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Diabetes in a dish: Modeling and phenotyping acute and chronic type 2 diabetes mellitus in vitro in rodent heart and skeletal muscle cells
Get PDFBackground: Diabetes mellitus is a metabolic disorder, characterized by elevated levels of blood glucose. Type 2 diabetes (T2D) accounts for >90% of cases and is a progressive disease with initially elevated insulin levels and insulin resistance (IR). This study aims to develop a novel method for simulating T2D in vitro, including its main aspects: Hyperglycemia, hyperlipidemia and variably elevated insulin levels. Skeletal and heart muscle cells are strongly affected by IR and chronic hyperglycemia.
Methods: We investigated IR, cellular respiration and mitochondrial function under different T2D-mimicking conditions in rodent skeletal (C2C12) and cardiac (H9C2) myotubes. Physiological control conditions included 5mM glucose (LG) with 20mM mannitol as osmotic controls (HM). To mimic hyperglycemia (HG), cells were exposed to 25mM glucose. Further treatment groups included the combination with insulin (I) (1nM, HGI), or palmitate (P) (75 or 150mM, HGP), or both (HGPI). After short-term (24h) or long-term (96h) exposure, we performed radioactive glucose-uptake assays and mitochondrial function assays using the Agilent Seahorse system. Ultrastructural analysis was performed using transmission electron microscopy.
Results: C2C12 and H9C2 cells treated short- or long-term with insulin and/or palmitate and HG became insulin resistant. In mitochondrial respiration assays C2C12 myotubes exposed to T2D-mimicking conditions showed similar maximal respiration rates compared to physiological controls, but significantly lower ATP linked respiration and spare respiratory capacity, implying more uncoupled respiration and mitochondrial dysfunction in skeletal muscle. In contrast, H9C2 myotubes showed elevated ATP linked respiration and maximal respiration upon exposure to T2D mimicking conditions, indicating better adaptation to stress and preferential lipid oxidation in cardiac muscle in a T2D environment. Both cell lines displayed elevated fractions of swollen mitochondria after T2D mimicking treatments.
Conclusions: Our stable, simple, and reproducible in vitro model of T2D causes IR, changes in ATP linked respiration, shifts in energetic phenotypes and mitochondrial morphology changes. These changes are consistent with what occurs in muscles of patients suffering from T2D. Our results support the relevance of T2D cell models that will be useful for experimental studies of pathomechanisms and screening for potential targets and therapeutic compounds also in other cell types affected by T2D.Hintergrund: Diabetes mellitus ist eine Stoffwechselerkrankung, gekennzeichnet durch erhöhte Blutzuckerspiegel. Typ-2-Diabetes (T2D) macht 90% der Fälle aus und ist durch anfangs erhöhte Insulinspiegel und eine progressive Insulinresistenz (IR) charakterisiert. Ziel dieser Studie ist die Entwicklung einer neuartigen Methode zur Simulation von T2D in vitro, einschließlich der wichtigsten Aspekte: Hyperglykämie, Hyperlipidämie und variabel erhöhte Insulinspiegel. Skelett- und Herzmuskelzellen sind von IR und chronischer Hyperglykämie betroffen. Methoden: Wir haben IR, Zellatmung und Mitochondrienfunktion in verschiedenen T2D-simulierenden Bedingungen in Skelett- (C2C12) und Herzmuskelzellen/Myotuben (H9C2) untersucht. Die physiologischen Kontrollbedingungen umfassten 5mM Glukose (LG) und 20mM Mannitol als osmotische Kontrolle (HM). Um eine Hyperglykämie (HG) zu simulieren, wurden die Zellen mit 25mM Glukose behandelt. Weitere Inkubationen umfassten die Kombination mit Insulin (I) (1nM, HGI) oder Palmitat (P) (75 oder 150mM, HGP) oder beidem (HGPI). Nach kurz- (24h) oder langfristiger (96h) Inkubation führten wir radioaktive Glukose-Aufnahme-Assays und mitochondriale Funktionstests mit dem Agilent Seahorse System durch. Ultrastrukturelle Analysen wurde mit Hilfe der Transmissionselektronenmikroskopie durchgeführt.
