Wyniki wyszukiwania

1

Molecular structure and biological function of von Willebrand factor

100%

Bykowska E.

Acta Biochimica Polonica

|

2007

|

tom 54

|

nr Supplement 4

2

Arterial angioplasty. Thrombosis and restenosis

100%

Badimon L., Chesebro J. H., Badimon J. J., Fuster V.

Journal of Physiology and Pharmacology. Supplement

|

1993

|

tom 44

|

nr 2

3

An age-related decrease in factor V Leiden frequency among Polish subjects

84%

Adler G., Parczewski M., Czerska E., Loniewska B., Kaczmarczyk M., Gumprecht J., Grzeszczak W., Szybinska A., Mossakowska M., Ciechanowicz A.

Journal of Applied Genetics

|

2010

|

tom 51

|

nr 3

Factor V Leiden (G1691A FV mutation) is a widely acknowledged risk factor of deep vein thrombosis, including pulmonary embolism as the most serious complication. However, its high prevalence of ~5% in the Caucasian population might be related to an unknown evolutionary advantage. It might exert a beneficial effect on the carrier, e.g. protecting women from excessive bleeding during labour or allowing increased survival in severe sepsis or with other inflammatory diseases. The aim of our study was to verify or contradict the hypothesis of a favourable association between the A allele (A1691) and longevity in the Polish population. For this purpose, the G1691A mutation was analyzed by PCR-RFLP in 1016 Poles: 400 neonates (187 female and 312 male), 184 healthy adults (129 female and 55 male), and 432 long-lived individuals (age ≥ 95 years: 343 women and 89 men). Frequencies of G1691A carriers and the A1691 allele in long-lived individuals (0.2% and 0.1%, respectively) were significantly lower than in neonates (4.2% and 2.2%, respectively) and adults (3.3% and 1.6%). The frequency of the G1691A factor V Leiden mutation decreased with age, which indicates a shorter survival time among A1691 allele carriers in the Polish population.

4

Nitric oxide as a modulator in platelet- and endothelium-dependent antithrombotic effect of eplerenone in diabetic rats

84%

Gromotowicz-Poplawska A., Kloza M., Aleksiejczuk M., Marcinczyk N., Szemraj J., Kozlowska H., Chabielska E.

Journal of Physiology and Pharmacology

|

2019

|

tom 70

|

nr 2

5

The phenomenon of neutrophil extracellular traps in vascular diseases

84%

Dabrowska D., Jablonska E., Garley M., Sawicka-Powierza J., Nowak K.

Archivum Immunologiae et Therapiae Experimentalis

|

2018

|

tom 66

|

nr 4

6

Artykuł dostępny w postaci pełnego tekstu - kliknij by otworzyć plik

Non-specific connective tissue dysplasia - a risk factor for postoperative thrombosis in the venous system of lower extremities

84%

Venher I., Kostiv S., Nenashko I.

Health Problems of Civilization

|

2016

|

tom 10

|

nr 2

Background. Deep vein thrombosis of lower extremities and pulmonary embolism have common pathogenic roots and are the most common cause of poor blood circulation. Several factors that contribute to the development of thrombosis in the venous system are identified and must be taken into consideration in the process of preparing for surgery. Material and methods. 472 patients were examined and operated in departments of surgery of municipal institution of Ternopil regional council Ternopil University Hospital in 2010-2014. In the process of surgical treatment thromboprophylaxis was applied according to sectoral protocols [1]. Results. In postoperative period t hrombotic process in the system IVC was diagnosed in 96 (20.34%) patients. The incidence of postoperative thrombosis in the IVC system was directly related to the risk of the venous thromboembolic complications. dysplasia; in 27 (45.1%) observations detected asthenic type of constitution, in 18 (36.6%) – hypermorbid syndrome, in 31 (57.7%) – varicose veins (class C1 – 27 cases, class C2 – 14 cases). In the laboratory study the indicators of metabolic products connective tissue level of total oxyproline exceeded the reference value at 41.77% (p <0.001), free oxyproline – by 46.85% (p <0.001), and bound oxyproline – 31.71% (p <0.001). Conclusions. Established that non-specific connective tissue dysplasia can be significant risk factor for postoperative venous thrombosis in the system inferior vena cava.

