A similar effect of fibrinogen on efficacy and safety of tenecteplase alteplase in acute ischemic cerebrovascular events (TRACE II) trial.

Background And Objectives: Hemostasis factors affecting clot patterns, particularly fibrinogen, may influence the effectiveness of intravenous thrombolysis (IVT). We aimed to investigate the impact of differences in fibrinogen plasma levels on the efficacy and safety of tenecteplase alteplase in an acute ischemic cerebrovascular events-II (TRACE-II) trial.

Methods: In a multi-center, prospective, open-label, end-point blinded, randomized, controlled trial.

Exploring Non-Coding RNA Regulation of the Blood-Brain Barrier in Neurodegenerative Diseases: A Systematic Review.

Neurodegenerative diseases (NDs) are characterized by progressive neuronal loss and dysfunction, leading to significant cognitive and motor impairments. The disruption of the blood-brain barrier (BBB) integrity, a key regulator of central nervous system homeostasis, emerges as a critical factor in the pathogenesis of these disorders. Accumulating evidence implicates non-coding RNAs, particularly microRNAs (miRNAs) and long non-coding RNAs (lncRNAs), in BBB regulation.

Relationship between homocysteine, vitamin B9, vitamin B12 levels methylenetetrahydrofolate reductase (C677T, A1298C) polymorphisms, and cryptogenic stroke in Tunisian adults´ patients: a case-control study.

Introduction: the relationship between elevated plasma homocysteine (Hcy) and stroke has been established, but this association remains indistinct in cryptogenic stroke in adults. Our aim is to investigate the association between homocysteine, vitamins B9 and B12, and cryptogenic stroke. Furthermore, to determine the correlation between methylenetetrahydrofolate reductase (MTHFR) polymorphism and biochemical levels in plasma.

Stroke Prognosis: The Impact of Combined Thrombotic, Lipid, and Inflammatory Markers.

Aim: D-dimer, lipoprotein (a) (Lp(a)), and high-sensitivity C-reactive protein (hs-CRP) are known predictors of vascular events; however, their impact on the stroke prognosis is unclear. This study used data from the Third China National Stroke Registry (CNSR-III) to assess their combined effect on functional disability and mortality after acute ischemic stroke (AIS).

Methods: In total, 9,450 adult patients with AIS were enrolled between August 2015 and March 2018.

Predicting 3-month poor functional outcomes of acute ischemic stroke in young patients using machine learning.

Background: Prediction of short-term outcomes in young patients with acute ischemic stroke (AIS) may assist in making therapy decisions. Machine learning (ML) is increasingly used in healthcare due to its high accuracy. This study aims to use a ML-based predictive model for poor 3-month functional outcomes in young AIS patients and to compare the predictive performance of ML models with the logistic regression model.

Ischemic Stroke in Young Tunisian Adults.

Introduction: Ischemic Stroke in young adults is a real public health problem; it's a major cause of disability, alters quality of life and has a great socio-economic impact.

Aim: determine risk factors and specify the etiology of arterial ischemic stroke in young Tunisian adults.

Methods: In this 5 years retrospective study (2015-2020), we included all young adults (18-50 years) admitted for arterial ischemic stroke (AIS).

MTHFR (C677T, A1298C), FV Leiden polymorphisms, and the prothrombin G20210A mutation in arterial ischemic stroke among young tunisian adults.

Arterial ischemic stroke (AIS) in young adults is less common in older adults, but the underlying pathogenesis and risk factors are more multi-faceted. The role of inherited thrombophilia such as 5, 10-methylenetetrahydrofolate reductase (MTHFR) gene polymorphism, (C677T and A1298C), factor V of Leiden (FVL) polymorphism, and the prothrombin G20210A mutations remains unclear. This study aims to evaluate the role of prothrombin genetic factor in AIS among young adults in Tunisia and to assess the synergistic effect between thrombogenic mutations in the pathogenesis of AIS.