The Experts below are selected from a list of 237 Experts worldwide ranked by ideXlab platform
Michael Obladen - One of the best experts on this subject based on the ideXlab platform.
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Complement and Contact Activation Related to Surfactant Response in Respiratory Distress Syndrome
Pediatric research, 1999Co-Authors: Mathias H. Wagner, Josef Sonntag, Evelyn Strauss, Michael ObladenAbstract:Complement and Contact Activation Related to Surfactant Response in Respiratory Distress Syndrome
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Complement and Contact Activation Related to Surfactant Response in Respiratory Distress Syndrome
Pediatric Research, 1999Co-Authors: Mathias H. Wagner, Josef Sonntag, Evelyn Strauss, Michael ObladenAbstract:The Activation of inflammation and coagulation cascades is part of the pathogenesis of adult respiratory distress syndrome (RDS). Previous studies have demonstrated Contact Activation in preterm infants with RDS, whereas no concordant results have been found with complement Activation. In this study, both systems were investigated in preterm infants with severe RDS and related to surfactant response. Thirty preterm newborns with severe respiratory distress (FiO_2 > 0.5), but with no evidence of infection or fetal acidosis, were studied. Eighteen healthy preterm newborns of similar gestational age and birth weight served as controls. The study group was divided into two subgroups, according to their response to a porcine natural surfactant 6 h after administration: responders (FiO_2 reduction > 50%) and poor responders (FiO_2 reduction ≤ 50%). C1q, C4, factor B, C3a, C5a, complement, and C1-inhibitor activity, as well as factor XIIa, were determined in blood samples, drawn 24 h after birth. Except for C1-inhibitor concentration and C1-inhibitor activity, all parameters for infants with severe RDS were different from controls. Complement precursor proteins were lower, and activated split products of the complement and Contact system were higher. Infants with a poor response after application of surfactant showed higher amounts of C3a, C5a, and factor XIIa but lower C1q and C4 levels compared with infants with a good response to surfactant. Activation of the complement and the Contact system was demonstrated in all respiratory distress patients. This Activation was more pronounced in poor responders to exogenous surfactant.
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Complement and Contact Activation in term neonates after fetal acidosis
Archives of disease in childhood. Fetal and neonatal edition, 1998Co-Authors: Josef Sonntag, Mathias H. Wagner, Evelyn Strauss, Michael ObladenAbstract:AIMS—To evaluate complement and Contact Activation after fetal acidosis. METHODS—Fifteen term neonates with hypoxic-ischaemic encephalopathy after umbilical arterial pH 7.20. Determinations of the complement function and C1-inhibitor activity were performed as kinetic tests 22-28 hours after birth. C1q, C1-inhibitor, and factor B concentrations were determined by radial immunodiffusion and those of C3a, C5a, and factor XIIa by enzyme immunoabsorbent assay. RESULTS—Median complement function (46 vs 73 %), C1q (4.3 vs 9.1 mg/dl), and factor B (5.2 vs 7.7 mg/dl) decreased after fetal acidosis. The activated split products C3a (260 vs 185 µg/l), C5a (5.0 vs 0.6 µg/l), and factor XIIa (3.2 vs 1.3 µg/l) increased in the neonates after fetal acidosis. No differences were found in the concentration and activity of C1-inhibitor. CONCLUSIONS—Complement and Contact Activation occurred in the newborns with hypoxic-ischaemic encephalopathy. Activation of these systems generates mediators which can trigger inflammation and tissue injury.
Thomas A. Horbett - One of the best experts on this subject based on the ideXlab platform.
