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Dissertations / Theses on the topic 'Hypoxic-ischemic injury'

Author: Grafiati

Published: 28 May 2022

Last updated: 30 July 2025

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1

Crooks, Suzanne. "Long-term neuropsychological and psychosocial outcomes of hypoxic-ischemic brain injury." Thesis, Queen's University Belfast, 2014. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.676279.

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Purpose: This study aimed to identify the long-term cognitive impairments arising from Hypoxic Ischaemic Brian Injury (HIBI) in a group of patients at least one year post insult. The long term psycho-social impact and carer burden associated with HIBI were also investigated. Method: A case series design was employed to facilitate detailed analysis of individual profiles. A battery of neuropsychological measures was administered to all participants. Cognitive domains assessed included premorbid and current IQ, visual and auditory recognition, immediate and delayed recall, auditory and visual at

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2

Dobrucki, Wawrzyniec L. "Nitrogen and Oxygen Radicals in Ischemic and Hypoxic Injury of the Brain." Ohio University / OhioLINK, 2003. http://rave.ohiolink.edu/etdc/view?acc_num=ohiou1057171850.

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3

Widerøe, Marius. "Magnetic Resonance Imaging of Hypoxic-Ischemic Brain Injury Development in the Newborn Rat." Doctoral thesis, Norges teknisk-naturvitenskapelige universitet, Institutt for laboratoriemedisin, barne- og kvinnesykdommer, 2012. http://urn.kb.se/resolve?urn=urn:nbn:no:ntnu:diva-17210.

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4

Leonardo, Christopher C. "The Role of Extracellular Matrix and Matrix-Degrading Proteases in Neonatal Hypoxic-Ischemic Injury." [Tampa, Fla] : University of South Florida, 2008. http://purl.fcla.edu/usf/dc/et/SFE0002587.

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5

Petrashenko, Viktoriia Oleksandrivna, D. Alper, Вікторія Олександрівна Петрашенко, and Виктория Александровна Петрашенко. "Diagnostical markers of perinatal hypoxic and ischemic injury of central nervous system at premature newborns." Thesis, Видавництво СумДУ, 2012. http://essuir.sumdu.edu.ua/handle/123456789/27542.

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6

Петрашенко, Вікторія Олександрівна, Виктория Александровна Петрашенко та Viktoriia Oleksandrivna Petrashenko. "Нейроспецифічна енолаза - ранній маркер тяжкості гіпоксично-ішемічного ураження ЦНС у недоношених новонароджених". Thesis, Видавництво СумДУ, 2012. http://essuir.sumdu.edu.ua/handle/123456789/27453.

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7

Редько, Олена Костянтинівна, Елена Константиновна Редько, Olena Kostiantynivna Redko, А. Сичона та А. Салех. "Комплексная терапия церебральной ишемии у доношенных новорожденных и кортексин". Thesis, Издательство СумГУ, 2012. http://essuir.sumdu.edu.ua/handle/123456789/27461.

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Включение кортексина в комплексную терапию гипоксически- ишемического поражения ЦНС у доношенных новорожденных позволяет быстрее восстановить соотношение процессов возбуждения и торможения, нормализовать неврологический статус и снизить сроки госпитализации. При цитировании документа, используйте ссылку http://essuir.sumdu.edu.ua/handle/123456789/27461

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8

Ranasinghe, Himani Sumudumalee. "Mechanisms underlying hypoxic ischemic injury to the developing brain: The significance of matrix metalloproteinase 2 and 9." Thesis, University of Auckland, 2009. http://hdl.handle.net/2292/4962.

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Perinatal hypoxic ischemic (HI) injury is a leading cause of long-term neurological complications in newborn babies. Matrix metalloproteinases (MMPs) are a family of endopeptidases that are capable of degrading the extracellular matrix (ECM) components. They are considered to be integral in many physiological processes. However, recently it has been demonstrated that the inappropriate activity of these proteases, particularly MMP-2 and 9, contribute to the pathogenesis of cerebral ischemia in the adult brain. Given that ECM disruption is frequently observed following injury to the developing

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Wang, Yanxin, and 王燕欣. "Hypoxic-ischemic injury in the neonatal rat model: prediction of irreversible infarction size by DiffusionWeighted MR Imaging." Thesis, The University of Hong Kong (Pokfulam, Hong Kong), 2005. http://hub.hku.hk/bib/B35757577.

