Journal articles: 'Hypoxic ischaemic brain injury'

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Howard, R. S., P. A. Holmes, and M. A. Koutroumanidis. "Hypoxic-ischaemic brain injury." Practical Neurology 11, no. 1 (January 13, 2011): 4–18. http://dx.doi.org/10.1136/jnnp.2010.235218.

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Gresoiu, Mihaela, and Silvana Christou. "Hypoxic ischaemic brain injury." Anaesthesia & Intensive Care Medicine 21, no. 6 (June 2020): 298–304. http://dx.doi.org/10.1016/j.mpaic.2020.03.009.

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Gray, Peter H., David I. Tudehope, John P. Masel, Yvonne R. Burns, Heather A. Mohay, Michael J. OʼCallaghan, and Gail M. Williams. "Perinatal Hypoxic-Ischaemic Brain Injury." Obstetrical & Gynecological Survey 49, no. 6 (June 1994): 389–90. http://dx.doi.org/10.1097/00006254-199406000-00010.

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Rocha-Ferreira, Eridan, and Mariya Hristova. "Plasticity in the Neonatal Brain following Hypoxic-Ischaemic Injury." Neural Plasticity 2016 (2016): 1–16. http://dx.doi.org/10.1155/2016/4901014.

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Hypoxic-ischaemic damage to the developing brain is a leading cause of child death, with high mortality and morbidity, including cerebral palsy, epilepsy, and cognitive disabilities. The developmental stage of the brain and the severity of the insult influence the selective regional vulnerability and the subsequent clinical manifestations. The increased susceptibility to hypoxia-ischaemia (HI) of periventricular white matter in preterm infants predisposes the immature brain to motor, cognitive, and sensory deficits, with cognitive impairment associated with earlier gestational age. In term infants HI causes selective damage to sensorimotor cortex, basal ganglia, thalamus, and brain stem. Even though the immature brain is more malleable to external stimuli compared to the adult one, a hypoxic-ischaemic event to the neonate interrupts the shaping of central motor pathways and can affect normal developmental plasticity through altering neurotransmission, changes in cellular signalling, neural connectivity and function, wrong targeted innervation, and interruption of developmental apoptosis. Models of neonatal HI demonstrate three morphologically different types of cell death, that is, apoptosis, necrosis, and autophagy, which crosstalk and can exist as a continuum in the same cell. In the present review we discuss the mechanisms of HI injury to the immature brain and the way they affect plasticity.

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Hage, Lory, Dusha Jeyakumaran, Jon Dorling, Shalini Ojha, Don Sharkey, Nicholas Longford, Neena Modi, Cheryl Battersby, and Chris Gale. "Changing clinical characteristics of infants treated for hypoxic-ischaemic encephalopathy in England, Wales and Scotland: a population-based study using the National Neonatal Research Database." Archives of Disease in Childhood - Fetal and Neonatal Edition 106, no. 5 (February 4, 2021): 501–8. http://dx.doi.org/10.1136/archdischild-2020-319685.

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BackgroundTherapeutic hypothermia is standard of care for babies with moderate/severe hypoxic-ischaemic encephalopathy and is increasingly used for mild encephalopathy.ObjectiveDescribe temporal trends in the clinical condition of babies diagnosed with hypoxic-ischaemic encephalopathy who received therapeutic hypothermia.DesignRetrospective cohort study using data held in the National Neonatal Research Database.SettingNational Health Service neonatal units in England, Wales and Scotland.PatientsInfants born from 1 January 2010 to 31 December 2017 with a recorded diagnosis of hypoxic-ischaemic encephalopathy who received therapeutic hypothermia for at least 3 days or died in this period.Main outcomesPrimary outcomes: recorded clinical characteristics including umbilical cord pH; Apgar score; newborn resuscitation; seizures and treatment on day 1. Secondary outcomes: recorded hypoxic-ischaemic encephalopathy grade.Results5201 babies with a diagnosis of hypoxic-ischaemic encephalopathy received therapeutic hypothermia or died; annual numbers increased over the study period. A decreasing proportion had clinical characteristics of severe hypoxia ischaemia or a diagnosis of moderate or severe hypoxic-ischaemic encephalopathy, trends were statistically significant and consistent across multiple clinical characteristics used as markers of severity.ConclusionsTreatment with therapeutic hypothermia for hypoxic-ischaemic encephalopathy has increased in England, Scotland and Wales. An increasing proportion of treated infants have a diagnosis of mild hypoxic-ischaemic encephalopathy or have less severe clinical markers of hypoxia. This highlights the importance of determining the role of hypothermia in mild hypoxic-ischaemic encephalopathy. Receipt of therapeutic hypothermia is unlikely to be a useful marker for assessing changes in the incidence of brain injury over time.

