Rashmi Sood

ORCID: 0000-0002-4523-9512
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About
Contact & Profiles
Research Areas
  • 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...

10.1084/jem.20070404 article EN The Journal of Experimental Medicine 2007-09-24

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...

10.1073/pnas.240315897 article EN Proceedings of the National Academy of Sciences 2000-11-14

<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...

10.4103/0973-6247.115577 article EN cc-by-nc-sa Asian Journal of Transfusion Science 2013-01-01

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....

10.1073/pnas.96.13.7467 article EN Proceedings of the National Academy of Sciences 1999-06-22

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...

10.1084/jem.20062566 article EN The Journal of Experimental Medicine 2007-04-16

10.1016/s0049-3848(09)70017-9 article EN Thrombosis Research 2009-01-01

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....

10.1182/bloodadvances.2018018853 article EN Blood Advances 2019-02-12

Mice reveal a link between maternal or fetal thrombophilia, uteroplacental thrombosis, hemorrhage, and placental abruption.

10.1126/sciadv.abb6196 article EN cc-by-nc Science Advances 2020-11-06
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