Wynik wyszukiwania w bazie Polska Bibliografia Lekarska GBL
Zapytanie:
TUTKA
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4
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1/4
Tytuł oryginału:
Nitric oxide and convulsions in 4-aminopyridine-treated mice.
Autorzy:
Tutka
Piotr,
Młynarczyk
Małgorzata,
Żółkowska
Dorota,
Kleinrok
Zdzisław,
Wielosz
Marian,
Czuczwar
Stanisław J.
Źródło:
Eur. J. Pharmacol. 2002: 437 (1/2) s.47-53, il., tab., bibliogr. s. 52-53
Sygnatura GBL:
312,088
Hasła klasyfikacyjne GBL:
farmacja
neurologia
Typ dokumentu:
praca doświadczalna
praca opublikowana za granicą
tytuł obcojęzyczny
Wskaźnik treści:
zwierzęta
myszy
Streszczenie angielskie:
We studied whether N**G-nitro-L-arginine (NNA), an inhibitor of nitric oxide (NO) synthase as well as L-arginine and molsidomine, two agents elevating NO, influenced convulsions caused by 4-aminopyridine, a K+ channel blocker in mice. NNA, in a dose known to decrease level of NO (40 mg kg -**1), enhanced the susceptibility to intraperitoneal (i.p.) and intracerebroventricular (i,c,v,) 4-aminopyride. L-arginine (500 mg kg -**1) and molsidomine (20 mg kg -**1) alone did not influence 4-aminopyridine-induced seizure activity. Surprisingly, the proconvulsant effect of NNA upon clonic and tonic seizures was potentiated by molsidomine (20 mg kg -**1). No influence of L-arginine on the proconvulsant effect of NNA was found. Taking into account the proconvulsant effect of NNA, an involvement of NO-mediated events in the mechanism of convulsive activity of 4-aminopyridine might by postulated, However, the ineffectiveness of L-arginine and molsidomine to suppress the convulsive activity of 4-aminopyridine as well as a paradoxical potentiation of the proconvulsant effect of NNA by molsidomine seem to exclude the impact of NO pathway on 4-aminopyridine-induced convulsions in mice. Our data suggest that the proconvulsant effect of NNA in this seizure model is caused by other, not related to NO, mechanisms.
2/4
Tytuł oryginału:
Molsidomine potentiates the protective activity of GYKI 52466, a non-NMDA antagonist, MK-801, a non-competitive NMDA antagonist, and riluzole against electroconvulsions in mice.
Autorzy:
Tutka
Piotr,
Olszewski
Krzysztof,
Woźniak
Małgorzata,
Kleinrok
Zdzisław,
Czuczwar
Stanisław J.,
Wielosz
Marian
Źródło:
Eur. Neuropsychopharmacol. 2002: 12 (4) s.321-326, tab., bibliogr. [35] poz.
Sygnatura GBL:
313,361
Hasła klasyfikacyjne GBL:
farmacja
neurologia
Typ dokumentu:
praca doświadczalna
praca opublikowana za granicą
tytuł obcojęzyczny
Wskaźnik treści:
zwierzęta
myszy
Streszczenie angielskie:
The influence of molsidomine, a donor of nitric oxide (NO), L-arginine, a substrate for NO synthesis, and NG-nitro-L-arginine (NNA), an inhibitor of NO synthase, on the protective activity of CGP 40116, GYKI 52466, MK-801, and riluzole against electroconvulsions was studied in mice. Molsidomine (100 mg kg-1; i.p.) potentiated the protective activity of GYKI 52466, MK-801, and riluzole but did not influence the protection offered by CGP 40116. In contrast to molsidomine, L-arginine (500 mg kg-1, i.p.) did not impair the protective activity of any anticonvulsant. In a dose of 40 mg kg-1, NNA administered i.p. did not afect the protection offered by any excitatory amino acid antagonists and riluzole. Combinations of molsidomine with either GYKI 52466 or MK-801 as well as riluzole did not cause a memory deficit in the passive avoidance task. However, the combined treatment of molsidomine with these anticonvulsant resulted in a motor impairment quantified by the chimney test. The lack of effect of L-arginine and NNA on the protective activity of excitatory amino acid antagonist suggests that molsidomine-evoked alterations in the protection provided by some excitatory amino acid antagonists against electroconvulsions are independent of the NO pathway.
3/4
Tytuł oryginału:
Rola tlenku azotu w doświadczalnych modelach drgawek i działaniu leków przeciwpadaczkowych u myszy : rozprawa habilitacyjna
Autorzy:
Tutka
Piotr; Akademia Medyczna Katedra Farmakologii, Zakład Farmakologii i Toksykologii w Lublinie
Źródło:
- Lublin, AM 2002, 138 s. : il., tab., bibliogr. s. 107-138, sum., 24 cm.
Sygnatura GBL:
735,548
Hasła klasyfikacyjne GBL:
farmacja
neurologia
Typ dokumentu:
praca doświadczalna
rozprawa habilitacyjna
Wskaźnik treści:
zwierzęta
myszy
4/4
Tytuł oryginału:
Exposure to environmental tobacco smoke and children health.
Autorzy:
Tutka
Piotr,
Wielosz
Marian,
Zatoński
Witold
Źródło:
Int. J. Occup. Med. Environ. Health 2002: 15 (4) s.325-335, bibliogr. 100 poz.
Sygnatura GBL:
306,313
Hasła klasyfikacyjne GBL:
otorynolaryngologia
pediatria
toksykologia
pulmonologia
Typ dokumentu:
tytuł obcojęzyczny
Wskaźnik treści:
ludzie
niemowlęta
dzieci 2-5 r.ż.
dzieci 6-12 r.ż.
dzieci 13-18 r.ż.
Streszczenie angielskie:
This paper reviews the investigations of the effects of pre- and/or postnatal exposure to environmental tobacco smoke (ETS) on children health reported in the literature. The evidence from epidemiolgical studies demonstrate that children's exposure to ETS is a risk factor for a variety of diseases, including respiratory disorders and middle ear disease. However, the current research base on the ETS-associated risks is still inadequate to fully support strategies, programs and policy development in this are. For example, it is not definitively determined what methods should be used for assessing ETS exposure and predicting potential healht risks of exposed children. Based ont the available data, we tired to find out which methods seem to be most desirable for quanitfying ETS exposure in children. It is our opinion that among all biomarkers, teh measurements of blood, saliva or urinary cotinine and hair nicotine are, as for today, the most specific and sensitive methods for an objective assessment of ETS exposure in children. A combination of the measurement of body fluids cotinine and hair nicotine with the questionnaire and interview-derived information seems to be the optimal method for assessing ets exposure in children.
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