TY  - JOUR
AU  - Dunjić Manevski, Sofija
AU  - Cumbo, Marija
AU  - Pruner, Iva
AU  - Gvozdenov, Maja
AU  - Tomić, Branko
AU  - Taxiarchis, Apostolos
AU  - Antović, Jovan
AU  - Đordjević, Valentina
PY  - 2023
UR  - https://onlinelibrary.wiley.com/doi/abs/10.1111/ijlh.14195
UR  - https://imagine.imgge.bg.ac.rs/handle/123456789/2199
AB  - Introduction Prothrombin Belgrade mutation is the result of the c.1787G>A substitution in the prothrombin gene. It is located in the antithrombin and sodium binding site and leads to impaired inactivation of thrombin by antithrombin, resulting in antithrombin resistance and thrombotic disorders. However, it negatively affects sodium binding and may have hypocoagulant effects. Considering that prothrombin Belgrade mutation mechanism is still not fully elucidated and that sodium binding is important for thrombin affinity towards fibrinogen, our aim was to determine whether this mutation affects fibrin clot formation and lysis. Methods Using HEK293T cell line, recombinant wild type and mutated prothrombin were generated by transient transfection. Samples that correspond to plasma of a non-carrier, heterozygous and homozygous carriers were reconstituted using prothrombin deficient plasma and recombinant proteins. Reconstituted samples were used in OHP assay (Overall Hemostasis Potential) to determine kinetic profiles of coagulation and fibrinolysis. Clot turbidity assay was performed to observe kinetics of clot formation and lysis more closely. Fibrin clots formed in reconstituted plasma samples were analyzed by confocal microscopy to determine density of fibrin network. Fibrin clots were additionally observed using electron microscopy to determine thickness of individual fibrin fibers. Results No significant difference found in OHP, OCP, OFP, and fibrin network density between wild type, heterozygous, and homozygous carrier reconstituted plasma samples. There were significant differences between samples for slope and slope time parameters in kinetic profiles and fibrin fiber thickness. Conclusions Results indicate that prothrombin Belgrade mutation has no significant impact on fibrinolysis, however it may affect kinetics of clot formation and its architecture.
T2  - International Journal of Laboratory Hematology
T1  - Effect of prothrombin Belgrade mutation, causing antithrombin resistance, on fibrin clot properties
VL  - n/a
DO  - 10.1111/ijlh.14195
ER  - 

@article{
author = "Dunjić Manevski, Sofija and Cumbo, Marija and Pruner, Iva and Gvozdenov, Maja and Tomić, Branko and Taxiarchis, Apostolos and Antović, Jovan and Đordjević, Valentina",
year = "2023",
abstract = "Introduction Prothrombin Belgrade mutation is the result of the c.1787G>A substitution in the prothrombin gene. It is located in the antithrombin and sodium binding site and leads to impaired inactivation of thrombin by antithrombin, resulting in antithrombin resistance and thrombotic disorders. However, it negatively affects sodium binding and may have hypocoagulant effects. Considering that prothrombin Belgrade mutation mechanism is still not fully elucidated and that sodium binding is important for thrombin affinity towards fibrinogen, our aim was to determine whether this mutation affects fibrin clot formation and lysis. Methods Using HEK293T cell line, recombinant wild type and mutated prothrombin were generated by transient transfection. Samples that correspond to plasma of a non-carrier, heterozygous and homozygous carriers were reconstituted using prothrombin deficient plasma and recombinant proteins. Reconstituted samples were used in OHP assay (Overall Hemostasis Potential) to determine kinetic profiles of coagulation and fibrinolysis. Clot turbidity assay was performed to observe kinetics of clot formation and lysis more closely. Fibrin clots formed in reconstituted plasma samples were analyzed by confocal microscopy to determine density of fibrin network. Fibrin clots were additionally observed using electron microscopy to determine thickness of individual fibrin fibers. Results No significant difference found in OHP, OCP, OFP, and fibrin network density between wild type, heterozygous, and homozygous carrier reconstituted plasma samples. There were significant differences between samples for slope and slope time parameters in kinetic profiles and fibrin fiber thickness. Conclusions Results indicate that prothrombin Belgrade mutation has no significant impact on fibrinolysis, however it may affect kinetics of clot formation and its architecture.",
journal = "International Journal of Laboratory Hematology",
title = "Effect of prothrombin Belgrade mutation, causing antithrombin resistance, on fibrin clot properties",
volume = "n/a",
doi = "10.1111/ijlh.14195"
}

