Relevant bibliographies by topics / Transient Ischemia

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  1. Journal articles
  2. Dissertations / Theses
  3. Books
  4. Book chapters
  5. Conference papers

Academic literature on the topic 'Transient Ischemia'

Author: Grafiati
Published: 4 June 2021
Last updated: 1 February 2022

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Journal articles on the topic "Transient Ischemia"

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Briones, Tess L., and Barbara Therrien. "Behavioral Effects of Transient Cerebral Ischemia." Biological Research For Nursing 1, no. 4 (April 2000): 276–86. http://dx.doi.org/10.1177/109980040000100404.

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CA1 neurons in the hippocampus, a brain structure involved in learning and memory, are selectively vulnerable to ischemic effects. In this study, the authors examined if duration of ischemia is directly related to extent of CA1 damage and degree of spatial learning deficit. Adult female Wistar rats received either 5-min or 10-min ischemia or sham surgery. Following recovery, rats were tested in the Morris water maze. Histological analysis showed moderate cell loss in CA1 (31%) and CA3 (12%) and minimal cell loss in CA2 (4%) with 5-min ischemia. Increased cell loss was seen in CA1 (68%), CA2 (16%), and CA3 (23%) with 10-min ischemia. Behavioral testing revealed that animals with 10-min ischemia have greater spatial learning deficits and they remain impaired across the test days compared to the 5-min ischemic group. Furthermore, degree of CA1 cell loss accounted for approximately 45% of the variance in spatial learning deficits in the ischemic group. The authors conclude that cell loss is largely confined to CA1 region in rats who received 5 and 10 min of ischemia and that increased ischemic duration results in persistent learning deficits in female rats; also, the degree of behavioral impairment is related to extent of CA1 cell loss.
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Hong, Kyung Pyo, Soon Ok Park, Jung Sik Park, Chong Yun Rim, Young Bahk Koh, and Young Lee. "Transient Myocardial Ischemia in Ischemic Heart Disease." Korean Circulation Journal 18, no. 1 (1988): 31. http://dx.doi.org/10.4070/kcj.1988.18.1.31.

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Matias-Guiu, J., A. Davalos, and A. Codina. "Transient global ischemia." Stroke 16, no. 1 (January 1985): 132–33. http://dx.doi.org/10.1161/str.16.1.132b.

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Nedergaard, Maiken, and Anker Jon Hansen. "Characterization of Cortical Depolarizations Evoked in Focal Cerebral Ischemia." Journal of Cerebral Blood Flow & Metabolism 13, no. 4 (July 1993): 568–74. http://dx.doi.org/10.1038/jcbfm.1993.74.

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Cortical tissue surrounding acute ischemic infarcts undergoes repetitive spontaneous depolarizations. It is unknown whether these events are episodes of spreading depression (SD) elicited by the elevated interstitial K+ ([K+]e) in the ischemic core or whether they are evoked by transient decreases of the local blood flow. Electrophysiologically, depolarization caused by SD or by ischemia (ID) can be distinguished by their characteristic patterns of [K+]e rise: During SD, [K+]e rises abruptly, while in ID, this fast rate of increase is preceded by a slow rate lasting minutes. To characterize the depolarizations, we occluded the right middle cerebral artery (MCA) in rats and inserted two K+-sensitive microelectrodes into the cortex surrounding the evolving infarct. Repeated increases in [K+]e arose spontaneously following MCA occlusion. [K+]e increased during these transients from a resting level of 3–6 to 60 m M. One-third of these transient increases in [K+]e were biphasic, consisting of a slow initial increase to 10–12 m M, which lasted for minutes, followed by an abrupt increase, a pattern characteristic of ID. The remaining two-thirds exhibited a steep monotonic increase in [K+]e (>10 s), characteristic of SD. The duration of the transients was a function of the pattern of [K+]e increase: ID-like transients lasted an average 10.7 ±5.1 min, whereas the duration of SD-like transients was 5.7 ± 3.4 min. Both types of K+ transients occurred in an apparently random fashion in individual animals. A K+ transient was never observed solely at one electrode. In 40% of the cases, the K+ transients occurred simultaneously at the two electrode sites, and in the remaining a temporal separation of 20–420 s was observed. Our data suggest that the majority of the spontaneous depolarizations evoked by focal ischemia are SD-like phenomena probably evoked by the high values of [K+]e or glutamate in the ischemic focus, while the rest are elicited by independent foci of low blood flow within the ischemic border areas.
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Prabhakaran, Shyam. "Reversible brain ischemia: lessons from transient ischemic attack." Current Opinion in Neurology 20, no. 1 (February 2007): 65–70. http://dx.doi.org/10.1097/wco.0b013e328013f445.

