992 resultados para 8-17 DNAzyme
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William F. Kopp, chairman.
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Dennis Chavez, chairman of subcommittee.
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Includes index.
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Trägerband: Inc. qu. 862; 'Polem. 295' oder 'Ref. Luther 796'; Vorbesitzer: Dominikanerkloster Frankfurt am Main
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Trägerbände: Ms. Barth. 52; Ms. Barth. 66; Vorbesitzer: St. Peter Urach; Bartholomaeusstift Frankfurt am Main
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O ato de ungir, do qual se origina o termo messias, era um costume dos povos do Antigo Oriente Médio e foi assimilado por Israel. O Antigo Testamento, porém, reinterpretou esta unção. Ele atribuiu ao rei, num primeiro momento, o título de ungido, maxiah;. Nesta perspectiva, o rei Davi foi aquele que deu origem à mentalidade messiânica em Israel. E a respeito da teologia messiânica, o profeta Isaías tornou-se um dos seus expoentes. Ele se dirige à classe alta de Jerusalém e propõe um Ungido de Javé em substituição ao rei da casa de Davi. Isto porque, o messianismo também se tornou um movimento de resistência frente a não observância da justiça e do direito, que culmina com a ausência da paz. Nesse sentido, Isaías apresenta também uma nova percepção do messianismo, a saber, uma ruptura com a casa de Davi (7,17). Este messias não estava sob os critérios humanos de um bom rei, forte e guerreiro, mas sob a direção do Espírito de Javé. Por isso, ele poderá ser um messias criança (7,14; 9,5). Esta dissertação tem, portanto, a finalidade de percorrer o caminho do surgimento do ungido, ou do ato de se ungir, até a concepção isaiânica de messias. Esse desenvolvimento mostrará, ao final do trabalho, a tipologia messiânica apresentada pelo profeta Isaías, a partir das perícopes de 7,10-17 e 8,23-9,6.(AU)
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O objeto de pesquisa desta dissertação são as perícopes de Isaías 7,10-17;8,23-9,6 e 11,1-9. Nelas encontra-se o cerne do pensamento messiânico de Isaías. É importante salientar que o messianismo isaiano parte da concepção de um messias que vem para governar a partir do direito e da justiça, e, assim, estabelecer a paz. O messianismo apresentado por este profeta não parte das esferas de poder da corte, mas dos pequenos e frágeis da sociedade, dotados do espírito de Javé. Há que se destacar que a profecia de Isaías é um divisor de águas no que concerne à teologia messiânica no Reino do Sul, especialmente nos profetas depois dele. Em Isaías, encontra-se a ruptura com as classes dominantes e com um messianismo bélico. A proposta deste profeta aponta para um messias frágil, mas que é movido pelo sopro, pelo movimento de Javé em suas ações. E assim, Isaías abre as portas para compreensão de um messias pobre, como retrata Zacarias, um messias servo, apresentado pelo Dêutero-Isaías, ou quem sabe um messias pastor, como proposto por Miquéias e Ezequiel e bem recebido pelas tradições do primeiro século (Jo 10,10). O messias em Isaías tem nomes e adjetivos : Imanuel, menino, raiz de Jessé, mas não tem rosto, não tem localização geográfica, não se enquadra em nenhum tipo messiânico desde o davidismo de Jerusalém. Este messias pode ser encontrado em qualquer época com qualquer rosto, por isso a importante releitura messiânica apresentada em textos do cristianismo nascente. Muitos deles inspirados na profecia isaiana do 8º. século a.C.
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The effects of a 15-mer antisense c-myc phosphorothioate modified oligodeoxynucleotide (OdN) upon the volume-sensitive Cl- current in ROS 17/2.8 cells were investigated using the whole-cell configuration of the patch clamp technique. At 5 microM, the OdN reversibly inhibited the current in a voltage- and time-dependent fashion. This was evident from the reduction in the peak current as assessed at the termination of each voltage pulse and an acceleration of the time-dependent inactivation present at strongly depolarised potentials. The kinetic modifications induced by the OdN suggest it may act by blocking the pore of open channels when the cell membrane potential is depolarised.
