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Stroke, Volume 56, Issue Suppl_1 , Page ATP356-ATP356, February 1, 2025. Background and Rationale:Acute hyperglycemia caused by cerebral ischemia occurs when there is a lack of oxygen, resulting in anaerobic glycolysis. We demonstrated that ischemia accelerates aging-like processes in the brain.
Stroke, Volume 56, Issue Suppl_1 , Page ATP376-ATP376, February 1, 2025. The study was aimed to test the effects of GSNO in ischemia/reperfusion (I/R) Injury through relieving thrombo-inflammation.Methods:Male C57BL/6 mice (n=160) were 10-week-old (20-25 g) at the time of surgery.
Stroke, Volume 56, Issue Suppl_1 , Page AWP395-AWP395, February 1, 2025. Introduction:Polymorphonuclear Neutrophils (PMNs) are the first blood-derived immune cells to respond in ischemia/reperfusion injury (I/RI). Mice were subject to 60 min or 90 min of ischemia to model strokes of varying severity.
Stroke, Volume 56, Issue Suppl_1 , Page ATP365-ATP365, February 1, 2025. Introduction:Polymorphonuclear leukocytes (PMNs) are among the first leukocytes recruited to the infarct following reperfusion in ischemic stroke. Infarct size was determined via triphenyl tetrazolium chloride staining.
Stroke, Volume 56, Issue Suppl_1 , Page ATP354-ATP354, February 1, 2025. Background:The selective autophagic removal of mitochondria, lysosomes, Golgi are termed mitophagy, lysophagy, Golgiphagy, respectively. Autophagic flux was examined by the buildup of p62 or ubiquitinated organelle protein.
Stroke, Volume 56, Issue Suppl_1 , Page AWP367-AWP367, February 1, 2025. Introduction:Ischemia reperfusion injury (IRI) is a paradoxical and deleterious consequence of current interventions for acute ischemic stroke (AIS).
Stroke, Volume 56, Issue Suppl_1 , Page AWP371-AWP371, February 1, 2025. The significance of cranial bone marrow-derived leukocytes following ischemic stroke in the setting of ischemia/reperfusion remains uncertain.
Stroke, Volume 56, Issue Suppl_1 , Page A113-A113, February 1, 2025. Background:Early detection and intervention of cerebral ischemia is critical to improving patient outcomes. This method has the potential to identify ischemic changes and facilitate expeditious intervention.
Stroke, Volume 56, Issue Suppl_1 , Page AWP399-AWP399, February 1, 2025. Background:The neuroinflammation triggered by acute cerebral ischemia can be mediated through inflammasome such as NLRP3 (NOD-like receptor family, pyrin domain containing 3) and ASC (apoptosis-associated speck-like protein).
Stroke, Volume 56, Issue Suppl_1 , Page ATP357-ATP357, February 1, 2025. Background:Despite the effectiveness of immediate treatment, such as thrombolytic therapy, after a stroke, many patients are unable to benefit due to time restrictions. However, treadmill training protected against these damages.
Stroke, Volume 56, Issue Suppl_1 , Page ATP395-ATP395, February 1, 2025. Introduction:Ischemic stroke is one of the leading causes of death in the United States and is a known risk factor for Alzheimers Disease (AD) development.
Stroke, Volume 56, Issue Suppl_1 , Page AWP370-AWP370, February 1, 2025. Approximately 30% of aneurysmal subarachnoid hemorrhage (aSAH) patients who survive the rupture develop delayed cerebral ischemia (DCI) 4 to 10 days following aSAH.
Stroke, Volume 56, Issue Suppl_1 , Page A157-A157, February 1, 2025. Experimental diffuse cortical ischemia was induced in Aldh1l1-Cre-ert2/MetRS-floxed mice via a 20-minute bilateral common carotid artery occlusion (BCCAO), followed by 3-week Anl water supplementation.
Stroke, Volume 56, Issue Suppl_1 , Page ATP368-ATP368, February 1, 2025. Ischemic stroke affects more than 600,000 Americans annually. Brain edema in the acute phase of ischemia-reperfusion primarily associates with early-stage neurovascular damage and plays a major role in poor outcomes of stroke.
Stroke, Volume 56, Issue Suppl_1 , Page AWP35-AWP35, February 1, 2025. Following SAH, neutrophils cause vascular occlusion via neutrophil extracellular traps (NETs) and NETs have been identified as a therapeutic target to prevent delayed cerebral ischemia in mice (DCI) with SAH. nucleosome.
