Wynik wyszukiwania w bazie Polska Bibliografia Lekarska GBL

Zapytanie: CHŁOPICKI
Liczba odnalezionych rekordów: 11



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1/11

Tytuł oryginału: Interactions between human platelets and eosinophils are mediated by selectin-P.
Autorzy: Jawień Jacek, Chłopicki Stefan, Gryglewski Ryszard J.
Źródło: Pol. J. Pharmacol. 2002: 54 (2) s.157-160, tab., bibliogr. 15 poz.
Sygnatura GBL: 313,156

Typ dokumentu:
  • tytuł obcojęzyczny
  • praca doświadczalna

    Wskaźnik treści:
  • ludzie

    Streszczenie angielskie: Mechanisms and biochemical consequences of platelet-neutrophil interactions are well known. In contrast, platelet-eosinophil interactions remain largely unexplored. The aim of this study was to assess whether platelets adhere to eosinophils, and to analyze whether selectin-P would mediate that phenomenon. Eosinophils and platelets were obtained from peripheral blood of healthy volunteers. Eosinophils were isolated using magnetic cell separation method. Platelets were isolated and washed. A number of "rosettes" (an eosinophil with more than 5 adherent platelets) per 100 eosinophils were examined in the eosinophil-platelet suspension. Addition of thrombin stimulated formation of "rosettes". Monoclonal antibodies against selectin-P almost completely prevented thrombin-stimulated formation of "rosettes". In summary, intercellular interaction between platelets and eosinophils are mediated by selectin-P. This phenomenon may be of importance in asthma and other atopic diseases.


    2/11

    Tytuł oryginału: Hypoxic pulmonary vasoconstriction in isolated blood-perfused rat lung; modulation by thromboxane A2, platelet-activating factor, cysteinyl leukotrienes and endothelin-1.
    Autorzy: Chłopicki Stefan, Bartuś Joanna B., Gryglewski Ryszard J.
    Źródło: Pol. J. Pharmacol. 2002: 54 (5) s.433-441, il., bibliogr. 49 poz.
    Sygnatura GBL: 313,156

    Hasła klasyfikacyjne GBL:
  • farmacja
  • kardiologia
  • pulmonologia

    Typ dokumentu:
  • praca doświadczalna
  • tytuł obcojęzyczny

    Wskaźnik treści:
  • zwierzęta
  • szczury

    Streszczenie angielskie: Recent evidence suggests that hypoxic pulmonary vasoconstriction (HPV) is mediated by hypoxia-induced closure of voltage-gated potassium channels in pulmonary vascular smooth muscle cells. It is also claimed that various vasoconstrictor mediators such as thromboxane A2 (TXA1), platelet activating factor (PAF), cysteinyl leukotrienes (cys-LTs) or endothelin-1 (ET-1) contribute to HPV. Their role, however, has not been unequivocally accepted. On the contrary, it is well known that endothelium-derived nitric oxide negatively modulates HPV. Since NO counteracts action of vasoconstrictor mediators, we tested the hypothesis that modulatory role of TXA2, PAF, cys-LTs and ET-1 in HPV would become apparent in absence of endogenous NO. For that purpose we assessed contribution of these mediators to HPV in the isolated blood-perfused rat lung pretreated with a nonselective NOS inhibitor, L-NAME. HPV, which was greatly augmented by L-NAME (300 ćM) alone, was inhibited neither by a TXA2 synthase inhibitor (Camonagrel, 300 ćM), nor by a PAF receptor antagonist (WEB 2170, 100 ćM), nor by an inhibitor of five-lipoxygenase-activating protein (MK 886, 10 ćM), nor by a non-selective ET-1 receptor antagonist (LU 302872, 30 ćM). In summary, in isolated blood-perfused rat lung, TXA2, PAF, cys-LTs and ET-1 seem not to be involved in HPV, whereas we confirm the dominant role of endogenous NO in blunting HPV.


    3/11

    Tytuł oryginału: Hartowanie serca przez niedokrwienie, a pochodne sulfonylomocznika w leczeniu cukrzycy.
    Autorzy: Chłopicki Stefan
    Źródło: Pol. Prz. Kardiol. 2002: 4 supl. 1: III Warszawskie Dni Farmakologii, Farmakoterapii i Farmakoekonomiki 2001 - materiały z konferencji s.51-57, il., bibliogr. 73 poz. - 3 Warszawskie Dni Farmakologii, Farmakoterapii i Farmakoekonomiki Warszawa 06-08.06. 2001
    Sygnatura GBL: 313,529