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Wyatt, JS. "Hypoxic-ischaemic injury of the neonatal brain." Fetal and Maternal Medicine Review 8, no. 2 (May 1996): 95–108. http://dx.doi.org/10.1017/s0965539500001522.

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Despite advances in obstetric and neonatal care, hypoxia-ischaemia remains as probably the commonest cause of severe disabling brain injury which occurs in the perinatal period. Although for the population as a whole, congenital brain abnormality and early fetal events are the most frequent antecedent of permanent neurodevelopmental disability, perinatal brain injury is an important and potentially preventable cause of severe and permanent handicap in both developed and developing countries.

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Howard, Robin S. "Hypoxic–ischaemic brain injury following cardiac arrest." Anaesthesia & Intensive Care Medicine 15, no. 4 (April 2014): 176–80. http://dx.doi.org/10.1016/j.mpaic.2014.01.014.

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Howard, Robin S. "Hypoxic–ischaemic brain injury following cardiac arrest." Anaesthesia & Intensive Care Medicine 18, no. 5 (May 2017): 244–48. http://dx.doi.org/10.1016/j.mpaic.2017.02.005.

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de Vries, Linda S., and Floris Groenendaal. "Patterns of neonatal hypoxic–ischaemic brain injury." Neuroradiology 52, no. 6 (April 14, 2010): 555–66. http://dx.doi.org/10.1007/s00234-010-0674-9.

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Gadian, D. G. "Developmental amnesia associated with early hypoxic-ischaemic injury." Brain 123, no. 3 (March 1, 2000): 499–507. http://dx.doi.org/10.1093/brain/123.3.499.

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Osredkar, Damjan, Hemmen Sabir, Mari Falck, Thomas Wood, Elke Maes, Torun Flatebø, Maja Puchades, and Marianne Thoresen. "Hypothermia Does Not Reverse Cellular Responses Caused by Lipopolysaccharide in Neonatal Hypoxic-Ischaemic Brain Injury." Developmental Neuroscience 37, no. 4-5 (2015): 390–97. http://dx.doi.org/10.1159/000430860.

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Introduction: Bacterial lipopolysaccharide (LPS) injection prior to hypoxia-ischaemia significantly increases hypoxia-ischaemic brain injury in 7-day-old (P7) rats. In addition, therapeutic hypothermia (HT) is not neuroprotective in this setting. However, the mechanistic aspects of this therapeutic failure have yet to be elucidated. This study was designed to investigate the underlying cellular mechanisms in this double-hit model of infection-sensitised hypoxia-ischaemic brain injury. Material and Methods: P7 rat pups were injected with either vehicle or LPS, and after a 4-hour delay were exposed to left carotid ligation followed by global hypoxia inducing a unilateral stroke-like hypoxia-ischaemic injury. Pups were randomised to the following treatments: (1) vehicle-treated pups receiving normothermia treatment (NT) (Veh-NT; n = 40), (2) LPS-treated pups receiving NT treatment (LPS-NT; n = 40), (3) vehicle-treated pups receiving HT treatment (Veh-HT; n = 38) and (4) LPS-treated pups receiving HT treatment (LPS-HT; n = 35). On postnatal day 8 or 14, Western blot analysis or immunohistochemistry was performed to examine neuronal death, apoptosis, astrogliosis and microglial activation. Results: LPS sensitisation prior to hypoxia-ischaemia significantly exacerbated apoptotic neuronal loss. NeuN, a neuronal biomarker, was significantly reduced in the LPS-NT and LPS-HT groups (p = 0.008). Caspase-3 activation was significantly increased in the LPS-sensitised groups (p < 0.001). Additionally, a significant increase in astrogliosis (glial fibrillary acidic expression, p < 0.001) was seen, as well as a trend towards increased microglial activation (Iba 1 expression, p = 0.051) in LPS-sensitised animals. Treatment with HT did not counteract these changes. Conclusion: LPS-sensitised hypoxia-ischaemic brain injury in newborn rats is mediated through neuronal death, apoptosis, astrogliosis and microglial activation. In this double-hit model, treatment with HT does not ameliorate these changes.