Stroke, Volume 56, Issue Suppl_1 , Page ATP233-ATP233, February 1, 2025. While nearly all stroke patients undergo neuroimaging during acute triage, many patients do not initially present to EVT-capable centers, and interhospital transfer for the EVT procedure can result in significant time delays. had vessel recanalization.
Stroke, Volume 56, Issue Suppl_1 , Page AWP398-AWP398, February 1, 2025. Background:White matter or axonal injury is a key predictor of long-term functional outcome following ischemic stroke in humans. However, this type of injury is significantly understudied in animal stroke research.
Stroke, Volume 56, Issue Suppl_1 , Page AWMP81-AWMP81, February 1, 2025. Background and purpose:Stroke as a world-wide prevalent disease, has brought a huge burden to health care and the national economy, accurate and fast stroke diagnosis can significantly increase reperfusion rate, mitigate disability, and reduce deaths.
Stroke, Volume 56, Issue Suppl_1 , Page ATP400-ATP400, February 1, 2025. Ischemic stroke is a leading cause of death and disability in the US, occurring when the blood supply to an area of the brain is disrupted. Using a combination of Gcamp voltage sensors and EEG. Using a combination of Gcamp voltage sensors and EEG.
Stroke, Volume 56, Issue Suppl_1 , Page ADP29-ADP29, February 1, 2025. Introduction:The potential role of tRNA derived fragment (tRF&tiRNA) in ischemic stroke remains largely unknown. Small RNA sequencing analyses were conducted to explore the differentially expressed tRNA derived fragments.
Stroke, Volume 56, Issue Suppl_1 , Page AWMP20-AWMP20, February 1, 2025. Background:Neuronal circuitry remodeling which compromises excitatory and inhibitory neurons is critical to improve neurological outcome after stroke.
Stroke, Volume 56, Issue Suppl_1 , Page AWP372-AWP372, February 1, 2025. Introduction:Recent advances in brain cytoprotection therapies following cerebral ischemia-reperfusion (I/R) injury have become an emerging interest.
Stroke, Volume 56, Issue Suppl_1 , Page AWP209-AWP209, February 1, 2025. Background:COVID-19, primarily a respiratory illness caused by SARS-CoV-2, is associated with vascular complications like ischemia due to endothelial injury, hypercoagulability, and inflammation.
Stroke, Volume 56, Issue Suppl_1 , Page AWMP115-AWMP115, February 1, 2025. Intro:Resources for studying stroke are limited to clinical trials with sparse access to physiological and biochemical details, and pre-clinical animal studies with limited relation to humans. International Stroke Conference, February 7-9 2024, Phoenix2.
Stroke, Volume 56, Issue Suppl_1 , Page ATP372-ATP372, February 1, 2025. Introduction:Ischemic stroke is highly heterogeneous, with patient-to-patient differences in infarct location, severity, and degree of reperfusion, among other factors.
Stroke, Volume 56, Issue Suppl_1 , Page ADP26-ADP26, February 1, 2025. The function of these novel RNAs within the post-stroke brain remains virtually unexplored. Results:We discovered 46 eSINE-RNAs upregulated in the cortex following MCAO, 33 of which were unique to stroke and not detected in the sham group.
Stroke, Volume 56, Issue Suppl_1 , Page A90-A90, February 1, 2025. Introduction:Post-Stroke Cognitive Impairment (PSCI) is increasingly recognized as a major factor in long-term disability. Therefore, new therapies that enhance post-stroke brain function (plasticity) are appealing in translational research.
Stroke, Volume 56, Issue Suppl_1 , Page AWP359-AWP359, February 1, 2025. Background:Mechanical thrombectomy has been associated with improved outcomes in patients with acute ischemic stroke. Investigating the post-reperfusion inflammatory milieu could provide valuable insights into the mechanisms that influence stroke outcomes.
Stroke, Volume 56, Issue Suppl_1 , Page ADP28-ADP28, February 1, 2025. Background:Microglia-mediated inflammatory response directly affects ischemic stroke outcome. Autophagy is crucial in inflammatory response after cerebral ischemia. Mass spectrometry was used to investigate the interaction of NLRC5 with other proteins.