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Nishijima, Yasuo, Kuniyasu Niizuma, Miki Fujimura, Yosuke Akamatsu, Hiroaki Shimizu, and Teiji Tominaga. "Consistent delayed unilateral neuronal death after modified transient focal cerebral ischemia in mice that mimics neuronal injury after transient global cerebral ischemia." Journal of Neurosurgery 123, no. 1 (July 2015): 243–53. http://dx.doi.org/10.3171/2014.9.jns14778.

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OBJECT Numerous studies have attempted to reveal the pathophysiology of ischemic neuronal injury using a representative transient global cerebral ischemia (tGCI) model in rodents; however, most of them have used gerbil or rat models. Recent advances in transgene and gene-knockout technology have enabled the precise molecular mechanisms of ischemic brain injury to be investigated. Because the predominant species for the study of genetic mutations is the mouse, a representative mouse model of tGCI is of particular importance. However, simple mouse models of tGCI are less reproducible; therefore, a more complex process or longer duration of ischemia, which causes a high mortality rate, has been used in previous tGCI models in mice. In this study, the authors aimed to overcome these problems and attempted to produce consistent unilateral delayed hippocampal CA1 neuronal death in mice. METHODS C57BL/6 mice were subjected to short-term unilateral cerebral ischemia using a 4-mm silicone-coated intraluminal suture to obstruct the origin of the posterior cerebral artery (PCA), and regional cerebral blood flow (rCBF) of the PCA territory was measured using laser speckle flowmetry. The mice were randomly assigned to groups of different ischemic durations and histologically evaluated at different time points after ischemia. The survival rate and neurological score of the group that experienced 15 minutes of ischemia were also evaluated. RESULTS Consistent neuronal death was observed in the medial CA1 subregion 4 days after 15 minutes of ischemia in the group of mice with a reduction in rCBF of < 65% in the PCA territory during ischemia. Morphologically degenerated cells were mostly positive for terminal deoxynucleotidyl transferase–mediated deoxyuridine triphosphate nick-end labeling and cleaved caspase 3 staining 4 days after ischemia. The survival rates of the mice 24 hours (n = 24), 4 days (n = 15), and 7 days (n = 7) after being subjected to 15 minutes of ischemia were 95.8%, 100%, and 100%, respectively, and the mice had slight motor deficits. CONCLUSIONS The authors established a model of delayed unilateral hippocampal neuronal death in C57BL/6 mice by inducing ischemia in the PCA territory using an intraluminal suture method and established inclusion criteria for PCAterritory rCBF monitored by laser speckle flowmetry. This model may be useful for investigating the precise molecular mechanisms of ischemic brain injury.
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Yang, Wei, Huaxin Sheng, David S. Warner, and Wulf Paschen. "Transient Global Cerebral Ischemia Induces a Massive Increase in Protein Sumoylation." Journal of Cerebral Blood Flow & Metabolism 28, no. 2 (June 13, 2007): 269–79. http://dx.doi.org/10.1038/sj.jcbfm.9600523.

