Results 21 to 30 of about 93,068 (305)
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.
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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
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Effects of hypoxia‐ischemia on monoamine metabolism in the immature brain [PDF]
Annals of Neurology, 1984 AbstractWe measured acute changes in monoamine metabolites in corpus striatum of immature rat pups exposed to hypoxiaischemia, hypoxia alone, or total global ischemia. Carotid ligations and two hours of 8% oxygen environment in 7‐day‐old pups led to asymmetrical turning behavior, a 70% decrease in endogenous striatal dopamine levels, and a 125 ...
Silverstein, Faye Sarah +1 more
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Establishment and identification of a hypoxia-ischemia brain damage model in neonatal rats. [PDF]
Biomed Rep, 2016 The present study was designed to set up a reliable model of severe hypoxia-ischemia brain damage (HIBD) in neonatal rats and several methods were used to identify whether the model was successful. A total of 40 healthy 7-day-old Sprague-Dawley rats were randomly divided into 2 groups: The sham-surgery group (n=18) and the HIBD model group (n=22).
Yao D +5 more
europepmc +4 more sources
Autophagy in hypoxia-ischemia induced brain injury: Evidences and speculations [PDF]
Autophagy, 2009 The interaction among autophagy, apoptosis and necrosis is complex and still a matter of debate. We have recently studied this interaction after neonatal hypoxia-ischemia (HI) in rats. We found that autophagic and apoptotic pathways were significantly increased at short times after HI in neuronal cells. 3-Methyladenine (3-MA) and wortmannin (WM), which
BALDUINI, WALTER +2 more
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A depletable pool of adenosine in area CA1 of the rat hippocampus [PDF]
, 2001 Adenosine plays a major modulatory and neuroprotective role in the mammalian CNS. During cerebral metabolic stress, such as hypoxia or ischemia, the increase in extracellular adenosine inhibits excitatory synaptic transmission onto vulnerable neurons via
Darren Caldwell +9 more
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Roles of nitric oxide in brain hypoxia-ischemia
Biochimica et Biophysica Acta (BBA) - Bioenergetics, 1999 A large body of evidence has appeared over the last 6 years suggesting that nitric oxide biosynthesis is a key factor in the pathophysiological response of the brain to hypoxia-ischemia. Whilst studies on the influence of nitric oxide in this phenomenon initially offered conflicting conclusions, the use of better biochemical tools, such as selective ...
Bolaños, Juan P, Almeida, Angeles
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A population of immature cerebellar parallel fibre synapses are insensitive to adenosine but are inhibited by hypoxia [PDF]
, 2011 The purine adenosine plays an important role in a number of physiological and pathological processes and is neuroprotective during hypoxia and ischemia.
Mark J. Wall +3 more
core +1 more source
The spectrum of Ischemia-induced white matter injury varies with age [PDF]
, 2013 Stroke is a neurological condition that targets the whole range of the human population, from the pre-term infant to the elderly and is a major cause of death worldwide (Ingall 2004).
Zammit, Christian +2 more
core +1 more source
Journal of Pharmacological Sciences, 2021 The blood–brain barrier (BBB) is mainly formed by brain capillary endothelial cells (BCECs) and is exposed to hypoxic environments under pathological conditions. The effects of hypoxia on the expression and activity of Ca2+-activated Cl− (ClCa) channels,
Takahisa Suzuki +4 more
doaj +1 more source