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Journal articles on the topic 'Hypoxic-ischemic injury'

Author: Grafiati

Published: 28 May 2022

Last updated: 30 July 2025

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1

Biagas, Katherine. "Hypoxic-ischemic brain injury." Current Opinion in Pediatrics 11, no. 3 (1999): 223–28. http://dx.doi.org/10.1097/00008480-199906000-00009.

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2

Xu, Xiaowen, Xinxin Wang, Li Zhang, et al. "Nicotinamide adenine dinucleotide treatment confers resistance to neonatal ischemia and hypoxia: effects on neurobehavioral phenotypes." Neural Regeneration Research 19, no. 12 (2024): 2760–72. http://dx.doi.org/10.4103/nrr.nrr-d-23-01490.

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JOURNAL/nrgr/04.03/01300535-202412000-00031/figure1/v/2024-04-08T165401Z/r/image-tiff Neonatal hypoxic-ischemic brain injury is the main cause of hypoxic-ischemic encephalopathy and cerebral palsy. Currently, there are few effective clinical treatments for neonatal hypoxic-ischemic brain injury. Here, we investigated the neuroprotective and molecular mechanisms of exogenous nicotinamide adenine dinucleotide, which can protect against hypoxic injury in adulthood, in a mouse model of neonatal hypoxic-ischemic brain injury. In this study, nicotinamide adenine dinucleotide (5 mg/kg) was intraperit

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3

Jha, Ruchira M., Aaron L. Berkowitz, and Joshua P. Klein. "Evolution of Hypoxic–Ischemic Injury." Neurohospitalist 3, no. 1 (2012): 46. http://dx.doi.org/10.1177/1941874412467807.

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4

Roland, Elke H., Kenneth Poskitt, Estela Rodriguez, Brian A. Lupton, and Alan Hill. "Perinatal Hypoxic-Ischemic Thalamic Injury." Obstetrical & Gynecological Survey 54, no. 3 (1999): 166–68. http://dx.doi.org/10.1097/00006254-199903000-00011.

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5

Boggio, Paulo Sérgio, Elizeu Coutinho de Macedo, Alvaro Pascual-Leone, Jose Maria Tormos Muñoz, José Salomáo SchWartzman, and Felipe Fregni. "Neuromodulation in hypoxic-ischemic injury." Brain Stimulation 2, no. 3 (2009): 179–81. http://dx.doi.org/10.1016/j.brs.2008.12.002.

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6

Povroznik, Jessica M., Elizabeth B. Engler-Chiurazzi, Tania Nanavati, and Paola Pergami. "Absolute lymphocyte and neutrophil counts in neonatal ischemic brain injury." SAGE Open Medicine 6 (January 1, 2018): 205031211775261. http://dx.doi.org/10.1177/2050312117752613.

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Objectives: This study aimed to identify differences in absolute neutrophils, lymphocytes, and neutrophil-to-lymphocyte ratio between neonates with two forms of ischemic brain injury, hypoxic-ischemic encephalopathy, and acute ischemic stroke, compared to controls. We also aimed to determine whether this neutrophil/lymphocyte response pattern is associated with disease severity or is a consequence of the effects of total-body cooling, an approved treatment for moderate-to-severe hypoxic-ischemic encephalopathy. Methods: A retrospective chart review of 101 neonates with hypoxic-ischemic encepha

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Davydenko, A. V. "GENE POLYMORPHISM AS A PREDICTOR DEVELOPMENT OF THE CHILDREN DISEASE." Актуальні проблеми сучасної медицини: Вісник Української медичної стоматологічної академії 22, no. 3-4 (2022): 225–30. http://dx.doi.org/10.31718/2077-1096.22.3.4.225.

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Neonates suffering from severe birth asphyxia may develop hypoxic ischemic encephalopathy and in some cases to permanent neurological damage. Around 20 – 50% of neonates with birth asphyxia who have hypoxic ischemic encephalopathy symptoms die in the neonatal period. Our study aims to clarify the role and impact of gene polymorphisms on the occurrence of hypoxic-ischemic encephalopathy. Hypoxic-ischaemic encephalopathy is a common cause of death and disability in newborns. It causes long-term or permanent damage, such as cerebral palsy, epilepsy, and certain forms of mental retardation. Autore

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8

Lai, Ming-Chi, and San-Nan Yang. "Perinatal Hypoxic-Ischemic Encephalopathy." Journal of Biomedicine and Biotechnology 2011 (2011): 1–6. http://dx.doi.org/10.1155/2011/609813.

