ArticleFrontiers in neurology2025
Overall leukocyte levels link risk factors to Von Willebrand factor and Neutrophil Extracellular Traps in stroke thrombi: a Structural Equation Modeling analysis.
Article in Frontiers in neurology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
1 citing paper in PubMed.
- Deep Vein Thrombosis Prevention in Acute Ischemic Stroke Patients with Lower Limb Paralysis: A Narrative Review.Journal of clinical medicine · 2026Review
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14 authors.
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Abstract
Background: Von Willebrand Factor (VWF) and Neutrophil Extracellular Traps (NETs) are involved in the inflammatory response during thrombi formation and are widely found in thrombi of Acute Ischemic Stroke (AIS) patients. Inflammation may mediate the relationship between cerebrovascular risk factors (such as blood glucose) and thrombi components. This study uses overall leukocyte levels to identify potential links between risk factors and VWF, NETs in thrombi. Methods: Thrombi samples and clinical data from 61 stroke patients treated at our hospital between 2017 and 2023 were collected. The Partial Least Squares Structural Equation Modeling (PLS-SEM) assessed direct and indirect associations, with leukocyte and its subtype counts as mediating variables, VWF and NETs as endogenous variables, and cerebrovascular risk factors as exogenous variables. Results: Heart dysfunction and blood glucose showed a significant negative indirect effect on VWF through the overall leukocyte levels (indirect effect = -0.119 and -0.118, Conclusion: Overall leukocyte levels mediate the influence of blood glucose levels, heart dysfunction, and vitamin B12 on content VWF in thrombi in stroke patients. VWF reduction correlates with elevated discharge NIHSS scores. These cerebrovascular factors may regulate the pathological process of AIS thrombosis through inflammatory responses, guiding further exploration of the underlying mechanisms and informing clinical strategies.
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