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&NA;. "Minocycline prevents hypoxic-ischaemic injury in neonatal brain." Inpharma Weekly &NA;, no. 1348 (July 2002): 9. http://dx.doi.org/10.2165/00128413-200213480-00018.

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Scott, R. J., and L. Hegyi. "Cell death in perinatal hypoxic-ischaemic brain injury." Neuropathology and Applied Neurobiology 23, no. 4 (August 1997): 307–14. http://dx.doi.org/10.1111/j.1365-2990.1997.tb01300.x.

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Scott, R. J., and L. Hegyi. "Cell death in perinatal hypoxic-ischaemic brain injury." Neuropathology and Applied Neurobiology 23, no. 4 (August 1997): 307–14. http://dx.doi.org/10.1046/j.1365-2990.1997.5598055.x.

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Gray, Peter H., David I. Tudehope, John P. Masel, Yvonne R. Burns, Heather A. Mohay, Micahel J. O'Callaghan, and Gail M. Williams. "PERINATAL HYPOXIC-ISCHAEMIC BRAIN INJURY: PRDICTION OF OUTCOME." Developmental Medicine & Child Neurology 35, no. 11 (November 12, 2008): 965–73. http://dx.doi.org/10.1111/j.1469-8749.1993.tb11578.x.

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Freeman, William D., Michelle L. Biewend, and Kevin M. Barrett. "Hypoxic-ischaemic brain injury (HIBI) after cardiopulmonary arrest." Current Anaesthesia & Critical Care 18, no. 5-6 (January 2007): 261–76. http://dx.doi.org/10.1016/j.cacc.2007.09.006.

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Wei, X. "Caffeic acid phenethyl ester prevents neonatal hypoxic-ischaemic brain injury." Brain 127, no. 12 (November 10, 2004): 2629–35. http://dx.doi.org/10.1093/brain/awh316.

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Cappellini, A. "Encefalopatia ipossico-ischemica." Rivista di Neuroradiologia 16, no. 3 (June 2003): 345–48. http://dx.doi.org/10.1177/197140090301600304.

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The term hypoxic-ischaemic encephalopathy, often used to cover the whole spectrum of perinatal brain damage, should be confined to neonatal suffering at term presenting specific physiopathological, clinical and radiological features. Most perinatal brain lesions are secondary to perinatal or post-natal hypoxic-ischaemic injury and can be classified on the basis of the predominant morphological characteristics (table 1). The different locations and morphological expression of brain damage in the premature infant and the neonate born at term reflect the different levels of brain maturation (table 2). These tables summarize the different pathogenetic and anatomopathological features of hypoxic-ischaemic lesions with clinical and radiological references in the premature infant and neonate born at term.

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Gunn, Alistair J., and Laura Bennet. "Timing still key to treating hypoxic ischaemic brain injury." Lancet Neurology 15, no. 2 (February 2016): 126–27. http://dx.doi.org/10.1016/s1474-4422(15)00386-5.

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Howard, R., M. Koutroumanidis, P. A. Holmes, A. Siddiqui, I. Tisopoulos, and D. Treacher. "PATH43 Hypoxic-ischaemic brain injury--MRI and EEG changes." Journal of Neurology, Neurosurgery & Psychiatry 81, no. 11 (October 22, 2010): e19-e19. http://dx.doi.org/10.1136/jnnp.2010.226340.11.

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Chotai, Niketa, Phua Hwee Tang, and Pratibha Agarwal. "Hypoxic Ischaemic Injury in an Immature Brain on MRI." Proceedings of Singapore Healthcare 19, no. 2 (June 2010): 163–65. http://dx.doi.org/10.1177/201010581001900212.

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Falck, Mari, Damjan Osredkar, Elke Maes, Torun Flatebø, Thomas Ragnar Wood, Hemmen Sabir, and Marianne Thoresen. "Hypothermic Neuronal Rescue from Infection-Sensitised Hypoxic-Ischaemic Brain Injury Is Pathogen Dependent." Developmental Neuroscience 39, no. 1-4 (2017): 238–47. http://dx.doi.org/10.1159/000455838.

