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350 results on '"Kronenberger, Bernd"'

1. Acute Cholangitis

Author

Kronenberger, Bernd, Mutignani, Massimiliano, editor, Albert, Jörg G., editor, and Fabbri, Carlo, editor

Published
2020
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4. Intrahepatic Stones

Author

Kronenberger, Bernd, Mutignani, Massimiliano, editor, Albert, Jörg G., editor, and Fabbri, Carlo, editor

Published
2020
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7. Supplementary Figure S2 from Improving Drug Penetrability with iRGD Leverages the Therapeutic Response to Sorafenib and Doxorubicin in Hepatocellular Carcinoma

Author

Schmithals, Christian, primary, Köberle, Verena, primary, Korkusuz, Hüdayi, primary, Pleli, Thomas, primary, Kakoschky, Bianca, primary, Augusto, Eduardo Alonso, primary, Ibrahim, Ahmed Atef, primary, Arencibia, Jose M., primary, Vafaizadeh, Vida, primary, Groner, Bernd, primary, Korf, Horst-Werner, primary, Kronenberger, Bernd, primary, Zeuzem, Stefan, primary, Vogl, Thomas J., primary, Waidmann, Oliver, primary, and Piiper, Albrecht, primary

Published
2023
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8. Data from Improving Drug Penetrability with iRGD Leverages the Therapeutic Response to Sorafenib and Doxorubicin in Hepatocellular Carcinoma

Author

Schmithals, Christian, primary, Köberle, Verena, primary, Korkusuz, Hüdayi, primary, Pleli, Thomas, primary, Kakoschky, Bianca, primary, Augusto, Eduardo Alonso, primary, Ibrahim, Ahmed Atef, primary, Arencibia, Jose M., primary, Vafaizadeh, Vida, primary, Groner, Bernd, primary, Korf, Horst-Werner, primary, Kronenberger, Bernd, primary, Zeuzem, Stefan, primary, Vogl, Thomas J., primary, Waidmann, Oliver, primary, and Piiper, Albrecht, primary

Published
2023
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30. Correction: Cyclic AMP induces transactivation of the receptors for epidermal growth factor and nerve growth factor, thereby modulating activation of MAP kinase, Akt, and neurite outgrowth in PC12 cells

Author

Piiper, Albrecht, Đikić, Ivan, Lutz, Manfred Paul, Leser, Jürgen, Kronenberger, Bernd, Elez, Robert, Cramer, Henning, Müller-Esterl, Werner, Zeuzem, Stefan, Piiper, Albrecht, Đikić, Ivan, Lutz, Manfred Paul, Leser, Jürgen, Kronenberger, Bernd, Elez, Robert, Cramer, Henning, Müller-Esterl, Werner, and Zeuzem, Stefan

Abstract

Erratum for: Cyclic AMP induces transactivation of the receptors for epidermal growth factor and nerve growth factor, thereby modulating activation of MAP kinase, Akt, and neurite outgrowth in PC12 cells.Journal of biological chemistry, 2002 Nov 15;277(46):43623-30. doi: 10.1074/jbc.M203926200. Epub 2002 Sep 5.

Published
2021

31. Cyclic AMP induces transactivation of the receptors for epidermal growth factor and nerve growth factor, thereby modulating activation of MAP kinase, Akt, and neurite outgrowth in PC12 cells

Author

Piiper, Albrecht, Đikić, Ivan, Lutz, Manfred Paul, Leser, Jürgen, Kronenberger, Bernd, Elez, Robert, Cramer, Henning, Müller-Esterl, Werner, Zeuzem, Stefan, Piiper, Albrecht, Đikić, Ivan, Lutz, Manfred Paul, Leser, Jürgen, Kronenberger, Bernd, Elez, Robert, Cramer, Henning, Müller-Esterl, Werner, and Zeuzem, Stefan

Abstract

In PC12 cells, a well studied model for neuronal differentiation, an elevation in the intracellular cAMP level increases cell survival, stimulates neurite outgrowth, and causes activation of extracellular signal-regulated protein kinase 1 and 2 (ERK1/2). Here we show that an increase in the intracellular cAMP concentration induces tyrosine phosphorylation of two receptor tyrosine kinases, i.e. the epidermal growth factor (EGF) receptor and the high affinity receptor for nerve growth factor (NGF), also termed Trk(A). cAMP-induced tyrosine phosphorylation of the EGF receptor is rapid and correlates with ERK1/2 activation. It occurs also in Panc-1, but not in human mesangial cells. cAMP-induced tyrosine phosphorylation of the NGF receptor is slower and correlates with Akt activation. Inhibition of EGF receptor tyrosine phosphorylation, but not of the NGF receptor, reduces cAMP-induced neurite outgrowth. Expression of dominant-negative Akt does not abolish cAMP-induced survival in serum-free media, but increases cAMP-induced ERK1/2 activation and neurite outgrowth. Together, our results demonstrate that cAMP induces dual signaling in PC12 cells: transactivation of the EGF receptor triggering the ERK1/2 pathway and neurite outgrowth; and transactivation of the NGF receptor promoting Akt activation and thereby modulating ERK1/2 activation and neurite outgrowth. Erratum in: Correction: Cyclic AMP induces transactivation of the receptors for epidermal growth factor and nerve growth factor, thereby modulating activation of MAP kinase, Akt, and neurite outgrowth in PC12 cells. Journal of biological chemistry 2020 Oct 23;295(43):14792. doi: 10.1074/jbc.AAC120.016177.

