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Relevant bibliographies by topics / Cerebral ischemia

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Academic literature on the topic 'Cerebral ischemia'

Author: Grafiati

Published: 4 June 2021

Last updated: 30 July 2024

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Journal articles on the topic "Cerebral ischemia"

1

Zhao, Ling, Qiwei Liao, Yueting Zhang, Shufen Tan, Shuqing Li, and Tingyu Ke. "Ischemic Postconditioning Mitigates Retinopathy in Tree Shrews with Diabetic Cerebral Ischemia." Journal of Diabetes Research 2020 (February 12, 2020): 1–10. http://dx.doi.org/10.1155/2020/6286571.

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Ischemic postconditioning (PC) is proved to efficiently protect diabetic patients with acute myocardial infarction from ischemia-reperfusion injury. We aimed to explore the protective roles of ischemic PC on diabetic retinopathy in tree shrews with diabetic cerebral ischemia. A diabetic tree shrew model was established through high-fat diet feeding combined with streptozotocin (STZ) injection, while cortical thrombotic cerebral ischemia was induced photochemically. Tree shrews were divided into the normal control group, sham operation group, diabetes mellitus group, diabetes mellitus+cerebral ischemia group, and diabetes mellitus+cerebral ischemia+PC group (in which the tree shrews with diabetic cerebral ischemia were treated with ischemic PC). H&E staining was used to examine the pathological changes in the retina, and immunohistochemistry was performed to determine the retinal expression of VEGF (vascular endothelial growth factor). The modeling resulted in 77% tree shrews with diabetes. Ischemic PC reduced the blood glucose levels in the tree shrews with diabetic cerebral ischemia. Tree shrews with diabetes had thinned retina with disordered structures, and these pathological changes were aggravated after cerebral ischemia. The retinopathy was alleviated after ischemic PC. Retina expression of VEGF was mainly distributed in the ganglion cell layer in tree shrews. Diabetes and cerebral ischemia increased retinal VEGF expression in a step-wise manner, while additional ischemic PC reduced retinal VEGF expression. Therefore, ischemic PC effectively alleviates retinopathy in tree shrews with diabetic cerebral ischemia, and this effect is associated with reduced retinal VEGF expression.

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Kanazawa, Masato, Tetsuya Takahashi, Masanori Ishikawa, Osamu Onodera, Takayoshi Shimohata, and Gregory J. del Zoppo. "Angiogenesis in the ischemic core: A potential treatment target?" Journal of Cerebral Blood Flow & Metabolism 39, no. 5 (March 6, 2019): 753–69. http://dx.doi.org/10.1177/0271678x19834158.

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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.

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Wang, Lei, Xu Zhang, Xiaoxing Xiong, Hua Zhu, Ran Chen, Shudi Zhang, Gang Chen, and Zhihong Jian. "Nrf2 Regulates Oxidative Stress and Its Role in Cerebral Ischemic Stroke." Antioxidants 11, no. 12 (November 30, 2022): 2377. http://dx.doi.org/10.3390/antiox11122377.

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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.

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Danilova, T. V. "Features of epilepsy in acute and chronic cerebral ischemia." Kazan medical journal 98, no. 6 (December 15, 2017): 877–83. http://dx.doi.org/10.17750/kmj2017-877.

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Aim. To study clinical features, functional and neuroimaging characteristics of the brain of patients with ischemic brain disease and epileptic seizures. Methods. 772 patients with acute and chronic cerebral ischemia (265 stroke patients with epileptic seizures and 174 patients with seizures on the background of chronic cerebral ischemia, and 203 patients with stroke and 130 patients with chronic cerebral ischemia without seizures) were comprehensively examined. The clinical neurological examination, electroencephalography, magnetic resonance imaging, ultrasound duplex scanning of extra- and intracranial arteries with the assessment of the level and degree of stenosis and cerebrovascular reactivity were carried out. Results. Focal seizures prevailed in patients with cerebral ischemia. In patients with epileptic seizures on the background of both ischemic stroke and chronic cerebral ischemia cortical localization of ischemic foci prevailed. Early epileptic seizures in patients with ischemic stroke developed with significantly more frequent localization of ischemic focus in the right hemisphere with the orientation vector of neuroimaging formation of the ischemic lesion in the caudal direction. In patients with chronic cerebral ischemia with epileptic seizures, along with frequent lesion of the cortex, more frequent damage of white matter of the brain was observed. In patients with acute and chronic ischemia of the brain with epileptic seizures, a higher incidence of stenosis of major arteries and predominance of impaired cerebrovascular reactivity in posterior cerebral circulation system were established. Conclusion. Multimodal examination of patients with acute and chronic cerebral ischemia allowed forming risk groups for epileptic seizures.

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Yamamoto, Kazumi, Fumiharu Akai, Toshiki Yoshimine, and Takehiko Yanagihara. "Immunohistochemical investigation of cerebral ischemia after middle cerebral artery occlusion in gerbils." Journal of Neurosurgery 67, no. 3 (September 1987): 414–20. http://dx.doi.org/10.3171/jns.1987.67.3.0414.

