Gotowa bibliografia na temat „Cerebral ischemia – Treatment”
Utwórz poprawne odniesienie w stylach APA, MLA, Chicago, Harvard i wielu innych
Spis treści
Zobacz listy aktualnych artykułów, książek, rozpraw, streszczeń i innych źródeł naukowych na temat „Cerebral ischemia – Treatment”.
Przycisk „Dodaj do bibliografii” jest dostępny obok każdej pracy w bibliografii. Użyj go – a my automatycznie utworzymy odniesienie bibliograficzne do wybranej pracy w stylu cytowania, którego potrzebujesz: APA, MLA, Harvard, Chicago, Vancouver itp.
Możesz również pobrać pełny tekst publikacji naukowej w formacie „.pdf” i przeczytać adnotację do pracy online, jeśli odpowiednie parametry są dostępne w metadanych.
Artykuły w czasopismach na temat "Cerebral ischemia – Treatment"
1
Kanazawa, Masato, Tetsuya Takahashi, Masanori Ishikawa, Osamu Onodera, Takayoshi Shimohata i Gregory J. del Zoppo. "Angiogenesis in the ischemic core: A potential treatment target?" Journal of Cerebral Blood Flow & Metabolism 39, nr 5 (6.03.2019): 753–69. http://dx.doi.org/10.1177/0271678x19834158.
Pełny tekst źródłaStreszczenie:
The ischemic penumbra is both a concept in understanding the evolution of cerebral tissue injury outcome of focal ischemia and a potential therapeutic target for ischemic stroke. In this review, we examine the evidence that angiogenesis can contribute to beneficial outcomes following focal ischemia in model systems. Several studies have shown that, following cerebral ischemia, endothelial proliferation and subsequent angiogenesis can be detected beginning four days after cerebral ischemia in the border of the ischemic core, or in the ischemic periphery, in rodent and non-human primate models, although initial signals appear within hours of ischemia onset. Components of the neurovascular unit, its participation in new vessel formation, and the nature of the core and penumbra responses to experimental focal cerebral ischemia, are considered here. The potential co-localization of vascular remodeling and axonal outgrowth following focal cerebral ischemia based on the definition of tissue remodeling and the processes that follow ischemic stroke are also considered. The region of angiogenesis in the ischemic core and its surrounding tissue (ischemic periphery) may be a novel target for treatment. We summarize issues that are relevant to model studies of focal cerebral ischemia looking ahead to potential treatments.
2
Siesjö, Bo K. "Pathophysiology and treatment of focal cerebral ischemia". Journal of Neurosurgery 77, nr 3 (wrzesień 1992): 337–54. http://dx.doi.org/10.3171/jns.1992.77.3.0337.
Pełny tekst źródłaStreszczenie:
✓ The mechanisms that give rise to ischemic brain damage have not been definitively determined, but considerable evidence exists that three major factors are involved: increases in the intercellular cytosolic calcium concentration (Ca++i), acidosis, and production of free radicals. A nonphysiological rise in Ca++i due to a disturbed pump/leak relationship for calcium is believed to cause cell damage by overactivation of lipases and proteases and possibly also of endonucleases, and by alterations of protein phosphorylation, which secondarily affects protein synthesis and genome expression. The severity of this disturbance depends on the density of ischemia. In complete or near-complete ischemia of the cardiac arrest type, pump activity has ceased and the calcium leak is enhanced by the massive release of excitatory amino acids. As a result, multiple calcium channels are opened. This is probably the scenario in the focus of an ischemic lesion due to middle cerebral artery occlusion. Such ischemic tissues can be salvaged only by recirculation, and any brain damage incurred is delayed, suggesting that the calcium transient gives rise to sustained changes in membrane function and metabolism. If the ischemia is less dense, as in the penumbral zone of a focal ischemic lesion, pump failure may be moderate and the leak may be only slightly or intermittently enhanced. These differences in the pump/leak relationship for calcium explain why calcium and glutamate antagonists may lack effect on the cardiac arrest type of ischemia, while decreasing infarct size in focal ischemia. The adverse effects of acidosis may be exerted by several mechanisms. When the ischemia is sustained, acidosis may promote edema formation by inducing Na+ and Cl− accumulation via coupled Na+/H+ and Cl−/HCO3− exchange; however, it may also prevent recovery of mitochondrial metabolism and resumption of H+ extrusion. If the ischemia is transient, pronounced intraischemic acidosis triggers delayed damage characterized by gross edema and seizures. Possibly, this is a result of free-radical formation. If the ischemia is moderate, as in the penumbral zone of a focal ischemic lesion, the effect of acidosis is controversial. In fact, enhanced glucolysis may then be beneficial. Although free radicals have long been assumed to be mediators of ischemic cell death, it is only recently that more substantial evidence of their participation has been produced. It now seems likely that one major target of free radicals is the microvasculature, and that free radicals and other mediators of inflammatory reactions (such as platelet-activating factor) aggravate the ischemic lesion by causing microvascular dysfunction and blood-brain barrier disruption. Solid experimental evidence exists that the infarct resulting from middle cerebral artery occlusion can be reduced by glutamate antagonists, by several calcium antagonists, and by some drugs acting on Ca++ and Na+ influx. In addition, published reports hint that qualitatively similar results are obtained with drugs whose sole or main effect is to scavenge free radicals. Thus, there is substantial experimental evidence that the ischemic lesions due to middle cerebral artery occlusion can be ameliorated by drugs, sometimes dramatically; however, the therapeutic window seems small, maximally 3 to 6 hours. This suggests that if these therapeutic principles are to be successfully applied to the clinical situation, patient management must change.
3
Wang, Lei, Xu Zhang, Xiaoxing Xiong, Hua Zhu, Ran Chen, Shudi Zhang, Gang Chen i Zhihong Jian. "Nrf2 Regulates Oxidative Stress and Its Role in Cerebral Ischemic Stroke". Antioxidants 11, nr 12 (30.11.2022): 2377. http://dx.doi.org/10.3390/antiox11122377.
Pełny tekst źródłaStreszczenie:
Cerebral ischemic stroke is characterized by acute ischemia in a certain part of the brain, which leads to brain cells necrosis, apoptosis, ferroptosis, pyroptosis, etc. At present, there are limited effective clinical treatments for cerebral ischemic stroke, and the recovery of cerebral blood circulation will lead to cerebral ischemia-reperfusion injury (CIRI). Cerebral ischemic stroke involves many pathological processes such as oxidative stress, inflammation, and mitochondrial dysfunction. Nuclear factor erythroid 2-related factor 2 (Nrf2), as one of the most critical antioxidant transcription factors in cells, can coordinate various cytoprotective factors to inhibit oxidative stress. Targeting Nrf2 is considered as a potential strategy to prevent and treat cerebral ischemia injury. During cerebral ischemia, Nrf2 participates in signaling pathways such as Keap1, PI3K/AKT, MAPK, NF-κB, and HO-1, and then alleviates cerebral ischemia injury or CIRI by inhibiting oxidative stress, anti-inflammation, maintaining mitochondrial homeostasis, protecting the blood–brain barrier, and inhibiting ferroptosis. In this review, we have discussed the structure of Nrf2, the mechanisms of Nrf2 in cerebral ischemic stroke, the related research on the treatment of cerebral ischemia through the Nrf2 signaling pathway in recent years, and expounded the important role and future potential of the Nrf2 pathway in cerebral ischemic stroke.
4
Siesjö, Bo K. "Pathophysiology and treatment of focal cerebral ischemia". Journal of Neurosurgery 108, nr 3 (marzec 2008): 616–31. http://dx.doi.org/10.3171/jns/2008/108/3/0616.
