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Sökning: L773:1098 9064 OR L773:0094 6176

  • Resultat 21-30 av 64
  • Föregående 12[3]4567Nästa
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21.
  • Fletcher-Sandersjoo, A, et al. (författare)
  • Clinical Significance of Vascular Occlusive Events following Moderate-to-Severe Traumatic Brain Injury: An Observational Cohort Study
  • 2022
  • Ingår i: Seminars in thrombosis and hemostasis. - : Georg Thieme Verlag KG. - 1098-9064 .- 0094-6176. ; 48:033, s. 301-308
  • Tidskriftsartikel (refereegranskat)abstract
    • Preventing hemorrhage progression is a potential therapeutic opportunity in traumatic brain injury (TBI) management, but its use has been limited by fear of provoking vascular occlusive events (VOEs). However, it is currently unclear whether VOE actually affects outcome in these patients. The aim of this study was to determine incidence, risk factors, and clinical significance of VOE in patients with moderate-to-severe TBI. A retrospective observational cohort study of adults (≥15 years) with moderate-to-severe TBI was performed. The presence of a VOE during hospitalization was noted from hospital charts and radiological reports. Functional outcome, using the Glasgow Outcome Scale (GOS), was assessed at 12 months posttrauma. Univariate and multivariate logistic regressions were used for endpoint assessment. In total, 848 patients were included, with a median admission Glasgow Coma Scale of 7. A VOE was detected in 54 (6.4%) patients, of which cerebral venous thrombosis was the most common (3.2%), followed by pulmonary embolism (1.7%) and deep vein thrombosis (1.3%). Length of ICU stay (p < 0.001), body weight (p = 0.002), and skull fracture (p = 0.004) were independent predictors of VOE. VOE development did not significantly impact 12-month GOS, even after adjusting for potential confounders using propensity score matching. In conclusion, VOE in moderate-to-severe TBI patients was relatively uncommon, and did not affect 12-month GOS. This suggests that the potential benefit of treating bleeding progression might outweigh the risks of VOE.
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23.
  • Hansson, Emma C., 1985, et al. (författare)
  • Antiplatelet Therapy, Platelet Function Testing, and Bleeding Complications in Cardiac Surgery Patients
  • 2017
  • Ingår i: Seminars in Thrombosis and Hemostasis. - : Georg Thieme Verlag KG. - 0094-6176 .- 1098-9064. ; 43:7, s. 699-705
  • Tidskriftsartikel (refereegranskat)abstract
    • Antiplatelet therapy with acetylsalicylic acid, alone or in combination with a P2Y(12) inhibitor, reduces thromboembolic events in patients with coronary artery disease but increases the risk for spontaneous and perioperative bleeding complications. Both the antiplatelet effect and the risk for bleeding complications are larger with the new generation P2Y(12) inhibitors prasugrel and ticagrelor than with clopidogrel. In this review, the perioperative handling of acetylsalicylic acid and the P2Y(12) inhibitors clopidogrel, prasugrel, and ticagrelor will be discussed. In addition, the concept of platelet function testing in the surgical setting will be covered.
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24.
  • He, S, et al. (författare)
  • Fibrin Network Porosity and Endo-/Exogenous Thrombin Cross-talk
  • 2021
  • Ingår i: Seminars in thrombosis and hemostasis. - : Georg Thieme Verlag KG. - 1098-9064 .- 0094-6176. ; 47:087, s. 775-786
  • Tidskriftsartikel (refereegranskat)abstract
    • The earliest assessment of fibrin network porosity used a liquid permeation system and confocal 3D microscopy, which was later replaced by scanning electron microscopy. Although the methods have extensively been applied in studies of health or disease, there remains debate on the choice of a proper clotting trigger. In this review, we assess published data and convey our opinions with regard to several issues. First, when the coagulation process is initiated by recombinant tissue factor (rTF) and phospholipids, the fibrin network porosity is regulated by the endogenous thrombin based on enzymatic activations of multiple coagulants. If purified thrombin (1.0 IU/mL) is employed as the clotting trigger, fibrin network porosity may be affected by exogenous thrombin, which directly polymerizes fibrinogen in plasma, and additionally by endogenous thrombin stemming from a “positive feedback loop” action of the added thrombin. Second, with use of either endogenous or exogenous thrombin, the concentration and clotting property of available fibrinogen both influence the fibrin network porosity. Third, in the assay systems in vitro, exogenous thrombin but not rTF-induced endogenous thrombin seems to be functional enough to activate factor XIII, which then contributes to a decrease in the fibrin network porosity. Fourth, fibrin network porosity determines the transport of fibrinolytic components into/through the clots and therefore serves as an indicator of the fibrinolysis potential in plasma.
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25.
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26.
