would enable analysis of serum. These preliminary findings suggest that LG3 could be a molecular mediator of neuroprotection afforded by exercise though further studies are required.
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Filiano, Anthony J. "The protective role of transglutaminase 2 in ischemic stroke." Thesis, Birmingham, Ala. : University of Alabama at Birmingham, 2009. https://www.mhsl.uab.edu/dt/2009p/filiano.pdf.
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Diniz, Deborath Lucia de Oliveira. "Ischemic stroke and "wake-up stroke": relations with obstructive sleep apnea and oxidative stress." Universidade Federal do CearÃ, 2015. http://www.teses.ufc.br/tde_busca/arquivo.php?codArquivo=13353.
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nÃo hÃStroke is the main cause of disability in the world and one of the main causes of death. Among the subtypes of ischemic stroke, there is found the called âwake-up strokeâ (WUS), defined as the ischemic stroke which is perceived by the patients upon waking and that occurs within 20 to 25% of strokes. Some studies show absence of differences between patients that wake up with deficits and patients that developed the deficit along the day. Patients from this subgroup tend to have an unfavorable evolution in relation to the other subtypes, being necessary depth on the study of the etiopathogenic mechanisms. Natural biological factors related to the circadian rhythm such as body temperature, hormonal levels and variability of the cardiac rhythm, among others, influences this process. The Obstructive Sleep Apnea syndrome (OSA) has appointed as an independent risk factor that worsens the prognostic. The study aims to evaluate the clinic-demographic characteristics from the cases with and without WUS e its relations with the OSA and the oxidative stress. Seventy patients, 57.1% being men with age between 32 and 80 years (58.5Â13.3) had been studying. WUS has observed in 24.3% of the patients. Hypertension (67.1%), diabetes (27.1%) and disturb of the lipid metabolism (22.8%) were frequent. Diabetes and previous physical inactivity were more common with WUS (p<0.05). In the total sample, 62.3% of the cases showed mild to moderate stroke (NIHSS<5). Excessive daytime somnolence (SED, Epworth Scale>10) was identified in 20% of the patients. There has not been difference among the groups with and without WUS in relation to the severity of stroke and the somnolence. Patients with somnolence were younger and more physical inactive (p<0.05). The individuals with alcoholism had the highest rate of somnolence (p=0.03). In this study, 29.6% of the cases showed OSA of mild intensity (Apnea and Hypopnea Index â AHI: 5
O Acidente Vascular Cerebral (AVC) à a principal causa de incapacidade no mundo e uma das principais causas de morte. Dentre os subtipos de AVC isquÃmico, encontra-se o chamado wake-up stroke (WUS), definido como o AVC isquÃmico que à percebido pelo paciente ao acordar, e que contam com aproximadamente 20 a 25% dos casos. Os dados de diversos estudos sÃo divergentes quanto à presenÃa de diferenÃas clÃnicas, radiolÃgicas e evolutivas entre os pacientes que acordaram com dÃficits e pacientes que os desenvolveram ao longo do dia, sendo necessÃrio aprofundamento no estudo do mecanismo etiopatogÃnico. Fatores biolÃgicos naturais relacionados ao ritmo circadiano tais como temperatura corporal, nÃveis hormonais, variabilidade do ritmo cardÃaco, entre outros, influenciam este processo. A SÃndrome da Apneia Obstrutiva do Sono (SAOS) tem sido apontada como um fator independente que piora o prognÃstico dos pacientes acometidos pela doenÃa cerebrovascular. O presente estudo tem por objetivo avaliar as caracterÃsticas clÃnico-demogrÃficas dos casos com e sem WUS e suas relaÃÃes com a SAOS e o estresse oxidativo, medido pelos nÃveis de substÃncias reativas ao Ãcido tiobarbitÃrico (TBARS) e nitrito. Foram estudados 70 pacientes sendo 57,1% homens com idade entre 32 e 80 anos (58,5Â13,3). Wake-up stroke foi observado 24,3% dos pacientes. HipertensÃo arterial sistÃmica (67,1%), diabetes (27,1%) e distÃrbio do metabolismo lipÃdico (22,8%) foram as comorbidades mais freqÃentes. Diabetes e sedentarismo foram mais comuns nos casos com WUS (p<0,05). Na amostra total, 62,3% dos casos apresentavam AVC, leve a moderado, (NIHSS<5). SonolÃncia excessiva diurna (SED, Escala de Epworth>10) foi identificada em 20% dos pacientes. NÃo houve diferenÃa entre os grupos com e sem WUS quanto à gravidade do AVC e grau de sonolÃncia. Pacientes com sonolÃncia eram mais jovens e mais sedentÃrios (p<0,05). Os indivÃduos com etilismo tinham maior grau de sonolÃncia (p=0,03). Neste estudo, 29,6% dos casos apresentavam SAOS de leve intensidade (Ãndice de Apneia e Hipopneia - IAH: 5
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Salmeron, Kathleen Elizabeth. "INVESTIGATIONS OF INTERLEUKIN-1 ALPHA AS A NOVEL STROKE THERAPY IN EXPERIMENTAL ISCHEMIC STROKE." UKnowledge, 2018. https://uknowledge.uky.edu/neurobio_etds/20.
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Stroke is a leading cause of death and disability worldwide. Although rapid recognition and prompt treatment have dropped mortality rates, most stroke survivors are left with permanent disability. Approximately 87% of all strokes result from the thromboembolic occlusion of the cerebrovasculature (ischemic strokes). Potential stroke therapeutics have included anti-inflammatory drugs, as well as many other targets with the goal of mitigating the acute and chronic inflammatory responses typically seen in an ischemic stroke. While these approaches have had great success in preclinical studies, their clinical translation has been less successful. Master inflammatory cytokines, such as IL-1, are of particular interest. IL-1’s isoforms, IL-1α and IL-1β, were long thought to have similar function. While IL-1β has been extensively studied in stroke, the role of IL-1α during post stroke inflammation has been overlooked. Because IL-1 inhibitors have been unsuccessful in clinical application, we reasoned that IL-1α may provide previously unknown benefits to the brain after injury. We hypothesized that IL-1α could be protective or even accelerate reparative processes in the brain such as producing new blood vessels (angiogenesis) or neurons (neurogenesis).
To test that IL-1α is protective after stroke, we tested IL-1α’s protective effects on primary cortical neurons in in vitro models of stroke. We showed that IL-1α was directly protective on primary cortical neurons in a dose-dependent fashion. We then performed mouse middle cerebral artery occlusion stroke studies to determine the safety of giving IL-1α in vivo. These studies showed that administering IL-1α acutely was neuroprotective. However, intravenous (IV) administration of IL-1α resulted in transient, hemodynamic changes following drug delivery. To minimize these systemic effects, we administered IL-1α intra-arterially (IA) directly into the stroke affected brain tissue, allowing us to significantly lower the concentration of administered IL-1α. In comparison to IV, IA IL-1α showed greater histological protection from ischemic injury as well as improved functional recovery following stroke, all without systemic side effects.