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10

Riparini, Giulia. "Perinatal Brain Injury: Mechanism and potential pharmacological therapies - The role of SIRT1 in the neuroprotective effect of Melatonin and of Endothelin-1 in Oligodendrocyte Progenitor Cell Development." Doctoral thesis, Urbino, 2018. http://hdl.handle.net/11576/2663578.

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11

Wang, Yanxin. "Hypoxic-ischemic injury in the neonatal rat model prediction of irreversible infarction size by Diffusion Weighted MR Imaging /." Click to view the E-thesis via HKUTO, 2005. http://sunzi.lib.hku.hk/hkuto/record/B35757577.

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12

Christophidis, Larissa Joy. "The roles of growth hormone and prolactin in the brain during development and recovery from hypoxic-ischemic injury." Thesis, University of Auckland, 2011. http://hdl.handle.net/2292/6781.

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Very preterm birth disrupts development of the brain and enhances its vulnerability to injury, resulting in neurological impairments ranging in severity from cerebral palsy to mild cognitive deficits. Currently there is no treatment available. Unilateral hypoxic-ischemia (HI) in the three day old rat is well established as a model of brain injury in infants born at 22 to 26 gestational weeks. However, it is inherently variable. I show that this injury results in short term neurological deficits which may be capitalised upon for allocation of pups into treatment studies. After it is inju

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13

Kendall, G. "The role of endotoxin, the TNF family of cytokines and intracellular pH in perinatal hypoxic-ischemic brain injury." Thesis, University College London (University of London), 2010. http://discovery.ucl.ac.uk/19212/.

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To explore the effect of endotoxin as a sensitising agent prior to neonatal hypoxiaischemia differing doses of endotoxin (E. coli lipopolysaccharide, LPS) were given to neonatal mice prior to hypoxia-ischemia, with sensitising effects noted at dosages of 0.3mg/kg of LPS or higher. Varying the time interval between endotoxin administration and hypoxia-ischemia demonstrated that LPS given between 4 and 12 hours before hypoxia-ischemia had a sensitising effect on subsequent hypoxia ischemia. In contrast, LPS given at the time of or 24 hours before hypoxia-ischemia did not. To help understand the

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14

Токарчук, Н. І., та І. В. Чигір. "Агвантар у комплексній терапії білково-енергетичної недостатності у дітей першого року життя із гіпоксично-ішемічним ушкодженням центральної нервової системи". Thesis, Сумський державний університет, 2015. http://essuir.sumdu.edu.ua/handle/123456789/43154.

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Білкoвo-енеpгетичнa недoстaтність (БЕН) є склaдним бaгaтoфaктopним захворюванням. Незважаючи на постійне зростання кількості та палітри метаболічних засобів, проблема удосконалення терапії БЕН залишається актуальною. Обов’язковою умовою терапії БЕН є метаболічна корекція, що дозволяє попередити прогресування захворювання.

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15

Lai, Pei-Chun, and 賴佩君. "Ceftriaxone attenuates hypoxic-ischemic brain injury in neonatal rat." Thesis, 2012. http://ndltd.ncl.edu.tw/handle/20603848098666369351.

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博士<br>慈濟大學<br>藥理暨毒理學碩士班/博士班<br>100<br>Perinatal brain injury is the leading cause of subsequent neurological disability in both term and preterm baby. Glutamate excitotoxicity is one of the major factors involved in perinatal hypoxic-ischemic encephalopathy (HIE). Glutamate transporter GLT1, expressed mainly in mature astrocytes, is the major glutamate transporter in the brain. HIE induced excessive glutamate release which is not reuptaked by immature astrocytes may induce neuronal damage. Compounds that enhance the expression of GLT1 may exert neuroprotective effect in HIE. In this study, we

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16

Sizonenko, Stéphane Vladimir. "Hypoxic-ischemic injury in the developing brain: pathogenesis and neuroprotection." 2002. http://hdl.handle.net/2292/3212.