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Perinatal hypoxic-ischemic encephalopathy (HIE) is an important cause of brain injury in the newborn and can result in long-term devastating consequences. Perinatal hypoxia is a vital cause of long-term neurologic complications varying from mild behavioural deficits to severe seizure, mental retardation, and/or cerebral palsy in the newborn. In the mammalian developing brain, ongoing research into pathophysiological mechanism of neuronal injury and therapeutic strategy after perinatal hypoxia is still limited. With the advent of promising therapy of hypothermia in HIE, this paper reviews the p

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9

Zhang, Ruilan, Zhenggang Zhang, and Michael Chopp. "Function of neural stem cells in ischemic brain repair processes." Journal of Cerebral Blood Flow & Metabolism 36, no. 12 (2016): 2034–43. http://dx.doi.org/10.1177/0271678x16674487.

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Hypoxic/ischemic injury is the single most important cause of disabilities in infants, while stroke remains a leading cause of morbidity in children and adults around the world. The injured brain has limited repair capacity, and thereby only modest improvement of neurological function is evident post injury. In rodents, embryonic neural stem cells in the ventricular zone generate cortical neurons, and adult neural stem cells in the ventricular–subventricular zone of the lateral ventricle produce new neurons through animal life. In addition to generation of new neurons, neural stem cells contri

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10

Carroll, J. "Stem cells for neonatal hypoxic-ischemic injury." Cell and Organ Transplantology 1, no. 1 (2013): 10–13. http://dx.doi.org/10.22494/cot.v1i1.44.

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Many types of adult stem cells have been used in pre-clinical situations to treat experimental hypoxic-ischemic (HI) injury in neonatal animals. Numerous laboratory reports have appeared in the literature indicating that this treatment is beneficial, and the route of cell administration does not appear to be critical. The success of treatment occurs with administration soon after the injury, and this early administration of the cells proximate to the time of injury appears to be decisive. The mechanism of benefit relates to preservation of intrinsic neurons at the site of injury rather than ce

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11

Khan, Muhammad Waleed, Ghazala Wahid, Rabeea Ihtesham, Uzma Badshah, Shaista Khan, and Samia Iftikhar. "TO DETERMINE THE DIAGNOSTIC ACCURACY OF TRANSCRANIAL ULTRASOUND IN THE DETECTION OF HYPOXIC ISCHEMIC INJURY IN NEONATES KEEPING MAGNETIC RESONANCE IMAGING AS A GOLD STANDARD." Khyber Journal of Medical Sciences 18, no. 1 (2025): 16–22. https://doi.org/10.70520/kjms.v18i1.519.

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Objective: To ascertain the accuracy of transcranial ultrasound diagnosis in the detection of hypoxic ischemic injury in neonates, keeping magnetic resonance imaging as the gold standard. Material & Methods: A cross-sectional study was conducted on 147 Male and female patients with an age range of 1-28 days in the Department of Radiology, Hayatabad Medical Complex, Peshawar, from 28 February 2023 to 28 August 2023 (06 months). The patients were suspected of hypoxic-ischemic injury, i.e., suffered from perinatal asphyxia. The diagnostic accuracy of transcranial sonography in detecting neona

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12

Zhao, Yijing, Tong Li, Zige Jiang, et al. "The miR-9-5p/CXCL11 pathway is a key target of hydrogen sulfide-mediated inhibition of neuroinflammation in hypoxic ischemic brain injury." Neural Regeneration Research 19, no. 5 (2023): 1084–91. http://dx.doi.org/10.4103/1673-5374.382860.

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Abstract JOURNAL/nrgr/04.03/01300535-202405000-00038/inline-graphic1/v/2023-09-28T063346Z/r/image-tiff We previously showed that hydrogen sulfide (H2S) has a neuroprotective effect in the context of hypoxic ischemic brain injury in neonatal mice. However, the precise mechanism underlying the role of H2S in this situation remains unclear. In this study, we used a neonatal mouse model of hypoxic ischemic brain injury and a lipopolysaccharide-stimulated BV2 cell model and found that treatment with L-cysteine, a H2S precursor, attenuated the cerebral infarction and cerebral atrophy induced by hypo

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13

Morgun, A. V., N. V. Kuvacheva, T. E. Taranushenko, et al. "CURRENT CONCEPTS OF PERINATAL ISCHEMIC INJURY IN THE BRAIN NEUROVASCULAR UNIT: MOLECULAR TARGETS FOR NEUROPROTECTION." Annals of the Russian academy of medical sciences 68, no. 12 (2013): 26–35. http://dx.doi.org/10.15690/vramn.v68i12.856.