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Perinatal infection increases the vulnerability of the neonatal brain to hypoxic-ischaemic (HI) injury. Hypothermia treatment (HT) does not provide neuroprotection after pre-insult inflammatory sensitisation by lipopolysaccharide (LPS), a gram-negative bacterial wall constituent. However, early-onset sepsis in term babies is caused by gram-positive species in more than 90% of cases, and neuro-inflammatory responses triggered through the gram-negative route (Toll-like receptor 4, TLR-4) are different from those induced through the gram-positive route via TLR-2. Whether gram-positive septicaemia sensitises the neonatal brain to hypoxia and inhibits the neuroprotective effect of HT is unknown. Seven-day-old Wistar rats (n = 178) were subjected to intraperitoneal injections of PAM3CSK4 (1 mg/kg, a synthetic TLR-2 agonist) or vehicle (0.9% NaCl). After an 8-h delay, the left carotid artery was ligated followed by 50 min of hypoxia (8% O2) at a rectal temperature of 36°C. Pups received a 5-h treatment of normothermia (NT, 37°C) or HT (32°C) immediately after the insult. Brains were harvested after 7 days' survival for hemispheric and hippocampal area loss analyses and immunolabelling of microglia (Iba1) and hippocampal neurons (NeuN). Normothermic PAM3CSK4-injected animals showed significantly more brain injury than vehicle animals (p = 0.014). Compared to NT, HT significantly reduced injury in the PAM3CSK4-injected animals, with reduced area loss (p < 0.001), reduced microglial activation (p = 0.006), and increased neuronal rescue in the CA1 region (p < 0.001). Experimental induction of a sepsis-like condition through the gram-positive pathway sensitises the brain to HI injury. HT was highly neuroprotective after the PAM3CSK4-triggered injury, suggesting HT may be neuroprotective in the presence of a gram-positive infection. These results are in strong contrast to LPS studies where HT is not neuroprotective.

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Alagappan, Dhivyaa, Deborah A. Lazzarino, Ryan J. Felling, Murugabaskar Balan, Sergei V. Kotenko, and Steven W. Levison. "Brain Injury Expands the Numbers of Neural Stem Cells and Progenitors in the SVZ by Enhancing Their Responsiveness to EGF." ASN Neuro 1, no. 2 (April 22, 2009): AN20090002. http://dx.doi.org/10.1042/an20090002.

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There is an increase in the numbers of neural precursors in the SVZ (subventricular zone) after moderate ischaemic injuries, but the extent of stem cell expansion and the resultant cell regeneration is modest. Therefore our studies have focused on understanding the signals that regulate these processes towards achieving a more robust amplification of the stem/progenitor cell pool. The goal of the present study was to evaluate the role of the EGFR [EGF (epidermal growth factor) receptor] in the regenerative response of the neonatal SVZ to hypoxic/ischaemic injury. We show that injury recruits quiescent cells in the SVZ to proliferate, that they divide more rapidly and that there is increased EGFR expression on both putative stem cells and progenitors. With the amplification of the precursors in the SVZ after injury there is enhanced sensitivity to EGF, but not to FGF (fibroblast growth factor)-2. EGF-dependent SVZ precursor expansion, as measured using the neurosphere assay, is lost when the EGFR is pharmacologically inhibited, and forced expression of a constitutively active EGFR is sufficient to recapitulate the exaggerated proliferation of the neural stem/progenitors that is induced by hypoxic/ischaemic brain injury. Cumulatively, our results reveal that increased EGFR signalling precedes that increase in the abundance of the putative neural stem cells and our studies implicate the EGFR as a key regulator of the expansion of SVZ precursors in response to brain injury. Thus modulating EGFR signalling represents a potential target for therapies to enhance brain repair from endogenous neural precursors following hypoxic/ischaemic and other brain injuries.

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Eklind, Saskia, Carina Mallard, Anna-Lena Leverin, Erik Gilland, Klas Blomgren, Inger Mattsby-Baltzer, and Henrik Hagberg. "Bacterial endotoxin sensitizes the immature brain to hypoxic-ischaemic injury." European Journal of Neuroscience 13, no. 6 (March 2001): 1101–6. http://dx.doi.org/10.1046/j.0953-816x.2001.01474.x.

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Fanaroff, A. A. "Caffeic Acid Phenethyl Ester Prevents Neonatal Hypoxic–Ischaemic Brain Injury." Yearbook of Neonatal and Perinatal Medicine 2006 (January 2006): 265–67. http://dx.doi.org/10.1016/s8756-5005(08)70345-7.