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In newborn infants, birth asphyxia represents the predominant cause of brain injury. These infants will later exhibit neurodevelopmental disabilities or a more major cerebral palsy. Prevention of adverse outcomes requires an understanding of the way in which these deficits develop. Endogenous protective mechanisms arising from the insult have opened new insights in neuroprotective strategies. Neurotrophic factors such as IGF-1 and its N-terminal tripeptide GPE have been shown to confer some neuroprotection after HI injury in the adult rodent. In the P21 rat brain after moderate HI injury, exog

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17

Lin, Wan-Ying, and 林宛瑩. "Anti-apoptotic mechanism of ischemic preconditioning against hypoxic-ischemic injury in the neonatal rat brain." Thesis, 2005. http://ndltd.ncl.edu.tw/handle/7j466r.

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碩士<br>國立成功大學<br>分子醫學研究所<br>93<br>Neonatal hypoxic-ischemic (HI) brain injury is a major cause of neonatal mortality and long-term disability. Currently, there are still no effective therapies against neonatal HI brain injury. A sublethal stress, such as a brief episode of ischemia, before a lethal injury may reduce neuronal death against subsequent lethal injury; a phenomenon called “preconditioning”. Elucidating the underlying mechanisms of preconditioning may provide potential neuroprotective therapy for neonatal HI brain injury. Permanent ligation of unilateral carotid artery followed by

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18

Chang, Kang-Fan, and 張綱凡. "LPS preconditioning mediates neuroprotection against hypoxic-ischemic injury in the neonatal rat brain." Thesis, 2004. http://ndltd.ncl.edu.tw/handle/91278671965730347711.

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碩士<br>國立成功大學<br>微生物及免疫學研究所<br>92<br>Perinatal hypoxic-ischemic (HI) brain injury is a major cause of neonatal mortality and long-term disability such as mental retardation, cerebral palsy, learning disability, and seizures. There are still no effective therapies against neonatal HI brain injury to date. A sublethal stress before a lethal injury can reduce the neuronal death, a phenomenon called “preconditioning”. Elucidating the underlying mechanisms of preconditioning may provide potential neuroprotective therapy for neonatal HI encephalopathy. 　　We first established a lipopolysaccharide (LPS

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19

Yi-ChingHsu and 許宜菁. "The mechanism of neurovascular damage in neonatal rat with hypoxic-ischemic brain injury." Thesis, 2014. http://ndltd.ncl.edu.tw/handle/89meyn.

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博士<br>國立成功大學<br>基礎醫學研究所<br>102<br>Brain cells are extremely sensitive to oxygen deprivation. Some brain cells actually start dying just under five minutes after their oxygen supply is cut. As a result, brain hypoxia can kill brain cells and rapidly cause severe brain damage. This is an emergency, and the sooner medical attention is given and the oxygen supply restored, the lower the chances of severe brain damage or death. Neonatal hypoxic-ischemic (HI) stress can lead to HI encephalopathy. There is still no effective drug against neonatal HI brain injury. Most neuroprotective agents have not

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20

Wu, Hsin-Chieh, and 吳欣潔. "The Effect of Neonatal Obesity on Hypoxic-ischemic Brain Injury in Rat Pups." Thesis, 2007. http://ndltd.ncl.edu.tw/handle/70012301530373508973.

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碩士<br>國立成功大學<br>分子醫學研究所<br>95<br>Perinatal hypoxic–ischemic (HI) brain damage remains a major cause of acute mortality and chronic neurologic morbidity in children. Obesity is a growing problem in modern society. Evidence has shown that obese adult persons suffer a higher risk of stroke and have worse prognosis than non-obese adults. Here, using a well-established HI brain injury model in neonatal rats, we first tested the hypothesis that the over-fed (OF) obese rat pups had a higher degree of HI brain injury compared with the normal-fed (NF) rat pups. 　　The OF group, defined by reducing the l

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21

Lu, Kwok-Tung, and 呂國棟. "Protection of Hippocampal Neurons from Hypoxic-Ischemic and Kainate-induced Neuronal Injury by Serotonin." Thesis, 1999. http://ndltd.ncl.edu.tw/handle/33854530548882428294.