Dunjić Manevski, S., Cumbo, M., Pruner, I., Gvozdenov, M., Tomić, B., Taxiarchis, A., Antović, J.,& Đordjević, V.. (2023). Effect of prothrombin Belgrade mutation, causing antithrombin resistance, on fibrin clot properties. in International Journal of Laboratory Hematology, n/a.
https://doi.org/10.1111/ijlh.14195

Dunjić Manevski S, Cumbo M, Pruner I, Gvozdenov M, Tomić B, Taxiarchis A, Antović J, Đordjević V. Effect of prothrombin Belgrade mutation, causing antithrombin resistance, on fibrin clot properties. in International Journal of Laboratory Hematology. 2023;n/a.
doi:10.1111/ijlh.14195 .

Dunjić Manevski, Sofija, Cumbo, Marija, Pruner, Iva, Gvozdenov, Maja, Tomić, Branko, Taxiarchis, Apostolos, Antović, Jovan, Đordjević, Valentina, "Effect of prothrombin Belgrade mutation, causing antithrombin resistance, on fibrin clot properties" in International Journal of Laboratory Hematology, n/a (2023),
https://doi.org/10.1111/ijlh.14195 . .

TY  - CONF
AU  - Dunjić, Sofija
AU  - Cumbo, Marija
AU  - Gvozdenov, Maja
AU  - Taxiarchis, Apostolos
AU  - Tomić, Branko
AU  - Antović, Jovan
AU  - Đorđević, Valentina
PY  - 2020
UR  - https://imagine.imgge.bg.ac.rs/handle/123456789/1635
AB  - Prothrombin Belgrade mutation is a result of the c.1787G>T
mutation in the prothrombin gene, which leads to the substitution of
Arg596 by Gln. This mutation is located in the antithrombin binding site
and leads to the impaired inactivation of thrombin by antithrombin and
antithrombin resistance, resulting in a thrombotic phenotype. Previous
studies have shown the complex mechanism of this mutation, manifested with higher endogenous thrombin potential, lower prothrombin
activity with normal prothrombin levels in carriers’ plasma.
C3  - Research and Practice in Thrombosis and Haemostasis
C3  - Research and Practice in Thrombosis and Haemostasis
T1  - The prothrombin Belgrade mutation causing antithrombin resistance does not affect fibrin clot formation
EP  - 1117
IS  - 1
SP  - 1117
VL  - 4
UR  - https://hdl.handle.net/21.15107/rcub_imagine_1635
ER  - 

@conference{
author = "Dunjić, Sofija and Cumbo, Marija and Gvozdenov, Maja and Taxiarchis, Apostolos and Tomić, Branko and Antović, Jovan and Đorđević, Valentina",
year = "2020",
abstract = "Prothrombin Belgrade mutation is a result of the c.1787G>T
mutation in the prothrombin gene, which leads to the substitution of
Arg596 by Gln. This mutation is located in the antithrombin binding site
and leads to the impaired inactivation of thrombin by antithrombin and
antithrombin resistance, resulting in a thrombotic phenotype. Previous
studies have shown the complex mechanism of this mutation, manifested with higher endogenous thrombin potential, lower prothrombin
activity with normal prothrombin levels in carriers’ plasma.",
journal = "Research and Practice in Thrombosis and Haemostasis, Research and Practice in Thrombosis and Haemostasis",
title = "The prothrombin Belgrade mutation causing antithrombin resistance does not affect fibrin clot formation",
pages = "1117-1117",
number = "1",
volume = "4",
url = "https://hdl.handle.net/21.15107/rcub_imagine_1635"
}

Dunjić, S., Cumbo, M., Gvozdenov, M., Taxiarchis, A., Tomić, B., Antović, J.,& Đorđević, V.. (2020). The prothrombin Belgrade mutation causing antithrombin resistance does not affect fibrin clot formation. in Research and Practice in Thrombosis and Haemostasis, 4(1), 1117-1117.
https://hdl.handle.net/21.15107/rcub_imagine_1635

Dunjić S, Cumbo M, Gvozdenov M, Taxiarchis A, Tomić B, Antović J, Đorđević V. The prothrombin Belgrade mutation causing antithrombin resistance does not affect fibrin clot formation. in Research and Practice in Thrombosis and Haemostasis. 2020;4(1):1117-1117.
https://hdl.handle.net/21.15107/rcub_imagine_1635 .

