Relevant bibliographies by topics / Oxidative Stress Acute brain injuries

Academic literature on the topic 'Oxidative Stress Acute brain injuries'

Author: Grafiati
Published: 10 December 2022
Last updated: 28 January 2023

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Journal articles on the topic "Oxidative Stress Acute brain injuries"

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Guo, Hanmu, Lexin Zheng, Heng Xu, Qiuyu Pang, Zhiyang Ren, Yuan Gao, and Tao Wang. "Neurobiological Links between Stress, Brain Injury, and Disease." Oxidative Medicine and Cellular Longevity 2022 (May 25, 2022): 1–17. http://dx.doi.org/10.1155/2022/8111022.

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Stress, which refers to a combination of physiological, neuroendocrine, behavioral, and emotional responses to novel or threatening stimuli, is essentially a defensive adaptation under physiological conditions. However, strong and long-lasting stress can lead to psychological and pathological damage. Growing evidence suggests that patients suffering from mild and moderate brain injuries and diseases often show severe neurological dysfunction and experience severe and persistent stressful events or environmental stimuli, whether in the acute, subacute, or recovery stage. Previous studies have shown that stress has a remarkable influence on key brain regions and brain diseases. The mechanisms through which stress affects the brain are diverse, including activation of endoplasmic reticulum stress (ERS), apoptosis, oxidative stress, and excitatory/inhibitory neuron imbalance, and may lead to behavioral and cognitive deficits. The impact of stress on brain diseases is complex and involves impediment of recovery, aggravation of cognitive impairment, and neurodegeneration. This review summarizes various stress models and their applications and then discusses the effects and mechanisms of stress on key brain regions—including the hippocampus, hypothalamus, amygdala, and prefrontal cortex—and in brain injuries and diseases—including Alzheimer’s disease, stroke, traumatic brain injury, and epilepsy. Lastly, this review highlights psychological interventions and potential therapeutic targets for patients with brain injuries and diseases who experience severe and persistent stressful events.
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Cavalli, Loredana, Lucia Briscese, Tiziana Cavalli, Paolo Andre, and Maria Chiara Carboncini. "Role of Acupuncture in the Management of Severe Acquired Brain Injuries (sABIs)." Evidence-Based Complementary and Alternative Medicine 2018 (September 12, 2018): 1–10. http://dx.doi.org/10.1155/2018/8107508.

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Acupuncture therapy has been used to treat several disorders in Asian countries and its use is increasing in Western countries as well. Current literature assessed the safety and efficacy of acupuncture in the acute management and rehabilitation of patients with neurologic disorders. In this paper, the role of acupuncture in the treatment of acute severe acquired brain injuries is described, acting on neuroinflammation, intracranial oedema, oxidative stress, and neuronal regeneration. Moreover, beneficial effects of acupuncture on subacute phase and chronic outcomes have been reported in controlling the imbalance of IGF-1 hormone and in decreasing spasticity, pain, and the incidence of neurovegetative crisis. Moreover, acupuncture may have a positive action on the arousal recovery. Further work is needed to understand the effects of specific acupoints on the brain. Allegedly concurrent neurophysiological measurements (e.g., EEG) may help in studying acupuncture-related changes in central nervous system activity and determining its potential as an add-on rehabilitative treatment for patients with consciousness disorders.
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Lee, Song-Hee, Min-Woo Lee, Dong-Gyun Ko, Bo-Young Choi, and Sang-Won Suh. "The Role of NADPH Oxidase in Neuronal Death and Neurogenesis after Acute Neurological Disorders." Antioxidants 10, no. 5 (May 7, 2021): 739. http://dx.doi.org/10.3390/antiox10050739.