To test that IL-1α could aid in neurorepair following stroke, we tested IL-1α’s ability to help damaged blood vessels repair in vitro. We found that IL-1α significantly increased brain endothelial cell activation, proliferation, migration, and capillary formation. We tested IL-1α’s proangiogenic properties in vivo by administering IL-1α three days following stroke. Delayed administration allowed us to separate IL-1α’s acute neuroprotective effects from potential subacute angiogenic effects. We found that mice receiving IL-1α performed significantly better on behavioral tests and also showed greater vascularization within the penumbra two weeks following stroke. We also found that IL-1α treated animals showed more endothelial activation than vehicle treated animals. Finally, our studies showed that IL-1α treated animals showed increased early-phase neurogenesis with evidence of increased proliferation at the subventricular zone suggesting that IL-1α’s beneficial effects are even more far-reaching than previously thought. In conclusion, our experiments suggest that the inflammatory cytokine IL-1α is neuroprotective and neuroreparative in experimental ischemic stroke and worthy of further study as a novel stroke therapy.
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Dykes, Angela. "Neuroprotective and Restorative Potential of Remote Ischemic Conditioning Following Stroke." Thesis, Université d'Ottawa / University of Ottawa, 2019. http://hdl.handle.net/10393/39354.
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Remote ischemic conditioning (RIC) is a noninvasive procedure where blood flow to a limb is repetitively reduced, sometimes called an “exercise memetic”. RIC delivered before (pre-RIC) or after (post-RIC) stroke is reportedly neuroprotective in preclinical stroke models. A review of the preclinical RIC literature revealed that studies almost exclusively use male subjects and a single stroke model (MCAO) that produces a large injury (~34% of hemisphere). To improve clinical translation, efficacy should be demonstrated in multiple stroke models and both sexes. Furthermore, the restorative potential of RIC (delivered past the neuroprotection window) to improve stroke recovery remains to be investigated. In male and female Sprague-Dawley rats (n=129) a standardized session (5min inflation, 5min deflation, 4 repetitions) of RIC was delivered using a pressurized cuff on the hindlimb. RIC was either delivered once 18h before, once 4hr acutely after or daily for 28 days beginning day 5 after endothelin-1 (ET-1) stroke. Infarct volumes were assessed 24hrs after stroke using MRI. To determine if RIC efficacy varied across stroke size, a hierarchical cluster analysis was used to divide rats into subgroups based on stroke size (small/large). RIC was effective in ET-1 which produced smaller strokes (“small”:5.2%, “large”:18.0% of hemisphere) than MCAO (~34%). This is more comparable to injury sizes seen clinically (4.5-14.0%). “Small” (42±4mm3) strokes were reduced by 39% (p=0.010, d=0.29) and “large” (146±8mm3) strokes were reduced by and 35% (p<.00001, d=1.41). Pre-RIC reduced infarct volume by 41% (p=<0.0001, d=0.92) versus 29% (p=0.009, d=0.43) in post-RIC. Interestingly, RIC is more effective in males, with double the infarct volume reduction of 46% (p<0.0001, d=0.94) compared with 23% (p=0.013, d=0.42) in females. Although RIC did not show restorative potential to improve motor stroke recovery, RIC is neuroprotective now with stronger clinically relevant evidence. RIC is effective across stroke models, stroke sizes and sex. Application of RIpreC to prevent stroke following a transient ischemic attack or recurrent stroke (especially in males with “large" strokes) would have the greatest potential.
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Madineni, Anusha. "Role of Cofilin, an Actin Cytoskeletal Protein, in Ischemic Conditions: Potential Therapeutic Target for Ischemic Stroke." University of Toledo Health Science Campus / OhioLINK, 2013. http://rave.ohiolink.edu/etdc/view?acc_num=mco1364331841.
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Maniskas, Michael E. "LOOKING TO THE FUTURE OF STROKE TREATMENT: COMBINING RECANALIZATION AND NEUROPROTECTION IN ACUTE ISCHEMIC STROKE." UKnowledge, 2016. http://uknowledge.uky.edu/neurobio_etds/17.
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Stroke is the 5th leading cause of death in the U.S. with 130,000 deaths and around 800,000 affected annually. Currently, there is a significant disconnect between basic stroke research and clinical stroke therapeutic needs. Few animal models of stroke target the large vessels that produce cortical deficits seen in the clinical setting. Also, current routes of drug administration, intraperitoneal and intravenous, do not mimic the clinical route of intra-arterial drug administration. To bridge this divide, we have retro-engineered a mouse model of stroke from the current standard of care for emergent large vessel occlusion (ELVO) stroke, endovascular thrombectomy, to include selective intra-arterial pharmacotherapy administration. Using the tandem transient common carotid and middle cerebral artery occlusion (MCAo) model to induce stroke, we threaded micro-angio tubing into the external carotid artery (ECA) towards the bifurcation of the common carotid and internal carotid arteries (CCA/ICA) allowing for the delivery of agents to the site of acute ischemia. Our model was optimized through a flow rate and injection volume study using carbon black ink injected through the intra-arterial model at different flow rates and injection volumes. The purpose of this study was to demonstrate that our injections were arriving at the site of ischemia and to improve injection volumes for future dosing while mitigating systemic side effects by preventing or minimizing systemic distribution. We determined that a flow rate of 2.5 µl/minute and injection volume of 10 µl was optimal. Next, we tested potential neuroprotective compounds nitroglycerin, verapamil, and a combination of verapamil and lubeluzole. Compounds were chosen for drug synergy and to target specific pathways in either an acute or delayed manner. Acute treatments included nitroglycerin and/or verapamil while delayed treatment included lubeluzole. The known mechanism of action for FDA approved nitroglycerin is through vessel dilation that results in increased blood flow to the treated region. A secondary mechanism of nitroglycerin is the production of nitric oxide, which has demonstrated antioxidant and anti-apoptotic effects when processed and released from cells surrounding the blood vessels. Verapamil, a calcium channel blocker, also FDA-approved for cerebral artery vasospasm: is thought to act by blocking the L-type calcium channels on the cell membrane from opening following membrane depolarization after insult. Finally, lubeluzole, also FDA-approved, is proposed to work as an NMDA modulator inhibiting the release of glutamate and nitric oxide synthase and blocking sodium and calcium channels. Through our stroke model we were able to demonstrate that each drug(s) showed a significant decrease in infarct volume and improved functional recovery while simultaneously minimizing potential systemic side effects suggesting that our stroke model may improve the preclinical validation of potential stroke therapies and help bridge the bench to bedside divide in developing new stroke therapies.