Ergebnisse: C2C12- und H9C2-Zellen, die kurz- oder langfristig mit Insulin und/oder Palmitat und HG behandelt wurden, wurden insulinresistent. In Tests zur mitochondrialen Atmung zeigten C2C12 Zellen, die T2D-simulierenden Bedingungen ausgesetzt waren, im Vergleich zu LG Kontrollen ähnliche maximale Atmungsraten, aber eine signifikant niedrigere ATP-Produktion und Reserve-Atmungskapazität, was auf vermehrt entkoppelte Atmung und mitochondriale Dysfunktion im Skelettmuskel hindeutet. H9C2 hingegen zeigten eine erhöhte ATP-Produktion und maximale Atmung, nachdem sie T2D-ähnlichen Bedingungen ausgesetzt waren, was auf eine bessere Stressanpassung und verstärkte Lipidoxidation des Herzmuskels in einer T2D-Umgebung hinweist. Beide Zelllinien zeigten erhöhte Fraktionen geschwollener Mitochondrien nach T2D-simulierenden Behandlungen.
Schlussfolgerungen: Unser stabiles, simples und reproduzierbares in vitro Modell von T2D bewirkt Insulinresistenz, Veränderungen in der ATP-Produktion, Verschiebungen in energetischen Phänotypen und eine veränderte Mitochondrienmorphologie. Diese Veränderungen stimmen mit dem überein, was in den Muskeln von Patienten mit T2D auftritt. Unsere Ergebnisse untermauern die Relevanz von T2D-Zellmodellen, die für experimentelle Studien von Pathomechanismen und das Screening nach potenziellen Targets und therapeutischen Wirkstoffen nützlich sein werden, auch in anderen von T2D betroffenen Zelltypen
Different roles of Regnase3 in resident macrophages and tubular epithelial cells in kidney disease
Get PDFAkutes Nierenversagen (ANV) ist eine häufige, jedoch schwere Erkrankung, die v.a. in klinischen Einrichtungen auftritt. ANV ist durch einen plötzlichen Rückgang der Nierenfunktion gekennzeichnet und wird durch den Anstieg des Serum-Kreatinin-Spiegels und die Abnahme der Urinausscheidung oder beides angezeigt. Die Prognose von ANV ist selbst für Überlebende schlecht, da viele Patienten nach einem schweren ANV eine chronische Niereninsuffizienz entwickeln können, was den Einsatz von Nierenersatzverfahren nowendig macht. Dies beeinträchtigt nicht nur die Lebensqualität der Patienten, sondern erhöht auch die Belastung für pflegende Angehörige und medizinische Kosten. Derzeit gibt es keine pharmazeutisch wirksamen präventiven oder therapeutischen Maßnahmen für ANV, es stehen lediglich Dialyse und unterstützende medizinische Versorgung zur Verfügung.
Ribonukleinsäure (Ribonucleic acid, RNA)-bindende Proteine (RBPs) sind eine Klasse von Proteinen, die eine entscheidende Rolle bei der Regulation der Genexpression spielen und bei einer Vielzahl von Erkrankungen beteiligt sind. Diese Proteine besitzen die Fähigkeit, unterschiedliche Transkripte zu binden und dadurch komplexe regulative Netzwerke zu bilden, die für die Erhaltung der Zellintegrität von entscheidender Bedeutung sind. Neuere Studien haben gezeigt, dass eine Reihe von RBPs an ANV beteiligt sind, darunter das kälteinduzierbare RNA-bindende Protein, humanes Antigen R, Pumilio und Y-Box-bindendes Protein. Regnase 3 ist ein Mitglied der Regnase RBP Familie und fördert Entzündungen, indem es die Expression vonTumor Nekrose Faktor (TNF) in Makrophagen erhöht und Interleukin 6 (IL6) in plasmazytoiden dendritischen Zellen unterdrückt. Trotz dieses Wissens ist die Bedeutung der Rolle, die Regnase 3 in renalen Tubuluszellen spielt, unbekannt. Wir haben die Hypothese aufgestellt, dass Regnase 3 sowohl in Makrophagen als auch in renalen Tubuluszellen eine Rolle spielt und Entzündungen und Tubulusreparatur in ANV beeinflusst.
