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Loss of Syndecan-1 Abrogates the Pulmonary Protective Phenotype Induced by Plasma After Hemorrhagic Shock.
Shock
September 2017
*Shock Trauma Center, University of Maryland School of Medicine, Baltimore, Maryland †Department of Anesthesia, University of Texas Health Science Center at Houston, Houston, Texas ‡Division of Respiratory Diseases, Children's Hospital, Harvard Medical School, Boston, Massachusetts.
Syndecan-1 (Sdc1) is considered a biomarker of injury to the endothelial glycocalyx following hemorrhagic shock, with shedding of Sdc1 deleterious. Resuscitation with fresh frozen plasma (FFP) has been correlated with restitution of pulmonary Sdc1 and reduction of lung injury, but the precise contribution of Sdc1 to FFPs protection in the lung remains unclear. Human lung endothelial cells were used to assess the time and dose-dependent effect of FFP on Sdc1 expression and the effect of Sdc1 silencing on in vitro endothelial cell permeability and actin stress fiber formation.
View Article and Find Full Text PDFPlasma-Mediated Gut Protection After Hemorrhagic Shock is Lessened in Syndecan-1-/- Mice.
Shock
November 2015
*Department of Pathology and Immunology, Baylor College of Medicine, Houston, Texas †Shock Trauma Center, University of Maryland, Baltimore, Maryland ‡Blood Systems Research Institute §Department of Surgery, University of California, San Francisco, California ||University of Texas Health Science Center at Houston, Houston, Texas ¶Division of Respiratory Diseases, Children's Hospital, Harvard Medical School, Boston, Massachusetts.
Article Synopsis
- The study shows that fresh frozen plasma (FFP) helps reduce lung inflammation and injury after hemorrhagic shock in the gut, linked to the protein syndecan-1.
- The effects of plasma on gut injury were tested using both normal mice and those lacking syndecan-1, revealing that the absence of this protein worsens gut damage.
- Additionally, resuscitation with FFP not only reduced gut inflammation and injury more than other treatments but also lowered levels of inflammation-related proteins TNFα and ADAM-17, suggesting a protective mechanism involving syndecan-1.
Syndecan-1 restitution by plasma after hemorrhagic shock.
J Trauma Acute Care Surg
June 2015
From the Shock Trauma Center (R.A.K.), University of Maryland, Baltimore, Maryland; and Blood Systems Research Institute and the University of California (S.P.), San Francisco, California.
Heparin, cell adhesion, and pathogenesis of inflammatory bowel disease.
Lancet
July 1999
Inflammatory Bowel Disease Research Group, St Mark's Hospital, Harrow, UK.
Tissue repair involves a close interplay between growth factors and cell adhesion molecules. The normal healing process may be disrupted by pathophysiological states such as inflammation, due to loss of growth factors, cell adhesion molecules, or both, which results in a reduced rate of healing. Such events may occur in inflammatory bowel disease during mucosal restitution.
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