Wynik wyszukiwania w bazie Polska Bibliografia Lekarska GBL

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1/5

Tytuł oryginału: Repeated imipramine and electroconvulsive shock increase ŕ1A-adrenoceptor mRNA level in rat prefrontal cortex.
Autorzy: Nalepa Irena, Kreiner Grzegorz, Kowalska Marta, Sanak Marek, Zelek-Molik Agnieszka, Vetulani Jerzy
Źródło: Eur. J. Pharmacol. 2002: 444 (3) s.151-159, il., tab., bibliogr. s. 158-159
Sygnatura GBL: 312,088

Hasła klasyfikacyjne GBL:
  • farmacja

    Typ dokumentu:
  • tytuł obcojęzyczny
  • praca doświadczalna
  • praca opublikowana za granicą

    Wskaźnik treści:
  • zwierzęta
  • szczury

    Streszczenie angielskie: ŕ1-Adrenoceptors have been implicated in the mechanism of action of antidepressants, but their action on specific receptor subtypes was rarely reported. We compared now the action of two prototypic antidepressant treatments: repeated imipramine and electroconvulsive shock, on the expression of the ŕ1A - and ŕ1B -adrenoceptor mRNAs and on the receptor density in rats. The mRNA expression was assessed by Northern blot in the prefrontal cortex and the hippocampus, the receptor density was measured by [3H] prazosin binding in the total cerbral cortex and hippocampus. In the cortex, both treatments elevated the ŕ1A -adrenoceptor mRNA and the expression of receptor protein. The expression of ŕ1B -adrenoceptor mRNA remained unaffected. In contrast, in the hippocampus, the antidepressant treatments augmented the density of ŕ1A -adrenoceptor protein without changing the level of its mRNA expression there. The results suggest that the ŕ1A -adrenoceptor subtype is specifically involved in the mechanism of action of classical antidepressant treatments.


    2/5

    Tytuł oryginału: Kaspazy i apoptoza: umrzyj i pozwól żyć.
    Tytuł angielski: Caspases and apoptosis: die and let live.
    Autorzy: Nalepa Grzegorz, Żukowska-Szczechowska Ewa
    Źródło: Wiad. Lek. 2002: 55 (1/2) s.100-106, bibliogr. 17 poz., sum.
    Sygnatura GBL: 301,774

    Wskaźnik treści:
  • ludzie

    Streszczenie polskie: Apoptoza (genetycznie zaprogramowana śmierć komorki) odgrywa ważną rolę w fizjologicznych procesach życiowych ludzkiego organizmu oraz w patogenezie wielu chorób, m.in. nowotworów złośliwych. Niezależnie od czynnika wywołującego samobójstwo komórki, w apoptozie zawsze uczestniczą enzymy proteolityczne, zwane kaspazami, które mogą zostać uaktywnione poprzez kilka różnych szlaków molekularnych. Bodźcem do uruchomienia kaskady kaspaz może być pobudzenie błonowych receptorow Fas lub TNF, uwolnienie cytochromu c z mitochondrium lub zetknięcie się komórki z granzymami wydzielanymi przez cytotoksyczne limfocyty T. Aktywne kaspazy przeprowadzają proteolizę wielu różnych białek uczestniczących w regulacji cyklu komórkowego (np. RB, MDM2), wykrywaniu uszkodzeń i naprawie DNA (np. DNA-PK, P53, PARP) oraz w utrzymywaniu prawidłowej struktury komórki (np. aktyna i laminy). Te zmiany zestawu białek znajdujących się w komórce stanowią bezpośrednie podłoże apoptozy. Lepsze zbadanie machanizmów regulujących aktywność kaspaz i sposobów działania tych enzymów pozwoli na dokładniejsze poznanie patogenezy nowotworów i innych schorzeń, a może nawet na opracowanie nowych, skuteczniejszych metod leczenia konwencjonalnego lub terapii genowej.

    Streszczenie angielskie: Apoptosis (genetically programmed cell death) plays a key role in human physiology and pathogenesis of various diseases, including cancer. A suicide of cell can be initiated by many different factors, but activation of caspases, which are a special class of proteolytic enzymes, is always involved in this process. Activation of caspases may be achieved by several molecular pathways; the best known stimuli triggering caspase cascade are stimulation of Fas or TNF receptors, release of cytochrome c from the cellular mitochondria and exposure to granzymes, which are secreted by cytotoxic T cells. Activated caspases digest many cellular proteins responsible for cell cycle regulation (e.g. RB. MDM2), DNA damage recognition and repair (e.g. DNA-PK, P53, PARP), and regulation of the cellular structure (e.g. actin and lamins). All these functional and structural protein modifications lead directly to apoptosis. Further research on the mechanisms controlling caspase activity and the modes of action will provided better insight into pathogenesis of cancer and other disorders. It may be even the first step to design new and more efficient methods of conventional tumor treatment or gene therapy.