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Lv, Yating. "Application of resting-state fMRI methods to acute ischemic stroke." Doctoral thesis, Universitätsbibliothek Leipzig, 2013. http://nbn-resolving.de/urn:nbn:de:bsz:15-qucosa-126910.
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Diffusion weighted imaging (DWI) and dynamic susceptibility contrast-enhanced (DSC) perfusion-weighted imaging (PWI) are commonly employed in clinical practice and in research to give pathophysiological information for patients with acute ischemic stroke. DWI is thought to roughly reflect the severely damaged infarct core, while DSC-PWI reflects the area of hypoperfusion. The volumetric difference between DWI and DSC-PWI is termed the PWI/DWI-mismatch, and has been suggested as an MRI surrogate of the ischemic penumbra. However, due to the application of a contrast agent, which has potentially severe side-effects (e.g., nephrogenic systemic fibrosis), the DSC-PWI precludes repetitive examinations for monitoring purposes. New approaches are being sought to overcome this shortcoming.
BOLD (blood oxygen-level dependent) signal can reflect the metabolism of blood oxygen in the brain and hemodynamics can be assessed with resting-state fMRI. The aim of this thesis was to use resting-state fMRI as a new approach to give similar information as DSC-PWI. This thesis comprises two studies:
In the first study (see Chapter 2), two resting-state fMRI methods, local methods which compare low frequency amplitudes between two hemispheres and a k-means clustering approach, were applied to investigate the functional damage of patients with acute ischemic stroke both in the time domain and frequency domain. We found that the lesion areas had lower amplitudes than contralateral homotopic healthy tissues. We also differentiated the lesion areas from healthy tissues using a k-means clustering approach.
In the second study (see Chapter 3), time-shift analysis (TSA), which assesses time delays of the spontaneous low frequency fluctuations of the resting-state BOLD signal, was applied to give similar pathophysiological information as DSC-PWI in the acute phase of stroke. We found that areas which showed a pronounced time delay to the respective mean time course were very similar to the hypoperfusion area.
In summary, we suggest that the resting-state fMRI methods, especially the time-shift analysis (TSA), may provide comparable information to DSC-PWI and thus serve as a useful diagnostic tool for stroke MRI without the need for the application of a contrast agent.
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Livne, Michelle [Verfasser]. "Imaging-based predictive modeling in acute ischemic stroke / Michelle Livne." Berlin : Medizinische Fakultät Charité - Universitätsmedizin Berlin, 2019. http://d-nb.info/117977891X/34.
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Seifert, Hilary. "The Inflammatory Response Initiated by the Spleen to Ischemic Stroke." Scholar Commons, 2013. http://scholarcommons.usf.edu/etd/4767.
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The peripheral immune system plays a role in delayed neural injury after stroke. This response originates from the spleen as splenectomy prior to middle cerebral artery occlusion (MCAO) in rats significantly reduces infarct volume in the brain. This research is based on the hypothesis that inhibiting the splenic response will reduce neurodegeneration after stroke. Studies in animals have implicated lymphocytes as the immune cell type that is detrimental following MCAO. Interferon gamma (IFNγ) has been identified as a pro-inflammatory cytokine that is also detrimental following stroke. IFNγ is important because it activates microglia and macrophages in a pro-inflammatory nature that increases neural injury following stroke. Therefore IFNγ was examined in the brain and the spleen following MCAO. IFNγ protein was elevated at 24 h in the spleen and at 72 h in the brain post MCAO. Microglia/macrophages become maximally activated at 72 h in the brain after MCAO. Splenectomy decreases the levels of IFNγ in the brain following MCAO. Systemic administration of IFNγ reversed the protective effects of splenectomy.
The cellular response to MCAO was examined next because of the difference in time between the spike in IFNγ in the spleen and the delayed increase in the brain. The cellular response from the spleen was studied by labeling splenocytes five days prior to MCAO with a fluorescein dye. Tissues were examined 48 and 96 h post MCAO or sham MCAO for fluorescence. These cells were released from the spleen into circulation at 48 h post MCAO and migrated to the brain where the cells produced IFNγ at 96 h post MCAO.
IFNγ appears to play a role in the splenic response to stroke. One protein that is up regulated by cells that have been activated by IFNγ, interferon-inducible protein 10 (IP-10) is part of the inflammatory cycle driven by IFNγ. IP-10 recruits more IFNγ producing T helper (Th) cells to the site of injury. IP-10 has the unique ability to attract Th1 cells, the pro-inflammatory Th cells, and inhibit Th2 cells, the anti-inflammatory Th cells. This leads to more IFNγ production as IFNγ is the signature cytokine of a Th1 response. IP-10 is significantly increased in the brain at 72 h post MCAO, similar to IFNγ expression. In the spleen IP-10 increased at 24 h and remained elevated out to 96 h following MCAO. IFNγ signaling was inhibited by utilizing an IFNγ neutralizing antibody administered beginning 24 h post MCAO. The IFNγ antibody treated group had decreased infarct volumes, IP-10 levels in the brain, and appeared to have decreased T cells in the ipsilateral hemisphere at 96 h post MCAO.
Following ischemic stroke splenocytes are released into circulation and migrate to the brain. They release IFNγ to activate microglia/macrophages in a proinflammatory phenotype causing an increase in IP-10 levels. IP-10 then potentiates the Th1 driven inflammation which inhibits the Th2 response. The elevated levels of IFNγ increase neural injury following MCAO. Blocking IFNγ selectively blocks the inflammatory facet of the immune response to reduce stroke induced neurodegeneration. This leaves the other immune responses intact and able to contribute to tissue repair, regeneration, and able to respond to infections. Selectively inhibiting IFNγ signaling is a promising stroke therapeutic.
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Tucker, Jessica Janice. "Predictors of Admission for Stroke or Transient Ischemic Attack Patients." ScholarWorks, 2019. https://scholarworks.waldenu.edu/dissertations/7257.
