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A new study has discovered what researchers say is the first drug to fully reproduce the effects of physical stroke rehabilitation in model mice, following from human studies.
BackgroundREST (Repressor‐Element 1 [RE1]‐silencing transcription factor) inhibits Na+/Ca2+exchanger‐1 (Ncx1) transcription in neurons through the binding of RE1 site on brain promoter(Br)after stroke. We identified a new putative RE1 site inNcx1heart promoter(Ht)sequence (Ht‐RE1) that participates in neuronalNcx1transcription.
Stroke is a major cause of mortality, morbidity and economic burden. Strokes can be thrombotic, embolic or haemorrhagic. The key risk factor for cardioembolic stroke is atrial fibrillation or flutter, and oral anticoagulation (OAC) is recommended in all but the lowest-risk patients with evidence of these arrhythmias.
Stroke, Volume 55, Issue Suppl_1 , Page AWP310-AWP310, February 1, 2024. Background:A major hallmark of stroke is the dysregulation of normal metabolic functions. These results support the hypothesis that PFKFB3 inhibitors may be used as a novel pharmacological treatment for reducing delayed cell death after ischemic stroke.
Patients with NVAF deemed appropriate for LAAX to reduce the risk of stroke and systemic embolism, will participate in this research effort. Stroke is a major concern for millions of people living with atrial fibrillation, and as physicians, we strive to deliver better outcomes for these patients." The acquisition of Laminar, Inc.
Stroke, Volume 56, Issue Suppl_1 , Page AWP339-AWP339, February 1, 2025. Background:Ischemic stroke triggers the metabolic reprogramming of cells in the infarct core and surrounding penumbra. Previous research in our lab supports a neuroprotective effect of PFKFB3 inhibition after stroke in young male mice.
Stroke, Volume 55, Issue Suppl_1 , Page AWP315-AWP315, February 1, 2024. Backgrounds:Our prior work demonstrated the potential of targeting miR-141-3p to mitigate ischemic stroke damage. Mice were sacrificed at 3 (acute) or 30 (chronic) days post-stroke.
Stroke, Volume 56, Issue Suppl_1 , Page ATP380-ATP380, February 1, 2025. Although progress has been made, the role of lipid metabolism following stroke remains unclear. Recent research on neurodegenerative diseases has highlighted a pathophysiological cascade characterized by abnormal lipid accumulation within the brain.
BackgroundAn increased risk of recurrent stroke is noted in patients with atrial fibrillation despite direct oral anticoagulant (DOAC) use. A total of 84 patients experienced recurrent ischemic stroke after switching to different oral anticoagulants, with a total follow‐up time of 14 years. 0.39] for apixaban, 0.23 [95% CI, 0.14–0.37]
Stroke, Volume 56, Issue Suppl_1 , Page AWP306-AWP306, February 1, 2025. 0.98; p=0.006) risk, but not ischemic stroke/subtypes (all p-values > 0.05). Introduction:Previous studies have suggested that increased body fat is associated with elevated cardiovascular disease (CVD) risk. Results were consistent in sensitivity analyses.
Stroke, Volume 56, Issue Suppl_1 , Page A57-A57, February 1, 2025. Background:Acute ischemic stroke is a leading cause of death and disability in the U.S. Patients with an initial Alberta Stroke Program Early CT Score (ASPECTS)>6 were compared to those with ASPECTS < 6.
Stroke, Volume 56, Issue Suppl_1 , Page ATP344-ATP344, February 1, 2025. In a mouse model of ischemic stroke, we found that Chrdl1 is excessively upregulated in astrocytes in the peri-infarct area during the post-stroke plasticity window (230 days post-stroke in the mouse).
Stroke, Volume 56, Issue Suppl_1 , Page AWP346-AWP346, February 1, 2025. Here we tested our hypothesis that pharmacological inhibition of TGFR2 in mice models of dementia may reduce RTN gliosis, breathing disorder and cognitive impairment.We In conclusion, pharmacological inhibition of TGFR2 improved cognition in AD and CAA mice.
