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Traumatic Brain Injury - DOAJ

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Last Updated: 18 May 2022

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Nutritional Support for Pediatric Severe Traumatic Brain Injury

Diete can aid in optimal recovery in critically ill children with significant traumatic brain injury. Children with sTBI experience a variety of physiological disorders in the acute post-injury period that can influence metabolic demand, resulting in nutritional requirements that may differ from those of other critically ill patients. Currently, there are relatively few studies investigating nutrition habits in PICU patients, and even fewer that focus on pediatric sTBI patients. According to available studies, modern neurocritical care practices can significantly reduce the predicted hypermetabolic state after sTBI, and that early enteral nutrition may be correlated with reduced morbidity and mortality. To improve outcomes, the Brain Trauma Foundation's most recent pediatric sTBI recommendations recommends the introduction of enteral nutrition within 72 hours.

Source link: https://doi.org/10.3389/fped.2022.904654


In situ forming and biocompatible hyaluronic acid hydrogel with reactive oxygen species-scavenging activity to improve traumatic brain injury repair by suppressing oxidative stress and neuroinflammation

The severity of neural repair and regeneration programs for traumatic brain injury rehabilitation are greatly limited by the harsh brain lesion microenvironment, including oxidative stress and hyper-inflammatory response. By dual-enzymatically crosslinking technology, antioxidant gallic acid-grafted hyaluronic acid was mixed with hyaluronic acid-tyramine polymer to produce an injectable hydrogel. The resulting HT/HGA hydrogel is biocompatible and has potent scavenging capability against DPPH and hydroxyl radicals. Under H2O2 insult, this hydrogel enhanced cell viability and reduced intracellular reactive oxygen species production under H2O2 insult. In-vivo injection of HT/HGA hydrogel significantly reduced malondialdehyde production and increased glutathione expression in lesion area after inflammatory Nrf2/HO-1 pathway activation. In addition, this hydrogel enhanced the inflammatory factor expression of IL-4, which aided in the microglia polarization to M2 phenotype.

Source link: https://doi.org/10.1016/j.mtbio.2022.100278


Brain age in chronic traumatic brain injury

Traumatic brain injury is attributed to a rise in the 'brain age' that may be triggered by atrophy in grey and white matter. We investigated whether "brain age" increases with years post injury and whether it is associated with injury severity, cognition, and functional outcome. TBI participants were predicted to have higher "brain age" than healthy controls. Greater brain age was associated with increased injury risk, according to post traumatic amnesia duration and Glasgow Coma Scale. A longitudinal study is required to see if TBI leads to a ‘one-off' decrease in brain age' or brain aging over time.

Source link: https://doi.org/10.1016/j.nicl.2022.103039


Postconcussion Syndrome / Disorder or Mild Traumatic Brain Injury: diagnostic issues and treatment

Traumatic brain injury at the younger end of the spectrum is more widespread than the moderate-severe spectrum. About 80% of traumatic brain injury cases involve Mild trauma [1]. Research into outcomes following traumatic brain injury at the younger end of the spectrum, the reliability of postconcussion syndrome/disorder, and treatment of signs associated with milder traumatic brain injuries are among the ongoing studies.

Source link: https://doi.org/10.47795/GAZR5504


circHtra1/miR-3960/GRB10 Axis Promotes Neuronal Loss and Immune Deficiency in Traumatic Brain Injury

Circular RNAs are abundant in the brain and contribute to central nervous system disorders, but the precise roles of circRNAs in human traumatic brain injury have yet to be established. Further tests revealed that circHtra1 behaves as a miR-3960 sponge and raises the expression of GRB10, which is involved in NK cell infiltration after TBI. circHtra1 has been reduced after brain insults were regulated circHtra1. Our findings reveal that circHtra1 contributes neuronal damage by sponging miR-3960 and banning GRB10 and apoptosis during brain insults.

Source link: https://doi.org/10.1155/2022/3522492


Management of paediatric traumatic brain injury in Sweden: a national cross-sectional survey

Abstract Background: In older studies, variations in management strategies for children with traumatic brain injury in Sweden have been discovered. This paper, therefore, seeks to outline existing paediatric TBI management techniques on a hospital/organizational level in Sweden. Respondents were found for all Swedish hospitals with an emergency department's child care system, who were notified via phone/mail before the survey was released. TBI of all ages and 66 responded 71 of the 76 identified hospitals treated patients with TBI of all ages and 66 responded. Nearly all hospitals have the ability to admit and observe children with TBI of various degrees, and virtually all centers have full access to neuroradiology. When it came to smaller hospitals, it was more common for nurses to discharge patients without doctor assessment when compared to smaller hospitals. Conclusions TBI management practices for children in Sweden also vary, with some of these differences persisting over time.