    Hasła klasyfikacyjne GBL:
  • endokrynologia
  • kardiologia
  • toksykologia

    Typ dokumentu:
  • praca związana ze zjazdem

    Wskaźnik treści:
  • ludzie


    4/11

    Tytuł oryginału: Eosinophil - epithelial cell interaction augments cysteinyl leukotrienes synthesis.
    Autorzy: Jawień J[acek], Chłopicki S., Olszanecki R., Lorkowska B., Gryglewski R. J.
    Źródło: J. Physiol. Pharmacol. 2002: 53 (1) s.127-132, il., bibliogr. 17 poz.
    Sygnatura GBL: 302,092

    Typ dokumentu:
  • praca doświadczalna
  • tytuł obcojęzyczny

    Wskaźnik treści:
  • ludzie
  • in vitro

    Streszczenie angielskie: Eosinophilis accumulation in the airways and sustained eosinophil-derived cysteinyl leukotrienes production repesent key elements of the inflammatory response seen in asthma. However, it is not known whether activated epithelial cells influence cysteinyl leukotrienes production by eosinophils from healthy valunteers. The aim of the present study was therefore to analyse the effects of interactions between non-atopic eosinophils and epithelial cells on cysteinyl leukotrienes production in vitro. We measured cysteinyl leukotrienes released by phorbol 12-myristate 13-acetate (PMA) - activated human eosinophils or epithelial cells (human bronchial epithelial cell line - BEAS-2B) cultured alone or together. While activated BEAS-2B cells barely formed leukotrienes (1.39 pg/ml ń 0.2) (n = 32), activated eosinophilis produced considerable amount of them (62.25 pg/ml ń 10.29) (n = 32). Interestingly, when activated eosinophils and epithelial cells were co-incubated, production of cysteinyl leukotrienes increased substantially (571.1 pg/ml ń 80.9) (n = 32). Thus, eosinophil-epithelial cell interactions, when occur, are associated with increased biosynthesis of cysteinyl leukotrienes.


    5/11

    Tytuł oryginału: No-dependent vasodilation induced by nebivolol in coronary circulation is not mediated by á-adrenoceptors or by 5 HT1A-receptors.
    Autorzy: Chłopicki S[tefan], Kozlovski V[alery] I., Gryglewski R. J.
    Źródło: J. Physiol. Pharmacol. 2002: 53 (4 p. 1) s.615-624, il., bibliogr. 19 poz., sum.
    Sygnatura GBL: 302,092

    Hasła klasyfikacyjne GBL:
  • kardiologia

    Typ dokumentu:
  • praca doświadczalna
  • tytuł obcojęzyczny

    Wskaźnik treści:
  • zwierzęta
  • Świnki morskie
  • in vitro

    Streszczenie angielskie: Nebivolol is a unique á1-adrenoceptor antagonist which possesses peripheral vasodilator properties dependent on endothelial NO. Nebivolol-induced release of NO was attributed to its L stereoisomer and to its ability to stimulate endothelial á2, á3 adrenoceptors or 5 HT1A receptors. Here, in the isolated guinea pig heart we analysed coronary vasodilator potency of L- and D-nebivolol and a possible role of á2, á3 adrenoceptors and 5-HT1A receptors in nebivolol-induced vasodilation. Surprisingly, we ound that not only L-nebivolol (3-30x10**-6 M) but also D-nebivolol (3-30x10**-6 M) induced coronary vasodilation, and both responses were inhibited by L-NAME (10**-4 M). In contrast with the stereoisomers of nebivolol, atenolol at the equimolar concentrations did induce slight casoconstriction. The nonselective á1/á2-adrenoceptor antagonist - nadolol (10-5 M). The selective á3-adrenoceptor antagonist - L 748337 (10**6 M) and the 5 HT1A receptor antagonist - NAN 190 (5 x 10**-6 M), none of them inhibited coronary vasodilation induced by D- and L-nebivolol. In summary, in the isolated guinea pig heart both D- and L-nebivolol act as coronary vasodilators. Coronary vasodilation induced by stereoisomers of nebivolol is mediated by endothelium-derived NO and does not depend on á2, á3 adrenoceptors or 5 HT1A receptors.