7

Atrial natiuretic peptide and brain natriuretic peptide changes after epicardial percutaneous left atrial appendage suture ligation using LARIAT device

84%

Bartus K., Podolec J., Lee R. J., Kapelak B., Sadowski J., Bartus M., Oles K., Ceranowicz P., Trabka R., Litwinowicz R.

Journal of Physiology and Pharmacology

|

2017

|

tom 68

|

nr 1

8

Neutrophil extracellular traps (NETs) - formation and implications

84%

Zawrotniak M., Rapala-Kozik M.

Acta Biochimica Polonica

|

2013

|

tom 60

|

nr 3

Neutrophils are cells of the immune system which freely circulate in blood vessels and are recruited to the inflammation sites when the human organism responds to microbial infections. One of the mechanisms of neutrophil action is the formation of neutrophil extracellular traps (NETs) The process of NET generation, called netosis, is a specific type of cell death, different from necrosis and apoptosis. NETs are formed by neutrophils upon contact with various bacteria or fungi as well as with activated platelets or under the influence of numerous inflammatory stimuli, and this process is associated with dramatic changes in the morphology of the cells. The main components of NETs, DNA and granular antimicrobial proteins, determine their antimicrobial properties. The pathogens trapped in NETs are killed by oxidative and non-oxidative mechanisms. On the other hand, it was also discovered that chromatin and proteases released into the circulatory system during NET formation can regulate procoagulant and prothrombotic factors and take part in clot formation in blood vessels. NETs have also been detected in lungs where they are involved in chronic inflammation processes in ALI/ARDS patients. Moreover, DNA-proteins complexes have been found in the airway fluids of cystic fibrosis patients where they can increase the viscosity of the sputum and have a negative impact on the lung functions. The DNA-complexed granular proteins and other proteins released by neutrophils during netosis lead to autoimmunity syndromes such as systemic lupus erythematosus (SLE), small-vessel vasculitis (SVV) or autoimmune diseases associated with the formation of autoantibodies against chromatin and neutrophil components. A possible involvement of NETs in metastasis is also considered.

9

The role of mTOR inhibitors and HMG-CoA reductase inhibitors on young and old endothelial cell functions, critical for re-endothelialisation after percutaneous coronary intervention: an in vitro study

84%

Korybalska K., Kawka E., Breborowicz A., Witkowski J.

Journal of Physiology and Pharmacology

|

2017

|

tom 68

|

nr 3

10

Acute ischemic stroke within the area of MCA from ICA thrombosis complicating moderate COVID-19 infection

84%

Kurys-Denis E., Prystupa A., Sak J.

Journal of Pre-Clinical and Clinical Research

|

2021

|

tom 15

|

nr 1

11

N-methylnicotinamide inhibits arterial thrombosis in hypertensive rats

84%

Mogielnicki A., Kramkowski K., Pietrzak L., Buczko W.

Journal of Physiology and Pharmacology

|

2007

|

tom 58

|

nr 3

There are few findings indicating that nicotinamide may potentially influence intravascular thrombosis. Interestingly, N-methylnicotinamide, one of the metabolites of nicotinamide - could be more potent than its parent compound. In the present study we have investigated the influence of N-methylnicotinamide on arterial thrombosis in normotensive and renovascular hypertensive rats. The contribution of platelets, coagulation and fibrinolytic systems in the mode of N-methylnicotinamide action was also determined. Furthermore, we examined the role of nitric oxide/prostacyclin in the mechanisms of N-methylnicotinamide action. N-methylnicotinamide, but not nicotinamide, administered intravenously into renovascular hypertensive rats developing electrically induced arterial thrombosis caused dose-dependent decrease of thrombus weight, collagen-induced platelet aggregation and plasma antigen/activity of plasminogen activator inhibitor - 1, without changing of occlusion time, routine coagulation parameters and plasma activity of tissue plasminogen activator. Indomethacin - an inhibitor of prostacyclin synthesis, completely abolished the antithrombotic and antiplatelet effect of N-methylnicotinamide, and the plasma level of 6-keto-PGF1alpha, prostacyclin metabolite, increased simultaneously with the inhibition of thrombus formation. Our study shows that N-methylnicotinamide via production/release of prostacyclin inhibits arterial thrombosis development. The antithrombotic effect of N-methylnicotinamide is accompanied by platelet inhibition and enhanced fibrinolysis, due to the decrease production of plasminogen activator inhibitor - 1.