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1. The effects of arachidonic acid upon the volume-sensitive Cl- current present in cultured osteoblastic cells (ROS 17/2.8) was studied using the whole-cell patch-clamp technique. 2. Arachidonate produced two distinct phases of inhibition, a rapid phase occurring within 10-15 s of application preceding a slower phase that occurred 2 min after onset of arachidonate superfusion. Accompanying the slower inhibitory phase was an acceleration of the time-dependent inactivation exhibited by the current at strongly depolarized potentials (> + 50 mV). The half-maximal inhibitory concentrations (IC50) were 177 +/- 31 and 10 +/- 4 microM for the two phases respectively. 3. Arachidonate was still effective in the presence of inhibitors of cyclo-oxygenase (indomethacin, 10 microM), lipoxygenase (nordihydroguaretic acid, 10-100 microM) and cytochrome P450 (SKF525A, 100 microM; ethoxyresorufin, 10 microM; metyrapone, 500 microM; piperonyl butoxide, 500 microM; cimetidine, 1 mM). The effects of arachidonate could not be produced by another cis unsaturated fatty acid, oleic acid. 4. Measurements of cell volume showed that arachidonate effectively inhibited the regulatory volume decrease elicited by ROS 17/2.8 cells in response to a reduction in extracellular osmolarity. 5. It is concluded that the volume-sensitive Cl- conductance in ROS 17/2.8 cells is directly modulated by arachidonate and may represent a physiological mechanism by which volume regulation can be controlled in these cells.
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1. During osmotic swelling, cultured osteoblastic cells (ROS 17/2.8) exhibited activation of large amplitude Cl- currents in the whole-cell configuration of the patch-clamp technique. Effects of hypotonic shock on cell volume and membrane conductance were rapidly reversed on return to isotonic conditions. 2. Voltage command pulses in the range -80 to +50 mV produce instantaneous activation of Cl- currents. At potentials more positive than +50 mV the current exhibited time-dependent inactivation. The instantaneous current-voltage relationship was outwardly rectifying. 3. The anion permeability sequence of the induced current was SCN- (2.2) > I- (1.9) > Br- (1.5) > Cl- (1.0) > F- (0.8) > gluconate- (0.2). This corresponds to Eisenman's sequence I. 4. The volume-sensitive Cl- current was effectively inhibited by the Cl- channel blockers 4,4'-diisothiocyanatostilbene-2,2-disulphonic acid (DIDS) and 5-nitro-2-(3-phenylpropylamino) benzoic acid (NPPB). Outward currents were more effectively suppressed by DIDS than inward currents. The concentrations for 50% inhibition (IC50) of outward and inward currents were 81 and 298 μM, respectively. NPPB was equally effective at inhibiting outward and inward currents (IC50 of 64 μM). The current was relatively insensitive to diphenylamine-2-carboxylate (DPC), 500 μM producing only 22.5 ± 4.0% inhibition. 5. Inhibitors of protein kinase A (H-89, 1 μM) and tyrosine kinase (tyrphostin A25, 200 μM) were without effect upon activation of Cl- currents in response to hypotonic shock. Under isotonic conditions, elevation of intracellular Ca2+ by ionomycin (1 μM) or activation of protein kinase C by 12-O-tetradecanoylphorbol 13-acetate (TPA, 0.1 μM) failed to evoke increases in basal Cl- conductance levels. 6. It is concluded that an outwardly rectifying Cl- conductance is activated upon osmotic swelling and may be involved in cell volume regulation of ROS 17/2.8 cells.
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Epidemiological studies previously identified cis-5,8,11,14,17-eicosapentaenoic acid (EPA) as the biologically active component of fish oil of benefit to the cardiovascular system. Although clinical investigations demonstrated its usefulness in surgical procedures, its mechanism of action still remained unclear. It was shown in this thesis, that EPA partially blocked the contraction of aortic smooth muscle cells to the vasoactive agents KCl and noradrenaline. The latter effect was likely caused by reducing calcium influx through receptor-operated channels, supporting a recent suggestion by Asano et al (1997). Consistently, EPA decreased noradrenaline-induced contractures in aortic tissue, in support of previous reports (Engler, 1992b). The observed effect of EPA on cell contractions to KCl was not simple due to blocking calcium influx through L-type channels, consistent with a previous suggestion by Hallaq et al (1992). Moreover, EPA caused a transient increase in [Ca2+]i in the absence of extracellular calcium. To resolve this it was shown that EPA increased inositol phosphate formation which, it is suggested, caused the release of calcium from an inositol phosphate-dependent internal binding site, possibly that of an intracellular membrane or superficial sarcoplasmic reticulum, producing the transient increase in [Ca2+]i. As it was shown that the cellular contractile filaments were not desensitised to calcium by EPA, it is suggested that the transient increase in [Ca2+]i subsequently blocks further cell contraction to KCl by activating membrane-associated potassium channels. Activation of potassium channels induces the cellular efflux of potassium ions, thereby hyperpolarising the plasma membrane and moving the membrane potential farther from the activation range for calcium channels. This would prevent calcium influx in the longer term and could explain the initial observed effect of EPA to block cell contraction to KCl.
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Trägerband: Ms. Ff. H. Ludolf II 1; Vorbesitzer: Hiob Ludolf
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Trägerband: Inc. qu. 869; Vorbesitzer: Magister Craffto; Dominikanerkloster Frankfurt am Main
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