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Your search keyword '"Nawrath, H."' showing total 280 results
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280 results on '"Nawrath, H."'

1. Abstracts

Author

Wammach, R., Fisch, M., Nawrath, H., Weihe, E., Hohenfellner, R., Tackett, Leslie D., Papadakis, Konstantionos, e. DePaepe, Monique, Wojcik, Louis J., Luks, Francois I., Caldamone, Anthony A., Rosch, W. H., Neuhuber, W. L., Schrott, K. M., Dik, P., de Jong, T. P. V. M., Sava, Perovic, Miroslav, Djordjevic, Hanna, Moneer K., Stock, Jeffrey A., Bellinger, Mark F., More land, Morey S., Schnook, Francis X., Duckett, John W., Jr., Lanchoney, Thomas, Canning, Douglas A., Salvador, Lima, V. C., Araujo, Luiz Alberto P., Montoro, Marisa, Fabio, O., Hensle, Terry W., Goluboff, Erik T., Fisch, Haryy, Strup, Stephen, Fabrizio, Michael, Filmer, R. Bruce, Noseworthy, John, Gearhart, John P., Perren, Fabienne, Frey, Peter, Gugenheim, J. J., Gonzales, E. T., Jr., Roth, D. R., Montagnino, B. A., Jani, Mihir M., Sponseller, Paul D., Jeffs, Robert D., Wakim, Alain, Miladi, Lotfi, Barbet, Jean-Patrick, Helardot, Pierre-George, Dubousset, Jean, Marsh, David W., Perlman, Elizabeth J., Mathews, Ranjiv, Jeffs, Robert, Husmann, Douglas A., Vandersteen, David R., McLorie, Gordon A., Churchill, Bernard M., Gearhart, John P., editor, and Mathews, Ranjiv, editor

Published
1999
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6. Wirkungsspektrum der Calciumantagonisten

Author

Nawrath, H., Buchborn, E., editor, Breithardt, G., editor, Brisse, Betty, editor, Jähnchen, E., editor, Kasper, W., editor, Knieriem, H.-J., editor, von Leitner, E.-R., editor, Lüderitz, B., editor, Matthiesen, P., II, editor, Mecking, D., editor, Meinertz, T., II, editor, Naumann d’Alnoncourt, C., editor, Nawrath, H., editor, Neuss, H., editor, Ostermeyer, J., editor, Schlepper, M., editor, Seipel, L., editor, Steinbeck, G., editor, Theisen, K., editor, Thormann, J., editor, Trenk, D., editor, and Tritthart, H. A., editor

Published
1983
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7. Wirkungsspektrum der Herzglykoside

Author

Nawrath, H., Buchborn, E., editor, Breithardt, G., editor, Brisse, Betty, editor, Jähnchen, E., editor, Kasper, W., editor, Knieriem, H.-J., editor, von Leitner, E.-R., editor, Lüderitz, B., editor, Matthiesen, P., II, editor, Mecking, D., editor, Meinertz, T., II, editor, Naumann d’Alnoncourt, C., editor, Nawrath, H., editor, Neuss, H., editor, Ostermeyer, J., editor, Schlepper, M., editor, Seipel, L., editor, Steinbeck, G., editor, Theisen, K., editor, Thormann, J., editor, Trenk, D., editor, and Tritthart, H. A., editor

Published
1983
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15. Voltage-Dependent Effects of Barnidipine in Rat Vascular Smooth Muscle

Author

Nawrath H, Korstanje C, and Jörg W. Wegener

Subjects
Male, medicine.medical_specialty, Patch-Clamp Techniques, Vascular smooth muscle, Barnidipine, Nifedipine, chemistry.chemical_element, Pharmacology, Calcium, Muscle, Smooth, Vascular, Rats, Sprague-Dawley, Internal medicine, medicine, Animals, Myocyte, Cells, Cultured, Chemistry, Dihydropyridine, Depolarization, Calcium Channel Blockers, Rats, Endocrinology, Mechanism of action, cardiovascular system, Female, medicine.symptom, Cardiology and Cardiovascular Medicine, medicine.drug
Abstract

