B
Birte Scholz
Researcher at University of Rostock
Publications - 4
Citations - 490
Birte Scholz is an academic researcher from University of Rostock. The author has contributed to research in topics: Wild type & Oxidative stress. The author has an hindex of 2, co-authored 3 publications receiving 427 citations.
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Journal ArticleDOI
Bacterial volatiles and their action potential
TL;DR: This review summarizes the presently known bioactive compounds and lists the wide panoply of effects possessed by organisms such as fungi, plants, animals, and bacteria to represent a source for new natural compounds that are interesting for man.
Journal ArticleDOI
Mutation of mitochondrial ATP8 gene improves hepatic energy status in a murine model of acute endotoxemic liver failure
Christian Eipel,Anke Hildebrandt,Birte Scholz,Lilianna Schyschka,Thomas Minor,Bernd Kreikemeyer,Saleh M. Ibrahim,Brigitte Vollmar +7 more
TL;DR: It is demonstrated that mutation in the ATPase subunit-8 partially protects mice against endotoxemic stress, most probably due to better hepatic energy status despite elevated oxidative stress, which may be an effective strategy to protect against sepsis-induced multiorgan dysfunction.
Journal ArticleDOI
The More the Better—Investigation of Polymethoxylated N-Carboranyl Quinazolines as Novel Hybrid Breast Cancer Resistance Protein Inhibitors
Philipp Stockmann,Lydia Kuhnert,Wencke Leinung,Cathleen Lakoma,Birte Scholz,Svetlana Paskas,Sanja Mijatović,Danijela Maksimović-Ivanić,Walther Honscha,Evamarie Hey-Hawkins +9 more
TL;DR: In this article , carboranyl quinazoline-based inhibitors of ABCG2 have been developed to reverse mitoxantrone (MXN) resistance in breast cancer resistance proteins.
Book ChapterDOI
Eine Mutation innerhalb der ATP8-Synthase verbessert den hepatischen Energiestatus im murinen Modell des akuten septischen Leberversagens
TL;DR: The data demonstrate that mutation in the ATPase subunit 8 partially protects mice under endotoxemic stress conditions most probably due to better hepatic energy status despite elevated overall oxidative stress, and underline the role of genetic polymorphisms in the pathophysiology of sepsis.