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✓ Progression and recovery of ischemic and postischemic damage after occlusion of the middle cerebral artery and subsequent reperfusion were investigated in the gerbil. This study was performed by immunohistochemical reaction testing for tubulin and creatine kinase BB-isoenzyme to visualize the neuronal structure and by immunohistochemical reaction testing for astroprotein (an astrocyte-specific protein) to visualize reactive astrocytes. The earliest ischemic lesion became visible in the frontoparietal cortex after 7 minutes of ischemia as a laminar loss of the reaction for tubulin involving the neuropil, neuronal perikarya, and dendrites. The earliest lesion in the caudoputamen evolved after 30 minutes of ischemia. After reestablishment of cerebral circulation, the immunohistochemical ischemic lesions in the neuronal structure disappeared if the ischemic period was 10 minutes or less and partially disappeared even after ischemia for 15 minutes in the cerebral cortex, while the postischemic lesion in the caudoputamen disappeared even after ischemia for 15 minutes. Reactive astrocytes were detected in the cerebral cortex and caudoputamen as early as 24 hours after reperfusion, both in the areas with and without the neuronal lesions. No lesion was identified in the hippocampus or thalamus. This experimental model is suitable for investigation of rapidly progressive regional ischemia in the cerebral cortex and for comparison with other regional or global cerebral ischemia in the gerbil or other animal species.

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Duarte, Sinésio Grace, Antônio Dorival Campos, and Benedicto Oscar Colli. "Functional evaluation of temporary focal cerebral ischemia: experimental model." Arquivos de Neuro-Psiquiatria 61, no. 3B (September 2003): 751–56. http://dx.doi.org/10.1590/s0004-282x2003000500009.

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OBJECTIVE: Despite cerebral ischemia being a frequent clinical pathologic state, the tolerance of neural tissue to oxygen absence and to reperfusion is controversial. This study aims to evaluate the effects of focal cerebral ischemia/reperfusion, by analyzing the mitochondrial respiration. METHOD: Sixty-four adult rats underwent focal cerebral ischemia by middle cerebral artery occlusion, during 15, 30 and 60 minutes, followed by 10 minutes or 19 hours of reperfusion. The effects of ischemia were analyzed measuring the O2 consumption by mitochondria in the ischemic and non-ischemic areas. RESULTS: There was compromise of the mitochondrial respiration after 30 and 60 minutes of ischemia, followed by 10 minutes of reperfusion but there was no alteration in this function after 19 hours of reperfusion. CONCLUSION: Compromise of the mitochondrial function occurred after 30 minutes of ischemia but, until one hour of ischemia, if the reperfusion was prolonged there was no evidence of ischemic/reperfusion injuries.

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Dong, Chao, Jiawei Li, Ming Zhao, Lin Chen, Xiaochen Zhai, Lingling Song, Jin Zhao, Qiang Sun, Jie Wu, and Xiaolu Xie. "Pharmacological Effect of Panax notoginseng Saponins on Cerebral Ischemia in Animal Models." BioMed Research International 2022 (August 4, 2022): 1–12. http://dx.doi.org/10.1155/2022/4281483.

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Panax notoginseng saponins (PNS), bioactive compounds, are commonly used to treat ischemic heart and cerebral diseases in China and other Asian countries. Most previous studies of PNS have focused on the mechanisms underlying their treatment of ischemic cardiovascular diseases but not cerebral ischemic diseases. This study sought to explore the pharmacological mechanisms underlying the effectiveness of PNS in treating cerebral ischemic diseases. Different experimental cerebral ischemia models (including middle cerebral artery occlusion (MCAO) and the blockade of four arteries in rats, collagen-adrenaline-induced systemic intravascular thrombosis in mice, thrombosis of carotid artery-jugular vein blood flow in the bypass of rats, and hypoxia tolerance in mice) were used to investigate the mechanisms underlying the actions of PNS on cerebral ischemia. The results indicated that (1) PNS improved neurological function and reduced the cerebral ischemia infraction area in MCAO rats; (2) PNS improved motor coordination function in rats with complete cerebral ischemia (blockade of four arteries), decreased Ca2+ levels, and ameliorated energy metabolism in the brains of ischemia rats; (3) PNS reduced thrombosis in common carotid artery-jugular vein blood flow in the bypass of rats; (4) PNS provided significant promise in antistroke hemiplegia and hypoxia tolerance in mice. In conclusion, PNS showed antagonistic effects on ischemic stroke, and pharmacological mechanisms are likely to be associated with the reduction of cerebral pathological damage, thrombolysis, antihypoxia, and improvement in the intracellular Ca2+ overload and cerebral energy metabolism.

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Han, Xue Mei, Hong Tao Wei, and Song Yan Liu. "Involvement of Erythropoietin Expression in Acupuncture Preconditioning-Induced Ischemic Tolerance." Advanced Materials Research 554-556 (July 2012): 1650–55. http://dx.doi.org/10.4028/www.scientific.net/amr.554-556.1650.