Um die mögliche Rolle von Regnase 3 bei Nierenschädigungen zu untersuchen, wurden eine Reihe von genetisch veränderten Mäusen im Hintergrund C57BL/6J hergestellt. Diese Mauslinien umfassten paired box gene 8 (Pax8)-reverse tetracycline transactivator (rTtA, Pax8rTtA), tetracycline resistance protein (TetO)-Cre (TetOCre), transgenic receptor activator of nuclear factor kappa-Β (Rank)-Cre (RankCre), and Regnase 3 floxed (Regnase3fl/fl) Mäuse. Diese genetisch veränderten Mäuse haben wir in einer Reihe von experimentellen Tiermodellen eingesetzt, um die Auswirkungen von Regnase 3 auf Nierenschädigung zu untersuchen, darunter ein unilaterales Nierenischämie-Reperfusionsmodel mit oder ohne Nephrektomie und ein Nephrocalcinose-induziertes Nierenschädigungsmodel. Zusätzlich haben wir in vitro-Modelle mit primären Nieren- und Entzündungszellen verwendet, um die Auswirkungen von Regnase 3 auf der Zellenebene zu studieren. Darüber hinaus haben wir single cell und bulk RNA-Sequenzierung durchgeführt, um die zugrundeliegenden Mechanismen der Funktion von Regnase 3 zu untersuchen.
Wir entdeckten, dass Regnase 3 in renalen Makrophagen nach ANV hoch exprimiert ist. Wir beobachteten, dass die Regnase 3-Expression positiv mit Phagozytose, Chemokinenproduktion und Monozytenreifung korrelieren. Darüber hinaus litten Rank-Regnase 3 Mäuse nach ANV aufgrund der Zunahme der CCR2-positiven Zellinfiltration im Vergleich zur Wildtyp-Kontrollgruppe mehr an Entzündung und Nierenschädigung. In vitro-Experimente zeigten, dass Regnase 3 an der Modulation der Makrophagenfunktion beteiligt ist, indem es die Polarisation von Makrophagen zu einem M1- und M2-Phänotyp bewirkt und die Zellmigration beeinflusst. Diese Ergebnisse deuten darauf hin, dass Regnase 3 bei der Makrophagenmigration und -infiltration nach ANV eine entscheidende Rolle spielt, die sowohol zur frühen Entzündungsphase nach ANV als auch der Progression zur chronischem Nierenversagen beiträgt.
Im nächsten Schritt wollten wir die Rolle von Regnase 3 im Kontext von Nierentubulusschädigung untersuchen. Wir beobachteten, dass Regnase 3 in gesunden Nierentubuli hoch exprimiert ist, aber die Expression nach Verletzung deutlich reduziert ist. Mittels in vivo- und in vitro-Experimenten fanden wir heraus, dass Regnase 3 eine entscheidende Rolle bei der Regulierung der frühen Apoptose, Zelltod, Proliferation und Wundheilung von tubulären Epithelzellen spielt. Diese Auswirkungen tragen zur Nierenverletzung bei postischemischen Nieren bei. Darüber hinaus entdeckten wir, dass Regnase 3-Defizienz Schutz vor ischämischem ANV bietet. Unsere Daten belegen, dass Regnase 3 prä-RNA erkennt und alternatives Splicing durch die Erhöhung des Anteils an gezielt übersprungenen Exonen und die Verringerung der Wahrscheinlichkeit gezielter behaltener Introne moduliert. Insgesamt deuten unsere Ergebnisse darauf hin, dass Regnase 3 eine wichtige Rolle bei ANV spielt und möglicherweise ein potenzielles Ziel für therapeutische Interventionen sein könnte.