Pełny tekst źródłaStreszczenie:
✓ This article examines the pathophysiology of lesions caused by focal cerebral ischemia. Ischemia due to middle cerebral artery occlusion encompasses a densely ischemic focus and a less densely ischemic penumbral zone. Cells in the focus are usually doomed unless reperfusion is quickly instituted. In contrast, although the penumbra contains cells “at risk,” these may remain viable for at least 4 to 8 hours. Cells in the penumbra may be salvaged by reperfusion or by drugs that prevent an extension of the infarction into the penumbral zone. Factors responsible for such an extension probably include acidosis, edema, K+/Ca++ transients, and inhibition of protein synthesis. Central to any discussion of the pathophysiology of ischemic lesions is energy depletion. This is because failure to maintain cellular adenosine triphosphate (ATP) levels leads to degradation of macromolecules of key importance to membrane and cytoskeletal integrity, to loss of ion homeostasis, involving cellular accumulation of Ca++, Na+, and Cl−, with osmotically obligated water, and to production of metabolic acids with a resulting decrease in intra- and extracellular pH. In all probability, loss of cellular calcium homeostasis plays an important role in the pathogenesis of ischemic cell damage. The resulting rise in the free cytosolic intracellular calcium concentration (Ca++) depends on both the loss of calcium pump function (due to ATP depletion), and the rise in membrane permeability to calcium. In ischemia, calcium influx occurs via multiple pathways. Some of the most important routes depend on activation of receptors by glutamate and associated excitatory amino acids released from depolarized presynaptic endings. However, ischemia also interferes with the intracellular sequestration and binding of calcium, thereby contributing to the rise in intracellular Ca++. A second key event in the ischemic tissue is activation of anaerobic glucolysis. The main reason for this activation is inhibition of mitochondrial metabolism by lack of oxygen; however, other factors probably contribute. For example, there is a complex interplay between loss of cellular calcium homeostasis and acidosis. On the one hand, a rise in intracellular Ca++ is apt to cause mitochondrial accumulation of calcium. This must interfere with ATP production and enhance anaerobic glucolysis. On the other hand, acidosis must interfere with calcium binding, thereby contributing to the rise in intracellular Ca++.
5
Siesjö, Bo K. "Pathophysiology and treatment of focal cerebral ischemia". Journal of Neurosurgery 77, nr 2 (sierpień 1992): 169–84. http://dx.doi.org/10.3171/jns.1992.77.2.0169.
Pełny tekst źródłaStreszczenie:
✓ This article examines the pathophysiology of lesions caused by focal cerebral ischemia. Ischemia due to middle cerebral artery occlusion encompasses a densely ischemic focus and a less densely ischemic penumbral zone. Cells in the focus are usually doomed unless reperfusion is quickly instituted. In contrast, although the penumbra contains cells “at risk.” these may remain viable for at least 4 to 8 hours. Cells in the penumbra may be salvaged by reperfusion or by drugs that prevent an extension of the infarction into the penumbral zone. Factors responsible for such an extension probably include acidosis, edema, K+/Ca++ transients, and inhibition of protein synthesis. Central to any discussion of the pathophysiology of ischemic lesions is energy depletion. This is because failure to maintain cellular adenosine triphosphate (ATP) levels leads to degradation of macromolecules of key importance to membrane and cytoskeletal integrity, to loss of ion homeostasis, involving cellular accumulation of Ca++, Na+, and Cl−, with osmotically obligated water, and to production of metabolic acids with a resulting decrease in intra- and extracellular pH. In all probability, loss of cellular calcium homeostasis plays an important role in the pathogenesis of ischemic cell damage. The resulting rise in the free cytosolic intracellular calcium concentration (Ca++) depends on both the loss of calcium pump function (due to ATP depletion), and the rise in membrane permeability to calcium. In ischemia, calcium influx occurs via multiple pathways. Some of the most important routes depend on activation of receptors by glutamate and associated excitatory amino acids released from depolarized presynaptic endings. However, ischemia also interferes with the intracellular sequestration and binding of calcium, thereby contributing to the rise in intracellular Ca++. A second key event in the ischemic tissue is activation of anaerobic glucolysis. The main reason for this activation is inhibition of mitochondrial metabolism by lack of oxygen; however, other factors probably contribute. For example, there is a complex interplay between loss of cellular calcium homeostasis and acidosis. On the one hand, a rise in intracellular Ca++ is apt to cause mitochondrial accumulation of calcium. This must interfere with ATP production and enhance anaerobic glucolysis. On the other hand, acidosis must interfere with calcium binding, thereby contributing to the rise in intracellular Ca++.
6
Han, Xue Mei, Hong Tao Wei i Song Yan Liu. "Involvement of Erythropoietin Expression in Acupuncture Preconditioning-Induced Ischemic Tolerance". Advanced Materials Research 554-556 (lipiec 2012): 1650–55. http://dx.doi.org/10.4028/www.scientific.net/amr.554-556.1650.
Pełny tekst źródłaStreszczenie:
Abstract Objective To investigate the expression of erythropoietin (EPO) after acupuncture preconditioning plus focal cerebral ischemia treatment. Methods Rat focal cerebral ischemia model and acupuncture preconditioning model were established. Animals were randomly assigned into different groups: control (focal cerebral ischemia) and acupuncture preconditioning plus focal cerebral ischemia, with 8 rats for each group. The expression of EPO after different treatments was determined by histological examination, immunohistochemistry and in situ hybridization. Results The mRNA and protein expressions of EPO could be detected in survival and necrotic neurons, glia as well as vascular endothelial cells. Focal cerebral ischemia promoted the expression of EPO. Significant enhanced EPO level was found in the ischemic peripheral zone after acupuncture preconditioning (P < 0.05). Conclusion Our results demonstrated that acupuncture preconditioning enhanced the expression of EPO in neurons, glia and vascular endothelial cells the ischemic peripheral zone, suggesting the involvement of EPO in acupuncture preconditioning-induced neuroprotection following focal cerebral ischemia. EPO may exert neuroprotective effects through promoting neurotrophic support and angiogenesis.
7
Song, Siying, Hao Wu, Xunming Ji i Ran Meng. "The BE COOL Treatments (Batroxobin, oxygEn, Conditioning, and cOOLing): Emerging Adjunct Therapies for Ischemic Cerebrovascular Disease". Journal of Clinical Medicine 11, nr 20 (20.10.2022): 6193. http://dx.doi.org/10.3390/jcm11206193.
Pełny tekst źródłaStreszczenie:
Ischemic cerebrovascular disease (ICD), the most common neurological disease worldwide, can be classified based on the onset time (acute/chronic) and the type of cerebral blood vessel involved (artery or venous sinus). Classifications include acute ischemic stroke (AIS)/transient ischemic attack (TIA), chronic cerebral circulation insufficiency (CCCI), acute cerebral venous sinus thrombosis (CVST), and chronic cerebrospinal venous insufficiency (CCSVI). The pathogenesis of cerebral arterial ischemia may be correlated with cerebral venous ischemia through decreased cerebral perfusion. The core treatment goals for both arterial and venous ICDs include perfusion recovery, reduction of cerebral ischemic injury, and preservation of the neuronal integrity of the involved region as soon as possible; however, therapy based on the current guidelines for either acute ischemic events or chronic cerebral ischemia is not ideal because the recurrence rate of AIS or CVST is still very high. Therefore, this review discusses the neuroprotective effects of four novel potential ICD treatments with high translation rates, known as the BE COOL treatments (Batroxobin, oxygEn, Conditioning, and cOOLing), and subsequently analyzes how BE COOL treatments are used in clinical settings. The combination of batroxobin, oxygen, conditioning, and cooling may be a promising intervention for preserving ischemic tissues.
8
Spetzler, Robert F. "Treatment of chronic cerebral ischemia". Surgical Neurology 23, nr 2 (luty 1985): 201. http://dx.doi.org/10.1016/0090-3019(85)90350-7.
Pełny tekst źródła
9
Ghosh, Nilanjan, Rituparna Ghosh, Zulfiqar A. Bhat, Vivekananda Mandal, Sitesh C. Bachar, Namsa D. Nima, Otimenyin O. Sunday i Subhash C. Mandal. "Advances in Herbal Medicine for Treatment of Ischemic Brain Injury". Natural Product Communications 9, nr 7 (lipiec 2014): 1934578X1400900. http://dx.doi.org/10.1177/1934578x1400900739.
Pełny tekst źródłaStreszczenie:
Ischemic brain injury is one of the leading causes of death worldwide and has attracted a lot of attention in the field of drug discovery. Cerebral ischemia is a complex pathological process involving a series of mechanisms, including generation of free radicals, oxidative stress, disruption of the membrane function, release of neurotransmitters and apoptosis. Thrombolytic therapy is the most effective therapeutic strategy, but the benefits are far from being absolute. Increased attention in the field of drug discovery has been focused on using natural compounds from traditional medicinal herbs for neuroprotection, which appears to be a promising therapeutic option for cerebral ischemia with minimal systemic adverse effects that could limit their long term use. The scenario calls for extensive investigations which can result in the development of lead molecules for neuroprotection in the future. In this context, the present review focuses on possible mechanisms underlying the beneficial effects of herbal drugs in patients with cerebral ischemic injury. Natural compounds have been demonstrated to have neurofunctional regulatory actions with antioxidative, anti-inflammatory, calcium antagonizing and anti-apoptotic activities. Among the several leads obtained from plant sources as potential neuroprotective agents, resveratrol, EGb761, curcumin and epigallocatechin-3-gallate have shown significant therapeutic benefits in cerebral ischemic conditions. However, ligustilide, tanshinone, scutellarin and shikonin are the few lead molecules which are under investigation for treatment of cerebral ischemia.
