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5. Forward Modeling of Coronal Mass Ejection Flux Ropes in the Inner Heliosphere with 3DCORE

Author

Möstl, C., Amerstorfer, T., Palmerio, E., Isavnin, A., Farrugia, C. J., Lowder, C., Winslow, R. M., Donnerer, J. M., Kilpua, E. K. J., Boakes, P. D., Department of Physics, and Space Physics Research Group

Subjects
DYNAMICS, space weather prediction, Solar Wind/Magnetosphere Interactions, EARTH, DST, Astrophysics::Solar and Stellar Astrophysics, Magnetospheric Physics, Research Articles, forward modeling, Solar/Planetary Relationships, Solar Physics, Astrophysics, and Astronomy, INSTRUMENT, magnetic flux ropes, MAGNETIC-FIELD, CLOUDS, Magnetic Storms and Substorms, geomagnetic storms, 115 Astronomy, Space science, EVOLUTION, History of Geophysics, Interplanetary Physics, Interplanetary Magnetic Fields, solar wind, SOLAR-WIND, Physics::Space Physics, MESSENGER, Space Weather, Coronal Mass Ejections, Natural Hazards, Research Article
Abstract

Forecasting the geomagnetic effects of solar storms, known as coronal mass ejections (CMEs), is currently severely limited by our inability to predict the magnetic field configuration in the CME magnetic core and by observational effects of a single spacecraft trajectory through its 3‐D structure. CME magnetic flux ropes can lead to continuous forcing of the energy input to the Earth's magnetosphere by strong and steady southward‐pointing magnetic fields. Here we demonstrate in a proof‐of‐concept way a new approach to predict the southward field B z in a CME flux rope. It combines a novel semiempirical model of CME flux rope magnetic fields (Three‐Dimensional Coronal ROpe Ejection) with solar observations and in situ magnetic field data from along the Sun‐Earth line. These are provided here by the MESSENGER spacecraft for a CME event on 9–13 July 2013. Three‐Dimensional Coronal ROpe Ejection is the first such model that contains the interplanetary propagation and evolution of a 3‐D flux rope magnetic field, the observation by a synthetic spacecraft, and the prediction of an index of geomagnetic activity. A counterclockwise rotation of the left‐handed erupting CME flux rope in the corona of 30° and a deflection angle of 20° is evident from comparison of solar and coronal observations. The calculated Dst matches reasonably the observed Dst minimum and its time evolution, but the results are highly sensitive to the CME axis orientation. We discuss assumptions and limitations of the method prototype and its potential for real time space weather forecasting and heliospheric data interpretation., Key Points A new semiempirical model (3DCORE) for simulating the propagation of coronal mass ejection magnetic flux ropes is introduced3DCORE is able to model the observations of a coronal mass ejection on 9–13 July 2013 observed at MESSENGER and WindSolar, coronagraph, and MESSENGER observations are used as constraints, resulting in a good match of the modeled and observed Dst index

Published
2018

13. Therapeutic drug monitoring (TDM) of the HIV drugs abacavir, atazanavir, darunavir, efavirenz, emtricitabine, lamivudine, lopinavir, and nevirapine

Author

Donnerer, J.

Subjects
ddc: 610, 610 Medical sciences, Medicine
Abstract

Aim: TDM helps to maintain optimal drug concentration for viral suppression and to avoid drug toxicity in the management of HIV infection. Compounds with sufficiently long half-lifes in plasma can be monitored at any time between dosing intervals. Single drug levels from routine clinical samples were[for full text, please go to the a.m. URL], 16. Jahreskongress für Klinische Pharmakologie

Published
2014
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18. Abstracts

