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Sonntag, S.

Publications and source records attributed to Sonntag, S..

5 recordsLinked to original sources

EegFun.jl: A Julia Package Tutorial for EEG Analysis

EegFun.jl is an open-source package for electroencephalography (EEG) analysis implemented in the Julia programming language. EegFun.jl provides a flexible framework for EEG research, covering data import from standard file formats, filtering and re-referencing, Independent Component Analysis (ICA) for artifact detection/correction, epoch extraction, and ERP averaging and visualisation. The Julia language provides the readability of a high-level scripting environment together with execution speeds comparable to compiled code. EegFun.jl combines interactive data visualization with high-performance execution, making large-scale analyses both efficient and easy. Here, we provide a brief overview and introductory tutorial of the core stages of the EEG analysis workflow to illustrate the package's capabilities. The package is freely available under the MIT license.

neuroscience↗

Interferons are the key cytokines acting on pancreatic islets in type 1 diabetes

The pro-inflammatory cytokines IFN, IFN{gamma}, IL-1{beta} and TNF may contribute to innate and adaptive immune responses during islet inflammation (insulitis) in type 1 diabetes (T1D). We used deep RNA-sequencing analysis to characterize the response of human pancreatic beta cells to each cytokine individually and compared the signatures obtained with those present in islets of individuals affected by T1D. IFN and IFN{gamma} had a much greater impact on the beta cell transcriptome when compared to IL-1{beta} and TNF. The IFN-induced gene signatures have a strong correlation with those observed in beta cells from T1D patients, and the level of expression of specific IFN-stimulated genes is positively correlated with proteins present in islets of these individuals, regulating beta cell responses to "danger signals" such as viral infections. These data suggest that IFN and IFN{gamma} are the central cytokines at the islet level in T1D, contributing to the triggering and amplification of autoimmunity.

immunology↗

Light-sheet microscopy of network activity in 3D neuronal systems

In vitro systems mimicking brain regions, brain organoids, are revolutionizing the neuroscience field. However, characterization of their electrical activity has remained a challenge as this requires readout at millisecond timescale in 3D at single-neuron resolution. While custom-built microscopes used with genetically encoded sensors are now opening this door, a full 3D characterization of organoid neural activity has not been performed yet, limited by the combined complexity of the optical and the biological system. Here, we introduce an accessible minimalistic light-sheet microscope to the neuroscience community. Designed as an add-on to a standard inverted microscope it can be assembled within one day. In contrast to existing simplistic setups, our platform is suited to record volumetric calcium traces. We successfully extracted 4D calcium traces at high temporal resolution by using a lightweight piezo stage to allow for 5Hz volumetric scanning combined with a processing pipeline for true 3D neuronal trace segmentation. As a proof of principle, we created a 3D connectivity map of a stem cell derived neuron spheroid by imaging its activity. Our fast, low complexity setup empowers researchers to study the formation of neuronal networks in vitro for fundamental and neurodegeneration research.

neuroscience↗

Viscoelastic properties of suspended cells measured with shear flow deformation cytometry

Numerous cell functions are accompanied by phenotypic changes in viscoelastic properties, and measuring them can help elucidate higher-level cellular functions in health and disease. We present a high-throughput, simple and low-cost microfluidic method for quantitatively measuring the elastic (storage) and viscous (loss) modulus of individual cells. Cells are suspended in a high-viscosity fluid and are pumped with high pressure through a 5.8 cm long and 200 {micro}m wide microfluidic channel. The fluid shear stress induces large, near ellipsoidal cell deformations. In addition, the flow profile in the channel causes the cells to rotate in a tank-treading manner. From the cell deformation and tank treading frequency, we extract the frequency-dependent viscoelastic cell properties based on a theoretical framework developed by R. Roscoe1 that describes the deformation of a viscoelastic sphere in a viscous fluid under steady laminar flow. We confirm the accuracy of the method using atomic force microscopy-calibrated polyacrylamide beads and cells. Our measurements demonstrate that suspended cells exhibit power-law, soft glassy rheological behavior that is cell cycle-dependent and mediated by the physical interplay between the actin filament and intermediate filament networks.

biophysics↗

A distinct pool of Nav1.5 channels at the lateral membrane of murine ventricular cardiomyocytes

BackgroundIn cardiac ventricular muscle cells, the presence of voltage-gated sodium channels Nav1.5 at the lateral membrane depends in part on the interaction between the dystrophin-syntrophin complex and the Nav1.5 C-terminal PDZ-domain-binding sequence Ser-Ile-Val (SIV motif). 1-Syntrophin, a PDZ-domain adaptor protein, mediates the interaction between Nav1.5 and dystrophin at the lateral membrane of cardiac cells. Using the cell-attached patch-clamp approach on cardiomyocytes expressing Nav1.5 in which the SIV motif is deleted ({Delta}SIV), sodium current (INa) recordings from the lateral membrane revealed an SIV-motif-independent INa. Since immunostainings have suggested that Nav1.5 is expressed in transverse (T-) tubules, this remaining INa might be conducted by channels in the T-tubules. Of note, a recent study using heterologous expression systems showed that 1-syntrophin also interacts with the Nav1.5 N-terminus, which may explain the SIV-motif independent INa at the lateral membrane of cardiomyocytes.\n\nAimTo address the role of 1-syntrophin in regulating the INa at the lateral membrane of cardiac cells.\n\nMethods and resultsPatch-clamp experiments in cell-attached configuration were performed on the lateral membranes of wild-type, 1-syntrophin knock-down, and {Delta}SIV ventricular mouse cardiomyocytes. Compared to wild-type, a reduction of the lateral INa was observed in myocytes from 1-syntrophin knockdown hearts. However, similar to {Delta}SIV myocytes, a remaining INa was still recorded. In addition, cell-attached INa recordings from lateral membrane did not differ significantly between non-detubulated and detubulated {Delta}SIV cardiomyocytes. Lastly, we obtained evidence suggesting that cell-attached patch-clamp experiments on the lateral membrane cannot record currents conducted by channels in T-tubules such as calcium channels.\n\nConclusionAltogether, these results suggest the presence of a sub-pool of sodium channels at the lateral membrane of cardiomyocytes that is independent of 1-syntrophin and the PDZ-binding motif of Na 1.5, located in membrane domains outside of T-tubules. The question of a T-tubular pool of Nav1.5 channels however remains open.

physiology↗