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Perinatal hypoxic-ischemic brain injury is a relevant medical and social problem. Among many pathological processes in the neonatal period perinatal hypoxic-ischemic injury is a major cause of further hemorrhage, necrotic and atrophic changes in the brain. This review presents recent data on the basic mechanisms of the hypoxic-ischemic brain injury along the concept of neurovascular unit (neurons, astrocytes, endothelial cells, pericytes) with the focus on alterations in cell-to-cell communication. Pathological changes caused by ischemia-hypoxia are considered within two phases of injury (isch

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14

Little, Deborah M., Marilyn F. Kraus, Catherine Jiam, et al. "Neuroimaging of hypoxic-ischemic brain injury." NeuroRehabilitation 26, no. 1 (2010): 15–25. http://dx.doi.org/10.3233/nre-2010-0532.

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15

Parish, Anjali, and Jatinder Bhatia. "Hypothermia for hypoxic–ischemic brain injury." Journal of Maternal-Fetal & Neonatal Medicine 22, no. 9 (2009): 719–21. http://dx.doi.org/10.3109/14767050902822237.

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16

Sladky, John T., and Lucy B. Rorke. "Perinatal Hypoxic/Ischemic Spinal Cord Injury." Pediatric Pathology 6, no. 1 (1986): 87–101. http://dx.doi.org/10.3109/15513818609025927.

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17

Perlman, J. M. "Pathogenesis of hypoxic-ischemic brain injury." Journal of Perinatology 27, S1 (2007): S39—S46. http://dx.doi.org/10.1038/sj.jp.7211716.

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18

Parish, Anjali, and Jatinder Bhatia. "Hypothermia for hypoxic-ischemic brain injury." Journal of Maternal-Fetal & Neonatal Medicine 22, no. 9 (2009): 719–21. http://dx.doi.org/10.1080/14767050902822237.

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19

Murphy, Eric J., and Lloyd A. Horrocks. "Mechanisms of hypoxic and ischemic injury." Molecular and Chemical Neuropathology 19, no. 1-2 (1993): 95–106. http://dx.doi.org/10.1007/bf03160171.

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20

Barkovich, A. James, and Danial Hallam. "Neuroimaging in perinatal hypoxic-ischemic injury." Mental Retardation and Developmental Disabilities Research Reviews 3, no. 1 (1997): 28–41. http://dx.doi.org/10.1002/(sici)1098-2779(1997)3:1<28::aid-mrdd5>3.0.co;2-t.

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21

Cordes, Isabel, Elke H. Roland, Alan Hill, and Brian A. Lupton. "Letter To The Editor." Pediatrics 97, no. 1 (1996): 152. http://dx.doi.org/10.1542/peds.97.1.152.

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The comments of Dr Badawi et al draw attention to some of the ambiguities in the current understanding of potential significant factors associated with peninatal hypoxic-ischemic cerebral injury. Experimental animal data has demonstrated clearly that intrapartum hypoxic-ischemic insult may result in cerebral injury.1,2 However, epidemiologic studies have raised concerns that this relationship may not be as prevalent as was believed earlier.3-5 Nevertheless, it is important to consider that even if only 10% to 15% of cases of cerebral palsy are related to intrapartum hypoxic-ischemic cerebral i

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22

Steinberg, Alexis. "Emergent Management of Hypoxic-Ischemic Brain Injury." CONTINUUM: Lifelong Learning in Neurology 30, no. 3 (2024): 588–610. http://dx.doi.org/10.1212/con.0000000000001426.

