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  • 1
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    Reduced ADAMTS13 in children with severe meningococcal sepsis is associated with severity and outcome
    Georg Thieme Verlag KG ; 2010
    In:  Thrombosis and Haemostasis Vol. 103, No. 06 ( 2010), p. 1181-1187
    Details
    In: Thrombosis and Haemostasis, Georg Thieme Verlag KG, Vol. 103, No. 06 ( 2010), p. 1181-1187
    Abstract: Multiple organ failure is a common feature of pediatric meningococcal sepsis and is associated with an imbalance of coagulation and fibrinolysis. This is partly due to an increased secretion of prothrombotic ultra-large von Willebrand factor (VWF) as the result of vascular endothelial damage. Another factor that may contribute is ADAMTS13, which converts VWF into smaller, less active, VWF multimers and thus influences VWF activity in plasma. We investigated the role of ADAMTS13 and VWF in the severity and outcome of sepsis. In 58 children with severe meningococcal sepsis we measured ADAMTS13 activity and antigen, VWF collagen binding activity (VWF:CB) and antigen levels (VWF:Ag), VWF propeptide and factor VIII at different time points during their stay in the paediatric intensive care unit. In the acute phase, both ADAMTS13 activity and antigen were decreased (median 23.4% and 33.7% of normal, respectively) and VWF:CB and VWF:Ag levels were strongly increased (325% and 348%, respectively.) ADAMTS13 antigen (23.9% vs. 34.6%; p=0.06) and VWF:CB (240% and 340% p 〈 0.001) were lower in non-survivors than in survivors. ADAMTS13 activity and VWF:CB were both correlated with the severity of the disease, as indicated by the Pediatric Risk of Mortality score (Rs= –0.38 and Rs= –0.50, p=0.01, respectively, p 〈 0.001). In the acute phase of severe sepsis decreased levels of ADAMTS13 and increased levels of VWF are observed, and the changes are related to severity of disease and outcome. This may contribute to the formation of microthrombi and the severity of thrombotic sequelae of sepsis.
    Type of Medium: Online Resource
    ISSN: 0340-6245 , 2567-689X
    URL: Article
    DOI: 10.1160/TH09-06-0376
    Language: English
    Publisher: Georg Thieme Verlag KG
    Publication Date: 2010
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  • 2
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    Age-related Differences in Outcome and Severity of DIC in Children with Septic Shock and Purpura
    Georg Thieme Verlag KG ; 1996
    In:  Thrombosis and Haemostasis Vol. 76, No. 06 ( 1996), p. 0932-0938
    Details
    In: Thrombosis and Haemostasis, Georg Thieme Verlag KG, Vol. 76, No. 06 ( 1996), p. 0932-0938
    Abstract: We studied the influence of age on mortality and severity of clotting abnormalities in 79 children (median age: 3.1 years) with meningococcal sepsis. Parameters of coagulation and fibrinolysis and plasma levels of cytokines were prospectively measured on admission. The mortality rate was 27%. The age of survivors was significantly different from that of non-survivors (p = 0.013). With the exception of FVII, vWF and t-PA, parameters of coagulation and fibrinolysis, as well as plasma cytokine levels were related to outcome. Patients were divided in two groups: younger and older than median age. The mortality in children ≤3.1 years was 40% versus 13% in children 〉 3.1 years (p = 0.006). In contrast to cytokine levels, which were not different between the two age groups, fibrinogen, prothrombin, factors V, VII, VIII, vWF, protein C, antithrombin, FDP, and the ratio PAI-l/t-PA were related to age, indicating a more severe coagulopathy in children ≤ 3.1 years despite a similar degree of inflammatory response. A relative deficiency of coagulation factors due to an immature state of the clotting system, as well as an inadequate fibrinolytic response, both related to age may have caused this more severe coagulative response in younger children, and may have contributed to the higher mortality rate.
