LEGO-Praktikum. Entwickeln, programmieren, optimieren: Berichte der Studierenden zum Projektseminar Elektrotechnik/Informationstechnik

Seit 2018 existiert die Open-Access-Schriftenreihe "LEGO-Praktikum. Entwickeln, programmieren, optimieren", in der studentische Beiträge veröffentlicht werden, die im Rahmen des Projektseminars Elektrotechnik/Informationstechnik (bzw. dem sogenannten "LEGO-Praktikum") an der gleichnamigen Fakultät entstanden sind. Am Ende dieses Seminars verfügen die Studierenden über Kenntnisse zur Programmierung mit MATLAB und können verschiedene Sensoren und Motoren ansteuern und regeln. Sie lernen das projektorientierte Arbeiten im Team, das mündliche Präsentieren ihrer eigenen Arbeit vor einer Gruppe und die schriftliche Dokumentation ihrer Ergebnisse in Form von kurzen Berichten, die in dieser Schriftenreihe veröffentlicht sind. Durch die praxisnahen Übungen mit LEGO-Bausätzen, die Vorträge und die schriftliche Ausarbeitung sind die Studierenden in der Lage, ihre Arbeiten wissenschaftlich kritisch zu hinterfragen und strukturiert zu dokumentieren

LEGO-Praktikum. Entwickeln, programmieren, optimieren: Berichte der Studierenden zum Projektseminar Elektrotechnik/Informationstechnik

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Characteristics of Müller glial cells in MNU-induced retinal degeneration.

Retinal Müller glial cells have been shown to undergo reactive gliosis in a variety of retinal diseases. Upregulation of glial fibrillary acidic protein (GFAP) is a hallmark of Müller cell activation. Reactive gliosis after retinal detachment or ischemia/reperfusion is characterized by hypertrophy and downregulation of inwardly rectifying K+ (Kir) currents. However, this kind of physiological alteration could not be detected in slowly progressing retinal degenerations. The photoreceptor toxin N-methyl-N-nitrosourea (MNU) leads to the rapid loss of cells in the outer nuclear layer and subsequent Müller cell activation. Here, we investigated whether Müller cells from MNU-treated mice exhibit reactive gliosis. We found that Müller cells showed increased GFAP expression and increased membrane capacitance, indicating hypertrophy. Membrane potential and Kir channel-mediated K+ currents were not significantly altered whereas Kir4.1 mRNA expression and Kir-mediated inward current densities were markedly decreased. This suggests that MNU-induced Müller cell gliosis is characterized by plasma membrane increase without alteration in the membrane content of Kir channels. Taken together, our findings show that Müller cells of MNU-treated mice are reactive and respond with a form of gliosis which is characterized by cellular hypertrophy but no changes in Kir current amplitudes

Involvement of A1 adenosine receptors in osmotic volume regulation of retinal glial cells in mice

PURPOSE: Osmotic swelling of Müller glial cells has been suggested to contribute to retinal edema. We determined the role of adenosine signaling in the inhibition of Müller cell swelling in the murine retina. METHODS: The size of Müller cell somata was recorded before and during perfusion of retinal sections and isolated Müller cells with a hypoosmolar solution. Retinal tissues were freshly isolated from wild-type mice and mice deficient in A(1) adenosine receptors (A(1)AR(-/-)), or cultured as whole-mounts for three days. The potassium conductance of Müller cells was recorded in isolated cells, and retinal slices were immunostained against Kir4.1. RESULTS: Hypotonic exposure for 4 min induced a swelling of Müller cell bodies in retinal slices from A(1)AR(-/-) mice but not wild-type mice. Pharmacological inhibition of A(1) receptors or of the ecto-5'-nucleotidase induced hypoosmotic swelling of Müller cells from wild-type mice. Exogenous adenosine prevented the swelling of Müller cells from wild-type but not A(1)AR(-/-) mice. The antiinflammatory corticosteroid, triamcinolone acetonide, inhibited the swelling of Müller cells from wild-type mice; this effect was blocked by an antagonist of A(1) receptors. The potassium conductance of Müller cells and the Kir4.1 immunolabeling of retinal slices were not different between A(1)AR(-/-) and wild-type mice, both in freshly isolated tissues and retinal organ cultures. CONCLUSIONS: The data suggest that autocrine activation of A(1) receptors by extracellularly generated adenosine mediates the volume homeostasis of Müller cells in the murine retina. The swelling-inhibitory effect of triamcinolone is mediated by enhancement of endogenous adenosine signaling