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hemocompatibility of treated polystyrene substrates Contact Activation platelet adhesion and procoagulant activity of adherent platelets
Journal of Biomedical Materials Research, 1998Co-Authors: J M Grunkemeier, Weibor Tsai, Thomas A. HorbettAbstract:Platelet adhesion to biomaterials is often used as an index of blood compatibility, but a more clinically relevant issue is whether the adherent platelets are able to promote clot formation (i.e., if they are in the procoagulant state). Platelets rapidly generate thrombin when they are in the procoagulant state and the Va/Xa complex is present. We found that adherent platelets are procoagulant by three different methods: binding of FITC–Annexin V, acceleration of thrombin generation in the presence of Xa, Va, and prothrombin; and clotting of recalcified plasma. In the clotting time studies, the effect of adherent platelets on TCPS was completely eliminated by the addition of Annexin V, which is known to bind tightly to procoagulant platelets. The degree of procoagulant activity of adherent platelets was determined by measuring thrombin generation rates in the presence of the clotting factors Va, Xa, and prothrombin and normalizing to the number of adherent platelets. Two key observations were made in these studies. First, the procoagulant activity of platelets adherent to untreated and to several types of treated polystyrenes, as well as to glass and PET, was much greater than the procoagulant activity of unstimulated bulk phase platelets. Little difference in the procoagulant activity of adherent platelets was observed among the materials tested, however. Second, the procoagulant activity of platelets prestimulated with ionophore and subsequently allowed to adhere to Plastek® M was much greater than when adherent platelets were stimulated by the adhesion event only. Measured values for platelet adhesion, platelet Activation, and Contact Activation of blood plasma are discussed in the context of their potential combined impact on blood clotting. © 1998 John Wiley & Sons, Inc. J Biomed Mater Res, 41, 657–670, 1998.
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hemocompatibility of treated polystyrene substrates Contact Activation platelet adhesion and procoagulant activity of adherent platelets
Journal of Biomedical Materials Research, 1998Co-Authors: J M Grunkemeier, Weibor Tsai, Thomas A. HorbettAbstract:Platelet adhesion to biomaterials is often used as an index of blood compatibility, but a more clinically relevant issue is whether the adherent platelets are able to promote clot formation (i.e., if they are in the procoagulant state). Platelets rapidly generate thrombin when they are in the procoagulant state and the VA/Xa complex is present. We found that adherent platelets are procoagulant by three different methods: binding of FITC-Annexin V, acceleration of thrombin generation in the presence of Xa, Va, and prothrombin; and clotting of recalcified plasma. In the clotting times studies, the effect of adherent platelets on TCPS was completely eliminated by the addition of Annexin V, which is known to bind tightly to procoagulant platelets. The degree of procoagulant activity of adherent platelets was determined by measuring thrombin generation rates in the presence of the clotting factors Va, Xa, and prothrombin and normalizing to the number of adherent platelets. Two key observations were made in these studies. First, the procoagulant activity of platelets adherent to untreated and to several types of treated polystyrenes, as well as to glass and PET, was much greater than the procoagulant activity of unstimulated bulk phase platelets. Little difference in the procoagulant activity of adherent platelets was observed among the materials tested, however. Second, the procoagulant activity of platelets prestimulated with ionophore and subsequently allowed to adhere to Plastek M was much greater than when adherent platelets were stimulated by the adhesion event only. Measured values for platelet adhesion, platelet Activation, and Contact Activation of blood plasma are discussed in the context of their potential combined impact on blood clotting.
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Contact Activation during incubation of five different polyurethanes or glass in plasma.
Journal of Biomedical Materials Research, 1995Co-Authors: K.w.h.j. Van Der Kamp, Kip D. Hauch, Jan Feijen, Thomas A. HorbettAbstract:During blood-material interaction, the enzymes factor XII fragment (factor XIIf) and kallikrein are generated (Contact Activation). In this study, the enzymatic activities of factor XIIf and kallikrein were examined with an assay based on the conversion of tripeptide-p-nitroanilide substrate. With the use of aprotinin to inhibit kallikrein, the proteolytic activities of factor XIIf and kallikrein could be separately determined. In this in vitro study, two commercially available polyurethanes, Pellethane and Biomer®; three custom synthesized polyurethanes; a biomerlike 2000 Mw polytetramethyleneoxide containing polyurethane (PU-2000); an octadecyl extended (ODCE) biomer-like 2000 Mw Polytetramethyleneoxide containing polyurethane (PU-2000-ODCE); a hard-segment polyurethane (HS-PU); and glass (reference material) were incubated in 25% diluted plasma. In both series of experiments, glass caused the highest amidolytic activities by factor XIIf and kallikrein compared with any of the polyurethanes. In contrast, within the polyurethane group of materials, lower amidolytic activities by factor XIIf and kallikrein were measured on the custom-made polyurethanes than on the commercially available polyurethanes, although the differences among the polyurethanes were small. In addition, the influence of different ratios of material surface to the plasma incubation volume was studied. An increased ratio of surface area over plasma volume resulted in reduced Contact Activation, suggesting that plasma components are the limiting factor.
