Abstract TP35: Estimation of Red Blood Cells in the Thrombus Using MRI. A Phantom Study with Predetermined Thrombus Components

Stroke ◽  
2017 ◽  
Vol 48 (suppl_1) ◽  
Author(s):  
Ana Paula Narata ◽  
Isabelle Filipiak ◽  
Richard Bibi ◽  
Jean Philippe Cottier ◽  
Kevin Janot

Background and Purpose: Better understanding about thrombus composition seems necessary, as treatment of acute ischemic stroke (AIS) is focus on clot chemical dissolution and mechanical extraction. We propose to evaluate whether magnetic resonance imaging (MRI) can differentiate white from red clots and estimate red blood cells percentage (RBC%) using clots with predetermined components and an index based on MRI signal intensity (SI). Material and Methods: 5 clots (A=100% fibrin, B=80% RBC, C=50% RBC, D=20% RBC, E=unknown) were fixed in gelatin-manganese solution and studied by: high-resolution 3D T1-weighted (T1MPR), T2-weighted turbo spin echo (T2TSE), T2-weighted gradient echo (T2GE), susceptibility weighted (SWI), fluid-attenuated inversion recovery (FLAIR) and diffusion weighted imaging (DWI) with apparent diffusion coefficient (ADC). SI index was calculated with clot SI and gelatin SI. Statistical analysis compared RBC-clots to fibrin-clot SI index and the correlation of RBC% and SI index in each MRI sequence. Results: Each red clot was different from clot A except clot D in FLAIR. Correlation between clots SI index and RBC concentration were found in T1MPR (r=-0.84), SWI (r=-0.79), T2GE (r=-0.72) and FLAIR (r=0.80). Linear regression resolution provided an indirect RBC estimation for clot E: 47.3 % in T1MPR, SWI 41.5%, T2GE 45.1% and FLAIR 50.9%. Histological analysis confirmed clot E composition. Conclusion: This in vitro study suggests that MRI can differentiate white from red clots except clots with low RBC% in FLAIR and also provide approximate RBC%.

2018 ◽  
Vol 251 (5-6) ◽  
pp. 735-745 ◽  
Author(s):  
Hanna Pruchnik ◽  
Aleksandra Włoch ◽  
Dorota Bonarska-Kujawa ◽  
Halina Kleszczyńska

2022 ◽  
Vol 140 ◽  
pp. 104281
Author(s):  
Toru Hyakutake ◽  
Hiroki Abe ◽  
Yohei Miyoshi ◽  
Manabu Yasui ◽  
Rina Suzuki ◽  
...  

2016 ◽  
Vol 255 ◽  
pp. 63-70 ◽  
Author(s):  
Jérôme Devoy ◽  
Antoine Géhin ◽  
Samuel Müller ◽  
Mathieu Melczer ◽  
Aurélie Remy ◽  
...  

2015 ◽  
Vol 492 (1-2) ◽  
pp. 55-64 ◽  
Author(s):  
Luca Flebus ◽  
François Lombart ◽  
Lucía Martinez-Jothar ◽  
Chantal Sevrin ◽  
Céline Delierneux ◽  
...  

1996 ◽  
Vol 85 (2) ◽  
pp. 220-224 ◽  
Author(s):  
RMW Moison ◽  
EJHA Hoof ◽  
PC Clahsen ◽  
D Zoeren-Grobben ◽  
HM Berger

Biomolecules ◽  
2020 ◽  
Vol 10 (10) ◽  
pp. 1448
Author(s):  
Alexey N. Semenov ◽  
Andrei E. Lugovtsov ◽  
Evgeny A. Shirshin ◽  
Boris P. Yakimov ◽  
Petr B. Ermolinskiy ◽  
...  

