Advances in diagnosis, treatments, and molecular mechanistic studies of traumatic brain injury

Lu, Chunyu; Xia, Jufeng; Wang, Bin; Wu, Yitian; Liu, Xiaohui; Zhang, Yong

doi:10.5582/bst.2015.01066

Cited by 7 publications

(5 citation statements)

References 108 publications

(93 reference statements)

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“…Despite recent advances in the management of trauma patients with multiple injuries [1], traumatic brain injury (TBI) remains a leading cause of morbidity and mortality in young people [2]. A patient’s neurological status after TBI is greatly dependent on numerous factors, including severity of injury (mild, moderate, or severe), mechanism (blunt or penetrating injury), and other patient factors [3].…”

Section: Introductionmentioning

confidence: 99%

Pharmacologic Neuroprotection for Functional Outcomes After Traumatic Brain Injury: A Systematic Review of the Clinical Literature

et al. 2016

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Introduction Traumatic brain injury (TBI) is a major cause of death and disability worldwide. The deleterious effects of secondary brain injury may be attenuated by early pharmacological therapy in the emergency room and intensive care unit (ICU). Current medical management of acute TBI is primarily supportive, aimed at reducing intracranial pressure (ICP) and optimizing cerebral perfusion. There are no pharmacological therapies to date that have been unequivocally demonstrated to improve neurological outcomes after TBI. Objectives The purpose of this systematic review was to evaluate the recent clinical studies from January 2013 through November 2015 that investigated neuroprotective functional outcomes of pharmacological agents after TBI. Methods The following databases were searched for relevant studies: MEDLINE (OvidSP January Week 1, 2013–November Week 2 2015), Embase (OvidSP 2013 January 1–2015 November 24), and the unindexed material in PubMed (National Library of Medicine/National Institutes of Health [NLM/NIH]). This systematic review included only full-length clinical studies and case series that included at least five patients and were published in the English language. Only studies that examined functional clinical outcomes were included. Results Twenty-five of 527 studies met our inclusion criteria, which investigated 15 independent pharmacological therapies. Eight of these therapies demonstrated possible neuroprotective properties and improved functional outcomes, of which five were investigated with randomized clinical trials: statins, N-acetyl cysteine (NAC), Enzogenol, Cerebrolysin, and nitric oxide synthase inhibitor (VAS203). Three pharmacological agents did not demonstrate neuroprotective effects, and four agents had mixed results. Conclusions While there is currently no single pharmacological therapy that will unequivocally improve clinical outcomes after TBI, several agents have demonstrated promising clinical benefits for specific TBI patients and should be investigated further.

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Section: Introductionmentioning

confidence: 99%

Pharmacologic Neuroprotection for Functional Outcomes After Traumatic Brain Injury: A Systematic Review of the Clinical Literature

et al. 2016

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“…Patient’s neurological status after TBI is greatly dependent on numerous factors, including severity of injury (mild, moderate or severe), mechanism (blunt or penetrating injury) and other patient factors ( 6 ). Glasgow Outcome Scale (GOS) is the mostly used to measure outcome after TBI.…”

Section: Introductionmentioning

confidence: 99%

Analysis on Short-Term Outcomes for Cerebral Protection Treatment in Post Severe Traumatic Brain Injury Patients: A Single Neurosurgical Centre Study

