Venous blood clot structure characterization using scattering operator

Author(s):  
Thibaud Berthomier ◽  
Ali Mansour ◽  
Luc Bressollette ◽  
Frederic Le Roy ◽  
Dominique Mottier
2017 ◽  
Vol 41 (S1) ◽  
pp. S479-S479
Author(s):  
N. Mistry ◽  
G. Sikka

IntroductionVenous thromboembolism (VTE) is a condition that causes a blood clot to form within the venous blood system. If this blood clot forms in the peripheral venous system it can cause symptoms such as calf pain and swelling. If this clot becomes dislodged, it may travel through the vessels into the pulmonary artery which can have much more severe consequences.ObjectivesThere has been a great deal of effort in recent years to increase the percentage of in-patients receiving a VTE assessment; and for those patients to receive appropriate VTE prophylaxis. VTE is a significant cause of inpatient deaths. This audit aims to compare current working practice to local standards and identify learning points.MethodsVTE and physical health assessment data was collected by checking electronic admission summaries from three acute psychiatric in-patient wards on a random date in 2016. The local pathway for the management of physical health and wellbeing states that the VTE assessment and Physical Health Assessment should be completed within 6 hours of admission. NICE guidelines also state that all patients should be assessed on admission, with a standard of 100%.Results60% of patients had a VTE assessment and 54% of patients had a physical health assessment done within 6 hours of admission.ConclusionsThis audit shows that the necessary standards are not met. Importance of these assessments has been communicated during induction programmes for all staff.Disclosure of interestThe authors have not supplied their declaration of competing interest.


Blood ◽  
1993 ◽  
Vol 82 (8) ◽  
pp. 2462-2469 ◽  
Author(s):  
JP Collet ◽  
J Soria ◽  
M Mirshahi ◽  
M Hirsch ◽  
FB Dagonnet ◽  
...  

Fibrinogen Dusart is a congenital dysfibrinogenemia (A-alpha 554 Arginine-->Cysteine) associated with severe thrombotic disorder, high incidence of thrombotic embolism, and abnormal fibrin polymerization. This thrombotic disorder was attributed to an abnormal clot thrombolysis with reduced plasminogen binding to fibrin and defective plasminogen activation by tissue plasminogen activator. The purpose of this work was to assess whether clot architecture could be involved in the thromboresistance of the fibrin Dusart and the high incidence of embolism. An important change in Dusart fibrin clot structure was identified with dramatic decrease of gel porosity (Ks), fiber diameters (d), and fiber mass-length ratios (mu) derived from permeation analysis. In addition, rigidity of the Dusart clot was found to be greatly increased compared with normal fibrin. We provide evidence that both thrombolysis resistance and abnormal rigidity of the fibrin Dusart are related to this abnormal architecture, which impairs the access of fibrinolytic enzymes to the fibrin and which is responsible for a brittle clot that breaks easily, resulting in a high incidence of embolism. Indeed, when restoring a normal clot structure by adding dextran 40 (30 mg/mL) before coagulation, clot thrombolysis and clot rigidity recovered normal values. This effect was found to be dose- dependent. We conclude that clot architecture is crucial for the propensity of blood clot to be degraded and that abnormal clot structure can be highly thrombogenic in vivo. The alpha-C domains of fibrinogen are determinant in fibrin clot structure.


1986 ◽  
Vol 60 (6) ◽  
pp. 1917-1922 ◽  
Author(s):  
M. Andrew ◽  
C. Carter ◽  
H. O'Brodovich ◽  
G. Heigenhauser

Components of the factor VIII complex increase and activation of the fibrinolytic system occur during exercise. The relation between the duration and intensity of exercise and the relative changes in the VIII complex and fibrinolytic system have not been previously examined. Five healthy male subjects were exercised with three protocols: a graded progressive exercise test to exhaustion on a cycle ergometer with 50-W increments every 4 min, steady-state exercise, 15 min at 5 and 125 W each, and an acute 30-s maximal exercise test on a cycle ergometer. Venous blood samples were drawn at base line, during the last 30 s of each power output in the graded exercise, at 5-min intervals for the steady-state exercise, and for up to 1 h after completion of exercise in all three protocols. At the maximum exercise intensities, increases in plasma lactate concentration ([La]), O2 uptake, and [H+] were observed. Components of the VIII complex [VIII procoagulant, VIII procoagulant antigen, VIII-related antigen (VIIIR:Ag), VIII ristocetin cofactor activity] abruptly rose at only the highest work intensities, whereas the whole blood clot lysis time began to gradually shorten much earlier at low work intensities. There were no qualitative changes in the factor VIIIR:Ag on crossed immunoelectrophoresis nor was there evidence of thrombin generation as determined by fibrinopeptide A generation. We conclude that during exercise the changes observed in the coagulation and fibrinolytic systems are related to the intensity of the exercise, which is reflected by increases in plasma [La] and [H+], and that the fibrinolytic system is activated before the changes in the VIII complex are observed.


