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Journal articles on the topic 'Cerebral ischemia stroke apoplexy'

Author: Grafiati

Published: 4 June 2021

Last updated: 1 February 2022

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1

Ahn, Jae-Min, Hyuk-Jin Oh, Jae-Sang Oh, and Seok-Mann Yoon. "Pituitary apoplexy causing acute ischemic stroke: Which treatment should be given priority." Surgical Neurology International 11 (May 16, 2020): 113. http://dx.doi.org/10.25259/sni_82_2020.

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Background: Pituitary apoplexy is syndrome of sudden onset of headache, visual loss, pituitary dysfunction, and altered consciousness. Pituitary apoplexy followed by acute cerebral ischemia is extremely rare. Here, we introduced the case of successful surgical resection of pituitary adenoma which induced acute cerebral ischemia. Case Description: A 78-year-old man with a known pituitary macroadenoma presented with decreased consciousness and left hemiparesis. Magnetic resonance image (MRI) and computed tomography (CT) showed large pituitary macroadenoma with hemorrhage and diffusion-perfusion

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2

Azizov, Miralim M. "Acute stroke in pituitary adenomas complicated by pituitary apoplexy." Russian Journal of Oncology 21, no. 3 (2016): 136–39. http://dx.doi.org/10.18821/1028-9984-2016-21-3-136-139.

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Pituitary apoplexy is a clinical syndrome that is manifested by headache, visual disturbances, ophthalmoplegia or impaired consciousness. It can develop as a result of necrosis or hemorrhage in the pituitary gland or in cases of pituitary tumors. A favorable prognosis is possible if early diagnosis and timely surgical treatment. Pituitary apoplexy complicated by the disorder of the cerebral circulation occurs relatively rare. We observed the female patient aged of 51 year with pituitary adenoma, clinical signs of which were sudden depression of consciousness, right hemiparesis and left-sided p

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Hu, Beilei, Songfang Chen, Ming Zou, Zhiyong He, Shengmin Shao, and Baohua Liu. "Effect of Extracellular Vesicles on Neural Functional Recovery and Immunologic Suppression after Rat Cerebral Apoplexy." Cellular Physiology and Biochemistry 40, no. 1-2 (2016): 155–62. http://dx.doi.org/10.1159/000452533.

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Background: Previous studies have demonstrated that mesenchymal stem cells (MSCs) can promote the recovery of neural function after cerebral apoplexy by secreting multiple cytokines. In addition, cell factor-derived extracellular vesicles play an important role in recovery of neural function. The aim of this study was to determine the effect of extracellular vesicles on neural functional recovery and brain tissue remodeling after cerebral apoplexy in a rat model. Methods: The rat models with local ischemic stroke was established and three random groups were created. In groups A and B, human bo

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Kornilova, A. A., O. V. Lagoda, and M. M. Tanashyan. "Cerebral Amyloid Angiopathy in Combination with Paroxysmal Atrial Fibrillation." Russian neurological journal 25, no. 4 (2020): 31–37. http://dx.doi.org/10.30629/2658-7947-2020-25-4-31-37.

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The present article addresses the definition of cerebral amyloid angiopathy (CAA) and its symptoms based on the analysis of the medical case; the issues of diagnosis and treatment of this pathology are discussed. The Boston criteria, which became the basis for diagnosis, study of clinical manifestations and progression of CAA and approaches to its therapy, are presented. Methods and modes of neuroimaging, including magnetic resonance imaging (MRI), which verify micro cerebral haemorrhage, are described. At the same time, the role and significance of cardiac arrhythmias in the genesis of ischem

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Wortham, Joy, Brenda Sandoval, Maureen Koops, Ramona Granda-Rodriguez, and Jan M. Bruder. "Giant Prolactinoma Causing Proptosis and Stroke." Journal of the Endocrine Society 5, Supplement_1 (2021): A584. http://dx.doi.org/10.1210/jendso/bvab048.1191.

