An old wives' tale, and strongly held dogma, maintains that one should be kept awake after a mild traumatic brain injury (mTBI) to prevent a coma. This, however, conflicts with the known benefits of sleep: repair and restoration. We therefore sought to examine the effects of sleep deprivation (SD) in the post-traumatic sleep period on post-concussion symptomology (PCS). Adolescent male and female rats were administered repetitive mTBIs (RmTBI) or sham injuries and were then assigned to 5 h of SD or left undisturbed. All animals were then tested using seven behavioral tasks validated to examine PCS, followed by analysis of serum cytokines, and quantitative real-time PCR for messenger RNA (mRNA) expression. Exposure to 3 SD epochs significantly impaired behavior in 4 of 7 of the measures, while RmTBI also produced dysfunction in 5 of 7 tests, but the effects of SD and RmTBI were not cumulative. SD induced long-lasting changes in serum levels of Tnf-α, IL6, and IL-1ß. mRNA expression in the pre-frontal cortex, hippocampus, hypothalamus, and anterior cingulate cortex was modified in response to SD and RmTBI; but similar to the behavioral measures, the mRNA changes were not cumulative. Consequently, we report that SD often produced impairments similar or worse than RmTBI, and sleep hygiene should become a priority for adolescent health.
Children and adolescents have the highest rates of traumatic brain injury (TBI), with mild TBI (mTBI) accounting for most of these injuries. This demographic also often suffers from post-injury symptomologies that may persist for months. Telomere length (TL) has previously been used as a marker for outcomes following repetitive mild TBI (RmTBI) and it may be possible that telomere elongation can reduce post-traumatic behavioral impairments. Telomerase activator-65 (TA-65) is a telomerase small-molecule activator purified from the root of Chinese herbs that has been anecdotally reported to have anti-aging and life-extending potential. We hypothesized that RmTBI would shorten TL but administration of TA-65 would reverse RmTBI-induced telomere shortening and behavioral deficits. Male and female Sprague-Dawley rats were orally administered TA-65 or a placebo substance for 30 consecutive days [postnatal day (P) 25-55]. Following the injury protocol (mTBIs on P33, 36, and 40), rats went through a behavioral test battery designed to examine symptomologies commonly associated with mTBI (balance and motor coordination, exploratory behavior, short-term working memory, and anxiety-and depressive-like behaviors). TL in ear and brain tissue (prefrontal cortex and hippocampus) and relative expression of TERT and Tep1 via qPCR were assessed 15 days following the last injury. We observed a heterogenous response between males and females, with TA65 administration resulting in increased mRNA expression of TERT and Tep1 in female rats that experienced RmTBI, which was accompanied by some functional recovery on motor behavior and footslips in the beam walk task and depressive-like behavior in the forced swim task.
Reduced order modeling has gained considerable attention in recent decades owing to the advantages offered in reduced computational times and multiple solutions for parametric problems. The focus of this manuscript is the application of model order reduction techniques in various engineering and scientific applications including but not limited to mechanical, naval and aeronautical engineering. The focus here is kept limited to computational fluid mechanics and related applications. The advances in the reduced order modeling with proper orthogonal decomposition and reduced basis method are presented as well as a brief discussion of dynamic mode decomposition and also some present advances in the parameter space reduction. Here, an overview of the challenges faced and possible solutions are presented with examples from various problems.
Repetitive mild traumatic brain injuries (RmTBIs) are increasingly recognized to have long-term neurological sequelae in a significant proportion of patients. Individuals that have had RmTBIs exhibit a variety of sensory, cognitive, or behavioral consequences that can negatively impact quality of life. Brain tissue oxygen levels (pO2) are normally maintained through exquisite regulation of blood supply to stay within the normoxic zone (18 to 30 mmHg in the rat hippocampus). However, during neurological events in which brain tissue oxygen levels leave the normoxic zone, neuronal dysfunction, and behavioral deficits have been observed, and are frequently related to poorer prognoses. The oxygenation response in the brain after RmTBIs/repeated concussions has been poorly characterized, with most preliminary research limited to the neocortex. Furthermore, the mechanisms by which RmTBIs impact changes to brain oxygenation and vice versa remains to be determined. In the current study we demonstrate that upon receiving RmTBIs, rats exhibit post-traumatic, electrographic seizures in the hippocampus, without behavioral (clinical) seizures, that are accompanied by a long-lasting period of hyperoxygenation. These electrographic seizures and the ensuing hyperoxic episodes are associated with deficits in working memory and motor coordination that were reversible through attenuation of the post-traumatic and postictal (post-seizure) hyperoxia, via administration of a vasoconstricting agent, the calcium channel agonist Bay K8644. We propose that the post-traumatic period characterized by brain oxygenation levels well above the normoxic zone, may be the basis for some of the common symptoms associated with RmTBIs.
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