2014 ◽  
Vol 112 (11) ◽  
pp. 901-908 ◽  
Author(s):  
Katherine Bridge ◽  
Helen Philippou ◽  
Robert Ariëns

SummaryFibrinogen is cleaved by thrombin to fibrin, which provides the blood clot with its essential structural backbone. As an acute phase protein, the plasma levels of fibrinogen are increased in response to inflammatory conditions. In addition to fibrinogen levels, fibrin clot structure is altered by a number of factors. These include thrombin levels, treatment with common cardiovascular medications, such as aspirin, anticoagulants, statins and fibrates, as well as metabolic disease states such as diabetes mellitus and hyperhomocysteinaemia. In vitro studies of fibrin clot structure can provide information regarding fibre density, clot porosity, the mechanical strength of fibres and fibrinolysis. A change in fibrin clot structure, to a denser clot with smaller pores which is more resistant to lysis, is strongly associated with cardiovascular disease. This pathological change is present in patients with arterial as well as venous diseases, and is also found in a moderate form in relatives of patients with cardiovascular disease. Pharmacological therapies, aimed at both the treatment and prophylaxis of cardiovascular disease, appear to result in positive changes to the fibrin clot structure. As such, therapies aimed at ‘normalising’ fibrin clot structure may be of benefit in the prevention and treatment of cardiovascular disease.


2021 ◽  
Author(s):  
Sachin M. Patil

Pulmonary embolism is an acute emergency due to the occlusion of the pulmonary arteries by a venous blood clot. The pathophysiology of pulmonary embolism follows Virchow\'s triad, which encompasses stasis in veins, increased coagulation, and vessel wall trauma. Pregnancy, major trauma or surgery, prolonged immobilization, obesity, medication, and inherited risks are important risks. It is an essential rule-out diagnosis in chest pain and dyspnea patients in the emergency room. It is also responsible for significant mortality if not diagnosed and treated promptly. Physicians utilize multiple algorithmic scores and calculators to supplement diagnosis along with a high degree of clinical suspicion at initial presentation. Clinical diagnosis involves utilizing multiple modalities, including D-dimer, troponin, arterial blood gas analysis, electrocardiogram, bedside echocardiogram, and imaging modalities such as venous duplex, chest computed tomography, ventilation-perfusion scans, and pulmonary angiogram. Some imaging modalities carry the risk of radiation and being invasive. The treatment can itself be short-term or lifelong based on the causative factor. Anticoagulants used in the therapy can itself cause devastating complications if not monitored appropriately. Despite adequate treatment, some of these patients progress to chronic disease resulting in secondary pulmonary hypertension.


2018 ◽  
Vol 114 (4) ◽  
pp. 978-991 ◽  
Author(s):  
Vijay Govindarajan ◽  
Shu Zhu ◽  
Ruizhi Li ◽  
Yichen Lu ◽  
Scott L. Diamond ◽  
...  

1997 ◽  
Vol 3 (S2) ◽  
pp. 233-234
Author(s):  
W. G. Jerome ◽  
R.R. Hantgan ◽  
S. Handt

A life threatening blood clot is the major cause of heart attacks. Thrombolytic therapy attempts to restore blood flow by activating the body's own fibrinolytic system at the site of the occlusive thrombus. However, for unknown reasons, therapy is unsuccessful in greater than 20% of patients. We have previously shown that the endothelial cells lining the wall of the vessel can play a substantial role in inhibiting clot lysis. This is due chiefly to the secretion of inhibitory molecules by endothelial cells. However, endothelial cells also have receptors for fibrin and little is known about how the direct interaction of fibrin with cells may influence lysis. To investigate this we have undertaken a series of microscopic studies to analyse the influence of endothelial cells on clot structure. We report here that endothelial cells can organize clot fibers into tight assemblies. We also show that, at least in culture, fibrin can act in concert with antithrombotic molecules to dramatically affect endothelial structure


Nanomaterials ◽  
2021 ◽  
Vol 11 (3) ◽  
pp. 674
Author(s):  
Long Bai ◽  
Peiru Chen ◽  
Bin Tang ◽  
Ruiqiang Hang ◽  
Yin Xiao

