Results 11 to 20 of about 112,633 (288)
Antimicrobial peptides and complement in neonatal hypoxia-ischemia induced brain damage [PDF]
Frontiers in Immunology, 2015 Hypoxic-ischemic encephalopathy (HIE) is a clinical condition in the neonate, resulting from oxygen deprivation around the time of birth. HIE affects 1-5/1000 live births worldwide and is associated with the development of neurological deficits ...
Hristova, M, Rocha-Ferreira, E
core +6 more sources
Single Dose Caffeine Protects the Neonatal Mouse Brain against Hypoxia Ischemia. [PDF]
PLoS ONE, 2017 In this randomized blinded study, we investigated caffeine 5 mg/kg treatment given directly after neonatal brain hypoxia ischemia. Brain morphology, behavior and key brain infiltrating immune populations were examined.
Max Winerdal +5 more
doaj +4 more sources
Hypoxia–ischemia in the immature brain [PDF]
Journal of Experimental Biology, 2004 SUMMARYThe immature brain has long been considered to be resistant to the damaging effects of hypoxia and hypoxia–ischemia (H/I). However, it is now appreciated that there are specific periods of increased vulnerability, which relate to the developmental stage at the time of the insult.
Susan J, Vannucci, Henrik, Hagberg
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Histology of Brain Trauma and Hypoxia-Ischemia [PDF]
Academic Forensic Pathology, 2018 Forensic pathologists encounter hypoxic-ischemic (HI) brain damage or traumatic brain injuries (TBI) on an almost daily basis. Evaluation of the findings guides decisions regarding cause and manner of death. When there are gross findings of brain trauma, the cause of death is often obvious.
Petra, Rahaman, Marc R, Del Bigio
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The Arginase Pathway in Neonatal Brain Hypoxia-Ischemia [PDF]
Developmental Neuroscience, 2018 Brain damage after hypoxia-ischemia (HI) occurs in an age-dependent manner. Neuroprotective strategies assumed to be effective in adults might have deleterious effects in the immature brain. In order to create effective therapies, the complex pathophysiology of HI in the developing brain requires exploring new mechanisms.
Jana Krystofova +4 more
openaire +4 more sources
Stem cells for brain repair in neonatal hypoxia–ischemia [PDF]
Child's Nervous System, 2013 Neonatal hypoxic-ischemic insults are a significant cause of pediatric encephalopathy, developmental delays, and spastic cerebral palsy. Although the developing brain's plasticity allows for remarkable self-repair, severe disruption of normal myelination and cortical development upon neonatal brain injury are likely to generate life-persisting sensory ...
Chicha, L., Smith, T., Guzman, R.
openaire +3 more sources
Efferocytosis Mediated Modulation of Injury after Neonatal Brain Hypoxia-Ischemia [PDF]
Cells, 2021 Neonatal brain hypoxia-ischemia (HI) is a leading cause of morbidity and long-term disabilities in children. While we have made significant progress in describing HI mechanisms, the limited therapies currently offered for HI treatment in the clinical setting stress the importance of discovering new targetable pathways.
Mike, Jana Krystofova +1 more
openaire +5 more sources
Cell Death in the Developing Brain after Hypoxia-Ischemia [PDF]
Frontiers in Cellular Neuroscience, 2017 Perinatal insults such as hypoxia-ischemia induces secondary brain injury. In order to develop the next generation of neuroprotective therapies, we urgently need to understand the underlying molecular mechanisms leading to cell death. The cell death mechanisms have been shown to be quite different in the developing brain compared to that in the adult ...
Claire Thornton +6 more
openaire +5 more sources
17β-Estradiol protects the neonatal brain from hypoxia–ischemia [PDF]
Experimental Neurology, 2007 Hypoxia-ischemia is relatively common in human infants. Hypoxia-ischemia can occur as a result of complications associated with prematurity or birth, frequently leading to altered brain development and cognitive and behavioral deficits that persist throughout life. Despite the relative frequency of neonatal hypoxic-ischemic encephalopathy, the immature
Joseph, Nuñez +5 more
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Alterations of CaMKII after hypoxia‐ischemia during brain development [PDF]
Journal of Neurochemistry, 2004 AbstractTransient brain hypoxia‐ischemia (HI) in neonates leads to delayed neuronal death and long‐term neurological deficits. However, the underlying mechanisms are incompletely understood. Calcium‐calmodulin‐dependent protein kinase II (CaMKII) is one of the most abundant protein kinases in neurons and plays crucial roles in synaptic development and ...
Kaixiong, Tang +3 more
openaire +2 more sources