12

Angiotensin II via AT1 receptor accelerates arterial thrombosis in renovascular hypertensive rats

84%

Kaminska M., Mogielnicki A., Stankiewicz A., Kramkowski K., Domaniewski T., Buczko W., Chabielska E.

Journal of Physiology and Pharmacology

|

2005

|

tom 56

|

nr 4

Although there are some in vitro evidence that angiotensin II (Ang II) may promote thrombosis, there is still no data concerning effect of Ang II on arterial thrombus formation. In the present study we have investigated the influence of Ang II on electrically induced arterial thrombosis in a common carotid artery of renovascular hypertensive rats. Furthermore, we examined if Ang II effect is mediated via AT1 receptor. We measured some coagulation and fibrinolytic parameters at the same time. Since platelets play crucial role in the initiation of arterial thrombosis their contribution in the mode of Ang II action was also determined. Intravenous infusion of Ang II caused significant increase in arterial thrombus weight, which was reversed by losartan, selective AT1 receptor antagonist. The prothrombotic effect of Ang II was accompanied by increase in haemostatic and decrease in fibrinolytic potential of rat plasma. While number of data has clearly demonstrated that Ang II can augment human platelets aggregation, at least in rats, platelets were not involved in the mechanism of Ang II action. Our study shows that Ang II via AT1 receptor accelerates arterial thrombosis in renovascular hypertensive rat, therefore may be considered as a risk factor of myocardial infarction or stroke.

13

Losartan inhibits the adhesion of rat platelets to fibrillar collagen - a potential role of nitric oxide and prostanoids

84%

Matys T., Chabielska E., Pawlak R., Kucharewicz I., Buczko W.

Journal of Physiology and Pharmacology

|

2000

|

tom 51

|

nr 4,1

14

P-selectin mediates adhesion of leucocytes, platelets, and cancer cells in inflammation, thrombosis, and cancer growth and metastasis

84%

Chen M., Geng J. G.

Archivum Immunologiae et Therapiae Experimentalis

|

2006

|

tom 54

|

nr 2

15

The pathophysiological hypothesis of homocysteine thiolactone-mediated vascular disease

67%

Jakubowski H.

Journal of Physiology and Pharmacology. Supplement

|

2008

|

tom 59

|

nr 9

155-167

16

Diagnostics in pulmonary hypertension

67%

Schannewll C. M., Steiner S., Strauer B.-E.

Journal of Physiology and Pharmacology. Supplement

|

2007

|

tom 58

|

nr 5

17

JAK2 mutation status, hemostatic risk factors and thrombophilic factors in essential thrombocythemia (ET) patients

67%

Sokolowska B., Nowaczynska A., Bykowska K., Chocholska S., Wejksza K., Walter-Croneck A., Gromek T., Kowalska A. M., Kandefer-Szerszen M., Dmoszynska A.

Folia Histochemica et Cytobiologica

|

2011

|

tom 49

|

nr 2

18

Flow cytometric analysis of CD55 and CD59 expression on blood cells in paroxysmal nocturnal haemoglobinuria

67%

Dworacki G., Sikora J., Mizera-Nyczak E., Trybus M., Mozer-Lisewska I., Czyz A., Zeromski J.

Folia Histochemica et Cytobiologica

|

2005

|

tom 43

|

nr 2

19

Antithrombotic effect of tissue and plasma type angiotensin converting enzyme inhibitors in experimental thrombosis in rats

67%

Wojewodzka-Zelazniakowicz M., Chabielska E., Mogielnicki A., Kramkowski K., Karp A., Opadczuk A., Domaniewski T., Malinowska-Zaprzalka M., Buczko W.

Journal of Physiology and Pharmacology

|

2006

|

tom 57

|

nr 2

This study compared the antihrombotic effect of plasma angiotensin converting enzyme inhibitors (ACE-Is): captopril (CAP), enalapril (ENA) and Tissue ACE-Is: perindopril (PER), quinapril (QUIN) in experimental venous and arterial thrombosis. Normotensive Wistar rats were treated p.o. with CAP (75 mg/kg), ENA (20 mg/kg), PER (2 mg/kg) and QUIN (3 mg/kg) for 10 days. The influence of ACE-Is on coagulation and fibrinolytic systems as well as platelet function was evaluated. The hypotensive effect of ACE-Is was equal in all groups. QUIN mantained the final carotid blood flow at the highest value in comparison to PER and plasma ACE-Is. The arterial thrombus weight was reduced in PER and QUIN groups while venous thrombus weight was also reduced after CAP. Tissue andplasma ACE-Is caused the inhibition of platelet adhesion and aggregation. A reduction of fibrin generation, prolongation of prothrombin time (PT), activated partial thromboplastin time (APTT) and shortening of euglobulin clot lysis time (ECLT) were observed after PER and QUIN treatment. In conclusion, given in equipotent hypotensive doses, Tissue ACE-Is exerted more pronounced antithrombotic effect than plasma ACE-Is in experimental thrombosis. The differences between Tissue and plasma ACE-Is in terms of their more pronounced inhibition of experimental thrombosis may be related to the intensified activation of fibrinolysis and inhibition of coagulation.

