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Wyszukujesz frazę "Rozalski, Marcin" wg kryterium: Autor

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    Wyświetlanie 1-4 z 4
    Tytuł:
    Znaczenie uwarunkowań genetycznych w dysfunkcjach układu hemostazy w cukrzycy - potencjalne czynniki ryzyka powikłań naczyniowych
    Significance of genetic po lymorphisms in haemostatic dysfunctions in diabetes mellitus - potential risk factors of vascular complications
    Autorzy:
    Watała, Cezary
    Boncler, Magdalena
    Różalski, Marcin
    Powiązania:
    https://bibliotekanauki.pl/articles/945055.pdf
    Data publikacji:
    1999
    Wydawca:
    Uniwersytet Łódzki. Wydawnictwo Uniwersytetu Łódzkiego
    Opis:
    The unambiguous determination of etiopathogenetic factors underlying the increased risk of vascular disease in diabetic patients remains to be established. Evidence accumulated hitherto points that such an increased risk might be a constellation of metabolic disorders and genetic background. Thus, the impairments in coagulation and fibrinolysis, which are believed to partly result from metabolic disorders encountered in diabetes, and genetic factors might be compounding in predisposing a diabetic individual to develop the late diabetic sequelae sooner. The role of the latter seems superior with respect to some dysfunctions in haemostasis. Hence, the monitoring of the frequency and distribution of genetic polymorphisms of selected haemostatic proteins might be promising in an attempt to define the reasons of altered haemostatic imbalance in patients with diabetes mellitus. Based on such a knowledge one could discriminate the groups of patients with high risk for the development of vascular disease, in whom pharmacological strategy to attenuate haemostatic impairments would be desirable.
    Źródło:
    Acta Universitatis Lodziensis. Folia Biochimica et Biophysica; 1999, 14
    0208-614X
    Pojawia się w:
    Acta Universitatis Lodziensis. Folia Biochimica et Biophysica
    Dostawca treści:
    Biblioteka Nauki
    Artykuł
    Tytuł:
    Adenosine diphosphate receptors on blood platelets - potential new targets for antiplatelet therapy
    Autorzy:
    Rozalski, Marcin
    Nocun, Marek
    Watala, Cezary
    Powiązania:
    https://bibliotekanauki.pl/articles/1041421.pdf
    Data publikacji:
    2005
    Wydawca:
    Polskie Towarzystwo Biochemiczne
    Tematy:
    P2Y12
    ADP antagonists
    ADP receptors
    P2Y1
    platelet
    antiplatelet therapy
    Opis:
    Platelets play a key role not only in physiological haemostasis, but also under pathological conditions such as thrombosis. Platelet activation may be initiated by a variety of agonists including thrombin, collagen, thromboxane or adenosine diphosphate (ADP). Although ADP is regarded as a weak agonist of blood platelets, it remains an important mediator of platelet activation evoked by other agonists, which induce massive ADP release from dense granules, where it occurs in molar concentrations. Thus, ADP action underlies a positive feedback that facilitates further platelet aggregation and leads to platelet plug formation. Additionally, ADP acts synergistically to other, even weak, agonists such as serotonin, adrenaline or chemokines. Blood platelets express two types of P2Y ADP receptors: P2Y_1 and P2Y_12. ADP-dependent platelet aggregation is initiated by the P2Y1 receptor, whereas P2Y_12 receptor augments the activating signal and promotes platelet release reaction. Stimulation of P2Y_12 is also essential for ADP-mediated complete activation of GPIIb-IIIa and GPIa-IIa, and further stabilization of platelet aggregates. The crucial role in blood platelet biology makes P2_Y12 an ideal candidate for pharmacological approaches for anti-platelet therapy.
    Źródło:
    Acta Biochimica Polonica; 2005, 52, 2; 411-415
    0001-527X
    Pojawia się w:
    Acta Biochimica Polonica
    Dostawca treści:
    Biblioteka Nauki
    Artykuł
    Tytuł:
    Inhibition of collagen-induced platelet reactivity by DGEA peptide.