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Approximately 11% of patients diagnosed with a stroke or a transient ischemic attack are readmitted to the hospital, creating a cost burden of nearly $2 billion per year for Medicare beneficiaries. Because researchers and policy makers consider hospital readmission for patients with strokes or transient ischemic attack to be an indicator for the delivery of quality care, the Centers for Medicare and Medicaid Services has imposed financial penalties of up to 3% of a hospital's Medicare reimbursement in 1 year for excessive readmissions, potentially impacting the financial sustainability of various healthcare organizations. The ecological systems theory allows for the understanding of how microsystems, mesosystems, exosystems, macrosystems, and chronosystems impact the development, influence, and predictability characteristics of a specific population serviced in a healthcare setting. This quantitative study analyzed cross-sectional data from the 2016 National Hospital Ambulatory Care Survey, using cross-tabulations with chi-square followed by multiple regression analyses. Overall, this study addressed the gap in the existing literature by examining admission rates for patients with the diagnoses of strokes or TIA and the association between ancillary service use, insurance status, and provider level evaluation. The study concluded that few predictors that exist between the independent and dependent variables, with the exception of the amount of laboratory tests ordered. Maintaining the financial reasonability by avoiding penalties for stroke or transient ischemic attack unnecessary admission from value-based purchasing, the implication for social change is maintaining access to care for patients by avoiding hospital closures.
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Kufner, Anna [Verfasser]. "PREDICT-STROKE: predicting response to thrombolysis in acute ischemic stroke patients using multiparametric MRI / Anna Kufner." Berlin : Medizinische Fakultät Charité - Universitätsmedizin Berlin, 2018. http://d-nb.info/1160514585/34.
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Guan, Ling. "Autonomic nervous system parameters to predict the occurrence of ischemic events after transient ischemic attack or minor stroke." Thesis, University of British Columbia, 2017. http://hdl.handle.net/2429/63274.
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The full abstract for this thesis is available in the body of the thesis, and will be available when the embargo expires.Medicine, Faculty of
Experimental Medicine, Division of
Medicine, Department of
Graduate
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MARIANI, JACOPO. "MULTICENTRE AND MULTISPECIES PRECLINICAL TRIAL OF REMOTE ISCHEMIC CONDITIONING IN ANIMAL MODEL OF ACUTE ISCHEMIC STROKE (TRICS–BASIC)." Doctoral thesis, Università degli Studi di Milano-Bicocca, 2023. https://hdl.handle.net/10281/403043.
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Il condizionamento ischemico remoto (RIC) risulta essere un candidato ideale per essere investigato in uno studio multicentrico volto al trattamento dell'ictus ischemico acuto (AIS). L’ efficacia terapeutica del RIC è stata dimostrata a livello preclinico, come riportato da precedenti studi ottenuti da singoli laboratori; ciò nonostante, gli studi clinici di fase II-III non hanno ancora fornito risultati soddisfacenti. TRICS Basic è definita come la fase preclinica del progetto TRICS, un Trial traslazionale multicentrico di Condizionamento Ischemico Remoto in modelli animali di Ictus Ischemico Acuto, sostenuto dell’Organizzazione Italiana sull’ictus (ISO), che ha previsto la collaborazione di 7 università e centri di ricerca italiani. TRICS Basic è uno studio preclinico multicentrico, randomizzato e consistente, oltre ad essere orientato alla pratica traslazionale. Lo studio include due specie animali (ratti e topi) ed entrambi i generi (maschi e femmine) sono ugualmente rappresentati. Lo scopo di questo progetto è quello di studiare l'efficacia del trattamento RIC in modelli preclinici di ictus ischemico acuto. Tutti gli animali allocati nel gruppo MCAo+ (soggetti ad ictus) sono stati sottoposti allo stesso tempo di occlusione (60min nei topi; 100min nei ratti). In particolare, il trattamento è stato applicato bloccando l'arteria femorale ipsilaterale per 10 minuti nei topi e 20 nei ratti. La valutazione dei risultati è stata eseguita in cieco, sia per quanto riguarda l’outcome funzionale dicotomizzato (risultato primario), che per la quantificazione del volume dell'infarto (risultato secondario) a 48 ore. Anche le analisi statistiche sono state eseguite in cieco e secondo un paradigma intention–to–treat. Durante la fase sperimentale iniziale, è stata effettuata una fase di armonizzazione, includendo tutti i centri coinvolti, al fine di ridurre le differenze di valutazione durante la valutazione neurocomportamentale. Dopo aver raggiunto l'obiettivo di interclass correlation (ICC)=0.60, imposto a priori dal protocollo pre–pubblicato, la vera fase sperimentale ha avuto inizio. La coorte sperimentale è composta da n=206 animali (n=110 topi e n=96 ratti) ma solo n=152 sono stati inclusi nell’analisi finale per il gruppo MCAo+ (n=81 topi; n=71 ratti). I risultati ottenuti hanno dimostrato che il RIC ha un effetto positivo a livello dell’outcome funzionale (+20% nei topi; +18% nei ratti) ed è in grado di ridurre l'area della lesione ischemica (-4,3% nei topi; -26,6% nei ratti) in entrambe le specie analizzate. Nonostante il consistente numero di animali utilizzati in questo studio, rispetto ai precedenti studi preclinici su questo trattamento, non abbiamo raggiunto la significatività statistica nei nostri due outcome principali, se confrontiamo le singole specie animali. Al contrario, analizzando tutti gli animali come un’unica specie, abbiamo ottenuto un risultato significativo in entrambi gli outcome. Ciò suggerisce che, analogamente agli studi clinici, una maggiore dimensione della popolazione avrebbe portato a risultati più significativi per quanto riguarda il miglioramento del deficit neurologico e la riduzione del volume dell’infarto, analizzando le singole specie.Remote ischemic conditioning (RIC) represents an ideal candidate to enter a multicenter trial for acute ischemic stroke (AIS) treatment, since previous results from single laboratories support its efficacy, but unfortunately phase II–III clinical trials still provided inconclusive results. TRICS–Basic is the preclinical trial in the TRICS project, a multicentre translational Trial of Remote Ischemic Conditioning in Acute Ischemic Stroke from the Italian Stroke Organization (ISO) Basic Science network, which consisted in the collaboration of 7 Italian institution. TRICS–Basic is a robust, translationally oriented, multicentre, randomized preclinical trial, which includes two animal species (rats and mice) and both male and female sexes are equally represented. The aim of this project was to investigate the efficacy of RIC treatment in AIS experimental models. All the animals in the MCAo+ groups were subjected to the same time of occlusion (60 min in mice; 100 min in rats). The treatment was applied by clamping the ipsilateral femoral artery for 10 min in mice and 20 min in rats. Blinded outcomes assessment was performed both for dichotomized functional neuroscore (primary outcome) and for infarct volume (secondary outcome) at 48 hours. Statistical analyses were performed in a blind status and according to an intention–to–treat paradigm. During the initial experimental period, we carried out a harmonization phase, including all the involved centres, in order to reduce the assessment bias during the neurobehavioral test evaluation. After we have reached the target of Inter class correlation (ICC) 30.60 imposed a priori by the protocol paper, we started the real experimental phase. The experimental cohort was composed by n=206 animals (n=110 mice and n=96 rats) but only n=168 were allocated in the MCAo+ groups (n=88 mice; n=80 rats) and n=152 animals were included in the study (n=78 mice; n=74 rats). The obtained data showed that RIC improve the good functional outcome (+20% in mice; +18% in rats) and reduce the area of ischemic injury (-4.3% in mice; -26.6% in rats) in both species. Despite the large number of animals used in this study and as compared to previous preclinical studies on RIC treatment, we did not reach the statistical significance in our two major outcomes, if we compare the single species alone. On the contrary, if we combine together all the animals, we obtained a significant result in both the analysed outcomes. This suggest that, similarly to clinical trials, a larger sample size would have resulted in more significant results in the functional and the infarct size outcomes single species analyses.