Mathias H. Wagner - One of the best experts on this subject based on the ideXlab platform.
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Complement and Contact Activation Related to Surfactant Response in Respiratory Distress Syndrome
Pediatric research, 1999Co-Authors: Mathias H. Wagner, Josef Sonntag, Evelyn Strauss, Michael ObladenAbstract:Complement and Contact Activation Related to Surfactant Response in Respiratory Distress Syndrome
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Complement and Contact Activation Related to Surfactant Response in Respiratory Distress Syndrome
Pediatric Research, 1999Co-Authors: Mathias H. Wagner, Josef Sonntag, Evelyn Strauss, Michael ObladenAbstract:The Activation of inflammation and coagulation cascades is part of the pathogenesis of adult respiratory distress syndrome (RDS). Previous studies have demonstrated Contact Activation in preterm infants with RDS, whereas no concordant results have been found with complement Activation. In this study, both systems were investigated in preterm infants with severe RDS and related to surfactant response. Thirty preterm newborns with severe respiratory distress (FiO_2 > 0.5), but with no evidence of infection or fetal acidosis, were studied. Eighteen healthy preterm newborns of similar gestational age and birth weight served as controls. The study group was divided into two subgroups, according to their response to a porcine natural surfactant 6 h after administration: responders (FiO_2 reduction > 50%) and poor responders (FiO_2 reduction ≤ 50%). C1q, C4, factor B, C3a, C5a, complement, and C1-inhibitor activity, as well as factor XIIa, were determined in blood samples, drawn 24 h after birth. Except for C1-inhibitor concentration and C1-inhibitor activity, all parameters for infants with severe RDS were different from controls. Complement precursor proteins were lower, and activated split products of the complement and Contact system were higher. Infants with a poor response after application of surfactant showed higher amounts of C3a, C5a, and factor XIIa but lower C1q and C4 levels compared with infants with a good response to surfactant. Activation of the complement and the Contact system was demonstrated in all respiratory distress patients. This Activation was more pronounced in poor responders to exogenous surfactant.
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Complement and Contact Activation in term neonates after fetal acidosis
Archives of disease in childhood. Fetal and neonatal edition, 1998Co-Authors: Josef Sonntag, Mathias H. Wagner, Evelyn Strauss, Michael ObladenAbstract:AIMS—To evaluate complement and Contact Activation after fetal acidosis. METHODS—Fifteen term neonates with hypoxic-ischaemic encephalopathy after umbilical arterial pH 7.20. Determinations of the complement function and C1-inhibitor activity were performed as kinetic tests 22-28 hours after birth. C1q, C1-inhibitor, and factor B concentrations were determined by radial immunodiffusion and those of C3a, C5a, and factor XIIa by enzyme immunoabsorbent assay. RESULTS—Median complement function (46 vs 73 %), C1q (4.3 vs 9.1 mg/dl), and factor B (5.2 vs 7.7 mg/dl) decreased after fetal acidosis. The activated split products C3a (260 vs 185 µg/l), C5a (5.0 vs 0.6 µg/l), and factor XIIa (3.2 vs 1.3 µg/l) increased in the neonates after fetal acidosis. No differences were found in the concentration and activity of C1-inhibitor. CONCLUSIONS—Complement and Contact Activation occurred in the newborns with hypoxic-ischaemic encephalopathy. Activation of these systems generates mediators which can trigger inflammation and tissue injury.
