Репозиторий Университета

© 2020 Sports Medicine Australia Objectives: Para athletes with brain impairment are affected by hypertonia, ataxia and athetosis, which adversely affect starting, sprinting and submaximal running. The aim was to identify and synthesise evidence from studies that have compared the biomechanics of runners with brain impairments (RBI) and non-disabled runners (NDR). Design: Systematic review. Methods: Five journal databases were systematically searched from inception to March 2020. Included studies compared the biomechanics of RBI (aged > 14 years) and NDR performing either block-starts, sprinting, or submaximal running. Results: Eight studies were included, analysing a total of 100 RBI (78M:22F; 18–38 years) diagnosed with either cerebral palsy (n = 44) or traumatic brain injury (n = 56). Studies analysed block-starts (n = 3), overground sprinting (n = 3) and submaximal running (n = 2), and submaximal treadmill running (n = 1). Horizontal velocity during starts, sprinting and self-selected submaximal speeds were lower in RBI. During sprinting and submaximal running, compared with NDR, RBI had shorter stride length, step length, and flight time, increased ground-contact time, increased cadence, and reduced ankle and hip range of motion. In submaximal running, RBI had decreased ankle-power generation at toe-off. Conclusions: There is limited research and small sample sizes in this area. However, preliminary evidence suggests that RBI had lower sprint speeds and biomechanical characteristics typical of submaximal running speeds in NDR, including increased ground-contact times and reduced stride length, step length, and flight times. Meaningful interpretation of biomechanical findings in RBI is impeded by impairment variability (type, severity and distribution), and methods which permit valid, reliable impairment stratification in larger samples are required.

© 2020 Sports Medicine Australia Objectives: Para athletes with brain impairment are affected by hypertonia, ataxia and athetosis, which adversely affect starting, sprinting and submaximal running. The aim was to identify and synthesise evidence from studies that have compared the biomechanics of runners with brain impairments (RBI) and non-disabled runners (NDR). Design: Systematic review. Methods: Five journal databases were systematically searched from inception to March 2020. Included studies compared the biomechanics of RBI (aged > 14 years) and NDR performing either block-starts, sprinting, or submaximal running. Results: Eight studies were included, analysing a total of 100 RBI (78M:22F; 18–38 years) diagnosed with either cerebral palsy (n = 44) or traumatic brain injury (n = 56). Studies analysed block-starts (n = 3), overground sprinting (n = 3) and submaximal running (n = 2), and submaximal treadmill running (n = 1). Horizontal velocity during starts, sprinting and self-selected submaximal speeds were lower in RBI. During sprinting and submaximal running, compared with NDR, RBI had shorter stride length, step length, and flight time, increased ground-contact time, increased cadence, and reduced ankle and hip range of motion. In submaximal running, RBI had decreased ankle-power generation at toe-off. Conclusions: There is limited research and small sample sizes in this area. However, preliminary evidence suggests that RBI had lower sprint speeds and biomechanical characteristics typical of submaximal running speeds in NDR, including increased ground-contact times and reduced stride length, step length, and flight times. Meaningful interpretation of biomechanical findings in RBI is impeded by impairment variability (type, severity and distribution), and methods which permit valid, reliable impairment stratification in larger samples are required.

© 2020 Elsevier Inc. Mitochondria are essential for neuronal function because they serve not only to sustain energy and redox homeostasis but also are harbingers of death. A dysregulated mitochondrial network can cascade until function is irreparably lost, dooming cells. TBI is most prevalent in the young and comes at significant personal and societal costs. Traumatic brain injury (TBI) triggers a biphasic and mechanistically heterogenous response and this mechanistic heterogeneity has made the development of standardized treatments challenging. The secondary phase of TBI injury evolves over hours and days after the initial insult, providing a window of opportunity for intervention. However, no FDA approved treatment for neuroprotection after TBI currently exists. With recent advances in detection techniques, there has been increasing recognition of the significance and roles of mitochondrial redox lipid signaling in both acute and chronic central nervous system (CNS) pathologies. Oxidized lipids and their downstream products result from and contribute to TBI pathogenesis. Therapies targeting the mitochondrial lipid composition and redox state show promise in experimental TBI and warrant further exploration. In this review, we provide 1) an overview for mitochondrial redox homeostasis with emphasis on glutathione metabolism, 2) the key mechanisms of TBI mitochondrial injury, 3) the pathways of mitochondria specific phospholipid cardiolipin oxidation, and 4) review the mechanisms of mitochondria quality control in TBI with consideration of the roles lipids play in this process.

© 2020 Elsevier Inc. Mitochondria are essential for neuronal function because they serve not only to sustain energy and redox homeostasis but also are harbingers of death. A dysregulated mitochondrial network can cascade until function is irreparably lost, dooming cells. TBI is most prevalent in the young and comes at significant personal and societal costs. Traumatic brain injury (TBI) triggers a biphasic and mechanistically heterogenous response and this mechanistic heterogeneity has made the development of standardized treatments challenging. The secondary phase of TBI injury evolves over hours and days after the initial insult, providing a window of opportunity for intervention. However, no FDA approved treatment for neuroprotection after TBI currently exists. With recent advances in detection techniques, there has been increasing recognition of the significance and roles of mitochondrial redox lipid signaling in both acute and chronic central nervous system (CNS) pathologies. Oxidized lipids and their downstream products result from and contribute to TBI pathogenesis. Therapies targeting the mitochondrial lipid composition and redox state show promise in experimental TBI and warrant further exploration. In this review, we provide 1) an overview for mitochondrial redox homeostasis with emphasis on glutathione metabolism, 2) the key mechanisms of TBI mitochondrial injury, 3) the pathways of mitochondria specific phospholipid cardiolipin oxidation, and 4) review the mechanisms of mitochondria quality control in TBI with consideration of the roles lipids play in this process.

© 2018, Media Sphera Publishing Group. All rights reserved. Inflammasomes are macromolecular complexes that contain many copies of receptors recognizing molecular patterns of pathogenic agents (PAMP) and damage-associated structures (DAMP), and also include molecules of adapter protein ASC and procaspase- 1. Activation of inflammasomes leads to the formation of active caspase-1 that, in turn, provides the maturation of pro-IL-1β and pro-IL-18 to IL-1β and IL-18. The latter cytokines play an important role in control of neuroinlfammation in the central nervous system contributing to the pathogenesis of a series of neurological, neurodegenerative and mental disorders. The review discusses the involvement of NLRP3 inflammasome and other their types in the development of the traumatic brain injury, ischemic and hemorrhagic stroke, brain tumors, CNS infections, Alzheimer’s and Parkinson’s diseases, epilepsy, amyotrophic lateral sclerosis, depressiver, and consequences of alcohol abuse. The elucidation of molecular mechanisms and signaling pathways controlled by inflammasomes will allow the development of new therapeutic measures for diseases, in which neuroinflammation plays a leading pathogenetic role.