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A new group of proteins, small ubiquitin-like modifier (SUMO) proteins, has recently been identified and protein sumoylation has been shown to play a major role in various signal transduction pathways. Here, we report that transient global cerebral ischemia induces a marked increase in protein sumoylation. Mice were subjected to 10 mins severe forebrain ischemia followed by 3 or 6 h of reperfusion. Transient cerebral ischemia induced a massive increase in protein sumoylation by SUMO2/3 both in the hippocampus and cerebral cortex. SUMO2/3 conjugation was associated with a decrease in levels of free SUMO2/3. After ischemia, protein levels of the SUMO-conjugating enzyme Ubc9 were transiently decreased in the cortex but not in the hippocampus. We also exposed HT22 cells to arsenite, a respiratory poison that impairs cytoplasmic function and induces oxidative stress. Arsenite exposure induced a marked rise in protein sumoylation, implying that impairment of cytoplasmic function and oxidative stress may be involved in the massive post-ischemic activation of SUMO conjugation described here. Sumoylation of transcription factors has been shown to block their activation, with some exceptions such as the heat-shock factor and the hypoxia-responsive factor, where sumoylation blocks their degradation, and the nuclear factor-κB (NF-κB) essential modulator where sumoylation leads to an activation of NF-κB. Because protein sumoylation is known to be involved in the regulation of various biologic processes, the massive post-ischemic increase in protein sumoylation may play a critical role in defining the final outcome of neurons exposed to transient ischemia.
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Ok, Engin, Zeki Yilmaz, Erhan Akgün, Erdoğan M. Sözüer, Yaşar Yeşilkaya, and Figen Öztürk. "Development of Collaterals in Intermittent and Permanent Ischemia of the Liver." HPB Surgery 10, no. 1 (January 1, 1996): 35–40. http://dx.doi.org/10.1155/1996/94108.

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The ischemia caused by hepatic dearterialization as therapy for hepatic malignancies is transient because of the rapid formation of collaterals. In order to prevent this transient repeated ischemia has been suggested.An experimental study was planned to compare the collateral occurrence in persistent ischemia and transient repeated ischeamia of the liver. Fourteen dogs (seven persistent ischemia, seven transient repeated ischemia) were used in this study. Hepatic dearterialization were performed in both groups. In the first group (persistent ischemia), the hepatic artery was ligated proximal to the gastroduodenal artery. In the second group (transient repeated ischemia), the hepatic artery was occluded externally in the same region as the first group by means of a device modified from 8 guage Foley catheter and after occlusion for one hour it was reopened. Occlusions were repeated twice in a day. Five dogs in the first group and six dogs in the second group completed a three weeks ischemia period and angiography were then performed in all. The dogs were sacrificed after the angiography and examined for possible abscess formation, arterial thrombosis, peritoneal adhesions and liver necrosis. After angiography, the two groups were also examined for collateral occurrence. Only one collateral occurred in the transient repeated ischemia group, but in the persistent ischemia group, collaterals occurred in all dogs. This difference between two groups is statistically significant (Fischer Absolute Chi Square Test, p=0.013).Transient repeated ischemia is superior to persistent ischemia because of fewer collaterals, but in practise, total dearterialization of the liver is impossible.
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Pang, Jinming, Toshifumi Itano, Kazunori Sumitani, Tetsuro Negi, and Osamu Miyamoto. "Electroacupuncture Attenuates Both Glutamate Release and Hyperemia After Transient Ischemia in Gerbils." American Journal of Chinese Medicine 31, no. 02 (January 2003): 295–303. http://dx.doi.org/10.1142/s0192415x03000977.

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Although many studies have indicated that electroacupuncture (EA) provides a neuroprotective effect against ischemic brain damage, the protective mechanism is not fully understood. Glutamate release and hippocampal blood flow in ischemia with EA were investigated to elucidate the neuroprotective mechanism of EA. Transient 5-minute ischemia was induced in gerbils. EA (7 Hz, 6 mA, for 30 minutes) delivered to the points called Fengfu (GV16) and Shendao (GV11) was administered pre-, intra- or post-ischemia. The procedure rescued hippocampal neurons from ischemic insult and significantly attenuated both ischemia-induced glutamate release and transient increase of cerebral blood flow (CBF) during reperfusion (hyperemia). Hyperemia as well as excessive glutamate after ischemia are regarded as important factors in brain damage as they lead to reperfusion injury. These results suggest that EA protects neurons by suppressing both glutamate release and reperfusion injury after ischemia.
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Lin, Baowan, Myron D. Ginsberg, Raul Busto, and Lin Li. "Hyperglycemic Transient Ischemia Induces Massive Neutrophil Deposition in Brain." Stroke 32, suppl_1 (January 2001): 353. http://dx.doi.org/10.1161/str.32.suppl_1.353-c.