    Type of Medium: Online Resource
    ISSN: 0340-6245 , 2567-689X
    URL: Article
    DOI: 10.1055/s-0038-1650688
    Language: English
    Publisher: Georg Thieme Verlag KG
    Publication Date: 1996
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  • 3
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    Twenty-two Years of Failure to Set Up Undisputed Assays to Detect Patients with the Antiphospholipid Syndrome
    Georg Thieme Verlag KG ; 2008
    In:  Seminars in Thrombosis and Hemostasis Vol. 34, No. 04 ( 2008-6), p. 347-355
    Details
    In: Seminars in Thrombosis and Hemostasis, Georg Thieme Verlag KG, Vol. 34, No. 04 ( 2008-6), p. 347-355
    Type of Medium: Online Resource
    ISSN: 0094-6176 , 1098-9064
    URL: Article
    DOI: 10.1055/s-0028-1085477
    Language: English
    Publisher: Georg Thieme Verlag KG
    Publication Date: 2008
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  • 4
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    The Prevalence of a Non-phospholipid-binding Form of β2-Glycoprotein I in Human Plasma : Consequences for the Development of Anti-β2-glycoprotein I Antibodies
    Georg Thieme Verlag KG ; 1998
    In:  Thrombosis and Haemostasis Vol. 80, No. 11 ( 1998), p. 791-797
    Details
    In: Thrombosis and Haemostasis, Georg Thieme Verlag KG, Vol. 80, No. 11 ( 1998), p. 791-797
    Abstract: The presence of antiphospholipid antibodies (aPL) is strongly correlated with venous and arterial thrombosis, fetal loss and thrombocytopenia. This relation is called the antiphospholipid syndrome (APS). It is well recognized that thrombosis related aPL are not directed against phospholipids alone, but to phospholipid bound plasma proteins like β2-glycoprotein I (β2GPI). aPL that need β2GPI for the binding to negatively charged phospholipids are called anti-β2GPI-antibodies. Recently, a mutation in the gene encoding β2GPI has been described, which results in an amino acid substitution Trp316 into Ser316. This Ser316-β2GPI did not bind to negatively charged phospholipids. Because only phospholipid bound β2GPI is recognized by human anti-β2GPI-antibodies, it might be argued that individuals carrying the Trp316Ser mutation are protected against the development of anti-β2GPI-antibodies. To investigate this hypothesis, the prevalence of the Trp316Ser mutation was measured in 170 systemic lupus erythematosus (SLE) patients and in 18 patients with the primary antiphospholipid syndrome (PAPS) and the mutation was correlated with the presence of anti-β2 GPI-antibodies. In the total patient group 1 homozygous patient and 21 heterozygous patients were found. The allele frequency of the mutation in SLE patients with anti-β2GPI-antibodies (0.063) was comparable to that found in SLE patients without anti-β2-GPI-antibodies (0.062). These results indicate that the heterozygous presence of Trp316Ser mutation does not prevent an individual from developing anti-β2GPI-antibodies. We showed that this can be explained by the concentration of Trp316-β2GPI in heterozygous patients, which is far above the minimal β2GPI level necessary for optimal phospholipid binding. In our single patient homozygous for the Trp316Ser mutation no binding of β2GPI to the phospholipid surface was detected and no anti-β2GPI-antibodies were present in the plasma of this patient. In conclusion, heterozygous Trp316Ser β2GPI persons are not protected against the development of anti-β2GPI-antibodies. To confirm that homozygotes do not develop anti-β2GPI-antibodies a very large population is needed, due to the relatively low prevalence of the mutation.
    Type of Medium: Online Resource
    ISSN: 0340-6245 , 2567-689X
    URL: Article
    DOI: 10.1055/s-0037-1615360
    Language: English
    Publisher: Georg Thieme Verlag KG
    Publication Date: 1998
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  • 5
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    Optimisation of lupus anticoagulant tests: should test samples always be mixed with normal plasma?