Stroke, Volume 55, Issue Suppl_1 , Page A15-A15, February 1, 2024. In this study, we investigated the effect of pharmacological activation of MerTK-mediated efferocytosis using the Gas6 in intracranial aneurysms.Methods:We used 10-week-old male C57BL/6J mice.
Stroke, Volume 56, Issue Suppl_1 , Page AWP392-AWP392, February 1, 2025. In our lab, we have shown that Ripk2 contributes to secondary injury following ischemic stroke due to neuroinflammation. Additionally, pharmacologically inhibiting Ripk2 is neuroprotective and reduces infarction and deficits after stroke.
Stroke, Volume 56, Issue Suppl_1 , Page ATP369-ATP369, February 1, 2025. In young mice, pharmacological activation or stimulation of the Vagus nerve has been shown to mitigate ischemic stroke injury by reducing brain and peripheral inflammation and oxidative stress.
Stroke, Volume 55, Issue Suppl_1 , Page AWP317-AWP317, February 1, 2024. We also used flow sorted Ly6C hi and low monocytes for phagocytic uptake study obtained from perilesional ipsilateral mouse brain tissue of P2X4R KO and littermate WT mice after 3 or 7 days of stroke. and 2-fold P<0.05 and 2-fold P<0.05
Stroke, Volume 55, Issue Suppl_1 , Page ATP320-ATP320, February 1, 2024. Background:The complement C3a receptor (C3aR) plays a prominent role in deleterious post-stroke neuroinflammation. We and others have shown that either genetic deficiency of C3aR or its pharmacological inhibition in rodents protects against ischemic brain injury.
Stroke, Volume 55, Issue Suppl_1 , Page AWP301-AWP301, February 1, 2024. We hypothesized that pharmacological inhibition of STAT3 activation in mice during the reperfusion phase after middle cerebral artery occlusion (MCAO) will lead to increased infarct size. Interestingly Stattic-treated mice had larger spleens (66.31 ± 5.40
Despite comprehensive anticoagulation protocols, discrepancies in pharmacologic responses due to patient-specific factors such as adherence to anticoagulation, renal function, and genetics suggest that imaging studies may still be critical for patient safety. Mortality rates within a year did not differ significantly between the two groups.
The 91 villages underwent random allocation into two arms: the control arm, encompassing 45 clusters, was subjected to non-pharmacological intervention (educational training on healthy lifestyle), whereas the intervention arm, comprising 46 clusters, received the non-pharmacological interventions in conjunction with a once-daily polypill tablet.
It is the main cause of lacunar stroke and a major source of vascular contributions to cognitive impairment and dementia. Knowledge gaps include initiating factors, molecular pathogenesis, relationships between arterial pathology and tissue damage, possible reversibility, pharmacological targets, and molecular biomarkers.
Stroke, Volume 55, Issue Suppl_1 , Page ATP312-ATP312, February 1, 2024. Traumatic brain injury (TBI) afflicts 70 million people worldwide annually and is the 3rd overall risk factor for developing Alzheimer's disease (AD), behind genetics and aging.
This miscommunication can cause blood to pool in the atria, increasing the risk of clot formation, which can then lead to strokes. AFib is associated with a fivefold increased risk of stroke, and it is also linked to heart failure, chronic fatigue, and other serious health issues.
Stroke, Ahead of Print. Subarachnoid hemorrhage is a critical neurological condition accounting for about 5% of all strokes, and survivors experience long-term cognitive deterioration and increased risk of dementia. Management techniques reviewed include long-term cognitive health, such as endovascular coiling and surgical clipping.
3 Patients with ASCVD are at a higher risk for major adverse cardiovascular events (MACE) including heart attack or myocardial infarction (MI), stroke, and cardiovascular (CV) death.4 mg) to reduce the risks of heart attack, stroke, coronary revascularization, and CV death.29 4 In the U.S. 22 In general, hsCRP values above 2.0
Stroke, Volume 55, Issue Suppl_1 , Page AWP51-AWP51, February 1, 2024. Background:Stroke is a debilitating condition and patients with acute stroke usually stays about a week in the acute hospital. The APN would identify stroke patients admitting to CH for further rehabilitation.
