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Julian Constantin Raimar Schulze zur Wiesch (1974-)

Arzt

Name	Julian Constantin Raimar Schulze zur Wiesch
Zeit	1974- (Lebensdaten)
Ort	Deutschland
Geschlecht	männlich
Akademischer Grad bzw. Titel	Dr. med.
Beruf	Arzt (charakteristischer Beruf)
Variante	Julian Constantin Raimar Schulze zur Wiesch Julian Constantin Raimar Schulze Zur Wiesch Julian Schulze zur Wiesch Julian Schulze zur Wiesch Julian Schulze Zur Wiesch Julian Constantin Raimar Schulze ZurWiesch (RAK alt) Julian Constantin Raimar Schulze ZurWiesch (RAK alt)
Beziehung	Universitätsklinikum Hamburg-Eppendorf
Weitere Angaben	Diss. Fachbereich Medizin, Hamburg, Univ., 2000 Univ. Hamburg, Medizinische Fak., Universitätsklinikum Hamburg-Eppendorf, Zentrum für Innere Medizin, I. Medizinische Klinik und Poliklinik
Datensatztyp	Person
GND-Nummer	122681487
Datensatz-ID	122681487
Beteiligt an alle anzeigen SARS-CoV-2 vaccination may mitigate dysregulation of IL-1/IL-18 and gastrointestinal symptoms of the post-COVID-19 condition A multicenter randomized-controlled trial of nucleos(t)ide analogue cessation in HBeAg-negative chronic hepatitis B Immune escape pathways from the HBV core18-27 CD8 T cell response are driven by individual HLA class I alleles Mechanisms of CD8+ T cell failure in chronic hepatitis E virus infection Bestimmung der Breite und Spezifität der Hepatitis Delta Virus (HDV)-spezifischen T-Zellantwort Human hepatitis D virus-specific T cell epitopes Treatment and re-treatment results of HCV patients in the DAA era Immediate versus deferred antiretroviral therapy in HIV-infected patients presenting with acute AIDS-defining events (toxoplasmosis, Pneumocystis jirovecii-pneumonia): a prospective, randomized, open-label multicenter study (IDEAL-study) HCV-specific CD4+ T cells of patients with acute and chronic HCV infection display high expression of TIGIT and other co-inhibitory molecules Mutations in hepatitis D virus allow it to escape detection by CD8+ T cells and evolve at the population level Assessment of the range of the HIV-1 infectivity enhancing effect of individual human semen specimen and the range of inhibition by EGCG The transhepatic endotoxin gradient is present despite liver cirrhosis and is attenuated after transjugular portosystemic shunt (TIPS) Antibody dynamics and spontaneous viral clearance in patients with acute hepatitis C infection in Rio de Janeiro, Brazil Das Nicht-Strukturprotein 3 des Hepatitis-C-Virus inhibiert die Funktionen des Proteinkinase C

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Katalog der Deutschen Nationalbibliothek

Julian Constantin Raimar Schulze zur Wiesch (1974-)

SARS-CoV-2 vaccination may mitigate dysregulation of IL-1/IL-18 and gastrointestinal symptoms of the post-COVID-19 condition

A multicenter randomized-controlled trial of nucleos(t)ide analogue cessation in HBeAg-negative chronic hepatitis B

Immune escape pathways from the HBV core18-27 CD8 T cell response are driven by individual HLA class I alleles

Mechanisms of CD8+ T cell failure in chronic hepatitis E virus infection

Bestimmung der Breite und Spezifität der Hepatitis Delta Virus (HDV)-spezifischen T-Zellantwort

Human hepatitis D virus-specific T cell epitopes

Treatment and re-treatment results of HCV patients in the DAA era

Immediate versus deferred antiretroviral therapy in HIV-infected patients presenting with acute AIDS-defining events (toxoplasmosis, Pneumocystis jirovecii-pneumonia): a prospective, randomized, open-label multicenter study (IDEAL-study)

HCV-specific CD4+ T cells of patients with acute and chronic HCV infection display high expression of TIGIT and other co-inhibitory molecules

Mutations in hepatitis D virus allow it to escape detection by CD8+ T cells and evolve at the population level

Assessment of the range of the HIV-1 infectivity enhancing effect of individual human semen specimen and the range of inhibition by EGCG

The transhepatic endotoxin gradient is present despite liver cirrhosis and is attenuated after transjugular portosystemic shunt (TIPS)

Antibody dynamics and spontaneous viral clearance in patients with acute hepatitis C infection in Rio de Janeiro, Brazil

Das Nicht-Strukturprotein 3 des Hepatitis-C-Virus inhibiert die Funktionen des Proteinkinase C