  • He, S, et al. (författare)
  • The Clotting Trigger Is an Important Determinant for the Coagulation Pathway In Vivo or In Vitro-Inference from Data Review
  • 2021
  • Ingår i: Seminars in thrombosis and hemostasis. - : Georg Thieme Verlag KG. - 1098-9064 .- 0094-6176. ; 47:061, s. 63-73
  • Tidskriftsartikel (refereegranskat)abstract
    • Blood coagulation comprises a series of enzymatic reactions leading to thrombin generation and fibrin formation. This process is commonly illustrated in a waterfall-like manner, referred to as the coagulation cascade. In vivo, this “cascade” is initiated through the tissue factor (TF) pathway, once subendothelial TF is exposed and bound to coagulation factor VII (FVII) in blood. In vitro, a diminutive concentration of recombinant TF (rTF) is used as a clotting trigger in various global hemostasis assays such as the calibrated automated thrombogram, methods that assess fibrin turbidity and fibrin viscoelasticity tests such as rotational thromboelastometry. These assays aim to mimic in vivo global coagulation, and are useful in assessing hyper-/hypocoagulable disorders or monitoring therapies with hemostatic agents. An excess of rTF, a sufficient amount of negatively charged surfaces, various concentrations of exogenous thrombin, recombinant activated FVII, or recombinant activated FIXa are also used to initiate activation of specific sub-processes of the coagulation cascade in vitro. These approaches offer important information on certain specific coagulation pathways, while alterations in pro-/anticoagulants not participating in these pathways remain undetectable by these methods. Reviewing available data, we sought to enhance our knowledge of how choice of clotting trigger affects the outcome of hemostasis assays, and address the call for further investigations on this topic.
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27.
  • Hedner, Ulla (författare)
  • Mechanism of action of factor VIIa in the treatment of coagulopathies.
  • 2006
  • Ingår i: Seminars in Thrombosis and Hemostasis. - : Georg Thieme Verlag KG. - 1098-9064 .- 0094-6176. ; 32 Suppl 1:Suppl. 1, s. 77-85
  • Tidskriftsartikel (refereegranskat)abstract
    • Recombinant factor VIIa (rFVIIa) has been developed for treatment of bleeding in patients with hemophilia who have inhibitors against factor VIII (FVIII) or FIX, and has been found to induce hemostasis during major orthopedic surgery. The use of rFVIIa treatment for hemophilia is a new concept and is based on the low-affinity binding of FVIIa to the surface of thrombin-activated platelets. Administration of pharmacologic doses of exogenous rFVIIa enhances thrombin generation on the platelet surface at the site of injury independently of the presence of FVIII or FIX. Pharmacologic doses of rFVIIa induce hemostasis not only in hemophilia patients, but also in patients with thrombocytopenia, functional platelet defects, and with profuse bleeding triggered by extensive surgery or trauma. The general mechanism of action of rFVIIa to induce hemostasis under these conditions may be its capacity to generate a tight fibrin hemostatic plug through increased thrombin generation. A tight fibrin plug will aid in resisting the overwhelming local release of fibrinolytic activity triggered by vast tissue damage occurring in extensive trauma. Local fibrinolytic activity also occurs in the gastrointestinal tract as well as during profuse postpartum bleeding. Pharmacologic doses of rFVIIa induce hemostasis in these cases also.
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28.
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29.
  • Karlsson, Ove (författare)
  • Experience of Point-of-Care Devices in Obstetrical Care
  • 2017
  • Ingår i: Seminars in Thrombosis and Hemostasis. - 0094-6176 .- 1098-9064. ; 43:4, s. 397-406
  • Forskningsöversikt (refereegranskat)abstract
    • Copyright © 2017 by Thieme Medical Publishers, Inc. During pregnancy and puerperium, there are pronounced hemostatic changes characterized by increased coagulability and decreased fibrinolysis. In addition, hemostasis can change dramatically during obstetric complications. Several reports have described substandard management of hemostatic defects in this setting and state the need for guidelines and better care. Point-of-care devices can assess hemostatic status and are especially suitable in perioperative settings. Using point-of-care devices, no time is required for transportation, allowing faster availability of results and providing potential for better care of the patient. This article will demonstrate the use of a viscoelastic method in six different patients; five with impaired hemostasis, and where the use of viscoelastic method contributes or should have contributed to better care. The cases represent patients with normal delivery; postpartum hemorrhage (PPH); PPH with low fibrinogen; placental abruption; preeclampsia with hemolysis, elevated liver enzymes, low platelet count syndrome; and finally, one patient with sepsis. This article also shows the need for good practices and good supervision to implement the devices in patient care.
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30.
  • Karpman, Diana, et al. (författare)
  • Pathophysiology of typical hemolytic uremic syndrome.
  • 2010
  • Ingår i: Seminars in Thrombosis and Hemostasis. - : Georg Thieme Verlag KG. - 1098-9064 .- 0094-6176. ; 36:6, s. 575-585
  • Tidskriftsartikel (refereegranskat)abstract
    • The typical form of hemolytic uremic syndrome (HUS) is associated with enterohemorrhagic ESCHERICHIA COLI (EHEC) infection. The disease process is initiated and perpetuated by interactions between the pathogen or its virulence factors and host cells, as well as the host response. During EHEC-associated HUS, alterations occurring at the intestinal mucosal barrier and in the circulation, as well as on endothelial cells and other target-organ cells, lead to cell activation and/or cytotoxicity, and trigger a prothrombotic state. This review summarizes current knowledge regarding the interactions of the pathogen and its virulence factors with cells in the intestine, bloodstream, kidney, and brain. Mechanisms of bacterial colonization, toxin circulation, and induction of target organ damage are discussed.
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