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P80 Acute hyperglycemia worsens neurological signs and accentuates neuropathology after ischemia, but the mechanisms are poorly understood. In this study, we tested whether polymorphonuclear leukocytes (neutrophils) might be contributory. Anesthetized, physiologically monitored Wistar rats underwent global forebrain ischemia for 12.5 min by bilateral carotid artery occlusions plus hypotension (45 mm Hg). To induce hyperglycemia, rats received 2.5 ml of 25% dextrose i.p. 30 min prior to ischemia. Normoglycemic rats received saline. Plasma glucose levels were 340±66 and 133 ±21 mg/dl, respectively (mean±SD). Animals were sacrificed at either 24 h or 3 days by perfusion-fixation with FAM. Brain sections were reacted for the immunohistochemical visualization of myeloperoxidase (MPO), a specific and quantitative marker of neutrophil activity in the brain. In sham rats and in normoglycemic-ischemic animals, almost no MPO-positive cells were identified. In marked contrast, brains of hyperglycemic-ischemic rats studied at 24 h contained dramatic accumulations of MPO-positive cells within pial and parenchymal blood vessels as well as within cortical and subcortical parenchyma. MPO-positivity was most robust in areas of severe injury (on H&E sections), but MPO cells were also observed in areas without overt injury. Intravascular MPO-positive cells commonly obstructed the vascular lumen. Following 3-d survival, MPO-positivity of hyperglycemic-ischemic brains had significantly decreased. In hyperglycemic brains studied at 24 h, median numbers of MPO-positive cells were increased by 130-fold in cortex and 110-fold in striatum above values in normoglycemic-ischemic rats. In summary, this study shows that preischemic hyperglycemia triggers the early and dramatic deposition of polymorphonuclear leukocytes in the postischemic brain, with neutrophil adherence to cerebral blood vessels and their migration into brain parenchyma following brief forebrain ischemia. These events may contribute to the enhanced tissue destruction, extension of infarction, and BBB disruption observed in hyperglycemic ischemia. Supported by NIH Grant NS05820.
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Dissertations / Theses on the topic "Transient Ischemia"

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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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Nishijima, Kazuaki. "In vivo evaluation of platelet-endothelial interactions after transient retinal ischemia." Kyoto University, 2003. http://hdl.handle.net/2433/148702.

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Eriksson, Rolf. "The Utility of Manganese for Magnetic Resonance Imaging of Transient Myocardial Ischemia." Doctoral thesis, Uppsala : Acta Universitatis Upsaliensis : Univ.-bibl. [distributör], 2005. http://urn.kb.se/resolve?urn=urn:nbn:se:uu:diva-5817.

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Platholi, Jimcy. "Regulation of protein phosphatase-1I : in transient global cerebral ischemia and reperfusion /." Access full-text from WCMC, 2008. http://proquest.umi.com/pqdweb?did=1528857081&sid=17&Fmt=2&clientId=8424&RQT=309&VName=PQD.

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Hirose, Fumitaka. "In vivo evaluation of retinal injury after transient ischemia in hypertensive rats." Kyoto University, 2006. http://hdl.handle.net/2433/143861.

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Tokime, Tomoo. "Neuroprotective effect of FK506, an immunosuppressant, on transient global ischemia in gerbil." Kyoto University, 1997. http://hdl.handle.net/2433/202178.

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Silva, Matthew S. "NMR characterization of changes in the apparent diffusion coefficient of water following transient cerebral ischemia." Link to electronic thesis, 2002. http://www.wpi.edu/Pubs/ETD/Available/etd-0327102-221251.

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Chapman, Courtney Myfanwy. "Novel pharmaceutical combination confers protection from delayed cell death following transient cerebral ischemia." Thesis, Montana State University, 2009. http://etd.lib.montana.edu/etd/2009/chapman/ChapmanC0509.pdf.

