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- Frebelius, S, et al.
(författare)
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Thrombin inhibition by antithrombin III on the subendothelium is explained by the isoform AT beta
- 1996
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Ingår i: Arteriosclerosis, thrombosis, and vascular biology. - : Ovid Technologies (Wolters Kluwer Health). - 1079-5642 .- 1524-4636. ; 16:10, s. 1292-1297
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Tidskriftsartikel (refereegranskat)abstract
- Balloon injury of the rabbit aorta results in thrombin coagulant activity on the injured vessel wall that causes fibrin formation. The anticoagulant activity of both the intact and injured vessel wall has been partly explained by glycosaminoglycans with heparin-like activity that augment the activity of antithrombin III (AT). AT exists in two isoforms, α and β. ATβ, which constitutes only 5% to 10% of AT in plasma, lacks one carbohydrate side chain, has higher affinity for glycosaminoglycans, and associates more readily with the subendothelium. This study evaluated whether AT can inhibit thrombin on the injured vessel wall and, if so, whether one of the isoforms is more effective then the other. The two isoforms were isolated from human plasma by heparin-Sepharose chromatography, and the purity was investigated by isoelectric focusing and crossed immunoelectrophoresis. Rabbits were subjected to balloon injury of the aorta; 3 hours after injury the aorta was excised. Thrombin coagulant activity on the aorta was measured by exposure to fibrinogen and thereafter by measuring the generation of fibrinopeptide A. Injured animals were treated with AT, ATα, or ATβ and were compared with control animals. AT was demonstrated on the injured vessel wall by using an immunohistochemical method. Animals receiving crude AT had significantly lower amounts of thrombin coagulant activity on the injured aortic wall than control animals, but ATα at a comparable dose had no effect. ATβ was given in the same dose as crude AT and also at a dose (10%) proportional to its presence in plasma. Animals receiving ATβ had significantly lower values of thrombin on the injured aortic wall than control animals. We conclude that the inhibitory effect of AT on thrombin coagulant activity on the injured vessel wall is explained by its ATβ content.
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- Sims, D. A., et al.
(författare)
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The He(γ,n) reaction: a potential testing ground for the alpha-particle wavefunction
- 1998
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Ingår i: Physics Letters B. - 0370-2693. ; 442:1-4, s. 43-47
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Tidskriftsartikel (refereegranskat)abstract
- Differential cross sections (σ(Eγ,θn)) for the He(γ,n) reaction have been measured at Eγ=50–71 MeV and θn=30–120°. These data are compared with theoretical predictions where a microscopic calculation of the He and He wavefunctions has been made within the Alt-Grassberger-Sandhas, integral-equation formalism.
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- Blomqvist, J E, et al.
(författare)
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Importance of bone graft quality for implant integration after maxillary sinus reconstruction
- 1998
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Ingår i: Oral Surgery, Oral Medicine, Oral Pathology, Oral Radiology and Endodontology. - 1079-2104. ; 86:3, s. 268-274
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Tidskriftsartikel (refereegranskat)abstract
- OBJECTIVE: The aim of this study was to determine whether bone quality, as assessed by osteometry and histologic parameters, can be used to predict implant integration in conjunction with maxillary sinus reconstruction. STUDY DESIGN: Twelve patients with severely atrophied maxillary alveolar processes were treated through use of a two-stage surgical reconstructive strategy with implant placement 4 months after bone grafting. Bone biopsy specimens taken from the iliac crest peroperatively and from the sinus inlay sites 1, 2, 4, 6, or 12 months postoperatively were analyzed by light microscopy and osteomorphometry. Bone mineral content was measured by osteometry. RESULTS: Osteometric and osteomorphometric data (trabecular bone volume [%], assessment of chromatin staining, and an osteocyte index) registered for the biopsy specimens were not statistically correlated with implant failure. CONCLUSIONS: Prognostic evaluation of implant survival is difficult. The tested methods did not contribute to the improvement of guidelines for the clinical handling of these patients.
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- Karpman, D, et al.
(författare)
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von Willebrand factor mediates increased platelet retention in recurrent thrombotic thrombocytopenic purpura
- 1997
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Ingår i: Thrombosis and Haemostasis. - 0340-6245. ; 78:6, s. 62-1456
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Tidskriftsartikel (refereegranskat)abstract
- The plasma cryoprecipitate of two brothers with recurrent thrombotic thrombocytopenic purpura (TTP) was previously found to mediate increased platelet retention and contain ultra-large von Willebrand factor (vWF) multimers during remissions. We conducted this study to examine if vWF is involved in the increased platelet retention in TTP. Platelet retention decreased when the patients' plasma was incubated with a monoclonal antibody directed to the vWF epitope which interacts with the platelet receptor glycoprotein Ib or when incubated with a Fab-fragment directed to the platelet receptor glycoprotein IIb/IIIa. Replacement of patient vWF with an equivalent concentration of a factor VIII/vWF concentrate containing no ultra-large vWF multimers was accompanied by a normalization of platelet retention. These results indicate that vWF is involved in the increased platelet retention. Analysis of polymorphic markers in the vWF gene demonstrated that a recessive mutation in this gene is unlikely.
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