scholarly journals Alkali treatment of microrough titanium surfaces affects macrophage/monocyte adhesion, platelet activation and architecture of blood clot formation

2011 ◽  
Vol 21 ◽  
pp. 430-444 ◽  
Author(s):  
V Milleret ◽  
◽  
S Tugulu ◽  
F Schlottig ◽  
H Hall
Keyword(s):  
Platelet Activation ◽  
Alkali Treatment ◽  
Blood Clot ◽  
Clot Formation ◽  
Monocyte Adhesion ◽  
Titanium Surfaces

scholarly journals The Prothrombotic Predominance in Metabolic Syndrome: A Complex Pathomechanism

2021 ◽  
Vol 2 (4) ◽  
pp. 4-9
Author(s):  
Fahmy Rusnanta ◽  
Mohammad Saifur Rohman
Keyword(s):  
Metabolic Syndrome ◽  
Platelet Activation ◽  
Fibrinolytic Activity ◽  
Preventive Measures ◽  
Blood Clot ◽  
Coagulation Factors ◽  
Cardiovascular Complications ◽  
Clot Formation ◽  
Premature Atherosclerosis ◽  
Clot Structure

Patients with metabolic syndrome (MS) have many cardiovascular complications related to atherothrombotic complications. MS contributes premature atherosclerosis, increases platelet activation, promotes coagulation factors, and reduces fibrinolytic activity. The last step in the atherothrombotic cascade is blood clot formation, and altered clot structure is a key role to determine cardiovascular complications. The MS, caused in part by an excess of atherosclerosis and in part by fibrinolytic dysfunction, is profoundly related to an excess of CVD. These combinations of factors involved in MS parameters contribute the increased propensity of people with MS to develop atherothrombosis and fibrinolysis. Awareness and preventive measures are important to improve outcomes in patients with MS.

The Haemocompatibility of Biomaterials In Vitro: Investigations on the Mechanism of the Whole-blood Clot Formation Test

1992 ◽  
Vol 20 (3) ◽  
pp. 390-395 ◽  
Author(s):  
Thomas Groth ◽  
Katrin Derdau ◽  
Frank Strietzel ◽  
Frank Foerster ◽  
Hartmut Wolf
Keyword(s):  
Whole Blood ◽  
Blood Clotting ◽  
Blood Clot ◽  
Formation Rate ◽  
Clot Formation ◽  
Coagulation Cascade ◽  
Contact Activation ◽  
Human Fibrinogen ◽  
Static Conditions

Twenty years ago Imai & Nose introduced a whole-blood clotting test for the estimation of haemocompatibility of biomaterials in vitro In our paper a modification of this assay is described and the mechanism of clot formation further elucidated. It was found that neither the inhibition of platelet function nor the removal of platelets from blood significantly changed the clot formation rate on glass and polyvinyl chloride in comparison to the rate tor whole blood. Scanning electron microscopy demonstrated that platelets were not involved in clot formation near the blood/biomaterial interface. Thus, it was concluded that the system of contact activation of the coagulation cascade dominates during clot formation under static conditions. The latter conclusion was supported by the fact that preadsorption of human serum albumin or human fibrinogen onto the glass plates used, decreased the clot formation rate in the same manner.

scholarly journals Anticoagulant Polyethylene Terephthalate Surface by Plasma-Mediated Fucoidan Immobilization

Polymers ◽  
2019 ◽  
Vol 11 (5) ◽  
pp. 750 ◽  
Author(s):  
Kadir Ozaltin ◽  
Marian Lehocky ◽  
Petr Humpolicek ◽  
Jana Pelkova ◽  
Antonio Di Martino ◽  
...  
Keyword(s):  
Polyethylene Terephthalate ◽  
Photoelectron Spectroscopy ◽  
Anticoagulant Activity ◽  
Blood Clot ◽  
Clot Formation ◽  
Thrombin Time ◽  
Air Plasma ◽  
Water Contact ◽  
Polymeric Biomaterials ◽  
Performance Surface

Biomaterial-based blood clot formation is one of the biggest drawbacks of blood-contacting devices. To avoid blood clot formation, their surface must be tailored to increase hemocompatibility. Most synthetic polymeric biomaterials are inert and lack bonding sites for chemical agents to bond or tailor to the surface. In this study, polyethylene terephthalate was subjected to direct current air plasma treatment to enhance its surface energy and to bring oxidative functional binding sites. Marine-sourced anticoagulant sulphated polysaccharide fucoidan from Fucus vesiculosus was then immobilized onto the treated polyethylene terephthalate (PET) surface at different pH values to optimize chemical bonding behavior and therefore anticoagulant performance. Surface properties of samples were monitored using the water contact angle; chemical analyses were performed by FTIR and X-ray photoelectron spectroscopy (XPS) and their anticoagulant activity was tested by means of prothrombin time, activated partial thromboplastin time and thrombin time. On each of the fucoidan-immobilized surfaces, anticoagulation activity was performed by extending the thrombin time threshold and their pH 5 counterpart performed the best result compared to others.