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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.

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Zeng, Xian-Si, Wen-Shuo Geng, Lei Chen, and Jin-Jing Jia. "Thioredoxin as a Therapeutic Target in Cerebral Ischemia." Current Pharmaceutical Design 24, no. 25 (November 8, 2018): 2986–92. http://dx.doi.org/10.2174/1381612824666180820143853.

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Background: Cerebral ischemia is a common cause of disability and death. Ischemic brain injury results from complex pathological processes, including oxidative stress, inflammation, and apoptosis. Thioredoxin( Trx) is an important multifunctional protein, which regulates cellular redox status. Increasing studies have demonstrated that Trx provides a neuroprotective role against cerebral ischemia-induced injury. Methods: A systematic search of PMC and the PubMed Database was conducted to summarize the protective effects of Trx against cerebral ischemia. Results: This article reviews the understanding of potential effects and mechanisms of Trx against cerebral ischemia, including the anti-oxidant, anti-apoptotic and anti-inflammatory effects, as well as the activation of prosurvival pathway. We also summarize that some natural compounds induce the expression of Trx, which is involved in their anti-ischemic effects. Conclusion: In conclusion, Trx has a potential neuroprotection in cerebral ischemia and may be very promising for clinical therapy of ischemic stroke in the future.

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Lee, Choong-Hyun, Tae-Kyeong Lee, Dae Won Kim, Soon Sung Lim, Il Jun Kang, Ji Hyeon Ahn, Joon Ha Park, et al. "Relationship between Neuronal Damage/Death and Astrogliosis in the Cerebral Motor Cortex of Gerbil Models of Mild and Severe Ischemia and Reperfusion Injury." International Journal of Molecular Sciences 23, no. 9 (May 3, 2022): 5096. http://dx.doi.org/10.3390/ijms23095096.

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Neuronal loss (death) occurs selectively in vulnerable brain regions after ischemic insults. Astrogliosis is accompanied by neuronal death. It can change the molecular expression and morphology of astrocytes following ischemic insults. However, little is known about cerebral ischemia and reperfusion injury that can variously lead to damage of astrocytes according to the degree of ischemic injury, which is related to neuronal damage/death. Thus, the purpose of this study was to examine the relationship between damage to cortical neurons and astrocytes using gerbil models of mild and severe transient forebrain ischemia induced by blocking the blood supply to the forebrain for five or 15 min. Significant ischemia tFI-induced neuronal death occurred in the deep layers (layers V and VI) of the motor cortex: neuronal death occurred earlier and more severely in gerbils with severe ischemia than in gerbils with mild ischemia. Distinct astrogliosis was detected in layers V and VI. It gradually increased with time after both ischemiae. The astrogliosis was significantly higher in severe ischemia than in mild ischemia. The ischemia-induced increase of glial fibrillary acidic protein (GFAP; a maker of astrocyte) expression in severe ischemia was significantly higher than that in mild ischemia. However, GFAP-immunoreactive astrocytes were apparently damaged two days after both ischemiae. At five days after ischemiae, astrocyte endfeet around capillary endothelial cells were severely ruptured. They were more severely ruptured by severe ischemia than by mild ischemia. However, the number of astrocytes stained with S100 was significantly higher in severe ischemia than in mild ischemia. These results indicate that the degree of astrogliosis, including the disruption (loss) of astrocyte endfeet following ischemia and reperfusion in the forebrain, might depend on the severity of ischemia and that the degree of ischemia-induced neuronal damage may be associated with the degree of astrogliosis.

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Dissertations / Theses on the topic "Cerebral ischemia"

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Keasey, Matthew P. "MicroRNAs in Cerebral Ischemia." Thesis, University of Bristol, 2010. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.526014.

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Molnar, Maria. "Hyperglycemia in Experimental Cerebral Ischemia." Doctoral thesis, Uppsala universitet, Anestesiologi och intensivvård, 2015. http://urn.kb.se/resolve?urn=urn:nbn:se:uu:diva-247763.

