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Thomas W. Wakefield

Researcher at University of Michigan

Publications -  407
Citations -  23278

Thomas W. Wakefield is an academic researcher from University of Michigan. The author has contributed to research in topics: Venous thrombosis & Thrombosis. The author has an hindex of 68, co-authored 395 publications receiving 20620 citations. Previous affiliations of Thomas W. Wakefield include Conrad Hotels & Scripps Research Institute.

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Book ChapterDOI

Management of Chronic Venous Disease and Varicose Veins in the Elderly

TL;DR: In an age 65 and older subset of total patients who underwent radiofrequency ablation alone versus RFA + TIPP (transilluminated powered phlebectomy), there was a trend toward a higher percentage of patients who had RFA alone, and in this elderly subset, Venous Clinical Severity Scores tended to improve more with R FA alone compared to RFA+TIPP, without a significant difference in complications between the two procedures.
Journal Article

Prothrombotic effects of thrombolytic therapy in a rat (Rattus norvegicus) model of venous thrombolysis

TL;DR: Thrombus size was decreased in the tPA-treated rats but not in those that received saline or plasmin, and levels of the prothrombotic marker plasma soluble P-selectin increased when pl asmin was administered, while thrombus structure and vein wall effects did not differ between groups.
Journal ArticleDOI

Use of Compression Therapy in Patients with Chronic Venous Insufficiency Undergoing Ablation Therapy: A Report from the American Venous Registry.

TL;DR: The subcutaneous tissue pressure is significantly elevated in limbs with symptomatic varicose veins, and increases with disease severity, and the highest intramuscular tissue pressure was seen in obstructive venous disease, but was also significantly increased in C5-6 patients more importantly in the C 5-6 post-thrombotic limbs.
Journal ArticleDOI

The histone methyltransferase MLL1/KMT2A in monocytes drives coronavirus-associated coagulopathy and inflammation

TL;DR: In this article , the histone methyltransferase Mixed Lineage Leukemia 1 (MLL1/KMT2A) is an important regulator of MO/Mφ expression of procoagulant and profibrinolytic factors such as tissue factor (F3; TF), urokinase (PLAU), and urogenase receptor (PLAUR) in non-infected and infected cells.