    Autorzy:
    Luzak, Boguslawa
    Golanski, Jacek
    Rozalski, Marcin
    Boncler, Magdalena
    Watala, Cezary
    Powiązania:
    https://bibliotekanauki.pl/articles/1043398.pdf
    Data publikacji:
    2003
    Wydawca:
    Polskie Towarzystwo Biochemiczne
    Tematy:
    collagen
    platelet receptor antagonists
    collagen receptors
    GPIaIIa
    DGEA
    platelet reactivity
    Opis:
    Direct interactions between collagen, the most thrombogenic component of the extracellular matrix, and platelet surface membrane receptors mediate platelet adhesion and induce platelet activation and aggregation. In this process two glycoproteins are crucial: integrin α2β1, an adhesive receptor, and GPVI, which is especially responsible for signal transduction. Specific antagonists of the collagen receptors are useful tools for investigating the complexity of platelet-collagen interactions. In this work we assessed the usefulness of DGEA peptide (Asp-Gly-Glu-Ala), the shortest collagen type I-derived motif recognised by the collagen-binding integrin α2β1, as a potential antagonist of collagen receptors. We examined platelet function using several methods including platelet adhesion under static conditions, platelet function analyser PFA-100TM, whole blood electric impedance aggregometry (WBEA) and flow cytometry. We found that DGEA significantly inhibited adhesion, aggregation and release reaction of collagen activated blood platelets. The inhibitory effect of DGEA on static platelet adhesion reached sub-maximal values at millimolar inhibitor concentrations, whereas the specific blocker of α2β1 - monoclonal antibodies Gi9, when used at saturating concentrations, had only a moderate inhibitory effect on platelet adhesion. Considering that 25-30% of total collagen binding to α2β1 is specific, we conclude that DGEA is a strong antagonist interfering with a variety of collagen-platelet interactions, and it can be recognised not only by the primary platelet adhesion receptor α2β1 but also by other collagen receptors.
    Źródło:
    Acta Biochimica Polonica; 2003, 50, 4; 1119-1128
    0001-527X
    Pojawia się w:
    Acta Biochimica Polonica
    Dostawca treści:
    Biblioteka Nauki
    Artykuł
    Tytuł:
    Cu,Zn-superoxide dismutase deficiency in mice leads to organ-specific increase in oxidatively damaged DNA and NF-κB1 protein activity
    Autorzy:
    Siomek, Agnieszka
    Brzoska, Kamil
    Sochanowicz, Barbara
    Gackowski, Daniel
    Rozalski, Rafal
    Foksinski, Marek
    Zarakowska, Ewelina
    Szpila, Anna
    Guz, Jolanta
    Bartlomiejczyk, Teresa
    Kalinowski, Bartlomiej
    Kruszewski, Marcin
    Olinski, Ryszard
    Powiązania:
    https://bibliotekanauki.pl/articles/1042730.pdf
    Data publikacji:
    2010
    Wydawca:
    Polskie Towarzystwo Biochemiczne
    Tematy:
    Cu,Zn-SOD deficiency
    NF-κB pathway
    oxidative stress
    Opis:
    Earlier experimental studies have demonstrated that: i) Cu,Zn-superoxide dismutase deficiency leads to oxidative stress and carcinogenesis; ii) dysregulation of NF-κB pathway can mediate a wide variety of diseases, including cancer. Therefore, we decided, for the first time, to examine the level of oxidative DNA damage and the DNA binding activity of NF-κB proteins in SOD1 knockout, heterozygous and wild-type mice. Two kinds of biomarkers of oxidatively damaged DNA: urinary excretion of 8-oxodG and 8-oxoGua, and the level of oxidatively damaged DNA were analysed using HPLC-GC-MS and HPLC-EC. The DNA binding activity of p50 and p65 proteins in a nuclear extracts was assessed using NF-κB p50/p65 EZ-TFA transcription factor assay. These parameters were determined in the brain, liver, kidney and urine of SOD1 knockout, heterozygous and wild-type mice. The level of 8-oxodG in DNA was higher in the liver and kidney of knockout mice than in wild type. No differences were found in urinary excretion of 8-oxoGua and 8-oxodG between wild type and the SOD1-deficient animals. The activity of the p50 protein was higher in the kidneys, but surprisingly not in the livers of SOD1-deficient mice, whereas p65 activity did not show any variability. Our results indicate that in Cu,Zn-SOD-deficient animals the level of oxidative DNA damage and NF-κB1 activity are elevated in certain organs only, which may provide some explanation for organ-specific ROS-induced carcinogenesis.
    Źródło:
    Acta Biochimica Polonica; 2010, 57, 4; 577-583
    0001-527X
    Pojawia się w:
    Acta Biochimica Polonica
    Dostawca treści:
    Biblioteka Nauki
    Artykuł
      Wyświetlanie 1-4 z 4

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