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Abstract Background: Although suprasellar and cavernous sinus invasion are common in giant prolactinomas, intra-orbital extension is extremely uncommon [1]. Even less reported are cases of giant prolactinomas causing cerebral ischemia or death. Clinical Case: A 51-year old woman presented to the ED with confusion, right-sided weakness and severe left eye proptosis with loss of vision. Five years prior, she underwent a partial transphenoidal resection for a macroprolactinoma due to acute vision changes with compression of the optic chiasm. Prior to surgery, prolactin level was elevated to 2,106

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Zou, Mingyang, Junjie Liao, Yurong Zeng, Qianwen Guan, and Bowen Lan. "Diagnostic Value of CT Angiography Combined with High-Resolution Magnetic Resonance Angiography in Vascular Lesions in Acute Stroke." Scientific Programming 2021 (September 11, 2021): 1–7. http://dx.doi.org/10.1155/2021/2274443.

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Cerebrovascular disease is increasing rapidly because of its high morbidity and high mortality, which is a serious threat to human health. For the early diagnosis and treatment of diseases, the CT vascular noise combined with high-resolution magnetic resonance angiography in acute cerebral apoplexy vascular disease is adopted. 150 patients with ischemic stroke were selected, which were admitted to the Department of Radiology, Huizhou Central People’s Hospital, from January 2020 to December 2020. All patients accepted digital subtraction angiography (DSA), magnetic resonance angiography (MRA),

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7

Ben-Nakhi, A., T. J. E. Muttikkal, V. N. K. Chavan, A. Yt Al-Turkomani, and R. Gupta. "Pituitary Apoplexy: A Rare Cause of Cerebral Infarction." Neuroradiology Journal 21, no. 5 (2008): 661–65. http://dx.doi.org/10.1177/197140090802100509.

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Pituitary apoplexy is usually the result of hemorrhagic infarction in pituitary adenoma. The clinical presentation of pituitary apoplexy varies widely and includes asymptomatic hemorrhage, classical pituitary apoplexy and even sudden death. Few cases of cerebral infarction associated with pituitary apoplexy have been reported in the literature. Pituitary apoplexy can cause narrowing of intracranial vessels by mechanical obstruction due to mass effect or by vasospasm resulting in cerebral ischemia. We report a case of pituitary apoplexy associated with cerebral infarction and the putative mecha

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8

Bettag, Christoph, Christoph Strasilla, Andreas Steinbrecher, and Rüdiger Gerlach. "Unilateral Tuberothalamic Artery Ischemia Caused by Pituitary Apoplexy." Journal of Neurological Surgery Part A: Central European Neurosurgery 79, no. 06 (2018): 550–54. http://dx.doi.org/10.1055/s-0038-1656514.

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Background and Importance Pituitary apoplexy (PA) occasionally occurs in patients with pituitary adenoma and may cause severe functional deficits. Headache, pituitary insufficiency, visual impairment, and cranial nerve palsies are the most frequent symptoms in patients with PA. Secondary cerebral ischemia develops in only a limited number of PA patients. Two pathogenic mechanisms were previously proposed. One states that ischemia may be due to major vessel encasement or to vessel compression, as a result of extended tumor growth. The second states that cerebral vasospasm following PA may cause

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9

Wang, Yang, Yongting Wang, and Guo-Yuan Yang. "MicroRNAs in Cerebral Ischemia." Stroke Research and Treatment 2013 (2013): 1–6. http://dx.doi.org/10.1155/2013/276540.

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The risk of ischemic stroke increases substantially with age, making it the third leading cause of death and the leading cause of long-term disability in the world. Numerous studies demonstrated that genes, RNAs, and proteins are involved in the occurrence and development of stroke. Current studies found that microRNAs (miRNAs or miRs) are also closely related to the pathological process of stroke. miRNAs are a group of short, noncoding RNA molecules playing important role in posttranscriptional regulation of gene expression and they have emerged as regulators of ischemic preconditioning and i

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10

Simard, J. Marc, Kevin N. Sheth, W. Taylor Kimberly, et al. "Glibenclamide in Cerebral Ischemia and Stroke." Neurocritical Care 20, no. 2 (2013): 319–33. http://dx.doi.org/10.1007/s12028-013-9923-1.