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Edwards, AD. "Protection against hypoxic-ischaemic cerebral injury in the developing brain." Perfusion 8, no. 1 (January 1993): 97–100. http://dx.doi.org/10.1177/026765919300800113.

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Peden, C. J., M. A. Rutherford, J. Sargentoni, I. J. Cox, D. J. Bryant, and L. M. S. Dubowitz. "PROTON SPECTROSCOPY OF THE NEONATAL BRAIN FOLLOWING HYPOXIC-ISCHAEMIC INJURY." Developmental Medicine & Child Neurology 35, no. 6 (November 12, 2008): 502–10. http://dx.doi.org/10.1111/j.1469-8749.1993.tb11680.x.

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Kane, Nick, and Agyepong Oware. "Somatosensory evoked potentials aid prediction after hypoxic–ischaemic brain injury." Practical Neurology 15, no. 5 (July 27, 2015): 352–60. http://dx.doi.org/10.1136/practneurol-2015-001122.

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Naithani, Manisha, and Ashish Kumar Simalti. "Biochemical Markers in Perinatal Asphyxia." Journal of Nepal Paediatric Society 31, no. 2 (May 6, 2011): 151–56. http://dx.doi.org/10.3126/jnps.v31i2.4155.

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Early assessment of the severity of an acute cerebral lesion secondary to hypoxia-ischemia or other pathologic conditions may provide a very useful basis for preventive or therapeutic decisions in pediatric patients. In the present review, we discuss the diagnostic and prognostic value of a series of biochemical parameters, with special reference to the diagnosis of neonatal HIE. Currently many specific biochemical markers of brain injury are being investigated to assess regional brain damage after perinatal asphyxia in neonates of which serum protein S-100β, brain-specific creatine kinase, neuron-specific enolase, IL6 and urinary uric acid levels appear promising in identifying patients with a risk of developing hypoxic-ischemic encephalopathy. Whether detection of elevated serum concentrations of these proteins reflects long-term neurodevelopmental impairment remains to be investigated. Key words: S-100; Brain specific creatine kinase; neuron specific enolase; IL6; urinary uric acid; hypoxic ischaemic cerebral injury. DOI: 10.3126/jnps.v31i2.4155 J Nep Paedtr Soc 2010;31(2):151-156

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Lee, Wei Ling Amelia, Adina T. Michael-Titus, and Divyen K. Shah. "Hypoxic-Ischaemic Encephalopathy and the Blood-Brain Barrier in Neonates." Developmental Neuroscience 39, no. 1-4 (2017): 49–58. http://dx.doi.org/10.1159/000467392.

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This review aims to highlight a possible relationship between hypoxic-ischaemic encephalopathy (HIE) and the disruption of the blood-brain barrier (BBB). Inflammatory reactions perpetuate a large proportion of cerebral injury. The extent of injury noted in HIE is not only determined by the biochemical cascades that trigger the apoptosis-necrosis continuum of cell death in the brain parenchyma, but also by the breaching of the BBB by pro-inflammatory factors. We examine the changes that contribute to the breakdown of the BBB that occur during HIE at a macroscopic, cellular, and molecular level. The BBB is a permeability barrier which separates a large majority of brain areas from the systemic circulation. The concept of a physiological BBB is based at the anatomical level on the neurovascular unit (NVU). The NVU consists of various cellular components that jointly regulate the exchanges that occur at the interface between the systemic circulation and the brain parenchyma. There is increased understanding of the contribution of the components of the NVU, e.g., astrocytes and pericytes, to the maintenance of this physiological barrier. We also explore the development of therapeutic options in HIE, such as harnessing the transport systems in the BBB, to enable the delivery of large molecules with molecular Trojan horse technology, and the reinforcement of the physical barrier with cell-based therapy which utilizes endothelial progenitor cells and stem cells.

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Howard, R. S., P. A. Holmes, A. Siddiqui, D. Treacher, I. Tsiropoulos, and M. Koutroumanidis. "Hypoxic-ischaemic brain injury: imaging and neurophysiology abnormalities related to outcome." QJM 105, no. 6 (February 9, 2012): 551–61. http://dx.doi.org/10.1093/qjmed/hcs016.

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Thornton, Claire, Adam Jones, Syam Nair, Afra Aabdien, Carina Mallard, and Henrik Hagberg. "Mitochondrial dynamics, mitophagy and biogenesis in neonatal hypoxic-ischaemic brain injury." FEBS Letters 592, no. 5 (December 25, 2017): 812–30. http://dx.doi.org/10.1002/1873-3468.12943.

