Search

Your search keyword '"Krönke M"' showing total 469 results
Start Over Author "Krönke M"
469 results on '"Krönke M"'

5. Utility of 18F-rhPSMA-7.3 PET for imaging of primary prostate cancer and pre-operative efficacy in N-staging of unfavorable intermediate to very high-risk patients validated by histopathology

Author

Langbein, T., additional, Wang, H., additional, Rauscher, I., additional, Krönke, M., additional, Knorr, K., additional, Wurzer, A., additional, Schwamborn, K., additional, Maurer, T., additional, Horn, T., additional, Haller, B., additional, Wester, H.J., additional, and Eiber, M., additional

Published
2022
Full Text
View/download PDF

6. Routinely Prepared Cells for Cytogenetic Analysis Stored at −20 °C for Several Years can be Used for RT-PCR-Based Detection of Chromosomal Aberrations in Leukemias

Author

Schafhausen, P., Schoch, R., Nickelsen, M., Haferlach, T., Jenisch, S., Weber-Matthiesen, K., Schlegelberger, B., Krönke, M., Gassmann, W., Löffler, H., Hiddemann, W., editor, Büchner, T., editor, Wörmann, B., editor, Ritter, J., editor, Creutzig, U., editor, Keating, M., editor, and Plunkett, W., editor

Published
1998
Full Text
View/download PDF

32. Singuläre Metastase in der PSMA-Liganden PET und niedriger PSA-Wert als präoperative Prädiktoren für gutes biochemisches Ansprechen nach PSMA-radioguided surgery beim rezidivierenden Prostatakarzinom

Author

Maurer, T, additional, Horn, T, additional, Rauscher, I, additional, Krönke, M, additional, Robu, S, additional, Wester, HJ, additional, Schottelius, M, additional, Haller, B, additional, Heck, MM, additional, Gschwend, JE, additional, Weber, W, additional, and Eiber, M, additional

Published
2019
Full Text
View/download PDF

37. Molecular Cloning of cDNA for the Human Interleukin-2 Receptor

Author

Greene, W. C., Depper, J. M., Crabtree, G. R., Rudikoff, S., Pumphrey, J., Robb, R. J., Krönke, M., Svetlik, P., Peffer, N. J., Waldmann, T. A., Leonard, W. J., Heimpel, H., editor, Huhn, D., editor, Mueller-Eckhardt, C., editor, Ruhenstroth-Bauer, G., editor, Neth, Rolf, editor, Gallo, Robert C., editor, Greaves, Melvyn F., editor, and Janka, Gritta, editor

Published
1985
Full Text
View/download PDF

38. p22phox C242T SNP inhibits inflammatory oxidative damage to endothelial cells and vessels

Author

Meijles, DN, Fan, LM, Ghazaly, MM, Howlin, Brendan, Krönke, M, Brooks, G, and Li, J-M

Subjects
cardiovascular system
Abstract

Background— T NADPH oxidase, by generating reactive oxygen species, is involved in the pathophysiology of many cardiovascular diseases and represents a therapeutic target for the development of novel drugs. A single-nucleotide polymorphism (SNP) C242T of the p22phox subunit of NADPH oxidase has been reported to be negatively associated with coronary heart disease (CHD) and may predict disease prevalence. However, the underlying mechanisms remain unknown.\ud \ud Methods and Results— Using computer molecular modelling we discovered that C242T SNP causes significant structural changes in the extracellular loop of p22phox and reduces its interaction stability with Nox2 subunit. Gene transfection of human pulmonary microvascular endothelial cells showed that C242T p22phox reduced significantly Nox2 expression but had no significant effect on basal endothelial O2.- production or the expression of Nox1 and Nox4. When cells were stimulated with TNFα (or high glucose), C242T p22phox inhibited significantly TNFα-induced Nox2 maturation, O2.- production, MAPK and NFκB activation and inflammation (all p

Published
2016

39. p22phox C242T Single-Nucleotide Polymorphism Inhibits Inflammatory Oxidative Damage to Endothelial Cells and Vessels

