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Hereditary and acquired protein S deficiencies are associated with low TFPI levels in plasma.
No full textJ Thromb Haemost. 2010 Feb;8(2):294-300. Epub 2009 Nov 30.
Hereditary and acquired protein S deficiencies are associated with low TFPI
levels in plasma.
Castoldi E, Simioni P, Tormene D, Rosing J, Hackeng TM.
Department of Biochemistry, CARIM, Maastricht University, Maastricht, the
Netherlands. [email protected]
BACKGROUND: Protein S and tissue factor pathway inhibitor (TFPI) act together in
down-regulating coagulation.
OBJECTIVE: To investigate the TFPI/protein S system in hereditary and acquired
protein S deficiency.
METHODS: Plasma antigen levels of protein S and full-length TFPI were determined
in heterozygous type I protein S-deficient individuals (n=35), patients on oral
anticoagulant treatment (OAT) (n=29), oral contraceptive (OC) users (n=10) and
matched controls. Thrombin generation was determined using calibrated automated
thrombography.
RESULTS: Full-length TFPI levels were lower in type I protein S-deficient
individuals (76.8+/-33.8%) than in age- and sex-matched controls (128.0+/-59.4%,
P<0.001). Among protein S-deficient individuals with thrombosis, those on OAT had
not only lower total protein S levels (25.7+/-8.2% vs. 54.7+/-8.2%, P<0.001), but
also lower full-length TFPI levels (52.6+/-15.0% vs. 75.4+/-22.9%, P=0.009) than
those not on OAT. Similarly, OC users had lower protein S (73.8+/-11.5% vs.
87.9+/-10.8%, P=0.005) and full-length TFPI levels (73.7+/-27.7% vs.
106.4+/-29.2%, P=0.007) than non-users. When triggered with tissue factor, plasma
from protein S-deficient individuals generated 3-5-fold more thrombin than
control plasma. The difference was only partially corrected by normalization of
the protein S level, full correction requiring additional normalization of the
TFPI level. Protein S-immunodepletion experiments indicated that free protein S
and full-length TFPI form a complex in plasma, and the protein S/TFPI interaction
was confirmed by surface plasmon resonance analysis.
CONCLUSIONS: Full-length TFPI binds to protein S in plasma and is reduced in
genetic and acquired protein S deficiency. The concomitant TFPI deficiency
substantially contributes to the hypercoagulable state associated with protein S
deficiency.
PMID: 20002538 [PubMed - indexed for MEDLINE
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No full textAnticoagulants in cirrhosis: main concerns
No full textManagement of anticoagulation in cirrhosis is challenging because of the concomitant risk of both thromboembolism and bleeding complications. Randomized controlled studies are lacking. Direct oral anticoagulants seem to be the most manageable option. However, for patients with Child C cirrhosis, the only safer anticoagulant strategy, currently, is low-molecular-weight heparin
NUMERICAL MODELLING OF BOND BEHAVIOUR IN RC STRUCTURES AFFECTED BY REINFORCEMENT CORROSION
No full textSteel corrosion in reinforced concrete structures leads to severe degradation processes which usually affect both the ultimate and serviceability limit state performance of the whole construction. Numerical modelling of such a behaviour requires effective non linear models able to capture all the main effects of corrosion (i.e. cracking, reduction in bond strength, reduction in steel cross-section, bond degradation, etc.). This paper discusses these topics by focusing on the effects of corrosion on bond behaviour. In particular, a coupled mechanicalenvironmental damage model is used to simulate the deterioration of concrete (i.e. cover cracking and reduction of mechanical properties), while the effects of corrosion on bond behaviour have been dealt with using two
different approaches, one based on a “frictional type” law and the other on a “damage type” law. A comparison between experimental pull-out test data and numerical results verifies that the proposed procedures can effectively simulate the effects of corrosion on bond behaviour, mainly for the “damage type” approach. Finally the numerical simulation of some experimental tests of corroded beam has been carried out
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