Zusammenfassend zeigen unsere Ergebnisse, dass Regnase3 eine wichtige Rolle in der Entwicklung von Nierenschäden in postischemischen Nieren spielt und somit ein potenzielles therapeutisches Ziel für die Behandlung von renalen IRI darstellt. Der Einfluss von Regnase3 auf Nierenschäden ist jedoch von der spezifischen Zelllinie abhängig. Unsere Forschung zeigt, dass das Löschen von Rank-Regnase3 zu einer Verschlimmerung von Nierenschäden durch eine Erhöhung der Makrophagenrekrutierung führt, während das Löschen von Pax8-Regnase3 zu einer Verbesserung von Nierenschäden durch seine Auswirkungen auf Zelltod und Wundheilungsfähigkeit von tubulären Epithelzellen führt und somit einen Schutz gegen ischämische ANV bietet. Daher ist die Rolle von Regnase3 in Nierenschäden stark von Standort und Zelllinie abhängig, was letztendlich den schädlichen oder nutzbringenden Einfluss auf Nierenschäden bestimmt.Acute kidney injury (AKI) is a prevalent yet severe condition that occurs in clinical settings. It is characterized by a sudden decline in kidney function, as indicated by an increase in serum creatinine (Scr) levels and a decrease in urine output, or both. The prognosis for AKI is poor, with many patients progressing to acute kidney disease, chronic kidney disease (CKD), and even end-stage kidney disease especially in those who were admitted to the intensive care unit. This not only negatively impacts patients' quality of life but also increases the burden on family caregivers and medical costs. Despite this, there are currently no effective preventive or therapeutic measures for AKI, with only dialysis and supportive medical care being available.
Ribonucleic acid (RNA)-binding proteins (RBPs) are a class of proteins that play a vital role in regulating gene expression and have been implicated in a wide range of diseases. These proteins possess the ability to bind and target multiple transcripts, forming intricate regulatory networks that are crucial for maintaining cellular integrity. Recent studies have revealed that a number of RBPs are involved in AKI, including the cold inducible RNA binding protein, human antigen R, Pumilio, and Y-box binding protein. Regnase3 is a member of the Regnase RBPs family and has been shown to promote inflammation by simultaneously increasing TNF in macrophages and repressing IL6 in plasmacytoid dendritic cells. Despite this knowledge, the full extent of the role played by Regnase3 in AKI remains largely unknown. Therefore, we hypothesized that Regnase3 plays a role in both macrophages and tubular epithelial cells, influencing inflammation and tubular repair in AKI.
In order to investigate the potential role of Regnase3 in kidney injury, a series of genetically-modified mice were developed on the C57BL/6J genetic background. These mice included the paired box gene 8 (Pax8)-reverse tetracycline transactivator (rTtA, Pax8rTtA), tetracycline resistance protein (TetO)-Cre (TetOCre), transgenic receptor activator of nuclear factor kappa-Β (Rank)-Cre (RankCre), and Regnase3 floxed (Regnase3fl/fl) mice. Using these genetically modified mice, we applied a range of experimental animal models to study the effects of Regnase3 on kidney injury, including unilateral kidney ischemia-reperfusion surgery with or without nephrectomy and nephrocalcinosis-related kidney injury. Additionally, we employed in vitro models utilizing primary cells to study Regnase3 on the cellular level. Furthermore, we utilized scRNA-seq and RNA-seq to investigate the underlying mechanisms of Regnase3's function.
We conducted a thorough investigation and discovered that the Regnase3 is highly expressed in macrophages located within the kidney after AKI. We observed that the expression levels of Regnase3 positively correlated with the functions of phagocytosis, chemokines, and monocyte maturation. Furthermore, Rank-Regnase3 mice suffered from more inflammation and kidney injury after AKI, characterized by an increase in CCR2 positive leukocyte infiltration when compared to the wildtype control group. Additionally, in vitro experiments revealed that Regnase3 is involved in modulating macrophage behavior, acting as a regulator of macrophage polarization towards an M1 and M2 phenotype and influencing the capacity of cell migration. These findings indicate that Regnase3 is essential in the migration of macrophages after AKI, which contribute to both early phase inflammation and progression towards AKI-CKD.
