Hemostatic Defect
Mostrando 1-12 de 14 artigos, teses e dissertações.
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1. Fibrin biopolymer as scaffold candidate to treat bone defects in rats
ABSTRACT Background: Bone tissue repair remains a challenge in tissue engineering. Currently, new materials are being applied and often integrated with live cells and biological scaffolds. The fibrin biopolymer (FBP) proposed in this study has hemostatic, sealant, adhesive, scaffolding and drug-delivery properties. The regenerative potential of an associat
J. Venom. Anim. Toxins incl. Trop. Dis. Publicado em: 04/11/2019
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2. Effect of collagen sponge and fibrin glue on bone repair
ABSTRACT The ability of hemostatic agents to promote bone repair has been investigated using in vitro and in vivo models but, up to now, the results are inconclusive. Objective In this context, the aim of this study was to compare the potential of bone repair of collagen sponge with fibrin glue in a rat calvarial defect model. Material and Methods Defect
J. Appl. Oral Sci.. Publicado em: 2015-12
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3. Hydroxyapatite and a New Fibrin Sealant Derived from Snake Venom as Scaffold to Treatment of Cranial Defects in Rats
Biomaterials are used as a promising alternative to bone grafts, including bioceramics whose composition resembles that of bone and fibrin sealants due to their hemostatic properties. The objective was to evaluate the repair of cranial defects in 40 rats, grafted with hydroxyapatite and a new fibrin sealant derived from snake venom. The animals were divided
Mat. Res.. Publicado em: 2015-02
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4. Simplified hemostatic technique during laparoscopic partial nephrectomy
INTRODUCTION: Laparoscopic partial nephrectomy (LPN) has gained popularity in recent years, although it remains a challenging procedure. Herein we describe our technique of renal defect closure using sutures as the sole means of hemostasis during LPN. SURGICAL TECHNIQUE: The kidney is approached transperitoneally in a standard fashion. After the renal artery
International braz j urol. Publicado em: 2012-02
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5. AlteraÃÃo bioquÃmica em fator de coagulaÃÃo como causa de trombose venosa profunda â relato de caso clÃnico
Deep venous thrombosis (DVT) in the pediatric population (0-18 year old) has been reported as lower than in adults. In almost half of the children, three or four risk factors for thrombosis are present simultaneously. Even in children with thromboembolic disturbance, thrombosis did not occur spontaneously; the hemostatic defect became apparent because thromb
Publicado em: 2006
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6. Effect of recombinant factor VIIa on the hemostatic defect in dogs with hemophilia A, hemophilia B, and von Willebrand disease.
Recombinant factor VIIa (rF.VIIa) is a two-chain procoagulant enzyme (Mr, approximately 50,000) active only when complexed with tissue factor in the extrinsic clotting system. We administered human rF.VIIa to hemophilic and von Willebrand disease (vWD) dogs to determine its hemostatic effectiveness and survival in the circulation. Hemophilia A dogs lacking f
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7. Physiological role of an endoperoxide in human platelets: hemostatic defect due to platelet cyclo-oxygenase deficiency.
The endoperoxide prostaglandin G2 (PGG2) induced platelet aggregation as well as the platelet release reaction (release of ADP and serotonin) when added to human platelet-rich plasma. Formation of a metabolite of PGG2 [8-(l-hydroxy-3-oxopropyl)-9,12L-dihydroxy-5,10-heptadecadienoic acid] and a lipoxygenase product [12L-hydroxy-5,8,10,14-eicosatetraenoic acid
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8. Influence of Cephalosporin Antibiotics on Blood Coagulation and Platelet Function
Administration of cephalothin to normal volunteers in maximal doses of 300 mg/kg per day resulted in a combined defect of platelet function and blood coagulation. No such abnormalities were evident after infusion of cefazolin or cephapirin at a maximal dosage of 200 mg/kg per day. The observed thrombocytopathy was similar to but less severe than that induced
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9. Reduced Platelet Thromboxane Formation in Uremia. EVIDENCE FOR A FUNCTIONAL CYCLOOXYGENASE DEFECT
A qualitative platelet abnormality and a bleeding tendency are frequently associated with renal failure and uremia. We demonstrated previously that uremic patients display an abnormal platelet aggregation to arachidonic acid and reduced malondialdehyde production in response to thrombin and arachidonic acid. The objectives of this investigation were: (a) to
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10. An inherited bleeding disorder linked to a defective interaction between ADP and its receptor on platelets. Its influence on glycoprotein IIb-IIIa complex function.
Much discussion has concerned the central role of ADP in platelet aggregation. We now describe a patient (M.L.) with an inherited bleeding disorder whose specific feature is that ADP induces a limited and rapidly reversible platelet aggregation even at high doses. Platelet shape change and other hemostatic parameters were unmodified. A receptor defect was in
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11. Tissue factor deficiency causes cardiac fibrosis and left ventricular dysfunction
Exposure of blood to tissue factor (TF) activates the extrinsic (TF:FVIIa) and intrinsic (FVIIIa:FIXa) pathways of coagulation. In this study, we found that mice expressing low levels of human TF (≈1% of wild-type levels) in an mTF−/− background had significantly shorter lifespans than wild-type mice, in part, because of spontaneous fatal hemorrhages.
National Academy of Sciences.
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12. Reduced thrombin binding and aggregation in Bernard-Soulier platelets.
Platelets from two patients with Bernard-Soulier disease showed a reduction in their ability to bind human thrombin. Thrombin binding studies in the high affinity range showed 1,500 sites for the Bernard-Soulier platelets as against 4,000 for normal controls. However, the dissociation constant was the same for both normals and patients (4.4 nM) indicating id