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Lin, Hannah. "Factors Associated with Mortality After Undergoing Thrombectomy for Acute Ischemic Stroke." eScholarship@UMMS, 2020. https://escholarship.umassmed.edu/gsbs_diss/1085.
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Background: Mechanical thrombectomy is the gold standard for treating patients with certain acute ischemic stroke (AIS) due to large vessel occlusion (LVO). However, even with major advancements and increasing procedural volumes, acute endovascular therapy remains a high-risk procedure with a considerable 90-day mortality rate, affected by a variety of factors.
Purpose: To investigate various clinical and procedural factors associated with 90-day mortality in patients undergoing mechanical thrombectomy for emergent treatment of AIS and determine which of these factors made unique contributions to post-thrombectomy prognosis.
Methods: We examined a prospective registry of 323 patients treated with endovascular thrombectomy for AIS between 2016 and 2019 at a high-volume comprehensive stroke center in central Massachusetts. We developed two multivariable logistic regression models adjusting for the contributions of baseline characteristics and recanalization parameters, to identify potential predictors of mortality at 90 days.
Results: Among 323 AIS patients treated with mechanical thrombectomy, the overall rate of successful recanalization was 86% and the overall post-procedure mortality rate was 29% by 90 days. After univariate analysis, a baseline multivariable model comprised of: history of stroke (OR 0.28, 95% CI 0.09 – 0.68), pre-stroke modified Rankin Scale (mRS 2: OR 3.75, 95% CI), severe admission National Institutes of Health Stroke Scale (NIHSS 21–42: OR 12.36, 95% CI 1.48 – 103.27), internal carotid artery (ICA) occlusion (OR 2.77, 95% CI 1.18 – 6.55), and posterior circulation occlusion (OR 2.69, 95% CI 1.06 – 6.83) was prognostic of 90-day mortality. A second multivariable model also found the procedural factors of: clot obtained after each pass (OR 0.49, 95% CI 0.24 – 1.00), successful recanalization (OR 0.21, 95% CI 0.06 – 0.8) and symptomatic intracranial hemorrhage (sICH; OR 17.89, 95% CI 5.22 – 61.29) to be identifiable predictors of post-thrombectomy mortality.
Conclusion: Death within 90 days after thrombectomy was increased among patients with higher pre-stroke disability, higher stroke severity on admission, ICA or posterior occlusion, and those with sICH complication. A history of stroke, clot extraction after each device pass, and successful recanalization are associated with decreased 90-day mortality. These identifiable contributors may inform patient selection, prognosis evolution, and shared decision-making regarding emergent thrombectomy for treatment of AIS.
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Kouwenhoven, Mathilde Cornelia Maria. "Matrix-degrading metalloproteinases and cytokines in multiple sclerosis and ischemic stroke /." Stockholm : Karolinska Univ. Press, 2001. http://diss.kib.ki.se/2001/91-7349-021-0/.
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Adali, Ayse Cinar. "Analysis Of Cytochrome P4501a1 Genetic Polymorphisms In Patients With Ischemic Stroke." Master's thesis, METU, 2011. http://etd.lib.metu.edu.tr/upload/12613041/index.pdf.
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ANALYSIS OF CYTOCHROME P4501A1 GENETIC
POLYMORPHISMS IN PATIENTS WITH ISCHEMIC STROKE
Adali, Ayse Çinar M.Sc., Department of Biochemistry Supervisor: Prof. Dr. Orhan Adali Co-Supervisor: Dr. Birsen Can Demirdö
gen January 2011, 179 pages Stroke is the third leading cause of death worldwide and results in serious disabilities. Cytochrome P450 1A1 gene (CYP1A1) is a highly polymorphic gene encoding its corresponding xenobiotic metabolizing enzyme which is responsible from the metabolism of carcinogenic polycyclic aromatic hydrocarbons (PAHs) that are engaged with the formation of free radicals. Atherosclerosis is a major cause of ischemic stroke and this pathology may be associated with the disruption of vascular homeostasis due to the formation of these chemicals. The main objective of this study was to investigate the coding region (A4889G) and non-coding region (T6235C) polymorphisms of the CYP1A1 gene as a risk factor for ischemic stroke. The study group in Turkish population consisted of 226 unrelated ischemic stroke patients and 113 control subjects. There was no statistically significant difference between the groups with respect to age and gender. Total blood samples were obtained from Gü
lhane Military Medical Academy Hospital, Neurology Department, Ankara. In stroke patients, hypertension, diabetes mellitus, smoking and obesity were at least 2 times more common and high density lipoprotein cholesterol (HDL-C) was significantly lower than controls. The frequency of mutant allele 4889G was 0.445 in patients and was nearly the same with controls. The frequency of mutant allele 6235C was 0.151 in patients and was significantly higher in controls (0.226, P=0.015). The risk of diabetic, smoker and obese individuals having ischemic stroke was significantly higher in 4889G allele carriers (AG+GG
Odds ratio
OR= 2.1, 2.4 and 3, respectively). The risk of hypertensive and diabetic individuals having ischemic stroke was higher in 6235TT genotypic people (OR= 3 and 2.2, respectively). On the contrary, the risk of smoker and obese individuals having ischemic stroke was significantly higher in 6235 C allele carriers (OR=5.3 and 3.7, respectively). Logistic regression analysis revealed that hypertension, smoking, levels of low density lipoprotein cholesterol (LDL-C) and HDL-C and 6235C allele were significant predictors of stroke. In this analysis, high level of LDL-C was found to be associated with almost 1.5-fold risk of ischemic stroke. On the other hand, HDL-C and having mutant 6235C allele decreased the risk of ischemic stroke 2.5 and 2-fold, respectively. This is the first study investigating the relation between A4889G polymorphism and stroke risk. Additionally, in Turkish population A4889G and T6235C polymorphisms were analyzed for the first time in terms of its relation to ischemic stroke. The present study demonstrated that the frequency of mutant 4889G allele was nearly the same in stroke patients and control subjects
whereas the frequency of mutant 6235 C allele was higher in control subjects than in stroke patients. Consequently, we decided that carrying mutant 4889 G allele does not constitute a risk for ischemic stroke and carrying mutant 6235C allele may have a protective effect against stroke.