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11

Huang, Judy, Urvashi M. Upadhyay, and Rafael J. Tamargo. "Inflammation in stroke and focal cerebral ischemia." Surgical Neurology 66, no. 3 (2006): 232–45. http://dx.doi.org/10.1016/j.surneu.2005.12.028.

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12

Schweizer, Sophie, Andreas Meisel, and Stefanie Märschenz. "Epigenetic Mechanisms in Cerebral Ischemia." Journal of Cerebral Blood Flow & Metabolism 33, no. 9 (2013): 1335–46. http://dx.doi.org/10.1038/jcbfm.2013.93.

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Treatment efficacy for ischemic stroke represents a major challenge. Despite fundamental advances in the understanding of stroke etiology, therapeutic options to improve functional recovery remain limited. However, growing knowledge in the field of epigenetics has dramatically changed our understanding of gene regulation in the last few decades. According to the knowledge gained from animal models, the manipulation of epigenetic players emerges as a highly promising possibility to target diverse neurologic pathologies, including ischemia. By altering transcriptional regulation, epigenetic modi

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13

CHINO, NAOKAZU. "Stroke impairment assessment set(SIAS).A new cerebral apoplexy functional evaluation method." Japanese Journal of Rehabilitation Medicine 31, no. 9 (1994): 603–7. http://dx.doi.org/10.2490/jjrm1963.31.603.

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14

Khan, Sibghat Ullah, Naveed Aslam Lashari, Nadia Irum Lakho, Ambreen Faisal, and Aamir Hussain. "CEREBRAL ISCHAEMIA AND STROKE;." Professional Medical Journal 24, no. 12 (2017): 1823–27. http://dx.doi.org/10.29309/tpmj/2017.24.12.564.

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Introduction: Colour Doppler sonography is a well-established widely available,noninvasive, cost effective and a reliable method for assessing cerebrovascular circulation.It has become a valuable completion of the sonographic workup in patients with cerebralischaemia and infarction. Its accuracy is close to angiography. Objectives: To determine thefrequency of significant carotid artery stenosis in patients of cerebral ischaemia/stroke and itscharacterized sonographic appearance of plaque. Study Design: Cross sectional study, basedon nonprobability convenience sample technique. Setting: Depart

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15

Dumont, Aaron S., and Avery J. Evans. "Introduction: Endovascular approaches to cerebral ischemia." Neurosurgical Focus 26, no. 3 (2009): E1. http://dx.doi.org/10.3171/2009.1.focus.mar09.intro.

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Thetreatment of stroke has rapidly evolved over the past decade, particularly as data concerning the natural history have emerged and endovascular treatment options have matured. Therapies for acute stroke have expanded as intraarterial thrombolysis and mechanical clot retrieval have been validated. Furthermore, angioplasty and stenting of intra- and extracranial vessels have evolved with the development of new devices coupled with increasing operator experience. Endovascular therapy is now a widely accepted treatment option for cerebral ischemia in many clinical situations.

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16

Kononets, O. M., O. V. Tkachenko, and O. O. Kamenetska. "Cerebral hemispheres – cerebellum – kidney interaction in patients with acute cerebral ischemia." Medicni perspektivi (Medical perspectives) 26, no. 1 (2021): 90–98. http://dx.doi.org/10.26641/2307-0404.2021.1.227941.

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The nervous system, in particular the autonomic one, is well known to constantly regulate the internal functioning of the body, adapting it to changeable external and internal environmental parameters. In particular, there is a close multiple-vector correlation between the nervous system and the kidneys. The aim of this study was to specify the mechanisms, clinical and paraclinical characteristics of the concomitant lesions of the nervous system and the kidneys in patients with acute stroke. This paper presents the case report of 215 patients, aged 70 ± 8.44, who suffered from ischemic stroke.