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Stroke is a leading cause of death and disability throughout the world; ischemia is the most common form of stroke. Medical procedures such as cardio-pulmonary bypass surgery can cause ischemic stroke can be caused. There are no treatments to limit neural impairment following stroke. The current research investigates neuroprotection offered by treatment with a novel drug combination consisting of Simvastatinâ„¢, Gemfibrozilâ„¢, Troglitazoneâ„¢, and Spironolactoneâ„¢. Animals were treated with the drug cocktail three weeks proceeding and one week subsequent to surgery. Ischemic insult was induced by clamping the carotid arteries for 5 min. Sham subjects underwent similar surgical procedures, but the carotids were not clamped. Twenty-four hrs following the surgical procedure locomotor activity was monitored in an open field for 5 min. Seven to fourteen days following ischemia or the sham procedure animals were sacrificed and sections containing the hippocampal CA1 region were mounted on slides and stained with cresyl violet. The CA1 region was rated on a 4-point scale for level of damage. Rodents generally show increased locomotor activity following transient global ischemia in an open field. In our study, ischemic animals that received vehicle demonstrated increased activity relative to the animals that received the drug treatment on all behavioral measures. Ischemic animals that received vehicle treatment had significantly more neural damage in the hippocampal CA1 region than ischemic animals receiving the drug. The appearance of neurons in the CA1 hippocampal regions of animals in the sham condition was not significantly different from ischemic animals in the drug treatment condition. It is concluded that the drug treatment is effective in offering neuroprotection during transient global ischemia. The next step is to characterize the biochemical mechanisms behind the neuroprotection conferred by the drug treatment. Contrasting the protein expression levels of animals receiving the vehicle treatment with animals receiving the drug treatment following an ischemic insult will assist in elucidating these pathways. Predictions are made regarding the biochemical mechanisms affected by the drug treatment based on previous research on the biochemical pathways affected by each pharmaceutical.
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Leung, Wai-chung. "Investigations into the role of endothelial endothelin-1 on transient focal cerebral ischemia." Click to view the E-thesis via HKUTO, 2007. http://sunzi.lib.hku.hk/hkuto/record/B39634127.

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Leung, Wai-chung, and 梁偉聰. "Investigations into the role of endothelial endothelin-1 on transient focal cerebral ischemia." Thesis, The University of Hong Kong (Pokfulam, Hong Kong), 2007. http://hub.hku.hk/bib/B39634127.

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Books on the topic "Transient Ischemia"

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Schaller, Bernhard. Endogenous neuroprotection. New York: Nova Science, 2008.

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International Conference on Cerebral Vasospasm (5th 1993 Edmonton, Alta. and Jasper, Alta.). Cerebral vasospasm: Proceedings of the Vth International Conference on Cerebral Vasospasm, Edmonton and Jasper, Alberta, Canada, May 17-21, 1993. Amsterdam: Elsevier, 1993.

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Tonchev, Anton B., George N. Chaldakov, and Tetsumori Yamashima. Distribution and Phenotype of Proliferating Cells in the Forebrain of Adult Macaque Monkeys after Transient Global Cerebral Ischemia. Berlin, Heidelberg: Springer Berlin Heidelberg, 2007. http://dx.doi.org/10.1007/978-3-540-39617-8.

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N, Tulenko Thomas, and Cox Robert H, eds. Recent advances in arterial diseases: Atherosclerosis, hypertension, and vasospasm : proceedings of the A.N. Richards Symposium, held in Philadelphia, Pennsylvania, May 10-11, 1984. New York: Liss, 1986.

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Heart and Stroke Foundation of Canada. Understanding transient ischemic attack (TIA). [Ottawa]: Heart and Stroke Foundation of Canada, 2000.

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Zoppo, Gregory J. Del. Innate inflammation and stroke. Edited by New York Academy of Sciences. Boston, Mass: Published by Blackwell Pub. on behalf of the New York Academy of Sciences, 2010.

