Neonatal Hypoxia Ischemia and Individual Differences in Neurodevelopmental Outcomes

Miguel, Patrícia Maidana; Silveira, Patrícia Pelufo

doi:10.1001/jamapediatrics.2020.0537

Cited by 2 publications

(3 citation statements)

References 7 publications

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“…Hypoxic stress is involved in not only physiological processes but also pathophysiological conditions such as ischemic stroke, cardiac ischemia, neonatal hypoxic-ischemic (H/I) encephalopathy, and cancer ( Hajizadeh et al, 2019 ; Chen et al, 2020 ; Miguel and Silveira, 2020 ; Severino et al, 2020 ). Normal neuron function is highly dependent on sufficient oxygen supply.…”

Section: Introductionmentioning

confidence: 99%

Deficiency in Neuroserpin Exacerbates CoCl2 Induced Hypoxic Injury in the Zebrafish Model by Increased Oxidative Stress

et al. 2021

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Protective strategy against hypoxic-ischemic (H/I) induced injury has been intensively discussed. Neuroserpin, an inhibitor for tissue plasminogen activator (tPA), has been proved a vital neuroprotective agent in cerebral ischemia mouse model and oxygen-glucose deprivation and reoxygenation (OGD/R) cell model. Neuroserpin is a promising therapeutic hint for neonatal hypoxic-ischemia injury. Here, we established a neuroserpin deficient zebrafish to study its role in CoCl2 chemically induced hypoxic injury. CoCl2 exposure was beginning at the embryonic stage. Development defects, neuronal loss, and vascular malformation was assessed by imaging microscopy. Neuroserpin deficient zebrafish showed more development defects, neuronal loss and vascular malformation compared to wide-type. Apoptosis and oxidative stress were evaluated to further identify the possible mechanisms. These findings indicate that neuroserpin could protective against CoCl2 induced hypoxic injury by alleviating oxidative stress.

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Section: Introductionmentioning

confidence: 99%

Deficiency in Neuroserpin Exacerbates CoCl2 Induced Hypoxic Injury in the Zebrafish Model by Increased Oxidative Stress

et al. 2021

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“…This results in a cognitive decline in the inhabitants of high-altitude areas, especially those who rapidly enter high altitudes. Indeed, cognitive decline correlates with altitude, duration, and task complexity (Miguel and Silveira, 2020;Cai et al, 2021). In the past, high-altitude health protection programs predominantly included health education, nocturnal oxygenation, adjustment of dietary composition, and advancement of work and rest times (Srivastava and Kumar, 1992;Wing-Gaia, 2014;Tan et al, 2021).…”

Section: Introductionmentioning

confidence: 99%

“…However, economic and technological developments, especially high-speed iteration of electronic equipment, have increased the complexity of work at high altitudes. This has led to a greater mental load in high-altitude workers, and traditional protection methods have had minimal effects on these types of work requiring a high cognitive load (Miguel and Silveira, 2020;Perosa et al, 2020;Wakhloo et al, 2020;Pang and Kim, 2021). Therefore, effective protection of cognitive function in high-altitude environments and improvements in mental work ability at high altitudes are urgent problems to be resolved.…”

Section: Introductionmentioning

confidence: 99%

Modulation of thalamic network connectivity using transcranial direct current stimulation based on resting-state functional magnetic resonance imaging to improve hypoxia-induced cognitive impairments

et al. 2022

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Hypoxic conditions at high altitudes severely affect cognitive functions such as vigilance, attention, and memory and reduce cognitive ability. Hence, there is a critical need to investigate methods and associated mechanisms for improving the cognitive ability of workers at high altitudes. This study aimed to use transcranial direct current stimulation (tDCS) to modulate thalamic network functional connectivity to enhance cognitive ability. We recruited 20 healthy participants that underwent hypoxia exposure in a hypoxic chamber at atmospheric pressure to simulate a hypoxic environment at 4,000 m. Participants received both sham and real stimulation. tDCS significantly improved the participants’ emotional status, including depression, fatigue, and energy level. These effects were sustained for more than 6 h (P < 0.05 at the second to fifth measurements). In addition, tDCS enhanced vigilance, but this was only effective within 2 h (P < 0.05 at the second and third measurements). Central fatigue was significantly ameliorated, and cerebral blood oxygen saturation was increased within 4 h (P < 0.05 at the second, third, and fourth measurements). Furthermore, functional connectivity results using the thalamus as a seed revealed enhanced connectivity between the thalamus and hippocampus, cingulate gyrus, and amygdala after tDCS. These results indicated that tDCS increased local cerebral blood oxygen saturation and enhanced thalamic network connectivity in a hypoxic environment, thereby improving vigilance, depression, fatigue, and energy levels. These findings suggest that tDCS may partially rescue the cognitive decline caused by hypoxia within a short period. This approach affords a safe and effective cognitive enhancement method for all types of high-altitude workers with a large mental load.

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Neonatal Hypoxia Ischemia and Individual Differences in Neurodevelopmental Outcomes

Cited by 2 publications

References 7 publications

Deficiency in Neuroserpin Exacerbates CoCl2 Induced Hypoxic Injury in the Zebrafish Model by Increased Oxidative Stress

Deficiency in Neuroserpin Exacerbates CoCl2 Induced Hypoxic Injury in the Zebrafish Model by Increased Oxidative Stress

Modulation of thalamic network connectivity using transcranial direct current stimulation based on resting-state functional magnetic resonance imaging to improve hypoxia-induced cognitive impairments

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