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Sharma, M. "Community intervention programs for acute ischemic stroke: Assessment by Markov model." Thesis, University of Ottawa (Canada), 2006. http://hdl.handle.net/10393/27296.
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Stroke is a common illness with significant morbidity and mortality. Thrombolysis is the only approved therapy for ischemic stroke. Current protocols utilize a three hour time window from symptom onset for treatment eligibility. Public education campaigns regarding the symptoms of stroke have been advocated as a means to increase the treatment rates. A Markov model was constructed to simulate the experience of a population at risk for stroke. The probabilities of clinical events and health state utilities were extracted from the literature or estimated. Systematic reviews of community interventions in stroke and chest pain were performed. Base case analysis suggests that community intervention is the preferred strategy. The preference was robust in the face of multiple sensitivity analyses. A small incremental gain of 56 minutes was noted in life expectancy with a gain of 69 minutes in quality-adjusted life expectancy and 56 minutes in discounted quality-adjusted life expectancy.
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Joseph, Elizabeth. "Barriers to timely administration of thrombolytics in acute ischemic stroke patients." Doctoral diss., University of Central Florida, 2012. http://digital.library.ucf.edu/cdm/ref/collection/ETD/id/4693.
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Stroke is a leading cause of long term disability in the United States. The therapeutic benefits of intravenous thrombolytics is time dependent in an acute ischemic stroke patient and is an important determinant of 90 day and one year functional outcomes. This study investigated areas in the stroke alert process of a community based primary stroke care center that resulted in the delay of administration of thrombolytics within 60 minutes of an acute ischemic stroke patient's arrival to the emergency room. A retrospective descriptive design was utilized and chart reviews were done on 40 patients that received thrombolytics in the emergency room. Patient characteristics and time variables associated with the various steps in the stroke alert process were extracted. Findings showed that only 7.5% of the patients received thrombolytics within the recommended 60 minutes, with the longest time interval associated with time from arrival to the emergency room to time of evaluation by teleneurologist. There were no significant differences in the characteristics of patients who received thrombolytics within 60 minutes and those patients that received thrombolytics after 60 minutes. Recommendations were made for changes in organizational and practice strategies to improve timely administration, and for future research involving the effects of quality improvement initiatives.D.N.P.
Doctorate
Nursing
College of Nursing
Nursing Practice DNP
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Alves, Allan Felipe Fattori. "Image processing for enhancement of ischemic stroke in computed tomography examinations." Botucatu, 2019. http://hdl.handle.net/11449/181997.
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Orientador: Diana Rodrigues PinaResumo: O acidente vascular cerebral (AVC) é uma das maiores causas de morte em todo o mundo. No Brasil, o AVC é a principal, sendo que em 2009, foi responsável por 10,2% das mortes registradas. A tomografia computadorizada (TC) e a ressonância magnética nuclear (RMN) são as duas principais técnicas de imagem usadas para detectar o AVC. A TC tem um custo menor e maior acessibilidade da população, por isso ainda é o principal método de avaliação do acidente vascular cerebral. A avaliação do cérebro comprometido é realizada de forma subjetiva e pode levar à dificuldades no diagnóstico. Esta pesquisa propõe a implementação de um algoritmo computacional, destacando regiões de AVC isquêmico. Diferentes métodos de processamento de imagem foram utilizados para melhorar a visualização do tecido isquêmico. Um conjunto de 41 tomografias retrospectivas obtidas na Faculdade Medicina de Botucatu foram utilizadas, divididas em 25 casos de AVC isquêmico e 16 pacientes controle. Os casos de AVC foram obtidos dentro de 4,5 horas após os primeiros sintomas. Após a seleção dos slices com a possível presença de AVC, tais slices foram somados resultando em um único slice com valores médios de forma a reduzir o ruído. Isto foi seguido por um modelo de decomposição variacional onde se mantiveram componentes de interesse da imagem. O método de maximização de expectativas foi aplicado para gerar imagens melhoradas. Determinamos um teste de desempenho de observadores em um ambiente clínico. A sensibilidade ge... (Resumo completo, clicar acesso eletrônico abaixo)
Abstract: Stroke is one of the highest causes of death worldwide. In Brazil, stroke is the leading cause of death, and in 2009, it was responsible for 10.2% of deaths recorded. Non-enhanced computed tomography (CT) and nuclear magnetic resonance imaging (MRI) are the two main imaging techniques used to detect stroke. CT has a lower cost and greater accessibility of the population, so it is still the main method used. In most cases, the assessment of the compromised brain area is performed subjectively and may lead to difficulties in diagnosis. This research work proposes an approach based on a computational algorithm, highlighting regions of ischemic stroke. Different image processing methods were used to enhance ischemic tissues. A set of 41 retrospective CT scans from Botucatu Medical School (Brazil) was used, divided into 25 cases of acute ischemic stroke and 16 normal patients. Stroke cases were obtained within 4.5 h of symptom onset. After selection of CT slices, image averaging was performed to reduce the noise. This was followed by a variational decomposition model and the expectation maximization method was applied to generate enhanced images. We determined a test to evaluate the performance of observers in a clinical environment with and without the aid of enhanced images. The overall sensitivity of the observer’s analysis was 64.5 % and increased to 89.6 % and specificity was 83.3 % and increased to 91.7 %. These results show the importance of a computational tool to assist n... (Complete abstract click electronic access below)
Doutor
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Fattori, Alves Allan Felipe. "Image Processing for Enhancement of Ischemic Stroke in Computed Tomography Examinations." Thesis, Orléans, 2019. http://www.theses.fr/2019ORLE2003.