High blood pressure, or hypertension , is a leading cause of heart attacks, strokes and death. “In most cases, these differences persisted at six-month follow up despite the addition of other antihypertensive treatments. No new serious safety concerns were observed.”
Cerebral arteriovenous malformations represent the most common form of vascular malformations and can cause recurrent bleeding and hemorrhagic stroke. This discovery provides a promising entry point for preventive pharmacological interventions. The current issue of the JCI features an article by Zhao et al.
Using mediation Mendelian randomization, we explored proteomic mediators of the effects of genetically proxied IL-6 signaling on coronary artery disease, large artery atherosclerotic stroke, and peripheral artery disease.
A new joint guideline from the American Heart Association (AHA), the American College of Cardiology (ACC) and nine other medical societies reports early diagnosis and treatment of peripheral artery disease is essential to improve outcomes and reduce amputation risk, heart attack, stroke and death for people with Peripheral Artery Disease (PAD).
Stroke, Volume 55, Issue Suppl_1 , Page A103-A103, February 1, 2024. Introduction:Damage in the ischemic core and penumbra after stroke affects patient prognosis. Microglia immediately respond to ischemic insult after stroke. However, the microglial heterogeneity and the underlying mechanisms remain unclear.
This miscommunication can cause blood to pool in the atria, increasing the risk of clot formation, which can then lead to strokes. AFib is associated with a fivefold increased risk of stroke, and it is also linked to heart failure, chronic fatigue, and other serious health issues.
AF increases the risk of stroke, heart failure, dementia, and hospitalization. However, studies on how obesity affects pharmacologic or interventional AF treatments are limited. Journal of the American Heart Association, Ahead of Print. ABSTRACTAtrial fibrillation (AF) is the most common cardiac arrhythmia.
Stroke, Volume 55, Issue Suppl_1 , Page AWP322-AWP322, February 1, 2024. Hyperhomocysteinemia (Hhcy), a metabolic disorder is recognized as a risk factor for ischemic stroke. However, the impact of Hhcy on stroke outcome is not known.
Stroke, Volume 56, Issue Suppl_1 , Page ATP189-ATP189, February 1, 2025. Contributing factors such as hypocholesterolemia and hypertension amplify the risk of ICH and subsequent hematoma expansion, underscoring the urgent need for effective interventions.
Stroke, Volume 56, Issue Suppl_1 , Page AWP31-AWP31, February 1, 2025. Neurovascular disorders- including stroke, brain aneurysm, and vascular malformations- strike an estimated seven million Americans annually and can lead to vascular pathologies, neurological disability, and death.
Stroke, Ahead of Print. The motivation for developing a suitable PRES model is 2-fold: to fill in knowledge gaps of the pathophysiological mechanisms involved, and to open new perspectives for clinical assessment of pharmacological targets to improve therapeutic management of PRES.
Stroke, Volume 56, Issue Suppl_1 , Page ATP364-ATP364, February 1, 2025. This suggests that intranasally targeting the NgR1 pathway may be a viable pharmacologic mechanism of facilitating neuronal recovery in patients exposed to air pollution.
Stroke, Volume 55, Issue Suppl_1 , Page AWMP114-AWMP114, February 1, 2024. CAA may lead to dementia and stroke; however effective options currently are very limited to treat or halt CAA progression. Pharmacological inhibition of EZH2 improved cognitive outcomes in CAA mice, suggesting a possible therapeutic target.
Stroke: Vascular and Interventional Neurology, Ahead of Print. BACKGROUNDLocal angiotensin activity is thought to play a critical role in arterial wall homeostasis and remodeling, and impaired arterial wall integrity contributes to the pathogenesis of subarachnoid hemorrhage (SAH).
Patients with a new or recurrent episode of ASCVD (angina, acute myocardial infarction, transient ischemic attack, stroke, or peripheral arterial disease) between 1-Jan-2017 and 31-Dec-2018 were included. The costs derived from pharmacological treatments were obtained from the NHS pricing nomenclator database ( [link] ).
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