10
Han, Xue Mei, Hong Tao Wei i Song Yan Liu. "Functional Role of HIF-1α in Hypoxic Preconditioning-Induced Neuroprotection against Focal Cerebral Ischemia". Advanced Materials Research 554-556 (lipiec 2012): 1762–67. http://dx.doi.org/10.4028/www.scientific.net/amr.554-556.1762.
Pełny tekst źródłaStreszczenie:
Objective To investigate the expression of HIF-1α after permenent focal cerebral ischemia and to explore the role of HIF-1α in hypoxic preconditioning-induced neuroprotection. Methods Rat focal cerebral ischemia model and hypoxic preconditioning models were established. Animals were randomly divided into four groups: healthy control, hypoxic preconditioning (3 h of 8% O2/92% N2 treatment), focal cerebral ischemia (6 h, 1 d, 3 d or 7 d) and hypoxic preconditioning + focal cerebral ischemia (6 h, 1 d, 3 d or 7 d). The expression of HIF-1α after different treatments was determined by histological examination, immunohistochemistry and in situ hybridization. Results The mRNA and protein expressions of HIF-1α could be detected in survival and necrotic neurons, glia as well as vascular endothelial cells. Hypoxic preconditioning significantly promoted the expression of HIF-1α after focal cerebral ischemia, especially in ischemic peripheral zone (P < 0.05).
Rozprawy doktorskie na temat "Cerebral ischemia – Treatment"
1
Yang, Di, i 楊荻. "Neuroprotective effects of lycium barbarum extracts in cerebral and retinal ischemia/reperfusion injury". Thesis, The University of Hong Kong (Pokfulam, Hong Kong), 2014. http://hdl.handle.net/10722/206738.
Pełny tekst źródłaStreszczenie:
Ischemic stroke is a devastating cerebrovascular disease resulting in high mortality rate and distressing sequelae such as hemiplegia, ataxia and even visual impairment. Retinal ischemia refers to a common pathological feature shared by many blinding diseases including retinal vascular occlusions, diabetic retinopathy, glaucoma, and retinopathy of prematurity. Ischemia/reperfusion injury is implicated in both of these pathological conditions, which greatly impact on one’s daily life. The eventual consequence of the insult is irreversible neuronal cell death and functional deterioration. Apart from current symptomatic treatment for these diseases, researchers and clinicians are dedicated to look for ideal neuroprotectant to meet the clinical needs. Traditional Chinese medicine has been received accumulating attention in recent years, and Lycium barbarum is one of them. The polysaccharides (LBP) utilized in the present study are the rich extracts of the fruit of Lycium barbarum that has been shown to exert many biological effects. This study aims to evaluate its protective effects in cerebral and retinal ischemia, which has not yet been fully investigated.
A well-established rodent model, middle cerebral artery occlusion, was utilized in the present study to mimic cerebral and retinal ischemia/reperfusion injury. In the study of cerebral ischemia, both pre-treatment and post-treatment of LBP were explored. Seven-day LBP pre-treatment revealed significant protection against neurological deficits and cerebral infarction. Besides, it attenuated cerebral edema and glial activation, as well as preserved blood-brain barrier integrity. Further study showed that these beneficial effects of LBP pre-treatment might act via anti-apoptosis, antioxidation and anti-inflammation. However, similar findings were not noted in LBP post-treatment experiments, possibly due to the timing of intervention.
In the investigation of retinal ischemia, the observation time was prolonged to 7 days after the insult. Electroretinogram was used to evaluate the functional alternation of retinal neurons. Sustained retinal dysfunction was induced by two-hour ischemia. LBP pre-treatment with continuous daily supplementation effectively alleviated visual dysfunction and protected the retina from morphological impairment including neuronal death, glial activation and blood-retinal barrier disruption. Similarly, these protective effects might be associated with the involvement of attenuation of apoptosis and oxidative stress.
In conclusion, LBP pre-treatment with continuous daily supplementation protected the brain and retina, both functionally and morphologically, from ischemia/reperfusion injury. This dosing regimen hold great promise in serving as a prophylactic neuroprotectant in patients at high risk for ischemic stroke, as well as preserving normal visual function and reducing irreversible neuronal death in ischemic retinopathies. Further studies on the active ingredients and underlying mechanisms would be informative for better application of LBP in clinical situation.published_or_final_version
Ophthalmology
Doctoral
Doctor of Philosophy
2
Chan, Chu-fung, i 陳柱峰. "Neuroprotective effects of granulocyte-colony stimulating factor in a mice stroke model". Thesis, The University of Hong Kong (Pokfulam, Hong Kong), 2007. http://hub.hku.hk/bib/B40687284.
Pełny tekst źródła
3
Xu, Mingjing, i 徐明婧. "Baicalin protects neural cells from cerebral ischemia reperfusion injury by scavenging peroxynitrite". Thesis, The University of Hong Kong (Pokfulam, Hong Kong), 2011. http://hub.hku.hk/bib/B47753110.
Pełny tekst źródłaStreszczenie:
Ischemic stroke is the leading cause of death and disability in human diseases all around the world. As effective treatment for ischemic stroke is still absent, seeking for new therapy is of great interest. Currently, several key pathological cascades following cerebral ischemia have been explored to develop further therapies. Among them, reactive nitrogen species (RNS) has been indicated to play a critical role in cerebral ischemia reperfusion injury. As one of the RNS, peroxynitrite contributes to the neural cell death and subsequent brain dysfunction in the process. Thus, development of antioxidants targeting on peroxynitrite could be an important strategy for the treatment of cerebral ischemia-reperfusion injury.
Baicalin is a polyphenolic compound isolated from roots of Scutellaria baicalensis. Baicalin exerted protective effects against cerebral ischemia-reperfusion injury but the mechanisms are not clear yet. In this study, we investigated the free radical scavenging ability and neuroprotective effects of baicalin. According to our results, baicalin neutralized DPPH radicals effectively. By using electron paramagnetic resonance (EPR) spin trapping technology and fluorescent probe DAF-2DA, we found that baicalin dose-dependently scavenged superoxide, but had very low effect on elimination of nitric oxide. The immunofluoresent results revealed that baicalin at the concentration of 50 M completely suppressed the nitrotyrosine formation induced by 3-morpholinylsydnoneimine chloride (SIN-1, a peroxynitrite donor) in neuroblastoma SH-SY5Y cells. Mass spetrum provided direct evidence of the peroxynitrite scavenging ability of baicalin. Using MTT assays, we found that baicalin totally reversed peroxynitrite-induced cytotoxicity in SH-SY5Y cells and protected SH-SY5Y cells in oxygen glucose deprivation (OGD) and following reoxygenation injury. Furthermore, in vivo experiments revealed that intravenous injection of baicalin exerted better neuroprotective effect than intraperitoneal administration in rats underwent middle cerebral artery occlusion (MCAO). After cerebral ischemia reperfusion, rats treated with 3 mg/kg of peroxynitrite decomposition catalyst (FeTMPyP) or 25 mg/kg of baicalin revealed a smaller size of infarction volume, suppressed neural cell death and reduced nitrotyrosine formation than MCAO rats. However, baicalin did not alter the expression of tight junction proteins, claudin-5 and ZO-1, in brain endothelial bEnd3 cell line treated with OGD following reoxygenation. In cerebral ischemia reperfusion rats, administration of FeTMPyP at the dosage of 3 mg/kg diminished the Evans blue leakage caused by blood brain barrier disruption, whereas treatment of baicalin did not show significant effect.
In conclusion, this study suggests that baicalin can scavenge peroxynitrite and protect neural cells from peroxynitrite-induced injury. Furthermore, baicalin could prevent brains from cerebral ischemia-reperfusion injury and the neuroprotective mechanisms are associated with the scavenging effects on peroxynitrite. These findings provide new insights into the antioxidant and neuroprotective properties of baicalin and indicate the potential application of baicalin for the treatment of ischemic stroke.published_or_final_version
Chinese Medicine
Master
Master of Philosophy
4
Khanasari, Parto S. "An investigation of the neuroprotective properties of fenamate NSAIDs, against experimental model of ischemic stroke". Scholarly Commons, 2007. https://scholarlycommons.pacific.edu/uop_etds/671.