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Cerebral ischemia is a life-threatening condition associated with a substantial morbidity and mortality. Hyperglycemia, a common coexisting phenomenon in both stroke and cardiac arrest (CA), may further aggravate ischemic brain injury. To date, the therapeutic possibilities are lim-ited and the search for new treatment modalities is warranted. One aspect of such a research could be to better understand the cerebral pathogenesis induced by hyperglycemic ischemia-reperfusion. We investigated the combination of ischemia and hyperglycemia in two experimental models of stroke and CA. The aims were to test the neuroprotective potential of the sulfonated nitrone 2-sulfophenyl-N-tert-butylnitrone (S-PBN) in focal hyperglycemic cerebral ischemia (1), to outline the short-terms effects of hyperglycemia in prolonged (2) and short CA (3) and to performed a global transcriptome analysis of brain from hyperglycemic and normoglycemic CA (4). In a stroke model rats were made hyperglycemic prior to transient middle cerebral artery oc-clusion and randomized to S-PBN or saline. We found that S-PBN may ameliorate hyperglyce-mic-ischemic brain damage by improving the neurological performance after 1 day of survival, but did not reduce the infarct size. To study the cerebral oxidative state and perfusion after CA, pigs were randomized and clamped at blood glucose levels of 8.5 ̶ 10.0 mmol/L (high) and 4.0 ̶ 5.5 mmol/L (normal), sub-jected to 12 ̶ min of CA, followed by 8 min of cardiopulmonary resuscitation (CPR), and ob-served for 180 min. Increased oxygenation was found at higher glucose levels measured by near-infrared light spec-troscopy after CA. Tendencies toward increased protein S100β and 15-keto-dihydro-prostaglandin F2α were observed in the hyperglycemic group. We hypothesized that in combination with a brief period of CA, the preischemic hyperglycemia would worsen the cerebral injury compared with normoglycemia. We used a glycemic protocol similar to that in Paper II, whereby pigs were subjected to 5 ̶ min of CA, followed by 8 min of CPR, and observed for 180 mins. An increased level of the cerebral marker S100β was found in hyperglycemic pigs compared with normoglycemic pigs after CA. Global transcriptome analysis using microarray analysis revealed a different early metabolic gene expression in hyperglycemic CA compared with normoglycemic CA.

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Christensen, Thomas. "Experimental focal cerebral ischemia : pathophysiology, metabolism and pharmacology of the ischemic penumbra /." Copenhagen, 2007. http://bvbr.bib-bvb.de:8991/F?func=service&doc_library=BVB01&doc_number=016143698&line_number=0001&func_code=DB_RECORDS&service_type=MEDIA.

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Thorén, Anna. "Astrocyte metabolism following focal cerebral ischemia /." Göteborg : Institute of Neuroscience and Physiology, The Sahlgrenska Academy, Göteborg University, 2006. http://hdl.handle.net/2077/744.

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Thomas, Sunu Samuel. "Murine models of cerebral ischemia, development of a mouse model of global cerebral ischemia; response of GluR2 knockout mice in a model of permanent focal cerebral ischemia." Thesis, National Library of Canada = Bibliothèque nationale du Canada, 2000. http://www.collectionscanada.ca/obj/s4/f2/dsk1/tape2/PQDD_0026/MQ50439.pdf.

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Li, Yan. "Inhibitory synpatic transmission in striatal neurons after transient cerebral ischemia." Connect to resource online, 2009. http://hdl.handle.net/1805/2021.

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Thesis (Ph.D.)--Indiana University, 2009.
Title from screen (viewed on December 1, 2009). Department of Anatomy and Cell Biology, Indiana University-Purdue University Indianapolis (IUPUI). Advisor(s): Zao C. Xu, Feng C. Zhou, Charles R. Yang, Theodore R. Cummins. Includes vitae. Includes bibliographical references (leaves 115-135).

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Karelina, Ekaterina. "MECHANISMS OF SOCIAL NEUROPROTECTION AFTER CEREBRAL ISCHEMIA." The Ohio State University, 2010. http://rave.ohiolink.edu/etdc/view?acc_num=osu1274922479.

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Adhami, Faisal. "Differential Adult and Neonatal Response to Cerebral Ischemia-Hypoxia." University of Cincinnati / OhioLINK, 2007. http://rave.ohiolink.edu/etdc/view?acc_num=ucin1196054266.

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Edrissi, Hamidreza. "Blood Brain Barrier Dysfunction in Chronic Cerebral Ischemia." Thesis, Université d'Ottawa / University of Ottawa, 2015. http://hdl.handle.net/10393/32531.

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Cerebral small vessel pathology is now known to be associated with the development of cognitive impairment and mild motor impairments such as gait disturbance in a variety of neurodegenerative diseases. This dissertation explores the hypothesis that blood brain barrier dysfunction is an early event in cerebral ischemia and contributes to the development of cerebral small vessel disease (CSVD). A common rodent model of CSVD is permanent bilateral common carotid artery occlusion in the rat. This model was used to study several aspects of the progression of CSVD including the timecourse of blood brain barrier permeability changes following the onset of ischemia, gait disturbance, the expression of tight junction proteins and cytokine expression. It was determined that BBB permeability was elevated for 2 weeks following BCCAO and ischemic rats displayed lower gait velocity. There was no change in expression of TJ proteins. However, ischemic rats had higher levels of some proinflammatory cytokines and chemokines in brain tissue with no obvious changes in plasma levels. The mechanisms underlying the increase in BBB permeability were studied in vitro using artificial barriers made of confluent rat brain microvascular endothelial cells. Cerebral ischemia has been reported to cause an increase in plasma toxicity, likely by elevating the numbers of circulating microparticles (MPs). MPs isolated from the plasma of ischemic rats were applied to artificial barriers where it was found that they act mainly as vectors of TNF-α signaling. MPs induce activation of caspase-3 and the Rho/Rho kinase pathways. It is concluded that most of the increase in barrier permeability is due to apoptosis and disassembly of actin cytoskeleton and disruption of adherens junctions IV and not an increase in transcellular transport. The effects of treatment with the type III phosphodiesterase inhibitor cilostazol on dye extravasation in the brain, glial activation, white matter damage and motor performance were evaluated. It was determined that cilostazol could improve the increased BBB permeability and gait disturbance and microglial activation in optic tract following BCCAO. Also, the effects of treatment with cilostazol on plasma toxicity in vivo (24h and 14d following BCCAO) and artificial barriers (in vitro) were assessed. It was found that cilostazol could reduce plasma toxicity at 24h and improve increased endothelial barrier permeability that is induced by MP treatment respectively. In summary BBB dysfunction occurs in the rat model of chronic cerebral hypoperfusion with no differences in expression of TJ proteins. There is a mild motor disturbance in the form of lower gait velocity following BCCAO. Cytokines released in brain tissue may be associated with pathological consequences following BCCAO while there is no significant difference in plasma levels and circulating MPs may play a role in BBB dysfunction.