An elevated concentration of fibrinogen in blood is a significant risk factor during many pathological diseases, as it leads to an increase in red blood cells (RBC) aggregation, resulting in hemorheological disorders. Despite the biomedical importance, the mechanisms of fibrinogen-induced RBC aggregation are still debatable. One of the discussed models is the non-specific adsorption of fibrinogen macromolecules onto the RBC membrane, leading to the cells bridging in aggregates. However, recent works point to the specific character of the interaction between fibrinogen and the RBC membrane. Fibrinogen is the major physiological ligand of glycoproteins receptors IIbIIIa (GPIIbIIIa or αIIββ3 or CD41/CD61). Inhibitors of GPIIbIIIa are widely used in clinics for the treatment of various cardiovascular diseases as antiplatelets agents preventing the platelets’ aggregation. However, the effects of GPIIbIIIa inhibition on RBC aggregation are not sufficiently well studied. The objective of the present work was the complex multimodal in vitro study of the interaction between fibrinogen and the RBC membrane, revealing the role of GPIIbIIIa in the specificity of binding of fibrinogen by the RBC membrane and its involvement in the cells’ aggregation process. We demonstrate that GPIIbIIIa inhibition leads to a significant decrease in the adsorption of fibrinogen macromolecules onto the membrane, resulting in the reduction of RBC aggregation. We show that the mechanisms underlying these effects are governed by a decrease in the bridging components of RBC aggregation forces.


2018 ◽  
Vol 1 (1) ◽  
pp. 1-20 ◽  
Author(s):  
Sudeshna Paul ◽  
Shamreen Naaz ◽  
Arnab Kumar Ghosh ◽  
Sanatan Mishra ◽  
Aindrila Chattopadhyay ◽  
...  

Oxidative stress is an important causative factor for a number of diseases. Phenylhydrazine (PHZ) is a widely accepted model for studying hemolytic anemia by induction of oxidative stress. In the present study, goat red blood cells (RBCs) were incubated in vitro with PHZ (1mM) to generate oxidative stress. To test whether melatonin exhibits protective effects on PHZ induced RBC damage and to explore its potential molecular mechanisms, different concentrations of melatonin (5, 10, 20 and 40 nmoles/ml) were also included. PHZ caused altered profiles on biomarkers of oxidative stress and antioxidative as well as glucose metabolic enzymes in RBCs. These alterations indicated a development of oxidative stress. Melatonin at a concentration of 40 nmoles/ml provided optimal protection against all alterations induced by PHZ. The important cellular membrane proteins, including spectrin and actin, were also damaged by PHZ and this led to RBC deformation similar to that of observed in severe β-thalassaemia; the RBC deformation was also prevented by melatonin. Binding profiles of melatonin with PHZ and ferrous iron indicated favorable binding of melatonin with both of them, respectively. Thus, in addition to the direct antioxidant and free radical scavenging capability, melatonin also inhibited iron overloading by chelating iron and binding with the PHZ. This action of melatonin further reduces free radical generation. Based on the results, melatonin may provide therapeutic relevance to ß-thalassemia and other hemolytic RBC disorders involving oxidative stress. 


2020 ◽  
Vol 20 (8) ◽  
pp. 1321-1327
Author(s):  
Saleh M. Abdullah ◽  
Hina Rashid

Background: Bisphenol A (BPA) is a xenobiotic that causes oxidative stress in various organs in living organisms. Blood cells are also an endpoint where BPA is known to cause oxidative stress. Blood cells, especially red blood cells (RBCs), are crucial for maintaining homeostasis and overall wellbeing of the organism. They are highly susceptible to oxidative stress induced by xenobiotics. However, there is limited data about the oxidative stress induced by BPA in blood, especially in red blood cells. This study was carried out to evaluate BPA induced oxidative stress in human RBCs in vitro and its amelioration by melatonin. Objective: To find if melatonin exerts a protective effect on the oxidative stress induced by the BPA in human red blood cells in vitro. Methods: The erythrocyte suspensions (2 ml) were divided into six groups and treated with 0, 50, 100, 150, 200, and 250 μg/ml of BPA. Another set of erythrocyte suspension with similar BPA treatment and 50 μM Melatonin per group was also set. Incubations lasted for 12 hrs in the dark. Lipid peroxidation, glutathione, glutathione reductase, catalase, and superoxide dismutase were measured as indicators of oxidative stress. Results: BPA caused a significant increase in lipid peroxidation. A decrease in GSH levels was also observed. The activities of all the studied antioxidants also decreased with BPA treatment. Melatonin was seen to mitigate the oxidative stress induced by BPA. Conclusion: Treatment of red blood cells with BPA caused an increase in oxidative stress, while melatonin decreased the induced oxidative stress.


2016 ◽  
Vol 307 ◽  
pp. 328-335 ◽  
Author(s):  
Aneta Maćczak ◽  
Monika Cyrkler ◽  
Bożena Bukowska ◽  
Jaromir Michałowicz

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