Published
2021

36. Correction: Cyclic AMP induces transactivation of the receptors for epidermal growth factor and nerve growth factor, thereby modulating activation of MAP kinase, Akt, and neurite outgrowth in PC12 cells.

Author

Piiper, Albrecht, primary, Dikic, Ivan, additional, Lutz, Manfred P., additional, Leser, Jürgen, additional, Kronenberger, Bernd, additional, Elez, Robert, additional, Cramer, Henning, additional, Müller-Esterl, Werner, additional, and Zeuzem, Stefan, additional

Published
2020
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43. Interleukin-22 predicts severity and death in advanced liver cirrhosis: a prospective cohort study

Author

Kronenberger Bernd, Rudloff Ina, Bachmann Malte, Brunner Friederike, Kapper Lisa, Filmann Natalie, Waidmann Oliver, Herrmann Eva, Pfeilschifter Josef, Zeuzem Stefan, Piiper Albrecht, and Mühl Heiko

Subjects
Interleukin-22, Liver cirrhosis, Liver-related complications, Hepatitis, Alcoholic liver disease, MELD, Medicine
Abstract

Abstract Background Interleukin-22 (IL-22), recently identified as a crucial parameter of pathology in experimental liver damage, may determine survival in clinical end-stage liver disease. Systematic analysis of serum IL-22 in relation to morbidity and mortality of patients with advanced liver cirrhosis has not been performed so far. Methods This is a prospective cohort study including 120 liver cirrhosis patients and 40 healthy donors to analyze systemic levels of IL-22 in relation to survival and hepatic complications. Results A total of 71% of patients displayed liver cirrhosis-related complications at study inclusion. A total of 23% of the patients died during a mean follow-up of 196 ± 165 days. Systemic IL-22 was detectable in 74% of patients but only in 10% of healthy donors (P < 0.001). Elevated levels of IL-22 were associated with ascites (P = 0.006), hepatorenal syndrome (P < 0.0001), and spontaneous bacterial peritonitis (P = 0.001). Patients with elevated IL-22 (>18 pg/ml, n = 57) showed significantly reduced survival compared to patients with regular (≤18 pg/ml) levels of IL-22 (321 days versus 526 days, P = 0.003). Other factors associated with reduced overall survival were high CRP (≥2.9 mg/dl, P = 0.005, hazard ratio (HR) 0.314, confidence interval (CI) (0.141 to 0.702)), elevated serum creatinine (P = 0.05, HR 0.453, CI (0.203 to 1.012)), presence of liver-related complications (P = 0.028, HR 0.258, CI (0.077 to 0.862)), model of end stage liver disease (MELD) score ≥20 (P = 0.017, HR 0.364, CI (0.159 to 0.835)) and age (P = 0.011, HR 0.955, CI (0.922 to 0.989)). Adjusted multivariate Cox proportional-hazards analysis identified elevated systemic IL-22 levels as independent predictors of reduced survival (P = 0.007, HR 0.218, CI (0.072 to 0.662)). Conclusions In patients with liver cirrhosis, elevated systemic IL-22 levels are predictive for reduced survival independently from age, liver-related complications, CRP, creatinine and the MELD score. Thus, processes that lead to a rise in systemic interleukin-22 may be relevant for prognosis of advanced liver cirrhosis.

Published
2012
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47. Current and future treatment options for HCV

Author

Kronenberger, Bernd, Zeuzem, Stefan, Kronenberger, Bernd, and Zeuzem, Stefan

Abstract

Aim of antiviral therapy of patients with chronic hepatitis C is the sustained elimination of the hepatitis C virus (HCV). The standard of care (SOC) is peginterferon alfa-2a/-2b with ribavirin for 48 weeks or 24 weeks in patients infected with HCV genotype 1 or 2/3, respectively. Overall, approximately half of the patients can be cured by SOC. Based on baseline viral load and the speed of virologic response during treatment, individualization of treatment duration is possible. However, this approach is not sufficient to substantially improve the sustained virologic response (SVR) rates. This goal can be achieved with new HCV specific inhibitors against the NS3/4A polymerase and the NS5B polymerase. Recent trials reported SVR rates in the order of 67-69% and 67-75% for the combination of SOC with the protease inhibitors telaprevir and boceprevir, respectively, in patients with HCV genotype 1 infection. Several new HCV specific inhibitors such as protease inhibitors, nucleoside and non-nucleoside polymerase inhibitors as well as non HCV specific compounds with anti-HCV activity such as cyclophilin inhibitors, silibinin, and nitazoxanide are currently in clinical evaluation. The review describes recent developments and discusses limitations posed by resistance development and drug toxicity.

Published
2019

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