Next, we aimed to examine the role of Regnase3 in the context of kidney and renal tubule injury. We observed that Regnase3 is highly expressed in healthy renal tubules, but its expression is significantly reduced following injury. Through in vivo and in vitro experiments, we found that Regnase3 controls early apoptosis, cell death, proliferation, and wound healing capability of tubular epithelial cells. These effects contribute to kidney injury in postischemic kidneys. Additionally, we discovered that the deletion of Regnase3 provides protection against ischemic AKI. Mechanistically, Regnase3 targets pre-RNA and modulates alternative splicing by increasing the proportion of targeted skipped exon events and decreasing the probability of targeted retained intron events. Overall, our findings indicate that Regnase3 plays a vital role in tubular epithelial cells in the response to kidney injury by regulating alternative splicing.
In summary, our findings indicate that Regnase3 contributes to kidney injury in postischemic kidneys. However, the impact of Regnase3 on kidney injury is contingent upon the specific cell lineage in question. Our research demonstrates that the deletion of Rank-Regnase3 leads to an exacerbation of kidney injury by increasing macrophage recruitment, whereas the deletion of Pax8-Regnase3 leads to an improvement in kidney injury through its effects on cell death and wound healing capability of tubular epithelial cells, providing protection against ischemic AKI. Therefore, the role of Regnase3 in kidney injury is highly dependent on the cell lineage, which ultimately determines the detrimental or beneficial impact on kidney injury
Effektivität von oral verabreichtem GS-441524 zur Behandlung von Katzen mit feliner infektiöser Peritonitis
Get PDFCellular and molecular mechanisms of tissue repair by fascia
Get PDFAging is an important factor affecting wound healing in the skin. Former research demonstrated that wound healing progresses slowly and is delayed in aging skin compared to adolescent skin. Aged and injured skin also tends to develop into chronic wounds, and that removing senescent cells from the skin can accelerate wound healing(Wilkinson and Hardman, 2020; Yousefzadeh et al., 2018). However, it has also been shown that senescent cells in the skin contribute to wound healing, ultimately leading to the formation of smaller scars. Therefore, it is unclear what the exact mechanism of aging is in affecting wound healing. In this study, we explored the differences and mechanisms between young and aged skin wounds using in vitro skin culture techniques, in vivo skin wound models, skin chimeric grafting experiments, in vitro cell transplantation experiments, real-time imaging techniques, three-dimensional imaging techniques, immunofluorescence staining and histological staining. The cumulative data indicates that the differences in wound healing dynamics between aged and young skin are due to the heterogeneity of fascia fibroblasts. Specifically, the differentiation capacity of fascia fibroblasts is greatly reduced in aging skin, leading to a decrease in fascia contractility and transport into wounds, which ultimately leads to slow skin wound closure and delayed wound healing. The use of a Wnt Signaling agonist (CHIR) can reactivate the differentiation capacity of aged fibroblasts, increasing the contractility capacity of aged fascia, accelerating the closure of aged wounds, and promoting wound healing. These finding explains how wound healing is slowed down during aging, revealing Wnt signaling can activate or reprogram aged fascial fibroblasts to promote wound healing, and provides a new basic research and translational perspectives to accelerate and improve wound healing of aged skin
Property prediction of energetic materials with the “Research output software for energetic materials based on observational modelling” RoseBoom©
Get PDFSince 2020, which is when the author of this thesis collected her first experiences with energetic materials 16.500 articles were published and registered by google scholar on “synthesis of new energetic materials”. This level of productivity and access to vast amounts of information was previously unheard of. In the early 1980s, home computers were just becoming possible and very few people had mobile phones. Researchers now face the challenge of sifting through a vast amount of information, with the crucial questions being about its reliability and practical use.
This thesis presents several innovations that enable researchers to access information from the literature in a selective and automated way. These innovations also allow for comparison using established models, leading to informed decisions made by experts.
The first chapter of this research serves as a comprehensive introduction to the concept of RoseBoom© and provides two examples of the application of RoseBoom© reported in literature. Chapter two delves into the development of RoseBoom©, a program that encapsulates the key discoveries of this research. The subsequent chapters consist of papers that provide detailed explanations of essential aspects of the study. Finally, the last chapter explores the wider scope of opportunities for advancing this field.
