- Blood Coagulation and Thrombosis Mechanisms
- Pregnancy and preeclampsia studies
- Maternal and fetal healthcare
- Hemophilia Treatment and Research
- Platelet Disorders and Treatments
- Coagulation, Bradykinin, Polyphosphates, and Angioedema
- Blood disorders and treatments
- Cardiovascular Issues in Pregnancy
- Myeloproliferative Neoplasms: Diagnosis and Treatment
- Chronic Myeloid Leukemia Treatments
- Blood groups and transfusion
- Ubiquitin and proteasome pathways
- Cancer-related gene regulation
- Sepsis Diagnosis and Treatment
- Acute Myeloid Leukemia Research
- Vitamin K Research Studies
- Erythrocyte Function and Pathophysiology
- Acute Lymphoblastic Leukemia research
- Congenital heart defects research
- Educational Assessment and Improvement
- Protein Degradation and Inhibitors
- Caveolin-1 and cellular processes
- Venous Thromboembolism Diagnosis and Management
- Congenital Diaphragmatic Hernia Studies
- Reflective Practices in Education
Medical College of Wisconsin
2005-2020
Institute of Cell Biology and Neurobiology
2019
Artemis Hospitals
2013
Versiti Blood Center of Wisconsin
2003-2008
University of North Carolina at Chapel Hill
2003
Eli Lilly (United States)
2003
Université Paris Cité
2003
Hôpital Cochin
2003
Assistance Publique – Hôpitaux de Paris
2003
Loyola University Medical Center
1999-2000
Activated protein C (APC) reduces mortality of severe sepsis patients but increases the risk serious bleeding. APC exerts anticoagulant activity by proteolysis factors Va/VIIIa. also antiinflammatory and antiapoptotic effects stabilizes endothelial barrier function APC-initiated cell signaling that requires two receptors, receptor (EPCR) protease-activated 1 (PAR1). The relative importance APC's various activities for efficacy in is unknown. We used engineering mouse genetically altered mice...
The E-26 transforming specific (ETS)-related gene, TEL , also known as ETV6 encodes a strong transcription repressor that is rearranged in several recurring chromosomal rearrangements associated with leukemia and congenital fibrosarcoma. nuclear phosphoprotein widely expressed all normal tissues. contains DNA-binding domain at the C terminus helix–loop–helix (also called pointed domain) N terminus. necessary for homotypic dimerization interaction ubiquitin-conjugating enzyme UBC9. Here we...
<b>Background:</b> Serological safety is an integral part of overall for blood banks. Emphasis on the use routinue Red Blood Cell (RBC) antibody screen test, at set time intervals, to reduce risks related alloantibodies. Also emphasis importance issuing antigen negative alloantibody positive patients. Effect using leucodepleted rate alloimmunization highlighted. The concept provision phenotypically matched suggested. <b>Materials and Methods:</b> Antibody test important select appropriate...
The E-26 transforming specific (ETS)-related gene TEL , also known as ETV6 is involved in a large number of chromosomal rearrangements associated with leukemia and congenital fibrosarcoma. encoded protein contains two functional domains: helix–loop–helix (HLH) domain (also pointed domain) located at the N terminus DNA-binding C terminus. HLH protein–protein interaction itself other members ETS family transcription factors such FLI1. factor, we others have shown that it repressor expression....
We describe a mouse model of fetal loss in factor V Leiden (FvL) mothers which is triggered when the maternal prothrombotic state coincides with gene defects that reduce activation protein C anticoagulant pathway within placenta. Fetal caused by disruption placental morphogenesis at stage labyrinth layer formation and occurs absence overt thrombosis, infarction, or perfusion defects. Platelet depletion elimination protease-activated receptor 4 (Par4) from mother allows normal placentation...
Abstract Tissue factor pathway inhibitor (TFPI) is a serine protease with multiple anticoagulant activities. The Kunitz1 (K1) domain of TFPI binds the active site VIIa and required for inhibition tissue (TF)/factor catalytic activity. Mice lacking K1 die in utero. highly expressed on trophoblast cells placenta. We used genetic strategies to selectively ablate exon 4 encoding embryo, while maintaining expression cells. This approach resulted expected Mendelian frequency domain–deficient mice....
Mice reveal a link between maternal or fetal thrombophilia, uteroplacental thrombosis, hemorrhage, and placental abruption.