Dunjić, Sofija, Cumbo, Marija, Gvozdenov, Maja, Taxiarchis, Apostolos, Tomić, Branko, Antović, Jovan, Đorđević, Valentina, "The prothrombin Belgrade mutation causing antithrombin resistance does not affect fibrin clot formation" in Research and Practice in Thrombosis and Haemostasis, 4, no. 1 (2020):1117-1117,
https://hdl.handle.net/21.15107/rcub_imagine_1635 .

TY  - JOUR
AU  - Pruner, Iva
AU  - Farm, Maria
AU  - Tomić, Branko
AU  - Gvozdenov, Maja
AU  - Kovač, Mirjana
AU  - Miljić, Predrag
AU  - Soutari, Nida Mahmoud Hourani
AU  - Antović, Aleksandra
AU  - Radojković, Dragica
AU  - Antović, Jovan P.
AU  - Đorđević, Valentina
PY  - 2020
UR  - https://imagine.imgge.bg.ac.rs/handle/123456789/1375
AB  - BACKGROUND: Thrombosis is a major global disease burden with almost 60% of cases related to underlying heredity and most cases still idiopathic. Synonymous single nucleotide polymorphisms (sSNPs) are considered silent and phenotypically neutral. Our previous study revealed a novel synonymous FII c.1824C gt  T variant as a potential risk factor for pregnancy loss, but it has not yet been associated with thrombotic diseases. METHODS: To determine the frequency of the FII c.1824C gt  T variant we have sequenced patients' DNA. Prothrombin RNA expression was measured by quantitative PCR. Functional analyses included routine hemostasis tests, western blotting and ELISA to determine prothrombin levels in plasma, and global hemostasis assays for thrombin and fibrin generation in carriers of the FII c.1824C gt  T variant. Scanning electron mi- croscopy was used to examine the structure of fibrin clots. RESULTS: Frequency of the FII c.1824C gt  T variant was significantly increased in patients with venous thromboembolism and cerebrovascular insult. Examination in vitro demonstrated increased expression of prothrombin mRNA in FII c.1824C gt  T transfected cells. Our ex vivo study of FII c.1824C gt  T carriers showed that the presence of this variant was associated with hyperprothrom-binemia, hypofibrinolysis, and formation of densely packed fibrin clots resistant to fibrinolysis. CONCLUSION: Our data indicate that FII c.1824C gt  T, although a synonymous variant, leads to the development of a prothrombotic phenotype and could represent a new prothrombotic risk factor. As a silent variant, FII c.1824C gt  T would probably be overlooked during genetic screening, and our results show that it could not be detected in routine laboratory tests.
PB  - Oxford Univ Press Inc, Cary
T2  - Clinical Chemistry
T1  - The Silence Speaks, but We Do Not Listen: Synonymous c.1824C  gt  T Gene Variant in the Last Exon of the Prothrombin Gene as a New Prothrombotic Risk Factor
EP  - 389
IS  - 2
SP  - 379
VL  - 66
DO  - 10.1093/clinchem/hvz015
ER  - 

