scholarly journals Minor neurological dysfunction and associations with motor function, general cognitive abilities, and behaviour in children born extremely preterm

2018 ◽  
Vol 60 (8) ◽  
pp. 826-832 ◽  
Author(s):  
Lina Broström ◽  
Brigitte Vollmer ◽  
Jenny Bolk ◽  
Eva Eklöf ◽  
Ulrika Ådén
2000 ◽  
Vol 42 (8) ◽  
pp. 508-514 ◽  
Author(s):  
Béatrice Larroque ◽  
Monique Kaminski ◽  
Phillipe Dehaene ◽  
Damien Subtil ◽  
Denis Querleu

2011 ◽  
Vol 53 (7) ◽  
pp. 641-646 ◽  
Author(s):  
MARIANNE DE JONG ◽  
MARJA PUNT ◽  
ERIK DE GROOT ◽  
RUUD B MINDERAA ◽  
MIJNA HADDERS-ALGRA

2010 ◽  
Vol 52 (12) ◽  
pp. 1127-1132 ◽  
Author(s):  
MARJA PUNT ◽  
MARIANNE DE JONG ◽  
ERIK DE GROOT ◽  
MIJNA HADDERS-ALGRA

2017 ◽  
Vol 38 (10) ◽  
pp. 1818-1827 ◽  
Author(s):  
Raghavendar Chandran ◽  
TaeHee Kim ◽  
Suresh L Mehta ◽  
Eshwar Udho ◽  
Vishal Chanana ◽  
...  

Uncontrolled oxidative stress contributes to the secondary neuronal death that promotes long-term neurological dysfunction following traumatic brain injury (TBI). Surprisingly, both NADPH oxidase 2 (NOX2) that increases and transcription factor Nrf2 that decreases reactive oxygen species (ROS) are induced after TBI. As the post-injury functional outcome depends on the balance of these opposing molecular pathways, we evaluated the effect of TBI on the motor and cognitive deficits and cortical contusion volume in NOX2 and Nrf2 knockout mice. Genetic deletion of NOX2 improved, while Nrf2 worsened the post-TBI motor function recovery and lesion volume indicating that decreasing ROS levels might be beneficial after TBI. Treatment with either apocynin (NOX2 inhibitor) or TBHQ (Nrf2 activator) alone significantly improved the motor function after TBI, but had no effect on the lesion volume, compared to vehicle control. Whereas, the combo therapy (apocynin + TBHQ) given at either 5 min/24 h or 2 h/24 h improved motor and cognitive function and decreased cortical contusion volume compared to vehicle group. Thus, both the generation and disposal of ROS are important modulators of oxidative stress, and a combo therapy that prevents ROS formation and potentiates ROS disposal concurrently is efficacious after TBI.


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