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ABSTRACT OBJECTIVE This article outlines interventions used to improve outcomes for patients with hypoxic-ischemic brain injury after cardiac arrest. LATEST DEVELOPMENTS Emergent management of patients after cardiac arrest requires prevention and treatment of primary and secondary brain injury. Primary brain injury is minimized by excellent initial resuscitative efforts. Secondary brain injury prevention requires the detection and correction of many pathophysiologic processes that may develop in the hours to days after the initial arrest. Key physiologic parameters important to secondary brain

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23

Koch, Joshua D., Darryl K. Miles, Jennifer A. Gilley, Cui-Ping Yang, and Steven G. Kernie. "Brief Exposure to Hyperoxia Depletes the Glial Progenitor Pool and Impairs Functional Recovery after Hypoxic-Ischemic Brain Injury." Journal of Cerebral Blood Flow & Metabolism 28, no. 7 (2008): 1294–306. http://dx.doi.org/10.1038/jcbfm.2008.15.

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Patterns of hypoxic-ischemic brain injury in infants and children suggest vulnerability in regions of white matter development, and injured patients develop defects in myelination resulting in cerebral palsy and motor deficits. Reperfusion exacerbates the oxidative stress that occurs after such injuries and may impair recovery. Resuscitation after hypoxic-ischemic injury is routinely performed using 100% oxygen, and this practice may increase the oxidative stress that occurs during reperfusion and further damage an already compromised brain. We show that brief exposure (30 mins) to 100% oxygen

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24

Jisa, Kyle A., Dillon D. Clarey, and Eric S. Peeples. "Magnetic Resonance Imaging Findings of Term and Preterm Hypoxic-Ischemic Encephalopathy: A Review of Relevant Animal Models and Correlation to Human Imaging." Open Neuroimaging Journal 12, no. 1 (2018): 55–65. http://dx.doi.org/10.2174/1874440001812010055.

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Background:Neonatal hypoxic-ischemic encephalopathy is brain injury caused by decreased perfusion and oxygen delivery that most commonly occurs in the context of delivery complications such as umbilical cord compression or placental abruption. Imaging is a key component for guiding treatment and prediction of prognosis, and the most sensitive clinical imaging modality for the brain injury patterns seen in hypoxic-ischemic encephalopathy is magnetic resonance imaging.Objective:The goal of this review is to compare magnetic resonance imaging findings demonstrated in the available animal models o

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25

Bernis, Maria E., Charlotte Hakvoort, Efe Nacarkucuk, et al. "Neuroprotective Effect of Clemastine Improved Oligodendrocyte Proliferation through the MAPK/ERK Pathway in a Neonatal Hypoxia Ischemia Rat Model." International Journal of Molecular Sciences 25, no. 15 (2024): 8204. http://dx.doi.org/10.3390/ijms25158204.

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Neonatal hypoxic-ischemic encephalopathy is the most common cause of long-term disability in term neonates, and white matter injury is the primary cause of cerebral palsy. Therapies that focus on the neuroprotection of myelination and oligodendrocyte proliferation could potentially ameliorate long-lasting neurological impairments after hypoxic-ischemic encephalopathy. Clemastine, a histamine H1 antagonist, has been shown to exert neuroprotective effects in multiple sclerosis and spinal cord injury by promoting oligodendrogenesis and re-myelination. In this study, we demonstrated the neuroprote

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26

Lu-Emerson, Christine, and Sandeep Khot. "Neurological sequelae of hypoxic-ischemic brain injury." NeuroRehabilitation 26, no. 1 (2010): 35–45. http://dx.doi.org/10.3233/nre-2010-0534.

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27

Sharp, Frank R., Ruiqiong Ran, Aigang Lu, et al. "Hypoxic preconditioning protects against ischemic brain injury." NeuroRX 1, no. 1 (2004): 26–35. http://dx.doi.org/10.1602/neurorx.1.1.26.

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28

Huang, Hsiu-Mei, Chao-Ching Huang, Pi-Lien Hung, and Ying-Chao Chang. "Hypoxic–ischemic retinal injury in rat pups." Pediatric Research 72, no. 3 (2012): 224–31. http://dx.doi.org/10.1038/pr.2012.74.

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29

Rivkin, Michael, and Joseph Volpe. "Hypoxic-Ischemic Brain Injury in the Newborn." Seminars in Neurology 13, no. 01 (1993): 30–39. http://dx.doi.org/10.1055/s-2008-1041104.

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30

du Plessis, Adré J., and Michael V. Johnston. "Hypoxic-ischemic Brain Injury in the Newborn." Clinics in Perinatology 24, no. 3 (1997): 627–54. http://dx.doi.org/10.1016/s0095-5108(18)30162-3.

