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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, 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.
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 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 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 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.
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 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.
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 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 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
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.
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.
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.
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.
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.
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 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.
BackgroundPoststroke depression (PSD) is a prevalent neuropsychiatric complication of stroke. HCN channels were downregulated by pharmacological inhibitor or neuronspecific adenoassociated virus. Journal of the American Heart Association, Ahead of Print. However, the mechanisms underlying PSD are still unclear.
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.
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.
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 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, 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: 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).
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, Volume 56, Issue Suppl_1 , Page ATP211-ATP211, February 1, 2025. Pharmacologic mitigators of neurotoxicity have the potential to lengthen this therapeutic window, extending the opportunity for favorable surgical outcomes.
Stroke, Ahead of Print. This study supports the need to investigate new pharmacological approaches added to thrombolysis to prevent NET formation or enhance their disruption, such as recombinant human DNase I (deoxyribonuclease I). BACKGROUND:Thrombosis is linked to neutrophil release of neutrophil extracellular traps (NETs).
Stroke, Volume 56, Issue Suppl_1 , Page ADP50-ADP50, February 1, 2025. Background:Local angiotensin activity is thought to play a critical role in arterial wall homeostasis and remodeling, which contributes to the pathogenesis of subarachnoid hemorrhage (SAH).
Stroke: Vascular and Interventional Neurology, Volume 3, Issue S2 , November 1, 2023. IntroductionThrombolysis with recombinant tissue plasminogen activator remains vital to acute ischemic stroke (AIS) therapy. The admission National Institutes of Health Stroke Scale scores (NIHSS) were similar. min, p=0.00021).
24 will focus on the following three current guideline updates: American College of Cardiology (ACC)/American Heart Association (AHA) Guidelines 2023 Atrial Fibrillation Guideline - Pharmacology II: Strokes vs. Bleeds, What Do the Guidelines Tell Us About Practical Management in A-fib? The Guidelines Sessions at ACC.24
During a median follow-up of 53 months, we recorded venous thromboembolism (VTE), ischemic stroke or myocardial infarction, along with major bleeding. We observed 4 (6.1%, 3 VTE and 1 ischemic stroke) thrombotic events in patients on apixaban and 12 events (14%, 9 VTE, 2 ischemic strokes and 1 myocardial infarction) in VKA patients.
Thrombosis continues to pose a significant challenge in cardiovascular and cerebrovascular diseases, contributing to severe health complications such as myocardial infarction, acute ischemic stroke, and venous thromboembolism.
Peripheral arterial disease (PAD) is the third leading cause of atherosclerotic morbidity after coronary heart disease and stroke yet is widely underdiagnosed and undertreated. Treatment of risk factors such as diabetes and cigarette smoking can benefit patients with PAD.
Stroke, Volume 56, Issue Suppl_1 , Page AWP364-AWP364, February 1, 2025. proposed an innovative thromboembolic stroke model in mice where murine thrombin is injected into the M2 segment of the middle cerebral artery (MCA) to induce arterial thrombosis. Introduction:In 2007, Orset et al.
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 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.
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.
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