In this thesis machine learning models, empirical models, and thermo-equilibrium codes are thoroughly tested and evaluated for the prediction of energetic materials. The limits and advantages of each method are carefully evaluated and should be considered. In Chapter 1.6, the experimental situation is assessed. An overview of various measurement techniques for detonation parameters is provided, along with recent research on using modeling tests with simpler experimental setups as an alternative method. Furthermore, the deviations in experimental measurements of detonation pressures have been analyzed. Chapter 1.7 provides a comparison of various unclassified software solutions for energetic materials, including RoseBoom©. These solutions compete in eight categories and are ranked based on the points they receive.
The fundamental concept of RoseBoom© is presented in Chapter 2.3. A thorough evaluation of empirical models for energetic materials presented in the literature is given in Chapter 2.1., which was revalidated for novel energetic materials. An update for performance prediction for mixtures is given in Chapter 2.2 along with the automated input of large molecule datasets from .csv files. In Chapter 2.7 and 4.2 currently available open-source chemical structure recognition tools are investigated for implementation in RoseBoom© which further improve the user’s experience. An update to the software for rocket propellants is given in Chapter 2.4, where the specific impulses of the ISPBKW code to two empirical models are compared. Including the application programming interface to the ISPBKW code, which allows it to be easily accessed using the RoseBoom©. In Chapter 2.5, the impact on the calculated detonation parameters was investigated by comparing the use of density and heat of formation predicted by RoseBoom2.2© to those published with corresponding molecules. A range of traditional models was tested for sensitivity to input value accuracy. This highlights the need for agreement on one software for predicting energetic material performance, starting with input values. It also increases trust in RoseBoom© predictions while raising awareness of uncertainties in published performance values. This motivated the author to conduct a study in chapter 2.6 investigating the prediction of enthalpies of sublimation and vaporization, as they are required to convert an enthalpy of formation value obtained from a gas phase calculation into a room temperature state.
The study presented in Chapter 1.5 aimed to determine whether complex machine learning models are necessary to predict material properties or if simple linear regression models can provide accurate predictions of thermochemical properties and density. The study analysed Joback's method in combination with statistical models, as well as the density predictions of Holden, Keshavarz, and Bondarchuk. Updated group increment tables for Joback's method were also included in the analysis. In the same chapter, a correlation between the plate dent test and Chapman-Jougett detonation pressure is presented, which would be an excellent candidate for lab-scale performance testing of novel energetic materials. Further studies like this are presented in Chapter 3 including the Ballistic Mortar test, the Trauzl Test, and the SSRT-Test. Chapter 4.1 is an example where some of the computational methods used in this thesis were applied to real-life problems
Astrocytic diazepam binding inhibitor instructs microglial synaptic engulfment in Lewy body dementia
Get PDFIn Lewy body dementia (LBD), loss of synapses is associated with reactive astrocytes and activated microglia. However, the interaction between these two major glial cell types and the subsequent implications on synaptic removal remain unclear. This study demonstrates that anomalous secretion of astrocyte-derived diazepam binding inhibitor (DBI), an endogenous ligand of the 18 kDa translocator protein (TSPO), facilitates excessive microglial phagocytosis of synaptic materials in a mouse model of LBD and in postmortem brains of patients with LBD-associated dementia. Additionally, evidence is presented suggesting that the decline of synaptic plasticity in LBD-associated dementia is dependent on the astrocytic DBI-microglial TSPO signaling pathway, as it can be mitigated by DBI knock-down or TSPO knock-out. These findings emphasize the significance of astrocyte-microglia interaction in regulating synaptic plasticity and propose the non-neuronal DBI-TSPO signaling pathway between these glial cells as potential therapeutic targets to improve synaptic pathology in LBD-associated dementia
Stress as a mediator of overeating and the effectiveness of mindfulness training as an intervention strategy
Get PDFProlonged exposure to stress implicates the physiological system, which can have adverse effects on many health-related domains, including eating behavior. As the global prevalence of chronic stress continues to rise, it is imperative to investigate an intervention to reduce stress and its accompanying diseases. Stress-induced overeating, for example, can lead to the accumulation of visceral fat tissue, thereby increasing the risk of developing metabolic and cardiovascular diseases such as type 2 diabetes and hypertension. Stress-eating can, therefore, not only severely impact physiological health but can also greatly reduce an individual’s quality of life. Mindfulness meditation, through its ability to regulate emotions and increase interoceptive awareness, could serve as a candidate to reduce stress as well as its subsequent maladaptive eating behavior. As the effects of stress and mindfulness can be observed on the behavioral and neuronal levels, the main aims of this dissertation project were threefold: 1) proof of concept: conduct a clinical trial to investigate the effectiveness of web-based mindfulness training and observe its corresponding neural correlates 2) identify the neural processing nodes fundamental for the sensory perception of food stimuli 3) conduct a clinical trial to investigate the effectiveness of a web-based, food-related, mindfulness training on stress-eating and observe its corresponding neural correlates.