Nutzung von Mantelwellensperren für die MR-geführte Mikrowellenablation

Bildgeführte, minimalinvasive Verfahren werden zur Biopsie suspekten Gewebes und dessen Behandlung eingesetzt. Eine weit verbreitete Methode für Letzteres sind thermoablative Verfahren wie beispielsweise die Mikrowellenablation (MWA). Mittels Bildgebung kann eine korrekte Platzierung einer für die MWA genutzten Elektrode überwacht werden. Die applizierten elektromagnetischen Felder führen aufgrund des Leistungsumsatzes im Gewebe zu einer starken Temperaturerhöhung. Studien haben gezeigt, dass unter Einhaltung eines Sicherheitssaumes von >5mm um den Tumor die Rezidivrate erheblich gesenkt werden kann [1]. Die Nutzung des MRTs bietet dazu die Möglichkeit Temperaturkarten zu erstellen, um einen geforderten Sicherheitsraum nachweisen zu können. Die MR-Bildgebung hat jedoch den Nachteil, äußerst anfällig gegenüber Interferenzen externer Geräte zu sein [2]. Eine mögliche Störquelle stellen hierbei Gleichtaktströme dar, welche sich auf den langen Zuleitungen zwischen MWA-Generator und Ablationselektrode bilden können. Um diese Gleichtaktströme zu dämpfen, gibt es in der MR-Bildgebung den Ansatz, nichtmagnetische Mantelwellensperren (MWS) zu verwenden [3]. Typischerweise wird hierfür ein geschirmter Leiter aufgewickelt und die resultierende Induktivität bildet mit einer an der Schirmung angebrachten Kapazität einen Schwingkreis, welche im Resonanzfall eine hohe Impedanz für den Gleichtaktstrom aufweist [4]. Die Effektivität der MWS hängt von deren Platzierung auf dem Kabel ab. Eine Neuplatzierung der MWS nach dem Anlöten am Kabelschirm ist mit einem erheblichen Aufwand in der MR-Umgebung verbunden [3]. Auch sollte beachtet werden, dass die Nutzung von Kabelzuleitungen für therapeutische Anwendungen den thermischen und chemischen Anforderungen einer klinischen Sterilisation genügen müssen. Durch das Anlöten der Kondensatoren der solenoiden MWS am Kabelschirm wird dieser Prozess erschwert. Alternative MWS sind zum Beispiel die Floating Cable Traps (FCTs). Bei diesen wird auf dem geschirmten Kabel ein koaxiales Leitersegment angebracht, dessen Innen- und Außenleiter an den Enden mit Kondensatoren abgeschlossen wird. Im Resonanzfall weist das koaxiale Leitersegment eine hohe Impedanz auf, welches zu einer Dämpfung des vom Schirm des Kabels in das koaxiale Leitersegment eingekoppelten Gleichtaktsignals führt. Die FCT bietet hierbei den Vorteil, dass diese Art der MWS nicht auf den Außenleiter eines Koaxialkabels angelötet werden muss. In diesem Paper soll ein Konzept vorgestellt werden, bei dem FCTs für den klinischen Einsatz einer Mikrowellenablation genutzt werden. Die Wirksamkeit wird mittels MR-Bildgebung überprüft

Disruption of Endogenous Purinergic Signaling Inhibits Vascular Endothelial Growth Factor- and Glutamate-Induced Osmotic Volume Regulation of Muller Glial Cells in Knockout Mice