Pełny tekst źródłaStreszczenie:
Stroke is a devastating neurological disease with limited treatment opportunities. Recent advances in understanding the underlying pathogenesis of cerebral ischemia support the involvement of multiple biochemical pathways in the development of the ischemic injury.
The work reported in this thesis was undertaken to investigate the hypothesis that fenamate NSAIDs have neuroprotective properties against ischemic stroke and to explore the underlying mechanisms for any efficacy.
Fenamates are non-selective inhibitors of cyclooxygenases. In addition, fenamates are antagonists of non-selective cation channels, subtype-selective modutators of GABAA receptors, weak inhibitors of glutaniate receptors and activators of some potassium channels, all potentially important in the pathogenesis of ischemic stroke, Mefenamic acid, a prototype fenamate, administered by intracerebroventricular (ICV) infusion, reduced the ischemic brain damage and edema volume in the middle cerebral artery occlusion model in male rats. Consistent with these results; systemic administration of mefenamic acid, by multiple intravenous injections, also reduced the ischemic damage and edema volume measured by morphometric analysis and as a function of brain water content. These are the first set of experiments to demonstrate a significant neuroprotective effect of a fenamate against an in vivo model of ischemic stroke.
In vitro, mefenamic acid was also shown to reduce glutamate-evoked cell death (excitotoxicity) in a concentration-dependent manner in cultured embryonic rat hippocampal neurons. Similarly, selected other fenamates also reduced excitotoxicity in the rank order (from highest): mefenamic acid > flufenamic acid ≥ meclofenamic acid > niflumic acid supporting the idea that this is a drug class action.
Three pharmacological properties of fenamates, cyclooxygenase inhibition, GABAA receptor modulation and potassium channel activation were investigated as the potential mechanism(s} for the neuroprotective effects of mefenamic acid against excitotoxicity. The experimental results suggest that these are not the primary mechanisms for neuroprotective effects of mefenamic acid against glutamate-evoked cell death.
Collectively, these data support the hypothesis that fenamate NSAIDs are neuroprotective against experimental models of cerebral ischemia and suggest they should be further investigated as potential pharmacological treatments for stroke.
5
Weiss, Miriam [Verfasser], Gerrit Alexander [Akademischer Betreuer] Schubert i Martin [Akademischer Betreuer] Wiesmann. "Endovascular rescue treatment for delayed cerebral ischemia after subarachnoid hemorrhage is safe and effective / Miriam Weiss ; Gerrit Alexander Schubert, Martin Wiesmann". Aachen : Universitätsbibliothek der RWTH Aachen, 2019. http://d-nb.info/1215927614/34.
Pełny tekst źródła
6
Boulos, Sherif. "Identification and characterisation of potential neuroprotective proteins induced by erythropoietin (EPO) preconditioning of cortical neuronal cultures". University of Western Australia. School of Biomedical and Chemical Sciences, 2008. http://theses.library.uwa.edu.au/adt-WU2008.0128.
Pełny tekst źródłaStreszczenie:
[Truncated abstract] Clinical therapeutic agents to directly inhibit ischaemic neuronal death are presently unavailable. One approach to developing therapeutics is based upon the identification of proteins up-regulated by 'preconditioning', a natural adaptive response utilised by the neural cells to counter damaging insults, such as ischaemia. Thus, my project aimed to firstly identify proteins differentially expressed following erythropoietin (EPO) mediated neuronal preconditioning and secondly to assess whether any of these proteins possessed neuroprotective activity using in vitro ischaemia like models. To achieve the first aim, it was shown that in vitro neuronal EPO preconditioning could: (i) induce cell signal changes in neuronal cultures, (ii) protect neurons against in vitro ischaemia and (iii) induce differential protein expression. Overall, 40 differentially expressed proteins were identified in cortical neuronal cultures following EPO preconditioning. In order to investigate the neuroprotective or neurodamaging activity of proteins induced by EPO preconditioning I developed an adenoviral expression system for use in neuronal cultures. To this end, I assessed the suitability of four promoters (cytomegalovirus [CMV], rous sarcoma virus [RSV], human synapsin 1 [hSYN1], rat synapsin 1 [rSYN1]) previously used to express proteins in neuronal cultures and demonstrated the superiority of the RSV promoter for this purpose. ... Finally, in order to validate this adenoviral expression system, I over-expressed the anti-apoptotic protein Bcl-XL in neuronal cultures and subsequently confirmed its neuroprotective activity in the in vitro ischaemia and oxidative stress models used in my project. Using this adenoviral vector system and the in vitro oxidative stress model I assessed a number of proteins up-regulated by EPO preconditioning. The results of this preliminary study indicated that cyclophilin A (CyPA), peroxiredoxin 2 (PRDX2) and superoxide dismutase 1 (SOD1) over-expression were neuroprotective. It was subsequently verified that adenoviral mediated over-expression of CyPA and PRDX2, v but not SOD1 in cortical neuronal cultures could protect neurons from in vitro ischaemia. I also confirmed that CyPA mRNA increased in the rat hippocampus in response to 3 minutes of global cerebral ischaemia. Interestingly, an increase in CyPA, PRDX2 or SOD1 protein was not observed in the same experimental paradigm. To investigate CyPA's mode of action I confirmed that cultured neurons, but not astrocytes, express the CyPA receptor, CD147. It was also demonstrated that administration of exogenous CyPA protein to neuronal cultures could protect neurons against oxidative and ischaemic injury. I further demonstrated that exogenous administration of CyPA induces a rapid and transient activation of the extracellular signal-regulated kinase (ERK) 1/2 pathway in neuronal cultures. From this observation, I have proposed that the extracellular mediated neuroprotective activity of CyPA occurs via CD147 receptor signalling and activation of ERK1/2 pro-survival pathways. Based on the findings reported in this thesis, the neuroprotective activities of PRDX2 and CyPA warrant further investigation as targets for the development of new therapies to treat cerebral ischaemia.
7
Rahman, Rosanna, i n/a. "Potential causes of the delayed neural damage observed post-stroke & the effects of epigallocatechin gallate administration". University of Otago. Department of Pharmacology & Toxicology, 2006. http://adt.otago.ac.nz./public/adt-NZDU20070508.122246.
Pełny tekst źródłaStreszczenie:
Stroke is the 3rd leading cause of death and the leading cause of major disability worldwide. Currently, there are no neuroprotective drugs approved for the acute treatment of ischaemic stroke. The vast majority of stroke therapeutics failed in clinical trials due to toxic side effects and/or a clinically irrelevant therapeutic window. This thesis is focused on exploiting the delayed neurodegeneration that occurs in the compromised penumbra, as these cells may be capable of being saved by therapeutic intervention in a clinically obtainable window. In order to investigate the ischaemic cascade and be able to draw conclusions that are applicable to humans, the international gold standard animal model for cerebral ischaemia, the filament insertion middle cerebral artery occlusion (MCAO) model, was established at the University of Otago. This model was validated under new laboratory conditions and employed adult male Sprague Dawley rats. After testing multiple occlusion lengths, it was concluded that a 2hr ischaemic period was sufficient to produce a consistent infarct of optimal size. It has been well documented that neuroinflammation contributes to much of the delayed progression of neural injury post-stroke. Therefore, the catechin (-)-epigallocatechin gallate (EGCG), which is an anti-inflammatory, anti-oxidant and free-radical scavenging agent was investigated in the MCAO model of stroke. 50mg/kg i.p. of EGCG or saline was administered immediately post-MCAO and animals were sacrificed at 72hr post-filament insertion. The results confirmed that treatment with EGCG was neuroprotective and non-toxic. However, EGCG also induced an over 50% increase in the risk of haemorrhagic conversions. The anti-platelet effects of EGCG and lack of toxicity suggests that the catechin may prove to be an efficacious prophylactic for stroke. The contrary findings for EGCG treatment led to the re-evaluation of the neuroinflammatory pathway for alternate mechanisms to target therapeutic interventions.