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Ng, Kit-ying. "Neuroprotective effects of adiponectin in focal cerebral ischemia." Click to view the E-thesis via HKUTO, 2007. http://sunzi.lib.hku.hk/hkuto/record/B39634371.

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Books on the topic "Cerebral ischemia"

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Walz, Wolfgang. Cerebral Ischemia. New Jersey: Humana Press, 1999. http://dx.doi.org/10.1385/0896035409.

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Hacke, Werner, Herman J. Gelmers, Michael Hennerici, and Günter Krämer. Cerebral Ischemia. Berlin, Heidelberg: Springer Berlin Heidelberg, 1991. http://dx.doi.org/10.1007/978-3-642-75548-4.

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Walz, Wolfgang, ed. Cerebral Ischemia. Totowa, NJ: Humana Press, 1999. http://dx.doi.org/10.1007/978-1-59259-479-5.

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Maier, Carolina M., and Gary K. Steinberg. Hypothermia and Cerebral Ischemia. New Jersey: Humana Press, 2003. http://dx.doi.org/10.1385/1592596533.

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Hartmann, Alexander, and Wolfgang Kuschinsky, eds. Cerebral Ischemia and Hemorheology. Berlin, Heidelberg: Springer Berlin Heidelberg, 1987. http://dx.doi.org/10.1007/978-3-642-71787-1.

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Hartmann, Alexander, and Wolfgang Kuschinsky, eds. Cerebral Ischemia and Calcium. Berlin, Heidelberg: Springer Berlin Heidelberg, 1989. http://dx.doi.org/10.1007/978-3-642-85863-5.

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Hartmann, Alexander, Wolfgang Kuschinsky, and Siegfried Hoyer, eds. Cerebral Ischemia and Dementia. Berlin, Heidelberg: Springer Berlin Heidelberg, 1991. http://dx.doi.org/10.1007/978-3-642-76208-6.

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1943-, Hartmann A., Kuschinsky Wolfgang 1944-, and Hoyer S. 1933-, eds. Cerebral ischemia and dementia. Berlin: Springer-Verlag, 1991.

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A, Schurr, and Rigor Benjamin M, eds. Cerebral ischemia and resuscitation. Boca Raton: CRC Press, 1990.

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A, Hartmann, and Kuschinsky W, eds. Cerebral ischemia and hemorheology. Berlin: Springer-Verlag, 1987.

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Book chapters on the topic "Cerebral ischemia"

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Iadecola, Costantino. "Mechanisms of Cerebral Ischemic Damage." In Cerebral Ischemia, 3–32. Totowa, NJ: Humana Press, 1999. http://dx.doi.org/10.1007/978-1-59259-479-5_1.

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Kondo, Yoichi. "Activated and Phagocytic Microglia." In Cerebral Ischemia, 251–69. Totowa, NJ: Humana Press, 1999. http://dx.doi.org/10.1007/978-1-59259-479-5_10.

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Irwin, Anna, and Wolfgang Walz. "Spreading Depression Waves as Mediators of Secondary Injury and of Protective Mechanisms." In Cerebral Ischemia, 35–44. Totowa, NJ: Humana Press, 1999. http://dx.doi.org/10.1007/978-1-59259-479-5_2.

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Kimelberg, Harold K. "Cell Swelling in Cerebral Ischemia." In Cerebral Ischemia, 45–67. Totowa, NJ: Humana Press, 1999. http://dx.doi.org/10.1007/978-1-59259-479-5_3.

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Morley, Paul, Joseph S. Tauskela, and Antoine M. Hakim. "Calcium Overload." In Cerebral Ischemia, 69–104. Totowa, NJ: Humana Press, 1999. http://dx.doi.org/10.1007/978-1-59259-479-5_4.

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Chan, Pak H. "Oxygen Radicals." In Cerebral Ischemia, 105–23. Totowa, NJ: Humana Press, 1999. http://dx.doi.org/10.1007/978-1-59259-479-5_5.

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Bruce-Keller, Annadora J., and Mark P. Mattson. "Mechanisms of Neuroprotective Cytokines." In Cerebral Ischemia, 125–42. Totowa, NJ: Humana Press, 1999. http://dx.doi.org/10.1007/978-1-59259-479-5_6.