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博士<br>國立成功大學<br>基礎醫學研究所<br>87<br>Abstract Serotonin (5-hydroxytryptamine, 5-HT) is an important neurotransmitter in the mammalian peripheral and central nervous systems. In the brain, most 5-HT-containing cells are located in the raphe nuclei which project to various brain regions including the hippocampus, amygdala, thalamus, prefrontal cortex and cerebellum. The hippocampal CA1 region is rich in 5-HT-containing terminals and expresses high density 5-HT1A receptors leads to a membrane hyperpolarization and inhibition of cell firing mediated via an increase in K+ conductance. Subseq

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22

Huang, Hsiu-Mei, and 黃修眉. "Hypoxic-Ischemic Retina Injury via Caspase-dependent and -Independent Apoptotic Death in Neonatal Rats." Thesis, 2012. http://ndltd.ncl.edu.tw/handle/77817324792861341219.

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碩士<br>長庚大學<br>臨床醫學研究所<br>101<br>Purpose: Visual loss associated with brain damage is currently the most common cause of visual impairment in children in developed countries. Hypoxic-ischemia (HI) injury is one of the most common causes for those neurological damages. We hypothesized that HI insult in the immature eyes per se may play a significant role in the visual impairment in those children. Vannucci model is one of the most widely used experimental paradigms to induce HI brain injury in rat pups. It remains to be determined the long-term functional and pathological sequalae of retina inju

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23

Scheepens, Arjan. "Studies on the GH/IGF axis in the infant rat brain following hypoxic ischemic injury." 1999. http://hdl.handle.net/2292/3200.

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Brain injuries, be they hypoxic, ischemic, traumatic or neurodegenerative result in permanent neurological deficit and presently there are few or no therapeutic interventions available. Recent research into how and why brain cells die after an insult has elucidated that a significant number of cells die in an apoptotic manner. Following a transient brain injury cells continue to die for upto 5 days after the insult thereby giving a window of opportunity for treatment. In response to injury, the brain produces a range of neurotrophic hormones including insulin-like growth factor 1 (IGF-I), whic

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Ming-YiHuang and 黃名儀. "Endothelial IRS-1 aggravates neurovascular damage after neonatal hypoxic-ischemic brain injury through increasing neuroinflammation." Thesis, 2015. http://ndltd.ncl.edu.tw/handle/nppwu2.

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碩士<br>國立成功大學<br>臨床醫學研究所<br>103<br>Perinatal hypoxic-ischemia (HI) is a major cause of neonatal mortality and long-term neurological morbidity among survivors. HI injury not only causes neuron death but also damages endothelial cells within neurovascular unit. Maintaining the integrity of whole neurovascular unit is required for proper brain function. Disruption of neurovascular unit, especially cerebral microvascular endothelial cells, leads to BBB perturbation and causes vasogenic cerebral edema and secondary neuronal damage, which eventually exacerbates long-term disability. Thus, there is a

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25

Ming-CheLee and 李明哲. "Inhibition of HDAC activity by sodium butyrate attenuates hypoxic-ischemic injury in the neonatal brain." Thesis, 2010. http://ndltd.ncl.edu.tw/handle/95704696191172209196.

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碩士<br>國立成功大學<br>分子醫學研究所<br>98<br>Background: Hypoxic-ischemia (HI) encephalopathy is a major cause of neonatal mortality and subsequent neurodevelopmental disability in the surviving infants, however, there is still no effective treatment. Recent studies have showed that increased histone acetylation by inhibitors of histone deacetylase (HDAC) protects against neurodegenerative disorders and acute cerebral ischemia in adult animals. The neuroprotective effect of HDAC inhibitors involves transcription activation through increasing histone acetylation of prosurvival genes. Hypothesis: This study

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Cerullo, Pierpaolo. "ROLE OF SODIUM/CALCIUM EXCHANGER IN NEURONAL DISFUNCTIONS FOLLOWING HYPOXIC-ISCHEMIC INJURY IN NEONATAL MICE." Tesi di dottorato, 2014. http://www.fedoa.unina.it/9954/1/cerullo_pierpaolo_26.pdf.

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Background: Hypoxic-ischemic encephalopathy (HIE) accounts for the majority of developmental, motor and cognitive deﬁcits in children, leading to life-long neurological impairments. Since (1) transient brain ischemia followed by reoxygenation alters ionic homeostasis in adult brain and the plasma membrane sodium/calcium exchanger (NCX) plays a fundamental role in the maintenance of ionic homeostasis during brain ischemia, we aim to demonstrate the involvement of NCX in the pathophysiology of HIE. Methods: Experimental HIE was induced in postnatal day 7 (P7) mice by unilateral elettrocoagulatio

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27

Dunlop, Kate. "Neuroprotective Effects of a Novel Apple Peel Extract AF4 in a Mouse Model of Hypoxic-Ischemic Brain Injury." 2011. http://hdl.handle.net/10222/13997.