    Georg Thieme Verlag KG ; 2014
    In:  Thrombosis and Haemostasis Vol. 112, No. 10 ( 2014), p. 736-742
    Details
    In: Thrombosis and Haemostasis, Georg Thieme Verlag KG, Vol. 112, No. 10 ( 2014), p. 736-742
    Abstract: Coagulation factor deficiencies are thought to interfere with the detection of the phospholipid-dependent coagulation inhibitor known as lupus anticoagulant (LA). Treatment with vitamin K antagonists (VKA) in particular, is thought to preclude accurate LA assessment. For this reason, the procedure to detect LA includes a mixing test, in which coagulation factor deficiencies are corrected by mixing samples with an equal volume of normal plasma. Despite these mixing tests, interpretation of LA test results is considered difficult in patients receiving high intensity VKA treatment. As a result, VKA treatment is often temporarily discontinued to allow LA assessment. However, whether coagulation factor deficiencies influence LA test results is unclear. We found that neither deficiency of a single coagulation factor, nor a functional coagulation factor deficiency due to high intensity VKA treatment, resulted in false positive dRVVT- or APTT-based (silica clotting time; SCT) LA test results. LA was readily detected in unmixed samples from VKA-treated LA-positive patients with both dRVVT and SCT reagents. VKA treatment caused an underestimation of the strength of the LA with SCT reagents, but did not lead to misclassification of LA status. Although mixing with normal plasma during both screen and confirm tests allowed more accurate assessment of the strength of the LA with SCT reagents in samples with an international normalised 〉 2.5, the mixing procedure itself lead to misclassification of LA in weakly positive samples from patients not treated with VKA. Based on these findings, we conclude that mixing studies are not necessary during LA-assessment.
    Type of Medium: Online Resource
    ISSN: 0340-6245 , 2567-689X
    URL: Article
    DOI: 10.1160/TH14-02-0122
    Language: English
    Publisher: Georg Thieme Verlag KG
    Publication Date: 2014
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  • 6
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    Antiphospholipid Antibody Positive Sera Enhance Endothelial Cell Procoagulant Activity – Studies in a Thrombosis Model
    Georg Thieme Verlag KG ; 1992
    In:  Thrombosis and Haemostasis Vol. 68, No. 03 ( 1992), p. 278-284
    Details
    In: Thrombosis and Haemostasis, Georg Thieme Verlag KG, Vol. 68, No. 03 ( 1992), p. 278-284
    Abstract: The effect of sera and IgG from 12 patients with systemic lupus erythematosus (SLE) on the endothelial cell (EC) procoagulant activity (PCA) was investigated in an in vitro thrombosis model. Six of the 12 SLE sera contained antiphospholipid antibodies (aPL). EC were stimulated for 8 h at 37° C with or without 50 pM tumor necrosis factor (TNF) in culture medium containing 20% patient or control serum. Then the endothelial cell matrix (ECM) was isolated and subsequently exposed in a perfusion chamber to circulating normal whole blood, anticoagulated with low molecular weight heparin (LMWH). The PCA of the ECM was determined as the amount of generated fibrinopeptide A (FPA) in samples taken before and after perfusion. Furthermore, cross sections were made of the perfused matrix and analyzed for platelet adhesion and aggregate formation. All six aPL containing sera induced a small, but significant increase of ECM procoagulant activity. When added in combination with a low dose of TNF (50 pM), a synergistic enhancement of ECM procoagulant activity was found. The FPA generation was increased to 150–614% from the values obtained after stimulation with TNF and control serum. Also a shift towards the formation of larger platelet thrombi was observed. After stimulation with TNF and patient serum the surface of ECM covered with large aggregates ( 〉 5 µm) was increased by 124–329% compared to the results obtained after stimulation with control serum and TNF. When patient sera were depleted from IgG the effects were strongly decreased. These data show that the potentiation of TNF-induced PCA formation by aPL containing sera from patients with SLE leads to enhanced thrombus formation in an in vitro thrombosis model. This may help explain the increased thrombotic tendency in these patients.