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31

Jacinto, Sergio J., Maria Gieron-Korthals, and Jose A. Ferreira. "PREDICTING OUTCOME IN HYPOXIC-ISCHEMIC BRAIN INJURY." Pediatric Clinics of North America 48, no. 3 (2001): 647–60. http://dx.doi.org/10.1016/s0031-3955(05)70332-1.

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32

Latchaw, Richard E., and Charles E. Truwit. "Imaging of perinatal hypoxic-ischemic brain injury." Seminars in Pediatric Neurology 2, no. 1 (1995): 72–89. http://dx.doi.org/10.1016/s1071-9091(05)80006-3.

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33

Tskitishvili, Ekaterine, Michelle Nisolle, Carine Munaut, et al. "Estetrol attenuates neonatal hypoxic–ischemic brain injury." Experimental Neurology 261 (November 2014): 298–307. http://dx.doi.org/10.1016/j.expneurol.2014.07.015.

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34

Sharp, Frank R., Ruiqiong Ran, Aigang Lu, et al. "Hypoxic preconditioning protects against ischemic brain injury." Neurotherapeutics 1, no. 1 (2004): 26–35. http://dx.doi.org/10.1007/bf03206565.

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35

Folkerth, Rebecca D. "Principles of Perinatal Hypoxic-Ischemic Brain Injury." Pathology Case Reviews 16, no. 5 (2011): 205–13. http://dx.doi.org/10.1097/pcr.0b013e31822987df.

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36

Bhatoe, Harjinder S. "The hypoxic-ischemic brain injury: Beyond semantics." Indian Journal of Neurotrauma 8, no. 2 (2011): 65–66. http://dx.doi.org/10.1016/s0973-0508(11)80001-8.

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37

Concepcion, Katherine R., and Lubo Zhang. "Corticosteroids and perinatal hypoxic-ischemic brain injury." Drug Discovery Today 23, no. 10 (2018): 1718–32. http://dx.doi.org/10.1016/j.drudis.2018.05.019.

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38

Sheng, Shiying, Jingzhong Huang, Yi Ren та ін. "Neuroprotection Against Hypoxic/Ischemic Injury: δ-Opioid Receptors and BDNF-TrkB Pathway". Cellular Physiology and Biochemistry 47, № 1 (2018): 302–15. http://dx.doi.org/10.1159/000489808.

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The delta-opioid receptor (DOR) is one of three classic opioid receptors in the opioid system. It was traditionally thought to be primarily involved in modulating the transmission of messages along pain signaling pathway. Although there were scattered studies on its other neural functions, inconsistent results and contradicting conclusions were found in past literatures, especially in terms of DOR’s role in a hypoxic/ischemic brain. Taking inspiration from the finding that the turtle brain exhibits a higher DOR density and greater tolerance to hypoxic/ischemic insult than the mammalian brain,

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39

Regmi, Pradeep Raj, Aalok Kumar Yadav, Bibek Koirala, Shreelal Yadav, and Isha Amatya. "Late Presentation of Hypoxic Injury of Brain in an Infant." Journal of Nepal Health Research Council 21, no. 2 (2023): 349–52. http://dx.doi.org/10.33314/jnhrc.v21i02.4451.

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Perinatal asphyxia is one of the leading causes of hypoxic-ischemic encephalopathy. In a developing country like Nepal, home delivery is the leading cause of perinatal asphyxia. Neuroimaging remains the diagnostic modality of choice. We present a case report of a 10-month-old infant who presented to the pediatric Out-patient-department with complaints of being unable to hold his head and unable to sit without support. Detailed history, physical examination, and developmental assessment along with lab investigation flash visual evoked potentials and Magnetic Resonance Imaging of the brain was p

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40

Volotko L. O. "NEUROSONOGRAPHIC STUDY OF CHILDREN WITH HYPOXIC-ISCHEMIC BRAIN IJURY." Science Review, no. 4(31) (April 30, 2020): 7–11. http://dx.doi.org/10.31435/rsglobal_sr/30042020/7050.