The temporal profile of the primary inducible enzymes nitric oxide synthase (NOS), cyclooxygenase (COX) and arginase (and their isoforms) were quantified 0, 3 and 7 days post-stroke. In both hemispheres, total NOS activity exhibited a significant and sustained up-regulation to 7 days post-occlusion. In the ipsilateral hemisphere at least half of the total increase was accounted for by inducible NOS (iNOS) expression. Arginase, which competes with NOS for L-arginine, demonstrated a delayed but significant increase in activity by day 7 in the infarcted hemisphere, thereby correlating well with the downward slope of NOS activity (illustrating the switch in the conversion pathway). COX activity was observably increased in the ipsilateral hemisphere, but the up-regulation did not reach significance by day 7. Alternately, the contralateral hemisphere displayed a significant decrease in activity by day 3. These results give conclusive evidence that the contralateral hemisphere is NOT an appropriate internal control and imply that NOS and COX inhibitors may prove to be efficacious for a much longer therapeutic window than current treatments. However, the delayed induction of COX activity may also indicate that this enzyme has a finite therapeutic window, as it may also stimulate remodelling of surviving neural networks. The prolonged up-regulation of inflammatory mediators implies that there may be an induction of an autoimmune component to the response. Therefore, the thymus (T) lymphocyte activation was quantified up to 14 days post-stroke. Cluster of differentiation (CD) 3⁺ T lymphocytes (equally contributed to by CD4⁺ and CD8⁺ T cells) exhibited a significant and sustained up-regulation in the infarcted region from day 3 up to at least day 14 post-ischaemia. Quantitative analysis of all cells present post-stroke determined that immune cells make up an average of 73% of all cells present in the 'peak' ischaemic areas. The CD4⁺ T helper cell response was delineated by double immunohistochemical labelling. Interferon-γ positively labelled with CD4⁺ T cells at days 3, 7 and 14 post-insult detailing a Th1-driven pro-inflammatory response. This evidence indicates that the autoimmune response is critical post-ischaemia and that it may be highly susceptible to modification by anti-inflammatory therapeutic intervention.
The primary downstream effect of the pro-inflammatory/immune cascade is apoptosis. The main organelle responsible for the 'go, no go' response to apoptotic factors is the mitochondria. In order to distinguish whether mitochondrial dysfunction was initiated shortly after ischaemia induction or if it was delayed, like the inflammatory/immune response, to a clinically relevant window, the temporal profile of mitochondrial complex inactivation was studied. It was found that mitochondrial membrane viability was impaired by day 3, followed by a significant decrease in respiratory complex activation and an increase in tissue injury by oxidative stress by 7 days post-ischaemia. These results indicate that targeting the early decrease in membrane viability or mitochondrial permeability transition pore opening combined with anti-apoptotic therapeutics, may attenuate the proceeding mitochondrial impairment in oxidative phosphorylation, reactive oxygen species generation and subsequent cell death cascades. The current investigations into the temporal profile and quantitative contributions of the inflammatory, immune and apoptotic mechanisms post-stroke highlight potential strategies for modulation by acute stroke therapeutics. Furthermore, the general knowledge amassed from these studies dictates the necessity of a new approach to therapeutic intervention. The acknowledgement of so many contributing systems suggests that in addition to a thrombolytic, a combination therapy involving multiple neuroprotectants should be employed to account for the multifaceted nature of the sequelae of ischaemic stroke.
8
Pütz, Volker, Matthias Weise, Rüdiger von Kummer i Georg Gahn. "Effective Treatment with Abciximab for Consecutive Bilateral Middle Cerebral Artery Occlusion". Saechsische Landesbibliothek- Staats- und Universitaetsbibliothek Dresden, 2014. http://nbn-resolving.de/urn:nbn:de:bsz:14-qucosa-135290.
Pełny tekst źródła
9
Pütz, Volker, Matthias Weise, Rüdiger von Kummer i Georg Gahn. "Effective Treatment with Abciximab for Consecutive Bilateral Middle Cerebral Artery Occlusion". Karger, 2006. https://tud.qucosa.de/id/qucosa%3A27636.
Pełny tekst źródła
10
Brodin, Camille. "De la paillasse au lit du patient, surmonter les problèmes de translation dans le domaine de l'AVC ischémique Single- and two- chain tissue plasminogen activator treatment differentially influence cerebral recovery after stroke Single- and two- chain tissue plasminogen activator treatment differentially influence cerebral recovery after stroke Cerebral blood flow correlates with ischemic brain lesion only when Stroke occurs awake: a preclinical model to bypass the translational roadblocks to clinic". Thesis, Normandie, 2019. http://www.theses.fr/2019NORMC427.
Pełny tekst źródłaStreszczenie:
Les défauts de translation des études précliniques vers les essais cliniques dans le domaine des AVC ischémiques et l'échec des développements thérapeutiques pourraient être expliqués par trois aspects : (1) le manque de compréhension des mécanismes des deux formes de rtPA, le traitement pharmacologique de l'AVC; (2) le manque d'outils adaptés d'imagerie de perfusion chez le petit animal et (3) l'influence de l'anesthésie sur l’effet des traitements testés dans les modèles animaux.Le tPA utilisé en clinique (Actilyse®) est un mélange de deux formes de tPA: une forme chaîne simple (sc-rtPA) et une double chaîne (tc-rtPA). Malgré des activités fibrinolytiques similaires, ces deux formes de tPA exercent des fonctions cérébrales distinctes influençant différemment la récupération des patients. Ainsi, nous avons décidé d'étudier en détail dans un modèle murin d'AVC thromboembolique les mécanismes pouvant expliquer ces effets divergents. Nous avons confirmé ces observations à savoir que sc-rtPA est bénéfique lorsqu'il est perfusé tôt après le début de l'AVC, alors que le tc-rtPA est délétère en raison d'une altération de la barrière hémato-encéphalique.L'imagerie en temps réel de la perfusion de l'ensemble du cerveau est un atout pour les études cliniques et précliniques. L'émergence des ultrasons ultra-rapides a conduit au développement du Doppler ultra-rapide et de la Microscopie de Localisation à Ultrasons (ULM), deux méthodes avec différents profils de résolutions spatio-temporelles et une excellente sensibilité aux petits flux sanguins. Nous avons combiné ces deux méthodes pour fournir un suivi longitudinal en 3D de la perfusion cérébrale dans un modèle murin d’AVC thromboembolique avec fibrinolyse par rtPA. Nos données montrent que le FUS et l’ULM présentent un intérêt majeur pour le pronostic précoce de l'AVC ischémique et de la réponse au traitement, avec une corrélation étroite entre la reperfusion précoce à 2h et la récupération tissulaire à 24h.Enfin, l’anesthésie utilisée en laboratoire interfère sur la lésion ischémique et les effets des molécules thérapeutiques testées. Nous nous sommes affranchis de ces effets en développant un nouveau modèle d’AVC ischémique chez des souris totalement éveillées. Le débit sanguin cérébral régional a été suivi par laser Doppler avant, pendant et 45min après le début de l’AVC. Le traitement par rtPA (à 20 min) est bénéfique dans les modèles d’AVC vigile et anesthésié, mais l'anesthésie est associée à un manque de corrélation entre la recanalisation et les volumes de lésion post-ischémie. Nous testons actuellement une molécule neuroprotectrice, qui était prometteuse avant d’échouer lors des essais cliniques (NXY-059), afin d’évaluer la pertinence de ce modèle novateur d’AVC pour les futures études pharmacologiques. Dans l’ensemble, ce travail fournit un panel de données précliniques innovantes pour améliorer nos chances de translation en clinique, incluant un modèle pertinent d'AVC thromboembolique chez des animaux vigiles et une méthode d'imagerie du pronostic précoce de réponse aux traitements vasculairesThe lack of translation between preclinical studies and clinical trials in the field of ischemic stroke and the failure of therapeutic developments could be explained by three aspects: (1) the lack of understanding the mechanism of the two forms of tPA, the pharmacological treatment in stroke; (2) the lack of optimized perfusion imaging tools for small animal and (3) the influence of anesthesia on treatment tested in animal models.tPA used in the clinical setting (Actilyse®) is a mix of two forms of tPA: single chain form (sc-rtPA) and two chains form (tc-rtPA). Despite similar fibrinolytic activities, these two forms exert distinct brain functions therefore influencing differentially the outcome patients. We then decided to further investigate in a relevant model of thromboembolic stroke in rodents, the mechanisms that can explain these differential effects. Here, we have confirmed differential outcomes of the two forms: whereas sc-rtPA is clearly beneficial when infused shortly after stroke onset, tc-rtPA is deleterious due to an increased alteration of the blood brain barrier integrity.Live imaging of cerebral perfusion of the whole brain is an asset for both clinical and preclinical studies. The emergence of ultrafast ultrasound led to the development of ultrafast Doppler (fUS) and Ultrasound Localization Microscopy (ULM), two methods with different sets of spatio-temporal resolutions and excellent sensitivity to small blood flows. We combined these two methods to provide a longitudinal monitoring of whole brain perfusion using the thromboembolic stroke model in mice with rtPA-induced reperfusion. Our data show that fUS and ULM are of major interest for early prognosis of ischemic stroke and response to treatment, with a tight correlation between early reperfusion at 2h and tissue recovery at 24h. Finally, we develop a relevant awake ischemic stroke model to test new therapies, avoiding interferences due to anesthesia commonly used during in vivo studies mice. The patern of the MCA was followed using Laser Doppler monitoring before, during and 45 min after the stroke onset. Although rtPA treatment is beneficial in both awake and anesthetized stroke models, anesthesia is associated with a lack of correlation between recanalization and stroke outcome. We are now testing a neuroprotective molecule, which was promising before failing in clinical trials (NXY-059), to assess the relevance of this innovative stroke model for future pharmacological studies. Altogether, we provide here a set of innovative pre-clinical data to improve our chance of translation to clinic, including a relevant model of thromboembolic stroke in awake animals and an early prognosis imaging method of response to vascular treatments
Książki na temat "Cerebral ischemia – Treatment"
1
Treatment of cerebral infarction: Experimental and clinical study. Wien: Springer-Verlag, 1987.