    Type of Medium: Online Resource
    ISSN: 0340-6245 , 2567-689X
    URL: Article
    DOI: 10.1055/s-0038-1656365
    Language: English
    Publisher: Georg Thieme Verlag KG
    Publication Date: 1992
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  • 7
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    Lupus Anticoagulant Activity Is Frequently Dependent on the Presence of β2-Glycoprotein I
    Georg Thieme Verlag KG ; 1992
    In:  Thrombosis and Haemostasis Vol. 67, No. 05 ( 1992), p. 499-502
    Details
    In: Thrombosis and Haemostasis, Georg Thieme Verlag KG, Vol. 67, No. 05 ( 1992), p. 499-502
    Abstract: Antiphospholipid antibodies (aPL) are defined by anticardioli-pin antibody (aCL) ELISA and prolongation of phospholipid dependent coagulation assays (lupus anticoagulant; LAC). For the binding of aCL to cardiolipin a cofactor, β2-glycoprotein I (β2-GPI), is necessary. We have investigated whether the same cofactor is essential for LAC activity. Plasma from 6 LAC positive patients and 3 controls was depleted from β2-GPI by means of affinity chromatography. From the 6 LAC positive plasmas, 4 became LAC negative (tested with dRWT) when β2-GPI was depleted and became positive again when purified β2-GPI (200 μg/ml) was added. A dose response curve showed that addition of 50 μg/ml β2-GPI to β2-GPI deficient patient plasma, led to a positive dRWT. Depletion of, and addition of β2-GPI to plasma from controls had no effect on the dRWT. Measurement of β2-GPI plasma levels in 19 LAC positive patients, 40 LAC negative patients and 15 controls showed no difference in β2-GPI levels. These results show that a combination of aPL and β2-GPI is essential not only for binding to cardiolipin, but also for LAC activity and imply that low β2-GPI levels ( 〈 50 μg/ml) can lead to false negative LAC tests. These observations may lead to new insights in the pathophysiological complications associated with aPL.
    Type of Medium: Online Resource
    ISSN: 0340-6245 , 2567-689X
    URL: Article
    DOI: 10.1055/s-0038-1648480
    Language: English
    Publisher: Georg Thieme Verlag KG
    Publication Date: 1992
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  • 8
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    The Case Manager: An Agent Controlling the Activation of Knowledge Sources in a FHIR-Based Distributed Reasoning Environment
    Georg Thieme Verlag KG ; 2023
    In:  Applied Clinical Informatics Vol. 14, No. 04 ( 2023-08), p. 725-734
    Details
    In: Applied Clinical Informatics, Georg Thieme Verlag KG, Vol. 14, No. 04 ( 2023-08), p. 725-734
    Abstract: Background Within the CAPABLE project the authors developed a multi-agent system that relies on a distributed architecture. The system provides cancer patients with coaching advice and supports their clinicians with suitable decisions based on clinical guidelines. Objectives As in many multi-agent systems we needed to coordinate the activities of all agents involved. Moreover, since the agents share a common blackboard where all patients' data are stored, we also needed to implement a mechanism for the prompt notification of each agent upon addition of new information potentially triggering its activation. Methods The communication needs have been investigated and modeled using the HL7-FHIR (Health Level 7-Fast Healthcare Interoperability Resources) standard to ensure proper semantic interoperability among agents. Then a syntax rooted in the FHIR search framework has been defined for representing the conditions to be monitored on the system blackboard for activating each agent. Results The Case Manager (CM) has been implemented as a dedicated component playing the role of an orchestrator directing the behavior of all agents involved. Agents dynamically inform the CM about the conditions to be monitored on the blackboard, using the syntax we developed. The CM then notifies each agent whenever any condition of interest occurs. The functionalities of the CM and other actors have been validated using simulated scenarios mimicking the ones that will be faced during pilot studies and in production. Conclusion The CM proved to be a key facilitator for properly achieving the required behavior of our multi-agent system. The proposed architecture may also be leveraged in many clinical contexts for integrating separate legacy services, turning them into a consistent telemedicine framework and enabling application reusability.