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Oxidative stress is a well-known common pathological process involved in mediating acute neurological injuries, such as stroke, traumatic brain injury, epilepsy, and hypoglycemia-related neuronal injury. However, effective therapeutic measures aimed at scavenging free reactive oxygen species have shown little success in clinical trials. Recent studies have revealed that NADPH oxidase, a membrane-bound enzyme complex that catalyzes the production of a superoxide free radical, is one of the major sources of cellular reactive oxygen species in acute neurological disorders. Furthermore, several studies, including our previous ones, have shown that the inhibition of NADPH oxidase can reduce subsequent neuronal injury in neurological disease. Moreover, maintaining appropriate levels of NADPH oxidase has also been shown to be associated with proper neurogenesis after neuronal injury. This review aims to present a comprehensive overview of the role of NADPH oxidase in neuronal death and neurogenesis in multiple acute neurological disorders and to explore potential pharmacological strategies targeting the NADPH-related oxidative stress pathways.
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Rjiba-Touati, K., I. Ayed-Boussema, Y. Guedri, A. Achour, H. Bacha, and S. Abid-Essefi. "Effect of recombinant human erythropoietin on mitomycin C-induced oxidative stress and genotoxicity in rat kidney and heart tissues." Human & Experimental Toxicology 35, no. 1 (March 2, 2015): 53–62. http://dx.doi.org/10.1177/0960327115577521.

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Mitomycin C (MMC) is an antineoplastic agent used for the treatment of several human malignancies. Nevertheless, the prolonged use of the drug may result in a serious heart and kidney injuries. Recombinant human erythropoietin (rhEPO) has recently been shown to exert an important cytoprotective effect in experimental brain injury and ischemic acute renal failure. The aim of the present work is to investigate the cardioprotective and renoprotective effects of rhEPO against MMC-induced oxidative damage and genotoxicity. Our results showed that MMC induced oxidative stress and DNA damage. rhEPO administration in any treatment conditions decreased oxidative damage induced by MMC. It reduced malondialdehyde and protein carbonyl levels. rhEPO ameliorated reduced glutathione plus oxidized glutathione modulation and the increased catalase activity after MMC treatment. Furthermore, rhEPO restored DNA damage caused by MMC. We concluded that rhEPO administration especially in pretreatment condition protected rats against MMC-induced heart and renal oxidative stress and genotoxicity.
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Zhang, Kaige, Yiming Jiang, Biyao Wang, Tiange Li, Dehao Shang, and Xinwen Zhang. "Mesenchymal Stem Cell Therapy: A Potential Treatment Targeting Pathological Manifestations of Traumatic Brain Injury." Oxidative Medicine and Cellular Longevity 2022 (June 15, 2022): 1–11. http://dx.doi.org/10.1155/2022/4645021.

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Traumatic brain injury (TBI) makes up a large proportion of acute brain injuries and is a major cause of disability globally. Its complicated etiology and pathogenesis mainly include primary injury and secondary injury over time, which can cause cognitive deficits, physical disabilities, mood changes, and impaired verbal communication. Recently, mesenchymal stromal cell- (MSC-) based therapy has shown significant therapeutic potential to target TBI-induced pathological processes, such as oxidative stress, neuroinflammation, apoptosis, and mitochondrial dysfunction. In this review, we discuss the main pathological processes of TBI and summarize the underlying mechanisms of MSC-based TBI treatment. We also discuss research progress in the field of MSC therapy in TBI as well as major shortcomings and the great potential shown.
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Park, Chang-Hyun, Ji Hoon Song, Su-Nam Kim, Ji Hwan Lee, Hae-Jeung Lee, Ki Sung Kang, and Hyung-Ho Lim. "Neuroprotective Effects of Tetrahydrocurcumin against Glutamate-Induced Oxidative Stress in Hippocampal HT22 Cells." Molecules 25, no. 1 (December 30, 2019): 144. http://dx.doi.org/10.3390/molecules25010144.