    3/5

    Tytuł oryginału: Modulation by cationic amphiphilic drugs of serine base-exchange, phospholipase D and intracellular calcium homeostasis in glioma C6 cells.
    Autorzy: Bobeszko Marta, Czajkowski Rafał, Wójcik Magdalena, Sabała Paweł, Lei Lingsheng, Nalepa Irena, Barańska Jolanta
    Źródło: Pol. J. Pharmacol. 2002: 54 (5) s.483-493, il., bibliogr. 37 poz.
    Sygnatura GBL: 313,156

    Hasła klasyfikacyjne GBL:
  • farmacja

    Typ dokumentu:
  • praca doświadczalna
  • tytuł obcojęzyczny

    Wskaźnik treści:
  • in vitro

    Streszczenie angielskie: We aimed to assess the effect of three drugs belonging to amphiphilic cations, imipramine, amitriptyline and propranolol, on lipid synthesis and intracellular calcium homeostasis in glioma C6 cells. Antidepressants, imipramine and amitriptyline, had a stimulatory effect on [14C]serine incorporation into phosphatidylserine. Similar effect was induced by propranolol, antidysrhythmic drug and an antagonist of á-adrenergic receptor, but not by isoproterenol, a selective agonist of this receptor. Stimulation of serine base-exchange activity by amphiphilic cations occured at concentration as low as 5 - 25 ćM that may be reached during clinical treatment. At much higher concentration (250 ćM), those drugs also stimulated phospholipase D-mediated synthesis of [14C]phosphatidylethanol and blocked phorbol ester-induced, protein kinase C-dependent phospholipase D activity. The latter effect already occurred at low (25 ćM) concentration of drugs. We have also shown that treatment of the cells with amphiphilic cations (1 mM) produced only a weak incrase in the intracellular Ca2+ concentration and did not affect Ca2+ release from the intracellular stores evoked by nucleotide receptor agonists, ATP and ADP. In contrast, this treatment strongly diminished an unspecific leak of Ca2+ from the endoplasmic reticulum caused by thapsigarin and ionomycin. Mianserin, which is not cationic amphiphilic drug, did not affect phosphatidylserine synthesis and phospholipase D activity and produced heterogenous and chaotic Ca2+ responses. Our results suggest that imipramine, amitriptyline and propranolol may modulate lipid synthesis and intracellular calcium signaling independently of theis action on membrane receptors, most probably by modification of the physicochemical properties of cell membranes.


    4/5

    Tytuł oryginału: Using reverse transcription and a competitive polymerase chain reaction for quantification of ŕ1B-adrenoceptor mRNA.
    Autorzy: Kreiner Grzegorz, Sanak Marek, Zelek-Molik Agnieszka, Nalepa Irena
    Źródło: Pol. J. Pharmacol. 2002: 54 (4) s.401-405, il., bibliogr. 10 poz.
    Sygnatura GBL: 313,156

    Hasła klasyfikacyjne GBL:
  • neurologia

    Typ dokumentu:
  • praca doświadczalna
  • komunikat
  • tytuł obcojęzyczny

    Wskaźnik treści:
  • zwierzęta
  • szczury
  • płeć męska

    Streszczenie angielskie: Molecular cloning studies have revealed the existence of three subtypes of ŕ1-adrenergic receptor (ŕ1-AR), namely ŕ1A, ŕ1B and ŕ1D. They are encoded by separate genes and have distinct pharmacological profiles. In rats' brain, the expression of mRNA for subtypes of an ŕ1-AR is partially structure-dependent. Our previous studies employing Northerm blot analysis of mRNA have shown that in the hippocapmus, where ŕ1A predominates, the ŕ1B receptor (ŕ1B-AR) was almost undetectable. The goal of the present study was to estabilish the method of reverse transcription and competitive polymerase chain reaction (RT-cPCR) to quantify a steady state level of ŕ1B-AR mRNA in the hippocampus, prefrontal cortex and thalamus, and to compare the ŕ1B-AR' pattern of expression with that revealed by Northern blot analysis. Our results have shown that ŕ1B-AR is similarly represented in the thalamus and prefrontal cortex. In the hippocampus, ten times lower expression of ŕ1B mRNA has been demonstrated with RT-cPCR, which was below a detection limit of Northern blot hybridization technique.


    5/5

    Tytuł oryginału: Effect of combined treatment with paroxetine and transcranial magnetic stimulation (TMS) on the mitogen-induced proliferative response of rat lymphocytes.
    Autorzy: Roman Adam, Vetulani Jerzy, Nalepa Irena
    Źródło: Pol. J. Pharmacol. 2002: 54 (6) s.633-639, il., bibliogr. 35 poz.
    Sygnatura GBL: 313,156

    Hasła klasyfikacyjne GBL:
  • psychiatria i psychologia
  • immunologia
  • farmacja
  • neurologia

    Typ dokumentu:
  • praca doświadczalna
  • tytuł obcojęzyczny

    Wskaźnik treści:
  • zwierzęta
  • szczury
  • in vitro

    Streszczenie angielskie: Depression is associated with abnormal functions of the immune system. In this study, we investigated how two modern antidepressant therapies, chronic treatment with transcranial magnetic stimulation (TMS) and administration of an antidepressant belonging to selective serotonin reuptake inhibitors (SSRI), paroxetine, affect the proliferative response of thymocytes and splenocytes stimulated in vitro with various mitogens. Paroxetine (10 mg/kg) and TMS (B=1.2 T, f= 30 Hz, t=330 s) were applied once daily for 12 consecutive days, while, if given jointly paroxetine was injected 30 min before TMS. The mitogens used were: concanavalin A (Con A), pokeweed mitogen (PWM) or lipopolysaccharide (LPS). While either treatment applied alone had no effect on proliferative response, the joint application of paroxetine and TMS significantly depressed it. The literature data suggest that pulsed magnetic field may directly inhibit mitogen-activated lymphocyte proliferation, which is also inhibited by the presence of high level of serotonin. The present results suggest that both effects are additive, and because of that application of both treatments, whose effects alone are insufficient to prompt the reaction, possibly because adaptative changes during chronic treatment, results in a significant inhibition of lymphocyte proliferation.

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