    Type of Medium: Online Resource
    ISSN: 1869-0327
    URL: Article
    DOI: 10.1055/a-2113-4443
    Language: English
    Publisher: Georg Thieme Verlag KG
    Publication Date: 2023
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  • 9
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    The Contribution of Anti-prothrombin-antibodies to Lupus Anticoagulant Activity : Discrimination between Functional and Non-functional Anti-prothrombin-antibodies
    Georg Thieme Verlag KG ; 1998
    In:  Thrombosis and Haemostasis Vol. 79, No. 04 ( 1998), p. 790-795
    Details
    In: Thrombosis and Haemostasis, Georg Thieme Verlag KG, Vol. 79, No. 04 ( 1998), p. 790-795
    Abstract: The presence of lupus anticoagulant (LAC) is strongly correlated with a history of thrombosis in patients with SLE. LAC activity can be caused by anti-prothrombin (FII)- and/or anti-β2glycoprotein I (β2GPI)-antibodies. In the present study, the contribution of anti-FII-antibodies to LAC activity was measured in 28 LAC positive plasmas. Plasmas were incubated with prothrombin or BSA, immobilized on CNBr-activated Sepharose, to absorb all anti-FII-antibodies. In 4 out of the 28 plasmas LAC activity was completely dependent on anti-FII-antibodies. In 7 out of the 28 plasmas, anti-FII-antibodies did not contribute to LAC activity. These anti-FII-antibodies can be regarded as non-functional antibodies. In the majority (17/28) of the samples, LAC activity within a single plasma was caused by a combination of antibodies with different specificities. Both dRVVT and KCT showed comparable sensitivity for the detection of functional anti-FII-antibodies. In conclusion, in most samples LAC activity is not caused by anti-FII-antibodies alone but by a combination of different types of antibodies. The presence of LAC activity and anti-FII-antibodies in one plasma does not automatically implicate that these antibodies are responsible for the LAC activity.
    Type of Medium: Online Resource
    ISSN: 0340-6245 , 2567-689X
    URL: Article
    DOI: 10.1055/s-0037-1615066
    Language: English
    Publisher: Georg Thieme Verlag KG
    Publication Date: 1998
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  • 10
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    Crossreactivity of Antibodies Directed against Cardiolipin, DNA, Endothelial Cells and Blood Platelets
    Georg Thieme Verlag KG ; 1990
    In:  Thrombosis and Haemostasis Vol. 63, No. 02 ( 1990), p. 169-173
    Details
    In: Thrombosis and Haemostasis, Georg Thieme Verlag KG, Vol. 63, No. 02 ( 1990), p. 169-173
    Abstract: The interrelationship of antibodies directed against cardiolipin (CL), double stranded DNA (dsDNA), endothelial cells (EC) and blood platelets was investigated. IgG fractions, reactive with these antigens, were isolated from the plasmas from 8 patients with systemic lupus erythematosus and tested for crossreactivity with anionic phospholipids (CL, phosphatidylserine, phos-phatidylinositol), zwitterionic phospholipids (phosphatidyl-ethanolamine, phosphatidylcholine), dsDNA, EC and platelets by enzyme-linked immunosorbent assays and for lupus anticoagulant (LAC) activity with a coagulation assay. Our results demonstrate the frequent occurrence of crossreactivity between antibodies to anionic phospholipids, EC and platelets. Crossreactivities between these antibodies and antibodies to dsDNA or zwitterionic phospholipids are exceptional. LAC activity was found in the anti-CL, anti-EC and anti-platelet fractions of only one patient. These findings support the hypothesis that subpopulations of antibodies directed against negatively charged phospholipids can bind to EC and blood platelets, which may have implications for the pathogenetic potential of antiphospholipid antibodies.
    Type of Medium: Online Resource
    ISSN: 0340-6245 , 2567-689X
    URL: Article
    DOI: 10.1055/s-0038-1645039
    Language: English
    Publisher: Georg Thieme Verlag KG
    Publication Date: 1990
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