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17

Smout, Jonathan, Alexander Dyker, Marcus Cleanthis, Gary Ford, Patrick Kesteven, and Gererd Stansby. "Platelet Function following Acute Cerebral Ischemia." Angiology 60, no. 3 (2009): 362–69. http://dx.doi.org/10.1177/0003319709332959.

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Background Studies have previously identified increased levels of platelet activation following acute ischemic stroke. In order to evaluate new antiplatelet agents and their combinations, there is a need for accurate measures of platelet activation. Methods Blood was taken from 17 patients within 24 hours of an acute ischemic stroke, and then at 3, 7, 14 and 42 days. For comparison, a group of 18 stable arteriopaths had identical tests performed. Platelet aggregation was measured using a free platelet counting technique, and platelet surface P-selectin and monocyte platelet aggregates (MPAs) w

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18

Pozzati, Eugenio, Giorgio Frank, Maria Teresa Nasi, and Giuliano Giuliani. "Pituitary Apoplexy, Bilateral Carotid Vasospasm, and Cerebral Infarction in a 15-Year-Old Boy." Neurosurgery 20, no. 1 (1987): 56–59. http://dx.doi.org/10.1227/00006123-198701000-00015.

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Abstract The authors report a case of pituitary apoplexy associated with oculomotor defects and focal cerebral signs; the visual pathways were intact. Computed tomography documented a mass of heterogeneous density within an enlarged sella turcica and a right parietal infarct. Angiograms revealed bilateral carotid spasm and occlusion of the right angular artery. Treatment was conservative. Control angiograms showed spontaneous resolution of the vasospasm and recanalization of the cortical artery. The patient made a complete neurological recovery; he needed only treatment with vasopressin due to

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19

Ouyang, Yi-Bing, Creed M. Stary, Guo-Yuan Yang, and Rona Giffard. "microRNAs: Innovative Targets for Cerebral Ischemia and Stroke." Current Drug Targets 14, no. 1 (2012): 90–101. http://dx.doi.org/10.2174/1389450111314010010.

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Ouyang, Yi-Bing, Creed M. Stary, Guo-Yuan Yang, and Rona Giffard. "microRNAs: Innovative Targets for Cerebral Ischemia and Stroke." Current Drug Targets 14, no. 1 (2013): 90–101. http://dx.doi.org/10.2174/138945013804806424.

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21

Wilkins, Heather M., та Russell H. Swerdlow. "TNFα in cerebral ischemia: another stroke against you?" Journal of Neurochemistry 132, № 4 (2015): 369–72. http://dx.doi.org/10.1111/jnc.13028.

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22

Karelina, Kate, Kathleen A. Stuller, Brant Jarrett, et al. "Oxytocin Mediates Social Neuroprotection After Cerebral Ischemia." Stroke 42, no. 12 (2011): 3606–11. http://dx.doi.org/10.1161/strokeaha.111.628008.

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Background and Purpose— The reduced incidence, morbidity, and mortality of stroke among humans with strong social support have been well-documented; however, the mechanisms underlying these socially mediated phenomena remain unknown, but may involve oxytocin (OT), a hormone that modulates some aspects of social behavior in humans and other animals. Methods— In the present study, adult male mice were socially isolated (housed individually) or socially paired (housed with an ovariectomized female); social pairing increased hypothalamic OT gene expression. To determine whether a causal relationsh

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23

Shin, Tae Hwan, Da Yeon Lee, Shaherin Basith, et al. "Metabolome Changes in Cerebral Ischemia." Cells 9, no. 7 (2020): 1630. http://dx.doi.org/10.3390/cells9071630.

