Home About us Contact
|
Home About us Contact | ||
|
|
||
L-Selectin Levels (l-selectin + level)
Selected AbstractsModulation of endothelial cell inflammatory integrins and stress markers with rh-factor VIIa in patients with advanced chronic hepatitis CJOURNAL OF VIRAL HEPATITIS, Issue 4 2003D. H. Van Thiel Summary. Individuals with chronic hepatitis C (CHC) progress to cirrhosis and hepatic cancer. Individuals with advanced CHC are coagulopathic and can manifest fibrinolysis. The coagulopathy is a consequence of hepatocytic dysfunction. The fibrinolysis represents a response to local endothelial cell injury, and is of a low-grade. Based upon this hypothesis, the effect of the infusion of recombinant human factor VIIa (rh-FVIIa) on endothelial cell inflammatory integrins and measures of endothelial stress were determined in 17 individuals with advanced CHC. Immediately prior to the infusion of rh-FVIIa, the plasma levels of tissue factor (TF), Thrombomodulin (TM), human soluble ICAM-1 (hs-ICAM-1), human soluble VCAM-1 (hs-VCAM-1), human soluble L-Selectin (hs-L-Selectin), the prothrombin time and the activated partial thromboplastin time were determined. The same parameters were assayed at 5, 10, 30, 120, 240 and 360 min after infusion. TF and TM levels were very high at baseline consistent with a vascular endothelial stress response. Similarly hs-ICAM-1, hs-VCAM-1 as well as L-Selectin levels were increased. Thirty minutes after the infusion, a marked reduction in ICAM-1 and VCAM-1 and to a lesser degree L-Selectin levels was observed. This reduction persisted for 360 min. No change in measures of fibrinolysis [plasminogen activator inhibitor-1 (PAI-1), total tissue factor pathway inhibitor (t-TFPI), activated tissue factor pathway inhibitor (TFPIa), d-dimers (DD), FSP and fibrinogen levels] occurred. In addition, no change in plasma Annexin-V was observed. Based upon these data it can be concluded that: (1) rh-FVIIa corrects the coagulopathy seen in advanced CHC; (2) reduces endothelial cell injury and/or stress as evidenced by the TF, TM, hs-ICAM-1 and hs-VCAM-1 levels in plasma; (3) these changes in coagulation occurred without inducing a propagated vascular thrombosis. [source] T lymphocyte rolling and recruitment into peripheral lymph nodes is regulated by a saturable density of L-selectin (CD62L)EUROPEAN JOURNAL OF IMMUNOLOGY, Issue 5 2007Elena Galkina Dr. Abstract L-selectin mediates tethering and rolling of lymphocytes in high endothelial venules (HEV) of lymph nodes (LN) and of leukocytes at inflammatory sites. We used transgenic mice expressing varying levels of wild-type or a non-cleavable mutant form of L-selectin on T cells to determine the relationship between L-selectin density, tethering and rolling, and migration into LN. T cells expressing supraphysiological levels of either wild-type or non-cleavable L-selectin showed rolling parameters similar to C57BL/6 T cells in hydrodynamic flow assays and during rolling in Peyer's patch HEV. In contrast, PMA- or antigen-activated T cells and L-selectin+/, T cells expressing subphysiological levels of L-selectin showed reduced numbers of rolling cells with increased rolling velocity. Short-term homing studies showed that elevated expression of L-selectin above physiological levels had no effect on T cell migration to LN; however, low L-selectin expression resulted in reduced T cell homing to LN. Thus, T lymphocyte migration into LN is regulated by the density of cell surface L-selectin. In addition, there is a saturable density of L-selectin required for optimal homing to PLN in C57BL/6 mice, the L-selectin level on circulating naive T cells promotes optimal homing, and increased expression above saturating levels promotes no further increase in T cell recruitment. [source] Selectin polymorphisms and perinatal morbidity in low-birthweight infantsACTA PAEDIATRICA, Issue 10 2006László Derzbach Abstracts Background: Studies have shown an association between altered expression of selectins and premature birth, early sepsis and bronchopulmonary dysplasia. Aim: To investigate the possible link between functional polymorphisms of the E-, P- and L-selectin genes and perinatal morbidity. Methods: We compared the genotype distribution of the E-selectin Ser128Arg, P-selectin Thr715Pro and L-selectin Pro213Ser polymorphisms in 125 low-birthweight singleton infants with those of 156 healthy term neonates. We also analysed the association of genotype with risk of sepsis and bronchopulmonary dysplasia. Results: We found no association between E-selectin or P-selectin polymorphisms and premature birth, nor did we find any association between E-selectin or P-selectin and early postnatal sepsis or bronchopulmonary dysplasia. Carriers of the 213Ser L-selectin allele were found to be more prevalent in low-birthweight infants, particularly in those with bronchopulmonary dysplasia. We found no association between the L-selectin polymorphism and early postnatal sepsis. Conclusion: Our results underline the importance of L-selectin in perinatal pathology, but further studies are needed to evaluate the alteration of L-selectin levels in carriers of the 213Ser allele and their possible contribution to premature birth and bronchopulmonary dysplasia. [source] | ||||||||||