ABSTRACT
BACKGROUND: In cases of massive hemorrhage in the US military, improved outcomes have been reported with the use of warm, fresh whole blood transfusions. Cold-stored low-titer type O whole blood (LTOWB) has become the preferred product for resuscitation of severe bleeding in deployed surgical units. Reports of LTOWB use in civilian trauma are becoming more frequent. CASE REPORT: We report our experience with emergency transfusion of LTOWB for a woman with massive postpartum hemorrhage. The patient had two previous cesarean section deliveries at term without complications. With her third elective cesarean section at term, blood loss during surgery was not excessive, but 3 to 4 hours later she had an estimated blood loss of 3600 mL. Despite measures to control the hemorrhage, she rapidly became hypotensive and tachycardic, and our massive transfusion protocol (MTP) was activated. The transfusion service had very recently incorporated LTOWB into Trauma Pack 1 of the MTP. She received two LTOWB units, after which her hemorrhaging ceased, blood pressure normalized, and she became alert. One hour later she received one unit of fresh frozen plasma and one unit of red blood cells (RBCs). The following morning she received one unit of crossmatched RBCs, for a hematocrit of 20.7%. She was discharged home on Day 4, and she remains healthy. CONCLUSIONS: This is the first report of which we are aware of massive postpartum hemorrhage treated using LTOWB. Our positive experience leads us to speculate that this approach could have a role in massive obstetric hemorrhage.
Subject(s)
ABO Blood-Group System/blood , Blood Preservation , Blood Transfusion , Postpartum Hemorrhage/therapy , Resuscitation , Adult , Female , Humans , Postpartum Hemorrhage/blood , Pregnancy , Severity of Illness IndexABSTRACT
INTRODUCTION: It was demonstrated that metallopanstimulin-1 (MPS-1, RPS27) inhibited the growth of tumors formed by head and neck squamous cell carcinoma cells and reduced paxillin gene expression. METHODS: The present study examined whether and how MPS-1 affects another type of cancer, multiple myeloma (CAG). Enhanced expression of MPS-1 dramatically inhibited CAG in vitro and in vivo. RESULTS: Overexpression of MPS-1 resulted in decreased fibroblast growth factor (FGF2) receptor 3 and impaired endogenous MAPK/ErK signaling. MAPK/ErK signaling was not stimulated by adding recombinant FGF2 to myeloma cells overexpressing MPS-1. CONCLUSIONS: These data suggest that MPS-1 suppresses CAG growth and that weakened FGF2 signaling may contribute to this effect.
Subject(s)
Metalloproteins/biosynthesis , Multiple Myeloma/metabolism , Nuclear Proteins/biosynthesis , RNA-Binding Proteins/biosynthesis , Receptor, Fibroblast Growth Factor, Type 3/antagonists & inhibitors , Ribosomal Proteins/biosynthesis , Animals , Apoptosis/physiology , Cell Growth Processes/physiology , Cell Line, Tumor , Culture Media, Conditioned , Fibroblast Growth Factors/metabolism , Gene Expression Profiling , Humans , MAP Kinase Signaling System , Male , Metalloproteins/genetics , Metalloproteins/pharmacology , Mice , Mice, Nude , Multiple Myeloma/genetics , Multiple Myeloma/pathology , Nuclear Proteins/genetics , Nuclear Proteins/pharmacology , RNA-Binding Proteins/genetics , RNA-Binding Proteins/pharmacology , Receptor, Fibroblast Growth Factor, Type 3/biosynthesis , Receptor, Fibroblast Growth Factor, Type 3/genetics , Ribosomal Proteins/genetics , Ribosomal Proteins/pharmacology , Signal Transduction , Transfection , Transplantation, HeterologousABSTRACT
Metallopanstimulin-1 (MPS-1) is a multifunctional ribosomal protein RPS27 that contains a zinc finger domain of the C(4) type. MPS-1 has been found to be increased in the sera of a number of different cancers, including head and neck squamous cell carcinoma (HNSCC). However, little is known about the effect of a high-level MPS-1 in regulating cancer cell behavior. In this study, we overexpressed MPS-1 protein in the HNSCC cell line UMSCC-1. We found MPS-1 distributes not only in the cytosol, but also in the nuclei. In addition, MPS-1 is secreted into the culture medium. In vitro and in vivo experiments show that growth of UMSCC-1 cells transfected with MPS-1 is dramatically inhibited. Moreover, we also found that with overexpressing MPS-1, UMSCC-1 cells were arrested on G0/G1 phase, cell proliferation rate was reduced, and tumor angiogenesis was impaired. Further gene array analysis, immunohistochemistry staining and Western blotting reveal that MPS-1 reduces paxillin mRNA and protein levels in UMSCC-1 cells both in vitro and in vivo. Together, these data indicate that when MPS-1 is overexpressed, it has an extraribosomal function as a strong inhibitor of HNSCC tumor cell growth, which may be exerted by reduced paxillin gene expression.