Josef Sonntag - One of the best experts on this subject based on the ideXlab platform.
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Complement and Contact Activation Related to Surfactant Response in Respiratory Distress Syndrome
Pediatric research, 1999Co-Authors: Mathias H. Wagner, Josef Sonntag, Evelyn Strauss, Michael ObladenAbstract:Complement and Contact Activation Related to Surfactant Response in Respiratory Distress Syndrome
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Complement and Contact Activation Related to Surfactant Response in Respiratory Distress Syndrome
Pediatric Research, 1999Co-Authors: Mathias H. Wagner, Josef Sonntag, Evelyn Strauss, Michael ObladenAbstract:The Activation of inflammation and coagulation cascades is part of the pathogenesis of adult respiratory distress syndrome (RDS). Previous studies have demonstrated Contact Activation in preterm infants with RDS, whereas no concordant results have been found with complement Activation. In this study, both systems were investigated in preterm infants with severe RDS and related to surfactant response. Thirty preterm newborns with severe respiratory distress (FiO_2 > 0.5), but with no evidence of infection or fetal acidosis, were studied. Eighteen healthy preterm newborns of similar gestational age and birth weight served as controls. The study group was divided into two subgroups, according to their response to a porcine natural surfactant 6 h after administration: responders (FiO_2 reduction > 50%) and poor responders (FiO_2 reduction ≤ 50%). C1q, C4, factor B, C3a, C5a, complement, and C1-inhibitor activity, as well as factor XIIa, were determined in blood samples, drawn 24 h after birth. Except for C1-inhibitor concentration and C1-inhibitor activity, all parameters for infants with severe RDS were different from controls. Complement precursor proteins were lower, and activated split products of the complement and Contact system were higher. Infants with a poor response after application of surfactant showed higher amounts of C3a, C5a, and factor XIIa but lower C1q and C4 levels compared with infants with a good response to surfactant. Activation of the complement and the Contact system was demonstrated in all respiratory distress patients. This Activation was more pronounced in poor responders to exogenous surfactant.
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Complement and Contact Activation in term neonates after fetal acidosis
Archives of disease in childhood. Fetal and neonatal edition, 1998Co-Authors: Josef Sonntag, Mathias H. Wagner, Evelyn Strauss, Michael ObladenAbstract:AIMS—To evaluate complement and Contact Activation after fetal acidosis. METHODS—Fifteen term neonates with hypoxic-ischaemic encephalopathy after umbilical arterial pH 7.20. Determinations of the complement function and C1-inhibitor activity were performed as kinetic tests 22-28 hours after birth. C1q, C1-inhibitor, and factor B concentrations were determined by radial immunodiffusion and those of C3a, C5a, and factor XIIa by enzyme immunoabsorbent assay. RESULTS—Median complement function (46 vs 73 %), C1q (4.3 vs 9.1 mg/dl), and factor B (5.2 vs 7.7 mg/dl) decreased after fetal acidosis. The activated split products C3a (260 vs 185 µg/l), C5a (5.0 vs 0.6 µg/l), and factor XIIa (3.2 vs 1.3 µg/l) increased in the neonates after fetal acidosis. No differences were found in the concentration and activity of C1-inhibitor. CONCLUSIONS—Complement and Contact Activation occurred in the newborns with hypoxic-ischaemic encephalopathy. Activation of these systems generates mediators which can trigger inflammation and tissue injury.
