Wynik wyszukiwania w bazie Polska Bibliografia Lekarska GBL

Zapytanie: OLSZANECKI
Liczba odnalezionych rekordów: 5



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1/5

Tytuł oryginału: Międzynarodowa Statystyczna Klasyfikacja Chorób i Problemów Zdrowotnych : rewizja dziesiąta : ICD-10 : kategorie 3-znakowe
Opracowanie edytorskie: Pająk Andrzej (red.), Brykczyńska Celina (tł.), Galicka-Latała Danuta (tł.), Kautsch Marcin (tł.), Kobayashi Maria (tł.), Kozierkiewicz Adam (tł.), Kunz Jerzy (tł.), Kwaśny-Krochin Beata (tł.), Namysłowska Irena (tł.), Nowak-Węgrzyn Anna (tł.), Olszanecki Piotr (tł.), Parnowski Tadeusz (tł.), Pawlęga Janusz (tł.), Pietruszewski Kazimierz (tł.), Piotrowski Andrzej (tł.), Pużyński Stanisław (tł.), Szelenberger Waldemar (tł.), Topór-Mądry Roman (tł.), Wciórka Jacek (tł.), Zaczek Anna (tł.).
Źródło: - Krakow, Fundacja Zdrowia Publicznego ; Uniwersyteckie Wydaw. Medyczne "Vesalius" 2002, 78 s. : il., 24 cm. - tyt. oryg. Classification of Diseases and Health Related Problems : tenth revision
Sygnatura GBL: 740,380

Wskaźnik treści:
  • ludzie

    2/5

    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.

    3/5

    Tytuł oryginału: Flavonoids and nitric oxide synthase.
    Autorzy: Olszanecki R[afał], Gębska A[nna], Kozlovski V. I., Gryglewski R. J.
    Źródło: J. Physiol. Pharmacol. 2002: 53 (4) p. 1 s.571-584, il., bibliogr. 38 poz.
    Sygnatura GBL: 302,092

    Hasła klasyfikacyjne GBL:
  • kardiologia

    Typ dokumentu:
  • praca doświadczalna

    Wskaźnik treści:
  • zwierzęta
  • myszy
  • Świnki morskie
  • in vitro

    Streszczenie angielskie: Induction of NOS-2 in macrophages and smooth muscles within vascular wall with concomittant suppression of endothelial NOS-3 activity is considered to be a hallmark of vascular inflammation that triggers atherogenesis. Accordingly, drugs designed to reverse these changes should not only support vaning function of NOS-3 but also suppress proinflammatory NO production by NOS-2. It means that using selective inhibitors of induction of NOS-2 (they spare ex definitione constitutive activity of NOS-3) is a more rational approach than using "selective" inhibitors of activity to previously induced NOS-2. First of all, those drugs are never sufficiently selective. In our work we tried to identify inhibitors of NOS-2 induction within the group of flavonoids, known stimulators of NOS-3 with putative antiatherogenic effects. Representatives of four main groups of flavonoids: flavonols (kaempferol, quercetin, rutin), flavones (apigenin, primuletin), flavanols (catechine) and flavones (hesperetin, hesperidin, naringenin) were tried on NOS-2 induction and activity in the in vitro model of LPS-treated macrophages (cell line J774.2). While none of these compounds inhibited activity of NOS-2, all with unexpectedly scattered potencies inhibited induction of NOS-2 protein in LPS-treated J774.2 cells, as evidenced by Western blotting technique. Subsequently, RT-PCR and Northern blotting methods revealed that so far the most potent compounds, kaempferol and apigenin, at micromolar concentrations did inhibit NOS-2 induction ...

    4/5

    Tytuł oryginału: Interleukin 1á induces functional prostaglandin E synthase in cultured human umbilical vein endothelial cells.
    Autorzy: Uracz W[ojciech], Uracz D[anuta], Olszanecki R[afał], Gryglewski R. J.
    Źródło: J. Physiol. Pharmacol. 2002: 53 (4 p. 1) s.643-654, il., bibliogr. 52 poz.
    Sygnatura GBL: 302,092

    Typ dokumentu:
  • praca doświadczalna
  • tytuł obcojęzyczny

    Wskaźnik treści:
  • ludzie
  • in vitro

    Streszczenie angielskie: Prostaglandin endoperoxide H2 (PGH2) is generated from arachidonic acid by either consitutive (COX)-1) or inducible (COX-2) cyclooxygenases. In arterial wall PGH2 is converted by PGI2 synthase (PGI-S) to prostacyclin (PGI2), and in plateles by thromboxane synthase (TX-S) to thromboxane (TXA2). Other prostanoids as PGD2, PGF2ŕ or PGE2 were belived to arise non-enzymatically from PGH2. Only recently , human prostaglandin E synthase (PGE-S) has been identified and cloned as a membrane bound, microsomal, glutathione-dependent inducible enzyme. Here we demonstrated that interleukin 1 á (IL-1á) is an inducer of COX-2 and PGE-S in human umbilical vein endothelial cells (HUVEC). Functional expression of PGE-S was measured at the level of specific mRNA by semi-quantitative RT-PCR, PGE-S protein was detected by Western blot in HUVEC, while PGE2 was measured by immunoassay in the supernatant. Actinomycin D, a classical transcription inhibitor, was used to prove that indeed IL-1á induced the functional PGE-S enzyme. PGE2 generation in HUVEC was inhibited by indomethacin, acetamoniphen and dexamethasone. In conclusion, we found that in cultured endothelial cells IL-1á induced as evidenced by the appearance of its transcript and its functional enzyme. The induction of endothelial PGE-S and COX-2 appeared to be and their transcripts were induced as fast as one might expect from immediate early genes. It means that IL-1á-triggered-PGE2 biosynthesis in endothelial cells is probably regulated by induction of both COX-2 and ...

    5/5

    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.

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