The results of this dissertation project were able to demonstrate mindfulness training-induced reductions in stress and anxiety, as well as increases in perceived mindfulness, flow state, and attention. Additionally, the results were able to provide initial insight into the application of web-based mindfulness training as an intervention for stress-eating behavior through the observed reductions in perceived food cravings as well as stress- and emotional-eating tendencies. Furthermore, changes observed on the behavioral level were accompanied by changes on the neuronal level thereby emphasizing the effectiveness of mindfulness training as an intervention strategy. Moreover, through the completion of an extensive meta-analysis, this dissertation was able to identify the neural processing nodes of the functional olfactory cortex, the results of which were utilized in subsequent neuroimaging analyses within the scope of this project.
In summary, this dissertation provides initial evidence of the effectiveness of web-based mindfulness training as an intervention strategy for stress as well as stress-eating behavior and should be considered for therapeutic or preventative treatment programs
Die Kunst der Beobachtung und die Beobachtung der Kunst
Get PDFErstmals wird die Darstellung kranker Kinder anhand von Werken der bildenden Kunst systematisch untersucht, bei denen man aufgrund des heutigen medizinischen Wissens medizinische Diagnosen stellen kann. Dies umfasst sowohl angeborene Erkrankungen (Ambras Syndrom, Angelman Syndrom, Epilepsie und Hydrocephalus, Herzfehler, Kleinwuchs, Prader-Willi Syndrom, siamesische Zwillinge und Trisomie 21) als auch Infektionskrankheiten (Croup, Diphtherie, Kinderlähmung, Mumps, Pest, Pocken, Sepsis, spanische Grippe, Syphilis, Tuberkulose und Typhus).
Es wurden Kunstwerke mit Kinderdarstellungen aus der Antike, dem Mittelalter, der Renaissance, dem Barock sowie dem 18., 19. und 20. Jahrhundert untersucht. Zu den analysierten Werken gehören unter anderem solche von Dürer, Mantegna, Raphael, Rubens, Velázquez, Rembrandt, Tiepolo, Murillo, Goya, Gauguin, Picasso und Dix. Dabei wurde die von Sir William Osler, einem Pionier der klinischen Medizin, entwickelte „Blickdiagnose“ angewendet.
Durch die Untersuchung der Kunstwerke unter einem medizinischen Blickwinkel werden neue Zusammenhänge zwischen der Geschichte der bildenden Kunst und der Geschichte der Medizin aufgezeigt, die für Kunsthistoriker genauso von Interesse sind wie für Mediziner.
Michael Vogel studierte Medizin an der Universität Münster. Die Promotion erfolgte 1979. 1989 Habilitation im Fach Kinderheilkunde an der Ludwig-Maximilians-Universität München, 1998 Ernennung zum außerplanmäßigen Professor. Nach Beendigung der ärztlichen Tätigkeit seit 2019 Studium der Kunstgeschichte an der LMU mit anschließender Promotion 2023.A systematic analysis of the presentation of sick children in artworks by making a medical diagnosis according to the contemporary medical knowledge is provided. The diagnoses include hereditary diseases such as Ambras syndrome, epilepsia and hydrocephalus, congenital heart disease, short stature, conjoined twins and trisomy 21 as well as infectious diseases like croup, diphtheria, mumps, plague, polio, smallpox, sepsis, Spanish flu, syphilis, tuberculosis and typhoid fever. Paintings and sculptures with presentation of children from antiquity, middle ages, renaissance, baroque, as well as from the 18th, 19th and 20th century were examined. Some of those analysed artworks were produced by Duerer, Mantegna, Raphael, Rubens, Velázquez, Rembrandt, Tiepolo, Murillo, Goya, Gauguin, Picasso and Dix. By examining art works applying a medical knowledge (a method pioneered by Sir William Osler) new relations between the history of medicine and art history could be discovered which are of interest to art historians as well as medical doctors.