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1970-, Giles Matthew F., and Rothwell Peter M, eds. Transient ischemic attack and stroke: Diagnosis, investigation, and management. Cambridge: Cambridge University Press, 2009.

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name, No. Stroke sourcebook: Basic consumer health information about stroke, including ischemic, hemorrhagic, transient ischemic attack (TIA) ... Detroit, MI: Omnigraphics, 2003.

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MD, Spencer Fredrick A., ed. Antithrombotic therapy in the prevention of ischemic stroke. Oxford: Oxford University Press, 2010.

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National Collaborating Centre for Chronic Conditions (Great Britain). Stroke: National clinical guideline for diagnosis and initial management of acute stroke and transient ischaemic attack (TIA). London: Royal College of Physicians, 2008.

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Book chapters on the topic "Transient Ischemia"

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Chierchia, Sergio. "Alpha-receptors and transient ischemia." In Silent Ischemia, 25–30. Heidelberg: Steinkopff, 1987. http://dx.doi.org/10.1007/978-3-662-12997-5_4.

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Niizuma, Kuniyasu, Hidenori Endo, Chikako Nito, D. Jeannie Myer, Gab Seok Kim, Teiji Tominaga, and Pak H. Chan. "Transient Global Cerebral Ischemia Model in Mice." In Springer Protocols Handbooks, 115–25. Totowa, NJ: Humana Press, 2009. http://dx.doi.org/10.1007/978-1-60327-185-1_10.

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Hagendorff, A., J. Grote, C. Haller, K. Zimmer, C. Dettmers, A. Nierhaus, and A. Hartmann. "The Effects of Transient and Long-Term Ischemia on Tissue PO2 in the Brain Cortex." In Cerebral Ischemia and Calcium, 111–19. Berlin, Heidelberg: Springer Berlin Heidelberg, 1989. http://dx.doi.org/10.1007/978-3-642-85863-5_14.

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Huber, Kurt, I. Lang, M. Joerg, P. Probst, and B. R. Binder. "Plasminogen activator inhibitor-1 and transient myocardial ischemia." In Predisposing Conditions for Acute Ischemic Syndromes, 59–69. Heidelberg: Steinkopff, 1989. http://dx.doi.org/10.1007/978-3-662-09434-1_7.

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Quyyumi, Arshed A. "Evaluation of Transient Myocardial Ischemia by Holter Monitoring." In Developments in Cardiovascular Medicine, 53–72. Boston, MA: Springer US, 1994. http://dx.doi.org/10.1007/978-1-4615-2628-5_5.

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Xu, Zao C. "Alterations of Synaptic Transmission Following Transient Cerebral Ischemia." In Neuronal and Vascular Plasticity, 117–34. Boston, MA: Springer US, 2003. http://dx.doi.org/10.1007/978-1-4615-0282-1_5.

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Siesjö, B. K., H. Uchino, T. Yoshimoto, B. R. Hu, and F. Shibasaki. "Mitochondrial Dysfunction and Maturation of Brain Damage After Transient Ischemia." In Maturation Phenomenon in Cerebral Ischemia IV, 229–39. Berlin, Heidelberg: Springer Berlin Heidelberg, 2001. http://dx.doi.org/10.1007/978-3-642-59446-5_27.

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Tomita, M., F. Gotoh, N. Tanahashi, M. Kobari, Y. Terayama, B. Mihara, and K. Ohta. "Intravascular RBC Aggregation and Transient Diminution of Cerebrovascular Volume Following Middle Cerebral Artery Occlusion in Cats." In Cerebral Ischemia and Hemorheology, 377–85. Berlin, Heidelberg: Springer Berlin Heidelberg, 1987. http://dx.doi.org/10.1007/978-3-642-71787-1_44.

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Ide, T., T. Morimoto, and T. Kirino. "Transient Ischemia Depletes Free Ubiquitin in the Gerbil Hippocampal CA1 Neurons." In Maturation Phenomenon in Cerebral Ischemia II, 93–97. Berlin, Heidelberg: Springer Berlin Heidelberg, 1997. http://dx.doi.org/10.1007/978-3-642-60546-8_12.