The effects of the dihydropyridine nifedipine and its more lipophilic congener, barnidipine, were investigated in smooth muscle preparations from the rat in resting and depolarizing conditions. Both drugs relaxed precontracted aortic rings more potently in depolarizing conditions, barnidipine being more potent than nifedipine. Currents through Ca 2+ channels in rat vascular smooth muscle cells (A7r5) and in isolated rat cardiomyocytes were reduced more potently by both drugs at a holding potential of-40 mV than at -80 mV. However, barnidipine and nifedipine were more effective in reducing the current in A7r5 cells than in cardiomyocytes. The IC 50 obtained in aortic rings and in A7r5 cells were similar for barnidipine but an order of magnitude different for nifedipine. The results show that, in depolarizing conditions, barnidipine was more effective than nifedipine. It is suggested that the higher potency of barnidipine acting in vascular smooth muscle is related to both a higher affinity to the inactivated state of vascular Ca 2+ channels and to a more lipophilic property as compared with nifedipine.

Published
2003

48. Effects of nitric oxide donors on cardiac contractility in wild-type and myoglobin-deficient mice.

Author

Schrader, J., Nawrath, H., Wegener, J. W., and Gödecke, A.

Subjects
*NITRIC oxide, *CARDIAC contraction, *MYOGLOBIN, *MYOCARDIUM, *GUANYLATE cyclase
Abstract

1 The effects of the nitric oxide (NO) donors S-nitroso-N-acetylpenicillamine (SNAP). sodium(Z)-1-(N,N-diethylamino)diazen-l-ium-1,2-diolate (DEA-NONOate), and (Z)-l-[N-(2-Aminoethyl)-N-(2-ammonioethyl)amino]diazen-l-ium-1,2-diolale (DETA-NONOate) on force of contraction (F[subc]) were studied in atrial and ventricular muscle strips obtained from wild-type (WT) and myoglobin-deficient (myo[sup-/-] mice. 2 SNAP slightly reduced F[subc] in preparations from WT mice at concentrations above 100 μM: this effect was more pronounced in myo[sup-/-] mice. 3 DEA-NONOate reduced F[sub c] in preparations from myo[sup-/-] mice to a larger extent than those from WT mice. 4 DETA-NONOate reduced F[subc] in preparations from myo[sup-/-] but not from WT mice. 5 Pre-incubation with an inhibitor of the soluble guanylyl cyclase (IH-[l,2,4]oxadiazolo[4.3-a]quinoxalin-l-one; 100μM) prevented the effects of SNAP, DEA-NONOate and DETA-NONOate on F[subc] in myo[sup-/-] mice. 6 It is suggested that,in physiological conditions. myoglobin acts as intracellular scavenger preventing NO from reaching its intracellular receptors in cardiomyocytes, whereas, in myoglobin-deficient conditions. NO is able to reduce contractility via activation of the soluble guanylyl cyclase/ cyclic GMP pathway. [ABSTRACT FROM AUTHOR]

Published
2002

50. The antigen self-presentation function of the cytotoxic T-cell clone 10BK.1 depends on reciprocal peptide presentation.

Author

Staege, M.S., Dick, T., Ertl, R., Jahnel, U., Nawrath, H., Rammensee, H.-G., and Reske-Kunz, A.B.

Subjects
T cells, ANTIGENS, CELL-mediated cytotoxicity, CD antigens, IMMUNOLOGY, CELL adhesion molecules
Abstract

Cells of the cytotoxic T-cell clone 10BK. 1 proliferate in response to ovalbumin (OVA) not only in the presence, but also in the absence, of antigen-presenting cells. This response is the consequence of reciprocal antigen presentation by two 10BK. I cells. At the single-cell level, we found antigeninduced changes in the cytosolic Ca2+ concentration ([Ca2+]1) only in 10BK.1 cells that had contact with another 10BK. 1 cell. This finding suggests that a single cell is unable to present the antigen to itself, and that two 10BK. 1 cells are necessary and adequate to present the antigen to each other. Our data indicate that 10BK.1 cells are not capable of processing the OVA molecule. The naturally processed peptide OVA257-264 is a very potent antigen for these cells. A corresponding peptide seems to be present not only in preparations of native OVA, but also in preparations of the commonly used peptide OVA258-276. This 19mer peptide does not bind with high affinity to the relevant Ks class I molecule. [ABSTRACT FROM AUTHOR]

Published
1994

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