Source link: https://doi.org/10.1186/s13049-022-01022-4


A Calixarene Assembly Strategy of Combined Anti-Neuroinflammation and Drug Delivery Functions for Traumatic Brain Injury Therapy

Excessive inflammation response promotes brain injury and delays brain repair in nervous system disorders, which can lead to brain injury and delays the recovery of neural function in nervous system disorders. In vitro and in vivo, we reviewed a number of calixarenes and found that among them, the self-assembling architecture of amphiphilic sulfonatocalix[8] arene's auto-assembling architecture had the most potent ability to reduce neuroinflammation. In addition, after applying the SC8A12C assemblies to the exposed brain tissue, we found that SC8A12C assemblies penetrated into the brain parenchyma and reduced the inflammatory factor storm, effectively ending neurobiological functions in a mouse model of traumatic brain injury.

Source link: https://doi.org/10.3390/molecules27092967


Nano-PSO Administration Attenuates Cognitive and Neuronal Deficits Resulting from Traumatic Brain Injury

Traumatic Brain Injury (TBI) is one of the most common causes of neurological impairment in young populations. In mice models of AD and genetic Creutzfeldt Jacob disease, a Nano formulation of Pomegranate seed oil [Nano-PSO] has been shown to first target the brain and then reduce memory loss and neuronal death in mice models of AD and genetic Creutzfeldt Jacob disease. Cognitive and behavioral decline are prevented by Nano-PSO delivery to mice before or after TBI application. SIRT1 and SYP protein postinjury were both elevated as a result of high amounts of Nano-PSO and SYP protein postinjury.

Source link: https://doi.org/10.3390/molecules27092725


Use of Hyperoncotic Human Albumin Solution in Severe Traumatic Brain Injury Revisited—A Narrative Review and Meta-Analysis

Patients with a serious traumatic brain injury suffer hypoalbuminemia and necessitate fluid resuscitation. Low serum albumin levels are corrected and aids in preventing euvolemia in non-brain-injured intensive care units and in perioperative patients. The infusion of hypooncotic HAS in patients with TBI has been correlated with adverse outcomes. The side effects of 4% HAS and the safety and effectiveness of hyperoncotic HAS used in the Lund model of TBI therapy require further investigation. 24 patients with hyperoncotic HAS were treated by the Lund method, out of 155 control patients compared to 59 out of 165 patients treated with the Lund scheme. Evidence pointing to a high risk of bias in patients with TBI shows that fluid control with hyperoncotic HAS may have a high risk of bias. TBI patients with TBI have randomized controlled trials, which may lead to changes in clinical practice guidelines for fluid management in patients with TBI.

Source link: https://doi.org/10.3390/jcm11092662


Abnormal Dorsal Caudate Activation Mediated Impaired Cognitive Flexibility in Mild Traumatic Brain Injury

Background: Mild traumatic brain injury is a significant yet less well known public health issue. Few studies have investigated neural causes of cognitive flexibility in mTBI patients using objective methods such as the psychological experiment paradigm. In addition, we performed mediation studies to determine the indirect effect of abnormal dorsal caudate activation on the relationship between information processing speed and cognitive flexibility in mTBI. mTBI patients had a longer reaction time in the task switching process than HCs, showing decreased cognitive flexibility. The reduced dCau activation had a significant effect on the relationship between information processing speed and cognitive flexibility in mTBI, according to Mediation's report. Conclusions: Normal dorsal caudate stimulation in mTBI mediates reduced cognitive flexibility, which suggests that dorsal caudate can play a crucial role in mTBI patients' cognitive flexibility.

Source link: https://doi.org/10.3390/jcm11092484

* Please keep in mind that all text is summarized by machine, we do not bear any responsibility, and you should always check original source before taking any actions

* Please keep in mind that all text is summarized by machine, we do not bear any responsibility, and you should always check original source before taking any actions