Author

Abdullah, Lubna H., Buchanan, K. D., Akopyan, T. N., Arzumanyan, A. M., Arutunyan, A. A., Berger, H., Oehme, P., Atkinson, M. E., Chaggar, J. S., Bailey, S. J., Featherstone, R. L., Jordan, C. C., Morton, I. K. M., Balfe, A., Skrabanek, P., Powell, D., Barja, F., Mathison, R., Huggel, H., Bittiger, H., Heid, J., Björkroth, Ulla, Rosell, Sune, Boyd, N. D., Anthony, M. P., Leeman, S. E., Briggs, I., Growcott, J. W., Jamieson, A., Tarpey, Ann V., Brodin, E., Meyerson, B. A., Brown, J. R., Hayes, A. G., Meecham, K. G., Tyers, M. B., Burcher, E., Bynke, G., Håkanson, R., Hörig, J., Cann, John R., Rahim, Iffat, Vatter, Albert, Stewart, John M., Cascieri, Margaret A., Liang, Tehming, Cheeseman, H. J., Pinnock, R. O., Henderson, G., Constantinidis, J., Bouras, C., Taban, C. H., Guntern, R., Couture, R., Cuello, A. C., Dalsgaard, C. -J., Jonsson, C. -E., Arvidsson, J., Risling, M., Hökfelt, T., Schultzberg, M., Vincent, S. R., Elfvin, L. -G., de Beaurepaire, R., Iversen, S. D., Delbro, D., Lisander, B., Fändriks, L., Andersson, S. A., Del Fiacco, M., Dessi, M. L., Levarvti, M. C., Del Rio, J., Naranjo, J. R., Domschke, S., Bloom, S. R., Adrian, T. E., Lux, G., Bryant, M. G., McGregor, G. P., Domschke, W., Donnerer, J., Barthó, L., Holzer, P., Lembeck, F., Skofitsch, G., Elliott, P. J., Bannon, M. J., Alpert, J. E., Ferri, G. -L, McGregor, G., Vezzadini, P., Labo, G., Polak, J. M., Fontaine-Perus, J. C., Chanconie, M., Foreman, J. C., Piotrowski, W., Fox, J. E. T., Daniel, E. E., Jury, J., Domoto, T., Berezin, I., Gaudino, G., Mondardini, L., Fasolo, A., Gazelius, B., Kahan, T., Panopoulos, P., Olgart, L., Gintzler, Alan R., Jaffe, Bernard M., Baron, Sheri A., GrÖnstad, K. O., Ahlman, H., Zinner, M. J., Jaffe, B. M., Yeo, C., Gu, J., Huang, W. M., lslam, K. N., Terenghi, G., Morrison, J., Güllner, H. -G., Haeusler, Guenther, Handelmann, Gail E., Selsky, Joyce H., Helme, R. D., White, D. M., Höfler, H., Heitzt, Ph. U., Auböck, L., Petsche, Ulrike, Lippe, Irmgard, Hylden, Janice L. K., Wilcox, George L., Inoue, Atsuko, Nakata, Yoshihiro, Segawa, Tomio, Jakubowska-Naziemblo, B., Potargowicz, E., Traczyk, W. Z., Cannon, D., Rohde, W., JancsÓ, G., Király, E., Karcsú, S., Szebeni, A., Bácsy, E., Jones, R. S. G., Olpe, H. -R., Wrightt, D. M., Jurna, I., Kerdelhué, B., Lenoir, V., Pasqualini, C., El Abed, A., Morel, G., Dubois, P., Hublot, P., Tartar, A., Klingmúller, D., Waltz, C., Kramer, H. J., Koop, H., Luster, W., Gropp, C., Havemenn, K., Arnold, R., Krause, James E., McKelvy, Jeffrey F., Krivoy, W., Couch, J., Strand, F., Leander, S., Folkers, K., Lee, C. M., Snyder, S. H., Lindberg, P., Dahlström, A., Lundberg, J. M., Lindefors, N., Ungerstedt, U., Liu-Chen, L. -Y., Liszczak, T., Mayberg, M. R., Moskowitz, M. A., Lundberg, Jan M., Saria, Alois, Brodin, Ernst, Martling, Claes-Roland, Hökfelt, Tomas, Lundblad, Lars, Änggård, Anders, McGeeney, K. F., O'Donnell, M. D., Blank, M. A., Manolas, K., Linger, W. G., Allen, J. M., Maggio, J. E., Sandberg, B. E. B., Bradley, C. V., Iversen, L. L., Santikarn, S., Williams, D. H., Hunter, J. C., Hanley, M. R., Magnusson, I., Thulin, L., Mandahl, Agneta, Bill, Anders, Manning, Maurice, Martensson, H., Akande, B., Stofer, P., Chappuis, G., Immer, H., Groog, P., Matthews, Margaret R., Connaughton, M., Moratalla, R., Nobin, Anders, Emson, Piers, Sundler, Frank, O'Donohue, T. L., Shults, C. W., Quirion, R., Moody, T. W., Chase, T. N., Otsuka, M., Konishi, S., Yanagisawa, M., Akagi, H., Otten, U., Rüegg, U. T., Pawlik, W., Konturek, S. J., Kania, J., Gustaw, P., Cosgrove, Patricia G., Pazoles, Christopher J., Priestley, J. V., Jensen, R. T., Pert, C. B., Regoli, D., Mizrahi, J., D'Orléans-Juste, P., Caranikas, S., Escher, E., Folkers, Karl, Rüegg, Urs T., Bishai, W. R., Saria, A., Rama Sastry, B. V., Jaiswal, Neelam, Tayeb, Osama S., Schultheiss, Hartmut, Hörig, Joachim, Scott, T. M., Shanahan, F., Befus, A. D., Fox, J., Denburg, J. A., Bienenstock, J., Sheppard, M. N., Kurian, S. S., Siegel, R. A., Weidenfeld, J., Globus, M., Melamed, E., Sjödin, L., Srivastava, G., Hall, Michael E., Suhar, A., Turk, V., Marks, N., Szkudlarek, U., Tarkkanen, A., Tervo, T., Tervo, K., Eränkö, L., Eränkö, O., Huang, W. -M., Morrison, J. F. B., Unger, W. G., Tessler, A., Himes, B. T., Murray, M., Goldberger, M. E., Torrens, Y., Beaujouan, J. C., Viger, A., Glowinski, J., Casanueva, F. F., Knuth, E., Havlicek, V., Friesen, H. G., Triepel, J., Weindl, A., Reinecke, M., Mader, J., Forssmann, W. G., Unger, Thomas, Becker, Hans, König, Manfred, Ganten, Detlev, Lang, Rudolf E., Vacca, L. L., Naftchi, N. E., Guan, X. -M., Ai, M. -K., Vijayan, E., Wang, Y. M., Mashford, M. L., Watson, Stephen P., Sandberg, Bengt E. B., Iversen, Leslie L., Weihe, E., Hartschuh, W., Kuchling, G., Winter, E. A., Keen, P., Yeo, C. J., Ylikoski, Jukka, Tervo, Timo, Tervo, Kaarina, Eränko, Liisa, and Cuello, Claudio