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Jang, Sung Ho, and You Sung Seo. "Recovery of Injured Optic Radiations in a Patient with Hypoxic-Ischaemic Brain Injury." Neuro-Ophthalmology 44, no. 4 (December 12, 2019): 270–73. http://dx.doi.org/10.1080/01658107.2019.1676263.

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Falck, Mari, Damjan Osredkar, Elke Maes, Torun Flatebø, Thomas Ragnar Wood, Lars Walløe, Hemmen Sabir, and Marianne Thoresen. "Hypothermia Is Neuroprotective after Severe Hypoxic-Ischaemic Brain Injury in Neonatal Rats Pre-Exposed to PAM3CSK4." Developmental Neuroscience 40, no. 3 (2018): 189–97. http://dx.doi.org/10.1159/000487798.

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Background: Preclinical research on the neuroprotective effect of hypothermia (HT) after perinatal asphyxia has shown variable results, depending on comorbidities and insult severity. Exposure to inflammation increases vulnerability of the neonatal brain to hypoxic-ischaemic (HI) injury, and could be one explanation for those neonates whose injury is unexpectedly severe. Gram-negative type inflammatory exposure by lipopolysaccharide administration prior to a mild HI insult results in moderate brain injury, and hypothermic neuroprotection is negated. However, the neuroprotective effect of HT is fully maintained after gram-positive type inflammatory exposure by PAM3CSK4 (PAM) pre-administration in the same HI model. Whether HT is neuroprotective in severe brain injury with gram-positive inflammatory pre-exposure has not been investigated. Methods: 59 seven-day-old rat pups were subjected to a unilateral HI insult, with left carotid artery ligation followed by 90-min hypoxia (8% O2 at Trectal 36°C). An additional 196 pups received intraperitoneal 0.9% saline (control) or PAM1 mg/kg, 8 h before undergoing the same HI insult. After randomisation to 5 h normothermia (NT37°C) or HT32°C, pups survived 1 week before they were sacrificed by perfusion fixation. Brains were harvested for hemispheric and hippocampal area loss analyses at postnatal day 14, as well as immunostaining for neuron count in the HIP CA1 region. Results: Normothermic PAM animals (PAM-NT) had a comparable median area loss (hemispheric: 60% [95% CI 33–66]; hippocampal: 61% [95% CI 29–67]) to vehicle animals (Veh-NT) (hemispheric: 58% [95% CI 11–64]; hippocampal: 60% [95% CI 19–68]), which is defined as severe brain injury. Furthermore, mortality was low and similar in the two groups (Veh-NT 4.5% vs. PAM-NT 6.6%). HT reduced hemispheric and hippocampal injury in the Veh group by 13 and 28%, respectively (hemispheric: p = 0.048; hippocampal: p = 0.042). HT also provided neuroprotection in the PAM group, reducing hemispheric injury by 22% (p = 0.03) and hippocampal injury by 37% (p = 0.027). Conclusion: In these experiments with severe brain injury, Toll-like receptor-2 triggering prior to HI injury does not have an additive injurious effect, and there is a small but significant neuroprotective effect of HT. HT appears to be neuroprotective over a continuum of injury severity in this model, and the effect size tapers off with increasing area loss. Our results indicate that gram-positive inflammatory exposure prior to HI injury does not negate the neuroprotective effect of HT in severe brain injury.

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Bale, Gemma, Subhabrata Mitra, Isabel de Roever, Magdalena Sokolska, David Price, Alan Bainbridge, Roxana Gunny, et al. "Oxygen dependency of mitochondrial metabolism indicates outcome of newborn brain injury." Journal of Cerebral Blood Flow & Metabolism 39, no. 10 (May 18, 2018): 2035–47. http://dx.doi.org/10.1177/0271678x18777928.

