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Function: require_once
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http://dx.doi.org/10.3324/haematol.2015.131227 | DOI Listing |
ASAIO J
December 2024
Division of Cardiology, Montefiore Medical Center, New York, New York.
Type II heparin-induced thrombocytopenia and thrombosis (type II HITT) is a rare but serious complication in patients receiving heparin for anticoagulation. In type II HITT, an immune-mediated reaction against platelet factor four-heparin complexes results in thrombocytopenia and an elevated risk of thrombosis. This poses significant challenges for patients with advanced heart failure requiring urgent left-ventricular assist device (LVAD) implantation.
View Article and Find Full Text PDFArthritis Res Ther
July 2024
Division of Rheumatology, Department of Internal Medicine, University of Michigan, 1150 W Medical Center Drive, Ann Arbor, MI, 48109, USA.
Objectives: Neutrophils and neutrophil extracellular traps (NETs) contribute to the vascular complications of multiple diseases, but their role in systemic sclerosis (SSc) is understudied. We sought to test the hypothesis that NETs are implicated in SSc vasculopathy and that treatment with prostacyclin analogs may ameliorate SSc vasculopathy not only through vasodilation but also by inhibiting NET release.
Methods: Blood from 125 patients with SSc (87 diffuse cutaneous SSc and 38 limited cutaneous SSc) was collected at a single academic medical center.
Clin Chim Acta
July 2024
Department of Pharmaceutical and Biomedical Sciences, College of Pharmacy, University of Rhode Island, Kingston, RI, United States. Electronic address:
Treprostinil (Remodulin®) is a Food and Drug Administration (FDA) approved prostacyclin analog to treat pulmonary arterial hypertension. Recently, treprostinil has been investigated to reduce ischemia-reperfusion injury (IRI) during transplantation, which currently has no approved treatment. A validated analytical method is necessary to measure treprostinil concentrations in biological specimens.
View Article and Find Full Text PDFSci Signal
February 2024
Vascular Biology Program, Boston Children's Hospital and Department of Surgery, Harvard Medical School, Boston, MA 02115, USA.
High-density lipoprotein (HDL) nanoparticles promote endothelial cell (EC) function and suppress inflammation, but their utility in treating EC dysfunction has not been fully explored. Here, we describe a fusion protein named ApoA1-ApoM (A1M) consisting of apolipoprotein A1 (ApoA1), the principal structural protein of HDL that forms lipid nanoparticles, and ApoM, a chaperone for the bioactive lipid sphingosine 1-phosphate (S1P). A1M forms HDL-like particles, binds to S1P, and is signaling competent.
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