@article{
author = "Pruner, Iva and Farm, Maria and Tomić, Branko and Gvozdenov, Maja and Kovač, Mirjana and Miljić, Predrag and Soutari, Nida Mahmoud Hourani and Antović, Aleksandra and Radojković, Dragica and Antović, Jovan P. and Đorđević, Valentina",
year = "2020",
abstract = "BACKGROUND: Thrombosis is a major global disease burden with almost 60% of cases related to underlying heredity and most cases still idiopathic. Synonymous single nucleotide polymorphisms (sSNPs) are considered silent and phenotypically neutral. Our previous study revealed a novel synonymous FII c.1824C gt  T variant as a potential risk factor for pregnancy loss, but it has not yet been associated with thrombotic diseases. METHODS: To determine the frequency of the FII c.1824C gt  T variant we have sequenced patients' DNA. Prothrombin RNA expression was measured by quantitative PCR. Functional analyses included routine hemostasis tests, western blotting and ELISA to determine prothrombin levels in plasma, and global hemostasis assays for thrombin and fibrin generation in carriers of the FII c.1824C gt  T variant. Scanning electron mi- croscopy was used to examine the structure of fibrin clots. RESULTS: Frequency of the FII c.1824C gt  T variant was significantly increased in patients with venous thromboembolism and cerebrovascular insult. Examination in vitro demonstrated increased expression of prothrombin mRNA in FII c.1824C gt  T transfected cells. Our ex vivo study of FII c.1824C gt  T carriers showed that the presence of this variant was associated with hyperprothrom-binemia, hypofibrinolysis, and formation of densely packed fibrin clots resistant to fibrinolysis. CONCLUSION: Our data indicate that FII c.1824C gt  T, although a synonymous variant, leads to the development of a prothrombotic phenotype and could represent a new prothrombotic risk factor. As a silent variant, FII c.1824C gt  T would probably be overlooked during genetic screening, and our results show that it could not be detected in routine laboratory tests.",
publisher = "Oxford Univ Press Inc, Cary",
journal = "Clinical Chemistry",
title = "The Silence Speaks, but We Do Not Listen: Synonymous c.1824C  gt  T Gene Variant in the Last Exon of the Prothrombin Gene as a New Prothrombotic Risk Factor",
pages = "389-379",
number = "2",
volume = "66",
doi = "10.1093/clinchem/hvz015"
}

Pruner, I., Farm, M., Tomić, B., Gvozdenov, M., Kovač, M., Miljić, P., Soutari, N. M. H., Antović, A., Radojković, D., Antović, J. P.,& Đorđević, V.. (2020). The Silence Speaks, but We Do Not Listen: Synonymous c.1824C  gt  T Gene Variant in the Last Exon of the Prothrombin Gene as a New Prothrombotic Risk Factor. in Clinical Chemistry
Oxford Univ Press Inc, Cary., 66(2), 379-389.
https://doi.org/10.1093/clinchem/hvz015

Pruner I, Farm M, Tomić B, Gvozdenov M, Kovač M, Miljić P, Soutari NMH, Antović A, Radojković D, Antović JP, Đorđević V. The Silence Speaks, but We Do Not Listen: Synonymous c.1824C  gt  T Gene Variant in the Last Exon of the Prothrombin Gene as a New Prothrombotic Risk Factor. in Clinical Chemistry. 2020;66(2):379-389.
doi:10.1093/clinchem/hvz015 .

Pruner, Iva, Farm, Maria, Tomić, Branko, Gvozdenov, Maja, Kovač, Mirjana, Miljić, Predrag, Soutari, Nida Mahmoud Hourani, Antović, Aleksandra, Radojković, Dragica, Antović, Jovan P., Đorđević, Valentina, "The Silence Speaks, but We Do Not Listen: Synonymous c.1824C  gt  T Gene Variant in the Last Exon of the Prothrombin Gene as a New Prothrombotic Risk Factor" in Clinical Chemistry, 66, no. 2 (2020):379-389,
https://doi.org/10.1093/clinchem/hvz015 . .

TY  - JOUR
AU  - Zong, Yanan
AU  - Pruner, Iva
AU  - Antović, Aleksandra
AU  - Taxiarchis, Apostolos
AU  - Vila, Zara Pons
AU  - Soutari, Nida
AU  - Mobarrez, Fariborz
AU  - Chaireti, Roza
AU  - Widengren, Jerker
AU  - Piguet, Joachim
AU  - Antović, Jovan P.
PY  - 2020
UR  - https://imagine.imgge.bg.ac.rs/handle/123456789/1302
AB  - Circulating microparticles (MPs) are procoagulant due to the surface containing phosphatidylserine (PS), which facilitates coagulation. We investigated if MPs improve hemostasis in HA plasma models. MPs isolated from pooled normal human plasma were added to severe, moderate and mild HA plasma models (0%, 2.5%, 20% FVIII). The MPs' effect on hemostasis was evaluated by calibrated automated thrombogram (CAT) and overall hemostasis potential (OHP) assays, while fibrin structure was imaged by standard confocal, stimulated emission depletion (STED) microscopy and scanning electron microscopy (SEM). MPs partially restored thrombin generation and fibrin formation in all HA plasma models. The procoagulant effect of MPs requires PS exposure, to a less extent of contact pathway activation, but not tissue factor exposure or in vitro stimulation of MPs. MPs partially normalized the fibrin structure, and using super-resolution STED, MPs attached to fibrin were clearly resolved. In summary, our results demonstrate that PS positive MPs could improve hemostasis in HA plasma models.
PB  - Nature Portfolio, Berlin
T2  - Scientific Reports
T1  - Phosphatidylserine positive microparticles improve hemostasis in in-vitro hemophilia A plasma models
IS  - 1
VL  - 10
DO  - 10.1038/s41598-020-64686-x
ER  - 