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Shuaib, Ashfaq. "The Role of Taurine in Cerebral Ischemia: Studies in Transient Forebrain Ischemia and Embolic Focal Ischemia in Rodents." In Advances in Experimental Medicine and Biology, 421–31. Boston, MA: Springer US, 2003. http://dx.doi.org/10.1007/978-1-4615-0077-3_51.

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Conference papers on the topic "Transient Ischemia"

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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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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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Nakamura, Kazuhiro, David Wright, Yasushi Kondoh, Shigenori Mizusawa, and Toshibumi Kinoshita. "Quantitative accuracy of delayed hyperperfusion in MRI of transient ischemia in rats." In 2008 30th Annual International Conference of the IEEE Engineering in Medicine and Biology Society. IEEE, 2008. http://dx.doi.org/10.1109/iembs.2008.4649284.

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Strano, A., G. Davi, I. Catalano, G. Francavilla, and A. Notarbartolo. "IS BETATHROMBOGLOBULIN (BTG) OF PROGNOSTIC VALUE IN PATIENTS WITH TRANSIENT CEREBRAL ISCHEMIA (TIA) ?" In XIth International Congress on Thrombosis and Haemostasis. Schattauer GmbH, 1987. http://dx.doi.org/10.1055/s-0038-1643055.

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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.
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Smrdel, A., and F. Jager. "Diurnal changes of heart rate and sympatho-vagal activity for temporal patterns of transient ischemia." In Computers in Cardiology, 2005. IEEE, 2005. http://dx.doi.org/10.1109/cic.2005.1588240.

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Kostic, Marko N., Sina Fakhar, Tom Foxall, Budimir S. Drakulic, and Mitchell W. Krucoff. "Evaluation of Novel ECG Signal Processing on Quantification of Transient Ischemia and Baseline Wander Suppression." In 2007 29th Annual International Conference of the IEEE Engineering in Medicine and Biology Society. IEEE, 2007. http://dx.doi.org/10.1109/iembs.2007.4352760.

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Ting, Chien-Yu, Ching-Hsiang Fan, and Chih-Kuang Yeh. "Detection of transient ischemia and hemorrhage in blood-brain barrier disruption by high-frequency ultrasound imaging." In 2010 IEEE Ultrasonics Symposium (IUS). IEEE, 2010. http://dx.doi.org/10.1109/ultsym.2010.5935913.

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Lun-De Liao, Meng-Lin Li, Hsin-Yi Lai, You-Yin Chen, and Nitish V. Thakor. "Study of neurovascular coupling functions for transient focal cerebral ischemia in rats using electrocorticography functional photoacoustic microscopy (ECoG-fPAM)." In 2013 35th Annual International Conference of the IEEE Engineering in Medicine and Biology Society (EMBC). IEEE, 2013. http://dx.doi.org/10.1109/embc.2013.6609871.

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Falk, E. A. "UNSTABLE ANGINA PECTORIS: PATHOLOGIC ASPECTS." In XIth International Congress on Thrombosis and Haemostasis. Schattauer GmbH, 1987. http://dx.doi.org/10.1055/s-0038-1643711.