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The study is aimed at neurosonographic characteristics of brain injury in newborn patients with perinatal hypoxic-ischemic injury of central nervous system, complicated with inflectional process (meningitis, ventriculitis). It is settled that brain immaturity, hydrocephalic syndrome, ischemia of the brain tissue and intraventricular hemorrhages are found 2 times more often in infants with perinatal hypoxic-ischemic injury of central nervous system, complicated with inflectional process. This fact generally characterizes disorders of the hemato-encephalic barrier and the development of destruct

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41

Luo, Fengbao, Jian Shi, Qianqian Shi, Xianlin Xu, Ying Xia, and Xiaozhou He. "Mitogen-Activated Protein Kinases and Hypoxic/Ischemic Nephropathy." Cellular Physiology and Biochemistry 39, no. 3 (2016): 1051–67. http://dx.doi.org/10.1159/000447812.

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Tissue hypoxia/ischemia is a pathological feature of many human disorders including stroke, myocardial infarction, hypoxic/ischemic nephropathy, as well as cancer. In the kidney, the combination of limited oxygen supply to the tissues and high oxygen demand is considered the main reason for the susceptibility of the kidney to hypoxic/ischemic injury. In recent years, increasing evidence has indicated that a reduction in renal oxygen tension/blood supply plays an important role in acute kidney injury, chronic kidney disease, and renal tumorigenesis. However, the underlying signaling mechanisms,

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42

Tunç, Gaffari, Elif Ünver Korğalı, Gülşah Ünsal, Muhammet Ali Mutlu, and Esra Akaydın Gültürk. "Mortality in patients with hypoxic ischemic encephalopathy treated with therapeutic hypothermia." Cukurova Medical Journal 50, no. 1 (2025): 47–55. https://doi.org/10.17826/cumj.1569520.

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Purpose: Hypoxic-ischemic encephalopathy is a heterogeneous clinical syndrome that occurs in the perinatal period and is characterized by altered consciousness or seizures, respiratory depression, and hypotension. The aim of this study was to evaluate mortality in hypoxic-ischemic encephalopathy patients receiving therapeutic hypothermia. Materials and Methods: The study included 97 hypoxic-ischemic encephalopathy cases who underwent therapeutic hypothermia in the Neonatal Intensive Care Unit. The cases were evaluated for mortality and were divided into two groups: group 1 (n: 9, non-survivors

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43

Recker, Rebecca, Arash Adami, Beatriz Tone, et al. "Rodent Neonatal Bilateral Carotid Artery Occlusion with Hypoxia Mimics Human Hypoxic-Ischemic Injury." Journal of Cerebral Blood Flow & Metabolism 29, no. 7 (2009): 1305–16. http://dx.doi.org/10.1038/jcbfm.2009.56.

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We report a new clinically relevant model of neonatal hypoxic-ischemic injury in a 10-day-old rat pup. Bilateral carotid artery occlusion and 8% hypoxia (1 to 15 mins, BCAO-H) was induced with varying degrees of injury (mild, moderate, severe), which was quantified using magnetic resonance imaging including diffusion-weighted and T2-weighted imaging at 24 h and 21/28 days. We developed a magnetic resonance imaging-based rat pup severity score and compared 3D ischemic injury volumes/rat pup severity score with histology and behavioral testing. At 24 h, hypoxic-ischemic injury was observed in 17

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44

Garcia-Alix, Alfredo, and Juan Arnaez. "Value of brain damage biomarkers in cerebrospinal fluid in neonates with hypoxic–ischemic brain injury." Biomarkers in Medicine 16, no. 2 (2022): 117–25. http://dx.doi.org/10.2217/bmm-2021-0381.

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Hypoxic–ischemic encephalopathy is one of the leading causes of death and neurological disability worldwide. A key issue in neonates with hypoxic–ischemic encephalopathy is accurately establishing the occurrence and severity of brain lesions soon after a perinatal hypoxic–ischemic event. This is crucial to help with prognosis; guide clinical decision-making, including the use of other therapies; and improve family counseling. Neurobiochemical markers may offer a quantitative approximation for estimating the severity of brain damage and identifying infants who have a high risk of further neurol

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45

Fu, Changchang, Yihui Zheng, Kun Lin, et al. "Neuroprotective effect of apigenin against hypoxic-ischemic brain injury in neonatal rats via activation of the PI3K/Akt/Nrf2 signaling pathway." Food & Function 12, no. 5 (2021): 2270–81. http://dx.doi.org/10.1039/d0fo02555k.

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46

Wang, Liping, Sijie Li, Sara Saymuah Stone, et al. "The Role of the lncRNA MALAT1 in Neuroprotection against Hypoxic/Ischemic Injury." Biomolecules 12, no. 1 (2022): 146. http://dx.doi.org/10.3390/biom12010146.