Published
1983
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25. Bradykinin-evoked sensitization of neuropeptide release from afferent neurons in the guinea-pig lung

Author

Schuligoi, R, Peskar, B A, Donnerer, J, and Amann, R

Subjects
Male, Calcitonin Gene-Related Peptide, Adrenergic beta-Antagonists, Guinea Pigs, Indomethacin, Neuropeptides, In Vitro Techniques, Bradykinin, Papers, Prostaglandins, Animals, Female, Neurons, Afferent, Lung, Histamine
Abstract

1. It has been shown that bradykinin (BK) causes sensitization of airway sensory neurons and an enhancement of the cough reflex in guinea-pigs. In the present study, the guinea-pig isolated perfused lung was used to investigate the possible enhancement by BK of histamine-evoked neuropeptide release from peripheral terminals of primary afferent neurons, and to determine the contribution of cyclooxygenase products of arachidonate metabolism to this effect. 2. The lung was perfused with oxygenated physiological salt solution containing peptidase inhibitors (thiorphan, bestatin and captopril, 1 microM each). BK and histamine were added to the perfusate for 10 and 5 min, respectively. 3. BK alone (0.1 microM) evoked the release of 10.35+/-2.4 fmol immunoreactive calcitonin gene-related peptide (CGRP), histamine alone (100 microM) evoked the release of 12.7+/-1.6 fmol CGRP. Stimulation with 100 microM histamine in the presence of 0.1 microM BK (added 5 min before histamine and present during histamine) evoked the release of 67.1+/-5.3 fmol CGRP. 4. Prostaglandin (PG) release was stimulated by BK (418+/-71 pmol 15-keto-13,14-dihydro-PGF2alpha and 345+/-59 pmol 6-keto-PGF1alpha), and, to a lesser extent, by histamine (36.1+/-7.4 pmol 15-keto-13,14-dihydro-PGF2alpha, and 24.6+/-3.9 pmol 6-keto-PGF1alpha). Prostaglandin release induced by histamine in the presence of BK was not significantly higher than with BK alone. 5. Indomethacin (5 microM) as well as the bradykinin B2 receptor antagonist HOE140 (icatibant, 1 microM) inhibited prostaglandin release following stimulation with histamine in combination with BK. CGRP release evoked by histamine in combination with BK was attenuated by indomethacin and HOE140 to 22.1+/-7.8 fmol and 16.4+/-3.8 fmol, respectively, significantly less than the value obtained in control experiments (67.1+/-5.3 fmol). 6. The results suggest that BK-induced stimulation of prostaglandin synthesis results in facilitation of histamine-evoked release of pro-inflammatory neuropeptides from afferent neurons, a mechanism that probably becomes relevant during inflammation, and that can be blocked by a bradykinin B2 receptor antagonist.