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Cerebral ischemia is caused by perturbations in blood flow to the brain that trigger sequential and complex metabolic and cellular pathologies. This leads to brain tissue damage, including neuronal cell death and cerebral infarction, manifesting clinically as ischemic stroke, which is the cause of considerable morbidity and mortality worldwide. To analyze the underlying biological mechanisms and identify potential biomarkers of ischemic stroke, various in vitro and in vivo experimental models have been established investigating different molecular aspects, such as genes, microRNAs, and protein

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24

ITOH, Masashi, and Takiko SHINDO. "Changes in cerebral apoplexy. From 1921 autopsy casses of stroke in 20 years." JOURNAL OF THE JAPANESE ASSOCIATION OF RURAL MEDICINE 36, no. 5 (1988): 1046–50. http://dx.doi.org/10.2185/jjrm.36.1046.

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25

YAMAMOTO, KEN'ICHI. "Preventive effect of Ca antagonist on stroke of cerebral apoplexy in stroke-prone spontaneously hypertensive rats (SHRSP)." Rinsho yakuri/Japanese Journal of Clinical Pharmacology and Therapeutics 21, no. 1 (1990): 109–10. http://dx.doi.org/10.3999/jscpt.21.109.

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26

Kobayashi, Shoutai. "Evidence of Cerebral Apoplexy in Japanese Patients from Asymptomatic Cerebral Infarction to Acute Stroke and Region Cooperation." Nihon Naika Gakkai Zasshi 99, no. 9 (2010): 2021–34. http://dx.doi.org/10.2169/naika.99.2021.

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Kobayashi, Shoutai. "Evidence of Cerebral Apoplexy in Japanese Patients from Asymptomatic Cerebral Infarction to Acute Stroke and Region Cooperation." Nihon Naika Gakkai Zasshi 99, Suppl (2010): 38a—42a. http://dx.doi.org/10.2169/naika.99.38a.

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Tapeinos, Christos, Matteo Battaglini, Attilio Marino, and Gianni Ciofani. "Smart diagnostic nano-agents for cerebral ischemia." Journal of Materials Chemistry B 8, no. 29 (2020): 6233–51. http://dx.doi.org/10.1039/d0tb00260g.

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Lin, Weili, and William J. Powers. "Oxygen metabolism in acute ischemic stroke." Journal of Cerebral Blood Flow & Metabolism 38, no. 9 (2017): 1481–99. http://dx.doi.org/10.1177/0271678x17722095.

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Gaining insights into brain oxygen metabolism has been one of the key areas of research in neurosciences. Extensive efforts have been devoted to developing approaches capable of providing measures of brain oxygen metabolism not only under normal physiological conditions but, more importantly, in various pathophysiological conditions such as cerebral ischemia. In particular, quantitative measures of cerebral metabolic rate of oxygen using positron emission tomography (PET) have been shown to be capable of discerning brain tissue viability during ischemic insults. However, the complex logistics

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Vaughan, Carl J., and Norman Delanty. "Neuroprotective Properties of Statins in Cerebral Ischemia and Stroke." Stroke 30, no. 9 (1999): 1969–73. http://dx.doi.org/10.1161/01.str.30.9.1969.

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Macha, Kosmas, Armin Marsch, Gabriela Siedler, et al. "Cerebral Ischemia in Patients on Direct Oral Anticoagulants." Stroke 50, no. 4 (2019): 873–79. http://dx.doi.org/10.1161/strokeaha.118.023877.

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Background and Purpose— In patients with ischemic stroke on therapy with vitamin K antagonists, stroke severity and clinical course are affected by the quality of anticoagulation at the time of stroke onset, but clinical data for patients using direct oral anticoagulants (DOACs) are limited. Methods— Data from our registry including all patients admitted with acute cerebral ischemia while taking oral anticoagulants for atrial fibrillation between November 2014 and October 2017 were investigated. The activity of vitamin K antagonists was assessed using the international normalized ratio on admi

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Kvistad, Christopher Elnan, Vojtech Novotny, Halvor Næss, et al. "Safety and predictors of stroke mimics in The Norwegian Tenecteplase Stroke Trial (NOR-TEST)." International Journal of Stroke 14, no. 5 (2018): 508–16. http://dx.doi.org/10.1177/1747493018790015.