Author

Meijles, DN, Fan, LM, Ghazaly, MM, Howlin, B, Krönke, M, Brooks, G, and Li, J-M

Abstract

BACKGROUND: The NADPH oxidase, by generating reactive oxygen species, is involved in the pathophysiology of many cardiovascular diseases and represents a therapeutic target for the development of novel drugs. A single-nucleotide polymorphism, C242T of the p22(phox) subunit of NADPH oxidase, has been reported to be negatively associated with coronary heart disease and may predict disease prevalence. However, the underlying mechanisms remain unknown. METHODS AND RESULTS: With the use of computer molecular modeling, we discovered that C242T single-nucleotide polymorphism causes significant structural changes in the extracellular loop of p22(phox) and reduces its interaction stability with Nox2 subunit. Gene transfection of human pulmonary microvascular endothelial cells showed that C242T p22(phox) significantly reduced Nox2 expression but had no significant effect on basal endothelial O2 (.-) production or the expression of Nox1 and Nox4. When cells were stimulated with tumor necrosis factor-α (or high glucose), C242T p22(phox) significantly inhibited tumor necrosis factor-α-induced Nox2 maturation, O2 (.-) production, mitogen-activated protein kinases and nuclear factor κB activation, and inflammation (all P

Published
2016

40. Diagnostische Wertigkeit der 68Gallium-PSMA PET/CT zu Beurteilung des Therapieansprechens von Patienten mit metastasiertem, hormonsensitivem Prostatakarzinom unter primärer Hormonchemotherapie

Author

Seitz, A.K., Krönke, M., Luther, S., Heck, M.M., Horn, T., Retz, M., Gschwend, J.E., Schwaiger, M., Eiber, M., and Maurer, T.

Subjects
ddc: 610, 610 Medical sciences, Medicine
Abstract

Hintergrund: Die Aussagekraft der konventionellen Bildgebung zur Beurteilung des Therapieansprechens bei Patienten (Pt.) mit metastasiertem Prostatakarzinom (PCa) unter Systemtherapie ist limitiert. Insbesondere die Abgrenzung einer Tumorprogression gegenüber therapieassoziierten Effekten gestaltet[zum vollständigen Text gelangen Sie über die oben angegebene URL], 42. Gemeinsame Tagung der Bayerischen Urologenvereinigung und der Österreichischen Gesellschaft für Urologie und Andrologie

Published
2016

48. Cytochrome c oxidase deficiency accelerates mitochondrial apoptosis by activating ceramide synthase 6.

Author

Schüll, S, Günther, SD, Brodesser, S, Seeger, JM, Tosetti, B, Wiegmann, K, Pongratz, C, Diaz, F, Witt, A, Andree, M, Brinkmann, K, Krönke, M, Wiesner, RJ, Kashkar, H, Schüll, S, Günther, SD, Brodesser, S, Seeger, JM, Tosetti, B, Wiegmann, K, Pongratz, C, Diaz, F, Witt, A, Andree, M, Brinkmann, K, Krönke, M, Wiesner, RJ, and Kashkar, H

Abstract

Although numerous pathogenic changes within the mitochondrial respiratory chain (RC) have been associated with an elevated occurrence of apoptosis within the affected tissues, the mechanistic insight into how mitochondrial dysfunction initiates apoptotic cell death is still unknown. In this study, we show that the specific alteration of the cytochrome c oxidase (COX), representing a common defect found in mitochondrial diseases, facilitates mitochondrial apoptosis in response to oxidative stress. Our data identified an increased ceramide synthase 6 (CerS6) activity as an important pro-apoptotic response to COX dysfunction induced either by chemical or genetic approaches. The elevated CerS6 activity resulted in accumulation of the pro-apoptotic C16 : 0 ceramide, which facilitates the mitochondrial apoptosis in response to oxidative stress. Accordingly, inhibition of CerS6 or its specific knockdown diminished the increased susceptibility of COX-deficient cells to oxidative stress. Our results provide new insights into how mitochondrial RC dysfunction mechanistically interferes with the apoptotic machinery. On the basis of its pivotal role in regulating cell death upon COX dysfunction, CerS6 might potentially represent a novel target for therapeutic intervention in mitochondrial diseases caused by COX dysfunction.

Published
2015

Catalog

Books, media, physical & digital resources
See catalog results