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Hypoxic and ischemic brain injury can cause neurological disability and mortality, and has become a serious public health problem worldwide. Long-chain non-coding RNAs are involved in the regulation of many diseases. Metastasis-related lung adenocarcinoma transcript 1 (MALAT1) is a type of long non-coding RNA (lncRNA), known as long intergenic non-coding RNA (lincRNA), and is highly abundant in the nervous system. The enrichment of MALAT1 in the brain indicates that it may be associated with important functions in pathophysiological processes. Accordingly, the role of MALAT1 in neuronal cell h

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47

Rosova, Ivana, and Jan A. Nolta. "Hypoxic Preconditioning Results in Increased Motility and Improved Therapeutic Potential of Human Mesenchymal Stem Cells in a Xenograft Hind Limb Ischemia Injury Model." Blood 110, no. 11 (2007): 217. http://dx.doi.org/10.1182/blood.v110.11.217.217.

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Abstract Disorders such as peripheral artery disease cause hypoxic areas in tissues. Work from our group and others shows that stem cells appear to have innate mechanisms to respond to hypoxic conditions by migrating to the region of damage, and releasing trophic factors which initiate regeneration. Many tissues activate hepatocyte growth factor (HGF) as a response to ischemic injury. Multiple progenitor cell types express cMet, an HGF receptor. Mesenchymal stem cells (MSC) have been shown to improve regeneration of injured tissues in vivo, but their mechanisms of homing to the site of injury

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48

Cai, Chen-chen, Jiang-hu Zhu, Li-xia Ye, et al. "Glycine Protects against Hypoxic-Ischemic Brain Injury by Regulating Mitochondria-Mediated Autophagy via the AMPK Pathway." Oxidative Medicine and Cellular Longevity 2019 (February 6, 2019): 1–29. http://dx.doi.org/10.1155/2019/4248529.

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Hypoxic-ischemic encephalopathy (HIE) is detrimental to newborns and is associated with high mortality and poor prognosis. Thus, the primary aim of the present study was to determine whether glycine could (1) attenuate HIE injury in rats and hypoxic stress in PC12 cells and (2) downregulate mitochondria-mediated autophagy dependent on the adenosine monophosphate- (AMP-) activated protein kinase (AMPK) pathway. Experiments conducted using an in vivo HIE animal model and in vitro hypoxic stress to PC12 cells revealed that intense autophagy associated with mitochondrial function occurred during i

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Vasiljevic, Brankica, Svjetlana Maglajlic-Djukic, Miroslava Gojnic, and Sanja Stankovic. "The role of oxidative stress in perinatal hypoxic-ischemic brain injury." Srpski arhiv za celokupno lekarstvo 140, no. 1-2 (2012): 35–41. http://dx.doi.org/10.2298/sarh1202035v.

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Abstract:

Introduction. The pathogenesis of perinatal hypoxic-ischemic brain damage is highly complex. Objective. The aim of this study was to assess the role of oxidative stress in hypoxic-ischemic brain injury and subsequent abnormal neurological outcome in infants with perinatal hypoxic-ischemic encephalopathy (HIE). We estimated perinatal oxidative brain damage measuring activity of glutathione peroxidase (GPX) in cerebrospinal fluid (CSF) as an indirect biomarker of free radical production during cerebral hypoxia-ischemia in correlation with the level of intracellular enzyme neuron specific enolase

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Jiao, Mengya, Qun Dong, Yiting Zhang, et al. "Neuroprotection of N-benzyl Eicosapentaenamide in Neonatal Mice Following Hypoxic–Ischemic Brain Injury." Molecules 26, no. 11 (2021): 3108. http://dx.doi.org/10.3390/molecules26113108.

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Maca (Lepidium meyenii) has emerged as a popular functional plant food because of its medicinal properties and nutritional value. Macamides, as the exclusively active ingredients found in maca, are a unique series of non-polar, long-chain fatty acid N-benzylamides with multiple bioactivities such as antifatigue characteristics and improving reproductive health. In this study, a new kind of macamide, N-benzyl eicosapentaenamide (NB-EPA), was identified from maca. We further explore its potential neuroprotective role in hypoxic–ischemic brain injury. Our findings indicated that treatment with bi

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