Stroke, Volume 56, Issue Suppl_1 , Page AWMP7-AWMP7, February 1, 2025. Background and objectives:Remote ischemic conditioning during cerebral ischemia ( PerRIC ) represents a new protection paradigm. Methods:Patients with suspected stroke < 8 hours of evolution and motor RACE > 0 were included.
Stroke, Volume 56, Issue Suppl_1 , Page AWMP87-AWMP87, February 1, 2025. Background:Complete recanalization, defined as modified Treatment in Cerebral Ischemia (mTICI) score of 2c or better, has been shown to be superior to mTICI 2b in terms of patient outcomes following stroke thrombectomy.
Stroke, Volume 56, Issue Suppl_1 , Page AWP213-AWP213, February 1, 2025. Intracerebral Hemorrhagic (ICH) stroke is the second most common type of stroke and its aftermath is often more severe than ischemia. Neural activity (Electrophysiological) data is collected pre/post stroke and during stimulation.
Stroke, Volume 56, Issue Suppl_1 , Page A162-A162, February 1, 2025. Background:Preceding respiratory tract infections (RTIs) caused by bacteria or viruses are associated with worse stroke outcomes, likely due to an exaggerated inflammatory immune response, endothelial dysfunction, platelet activation, and coagulopathy.
Stroke, Volume 56, Issue Suppl_1 , Page AWP402-AWP402, February 1, 2025. Background:Patients with hypertension (HTN) are almost 3 times more likely to have a stroke than non-hypertensive individuals. Middle Cerebral Artery Occlusion was used to induce focal ischemia/reperfusion injury (I/R). fold), IL-6 (3.3-fold),
Stroke, Volume 56, Issue Suppl_1 , Page A34-A34, February 1, 2025. Introduction:Neuroinflammation plays a major role in post-stroke neuronal injury. Meanwhile, post-stroke microstructural degradation of white matter (WM) fibers can be observed using fixel-based analysis (FBA) of diffusion MRI (dMRI).
Stroke, Volume 56, Issue Suppl_1 , Page ATP392-ATP392, February 1, 2025. Diabetes is a widespread disease, and stroke is one of the serious complications of diabetes. Thus, we evaluated cerebral blood flow up to 7 days post-ischemia in RH-exposed ITD rats using laser speckle imaging.
Stroke, Volume 56, Issue Suppl_1 , Page AWMP9-AWMP9, February 1, 2025. Background:Remote ischemic conditioning (RIC) with transient cycles of limb ischemia and reperfusion is a safe and promising neuroprotective therapy in acute ischemic stroke (AIS).
Stroke, Volume 56, Issue Suppl_1 , Page ATP367-ATP367, February 1, 2025. Elucidating the mechanisms of IPC is a critical challenge in the stroke field. We also provide data demonstrating how ischemia/reperfusion and innate immune signaling affect STAT1 phosphorylation signaling dynamics in microglia in vitro.
Stroke, Volume 56, Issue Suppl_1 , Page AWP366-AWP366, February 1, 2025. Our previous studies have suggested that the X escapee genesKdm6aandKdm5cwere involved in microglial activation after stroke in aged mice. Infarct volume and behavioral deficits were quantified 3 days after stroke.
Stroke, Volume 56, Issue Suppl_1 , Page ATP338-ATP338, February 1, 2025. Background):Stroke has become a leading cause of mortality and disability worldwide. However, if specific components in CSF could contribute to functional recovery during chronic phase of ischemic stroke remains unclear.
Stroke, Volume 56, Issue Suppl_1 , Page ATP337-ATP337, February 1, 2025. These data suggest that the gut may be implicated in IGF-1-mediated effects on stroke-induced cognitive impairment. Doxycycline was administered 4h later and IGF-1 was given ip at 4 and 24 h post-stroke.
Stroke, Volume 56, Issue Suppl_1 , Page AWMP93-AWMP93, February 1, 2025. Background:Chronic total internal carotid artery occlusion (CTO) can be associated with a high (22-25%) annual risk of stroke with limited therapeutic options. All TIA, stroke, death, and MI were recorded during follow-up. risk of restenosis.
Stroke, Volume 56, Issue Suppl_1 , Page ATP349-ATP349, February 1, 2025. Background:Inflammation, a key player in both acute and chronic cerebral ischemia, is activated in brain tissues by bilateral carotid stenosis (BCAS)- induced chronic cerebral hypoperfusion.
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