@article{
author = "Zong, Yanan and Pruner, Iva and Antović, Aleksandra and Taxiarchis, Apostolos and Vila, Zara Pons and Soutari, Nida and Mobarrez, Fariborz and Chaireti, Roza and Widengren, Jerker and Piguet, Joachim and Antović, Jovan P.",
year = "2020",
abstract = "Circulating microparticles (MPs) are procoagulant due to the surface containing phosphatidylserine (PS), which facilitates coagulation. We investigated if MPs improve hemostasis in HA plasma models. MPs isolated from pooled normal human plasma were added to severe, moderate and mild HA plasma models (0%, 2.5%, 20% FVIII). The MPs' effect on hemostasis was evaluated by calibrated automated thrombogram (CAT) and overall hemostasis potential (OHP) assays, while fibrin structure was imaged by standard confocal, stimulated emission depletion (STED) microscopy and scanning electron microscopy (SEM). MPs partially restored thrombin generation and fibrin formation in all HA plasma models. The procoagulant effect of MPs requires PS exposure, to a less extent of contact pathway activation, but not tissue factor exposure or in vitro stimulation of MPs. MPs partially normalized the fibrin structure, and using super-resolution STED, MPs attached to fibrin were clearly resolved. In summary, our results demonstrate that PS positive MPs could improve hemostasis in HA plasma models.",
publisher = "Nature Portfolio, Berlin",
journal = "Scientific Reports",
title = "Phosphatidylserine positive microparticles improve hemostasis in in-vitro hemophilia A plasma models",
number = "1",
volume = "10",
doi = "10.1038/s41598-020-64686-x"
}

Zong, Y., Pruner, I., Antović, A., Taxiarchis, A., Vila, Z. P., Soutari, N., Mobarrez, F., Chaireti, R., Widengren, J., Piguet, J.,& Antović, J. P.. (2020). Phosphatidylserine positive microparticles improve hemostasis in in-vitro hemophilia A plasma models. in Scientific Reports
Nature Portfolio, Berlin., 10(1).
https://doi.org/10.1038/s41598-020-64686-x

Zong Y, Pruner I, Antović A, Taxiarchis A, Vila ZP, Soutari N, Mobarrez F, Chaireti R, Widengren J, Piguet J, Antović JP. Phosphatidylserine positive microparticles improve hemostasis in in-vitro hemophilia A plasma models. in Scientific Reports. 2020;10(1).
doi:10.1038/s41598-020-64686-x .

Zong, Yanan, Pruner, Iva, Antović, Aleksandra, Taxiarchis, Apostolos, Vila, Zara Pons, Soutari, Nida, Mobarrez, Fariborz, Chaireti, Roza, Widengren, Jerker, Piguet, Joachim, Antović, Jovan P., "Phosphatidylserine positive microparticles improve hemostasis in in-vitro hemophilia A plasma models" in Scientific Reports, 10, no. 1 (2020),
https://doi.org/10.1038/s41598-020-64686-x . .