    6/11

    Tytuł oryginału: Synthesis and thrombolytic activity of new thienopyrimidinone derivatives.
    Autorzy: Dupin J. P., Gryglewski R. J., Gravier D., Hou G., Casadebaig F., Swies J., Chłopicki S[tefan]
    Źródło: J. Physiol. Pharmacol. 2002: 53 (4 p. 1) s.625-634, il., tab., bibliogr. 25 poz.
    Sygnatura GBL: 302,092

    Hasła klasyfikacyjne GBL:
  • farmacja
  • kardiologia

    Typ dokumentu:
  • praca doświadczalna
  • tytuł obcojęzyczny

    Wskaźnik treści:
  • zwierzęta
  • szczury

    Streszczenie angielskie: It has been observed that ticlopidine and clopidogrel show, apart from their delayed antiplatelet properties, an immediate and transient thombolytic action related to the ability of these thienopyridines to stimulate the secretory function of vascular endothelium. With the objective to construct new molecules with identical thrombolytic potency but at a higher level, we carried out different structural modifications in the thienopyridine chemical molecule to conclude that the presence of a second N atom in the pyridine cycle (yielding pyrimidine moiety) and the presence of an additional cycle fused to the thienyl ring would lead to enhanced thrombolytic effects. Here we report the six-step synthesis of a series of new benzothienopyrimidinone derivatives characterized by this searched for potent thrombolytic activity. The pharmacological assay used anaesthetised Wistar rats with extracorporal circulation in which arterial blood superfused thrombi adhering to a strip of collagen. Weight of thrombi was continously monitored. Six compounds of the series were much more potent thrombolytic agents than their thienopyridine references: the effective thrombolytic dose that produced 30 p.c. of maximum thrombolysis (ED 30) was at a range of 8 to 170 ćg kg**-1 as compared with ED30 values of 16000 to 20000 ćg kg**-1 for clopidogrel and ticlopidine respectively. Especially with the most active compound, this difference in the threshold thrombolytic dose, giving an intnsity of action higher by three orders of magnitude, was ....


    7/11

    Tytuł oryginału: Paradoxical augumentation of bradykinin-induced vasodilatation by xanthine/xanthine oxidase-derived free radicals in isolated guinea pig heart.
    Autorzy: Olszanecki R[afał], Kozlovski V[alery] I., Chłopicki S[tefan], Gryglewski R. J.
    Źródło: J. Physiol. Pharmacol. 2002: 53 (4 p. 1) s.689-699, il., tab., bibliogr. 42 poz.
    Sygnatura GBL: 302,092

    Hasła klasyfikacyjne GBL:
  • farmacja
  • kardiologia

    Typ dokumentu:
  • praca doświadczalna
  • tytuł obcojęzyczny

    Wskaźnik treści:
  • zwierzęta
  • Świnki morskie
  • in vitro

    Streszczenie angielskie: Increased generation of reactive oxygen species contribute to endothelial dysfunction in atherosclerosis, hypertension and heart failure. Recently, it was suggested that bursts of superoxide anions may inactivate endothelial surface-bound enzymes such as angiotensin converting enzyme (ACE). Here, we tested effects of xanthine/xanthine oxidase-derived superoxide anions on vascular responses and ACE activity in the isolated guinea pig heart. We anlysed effects of intracoronary infusion of low concentration of xanthine oxidase (10 mU/ml) in the presence of xanthine (0,5 mM) (X/XO) on bradykinin, other endothelium-dependent and independent vasodilators (acetylcholine, ADP, SNAP), as well as vasoconstrictor responses to angiotensin I and angiotensin II. Surprisingly, X/XO significantly augumented coronary response to bradykinin without an effect on response to ADP, acetylcholine, SNAP, angiotensin I and angiotensin II. In contrast, inhibition of ACE by perindoprilate (100 nM) resulted in augumentation of bradykinin-induced vasodialidation as well as diminution of angiotensin I-evoked vasoconstriction without an influence on other responses. In summary, in the isolated guinea pig heart, X/XO-derived free radicals selectivity augumented coronary vasodilator response to bradykinin, which cannot be explained by X/XO-induced derangement of ACE. The mechanism of this paradoxical phenomenon, which might represent a defensive response of the coronary circulation to oxidative stress requires further investigations.


    8/11

    Tytuł oryginału: Ultrastructural alterations of endothelium covering advanced atherosclerotic plaque in human carotid artery visualised by scanning electron microscope.
    Autorzy: Walski M., Chłopicki S[tefan], Celary-Walska R., Frontczak-Baniewicz M.
    Źródło: J. Physiol. Pharmacol. 2002: 53 (4 p. 1) s.713-723, il., bibliogr. 29 poz.
    Sygnatura GBL: 302,092

    Hasła klasyfikacyjne GBL:
  • kardiologia

    Typ dokumentu:
  • praca kliniczna
  • tytuł obcojęzyczny

    Wskaźnik treści:
  • ludzie
  • dorośli 45-64 r.ż.
  • dorośli = 65 r.ż.
  • płeć męska
  • płeć żeńska

