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Adenosine Diphosphate

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A. Rodríguez-acosta – One of the best experts on this subject based on the ideXlab platform.

  • Inhibition of adrenaline and Adenosine Diphosphate induced platelet aggregation by Lansberg’s hognose pit viper (Porthidium lansbergii hutmanni) venom
    Annals of Hematology, 2007
    Co-Authors: J. C. Lopez-johnston, N. De Bosch, H. Scannone, A. Rodríguez-acosta

    Abstract:

    The haemostatic components of venom from the genus Porthidium has been poorly studied, although it is known that severe manifestations occur when humans are envenomed, which include invasive oedema and disseminated ecchymosis. The effects of venom on blood platelets are commonly studied and are normally carried out with platelet-rich plasma (PRP). A series of crude venom dilutions was used to determine the effects of Adenosine Diphosphate (2 μM) and adrenaline (11 μM) induced platelet aggregation. Venom of Porthidium lansbergii hutmanni was fractioned by anionic exchange chromatography, and the fractions were also used to determine the 50% inhibition of Adenosine Diphosphate (ADP) and adrenaline-induced platelet aggregating dose (AD50). Crude venom has more effect in inhibiting adrenaline-induced aggregation (AD50 = 0.0043 μg) followed by the Adenosine Diphosphate (AD50 = 17 μg). Peaks I and II obtained by chromatography also inhibited adrenaline-induced platelet aggregation with an AD50 of 3.2 and 0.013 μg, respectively, and both peaks inhibited ADP-induced platelet aggregation with an AD50 of 10 μg. The main purpose of this work was to characterise the in vitro effects caused by P. lansbergii hutmanni crude venom and its fractions on the platelet aggregation mediated by adrenaline and ADP agonists.

  • Inhibition of adrenaline and Adenosine Diphosphate induced platelet aggregation by Lansberg’s hognose pit viper (Porthidium lansbergii hutmanni) venom
    Annals of Hematology, 2007
    Co-Authors: J. C. Lopez-johnston, N. De Bosch, H. Scannone, A. Rodríguez-acosta

    Abstract:

    The haemostatic components of venom from the genus Porthidium has been poorly studied, although it is known that severe manifestations occur when humans are envenomed, which include invasive oedema and disseminated ecchymosis. The effects of venom on blood platelets are commonly studied and are normally carried out with platelet-rich plasma (PRP). A series of crude venom dilutions was used to determine the effects of Adenosine Diphosphate (2 microM) and adrenaline (11 microM) induced platelet aggregation. Venom of Porthidium lansbergii hutmanni was fractioned by anionic exchange chromatography, and the fractions were also used to determine the 50% inhibition of Adenosine Diphosphate (ADP) and adrenaline-induced platelet aggregating dose (AD50). Crude venom has more effect in inhibiting adrenaline-induced aggregation (AD50 = 0.0043 microg) followed by the Adenosine Diphosphate (AD50 = 17 microg). Peaks I and II obtained by chromatography also inhibited adrenaline-induced platelet aggregation with an AD50 of 3.2 and 0.013 microg, respectively, and both peaks inhibited ADP-induced platelet aggregation with an AD50 of 10 microg. The main purpose of this work was to characterise the in vitro effects caused by P. lansbergii hutmanni crude venom and its fractions on the platelet aggregation mediated by adrenaline and ADP agonists.

J. C. Lopez-johnston – One of the best experts on this subject based on the ideXlab platform.

  • Inhibition of adrenaline and Adenosine Diphosphate induced platelet aggregation by Lansberg’s hognose pit viper (Porthidium lansbergii hutmanni) venom
    Annals of Hematology, 2007
    Co-Authors: J. C. Lopez-johnston, N. De Bosch, H. Scannone, A. Rodríguez-acosta

    Abstract:

    The haemostatic components of venom from the genus Porthidium has been poorly studied, although it is known that severe manifestations occur when humans are envenomed, which include invasive oedema and disseminated ecchymosis. The effects of venom on blood platelets are commonly studied and are normally carried out with platelet-rich plasma (PRP). A series of crude venom dilutions was used to determine the effects of Adenosine Diphosphate (2 μM) and adrenaline (11 μM) induced platelet aggregation. Venom of Porthidium lansbergii hutmanni was fractioned by anionic exchange chromatography, and the fractions were also used to determine the 50% inhibition of Adenosine Diphosphate (ADP) and adrenaline-induced platelet aggregating dose (AD50). Crude venom has more effect in inhibiting adrenaline-induced aggregation (AD50 = 0.0043 μg) followed by the Adenosine Diphosphate (AD50 = 17 μg). Peaks I and II obtained by chromatography also inhibited adrenaline-induced platelet aggregation with an AD50 of 3.2 and 0.013 μg, respectively, and both peaks inhibited ADP-induced platelet aggregation with an AD50 of 10 μg. The main purpose of this work was to characterise the in vitro effects caused by P. lansbergii hutmanni crude venom and its fractions on the platelet aggregation mediated by adrenaline and ADP agonists.

  • Inhibition of adrenaline and Adenosine Diphosphate induced platelet aggregation by Lansberg’s hognose pit viper (Porthidium lansbergii hutmanni) venom
    Annals of Hematology, 2007
    Co-Authors: J. C. Lopez-johnston, N. De Bosch, H. Scannone, A. Rodríguez-acosta

    Abstract:

    The haemostatic components of venom from the genus Porthidium has been poorly studied, although it is known that severe manifestations occur when humans are envenomed, which include invasive oedema and disseminated ecchymosis. The effects of venom on blood platelets are commonly studied and are normally carried out with platelet-rich plasma (PRP). A series of crude venom dilutions was used to determine the effects of Adenosine Diphosphate (2 microM) and adrenaline (11 microM) induced platelet aggregation. Venom of Porthidium lansbergii hutmanni was fractioned by anionic exchange chromatography, and the fractions were also used to determine the 50% inhibition of Adenosine Diphosphate (ADP) and adrenaline-induced platelet aggregating dose (AD50). Crude venom has more effect in inhibiting adrenaline-induced aggregation (AD50 = 0.0043 microg) followed by the Adenosine Diphosphate (AD50 = 17 microg). Peaks I and II obtained by chromatography also inhibited adrenaline-induced platelet aggregation with an AD50 of 3.2 and 0.013 microg, respectively, and both peaks inhibited ADP-induced platelet aggregation with an AD50 of 10 microg. The main purpose of this work was to characterise the in vitro effects caused by P. lansbergii hutmanni crude venom and its fractions on the platelet aggregation mediated by adrenaline and ADP agonists.

Csaba Szabo – One of the best experts on this subject based on the ideXlab platform.

  • peroxynitrite production and activation of poly Adenosine Diphosphate ribose synthetase in spinal cord injury
    Annals of Neurology, 1999
    Co-Authors: Gwen S Scott, Lyn B Jakeman, Bradford T Stokes, Csaba Szabo

    Abstract:

    Peroxynitrite formation and the subsequent activation of the nuclear enzyme, poly (Adenosine Diphosphate [ADP]-ribose) synthetase (PARS), has been implicated in the pathogenesis of several neurodegenerative disorders. Here, we demonstrate that nitrotyrosine, an indicator of peroxynitrite generation, and poly (ADP) ribose, a marker of PARS activation, were selectively localized within tissues from spinal cord-injured rats. Our data implicate a role for peroxynitrite production and PARS activation in the development of spinal cord trauma.