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Background Stroke mimics are frequently treated with thrombolysis in clinical practice and thrombolytic trials. Although alteplase in stroke mimics has proven to be safe, safety of tenecteplase in stroke mimics has not been assessed in an ischemic stroke study setting. We aimed to assess clinical characteristics and safety of stroke mimics treated with thrombolysis in the Norwegian Tenecteplase Stroke Trial. We also aimed to identify possible predictors of stroke mimics as compared to patients with acute cerebral ischemia. Methods Norwegian Tenecteplase Stroke Trial was a phase-3 trial investi

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Bhatt, Archit, Muhammad U. Farooq, Sailaja Enduri, et al. "Clinical Significance of Serum Zinc Levels in Cerebral Ischemia." Stroke Research and Treatment 2010 (2010): 1–4. http://dx.doi.org/10.4061/2010/245715.

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Background. Zinc mediates several vital physiological, enzymatic and cellular functions. The association between serum zinc and stroke outcome has not been previously evaluated.Methods. This single center retrospective study was conducted on consecutive stroke () and TIA () patients. We sought to determine whether serum zinc concentrations in patients with acute ischemic strokes were associated with stroke severity and poor functional status at discharge, respectively.Results. Overall, out of the 224 patients analyzed (mean age 67 years), 35.7% patients had low zinc levels (65 mcg/dL). Patient

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Graham, Steven H., and Jun Chen. "Programmed Cell Death in Cerebral Ischemia." Journal of Cerebral Blood Flow & Metabolism 21, no. 2 (2001): 99–109. http://dx.doi.org/10.1097/00004647-200102000-00001.

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Programmed cell death (PCD) is an ordered and tightly controlled set of changes in gene expression and protein activity that results in neuronal cell death during brain development. This article reviews the molecular pathways by which PCD is executed in mammalian cells and the potential relation of these pathways to pathologic neuronal cell death. Whereas the classical patterns of apoptotic morphologic change often do not appear in the brain after ischemia, there is emerging biochemical and pharmacologic evidence suggesting a role for PCD in ischemic brain injury. The most convincing evidence

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Meadows, Kristy L. "Experimental models of focal and multifocal cerebral ischemia: a review." Reviews in the Neurosciences 29, no. 6 (2018): 661–74. http://dx.doi.org/10.1515/revneuro-2017-0076.

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AbstractRodent and rabbit stroke models have been instrumental in our current understanding of stroke pathophysiology; however, translational failure is a significant problem in preclinical ischemic stroke research today. There are a number of different focal cerebral ischemia models that vary in their utility, pathophysiology of causing disease, and their response to treatments. Unfortunately, despite active preclinical research using these models, treatment options for ischemic stroke have not significantly advanced since the food and drug administration approval of tissue plasminogen activa

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Danilova, T. V. "Features of epilepsy in acute and chronic cerebral ischemia." Kazan medical journal 98, no. 6 (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 i

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Li, T. Q., Z. G. Chen, and T. Hindmarsh. "Diffusion-weighted MR imaging of acute cerebral ischemia." Acta Radiologica 39, no. 5 (1998): 460–73. http://dx.doi.org/10.1080/02841859809172209.

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Diffusion-weighted MR imaging has been used in studies on experimental animal models and on patients with acute cerebral ischemia. Compared with CT and conventional MR techniques, diffusion-weighted imaging can provide earlier and more precise detection of the location and the extent of an ischemic lesion during the critical first few hours after the onset of stroke Quantitative apparent diffusion coefficient (ADC) mapping of the brain water can also be carried out by recording a series of diffusion-weighted images with different amplitudes of the displacement encoding gradients. ADC maps can

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Barber, Philip A., Roland N. Auer, Alastair M. Buchan, and Garnette R. Sutherland. "Understanding and managing ischemic stroke." Canadian Journal of Physiology and Pharmacology 79, no. 3 (2001): 283–96. http://dx.doi.org/10.1139/y00-125.