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In the central nervous system, glutamate is a major excitable neurotransmitter responsible for many cellular functions. However, excessive levels of glutamate induce neuronal cell death via oxidative stress during acute brain injuries as well as chronic neurodegenerative diseases. The present study was conducted to examine the effect of tetrahydrocurcumin (THC), a major secondary metabolite of curcumin, and its possible mechanism against glutamate-induced cell death. We prepared THC using curcumin isolated from Curcuma longa (turmeric) and demonstrated the protective effect of THC against glutamate-induced oxidative stress in HT22 cells. THC abrogated glutamate-induced HT22 cell death and showed a strong antioxidant effect. THC also significantly reduced intracellular calcium ion increased by glutamate. Additionally, THC significantly reduced the accumulation of intracellular oxidative stress induced by glutamate. Furthermore, THC significantly diminished apoptotic cell death indicated by annexin V-positive in HT22 cells. Western blot analysis indicated that the phosphorylation of mitogen-activated protein kinases including c-Jun N-terminal kinase, extracellular signal-related kinases 1/2, and p38 by glutamate was significantly diminished by treatment with THC. In conclusion, THC is a potent neuroprotectant against glutamate-induced neuronal cell death by inhibiting the accumulation of oxidative stress and phosphorylation of mitogen-activated protein kinases.
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Monsel, Antoine, Ying-gang Zhu, Stephane Gennai, Qi Hao, Jia Liu, and Jae W. Lee. "Cell-based Therapy for Acute Organ Injury." Anesthesiology 121, no. 5 (November 1, 2014): 1099–121. http://dx.doi.org/10.1097/aln.0000000000000446.

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Abstract Critically ill patients often suffer from multiple organ failures involving lung, kidney, liver, or brain. Genomic, proteomic, and metabolomic approaches highlight common injury mechanisms leading to acute organ failure. This underlines the need to focus on therapeutic strategies affecting multiple injury pathways. The use of adult stem cells such as mesenchymal stem or stromal cells (MSC) may represent a promising new therapeutic approach as increasing evidence shows that MSC can exert protective effects following injury through the release of promitotic, antiapoptotic, antiinflammatory, and immunomodulatory soluble factors. Furthermore, they can mitigate metabolomic and oxidative stress imbalance. In this work, the authors review the biological capabilities of MSC and the results of clinical trials using MSC as therapy in acute organ injuries. Although preliminary results are encouraging, more studies concerning safety and efficacy of MSC therapy are needed to determine their optimal clinical use. (Anesthesiology 2014; 121:1099-121)
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Zheng, Yijun, and Duming Zhu. "Molecular Hydrogen Therapy Ameliorates Organ Damage Induced by Sepsis." Oxidative Medicine and Cellular Longevity 2016 (2016): 1–6. http://dx.doi.org/10.1155/2016/5806057.

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Since it was proposed in 2007, molecular hydrogen therapy has been widely concerned and researched. Many animal experiments were carried out in a variety of disease fields, such as cerebral infarction, ischemia reperfusion injury, Parkinson syndrome, type 2 diabetes mellitus, metabolic syndrome, chronic kidney disease, radiation injury, chronic hepatitis, rheumatoid arthritis, stress ulcer, acute sports injuries, mitochondrial and inflammatory disease, and acute erythema skin disease and other pathological processes or diseases. Molecular hydrogen therapy is pointed out as there is protective effect for sepsis patients, too. The impact of molecular hydrogen therapy against sepsis is shown from the aspects of basic vital signs, organ functions (brain, lung, liver, kidney, small intestine, etc.), survival rate, and so forth. Molecular hydrogen therapy is able to significantly reduce the release of inflammatory factors and oxidative stress injury. Thereby it can reduce damage of various organ functions from sepsis and improve survival rate. Molecular hydrogen therapy is a prospective method against sepsis.
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Javaid, Sana, Talha Farooq, Zohabia Rehman, Ammara Afzal, Waseem Ashraf, Muhammad Fawad Rasool, Faleh Alqahtani, et al. "Dynamics of Choline-Containing Phospholipids in Traumatic Brain Injury and Associated Comorbidities." International Journal of Molecular Sciences 22, no. 21 (October 20, 2021): 11313. http://dx.doi.org/10.3390/ijms222111313.