Background/Aims: Osmotic swelling of Müller cells is a common phenomenon in animal models of ischemic and diabetic retinopathies. Müller cells possess a swelling-inhibitory purinergic signaling cascade which can be activated by various receptor ligands including vascular endothelial growth factor (VEGF) and glutamate. Here, we investigated whether deletion of P2Y1 (P2Y1R) and adenosine A1 receptors (A1AR), and of inositol-1,4,5-trisphosphate-receptor type 2 (IP3R2), in mice affects the inhibitory action of VEGF and glutamate on Müller cell swelling. Methods: The cross-sectional area of Müller cell somata was recorded after a 4-min superfusion of retinal slices with a hypoosmotic solution. Results: Hypoosmolarity induced a swelling of Müller cells from P2Y1R-/-, A1AR-/- and IP3R2-/- mice, but not from wild-type mice. Swelling of wild-type Müller cells was induced by hypoosmotic solution containing barium chloride. Whereas VEGF inhibited the swelling of wild-type Müller cells, it had no swelling-inhibitory effect in cells from A1AR-/- and IP3R2-/- mice. Glutamate inhibited the swelling of wild-type Müller cells but not of cells from P2Y1R-/-, A1AR-/- and IP3R2-/- animals. Conclusion: The swelling-inhibitory effects of VEGF and glutamate in murine Müller cells is mediated by transactivation of P2Y1R and A1AR, as well as by intracellular calcium signaling via activation of IP3R2

Characteristics of Müller glial cells in MNU-induced retinal degeneration

Retinal Müller glial cells have been shown to undergo reactive gliosis in a variety of retinal diseases. Upregulation of glial fibrillary acidic protein (GFAP) is a hallmark of Müller cell activation. Reactive gliosis after retinal detachment or ischemia/reperfusion is characterized by hypertrophy and downregulation of inwardly rectifying K+ (Kir) currents. However, this kind of physiological alteration could not be detected in slowly progressing retinal degenerations. The photoreceptor toxin N-methyl-N-nitrosourea (MNU) leads to the rapid loss of cells in the outer nuclear layer and subsequent Müller cell activation. Here, we investigated whether Müller cells from MNU-treated mice exhibit reactive gliosis. We found that Müller cells showed increased GFAP expression and increased membrane capacitance, indicating hypertrophy. Membrane potential and Kir channel-mediated K+ currents were not significantly altered whereas Kir4.1 mRNA expression and Kir-mediated inward current densities were markedly decreased. This suggests that MNU-induced Müller cell gliosis is characterized by plasma membrane increase without alteration in the membrane content of Kir channels. Taken together, our findings show that Müller cells of MNU-treated mice are reactive and respond with a form of gliosis which is characterized by cellular hypertrophy but no changes in Kir current amplitudes

Predicting food craving in everyday life through smartphone-derived sensor and usage data

BackgroundFood craving relates to unhealthy eating behaviors such as overeating or binge eating and is thus a promising target for digital interventions. Yet, craving varies strongly across the day and is more likely in some contexts (external, internal) than in others. Prediction of food cravings ahead of time would enable preventive interventions.ObjectiveThe objective of this study was to investigate whether upcoming food cravings could be detected and predicted from passive smartphone sensor data (excluding geolocation information) without the need for repeated questionnaires.MethodsMomentary food craving ratings, given six times a day for 14 days by 56 participants, served as the dependent variable. Predictor variables were environmental noise, light, device movement, screen activity, notifications, and time of the day recorded from 150 to 30 min prior to these ratings.ResultsIndividual high vs. low craving ratings could be predicted on the test set with a mean area under the curve (AUC) of 0.78. This outperformed a baseline model trained on past craving values in 85% of participants by 14%. Yet, this AUC value is likely the upper bound and needs to be independently validated with longer data sets that allow a split into training, validation, and test sets.ConclusionsCraving states can be forecast from external and internal circumstances as these can be measured through smartphone sensors or usage patterns in most participants. This would allow for just-in-time adaptive interventions based on passive data collection and hence with minimal participant burden