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Transient or permanent focal brain injury following acute thromboembolic occlusion develops from a complex cascade of pathophysiological events. The processes of excitotoxicity, peri-infarct depolarisation, inflammation, and apoptosis within the ischemic penumbra are proposed. While the translation of therapeutic agents from the animal models to human clinical trials have been disappointing, there remains an atmosphere of optimism as a result of the development of new diagnostic and therapeutic approaches, which include physiological, as opposed to pharmacological, intervention. This article p

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Petrov, M. G., S. S. Kucherenko, and M. P. Topuzova. "Hemorrhagic transformation of ischemic stroke." "Arterial’naya Gipertenziya" ("Arterial Hypertension") 27, no. 1 (2021): 41–50. http://dx.doi.org/10.18705/1607-419x-2021-27-1-41-50.

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The article reviews the problem of hemorrhagic transformation (HT) of ischemic stroke. The frequency and relevance of this complication in clinical practice is high considering the widespread implementation of cerebral recanalization methods: intravenous thrombolytic therapy and intravascular thromboembolectomy. The etiology and pathogenesis, as well as alternative mechanisms underlying the development of HT are also discussed. The probability of HT increases in case of extensive cerebral ischemia commonly associated with cardiac embolism. The role of spontaneous and medication-induced arteria

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Kurita, Naohide, Kazuo Yamashiro, Takuma Kuroki, et al. "Metabolic endotoxemia promotes neuroinflammation after focal cerebral ischemia." Journal of Cerebral Blood Flow & Metabolism 40, no. 12 (2020): 2505–20. http://dx.doi.org/10.1177/0271678x19899577.

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Lipopolysaccharide (LPS) is a major component of the outer membrane of Gram-negative bacteria and a potent inflammatory stimulus for the innate immune response via toll-like receptor (TLR) 4 activation. Type 2 diabetes is associated with changes in gut microbiota and impaired intestinal barrier functions, leading to translocation of microbiota-derived LPS into the circulatory system, a condition referred to as metabolic endotoxemia. We investigated the effects of metabolic endotoxemia after experimental stroke with transient middle cerebral artery occlusion (MCAO) in a murine model of type 2 d

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Cipolla, Marilyn J. "Thomas Willis Lecture." Stroke 52, no. 7 (2021): 2465–77. http://dx.doi.org/10.1161/strokeaha.121.034620.

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Cerebral infarction or ischemic death of brain tissue, most notably neurons, is a primary response to vascular occlusion that if minimized leads to better stroke outcome. However, many cell types are affected in the brain during ischemia and reperfusion, including vascular cells of the cerebral circulation. Importantly, the structure and function of all brain vascular segments are major determinants of the depth of ischemia during the occlusion, the extent of collateral flow (and therefore amount of potentially salvageable tissue) and the degree of reperfusion. Thus, appropriate function of th

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Martín, Abraham, Emilie Macé, Raphael Boisgard, et al. "Imaging of Perfusion, Angiogenesis, and Tissue Elasticity after Stroke." Journal of Cerebral Blood Flow & Metabolism 32, no. 8 (2012): 1496–507. http://dx.doi.org/10.1038/jcbfm.2012.49.

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Blood flow interruption in a cerebral artery causes brain ischemia and induces dramatic changes of perfusion and metabolism in the corresponding territory. We performed in parallel positron emission tomography (PET) with [15O]H2O, single photon emission computed tomography (SPECT) with [99mTc]hexamethylpropylene-amino-oxime ([99mTc]HMPAO) and ultrasonic ultrafast shear wave imaging (SWI) during, immediately after, and 1, 2, 4, and 7 days after middle cerebral artery occlusion (MCAO) in rats. Positron emission tomography and SPECT showed initial hypoperfusion followed by recovery at immediate r

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Hong, Pu, Feng-Xian Li, Ruo-Nan Gu, et al. "Inhibition of NLRP3 Inflammasome Ameliorates Cerebral Ischemia-Reperfusion Injury in Diabetic Mice." Neural Plasticity 2018 (2018): 1–8. http://dx.doi.org/10.1155/2018/9163521.