Znajdź pełny tekst źródła
2
Noé, Battistini, red. Acute brain ischemia: Medical and surgical therapy. New York: Raven Press, 1986.
Znajdź pełny tekst źródła
3
1931-, Robertson James T., Nowak Thaddeus S i Princeton Conference on Cerebrovascular Disease (20th : 1996 : Memphis, Tenn.), red. Frontiers in cerebrovascular disease: Mechanisms, diagnosis, and treatment. Armonk, NY: Futura Pub. Co., 1998.
Znajdź pełny tekst źródła
4
M, Maier Carolina, i Steinberg Gary K, red. Hypothermia and cerebral ischemia: Mechanisms and clinical applications. Totowa, N.J: Humana Press, 2004.
Znajdź pełny tekst źródła
5
Eric, Kasner Scott, i Gorelick Philip B, red. Prevention and treatment of ischemic stroke. Philadelphia: Butterworth-Heinemann, 2004.
Znajdź pełny tekst źródła
6
1946-, Feuerstein Giora Z., red. Inflammation and stroke. Basel: Birkhäuser, 2001.
Znajdź pełny tekst źródła
7
M, Barnett Henry J., i Hachinski Vladimir, red. Cerebral ischemia: Treatment and prevention. Philadelphia: Saunders, 1992.
Znajdź pełny tekst źródła
8
Therapeutic Strategies In Cerebral Ischemia. Clinical Pub, 2011.
Znajdź pełny tekst źródła
9
R, Caplan Louis, red. Brain ischemia: From basic science to treatment. London: Springer-Verlag, 1994.
Znajdź pełny tekst źródła
10
(Editor), J. Bogousslavsky, D. Guez (Editor) i Jose Biller (Editor), red. Cerebral Ischemia: From Pathophysiology to Treatment - Journal: Cerebrovascular Diseases, Suppl. 1, 1991 (Cerebral Ischemia). S. Karger AG (Switzerland), 1991.
Znajdź pełny tekst źródłaCzęści książek na temat "Cerebral ischemia – Treatment"
1
Hacke, Werner, Herman J. Gelmers, Michael Hennerici i Günter Krämer. "Treatment and Prophylaxis". W Cerebral Ischemia, 189–222. Berlin, Heidelberg: Springer Berlin Heidelberg, 1991. http://dx.doi.org/10.1007/978-3-642-75548-4_6.
Pełny tekst źródła
2
Hayashi, Nariyuki, i Dalton W. Dietrich. "Global and Focal Cerebral Ischemia". W Brain Hypothermia Treatment, 7–8. Tokyo: Springer Japan, 2004. http://dx.doi.org/10.1007/978-4-431-53953-7_2.
Pełny tekst źródła
3
O’Brien, M. D. "Academic Hemianopia and the Treatment of Cerebrovascular Disease". W Cerebral Ischemia and Calcium, 3–6. Berlin, Heidelberg: Springer Berlin Heidelberg, 1989. http://dx.doi.org/10.1007/978-3-642-85863-5_1.
Pełny tekst źródła
4
Soyka, D. "Treatment of Acute Migraine Attacks with Intravenous Flunarizine". W Cerebral Ischemia and Calcium, 403–9. Berlin, Heidelberg: Springer Berlin Heidelberg, 1989. http://dx.doi.org/10.1007/978-3-642-85863-5_53.
Pełny tekst źródła
5
Meyer, J. S., J. Lotfi i M. Kobari. "Treatment of Migraine and Cluster Headache with Calcium Antagonists". W Cerebral Ischemia and Calcium, 410–18. Berlin, Heidelberg: Springer Berlin Heidelberg, 1989. http://dx.doi.org/10.1007/978-3-642-85863-5_54.
Pełny tekst źródła
6
Bowen, D. M., P. T. Francis, S. L. Lowe, M. N. Pangalos, A. W. Procter i J. E. Steele. "Alzheimer’s Disease: Role of Energy Metabolism and Treatment of Symptoms". W Cerebral Ischemia and Dementia, 87–93. Berlin, Heidelberg: Springer Berlin Heidelberg, 1991. http://dx.doi.org/10.1007/978-3-642-76208-6_11.
Pełny tekst źródła
7
Vorstrup, S., O. B. Paulson i A. Andersen. "CBF Decreases in Ischemic Areas After Calcium Antagonist Treatment in Acute Stroke". W Cerebral Ischemia and Calcium, 378–83. Berlin, Heidelberg: Springer Berlin Heidelberg, 1989. http://dx.doi.org/10.1007/978-3-642-85863-5_49.
Pełny tekst źródła
8
Böker, D. K., i R. Wüllenweber. "Treatment of Symptomatic Cerebral Vasospasm After Subarachnoid Hemorrhage by Intraarterial Perfusion with Nimodipine". W Cerebral Ischemia and Calcium, 547–55. Berlin, Heidelberg: Springer Berlin Heidelberg, 1989. http://dx.doi.org/10.1007/978-3-642-85863-5_68.
Pełny tekst źródła
9
Teasdale, G. M., J. D. Pickard, G. Murray, R. Illingworth, M. D. M. Shaw, P. Foy, P. Humphrey i in. "Treatment of Subarachnoid Hemorrhage with Oral Nimodipine: Preliminary Report of the British Aneurysm Trial". W Cerebral Ischemia and Calcium, 563–67. Berlin, Heidelberg: Springer Berlin Heidelberg, 1989. http://dx.doi.org/10.1007/978-3-642-85863-5_70.
Pełny tekst źródła
10
Yenari, Midori A., David C. Tong i Gregory W. Albers. "Glycine Antagonists for Treatment of Ischemic Brain Injury". W Clinical Pharmacology of Cerebral Ischemia, 127–51. Totowa, NJ: Humana Press, 1997. http://dx.doi.org/10.1007/978-1-59259-472-6_6.
Pełny tekst źródłaStreszczenia konferencji na temat "Cerebral ischemia – Treatment"
1
Киреева, Виктория, Viktoriya Kireeva, Ю. Усольцев, Yu Usolcev, Ж. Капустенская, Zh Kapustenskaya, Е. Кожевникова i in. "Intermediate results 2016 of a search study of translational diagnostic methods Mitochondrial dysfunction in patients with chronic myocardial ischemia and/or head Brain". W Topical issues of translational medicine: a collection of articles dedicated to the 5th anniversary of the day The creation of a department for biomedical research and technology of the Irkutsk Scientific Center Siberian Branch of RAS. Москва: INFRA-M Academic Publishing LLC., 2017. http://dx.doi.org/10.12737/conferencearticle_58be81ec94893.
