Prenatal electronic cigarette exposure decreases brain glucose utilization and worsens outcome in offspring hypoxic–ischemic brain injury

2020 ◽  
Vol 153 (1) ◽  
pp. 63-79 ◽  
Author(s):  
Ali E. Sifat ◽  
Saeideh Nozohouri ◽  
Heidi Villalba ◽  
Abdullah Al Shoyaib ◽  
Bhuvaneshwar Vaidya ◽  
...  
Keyword(s):  
Brain Injury ◽  
Glucose Utilization ◽  
Electronic Cigarette ◽  
Ischemic Brain Injury ◽  
Ischemic Brain ◽  
Brain Glucose ◽  
Hypoxic Ischemic Brain Injury ◽  
Brain Glucose Utilization

scholarly journals Maternal Electronic Cigarette Use Can Enhance Offspring Susceptibility to Hypoxic‐Ischemic Brain Injury

2019 ◽  
Vol 33 (S1) ◽  
Author(s):  
Ali Ehsan Sifat ◽  
Saeideh Nozohouri ◽  
Heidi Villalba ◽  
Bhuvaneshwar Vaidya ◽  
Thomas Abbruscato
Keyword(s):  
Brain Injury ◽  
Electronic Cigarette ◽  
Ischemic Brain Injury ◽  
Cigarette Use ◽  
Ischemic Brain ◽  
Hypoxic Ischemic Brain Injury

Postnatal hypoxic-ischemic brain injury alters mechanisms mediating neuronal glucose transport

2004 ◽  
Vol 286 (2) ◽  
pp. R273-R282 ◽  
Author(s):  
Ann Zovein ◽  
Judy Flowers-Ziegler ◽  
Shanthie Thamotharan ◽  
Don Shin ◽  
Raman Sankar ◽  
...  
Keyword(s):  
Brain Injury ◽  
Glucose Uptake ◽  
Glucose Transporter ◽  
Synapsin I ◽  
Ischemic Brain Injury ◽  
Ischemic Brain ◽  
Brain Glucose ◽  
Modest Increase ◽  
Hypoxic Ischemia ◽  
Hypoxic Ischemic Brain Injury

We examined the effect of hypoxic ischemia and hypoxia vs. normoxia on postnatal murine brain substrate transporter concentrations and function. We detected a transient increase in the neuronal brain glucose transporter isoform (GLUT-3) in response to hypoxic ischemia after 4 h of reoxygenation. This increase was associated with no change in GLUT-1 (blood-brain barrier/glial isoform), monocarboxylate transporter isoforms 1 and 2, synapsin I (neuronal marker), or Bax (proapoptotic protein) but with a modest increase in Bcl-2 (antiapoptotic mitochondrial protein) protein concentrations. At 24 h of reoxygenation, the increase in GLUT-3 disappeared but was associated with a decline in Bcl-2 protein concentrations and the Bcl2:Bax ratio, an increase in caspase-3 enzyme activity (apoptotic effector enzyme), and extensive DNA fragmentation, which persisted later in time (48 h) only in the hippocampus. Hypoxia alone in the absence of ischemia was associated with a transient but modest increase in GLUT-3 and synapsin I protein concentrations, which did not cause significant apoptosis and/or necrosis. Assessment of glucose transporter function by 2-deoxyglucose (2-DG) uptake using two distinct techniques, namely positron emission tomography (PET) and the modified Sokoloff method, revealed a discrepancy due to glucose uptake by extracranial Harderian glands that masked the accurate detection of intracranial brain glucose uptake by PET scanning. The modified Sokoloff method assessing 2-DG uptake revealed that the transient increase in GLUT-3 was critical in protecting against a decline in brain glucose uptake. We conclude that hypoxic-ischemic brain injury is associated with transient compensatory changes targeted at protecting glucose delivery to fuel cellular energy metabolism, which then may delay the processes of apoptosis and cell necrosis.

Trace Fear Conditioning Detects Hypoxic-Ischemic Brain Injury in Neonatal Mice

2011 ◽  
Vol 33 (3-4) ◽  
pp. 222-230 ◽  
Author(s):  
Katarina Järlestedt ◽  
Alison L. Atkins ◽  
Henrik Hagberg ◽  
Marcela Pekna ◽  
Carina Mallard
Keyword(s):  
Brain Injury ◽  
Fear Conditioning ◽  
Ischemic Brain Injury ◽  
Ischemic Brain ◽  
Neonatal Mice ◽  
Trace Fear Conditioning ◽  
Hypoxic Ischemic Brain Injury ◽  
Trace Fear

Minocycline: A neuroprotective agent for hypoxic-ischemic brain injury in the neonate?

2009 ◽  
Vol 87 (3) ◽  
pp. 599-608 ◽  
Author(s):  
Kathryn M. Buller ◽  
Michelle L. Carty ◽  
Hanna E. Reinebrant ◽  
Julie A. Wixey
Keyword(s):  
Brain Injury ◽  
Ischemic Brain Injury ◽  
Ischemic Brain ◽  
Neuroprotective Agent ◽  
Hypoxic Ischemic Brain Injury

Focal protein synthesis inhibition in a model of neonatal hypoxic-ischemic brain injury

1987 ◽  
Vol 95 (2) ◽  
pp. 277-289 ◽  
Author(s):  
Barney E. Dwyer ◽  
Robert N. Nishimura ◽  
Clydette L. Powell ◽  
Susan L. Mailheau
Keyword(s):  
Protein Synthesis ◽  
Brain Injury ◽  
Ischemic Brain Injury ◽  
Protein Synthesis Inhibition ◽  
Ischemic Brain ◽  
Synthesis Inhibition ◽  
Hypoxic Ischemic Brain Injury
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