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Sustained activation of NLRP3 inflammasome is closely related to diabetes and stroke. However, it is unknown whether NLRP3 inflammasome plays an essential role in stroke in diabetes. We aim to investigate the effect and the potential mechanism of NLRP3 inflammasome in diabetic mice with cerebral ischemia-reperfusion injury. A type 2 diabetic mouse model was induced by a high-fat diet and streptozotocin (STZ). Diabetic mice received MCC950 (the specific molecule NLRP3 inhibitor) or vehicle 60 minutes before the middle cerebral artery occlusion (MCAO) and reperfusion. MCC950 reduced the neurolog

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Pihlasviita, Saana, Olli S. Mattila, Juhani Ritvonen, et al. "Diagnosing cerebral ischemia with door-to-thrombolysis times below 20 minutes." Neurology 91, no. 6 (2018): e498-e508. http://dx.doi.org/10.1212/wnl.0000000000005954.

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ObjectivesTo clarify diagnostic accuracy and consequences of misdiagnosis in the admission evaluation of stroke-code patients in a neurologic emergency department with less than 20-minute door-to-thrombolysis times.MethodsAccuracy of admission diagnostics was studied in an observational cohort of 1,015 stroke-code patients arriving by ambulance as candidates for recanalization therapy between May 2013 and November 2015. Immediate admission evaluation was performed by a stroke neurologist or a neurology resident with dedicated stroke training, primarily utilizing CT-based imaging.ResultsThe rat

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Hariri, Robert J., Elizabeth L. Supra, John Paul Roberts, and Michael H. Lavyne. "Effect of naloxone on cerebral perfusion and cardiac performance during experimental cerebral ischemia." Journal of Neurosurgery 64, no. 5 (1986): 780–86. http://dx.doi.org/10.3171/jns.1986.64.5.0780.

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✓ Transient global cerebral ischemia (TGI) was induced in awake rats using the “four-vessel” occlusion model of Pulsinelli and Brierley. Blood pressure, arterial blood gases, cerebral blood flow, and cardiac output were measured during the acute (up to 2 hours) and chronic (2 to 72 hours) postischemic time periods. Coincident with the onset of TGI, cardiac output and caudate blood flow were depressed. The former returned to baseline within 30 minutes after the conclusion of TGI, and the latter progressed to hyperemia at 12 hours (81.8 ± 4.9 vs 68.6 ± 3.9 ml/min/100 gm tissue (mean ± standard e

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Bacigaluppi, Marco. "Animal Models of Ischemic Stroke. Part Two: Modeling Cerebral Ischemia." Open Neurology Journal 4, no. 1 (2010): 34–38. http://dx.doi.org/10.2174/1874205x01004010034.

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Sironi, Luigi, Elena Tremoli, Ingrid Miller, et al. "Acute-Phase Proteins Before Cerebral Ischemia in Stroke-Prone Rats." Stroke 32, no. 3 (2001): 753–60. http://dx.doi.org/10.1161/01.str.32.3.753.

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Kawano, T., K. Tsutsumi, H. Miyake, and K. Mori. "Striatal dopamine in acute cerebral ischemia of stroke-resistant rats." Stroke 19, no. 12 (1988): 1540–43. http://dx.doi.org/10.1161/01.str.19.12.1540.

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Josephson, S. Andrew, Stephen L. Hauser, and S. Claiborne Johnston. "Malignant middle cerebral artery stroke: Where ischemia meets the scalpel." Annals of Neurology 68, no. 4 (2010): A6—A8. http://dx.doi.org/10.1002/ana.22265.

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Jiao, Yang, Yuze Cao, Xiaoyu Lu, et al. "Xanthohumol protects neuron from cerebral ischemia injury in experimental stroke." Molecular Biology Reports 47, no. 4 (2020): 2417–25. http://dx.doi.org/10.1007/s11033-019-05128-4.

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