20

Sphingosine 1-phosphate is a blood constituent released from activated platelets, possibly playing a variety of physiological and pathophysiological roles

67%

Igarashi Y., Yatomi Y.

Acta Biochimica Polonica

|

1998

|

tom 45

|

nr 2

We have found that sphingosine 1-phosphate (Sph-1-P) acts as an autocrine stimulator of platelets, being abundantly stored in platelets and released extracellularly, and that its exogenous addition induces platelet activation (Yatomi et al., Blood 1995, 86, 193-202) through a specific receptor on the platelet surface (Yatomi et al., J. Biol. Chem. 1997, 272, 5291-5297). Very recently, we identified Sph-1-P as a normal constituent of human plasma and serum. Sph-1-P levels in plasma and serum were 191±79 and 484±82 pmol/ml (mean ±S.D., n = 8), respectively. Platelets are most likely the source of Sph-1-P discharged during blood clotting, since they abundantly store Sph-1-P as compared with other blood cells, and release considerable amounts of stored Sph-1-P extracellularly upon stimulation. The Sph-1-P released from activated platelets may be involved in a variety of physiological processes, including thrombosis, atherosclerosis, and wound healing. Moreover, we often observed that Sph-1-P injection into mice (iv., 10 mg/kg) caused immediate rigor and death. This may be related to the recent observations from an other laboratory that nanomolar concentrations of Sph-1-P affected atrial myocyte K+ channel. These observations taken together strongly suggest pathophysiological roles of the released Sph-1-P in the blood. As one example, we found that Sph-1-P content in the plasma of platelet concentrates correlated with poor platelet increments after transfusion and with the occurence of transfusion reactions in patients.

Ograniczanie wyników

Molecular structure and biological function of von Willebrand factor

Arterial angioplasty. Thrombosis and restenosis

An age-related decrease in factor V Leiden frequency among Polish subjects

Nitric oxide as a modulator in platelet- and endothelium-dependent antithrombotic effect of eplerenone in diabetic rats

The phenomenon of neutrophil extracellular traps in vascular diseases

Non-specific connective tissue dysplasia - a risk factor for postoperative thrombosis in the venous system of lower extremities

Atrial natiuretic peptide and brain natriuretic peptide changes after epicardial percutaneous left atrial appendage suture ligation using LARIAT device

Neutrophil extracellular traps (NETs) - formation and implications

The role of mTOR inhibitors and HMG-CoA reductase inhibitors on young and old endothelial cell functions, critical for re-endothelialisation after percutaneous coronary intervention: an in vitro study

Acute ischemic stroke within the area of MCA from ICA thrombosis complicating moderate COVID-19 infection

N-methylnicotinamide inhibits arterial thrombosis in hypertensive rats

Angiotensin II via AT1 receptor accelerates arterial thrombosis in renovascular hypertensive rats

Losartan inhibits the adhesion of rat platelets to fibrillar collagen - a potential role of nitric oxide and prostanoids

P-selectin mediates adhesion of leucocytes, platelets, and cancer cells in inflammation, thrombosis, and cancer growth and metastasis

The pathophysiological hypothesis of homocysteine thiolactone-mediated vascular disease

Diagnostics in pulmonary hypertension

JAK2 mutation status, hemostatic risk factors and thrombophilic factors in essential thrombocythemia (ET) patients

Flow cytometric analysis of CD55 and CD59 expression on blood cells in paroxysmal nocturnal haemoglobinuria

Antithrombotic effect of tissue and plasma type angiotensin converting enzyme inhibitors in experimental thrombosis in rats

Sphingosine 1-phosphate is a blood constituent released from activated platelets, possibly playing a variety of physiological and pathophysiological roles