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The incidences of traumatic brain injuries (TBIs) are increasing globally because of expanding population and increased dependencies on motorized vehicles and machines. This has resulted in increased socio-economic burden on the healthcare system, as TBIs are often associated with mental and physical morbidities with lifelong dependencies, and have severely limited therapeutic options. There is an emerging need to identify the molecular mechanisms orchestrating these injuries to life-long neurodegenerative disease and a therapeutic strategy to counter them. This review highlights the dynamics and role of choline-containing phospholipids during TBIs and how they can be used to evaluate the severity of injuries and later targeted to mitigate neuro-degradation, based on clinical and preclinical studies. Choline-based phospholipids are involved in maintaining the structural integrity of the neuronal/glial cell membranes and are simultaneously the essential component of various biochemical pathways, such as cholinergic neuronal transmission in the brain. Choline or its metabolite levels increase during acute and chronic phases of TBI because of excitotoxicity, ischemia and oxidative stress; this can serve as useful biomarker to predict the severity and prognosis of TBIs. Moreover, the effect of choline-replenishing agents as a post-TBI management strategy has been reviewed in clinical and preclinical studies. Overall, this review determines the theranostic potential of choline phospholipids and provides new insights in the management of TBI.
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Rodrigues, Cecilia M. P., Stephen R. Spellman, Susana Solá, Andrew W. Grande, Cheryle Linehan-Stieers, Walter C. Low, and Clifford J. Steer. "Neuroprotection by a Bile Acid in an Acute Stroke Model in the Rat." Journal of Cerebral Blood Flow & Metabolism 22, no. 4 (April 2002): 463–71. http://dx.doi.org/10.1097/00004647-200204000-00010.

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Tauroursodeoxycholic acid (TUDCA), a hydrophilic bile acid, is a strong modulator of apoptosis in both hepatic and nonhepatic cells, and appears to function by inhibiting mitochondrial membrane perturbation. Excitotoxicity, metabolic compromise, and oxidative stress are major determinants of cell death after brain ischemia-reperfusion injury. However, some neurons undergo delayed cell death that is characteristic of apoptosis. Therefore, the authors examined whether TUDCA could reduce the injury associated with acute stroke in a well-characterized model of transient focal cerebral ischemia. Their model of middle cerebral artery occlusion resulted in marked cell death with prominent terminal deoxynucleotidyl transferase-mediated 2′-deoxyuridine 5′-triphosphate-biotin nick end labeling (TUNEL) within the ischemic penumbra, mitochondrial swelling, and caspase activation. Tauroursodeoxycholic acid administered 1 hour after ischemia resulted in significantly increased bile acid levels in the brain, improved neurologic function, and an approximately 50% reduction in infarct size 2 and 7 days after reperfusion. In addition, TUDCA significantly reduced the number of TUNEL-positive brain cells, mitochondrial swelling, and partially inhibited caspase-3 processing and substrate cleavage. These findings suggest that the mechanism for in vivo neuroprotection by TUDCA is, in part, mediated by inhibition of mitochondrial perturbation and subsequent caspase activation leading to apoptotic cell death. Thus, TUDCA, a clinically safe molecule, may be useful in the treatment of stroke and possibly other apoptosis-associated acute and chronic injuries to the brain.
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Dissertations / Theses on the topic "Oxidative Stress Acute brain injuries"

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Kehl, Christian Verfasser], Christine R. [Akademischer Betreuer] Rose, and Dieter [Akademischer Betreuer] [Willbold. "Astrocyte calcium signaling under oxidative stress in acute and cultured brain tissue slices / Christian Kehl. Gutachter: Christine R. Rose ; Dieter Willbold." Düsseldorf : Universitäts- und Landesbibliothek der Heinrich-Heine-Universität Düsseldorf, 2012. http://d-nb.info/102935023X/34.

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Kehl, Christian [Verfasser], Christine R. Akademischer Betreuer] Rose, and Dieter [Akademischer Betreuer] [Willbold. "Astrocyte calcium signaling under oxidative stress in acute and cultured brain tissue slices / Christian Kehl. Gutachter: Christine R. Rose ; Dieter Willbold." Düsseldorf : Universitäts- und Landesbibliothek der Heinrich-Heine-Universität Düsseldorf, 2012. http://d-nb.info/102935023X/34.

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Chen, Ruo-Dong, and 陳若冬. "Exploring uncoupling proteins and anti-oxidative stress mechanisms under acute cold exposure in adult zebrafish brain." Thesis, 2010. http://ndltd.ncl.edu.tw/handle/04340409043374410236.