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Nowak, Thaddeus S., and Marika Kiessling. "Reprogramming of Gene Expression After Ischemia." In Cerebral Ischemia, 145–215. Totowa, NJ: Humana Press, 1999. http://dx.doi.org/10.1007/978-1-59259-479-5_7.

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Abe, Koji. "Neurons." In Cerebral Ischemia, 217–32. Totowa, NJ: Humana Press, 1999. http://dx.doi.org/10.1007/978-1-59259-479-5_8.

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Jabs, Ronald, Lane K. Bekar, and Wolfgang Walz. "Reactive Astrogliosis in the Injured and Postischemic Brain." In Cerebral Ischemia, 233–49. Totowa, NJ: Humana Press, 1999. http://dx.doi.org/10.1007/978-1-59259-479-5_9.

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Conference papers on the topic "Cerebral ischemia"

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Fisher, M., and R. Francis. "ALTERED COAGULATION IN CEREBRAL ISCHEMIA PATIENTS." In XIth International Congress on Thrombosis and Haemostasis. Schattauer GmbH, 1987. http://dx.doi.org/10.1055/s-0038-1644345.

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We investigated coagulation changes in a group of patients with cerebral ischemia, ranging from transient ischemic attacks to cerebral infarction. Patients were studied acutely (within 72 hours of onset of ischemia) and again approximately 2 months following the initial examination. We evaluated platelet activation, fibrin generation, and fibrinolysis by measuring plasma beta-thromboglobulin (BTG), fibrinopeptide A (FPA), and fibrinopeptide B-beta 1-42 (FPB), respectively. We compared measurements in cerebral ischemia patients with a group of age -and sex-matched neurological inpatients without vascular disease ("patient controls") and a similarly matched group of normal volunteers ("normal controls"). BTG levels for 90 patients studied acutely were not significantly different compared to 58 of the same patients studied 2 months later, 16.4 ± 11.3 ng/ml (mean ± SD) versus 17.5 ± 10.2 ng/ml. Both values were significantly increased (p< .05) compared to normal controls (12.2 ± 6.5 ng/ml, n = 44); patient controls (13.2 ± 7.6 ng/ml, n = 18) were not significantly different from normals. In contrast, FPA measurements were significantly increased in acute patients compared to normals (3.3 ± 5.8 versus 1.0 ± 1.7 ng/ml, p< .05) while FPA levels 2 months post-ischemia (0.6 ± 0.9 ng/ml) were no different than normals. FPB measurements were not significantly different among either acute patients (6.5 ± 2.4 pmol/ml) or patients 2 months post-ischemia (4.8 ± 1.5 pmol/ml) compared to normals (6.5 ± 1.8 pmol/ml).In summary, we have found, among cerebral ischemia patients, sustained increases in BTG, acute increases in FPA, and normal FPB. These findings are compatible with a model of cerebral ischemia consisting of acutely increased fibrin generation without concomitant increased fibrinolytic activity, superimposed on a background of increased platelet activation.

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Khodanovich, M. Yu, and A. A. Kisel. "Animal models of cerebral ischemia." In NEW OPERATIONAL TECHNOLOGIES (NEWOT’2015): Proceedings of the 5th International Scientific Conference «New Operational Technologies». AIP Publishing LLC, 2015. http://dx.doi.org/10.1063/1.4936032.

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Lee, Gija, Seokkeun Choi, Sungwook Kang, Samjin Choi, Jeonghoon Park, Dong Hyun Park, Youngho Park, Kyungsook Kim, Bermseok Oh, and Hunkuk Park. "Changes in Extracellular Glutamate Release on Repetitive Transient Occlusion in Global Ischemia Model." In ASME 2009 Summer Bioengineering Conference. American Society of Mechanical Engineers, 2009. http://dx.doi.org/10.1115/sbc2009-206602.

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During the operation, surgeons in neurosurgical area usually performed the multiple temporary occlusions of parental artery which may induce the neuronal damage. It is generally thought that neuronal damage by cerebral ischemia is associated with extracellular concentrations of the excitatory amino acids. In this experiment, we measured the dynamics of extracellular glutamate release in 11 vessel occlusion (VO) model during repeated within short interval. Changes in cerebral blood flow were monitored by laser-Doppler flowmetry simultaneously with cortical glutamate level measured by amperometric biosensor. During ischemia, the peak level of glutamate release was gradually decreased as 112.38±26.21 μM in first period, 82.63±18.50 μM in second period, and 48.58±11.89 μM in third period. The time interval between the ischemia induction and the beginning of glutamate release was increased as 106.7 ± 10.89 (sec) at first attack, 139.11 ± 3.87 (sec) in second attack, 169.00 ± 14.56 (sec) in third ischemic period. From the results of real-time monitoring about glutamate release in 11-VO model during repetitive ischemic episode, it was demonstrated that repetitive ischemia induced less glutamate release from neuronal cell than single ischemia due to endogeneous protective mechanism which delayed glutamate release time in later ischemic injury.