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The neuroprotective effects of AF4, a flavonoid-enriched extract derived from the peel of Northern Spy apples (containing quercetin-3-O-glucoside, quercetin-3-O-galactoside, quercetin-3-O-rhamnoside, quercetin-3-O-rutinoside, epicatechin, and cyanidin-3-O-galactoside) were examined by assessing neuronal loss and motor impairment resulting from hypoxic-ischemic (HI) brain injury in adult C57BL/6 mice. Relative to vehicle treatment (water, 10mL/kg/day), oral administration of AF4 (50 mg/kg/day) for 3 days reduces HI-induced neuronal loss in the striatum and hippocampus, motor impairments, and re

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28

Guan, Jian. "Insulin-like growth factor-1 after hypoxic-ischemic brain injury: effects and modes of action on neuronal survival." 1996. http://hdl.handle.net/2292/3116.

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Insulin/insulin-like growth factor (IGF)s naturally occur in the central nervous system (CNS) and have an important role in cell proliferation and differentiation during brain development and maturation. IGFs, IGF binding protein (IGFBP)s and their receptors are expressed in damaged brain regions suggesting a role for the IGFs system after brain injury. It is now known that neurons can die some hours, even days after an injury. This programmed death is termed delayed neuronal death (DND). The process of DND might provide a therapeutic window of opportunity for insulin/IGFs to reduce brain dama

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29

Dunlop, Kate Elizabeth. "Neuroprotective Effects of a Novel Apple Peel Extract AF4 in a Mouse Model of Hypoxic-Ischemic Brain Injury." 2011. http://hdl.handle.net/10222/15722.

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The neuroprotective effects of AF4, a flavonoid-enriched extract derived from the peel of Northern Spy apples (containing quercetin-3-O-glucoside, quercetin-3-O-galactoside, quercetin-3-O-rhamnoside, quercetin-3-O-rutinoside, epicatechin, and cyanidin-3-O-galactoside) were examined by assessing neuronal loss and motor impairment resulting from hypoxic-ischemic (HI) brain injury in adult C57BL/6 mice. Relative to vehicle treatment (water, 10mL/kg/day), oral administration of AF4 (50 mg/kg/day) for 3 days reduces HI-induced neuronal loss in the striatum and hippocampus, motor impairments, and re

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30

FitriHandayani and 蘇涵亭. "Protection of neurovascular structure from hypoxic-ischemic brain injury by different progenitor cells derived from adipose-derived stem cell." Thesis, 2014. http://ndltd.ncl.edu.tw/handle/ykhwz8.

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碩士<br>國立成功大學<br>細胞生物與解剖學研究所<br>102<br>Adipose-derived stem cells (ASCs) show promise for regenerative medicine researches and able to differentiate into either endothelial or neuronal lineages. The current study aimed to investigate the therapeutic potential of human adipose-derived stem cell for hypoxic-ischemic (HI) brain injury. The HI brain injury was created by right common carotid artery ligation and then exposure to hypoxia (8% O2) for 2h. The human ASCs were differentiated into NPCs and EPCs by culturing ASCs in the chitosan and shear stress microenvironments. The rat pups were divided

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31

Сокол, Єлизавета Олександрівна, та Yelyzaveta Oleksandrivna Sokol. "Фізична терапія та ерготерапія для дітей раннього віку з наслідками гіпоксично-ішемічного ураження головного мозку". Master's thesis, 2020. http://repository.sspu.edu.ua/handle/123456789/9873.

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У дослідженні теоретично і практично обґрунтовано застосування комплексної програми фізичної терапії та ерготерапії для дітей раннього віку з наслідками гіпоксично-ішемічного ураження головного мозку. Визначено найбільш ефективні засоби фізичної терапії та ерготерапії для корекції психомоторних порушень у дітей раннього віку з наслідками гіпоксично-ішемічного ураження головного мозку. Описано та розкрито алгоритм побудови комплексної програми фізичної терапії та ерготерапії, яка включала кінезіотерапію, міофасціальний масаж, фізіотерапевтичні процедури, сенсорну інтеграцію і векторне кінезіоте

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