Published
1998

47. The NK1 Receptor Antagonist SR140333 Inhibits Capsaicin-Induced ERK Phosphorylation in Sensory Neurons.

Author

Donnerer, J. and Liebmann, I.

Subjects
*SENSORY neurons, *PHOSPHORYLATION, *CHEMICAL reactions, *PROTEIN kinases, *PHOSPHOTRANSFERASES, *NERVE growth factor
Abstract

Primary sensory neurons respond to a vigorous excitation via the capsaicin receptor/TRPV1 cation channel by a phosphorylation of the Jak/STAT pathway as measured by phospho-STAT3, and of the Ras/Raf-MAPK pathway as measured by phospho-MAPK/ERK1/2. In the present investigation a possible involvement of NK1 receptors in the capsaicin-induced activation of these signal transduction pathways was investigated by protein extraction and Western immunoblotting. Phospho-MAPK/ERK1/2 and phospho-STAT3 were determined in the dorsal root ganglia (DRG) and in the sciatic nerve of rats at 3 and 6 h following a systemic capsaicin treatment without or with the pretreatment of the selective NK1 receptor antagonist SR140333 (1 mg/kg s.c.; 3 h before capsaicin). Capsaicin evoked a threefold increase in phospho-ERK in the sciatic nerve and a two- to threefold increase in the DRG at 3 h and 6 h after the treatment. SR140333 markedly attenuated the capsaicin-induced increase in phosphorylated ERK. In the sciatic nerve the difference was significant at each individual time point (3 and 6 h, p < 0.001). In the DRG the difference was significant when the data at 3 h and 6 h were combined (p < 0.05), but not when individual time points were considered. Capsaicin evoked a four- to fivefold increase in phospho-STAT3 in the sciatic nerve and a twofold increase in the DRG at 3 and 6 h after the treatment. SR140333 less markedly attenuated the capsaicin-induced increase in phosphorylated STAT3: whereas in the sciatic nerve the difference was significant when the data at 3 h and 6 h were combined (p < 0.05), no such treatment effect of SR140333 was observed in the DRG. The expression of TRPV1 mRNA, a specific marker of capsaicin-sensitive small sensory neurons, was investigated by RT-PCR 4 days after the capsaicin treatment. Treatment of rats with SR140333 had no influence on the long-term downregulation of TRPV1 mRNA by capsaicin. Based on the present results and previous findings it can be postulated that the capsaicin-induced ERK phosphorylation in sensory neurons is not a direct effect by capsaicin, but that rather substance P release from the stimulated sensory neurons with an NK1-mediated nerve growth factor (NGF) production is involved. Copyright © 2006 S. Karger AG, Basel [ABSTRACT FROM AUTHOR]

Published
2006
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49. The non-peptide NK1 receptor antagonist SR140333 produces long-lasting inhibition of neurogenic inflammation, but does not influence acute chemo- or thermonociception in rats

Author

Amann, R., Schuligoi, R., Holzer, P., and Donnerer, J.

Abstract

In anaesthetized rats, the neurokinin (NK)1 receptor antagonist SR140333 (10–1000 µg/kg) stereoselectively inhibited mustard oil-induced plasma protein extravasation in the dorsal skin of the hind paw. After s.c. administration of SR140333, inhibition of plasma protein extravasation was maximal 3 h after injection. A dose of 0.1 mg/kg i.v. or 1.0 mg/kg s.c. produced long-lasting inhibition which was still significant 24 h after treatment.

Published
1995
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