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碩士
國立臺灣大學
動物學研究所
98
Exposure to fluctuating temperatures accelerates the mitochondrial respiration and increases the formation of mitochondrial reactive oxygen species (ROS) in ectothermic vertebrates including fish. Excess ROS production by intensively respiring mitochondria results in cellular damages, but mild uncoupling mechanism and enzymatically antioxidant adjustments can defense the oxidative stress. However, neuronal defense pathway against oxidative stress in fish brain upon cold stress is unclear so far. In this study, five members of uncoupling proteins (UCPs) of zebrafish (Danio rerio) were clearly annotated and identified. Effects of acute cold exposure (from 28 °C to 18 °C) on brains’ zucp mRNA expressions and oxidative stress parameters were measured. Except the zucp1, transcripts of other four zucps would be affected by acute 18 °C exposure. Concentrations of cellular protein carbonyl groups (biomarkers of oxidative stress) were significantly increased after cold exposure. Following the cold exposure, anti-oxidative stress parameters, activities of superoxide dismutase (SOD) and transcripts of catalase (CAT), were increased. All the mRNA levels of zppar homologs were also found to change after 18 °C exposure. The axis of peroxisome proliferator-activated receptor (PPAR) and UCPs is involved in the defense pathways against ROS. In addition, the similar expression patterns of PPAR and antioxidant enzymes were also found in this study. Furthermore, indicators of the cellular redox situation, glutathione redox ratio and glutathione content, were maintained constant. Taken all together, stimulation of the PPAR-UCP axis results in mitochondrial mild uncoupling, biogenesis activation, and reduction of ROS. Apart from the antioxidant enzymes, this mechanism may be one of the defense pathways for anti-oxidative stress, regulating metabolic balance, and maintaining cellular homeostasis in ectothermic zebrafish brain upon stressful cold exposure.
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Books on the topic "Oxidative Stress Acute brain injuries"

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Veasey, Sigrid C. Oxidative Neural Injury. Totowa, NJ: Humana Press, 2009.

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Dietrich, W. Dalton. Physiologic Modulators of Neural Injury After Brain and Spinal Cord Injury. Edited by David L. Reich, Stephan Mayer, and Suzan Uysal. Oxford University Press, 2017. http://dx.doi.org/10.1093/med/9780190280253.003.0001.

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Brain and spinal cord injury are leading causes of death and long-term disability, producing diverse burdens for the affected individuals, their families, and society. Such injuries, including traumatic brain injury, stroke, subarachnoid hemorrhage, and spinal cord injury, have common patterns of neuronal cell vulnerability that are associated with a complex cascade of pathologic processes that trigger the propagation of tissue damage beyond the acute injury. Secondary injury mechanisms, including oxidative stress, edema formation, changes in cerebral blood flow and vessel reactivity, metabolic and blood–brain barrier disruption, and neuroinflammation, are therefore important therapeutic targets. Several key physiological parameters require monitoring and intensive management during various phases of treatment to ameliorate secondary injury mechanisms and potentially protect against further neuronal injury. This chapter reviews the core physiological targets in the management of brain and spinal cord injury and relates them to secondary injury mechanisms and outcomes.
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Veasey, Sigrid C. Oxidative Neural Injury. Humana Press, 2010.

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Book chapters on the topic "Oxidative Stress Acute brain injuries"

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Clardy, S. L., X. Wang, W. Zhao, W. Liu, G. A. Chase, J. L. Beard, B. True Felt, and J. R. Connor. "Acute and chronic effects of developmental iron deficiency on mRNA expression patterns in the brain." In Oxidative Stress and Neuroprotection, 173–96. Vienna: Springer Vienna, 2006. http://dx.doi.org/10.1007/978-3-211-33328-0_19.

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Bayir, Hülya, and Valerian E. Kagan. "Free Radicals and Acute Brain Injury: Mechanisms of Oxidative Stress and Therapeutic Potentials." In Brain Injury, 115–44. Boston, MA: Springer US, 2001. http://dx.doi.org/10.1007/978-1-4615-1721-4_6.

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Ayer, R. E., and J. H. Zhang. "Oxidative stress in subarachnoid haemorrhage: significance in acute brain injury and vasospasm." In Acta Neurochirurgica Supplement, 33–41. Vienna: Springer Vienna, 2008. http://dx.doi.org/10.1007/978-3-211-75718-5_7.