Implant surfaces with a nanoscaled pattern can dominate the blood coagulation process resulting in a defined clot structure and its degradation behavior, which in turn influence cellular response and the early phase of osseointegration. Long non-coding (Lnc) RNAs are known to regulate many biological processes in the skeletal system; however, the link between the LncRNA derived from the cells within the clot and osseointegration has not been investigated to date. Hence, the sequence analysis of LncRNAs expressed within the clot formed on titania nanotube arrays (TNAs) with distinct nano-scaled diameters (TNA 15 of 15 nm, TNA 60 of 60 nm, TNA 120 of 120 nm) on titanium surfaces was profiled for the first time. LncRNA LOC103346307, LOC103352121, LOC108175175, LOC103348180, LOC108176660, and LOC108176465 were identified as the pivotal players in the early formed clot on the nano-scaled surfaces. Further bioinformatic prediction results were used to generate co-expression networks of LncRNAs and mRNAs. Gene Ontology and Kyoto Encyclopedia of Genes and Genomes pathway analyses revealed that distinct nano-scaled surfaces could regulate the biological functions of target mRNAs in the clot. LOC103346307, LOC108175175, and LOC108176660 upregulated mRNAs related to cell metabolism and Wnt, TGF-beta, and VEGF signaling pathways in TNA 15 compared with P-Ti, TNA 60, and TNA 120, respectively, whereas LOC103352121, LOC103348180, and LOC108176465 downregulated mRNAs related to bone resorption and inflammation through negatively regulating osteoclast differentiation, TNF, and NF-kappa signaling pathways. The results indicated that surface nano-scaled characteristics can significantly influence the clot-derived LncRNAs expression profile, which affects osseointegration through multiple signaling pathways of the targeted mRNAs, thus paving a way for better interpreting the link between the properties of a blood clot formed on the nano-surface and de novo bone formation.


2020 ◽  
Vol 26 (5) ◽  
pp. 406-409
Author(s):  
Bilal Demirhan ◽  
İhsan Kısadere ◽  
Mehmet Kılıç ◽  
Süleyman Patlar ◽  
Mehmet Günay ◽  
...  

ABSTRACT Introduction: Evaluation of health status and physical condition of Kyrgyz Judo Athletes before the Olympic Games. Objective: To evaluate changes in hematological, biochemical and blood gas values of athletes during the training period. Methods: Eight elite athletes (n=8 men), participated to the study. Before and after the exercise periods (baseline, 3rd month and 6th month), blood samples were taken, to determine plasma red blood cell (RBC), white blood cell (WBC), blood clot cell (PLT), granulocyte (NOTR) and agranulocyte (LNF) counts, hemoglobin (HGB) and hematocrit (HCT) values, mean corpuscular volume (MCV), mean corpuscular hemoglobin concentration (MCHC), and venous blood pH, PO2, PCO2, SAT O2, HCO3, BE, Na, K, Cl values. In addition, serum glucose (Glu), total protein (TP), total cholesterol (TC), HDL cholesterol, triglyceride (Trig), blood urea nitrogen (BUN), creatinine (Creat), lactate dehydrogenase (LDH) and creatine phosphokinase (CPK) values were measured. Results: Although, the athletes’ WBC and LNF counts increased significantly (p<0.05) in post-exercise periods, no statistical significance (p>0.05) was found in the other hematological parameters. Blood pH, pCO2, HCO3 and BE values decreased (P<0.05) after the exercise periods. Conclusion: The effects of exercise on judo athletes were evaluated before the Olympics. Level of Evidence III; Case-control study.


eLife ◽  
2021 ◽  
Vol 10 ◽  
Author(s):  
Helen McPherson ◽  
Cedric Duval ◽  
Stephen R Baker ◽  
Matthew S Hindle ◽  
Lih T Cheah ◽  
...  

Fibrinogen is essential for blood coagulation. The C-terminus of the fibrinogen α-chain (αC-region) is composed of an αC-domain and αC-connector. Two recombinant fibrinogen variants (α390 and α220) were produced to investigate the role of subregions in modulating clot stability and resistance to lysis. The α390 variant, truncated before the αC-domain, produced clots with a denser structure and thinner fibres. In contrast, the α220 variant, truncated at the start of the αC-connector, produced clots that were porous with short, stunted fibres and visible fibre ends. These clots were mechanically weak and susceptible to lysis. Our data demonstrate differential effects for the αC-subregions in fibrin polymerisation, clot mechanical strength, and fibrinolytic susceptibility. Furthermore, we demonstrate that the αC-subregions are key for promoting longitudinal fibre growth. Together, these findings highlight critical functions of the αC-subregions in relation to clot structure and stability, with future implications for development of novel therapeutics for thrombosis.


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