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Unstable angina pectoris represents a common and important manifestation of acute ischemic heart disease encompassing the broad spectrum of clinical syndromes between stable effort angina and acute myocardial infarction. This group of patientsisfar from uniform concerning underlying pathogenetic mechanisms and prognosis, but generally the risk of infarction or deathis increased during the unstable period. Most patients are presenting with new or worsening effort angina or angina at rest,and especially patients with rest anginaassociated with transient ECG changes seem to constitute a high risk subgroup. Transient reductions in coronary blood flow,rather than increases in myocardial oxygen demand, seem to play the major role in rest angina, indicating an underlying 'dynamic' coronary stenosis.Furthermore, unstable angina seems to beagood clinicalmarker for actively progressing coronary-artery disease.Pathologically, a rapidly evolving coronary-artery lesion represented by a disrupted atherosclerotic plaque with variable degree of plaque hemorrhage and luminalthrombosis usually is present in patientscoming to autopsy after a period of rest angina. The thrombus at the rupture site may be mural and limited (just sealing therupture) or occlusive depending on the degree of preexisting atherosclerotic stenosis. An occlusive thrombus is seldom seen over ruptured plaques causing less tha15% stenosis (histologic area stenosis), but is found with increasing frequency when stenosis severety increases beyond 15%.Most occlusive thrombi have a layered structure with thrombus material of differing age indicating an episodic growth by repeated mural deposits. Aggregated platelets usually can be identified in the mostrecent part of the thrombus, while older parts are more homogeneous due to fibrin infiltration/stabilization. Additionally,microemboli and microinfarcts are frequently found in the myocardium downstream tocoronary thrombi. So, the period of unstable angina preceding a fatal heart attackseems to be characterized by an ongoing thrombotic process in a major coronary artery where recurrent mural thrombus formation alternates with intermittent thrombus fragmentation and peripheral embolization. Such a dynamic thrombosis (with or without a concomitant focal vasospastic phenomenon) at the site of an unstable (ruptured) atherosclerotic lesion obviously may lead to the other clearly thrombus-related acute ischemic events: myocardial infarction or sudden death.Clinical studies using coronary angiography and coronary angioscopy during the acute phase of unstable angina have revealed a high frequency of ulcerated (unstable) atherothrombotic lesion in arteries responsible for the acute ischemia. Furthermore, episodic platelet activation (usually associated with chest pain) has recently been demonstrated in patients with unstable angina.The mechanism underlying pain/ischemia(predominantly spasm?) and the rapid plaque progression (plaque hemorr.hage/luminal thrombosis?) during unstable angina maydiffer. Accordingly, therapy directed against a possible spasm (nitrates, calcium antagonists) usually relieves pain effectively without having any documented effect on infarction/survival, while antithr-ombotic therapy (aspirin, heparin) clearlyimproves the prognosis without apparent antianginal effect. Therefore, with the objective not only of relieving pain but also of improving the prognosis, more attention should be paid to the potentially fatal thrombotic process that apparently isgoing on in a major coronary artery of many patients with unstable angina.
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Terres, W., W. Kupper, C. Hamm, and W. Bleifeld. "RESTING MYOCARDIAL ISCHEMIA AFTER INTRAVENOUS INFUSION OF BM 13.177, A THROMBOXANE RECEPTOR ANTAGONIST." In XIth International Congress on Thrombosis and Haemostasis. Schattauer GmbH, 1987. http://dx.doi.org/10.1055/s-0038-1643466.

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We conducted a double blind placebo controlled trial of BM 13.177, a thromboxane receptor antagonist, given intravenously in patients (PTS) with stenoses >70 % of the left anterior descending coronary artery and stable exertional angina pectoris (AP). The study had to be stopped after enrollment of 8 PTS, because 2 had developed resting AP after initiation of the study medication. Both proved to belong to the 4 PTS who had received BM 13.177 (12.5 mg/min). While in one PT, AP was mild, transient and associated with only slight decreases in coronary sinus blood flow (CSBF) and myocardial lactate extraction (MLE), in the other, AP was severe and persisted for 30 minutes in spite of antianginal therapy. Severe clinical symptoms in this PT were associated with a marked fall in MLE from +24 to -121 %. Two PTS under BM 13.177 and 4 on placebo underwent supraventricular stimulation. For both groups, no change in clinical symptoms, CSBF or MLE occured in comparison to a former control stimulation without medication. BM 13.177 led to an inhibition of ex vivo platelet aggregation induced by collagen 1 pg/ml (mean reduction in rate of aggregation by 41 %, p< 0.05), while aggregation was not influenced with collagen 5 μg/ml or ADP. This effect of BM on platelets is explained by its thromboxane receptor blocking properties. The induction of resting myocardial ischemia, however, in 2 of 4 PTS with formerly stable exertional AP may have been the result of either a coronary steal mechanism or an intrinsic stimulation of vascular thromboxane receptors, followed by coronary vasoconstriction.
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