The Long-term influences of Age-At-Injury on Neuroinflammation and neuronal Apoptosis following Traumatic Brain Injury in Pediatric and Adulthood Mice.

Objective: The study aims to investigate the long-term impacts of traumatic brain injury (TBI) on neuroinflammation and neuronal apoptosis in pediatric and adult mice, specifically focusing on how age-at-injury influences these processes.

Methods: Controlled cortical impact (CCI) was used to induce TBI in pediatric (21-25 days old) and adult (8-12 weeks old) C57Bl/6 male mice. Neuroinflammation was evaluated through immunoreactivity for Iba-1 and GFAP, while apoptosis was assessed using markers such as Bax, Bcl- 2, and pro-caspase-3.

Secondary hypoxic ischemia alters neurobehavioral outcomes, neuroinflammation, and oxidative stress in mice exposed to controlled cortical impact.

Objective: Hypoxic ischemia (HI) is a secondary insult that can cause fatal neurologic outcomes after traumatic brain injury (TBI), ranging from mild cognitive deficits to persistent vegetative states. We here aimed to unravel the underlying pathological mechanisms of HI injury in a TBI mouse model.

Methods: Neurobehavior, neuroinflammation, and oxidative stress were assessed in a mouse model of controlled cortical impact (CCI) injury followed by HI.

Relationships between serum levels of lactate dehydrogenase and neurological outcomes of patients who underwent targeted temperature management after out-of-hospital cardiac arrest.

This study aimed to evaluate times for measuring serum lactate dehydrogenase levels (SLLs) to predict neurological prognosis among out-of-hospital cardiac arrest (OHCA) survivors.This retrospective study examined patients who experienced OHCA treated with targeted temperature management (TTM). The SLLs were evaluated at the return of spontaneous circulation (ROSC) and at 24, 48, and 72 hours later.