Pełny tekst źródłaStreszczenie:
Purpose of the study. To rate prognostic properties of changes in mitochondrial DNA concentration in the blood plasma of patients with chronic cerebral ischemia and ischemic heart disease in relation to the disease and the effectiveness of the therapy. Materials and methods. The study involved patients suffering from coronary heart disease (CHD) and chronic cerebral ischemia (CCI) with stable and unstable atherosclerotic plaques, who have signed informed consent to the data processing within the framework of scientific research. The patients were admitted to the hospital for examination and treatment of CHD and CCI in Cardiology and Neurology Unit of the Hospital of ISC SB RAS. The subjects underwent laboratory and instrumental examination and analysis of the level of free circulating serum mitochondrial DNA by real-time PCR (copies/ml). The examination results considered as satisfactory were compared with the mtDNA levels before and after the treatment. Results. The average value of the mtDNA levels before and after the treatment in patients of neurological and cardiological profile were significantly different: 1 093 686 copies/ml vs 418 046 copies/ml, respectively (p = 0.02). Unlike women, men mtDNA levels statistically significantly (p = 0.03) decreased after the treatment. We revealed statistically significant differences in mtDNA level indicators before and after the treatment, depending on the definition of the series (p = 0.0010) for rank test Kruskal – Wallis test. The results of the proposed research will help to identify prognostic factors of destabilization of cell damage and plaques in endothelial dysfunction, atherosclerosis and its complications, to conduct clinical test of the method for predicting and diagnostics of cellular damage in chronic ischemia on a background of atherosclerosis.
2
Zhu, Liang, i Axel J. Rosengart. "Cooling Penetration Surrounding an Intra-Parenchymal Cooling Probe in Hypothermia Treatment for Ischemia or Head Injury Patients: Theoretical Analyses". W ASME 2004 International Mechanical Engineering Congress and Exposition. ASMEDC, 2004. http://dx.doi.org/10.1115/imece2004-61109.
Pełny tekst źródłaStreszczenie:
Inducing hypothermia to brain tissue after brain ischemia or head injury has been demonstrated beneficial to the patients. Clinical studies have shown that even 1 or 2°C temperature reduction in brain tissue can be protective [Dietrich 1992]. On the contrary, fever-induced hyperthermia can worsen the neurological outcome in an animal model after cerebral ischemia. It is of clinical importance to understand the temperature distribution in brain during brain hypothermia.
3
Sazonova, O. B., i E. M. Troshina. "REFLECTION IN THE EEG OF DISORDERS OF CEREBRAL HEMODYNAMICS IN CHRONIC CEREBRAL ISCHEMIA IN CHILDREN". W NOVEL TECHNOLOGIES IN MEDICINE, BIOLOGY, PHARMACOLOGY AND ECOLOGY. Institute of information technology, 2022. http://dx.doi.org/10.47501/978-5-6044060-2-1.368-375.
Pełny tekst źródłaStreszczenie:
The paper presents the results of a study of the bioelectrical activity of the brain in 77 patients aged 2 to 18 years old with chronic cerebral ischemia, due to pathology of the main arteries of the brain, observed and operated in the Institute of Neurosurgery of N.N. Burdenko from 2012. The study showed the role of EEG in assessing the functional state of the brain in chil-dren with chronic cerebrovascular insufficiency of various etiopathogenesis in children, de-pending on the age of the child. Comparison of EEG data in extra- and intracranial cerebral vascular pathology was performed. Revealed more pronounced changes with steno-occlusive disorders in the intracranial arteries. EEG is dominated by slow forms of activity or their combination with acute potentials. Extracranial pathology led to the predominance of signs of irritation in the bioelectric picture of the brain: accelerated, pointed alpha rhythm, acute potentials, frequent fluctuations. Detailed clinical and neurophysiological examination using EEG served as a rationale for diagnosis, determination of treatment tactics and indications and contraindications for surgical intervention.
4
Silva, Tibério Alves da, Ana Carolina Soares de Lira, Bárbara Letícia Barreto Ramos Aragão i Luciana Karla, Dayanna Grazielle Maia Viana. "Carotid endarterectomy as the treatment of choice for clearing the internal carotid artery in transitional ischemic attacks". W XIII Congresso Paulista de Neurologia. Zeppelini Editorial e Comunicação, 2021. http://dx.doi.org/10.5327/1516-3180.303.
Pełny tekst źródłaStreszczenie:
Introduction: TIAs are ischemia, caused by stenosis of the carotid and vertebral arteries. Those who have a TIA are at risk of ischemic stroke and myocardial infarction, with carotid endarterectomy being an intervention. Objective: To analyze the benefits of carotid endarterectomy using drugs. Methods: Literature review, in bases such as PUBMED, MEDLINE, descriptors: “Endarterectomy”, “Ischemic Attack”, with operator “AND” and “OR”. Those with two descriptors were selected in the summary and date between 2010-2020, English / Portuguese language, resulting in: 17 articles. Results: The internal carotid artery (ICA) is located in the neck as a branch of the common carotid artery, being one of its branches the middle cerebral artery (MCA), the main artery affected in strokes and TIAs. Thus, ACI ischemia causes a risk of thrombosis in MCA, the treatment of carotid stenosis requires drugs to prevent atheroma, as well as antiplatelet drugs to reduce embolic events¹. In some cases, carotid endarterectomy or carotid stent implantation is complementary. Therefore, patients with TIA or stroke, who have “transient, fluctuating or persistent unilateral motor weakness or speech disorder or eye symptoms”, should undergo endarterectomy if they have moderate-severe stenosis of the extracranial internal carotid artery in the first days of presentation². Thus, endarterectomy is the treatment of choice and stenting should only be offered to symptomatic patients. Conclusion: Therefore, endarterectomy has been shown to be safe for patients with internal carotid artery stenosis, indicating the prevalence in relation to the stent.
5
Pastorio, Indianara Keila, Nayara Christina de Lima Curti, Francine de Paula Roberto Domingos, Sayuri Aparecida Hirayama, Lorena Dias Araújo, Rafael de Almeida, Marilia Pires de Sousa e. Silva i William de Souza Delfim. "Post-traumatic vertebral artery dissection". W XIII Congresso Paulista de Neurologia. Zeppelini Editorial e Comunicação, 2021. http://dx.doi.org/10.5327/1516-3180.515.
Pełny tekst źródłaStreszczenie:
Introduction: Vertebral artery dissections are responsible for 2% of all ischemic strokes and correspond to more than 25% of events in young adults. Its main etiologies, such as spontaneous and traumatic, which compromise the structural integrity of the arterial wall, allowing blood to accumulate between the layers of the vessel as an intramural hematoma, which can progress to stenosis or luminal occlusion in stroke. Case report: We attended a woman, 29 years old, who suffered a mild trauma in the cervical region during weight training in the gym presenting symptoms hours after the accident, a sudden headache of strong intensity irradiated to cervical, which evolves to a picture of cerebral ischemia characterized by changes in balance and coordination. The diagnosis was confirmed through complementary examinations of cranial tomography and angiotomography and treatment was composed by a combination of aspirin and clopidogrel with favorable evolution of the condition. Conclusion: The report illustrates that the change in cerebral circulation due to ischemia can occur either suddenly or even days after the injury, and it is likely that many cases classified as “spontaneous” without identifying the cause, may have been caused by minor trauma. In general, there is a good prognosis if early recognition and correct management.
6
Brandão, André Iglesias, Luiz Paulo Bastos Vasconcelos, Carolina de Almeida e. Silva, Raul de Barros Valente, Danilo Jorge da Silva, Pedro Ivo Machado Campos de Araujo Costa, Matheus Henrique Freitas Silva i in. "Brain Ischemia associated with COVID-19 and PFO - Case Report". W XIII Congresso Paulista de Neurologia. Zeppelini Editorial e Comunicação, 2021. http://dx.doi.org/10.5327/1516-3180.287.
Pełny tekst źródłaStreszczenie:
Context: COVID19 has better known respiratory impacts than cardiovascular1 and high D-dimer as the most significant coagulation parameter2 . Otherwise, paradoxical embolism due to Patent Foramen Ovale (PFO) and Ischaemic Cerebral Vascular Accident (iCVA) mechanisms associated are poorly documented3, 4 . We aimed to report an associated case of iCVA and PFO and highlight COVID19 hypercoagulability triggering thromboembolisms. Case report: CTT, 76y, female, hypertensive, former-smoker was hospitalized with right-hemiplegia, transcortical aphasia, dysarthria by iCVA and evolved with headache, odynophagia, fever, chills. RT-PCR-SARS-Cov2: positive; chestCT: 25% bilateral pulmonary involvement, ground-glass opacities. 8days later, was transferred to ICU-COVID-HU-UFJF; D-dimer=827. In 30days, went to ward with O2-dependent pulmonary sequelae; CT-angiography excluded Pulmonary Thromboembolism. Searched iCVA mechanism, ECO detected PFO=2.8mm and Interatrial Septum aneurysm. Prescribed anticoagulants. Subsequently, presented right-clonus, further previous RankinScale=5. Requested brain-MRI pointed lobar hemorrhage with mass effect in recent iCVA’s territory (left-Middle Cerebral Artery). After 10days, a head-CT evidenced partial resorption and reduced mass effect. Patient was discharged taking rivaroxabana. Conclusions: Retrospectively, we suspected that COVID19 hypercoagulability triggered Deep Vein Thrombosis and the consequent PFO paradoxical embolism, which caused iCVA. Therefore, vascular pathologies in COVID19 deserve further studies. Treatment for secondary prevention in iCVA by PFO is uncertain3 .