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There is a need for a method of real-time assessment of brain metabolism during neonatal hypoxic-ischaemic encephalopathy (HIE). We have used broadband near-infrared spectroscopy (NIRS) to monitor cerebral oxygenation and metabolic changes in 50 neonates with HIE undergoing therapeutic hypothermia treatment. In 24 neonates, 54 episodes of spontaneous decreases in peripheral oxygen saturation (desaturations) were recorded between 6 and 81 h after birth. We observed differences in the cerebral metabolic responses to these episodes that were related to the predicted outcome of the injury, as determined by subsequent magnetic resonance spectroscopy derived lactate/N-acetyl-aspartate. We demonstrated that a strong relationship between cerebral metabolism (broadband NIRS-measured cytochrome-c-oxidase (CCO)) and cerebral oxygenation was associated with unfavourable outcome; this is likely to be due to a lower cerebral metabolic rate and mitochondrial dysfunction in severe encephalopathy. Specifically, a decrease in the brain tissue oxidation state of CCO greater than 0.06 µM per 1 µM brain haemoglobin oxygenation drop was able to predict the outcome with 64% sensitivity and 79% specificity (receiver operating characteristic area under the curve = 0.73). With further work on the implementation of this methodology, broadband NIRS has the potential to provide an early, cotside, non-invasive, clinically relevant metabolic marker of perinatal hypoxic-ischaemic injury.

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McNeill, Alisdair. "Expression of apolipoprotein-E in human perinatal brain after hypoxic-ischaemic injury." Pathology 37, no. 3 (June 2005): 256–58. http://dx.doi.org/10.1080/00313020500099007.

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McNeill, Heather, Christopher Williams, Jian Guan, Michael Dragunow, Patricia Lawlor, Ernest Sirimanne, Karoly Nikolics, and Peter Gluckman. "Neuronal rescue with transforming growth factor-β1 after hypoxic-ischaemic brain injury." NeuroReport 5, no. 8 (April 1994): 901–4. http://dx.doi.org/10.1097/00001756-199404000-00012.

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Cooper, Chris E. "In vivo measurements of mitochondrial function and cell death following hypoxic/ischaemic damage to the new-born brain." Biochemical Society Symposia 66 (September 1, 1999): 123–40. http://dx.doi.org/10.1042/bss0660123.

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Critically impaired gas exchange to the brain due to decreased oxygen (hypoxia) or reduced blood flow (ischaemia) is a major cause of brain injury in the perinatal period. There is an accumulating body of evidence suggesting that the irreversible cellular damage in the neonatal brain that occurs subsequent to an hypoxic/ischaemic insult is at the level of the mitochondria. Much of this evidence has been obtained by novel non-invasive measurements of mitochondrial function in vivo. This review focuses on four techniques: near-infrared spectroscopy, magnetic resonance spectroscopy, magnetic resonance imaging and electron paramagnetic resonance spectroscopy. The advantages and disadvantages of these in vivo methods are described in patients and animal models. The picture that emerges is of a slow (1-2 day) energy failure, occurring at the level of the brain mitochondria and leading to a primarily apoptotic cell death. Moderate post-insult hypothermia prevents this damage by an unknown mechanism. It is stressed that isolated cell studies alone are not sufficient to understand the processes occurring at the biochemical and physiological levels. The use of the non-invasive techniques described to understand the biochemistry occurring in vivo is therefore an invaluable aid in integrating cellular and organismal studies of the role of mitochondria in cell death.

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Rener-Primec, Z., K. Esih, K. Goričar, and V. Dolžan. "PP06.14 – 2591: Antioxidative enzyme polymorphisms and sequelae after neonatal hypoxic-ischaemic brain injury." European Journal of Paediatric Neurology 19 (May 2015): S55. http://dx.doi.org/10.1016/s1090-3798(15)30180-x.

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Vollmer, Brigitte. "Severe neonatal hypoxic‐ischaemic brain injury: still an important cause of infantile spasms." Developmental Medicine & Child Neurology 62, no. 1 (November 2019): 9. http://dx.doi.org/10.1111/dmcn.14386.

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Rosa, Nicola, Livio Vitiello, and Maddalena De Bernardo. "Optic nerve sheath diameter measurement in hypoxic ischaemic brain injury after cardiac arrest." Resuscitation 138 (May 2019): 310–11. http://dx.doi.org/10.1016/j.resuscitation.2019.01.043.

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Whitelaw, Andrew. "Systematic review of therapy after hypoxic-ischaemic brain injury in the perinatal period." Seminars in Neonatology 5, no. 1 (February 2000): 33–40. http://dx.doi.org/10.1053/siny.1999.0113.

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Jellema, RK, TGAM Wolfs, V. Lima Passos, A. Zwanenburg, DRMG Ophelders, E. Kuypers, AHN Hopman, et al. "O-061 Cell-based Therapy For Hypoxic-ischaemic Injury In The Preterm Brain." Archives of Disease in Childhood 99, Suppl 2 (October 2014): A45.2—A45. http://dx.doi.org/10.1136/archdischild-2014-307384.129.