Michael Vogel studied Medicine at Münster University. He graduated as MD in 1979. In 1989 he wrote his PhD thesis in paediatrics and in 1998 he became professor of paediatrics. He stopped practising paediatrics in 2019, studied art history and wrote his doctoral thesis in art history in 2023
Ich seh‘ doch so, wie du nicht siehst!
Get PDFVisuelle Wahrnehmungsstörungen bei Kindern und Jugendlichen im Sinne eines CVI (cerebral visual impairment) führen zu erheblichen Einschränkungen im schulischen und alltäglichen Verhalten. Häufig betroffen sind die visuelle Exploration und Suche sowie die visuelle Wort- und Textverarbeitung. Dies führt im (Schul-)Alltag zu Schwierigkeiten im visuellen Überblick und Lesen.
Die vorliegende Studie präsentiert Erkenntnisse zur Förderung von Kompensationsstrategien bei diesen Beeinträchtigungen. An einer Stichprobe von 61 Kindern und Jugendlichen im Alter von sechs bis 17 Jahren wurden Wirksamkeit und Spezifität zweier standardisierter, spezifischer und software-basierter Trainingsprogramme für die Teilleistungen visueller Überblick und visuelle Wort- und Textverarbeitung evaluiert.
Auf Grundlage des prozeduralen Lernens führten die Trainingsprogramme zu signifikanten Verbesserungen in der Genauigkeit und Geschwindigkeit des visuellen Suchverhaltens sowie der visuellen Wort- und Textverarbeitung. Diese Fortschritte wurden auch im Alltag subjektiv von den Kindern, Jugendlichen und Eltern erkannt. Die Förderungen bieten somit eine wertvolle Unterstützung für die leichtere Bewältigung des (Schul-)Alltags und tragen zur Verbesserung der psychischen Gesundheit von Kindern und Jugendlichen mit CVI bei.
Anna Myriam Lippenberger studierte Psychologie an der Ludwig-Maximilians-Universität (LMU) München sowie an der Université de Montréal und promovierte im Schwerpunkt Klinische Neuropsychologie. Sie war wissenschaftliche Mitarbeiterin an der LMU sowie Stipendiatin des Cusanuswerks, Bischöfliche Studienförderung. Sie leitet die CVI-Beratungsstelle am Sehbehinderten- und Blindenzentrum Südbayern.Visual perception disorders in children and adolescents with CVI (cerebral visual impairment) lead to significant limitations in academic and everyday behavior. Frequently affected subskills include visual exploration and search, as well as visual word and text processing. This results in difficulties with visual overview and reading.
The present study provides insights into promoting compensatory strategies for these impairments. In a sample of 61 children and adolescents aged six to 17 years, the effectiveness and specificity of two standardized, specific, and software-based training programs for visual overview and visual word and text processing were evaluated.
Based on procedural learning, the trainings led to significant improvements in the accuracy and speed of visual search behavior, as well as visual word and text processing. These improvements were also subjectively observed in daily life by the children, adolescents, and parents. The interventions thus provide valuable support for easier management of (academic) life and contribute to improving the mental health of children and adolescents with CVI.
Anna Myriam Lippenberger studied psychology at Ludwig Maximilian University (LMU) Munich, as well as at the Université de Montréal, and obtained her PhD with a focus on clinical neuropsychology. She worked as a research associate at LMU and was a Cusanuswerk scholarship recipient. She heads the CVI counseling center at the Center for the Visually Impaired and Blind in Southern Bavaria