Muhammad Mustafa,

Ab Mukmin,

Mazlan

et al. 2024

MJMS

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Background: Severe traumatic brain injury (TBI) is a leading cause of disability worldwide and cerebral protection (CP) management might determine the outcome of the patient. CP in severe TBI is to protect the brain from further insults, optimise cerebral metabolism and prevent secondary brain injury. This study aimed to analyse the short-term Glasgow Outcome Scale (GOS) at the intensive care unit (ICU) discharge and a month after ICU discharge of patients post CP and factors associated with the favourable outcome. Methods: This is a prospective cohort study from January 2021 to January 2022. The short-term outcomes of patients were evaluated upon ICU discharge and 1 month after ICU discharge using GOS. Favourable outcome was defined as GOS 4 and 5. Generalised Estimation Equation (GEE) was adopted to conduct bivariate GEE and subsequently multivariate GEE to evaluate the factors associated with favourable outcome at ICU discharge and 1 month after discharge. Results: A total of 92 patients with severe TBI with GOS of 8 and below admitted to ICU received CP management. Proportion of death is 17% at ICU discharge and 0% after 1 month of ICU discharge. Proportion of favourable outcome is 26.1% at ICU discharge and 61.1% after 1 month of ICU discharge. Among factors evaluated, age (odds ratio [OR] = 0.96; 95% CI: 0.94, 0.99; P = 0.004), duration of CP (OR = 0.41; 95% CI: 0.20, 0.84; P = 0.014) and hyperosmolar therapy (OR = 0.41; CI 95%: 0.21, 0.83; P = 0.013) had significant association. Conclusion: CP in younger age, longer duration of CP and patient not receiving hyperosmolar therapy are associated with favourable outcomes. We recommend further clinical trial to assess long term outcome of CP.

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“…Traumatic brain injury (TBI) results from an impact to the head that disrupts normal brain function. Severe TBI can cause permanent brain damage or death [1]. Diffuse axonal injury (DAI) is a typical pathological change after TBI and is closely associated with clinical prognosis [2].…”

Section: Introductionmentioning

confidence: 99%

“…Severe TBI can cause permanent brain damage or death [1]. Diffuse axonal injury (DAI) is a typical pathological change after TBI and is closely associated with clinical prognosis [2].…”

Section: Introductionmentioning

confidence: 99%

Mechanisms Underlying H2O2-Evoked Carbonyl Modification of Cytoskeletal Protein and Axon Injury in PC-12 Cells

Zhang

Li²,

Zhang

et al. 2018

Cell Physiol Biochem

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Background/Aims: To investigate the mechanism that enables oxidative stress and cytoskeleton protein carbonylation to contribute to axonal dysfunction in traumatic brain injury (TBI). Methods: We created an in vitro model of neuronal oxidative damage by exposing a neuron-like cell line (PC-12) to different concentrations (100 μM, 200 μM, and 300 μM) of H₂O₂ for 24 h or 48 h. Carbonyl modification of cytoskeletal proteins (β-actin and β-tubulin) and its impact on β-actin/β-tubulin filament dynamics were determined by enzyme-linked immunosorbent assay, immunostaining, and western blotting. Depolymerization of β-actin/β-tubulin filaments was evaluated using the monomer/polymer ratio of each protein via western blotting. Phosphorylation of the neurofilament heavy chain (P-NFH) was used as an axonal injury marker and detected by immunostaining. Results: Our results showed that H₂O₂ treatment led to increased oxidative stress in PC-12 cells, as indicated by the increased generation of malondialdehyde and 8-hydroxydeoxyguanosine and decreased intracellular glutathione levels. H₂O₂ treatment also increased carbonyl modification of total proteins and cytoskeleton proteins β-actin/β-tubulin, which occurred concurrently with the suppression of proteasome activity. Moreover, H₂O₂ treatment increased the generation of the axonal injury marker P-NFH, and depolymerization of the β-actin/β-tubulin filaments was indicated by increased monomer/polymer ratios of each protein. Lastly, overexpression of the proteasome β5 subunit in PC-12 cells significantly reduced the H₂O₂-induced accumulation of carbonylated β-actin/ β-tubulin, P-NFH, and β-actin/β-tubulin depolymerization. Conclusions: We concluded that carbonylation of cytoskeleton proteins could lead to depolymerization of their filaments and axonal injury, and proteasome suppression contributes to the accumulation of carbonylated proteins under oxidative conditions.

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Advances in diagnosis, treatments, and molecular mechanistic studies of traumatic brain injury

Cited by 7 publications

References 108 publications

Pharmacologic Neuroprotection for Functional Outcomes After Traumatic Brain Injury: A Systematic Review of the Clinical Literature

Pharmacologic Neuroprotection for Functional Outcomes After Traumatic Brain Injury: A Systematic Review of the Clinical Literature

Analysis on Short-Term Outcomes for Cerebral Protection Treatment in Post Severe Traumatic Brain Injury Patients: A Single Neurosurgical Centre Study

Mechanisms Underlying H2O2-Evoked Carbonyl Modification of Cytoskeletal Protein and Axon Injury in PC-12 Cells

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