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Your search keyword '"Bettina Kunz"' showing total 2 results
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2 results on '"Bettina Kunz"'

1. A Unified Approach to the Calculation of Self- and Mutual-Inductance for Coaxial Coils in Air

Author

Bettina Kunz, Ignacio Lope, W.H. Wolfle, Maeve Duffy, Jun Zhang, and William Gerard Hurley

Subjects
Leakage inductance, Tesla coil, Engineering, Allgemeines, Sonstiges, business.industry, Equivalent series inductance, Electrical engineering, Electrical reactance, Topology, Inductive coupling, Kinetic inductance, law.invention, Inductance, law, Wireless power transfer, Electrical and Electronic Engineering, business
Abstract

This paper extends a previous formula for the mutual inductance between single-turn coils to include all coils in air with rectangular cross sections, without any restrictions on the dimensions (including overlapping coils). The formula is compared with a wide spectrum of examples from the literature and agreement is excellent in every case. Experimental results are presented to validate the formula for both solenoid and disk coils. The formula is relevant to coreless transformers, inductive coupling, wireless power transfer, and leakage inductance in resonant converters.

Published
2015

2. Notch signaling drives development of Barrett’s metaplasia from Dclk1-positive epithelial tuft cells in the murine gastric mucosa

Author

Bettina Kunze, Moritz Middelhoff, H. Carlo Maurer, Tatiana Agibalova, Akanksha Anand, Anne-Marie Bührer, Hsin-Yu Fang, Theresa Baumeister, Katja Steiger, Julia Strangmann, Roland M. Schmid, Timothy C. Wang, and Michael Quante

Subjects
Medicine, Science
Abstract

Abstract Barrett’s esophagus (BE) is a precursor to esophageal adenocarcinoma (EAC), but its cellular origin and mechanism of neoplastic progression remain unresolved. Notch signaling, which plays a key role in regulating intestinal stem cell maintenance, has been implicated in a number of cancers. The kinase Dclk1 labels epithelial post-mitotic tuft cells at the squamo-columnar junction (SCJ), and has also been proposed to contribute to epithelial tumor growth. Here, we find that genetic activation of intracellular Notch signaling in epithelial Dclk1-positive tuft cells resulted in the accelerated development of metaplasia and dysplasia in a mouse model of BE (pL2.Dclk1.N2IC mice). In contrast, genetic ablation of Notch receptor 2 in Dclk1-positive cells delayed BE progression (pL2.Dclk1.N2fl mice), and led to increased secretory cell differentiation. The accelerated BE progression in pL2.Dclk1.N2IC mice correlated with changes to the transcriptomic landscape, most notably for the activation of oncogenic, proliferative pathways in BE tissues, in contrast to upregulated Wnt signalling in pL2.Dclk1.N2fl mice. Collectively, our data show that Notch activation in Dclk1-positive tuft cells in the gastric cardia can contribute to BE development.

Published
2021
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