scholarly journals Role of Endothelial Cells in Acute and Chronic Thrombosis

2019 ◽  
Vol 39 (02) ◽  
pp. 128-139 ◽  
Author(s):  
Magdalena L. Bochenek ◽  
Katrin Schäfer
Keyword(s):  
Endothelial Cells ◽  
Platelet Activation ◽  
Thrombus Formation ◽  
Blood Clot ◽  
Vascular Occlusion ◽  
Coagulation Factors ◽  
Activated Platelets ◽  
Endothelial Cell Response ◽  
Von Willebrand

AbstractHaemostasis encompasses a set of strictly regulated actions, such as vasoconstriction, platelet activation and blood coagulation. Endothelial cells play a crucial role in all of these processes and are an integral part of the vascular response to injury resulting in thrombus formation. Healthy endothelium expresses mediators to prevent platelet activation, including prostacyclin and nitric oxide, and to inhibit coagulation, such as thrombomodulin or RNase1. Upon activation, endothelial cells expose von Willebrand factor, integrins and other receptors to interact with activated platelets, erythrocytes and coagulation factors, respectively, resulting in blood clot formation. The endothelial cell response to cytokines and growth factors released from activated platelets and immune cells abundantly present in arterial and venous thrombi also plays an important role for thrombus resolution, whereas failure to completely resolve thrombi may initiate fibrotic remodelling and chronic vascular occlusion both in the arterial and venous tree. Therefore, endothelial cells are increasingly recognized as potential target to prevent thrombotic events and to accelerate thrombus resolution. Here, we discuss recent publications from our group in the context of other studies on the role of the endothelium during acute and chronic thrombotic events.

Effect of Progesterone and Synthetic Progestins on Whole Blood Clot Formation and Erythrocyte Structure

2017 ◽  
Vol 23 (3) ◽  
pp. 607-617 ◽  
Author(s):  
Albe C. Swanepoel ◽  
Odette Emmerson ◽  
Etheresia Pretorius
Keyword(s):  
Whole Blood ◽  
Blood Clot ◽  
Thrombotic Event ◽  
Clot Formation ◽  
Erythrocyte Aggregation ◽  
Erythrocyte Morphology ◽  
Increased Risk ◽  
Blood Clots ◽  
Membrane Ultrastructure

AbstractCombined oral contraceptive (COC) use is a risk factor for venous thrombosis (VT) and related to the specific type of progestin used. VT is accompanied by inflammation and pathophysiological clot formation, that includes aberrant erythrocytes and fibrin(ogen) interactions. In this paper, we aim to determine the influence of progesterone and different synthetic progestins found in COCs on the viscoelasticity of whole blood clots, as well as erythrocyte morphology and membrane ultrastructure, in an in vitro laboratory study. Thromboelastography (TEG), light microscopy, and scanning electron microscopy were our chosen methods. Our results point out that progestins influence the rate of whole blood clot formation. Alterations to erythrocyte morphology and membrane ultrastructure suggest the presence of eryptosis. We also note increased rouleaux formation, erythrocyte aggregation, and spontaneous fibrin formation in whole blood which may explain the increased risk of VT associated with COC use. Although not all COC users will experience a thrombotic event, individuals with a thrombotic predisposition, due to inflammatory or hematological illness, should be closely monitored to prevent pathological thrombosis.

Role of factor XIII in fibrin clot formation and effects of genetic polymorphisms

Blood ◽  
2002 ◽  
Vol 100 (3) ◽  
pp. 743-754 ◽  
Author(s):  
Robert A. S. Ariëns ◽  
Thung-Shenq Lai ◽  
John W. Weisel ◽  
Charles S. Greenberg ◽  
Peter J. Grant
Keyword(s):  
Genetic Polymorphisms ◽  
Factor Xiii ◽  
Blood Clot ◽  
Site Directed Mutagenesis ◽  
Clot Formation ◽  
Factor Xiiia ◽  
Clotting Factors ◽  
Functional Features

Abstract Factor XIII and fibrinogen are unusual among clotting factors in that neither is a serine protease. Fibrin is the main protein constituent of the blood clot, which is stabilized by factor XIIIa through an amide or isopeptide bond that ligates adjacent fibrin monomers. Many of the structural and functional features of factor XIII and fibrin(ogen) have been elucidated by protein and gene analysis, site-directed mutagenesis, and x-ray crystallography. However, some of the molecular aspects involved in the complex processes of insoluble fibrin formation in vivo and in vitro remain unresolved. The findings of a relationship between fibrinogen, factor XIII, and cardiovascular or other thrombotic disorders have focused much attention on these 2 proteins. Of particular interest are associations between common variations in the genes of factor XIII and altered risk profiles for thrombosis. Although there is much debate regarding these observations, the implications for our understanding of clot formation and therapeutic intervention may be of major importance. In this review, we have summarized recent findings on the structure and function of factor XIII. This is followed by a review of the effects of genetic polymorphisms on protein structure/function and their relationship to disease.

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