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Musienko, Julia I., and Natalia I. Nechipurenko. "Infrared laser hemotherap in cerebral ischemia modeling." In European Conference on Biomedical Optics. Washington, D.C.: OSA, 2003. http://dx.doi.org/10.1364/ecbo.2003.5142_200.

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Musienko, Julia I., and Natalia I. Nechipurenko. "Infrared laser hemotherapy in cerebral ischemia modeling." In European Conference on Biomedical Optics 2003, edited by Rudolf W. Steiner. SPIE, 2003. http://dx.doi.org/10.1117/12.501113.

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Ignatieva, Olga I., and Natalia G. Tokareva. "Cognitive impairments in patients with chronic cerebral ischemia." In Innovations in Medical Science and Education. Dela Press Publishing House, 2022. http://dx.doi.org/10.56199/dpcsms.utii3716.

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Cognitive impairments, such as memory and intelligence, attention and mental performance, usually suffer in diffuse brain damage, in particular in chronic cerebral ischemia. However, they can also occur in focal brain lesions, such as cerebral infarcts, reaching the degree of dementia. The aim of the study was to investigate the peculiarities of non-dementia cognitive disorders in patients with the consequences of cerebral infarction. We examined 30 patients with chronic cerebral ischemia with cerebral infarction at the age of 58-66 years (M=62.4) and a similar comparison group was chosen. The main results of the cognitive status assessment in patients with CHEM with suffered cerebral infarction showed a decrease in short-term visual and figurative memory, more so in men and with increasing age. There were also decreased productivity of attention, decreased level of abstract thinking, and weakened connection between logical thinking and attention, more pronounced in men and in the older age group. With a disease duration of more than 3 years, the volume of figurative memory and the abstract component of thinking decreased. The main conclusions are: cognitive disorders developing against the background of CIM worsen to a greater extent in men, in persons older than 60 years and in 3 years from the moment of cerebral infarction; short-term medication therapy has no significant effect on cognitive dysfunction, the significance of these results determines the need for long-term, at least 6 months, rehabilitative medication therapy.

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Palaniswamy, Sangeetha, Venkatapura Ramesh, Rita Christopher, and Dhananjaya Bhat. "A0022 Effect of Remote Ischemic Preconditioning on Cerebral Vasospasm and Biomarkers of Cerebral Ischemia in Aneurysmal Subarachnoid Hemorrhage." In 20th Annual Conference of Indian Society of Neuroanaesthesiology and Critical Care (ISNACC). Thieme Medical and Scientific Publishers Private Ltd., 2019. http://dx.doi.org/10.1055/s-0039-1684129.

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Soltanian-Zadeh, Hamid, Rabih Hammoud, Michael A. Jacobs, Suresh C. Patel, Panayiotis D. Mitsias, Mamatha Pasnoor, Robert Knight, Zhang G. Zheng, Mei Lu, and Michael Chopp. "Tissue characterization in cerebral ischemia using multiparameter MRI." In Medical Imaging 2001, edited by Chin-Tu Chen and Anne V. Clough. SPIE, 2001. http://dx.doi.org/10.1117/12.428162.

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Khodanovich, M. Yu. "Reparative neurogenesis after cerebral ischemia: Clinical application prospects." In NEW OPERATIONAL TECHNOLOGIES (NEWOT’2015): Proceedings of the 5th International Scientific Conference «New Operational Technologies». AIP Publishing LLC, 2015. http://dx.doi.org/10.1063/1.4935997.

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Monreal, M., E. Lafoz, M. Foz, and J. Monasterio. "ASPIRIN AND THE KIDNEY IN PATIENTS WITH CEREBRAL ISCHEMIA." In XIth International Congress on Thrombosis and Haemostasis. Schattauer GmbH, 1987. http://dx.doi.org/10.1055/s-0038-1644827.

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The acceptance of aspirin therapy for prevention of cerebral ischemia is based onpositive results of several large clinicaltrials, and the usual dose is 1000-1500 mg/day. Several recent reports emphasize the adverse effects of aspirin and other nonsteroidal anti-inflamatory agents on renal function. We examined wether two extreme doses of aspirin (60 mg vs 1200 mg/day) could alter renal function in patients recently admitted to hospital with cerebral ischemia. We studied 33 patients with cerebralischemia and no history of ingestion of aspirin nor other drugs two weeks prior to admission. During the first 5 days all patients received a 50 mEq sodium diet and no drugs, while during the second 5 days (trial) the patients were randomly assigned (double blind) to placebo, aspirin 20 mg or aspirin 400 mg, 3 times daily, with meals.Overall, body weight increased by 650 gin patients taking 1400 mg/day of aspirin (p≺0,01), but not in patients taking 60 mg/day. Also increases in systolic and diastolic blood pressure did not reach significant differences. While waiting morereports, aspirin at doses near 1000 mg should be administered cautiously in sodium restricted patients with cerebral ischemia.Acute water retention may be specially troublesome.