7
Strano, A., G. Davi, I. Catalano, G. Francavilla i A. Notarbartolo. "IS BETATHROMBOGLOBULIN (BTG) OF PROGNOSTIC VALUE IN PATIENTS WITH TRANSIENT CEREBRAL ISCHEMIA (TIA) ?" W XIth International Congress on Thrombosis and Haemostasis. Schattauer GmbH, 1987. http://dx.doi.org/10.1055/s-0038-1643055.
Pełny tekst źródłaStreszczenie:
TIA and stroke have for a long time been recognized as being associated with various abnormalities in platelet function.Plasma levels of BTG, a marker of platelet release reaction, have been found raised in TIA patients. However plasma measurements can be influenced by venipuncture or handling of the samples Therefore we measured urinary BTG levels and compared plasma and urinary levels of this protein in 18 patients with TIA and 18 controls of equivalent age (41-68 years) and sex.Plasma BTG levels were not different between TIA subjects (24.1 ± 8.6 ng/ml) and controls (20.2 ± 6.4 ng/ml). Urinary BTG levels were significantly different between TIA patients (0.72 ± 0.24 ng/ml) and controls (0.28 ± 0.09 ng/ml) and platelets from TIA patients were more sensitive to ADP than those from controls.After 6 months of ticlopidine administration urinary BTG levels in TIA patients fell to within normal ranges, plasma BTG values remained in the normal range and the the AC50 for ADP was significantly increased.We conclude that only urinary BTG levels may have diagnostic usefulness to evaluate a slight but continous platelet activation of circulating platelets, for istance, by ulcerated plaques in cranial arteries. The interpretation of elevated plasma BTG levels is hampered by the influence of the blood sampling technique which may give rise to false high levels due to platelet release during or after blood sampling. Urinary BTG levels provide a means for following the effects of therapy.In 4 patients,in whom ischemic attacks occured during the course of treatment, urinary and plasma BTG were not higher than in subjects in whom no further events occured. Therefore our data suggest that measurements of urinary and plasma BTG values have no prognostic value in TIA patients.
8
Signorelli, C. D., A. Giaquinta, G. Iofrida, G. Donato, Fr Signorelli, C. Bellecci, T. Lo Feudo, P. Gaudio i M. Gelfusa. "Surgical treatment of cerebral ischemia by means of diode laser: first experimental results and comparison with theoretical model." W European Conference on Biomedical Optics. Washington, D.C.: OSA, 2007. http://dx.doi.org/10.1364/ecbo.2007.6632_7.
Pełny tekst źródła
9
Signorelli, C. D., A. Giaquinta, G. Iofrida, G. Donato, Fr Signorelli, C. Bellecci, T. Lo Feudo, P. Gaudio i M. Gelfusa. "Surgical treatment of cerebral ischemia by means of diode laser: first experimental results and comparison with theoretical model". W European Conference on Biomedical Optics, redaktor Alfred Vogel. SPIE, 2007. http://dx.doi.org/10.1117/12.728256.
Pełny tekst źródła
10
Depieri, Lorena Dellagnesi, i Lorena Souza Viana. "Case report: Intracranial Arterial Dolichoectasia". W XIII Congresso Paulista de Neurologia. Zeppelini Editorial e Comunicação, 2021. http://dx.doi.org/10.5327/1516-3180.739.
Pełny tekst źródłaStreszczenie:
Introduction: Intracranial arterial dolichoectasia (IADE) is a diameter increase and/ or a long and tortuous path in one or more Intracranial arterial. Most patients keep asymptomatic and eventually present neurological complications (ischemia, bleeding or compression of adjacent structures). At around 12% of the patients with stroke present this kind of intracranial dilated, which 80% are in the posterior cerebral circulation, mainly in basilar artery. Objective: Report an unusual case of IADE refractory to the clinical treatment. Method: The information was obtained by reviewing the medical record, after the patient’s consent. Result: Patient, 51, male, hypertensive and dyslipidemic, with abdominal aortic aneurysm surgery and an incidental diagnosis in 2015 of fusiform basilar artery aneurysm, presented in March 2020 after cervical flexion, dysarthria, horizontal diplopia when looking to the right and ptosis to the left. The computed cranial angiotomography showed a basilar artery of 1.8 cm diameter fusiform aneurysm, compressing the pons and medulla oblongata, with no signs of ischemia or bleeding. He was discharged from hospital with clopidogrel without deficits, however, after 30 days, manifested a new focal neurological deficit with spontaneous remission. During the investigation a skull resonance was presented without ischemia, transcranial doppler with circulatory delay and without embolization. In view of the recurrence, an exchange in clopidogrel for ticagrelor was decided, which was kept stable for 30 days. Conclusion: IADE may be an incidental finding or even a life-threatening illness. Thus, these cases remain a major challenge in clinical practice and in interventional radiology.
Raporty organizacyjne na temat "Cerebral ischemia – Treatment"
1
Wu, Xiaoqi, Maoxia Fan, Yaobo Pan i Dona Guo. Quality of Evidence Supporting the Effects of Ginkgo Terpene Lactone Preparations in Ischemic Stroke: An Overview of Systematic Reviews and Meta-Analyses. INPLASY - International Platform of Registered Systematic Review and Meta-analysis Protocols, wrzesień 2022. http://dx.doi.org/10.37766/inplasy2022.9.0124.
Pełny tekst źródłaStreszczenie:
Review question / Objective: 2.2.1 Type of studies SRs/MAs of Randomized Controlled Trials (RCTs) of GTLP for IS in any language. 2.2.2 Type of Participants Included patients were diagnosed with IS according to international or national standards, regardless of race, age, gender, time of onset, and source of cases. 2.2.3 Type of Intervention The intervention method in the control group was routine treatment, and the intervention method in the intervention group was GTLP treatment or GTLP combined with the treatment of the control group. 2.2.4 Types of outcomes Conclusions at least need to include clinical efficacy analysis and National Institute of Health Stroke Scale (NIHSS). Condition being studied: Stroke is the second leading cause of death and third leading cause of disability globally.Among them, ischemic stroke (IS) accounts for 70% of all stroke types. It is a central nervous system disease caused by cerebral blood circulation disorder, ischemia and hypoxia .The incidence rate is high and increasing year by year, the age of onset is younger, the disability rate is high, and most patients have different degrees of limb motor dysfunction.In order to reduce the burden of stroke on the society and the patient's family, many articles proposed to strengthen the primary stroke prevention - behavior change and drug intervention.
2
Yu, Beibei, Yongfeng Zhang i Shouping Gong. Effects of miRNA-modified exosomes alleviate cerebral ischemic reperfusion injury in Pre-clinical Studies: A Meta-analysis. INPLASY - International Platform of Registered Systematic Review and Meta-analysis Protocols, maj 2022. http://dx.doi.org/10.37766/inplasy2022.5.0062.
Pełny tekst źródłaStreszczenie:
Review question / Objective: The purpose of this study was to investigate the effect of miRNA-modified exosomes in alleviating cerebral ischemic reperfusion injury compared with the non-treatment group. The research object is an animal model of middle cerebral artery occlusion. The research method is a controlled study. The primary outcome of this study was infarct volume, and the secondary outcome was neurobehavioral performance. Main outcome(s): The primary outcome of this study was Infarct volumes，which was measured by 2,3,5-triphenyltetranzolium chloride (TTC) staining. And it was calculated as followed: Infarct volume % = lesion area of each section = (contralateral hemisphere area/ipsilateral hemisphere area) × ipsilateral lesion area. Neurobehavioral performance was the secondary outcome, and was assessed by three scoring scales: modified neurological severity score (mNSS), Longa scoring system and neurological deficit score (NDS).