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L’Accident Vasculaire Cérébral (AVC) est l'une des principales causes de décès dans le monde. Le scanner et l'Imagerie par Résonance Magnétique (IRM) sont les deux principales techniques d'imagerie utilisées pour détecter les AVC. L’examen par scanner reste donc la principale méthode de diagnostic. Dans la plupart des cas, l'évaluation de la région cérébrale compromise est effectuée de manière subjective et peut entraîner des difficultés pour déterminer la région atteinte. Ce travail de thèse propose une approche basée sur un algorithme permettant de mettre en évidence les régions atteintes d’AVC ischémique dans les examens de scanner rétrospectifs. Différentes méthodes de traitement des images ont été utilisées pour réhausser les régions des tissus ischémiques. Afin de permettre aux médecins moins expérimentés de détecter de manière fiable les signes précoces AVC, une nouvelle approche est proposée pour améliorer la perception visuelle de l’accident ischémique cérébral. Une série de 41 images scanner rétrospectifs ont été utilisées, réparties en 25 cas d’AVC ischémiques et 16 patients normaux. Les cas d'AVC ont été obtenus dans les 4,5 heures suivant l'apparition des symptômes. Après la sélection des coupes importantes, une moyenne d'image est effectuée pour réduire le bruit. Ensuite, un modèle de décomposition variationnelle est appliqué afin de conserver la composante pertinente de l'image. Enfin, un algorithme d’espérance-maximisation est appliqué. Un test est proposé afin d’évaluer la performance des observateurs dans un environnement clinique avec et sans l'aide d'images rehaussées. La sensibilité globale de l'analyse de l'observateur a été améliorée de 64,5% à 89,6% et la spécificité de 83,3% à 91,7%. Ces résultats montrent l'importance d'un outil informatique d'aide à la décision en neuroradiologie, notamment dans les situations critiques telles que le diagnostic d'accident ischémique cérébralStroke is one of the highest causes of death worldwide. Non-enhanced computed tomography (CT) and nuclear magnetic resonance imaging (MRI) are the two main imaging techniques used to detect stroke. CT has a lower cost and greater accessibility of the population, so it is still the main method used. In most cases, the assessment of the compromised brain area is performed subjectively and may lead to difficulties in diagnosis. This research proposes an approach based on a computational algorithm, highlighting regions of ischemic stroke. Different image processing methods were used to enhance ischemic tissues. A set of 41 retrospective CT scans from Botucatu Medical School (Brazil) was used, divided into 25 cases of acute ischemic stroke and 16 normal patients. Stroke cases were obtained within 4.5 h of symptom onset. After selection of CT slices, image averaging was performed to reduce the noise. This was followed by a variational decomposition model and the expectation maximization method was applied to generate enhanced images. We determined a test to evaluate the performance of observers in a clinical environment with and without the aid of enhanced images. The overall sensitivity of the observer’s analysis was 64.5 % and increased to 89.6 % and specificity was 83.3 % and increased to 91.7 %. These results show the importance of a computational tool to assist neuroradiology decisions, especially in critical situations such as the diagnosis of ischemic stroke
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Атаман, Олександр Васильович, Александр Васильевич Атаман, Oleksandr Vasylovych Ataman, Євген Іванович Дубовик, Евгений Иванович Дубовик, Yevhen Ivanovych Dubovyk, and E. A. Garbuzova. "Frequencies of VKORC1 G3730A genetic variants in ischemic atherothrombotic stroke patients." Thesis, Sumy State University, 2015. http://essuir.sumdu.edu.ua/handle/123456789/41263.
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Lee, Ming Hsien, and 李明憲. "Intelligent early ischemic stroke detection system." Thesis, 2013. http://ndltd.ncl.edu.tw/handle/22ah82.
Full textAbstract:
碩士中山醫學大學
醫學資訊學系碩士班
101
In this thesis, we propose an intelligent early ischemic stroke detection system. It can help doctor to diagnosis. The system will be divided into three parts. First, the input Computed Tomography (CT) image will be performed preprocessing. The preprocessing step includes contrast enhancement using cubic curve, and extraction brain tissue using morphology technology in the image processing. The second, the brain tissue area will be segmented using Unsupervised Features region growing algorithm (UFRGA). Its goal is to distinguish the white matter and gray matter in the brain area. Finally, we use a simple position coincidence method to coincide the intensity according to the intensity of areas obtained by our proposed method. Hence, the brain stroke area will be found out. In the experiment result, we invite the two radiologists to help us to test our proposed system. And, the three statistic indices and an empirical evaluation index are used to evaluate our proposed system. From the result, we know that our proposed system can aided radiologist to increase themselves success rate to 64% up and the sensitivity of the system is 85.55%. The empirical evaluation index (Object-level Consistency Error, OCE) is 0.8678.
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Shiau, Ya-Fang, and 蕭雅方. "Secondary Prevention of Stroke and Death by Antiplatelet Therapies in Patients with Ischemic Stroke or Transient Ischemic Attack." Thesis, 2009. http://ndltd.ncl.edu.tw/handle/40974352691683728861.
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碩士臺北醫學大學
藥學研究所
97
Abstract Background Patients survived from ischemic stroke or transient ischemic attack (TIA) are high risk population for recurrent stroke. Antiplatelet agents, such as aspirin, the combination of aspirin plus extended-release dipyridamole (ASA-ERDP) and clopidogrel, are the first-line antiplatelet therapies for prevention of recurrent stroke in patients with ischemic stroke or TIA. Based on previous reports, the more expensive agents such as ASA-ERDP and clopidogrel are more effective than aspirin alone for the secondary prevention of stroke. However, most of the previous clinical trials fail to compare head-to-head directly three antiplatelet agents for the risk of recurrent stroke or other ischemic events. The aim of the present study was to investigate which antiplatelet therapy is the most effective in reducing the risk of recurrent stroke or death for patients with ischemic stroke or TIA in Taiwan. Method In this retrospective study, the patients’ data were obtained from the databank of Taiwan Stroke Registry, for analyzing subsequent risks in patients suffering from prior ischemic stroke or TIA. Patients in this study were treated with one of the following antiplatelet therapies such as (1) aspirin alone (Group A), (2) either the combination of aspirin plus dipyridamole or Aggrenox® (Group A plus D), and (3) clopidogrel alone (Group C). The primary outcomes were recurrent stroke and death within one month, three months, and six months after the onset of ischemic stroke or TIA. The subgroup analyses were performed for the primary outcomes with the baseline features, including five TOAST (Trial of Org 10172 in Acute Stroke Treatment) subtypes of ischemic stroke, history of atrial fibrillation, and patients with upper gastrointestinal bleeding. The statistical methods of the Kaplan-Meier method and the Cox proportional hazards regression model were used to analyze the results. Results A total of 10,792 patients were collected in this study. The final patient numbers for each therapy groups of A, A plus D, and C were 7,377, 1,902, and 1,513 patients, respectively. The patients of group C were associated with history of heart disease (40%) or prior stroke (40%), all of which were greater than other two groups. A total of 251 patients suffered recurrent stroke during six months after prior ischemic stroke or TIA. About 2.20% of group A patients, 2.47% of group A plus D patients, and 2.71% of group C patients developed recurrent stroke within six months after ischemic stroke or TIA. After adjusting baseline characteristics, the hazard ratios for recurrent stroke among three treatment groups did not reach statistical significance (p > 0.05). During the six-month period of follow-up, 368 patients died for unknown reason. The mortality rate of group A, group A plus D, and group C were 2.91%, 2.79%, and 6.61%, respectively. A significant two fold higher mortality rate was observed in group C (p < 0.001). After adjusting baseline features (e.g., age, heart disease, previous stroke), the hazard ratios for death among three treatment groups were not different significantly (p > 0.05). Subgroup analyses of five TOAST subtypes and the history of atrial fibrillation revealed that neither group A plus D treatment nor group C therapy produced a significant effect on the risk of recurrent stroke or death compared with group A (p > 0.05). However, a confirmatory finding was that patients with upper gastrointestinal bleeding in group C after receiving clopidogrel treatment had less risk of death than those in group A after receiving aspirin alone treatment within the first month after the onset of ischemic stroke or TIA (p = 0.039). Consistent with primary outcomes, subgroup analyses for recurrent stroke or death between group A plus D and group C also indicated that there were no statistically significant differences (p > 0.05). Conclusion Based on the previous clinical reports, approximately 7% ischemic stroke patients without antiplatelet therapies developed recurrent stroke within six months. In the present study, aspirin alone, the combination of aspirin plus dipyridamole, and clopidogrel alone were effective in the prevention of recurrent stroke or death in Taiwanese patients with ischemic stroke or TIA; patients who received antiplatelet treatments in this study decreased the risk of recurrent stroke to about 2.5%. With this evidence-based information in mind, aspirin monotherapy is recommended to be prescribed as the first-line antiplatelet therapy for secondary prevention of stroke unless patients are allergy to or intolerant of aspirin (e.g., upper gastrointestinal bleeding). Another important reason to use aspirin as initial therapy is the relative low cost of aspirin, which can lead to better long-term adherence in medication use. Further, for ischemic stroke patients with the complication of hemorrhage at any sites, the choice of drug for secondary prevention of stroke is clopidogrel, instead of aspirin-containing agents.