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Reports on the topic "Cerebral ischemia"

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Oeltgen, Peter R. Neuroprotective Effects of Opioid-Like Hibernation Factors in Cerebral Ischemia. Fort Belvoir, VA: Defense Technical Information Center, March 2004. http://dx.doi.org/10.21236/ada424443.

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TU, LANG, Yimiao Luo, Xinyi Xu, Huiling Xiong, Sihan Hu, and Xiao Ma. Constructing evidence for the treatment of cerebral ischemia-reperfusion injury with ligustrazine: a preclinical meta-analysis. INPLASY - International Platform of Registered Systematic Review and Meta-analysis Protocols, June 2023. http://dx.doi.org/10.37766/inplasy2023.6.0002.

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Wu, Xiaoqi, Maoxia Fan, Yaobo Pan, and 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, September 2022. http://dx.doi.org/10.37766/inplasy2022.9.0124.

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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.

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He, Miao, Sen Wang, Jing You, Jing Shi, Yanbing Yin, and Weirong Li. Neuroprotective effects of resveratrol against cerebral ischemia/reperfusion injury through anti-oxidant and anti-inflammatory mechanisms：A Systematic Review and Meta-Analysis in Rodents. INPLASY - International Platform of Registered Systematic Review and Meta-analysis Protocols, August 2022. http://dx.doi.org/10.37766/inplasy2022.8.0059.

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Xu, Fangyuan, Qiqi Yang, Wei Huang, and Zhenzhen Liu. The protective effect of acupuncture at Baihui acupoint (DU 20) for cerebral ischemia-reperfusion injury in rat models: a protocol for a systematic review and meta-analysis. INPLASY - International Platform of Registered Systematic Review and Meta-analysis Protocols, March 2021. http://dx.doi.org/10.37766/inplasy2021.3.0114.

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Yu, Beibei, Yongfeng Zhang, and 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, May 2022. http://dx.doi.org/10.37766/inplasy2022.5.0062.

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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).

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Huang, Wei, Dahong Yang, Danyang Fan, Chao Hou, and Wanqian Liu. Prognostic value of net water uptake in acute ischemic stroke: a protocol for a systematic review and meta-analysis. INPLASY - International Platform of Registered Systematic Review and Meta-analysis Protocols, December 2021. http://dx.doi.org/10.37766/inplasy2021.12.0077.

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Review question / Objective: The purpose of this protocol is to present a transparent and clear methodology for performing a systematic review and meta-analysis of the available literature aimed to answer the following question: among patients with acute ischemic stroke due to large vessel occlusion, is net water uptake (NWU), as measured in CT images, associated with (i) cerebrovascular complications, including malignant cerebral edema, secondary intracerebral hemorrhage, and (ii) post-stroke functional outcome as measured by the modified Rankin Scale. Condition being studied: Currently, the association between net water uptake with cerebrovascular complications or post-stroke functional outcomes is not well defined. Broocks found that NWU based on CT was an important marker for malignant edema in LVO patients and independently associated with clinical prognosis. Additionally, Nawabi indicated that a higher degree of NWU was a predictor of intracranial hemorrhage in patients with acute ischemic stroke treated with mechanical thrombectomy. Thus, a higher NWU might contribute to the development of stroke complications and poorer outcomes. However, no systematic review and meta-analysis to quantitatively summarize this evidence and help establish the predictive value of NWU in patients with acute ischemic stroke.

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Wang, Kai, Zhiguo Lv, Peng Xu, Baitong Wang, Aanqi Hou, Tianye Lan, Dongmei Zhang, and Jian Wang. Relevance of dynamic cerebral autoregulation after acute ischemic stroke with prognosis: A protocol for systematic review and meta-analysis. INPLASY - International Platform of Registered Systematic Review and Meta-analysis Protocols, January 2022. http://dx.doi.org/10.37766/inplasy2022.1.0056.

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Guan, Peiyu, Dingkun Gui, and Youhua Xu. Evaluation on the efficacy and safety of Panax notoginseng saponins in the treatment of stroke among elderly people - A systematic review and meta-analysis of 206 randomized controlled trials. INPLASY - International Platform of Registered Systematic Review and Meta-analysis Protocols, March 2023. http://dx.doi.org/10.37766/inplasy2023.3.0042.

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Review question / Objective: Population: The symptoms of the population were in line with the relevant diagnostic criteria for stroke both at home and abroad, and were confirmed as ischemic stroke by medical imaging tests such as MRI or CT.The subject groups were older adults with an average age of over 60, regardless of gender or race. Intervention: Intervention involves single use of PNS or combined use of PNS and WM or PNS and Treatment as usual (TAU). Comparator: All the patients in the controlled group underwent conventional routine treatment to improve their cerebral blood supply and drug treatment. Outcomes: Measurement for the outcomes should be clearly defined and includes at least one of the below items: neurological deficit score, the clinical response rate and assessment of Activities of daily living (ADLs). Study design: All the included studies were RCTs or clinical controlled trials. The study design adopted RCT.

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