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Complement and Contact Activation During Cardiovascular Operations in Infants
The Annals of thoracic surgery, 1998Co-Authors: Josef Sonntag, Ingo Dähnert, Brigitte Stiller, Roland Hetzer, Peter LangeAbstract:Abstract Background . By comparing the results of cardiac operations with or without cardiopulmonary bypass (CPB) in infants in a prospective study, we sought to determine which part of the postoperative systemic inflammatory response was caused by CPB. Methods . Thirty-five patients were divided into two groups: 11 infants operated on without CPB and 24 infants operated on with CPB. Blood samples were drawn before, during, and after the operation. We assessed complement function and the concentrations or activities of C1q, C3, C4, C1 inhibitor, factor B, the activated split product C3a, and prekallikrein and factor XIIa of the Contact system. Results . All of the patients exhibited a decrease of complement proteins. This was greater in infants who underwent CPB. A increase in C3a and factor XIIa and changes in prekallikrein activity occurred only in infants during CPB. Conclusions . Complement Activation occurs in all infants, but is significantly higher in the group with CPB. Contact Activation only occurs in patients who undergo CPB. Thus, the inflammatory response is caused by the use of a CPB circuit and to a lesser degree by surgical procedures and anesthesia.
Evelyn Strauss - One of the best experts on this subject based on the ideXlab platform.
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Complement and Contact Activation Related to Surfactant Response in Respiratory Distress Syndrome
Pediatric research, 1999Co-Authors: Mathias H. Wagner, Josef Sonntag, Evelyn Strauss, Michael ObladenAbstract:Complement and Contact Activation Related to Surfactant Response in Respiratory Distress Syndrome
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Complement and Contact Activation Related to Surfactant Response in Respiratory Distress Syndrome
Pediatric Research, 1999Co-Authors: Mathias H. Wagner, Josef Sonntag, Evelyn Strauss, Michael ObladenAbstract:The Activation of inflammation and coagulation cascades is part of the pathogenesis of adult respiratory distress syndrome (RDS). Previous studies have demonstrated Contact Activation in preterm infants with RDS, whereas no concordant results have been found with complement Activation. In this study, both systems were investigated in preterm infants with severe RDS and related to surfactant response. Thirty preterm newborns with severe respiratory distress (FiO_2 > 0.5), but with no evidence of infection or fetal acidosis, were studied. Eighteen healthy preterm newborns of similar gestational age and birth weight served as controls. The study group was divided into two subgroups, according to their response to a porcine natural surfactant 6 h after administration: responders (FiO_2 reduction > 50%) and poor responders (FiO_2 reduction ≤ 50%). C1q, C4, factor B, C3a, C5a, complement, and C1-inhibitor activity, as well as factor XIIa, were determined in blood samples, drawn 24 h after birth. Except for C1-inhibitor concentration and C1-inhibitor activity, all parameters for infants with severe RDS were different from controls. Complement precursor proteins were lower, and activated split products of the complement and Contact system were higher. Infants with a poor response after application of surfactant showed higher amounts of C3a, C5a, and factor XIIa but lower C1q and C4 levels compared with infants with a good response to surfactant. Activation of the complement and the Contact system was demonstrated in all respiratory distress patients. This Activation was more pronounced in poor responders to exogenous surfactant.
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Complement and Contact Activation in term neonates after fetal acidosis
Archives of disease in childhood. Fetal and neonatal edition, 1998Co-Authors: Josef Sonntag, Mathias H. Wagner, Evelyn Strauss, Michael ObladenAbstract:AIMS—To evaluate complement and Contact Activation after fetal acidosis. METHODS—Fifteen term neonates with hypoxic-ischaemic encephalopathy after umbilical arterial pH 7.20. Determinations of the complement function and C1-inhibitor activity were performed as kinetic tests 22-28 hours after birth. C1q, C1-inhibitor, and factor B concentrations were determined by radial immunodiffusion and those of C3a, C5a, and factor XIIa by enzyme immunoabsorbent assay. RESULTS—Median complement function (46 vs 73 %), C1q (4.3 vs 9.1 mg/dl), and factor B (5.2 vs 7.7 mg/dl) decreased after fetal acidosis. The activated split products C3a (260 vs 185 µg/l), C5a (5.0 vs 0.6 µg/l), and factor XIIa (3.2 vs 1.3 µg/l) increased in the neonates after fetal acidosis. No differences were found in the concentration and activity of C1-inhibitor. CONCLUSIONS—Complement and Contact Activation occurred in the newborns with hypoxic-ischaemic encephalopathy. Activation of these systems generates mediators which can trigger inflammation and tissue injury.