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Miller, Suzanne L., and David W. Walker. "The challenge of protecting the perinatal brain against hypoxic ischaemic injury - hasten slowly." Journal of Physiology 592, no. 3 (January 31, 2014): 425–26. http://dx.doi.org/10.1113/jphysiol.2013.268888.

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Azzopardi, D., J. S. Wyatt, E. B. Cady, P. A. Hamilton, D. T. Delpy, P. L. Hope, A. L. Stewart, and E. O. R. Reynolds. "PROGNOSIS OF INFANTS WITH HYPOXIC-ISCHAEMIC BRAIN INJURY ASSESSED BY MAGNETIC RESONANCE SPECTROSCOPY." Pediatric Research 22, no. 2 (August 1987): 220. http://dx.doi.org/10.1203/00006450-198708000-00044.

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Guan, Jian, Stephen J. M. Skinner, Erica J. Beilharz, Ke M. Hua, Stephen Hodgkinson, Peter D. Gluckman, and Chris E. Williams. "The movement of IGF-I into the brain parenchyma after hypoxic-ischaemic injury." NeuroReport 7, no. 2 (January 1996): 632–36. http://dx.doi.org/10.1097/00001756-199601310-00061.

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Suryana, Eurwin, and Nicole M. Jones. "The effects of hypoxic preconditioning on white matter damage following hypoxic‐ischaemic injury in the neonatal rat brain." International Journal of Developmental Neuroscience 37, no. 1 (July 4, 2014): 69–75. http://dx.doi.org/10.1016/j.ijdevneu.2014.06.007.

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Griesmaier, E., K. Medek, M. J. Gross, G. Schlager, M. Keller, U. Kiechl-Kohlendorfer, and M. Urbanek. "Repetitive Administration of Levetiracetam does not Reduce Hypoxic-Ischaemic Brain Injury in Newborn Mice." Pediatric Research 70 (November 2011): 649. http://dx.doi.org/10.1038/pr.2011.874.

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Wyatt, J. S., A. D. Edwards, D. Azzopardi, and E. O. Reynolds. "Magnetic resonance and near infrared spectroscopy for investigation of perinatal hypoxic-ischaemic brain injury." Archives of Disease in Childhood 64, no. 7 Spec No (July 1, 1989): 953–63. http://dx.doi.org/10.1136/adc.64.7_spec_no.953.

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Allemand, D., F. Allemand, F. Cortesi, A. Costa, V. Labellarte, and C. Vagnoni. "Evoluzione neuropsichiatrica a lungo termine in soggetti con encefalopatia ipossico-ischemica neonatale." Rivista di Neuroradiologia 16, no. 3 (June 2003): 535–37. http://dx.doi.org/10.1177/197140090301600340.

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Abstract:

We studied the neuropsychiatric evolution at school age in a population of children born at term with perinatal asphyxia, focusing on the assessment of cognitive disorders and psychopathological problems such as anxiety, depression and behavioural disorders. The cohort comprised 33 children aged between seven and 12 years, born at term and presenting hypoxic-ischaemic encephalopathy at birth. History-taking and neurological examination were done (according to Towen) and the following tests administered: WISC-R, test CBCL, childhood anxiety scale (Busnelli), CDI (Kovacs). A control group consisted of children aged between eight and 12 years without perinatal suffering. Results disclosed a number of evolutive disorders even though patients with severe neuromotor deficit were excluded from the study. Disorders included minor neurological syndromes, specific language and learning disorders, positivity on the scale for anxiety and depression: in particular 50% of the sample with minor neurological syndrome had symptoms of anxiety and depression. We divided the neonatal hypoxic-ischaemic encephalopathy into three degrees on the basis of brain scan and neurological examination. Relating the degree of neonatal hypoxic-ischaemic encephalopathy to some neuropsychological and psychiatric variables (cognitive level, anxiety, depression), only the correlation with anxiety was significant: the incidence of anxiety symptoms at school age was greater in the intermediate degree of neonatal hypoxic-ischaemic encephalopathy. Our findings further support the postulated link between neurological injury/dysfunction (perinatal asphyxia) and the subsequent onset of psychiatric and/or neuropsychological disorders.

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Journal articles on the topic 'Hypoxic ischaemic brain injury'

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