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Hsu, Cheng-Hsien, and 徐正憲. "Anisotropy Diffusion Index on Ischemic Stroke Patients." Thesis, 2006. http://ndltd.ncl.edu.tw/handle/59345755341799425872.
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碩士逢甲大學
自動控制工程所
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Diffusion weighted images (DWI) and Diffusion tensor images (DTI) have been used to evaluate the status of water diffusion in brain tissue. DTI provides more information about the orientation of the white matter tract of the brain especially. In addition to the information of the apparent diffusion coefficient (ADC), fractional anisotropy (FA) and orientation of the fibers, other geometric diffusion indicators such as CL, CP and CS corresponding to linear, planar and spherical morphology could be derived from the DTI measurements. Previous researchers have focused on the ADC, FA and other anisotropic indices of the ischemic cerebral infarction. The change of geometric parameters after infarction, however, has not been investigated up to data. The aim of this research is to compare the difference the change of geometric parameters between infarct and healthy brain tissue. We added the DTI sequences to healthy volunteers and ischemic stroke patients to get ADC, FA and geometric indices. The geometric distribution of both infarct and healthy brain tissue are displayed on the three-phase (3P) tensor diagram. The result shows that, on healthy subjects, the gray matter has high value on CS and lowers on CL and CP parameters (lie on top of the 3P diagram), while the white matter has higher value on CL and lower CP and CS (lie on left lower corner of 3P diagram). After infarction, the gray matter and white matter both show less anisotropy and raised CS index.
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白其卉. "A case-control study of ischemic stroke." Thesis, 2000. http://ndltd.ncl.edu.tw/handle/71992074777342533018.
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Pereira, Nuno Álvaro Andrez. "Management of Acute Ischemic Stroke - Endovascular Approach." Master's thesis, 2017. https://hdl.handle.net/10216/104170.
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Pereira, Nuno Álvaro Andrez. "Management of Acute Ischemic Stroke - Endovascular Approach." Dissertação, 2017. https://hdl.handle.net/10216/104170.
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Machado, Livia Sampaio. "Minocycline vascular protection after acute ischemic stroke." 2009. http://purl.galileo.usg.edu/uga%5Fetd/machado%5Flivia%5Fs%5F200905%5Fphd.
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Thesis (Ph. D.)--University of Georgia, 2009.Directed by Susan Fagan. Includes an article published in BMC neuroscience and an article submitted to Stroke. Includes bibliographical references (leaves 94-98).
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Lin, Longting. "Whole-brain CTP in acute ischemic stroke." Thesis, 2015. http://hdl.handle.net/1959.13/1310399.
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Research Doctorate - Doctor of Philosophy (PhD)Perfusion imaging technology not only enables stroke diagnosis by identifying the ischemic lesion earlier, but also helps the clinician to make treatment decisions by further classifying the ischemic lesion into salvageable tissue and non-salvageable tissue. The imaging of salvageable tissue, penumbra, provides a direct target for reperfusion treatment. However, the accuracy of penumbra measurement with perfusion imaging has been questioned, especially with CT perfusion (CTP). Perfusion images, acquired on earlier generation instruments such as the16 or 64-detector scanners, have limited coverage of potentially ischemic brain, a factor recognised to reduce the accuracy of penumbra measurement. This limitation can be overcome by the advance in technology. The new generation “mega-detector” scanners, such as 320-detector Toshiba Aquilion One, provide whole brain coverage of 160mm from skull base to vertex. In this thesis, I presented a series of studies aiming to evaluate the utility of whole-brain CTP in acute ischemic stroke. The first study was to derive the optimal penumbra measurement on whole-brain CTP with the reference of ischemic tissue outcome, and the second study was to test the penumbra measurement of whole-brain CTP in predicting clinical patient outcome. The two studies found that only with the threshold setting at Tmax>6s or DT>3s, did the whole-brain CTP achieve high accuracy (>99%) in delineating acute ischemic penumbra and good sensitivity (>80%) in predicting favourable clinical outcome. It was also confirmed that the accuracy of penumbra measurement was comprised when the brain coverage of CTP decreased from 160mm to 20mm. Following two studies examined the utility of whole-brain CTP in the clinical setting. Firstly, CTP was compared to MRP, the perfusion modality that has already been well used in clinic. This work demonstrated that with whole brain coverage, CTP was as effective as MPR in measuring the acute penumbra and in selecting patients for reperfusion treatment. Secondly, a case by case review was carried out to assist clinicians in the interpretation CTP output. In conclusion, findings of this thesis support the usage of whole-brain CTP in acute ischemic stroke. Noticeably, the conclusion only applies to patients with anterior circulation stroke. Whole-brain CTP might also have advantage in detecting ischemic lesions in posterior circulation territory, which require studies to prove it in the future.