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Chang, Chen-Kuei, Ching-Ping Chang, Shyun-Yeu Liu, and Mao-Tsun Lin. "Oxidative stress and ischemic injuries in heat stroke." In Progress in Brain Research, 525–46. Elsevier, 2007. http://dx.doi.org/10.1016/s0079-6123(06)62025-6.

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"Interplay Between Oxidative Stress and Calcium Homeostasis in Acute Neuronal Damage and Neurodegenerative Disease." In Free Radicals in Brain Pathophysiology, 220–39. CRC Press, 2000. http://dx.doi.org/10.1201/9781482270167-12.

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Ghosh, Samit. "Kidney Injuries in Sickle Cell Disease." In Sickle Cell Disease [Working Title]. IntechOpen, 2022. http://dx.doi.org/10.5772/intechopen.102839.

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Sickle cell disease (SCD), characterized by the presence of unstable sickle hemoglobin in the homozygous state (HbSS), results in progressive organ damage and early mortality with the median age of death in the 40s. The kidney is one of the most severely affected organs in SCD. Kidney diseases gradually develop in individuals with SCD. Microalbuminuria is evident in childhood, progressing to apparent proteinuria, deteriorating glomerular filtration rate (GFR) in early adulthood. While CKD becomes prevalent in adults. Moreover, among SCD patients, exacerbation of anemia is an independent risk factor for acute kidney injury (AKI) which is a predisposing factor for CKD and End Stage Renal Diseases (ESRD), altogether contributing to 16–18% mortality among this patients’ population. The pathogenesis of renal diseases in SCD is not completely understood. While epidemiological studies have shown a strong association between rate of hemolysis, severity of anemia and CKD, intrinsic inflammatory, oxidative and hypercoagulative stress that contribute to the characteristic endothelial dysfunction also promotes development of renal diseases in SCD. This chapter will elaborately discuss current research on the pathogenesis of AKI, AKI-to-CKD transition and future research perspectives for development of novel therapeutic strategies.
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Y. Kuo, Grace, Fawaz Philip Tarzi, Stan Louie, and Roy A. Poblete. "Neuroinflammation in Traumatic Brain Injury." In Traumatic Brain Injury [Working Title]. IntechOpen, 2022. http://dx.doi.org/10.5772/intechopen.105178.

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Neuroinflammation following traumatic brain injury (TBI) is an important cause of secondary brain injury that perpetuates the duration and scope of disease after initial impact. This chapter discusses the pathophysiology of acute and chronic neuroinflammation, providing insight into factors that influence the acute clinical course and later functional outcomes. Secondary injury due to neuroinflammation is described by mechanisms of action such as ischemia, neuroexcitotoxicity, oxidative stress, and glymphatic and lymphatic dysfunction. Neurodegenerative sequelae of inflammation, including chronic traumatic encephalopathy, which are important to understand for clinical practice, are detailed by disease type. Prominent research topics of TBI animal models and biomarkers of traumatic neuroinflammation are outlined to provide insight into the advances in TBI research. We then discuss current clinical treatments in TBI and their implications in preventing inflammation. To complete the chapter, recent research models, novel biomarkers, and future research directions aimed at mitigating TBI will be described and will highlight novel therapeutic targets. Understanding the pathophysiology and contributors of neuroinflammation after TBI will aid in future development of prophylaxis strategies, as well as more tailored management and treatment algorithms. This topic chapter is important to both clinicians and basic and translational scientists, with the goal of improving patient outcomes in this common disease.
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Hainline, Brian, Lindsey J. Gurin, and Daniel M. Torres. "Anxiety Following Concussion." In Concussion, edited by Brian Hainline, Lindsey J. Gurin, and Daniel M. Torres, 105–10. Oxford University Press, 2019. http://dx.doi.org/10.1093/med/9780190937447.003.0016.

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Anxiety symptoms are common following concussion but do not indicate more severe brain injury. In the acute post-concussion state, it is common to feel irritable, more emotional, and to have difficulty falling asleep, which are non-specific symptoms commonly observed in anxiety disorders. Concussion injuries sometimes occur in a psychically charged environment, which may potentiate acute anxiety disorder or post-traumatic stress disorder. These disorders can then potentiate prolonged post-concussion persistent symptoms. It is important to differentiate between post-concussion anxiety symptoms and the development of an anxiety disorder. Nonpharmacologic and pharmacologic management, as needed, should address the specific anxiety manifestations.
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Yi, Sophia C., Brian P. Lemkuil, and Piyush Patel. "Principles of Neuroprotection." In Oxford Textbook of Neuroscience and Anaesthesiology, edited by George A. Mashour and Kristin Engelhard, 77–92. Oxford University Press, 2019. http://dx.doi.org/10.1093/med/9780198746645.003.0007.