TY  - JOUR
AU  - Petković, Anica
AU  - Al-Khalili, Faris
AU  - Antović, Aleksandra
AU  - Ammar, Majeed
AU  - Pruner, Iva
AU  - Vranić, Aleksandra
AU  - Soutari, Nida
AU  - Zdravković, Nebojša
AU  - Malmstrom, Rickard E.
AU  - Jakovljević, Vladimir
AU  - Antović, Jovan P.
PY  - 2020
UR  - https://imagine.imgge.bg.ac.rs/handle/123456789/1345
AB  - The study was aimed to evaluate the effects of two standard doses of rivaroxaban and dabigatran on global hemostatic assays in patients with atrial fibrillation. The study included 52 patients treated with rivaroxaban (15/20 mg), 50 on dabigatran (110/150 mg) and 20 healthy individuals. Platelet-poor plasma was used for determination of three global hemostatic assays, namely endogenous thrombin potential (ETP), calibrated automated thrombogram (CAT) and overall hemostasis potential (OHP). Rivaroxaban and dabigatran reduced ETP (P lt 0.01) although OHP (P lt 0.05) was diminished only by dabigatran. Strong correlations were noticed between ETP parameters and the plasma concentrations of rivaroxaban (ETP, rUS0.51; c-max, rUS0.85; t-lag, rU0.83; t-max, rU0.66) as well as with plasma concentration of dabigatran (ETP, rUS0.75; c-max, rUS0.74; t-lag, rU0.73; t-max, rU0.52). Analysis of dabigatran concentrations under 50 ng/ml showed that ETP parameter has area under the concentration-time curvereceiver operating characteristic value of 0.879 (95% confidence interval 0.776-0.980). Dabigatran treatment paradoxically increased area under the concentration-time curve and peak values although rivaroxaban decreased peak values (P lt 0.01). However, significant correlation between CAT parameters and plasma concentration of both direct oral anticoagulants was not observed. We confirmed that the CAT assay is inappropriate for estimation of dabigatran effects and is not fully sensitive as regards rivaroxaban. The ETP assay can potentially be the appropriate method for estimation of global hemostatic capacity as regards both direct oral anticoagulants. The role of OHP needs to be confirmed in additional studies. ETP parameter of chromogenic assay has promising potential in exclusion of high plasma concentrations of dabigatran.
PB  - Lippincott Williams & Wilkins, Philadelphia
T2  - Blood Coagulation & Fibrinolysis
T1  - Effects of rivaroxaban and dabigatran on global hemostasis in patients with atrial fibrillation
EP  - 252
IS  - 4
SP  - 243
VL  - 31
DO  - 10.1097/MBC.0000000000000907
ER  - 

@article{
author = "Petković, Anica and Al-Khalili, Faris and Antović, Aleksandra and Ammar, Majeed and Pruner, Iva and Vranić, Aleksandra and Soutari, Nida and Zdravković, Nebojša and Malmstrom, Rickard E. and Jakovljević, Vladimir and Antović, Jovan P.",
year = "2020",
abstract = "The study was aimed to evaluate the effects of two standard doses of rivaroxaban and dabigatran on global hemostatic assays in patients with atrial fibrillation. The study included 52 patients treated with rivaroxaban (15/20 mg), 50 on dabigatran (110/150 mg) and 20 healthy individuals. Platelet-poor plasma was used for determination of three global hemostatic assays, namely endogenous thrombin potential (ETP), calibrated automated thrombogram (CAT) and overall hemostasis potential (OHP). Rivaroxaban and dabigatran reduced ETP (P lt 0.01) although OHP (P lt 0.05) was diminished only by dabigatran. Strong correlations were noticed between ETP parameters and the plasma concentrations of rivaroxaban (ETP, rUS0.51; c-max, rUS0.85; t-lag, rU0.83; t-max, rU0.66) as well as with plasma concentration of dabigatran (ETP, rUS0.75; c-max, rUS0.74; t-lag, rU0.73; t-max, rU0.52). Analysis of dabigatran concentrations under 50 ng/ml showed that ETP parameter has area under the concentration-time curvereceiver operating characteristic value of 0.879 (95% confidence interval 0.776-0.980). Dabigatran treatment paradoxically increased area under the concentration-time curve and peak values although rivaroxaban decreased peak values (P lt 0.01). However, significant correlation between CAT parameters and plasma concentration of both direct oral anticoagulants was not observed. We confirmed that the CAT assay is inappropriate for estimation of dabigatran effects and is not fully sensitive as regards rivaroxaban. The ETP assay can potentially be the appropriate method for estimation of global hemostatic capacity as regards both direct oral anticoagulants. The role of OHP needs to be confirmed in additional studies. ETP parameter of chromogenic assay has promising potential in exclusion of high plasma concentrations of dabigatran.",
publisher = "Lippincott Williams & Wilkins, Philadelphia",
journal = "Blood Coagulation & Fibrinolysis",
title = "Effects of rivaroxaban and dabigatran on global hemostasis in patients with atrial fibrillation",
pages = "252-243",
number = "4",
volume = "31",
doi = "10.1097/MBC.0000000000000907"
}