    Streszczenie angielskie: Human atherosclerotic plaque morphology at its various stages was extensively documented using light microscopy. However, much less is known of the ultrastructure of the human atherosclerotic plaque, in particular of ultrastructure of endothelial cells in atherosclerosis. Here, we annalysed alterations of endothelial cells covering advanced atherosclerotic plaque in carotid artery using scanning electron microscope. Examination was performed on specimens from atherosclerotic lesions of the interior carotid artery, collected from 8 patients who had undergone endarterectomy. We found wide spectrum of pathological alternations of the luminal surface of atherosclerotic plaque. In dominant part of the vessel, endothelial layer was preserved but displayed pronounced irregularities in endothelial architecture including appearance of cuboidal cells. Some endothelial cells were covered by numerous microvilli and/or contained "craters" disupting continuous surface of the endothelium. Platelets and leukocytes adhering to endothelium were frequently observed. There were also areas of the vessel lumen with endothelial denudation, in which the subendothelial surface containing fibrin proteins and collagen fibrils were visible. Interestingly, signs of proliferation of endothelial cells tending to cover the partially denuded vessel were observed. In summary, in scanning electron microscope, preserved endothelial cells of advanced atherosclerotic plaque displayed pronounced pathology; whether any of these changes represent the ultrastructural correlate of endothelial dysfunction remains to be estabilished.


    9/11

    Tytuł oryginału: Farmakologia śródbłonka.
    Autorzy: Chłopicki Stefan, Gryglewski Ryszard P.
    Źródło: Kardiol. Pol. 2002: 57 supl. 4 s.IV-5 - IV-15, il., bibliogr. 69 poz.
    Sygnatura GBL: 313,397

    Hasła klasyfikacyjne GBL:
  • kardiologia

    Typ dokumentu:
  • praca związana ze zjazdem

    Wskaźnik treści:
  • ludzie


    10/11

    Tytuł oryginału: Tlenek azotu we wstrząsie septycznym - winowajca czy obrońca?
    Autorzy: Chłopicki Stefan
    Źródło: Kardiol. Pol. 2002: 57 supl. 4 s.IV-99 - IV-107, il., bibliogr. 54 poz.
    Sygnatura GBL: 313,397

    Typ dokumentu:
  • praca związana ze zjazdem

    Wskaźnik treści:
  • ludzie


    11/11

    Tytuł oryginału: Wybiórcze inhibitory COX-2 - nowa klasa niesteroidowych leków przeciwzapalnych.
    Tytuł angielski: COX-2 inhibitors - a new class of anti-inflammatory drugs.
    Autorzy: Chłopicki Stefan
    Źródło: Probl. Ter. Monitor. 2002: 13 supl. 1: VII Zjazd Towarzystwa Terapii Monitorowanej s.3-11, il., tab., bibliogr. 41 poz., sum. - 7 Zjazd Towarzystwa Terapii Monitorowanej pt. Farmakoterapia skuteczna i bezpieczna Spała 13-15.09. 2001
    Sygnatura GBL: 312,913

    Hasła klasyfikacyjne GBL:
  • farmacja

    Typ dokumentu:
  • praca związana ze zjazdem

    Wskaźnik treści:
  • ludzie

    Streszczenie polskie: Od wielu lat w farmakoterapii objawów zapalenia stosuje się niesteroidowe leki przeciwzapalne )NLPZ), których mechanizm działania polega na zahamowaniu aktywności cyklooksygenazy. Stosowanie tych leków obok skutków przeciwzapalnych wywołuje jednak również wiele działań niepożądanych. 10 lat temu odkryto, że istnieją dwie izoformy cyklooksygenazy. Działania uboczne NLPZ przypisano zahamowaniu pierwszej z nich (COX-1), a terapeutyczne zahamowaniu drugiej (COX-2). W artykule podjęto próbę podsumowania jaką rolę w ustroju odgrywają COX-1 i COX-2 oraz jakie rysują się kliniczne zastosowania dla wybiórczych inhibitorów COX-2.

    Streszczenie angielskie: mon steroidal anti-inflammatory drugs (NSAIDs) have been used to treated symptoms of inflammation for decades. The mechanism of action of NSAID involves inhibition of cyclooxygenase. Aparat from their anti-inflammatory action NSAIDs induce various adverse effects. When second isoform of cyclooxygenase was discovered (COX-2), it was proposed that adverse effects of NSAIDs may result from the inhibition of COx-1, while therapeutic action of NSAIDs may come from the inhibition of COX-2. The present review assesses the physiological and pathophysiological roles of COX-1 and COX-2 as well as the potential use of selective COX-2 inhibitors.

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