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This chapter on the principles of neuroprotection includes information on cerebral metabolism, energy failure and pathophysiologic mechanisms, oxidative stress, acidosis, cell death, and difficulties encountered in the translation of neuroprotective strategies from animals to humans. It also covers peri-operative neuroprotective strategies (including barbiturates, volatile anaesthetics, etomidate, propofol, ketamine, and xenon), physiologic management and neuroprotection (including systemic temperature, neonatal hypothermia, induced hypothermia after cardiac arrest, hypothermia and spinal cord injury, hypothermia and traumatic brain injury (TBI), hypothermia and focal ischaemic stroke, arterial oxygen tension, arterial carbon dioxide tension, glucose management, cerebral perfusion pressure, and tPA). Finally, it covers interventional procedures (including mechanical thrombectomy) to treat acute ischaemic stroke.
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Cristina S. Franco, Edna, Marcelo Marques Cardoso, Celice Cordeiro de Souza, Michelle Castro da Silva, Carolina Ramos dos Santos, and Walace Gomes-Leal. "Microglial Plasticity Contributes to Recovery of Bone Marrow Mononuclear Cells during Experimental Stroke." In Macrophages. IntechOpen, 2021. http://dx.doi.org/10.5772/intechopen.95433.

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Brain stroke is an acute neural disorder characterized by obstruction (ischemic) or rupture (hemorrhagic) of blood vessels causing neural damage and subsequent functional impairment. Its pathophysiology is complex and involves a multitude of pathological events including energetic collapse, excitotoxicity, oxidative stress, metabolic acidosis, cell death and neuroinflammation. Despite its clinical importance, there is no effective pharmacological therapies available to diminish secondary damage avowing functional deficits. Considering the failure of pharmacological approaches for stroke, cell therapy came as promising alternative. Different cell types have been investigated in different experimental models with promising results. An important issue regarding the transplantation of stem cells into the damaged CNS tissue is how the pathological environment influences the transplanted cells. It has been established that an exacerbated inflammation in the pathological environment is detrimental to the survival of the transplanted stem cells. This prompted us to develop an experimental strategy to improve the therapeutic actions of bone marrow mononuclear cells (BMMCs) transplanted into the acute phase of brain stroke by modulating microglial activation with minocycline. In this chapter, we first review the basic pathophysiology of ischemic stroke with emphasis on the role of microglia to the pathological outcome. We then review the experimental approach of modulating microglia activation in order to enhance therapeutic actions of BMMCS for experimental stroke. We suggest that such an approach may be applied as an adjuvant therapy to control excessive neuroinflammation in the pathological environment allowing acute transplants and improving therapeutic actions of different kind of stem cells.
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Conference papers on the topic "Oxidative Stress Acute brain injuries"

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Sorokina, E. G., O. V. Karaseva, S. A. Afanasyeva, O. V. Globa, Z. B. Semenova, V. P. Reutov, and V. G. Pinelis. "MODIFIED ALBUMIN AS AN INDICATOR OF OXIDATIVE STRESS IN ISCHEMIC-HYPOXIC INJURIES OF THE BRAIN AND VARIOUS ORGANS." In NOVEL TECHNOLOGIES IN MEDICINE, BIOLOGY, PHARMACOLOGY AND ECOLOGY. Institute of information technology, 2022. http://dx.doi.org/10.47501/978-5-6044060-2-1.301-310.

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The article discusses the literature data on the relationship of modified albumin by ishemia (IMA) and nitrosative stress (nitroalbumin/nitrotyrosine) to the ischemic/hypoxic damage of the brain and other organs. Data on the association of an increase in the content of IMA with a violation of the binding of serum albumin of metals, which is observed in processes accompanied by oxidative oxygen and nitrosative stress, are presented.
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