Petković, A., Al-Khalili, F., Antović, A., Ammar, M., Pruner, I., Vranić, A., Soutari, N., Zdravković, N., Malmstrom, R. E., Jakovljević, V.,& Antović, J. P.. (2020). Effects of rivaroxaban and dabigatran on global hemostasis in patients with atrial fibrillation. in Blood Coagulation & Fibrinolysis
Lippincott Williams & Wilkins, Philadelphia., 31(4), 243-252.
https://doi.org/10.1097/MBC.0000000000000907

Petković A, Al-Khalili F, Antović A, Ammar M, Pruner I, Vranić A, Soutari N, Zdravković N, Malmstrom RE, Jakovljević V, Antović JP. Effects of rivaroxaban and dabigatran on global hemostasis in patients with atrial fibrillation. in Blood Coagulation & Fibrinolysis. 2020;31(4):243-252.
doi:10.1097/MBC.0000000000000907 .

Petković, Anica, Al-Khalili, Faris, Antović, Aleksandra, Ammar, Majeed, Pruner, Iva, Vranić, Aleksandra, Soutari, Nida, Zdravković, Nebojša, Malmstrom, Rickard E., Jakovljević, Vladimir, Antović, Jovan P., "Effects of rivaroxaban and dabigatran on global hemostasis in patients with atrial fibrillation" in Blood Coagulation & Fibrinolysis, 31, no. 4 (2020):243-252,
https://doi.org/10.1097/MBC.0000000000000907 . .

TY  - JOUR
AU  - Miković, Danijela
AU  - Pruner, Iva
AU  - Antović, Jovan P.
AU  - Chaireti, Roza
PY  - 2019
UR  - https://imagine.imgge.bg.ac.rs/handle/123456789/1280
PB  - Pergamon-Elsevier Science Ltd, Oxford
T2  - Thrombosis Research
T1  - Presence of thrombophilia and levels of coagulation factors, coagulation inhibitors and TAFI do not affect global haemostasis or bleeding phenotype in patients with haemophilia A
EP  - 3
SP  - 1
VL  - 173
DO  - 10.1016/j.thromres.2018.11.008
ER  - 

@article{
author = "Miković, Danijela and Pruner, Iva and Antović, Jovan P. and Chaireti, Roza",
year = "2019",
publisher = "Pergamon-Elsevier Science Ltd, Oxford",
journal = "Thrombosis Research",
title = "Presence of thrombophilia and levels of coagulation factors, coagulation inhibitors and TAFI do not affect global haemostasis or bleeding phenotype in patients with haemophilia A",
pages = "3-1",
volume = "173",
doi = "10.1016/j.thromres.2018.11.008"
}

Miković, D., Pruner, I., Antović, J. P.,& Chaireti, R.. (2019). Presence of thrombophilia and levels of coagulation factors, coagulation inhibitors and TAFI do not affect global haemostasis or bleeding phenotype in patients with haemophilia A. in Thrombosis Research
Pergamon-Elsevier Science Ltd, Oxford., 173, 1-3.
https://doi.org/10.1016/j.thromres.2018.11.008

Miković D, Pruner I, Antović JP, Chaireti R. Presence of thrombophilia and levels of coagulation factors, coagulation inhibitors and TAFI do not affect global haemostasis or bleeding phenotype in patients with haemophilia A. in Thrombosis Research. 2019;173:1-3.
doi:10.1016/j.thromres.2018.11.008 .

Miković, Danijela, Pruner, Iva, Antović, Jovan P., Chaireti, Roza, "Presence of thrombophilia and levels of coagulation factors, coagulation inhibitors and TAFI do not affect global haemostasis or bleeding phenotype in patients with haemophilia A" in Thrombosis Research, 173 (2019):1-3,
https://doi.org/10.1016/j.thromres.2018.11.008 . .