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Interaktionale Bibeldidaktik initiiert Praktiken und Prozesse der Selbst-Einschrei-bung in Bibeltexte. Im Kontext einer zunehmend visuell geprägten Gesellschaft, die sich für SchülerInnen im Raum von Social Media-Plattformen vollzieht, stel-len sich auch an die Religionsdidaktik im Kontext einer mediatisierten Gesell-schaft neue Herausforderungen, die in diesem Beitrag für die textgebundene Bibeldidaktik aktualisiert werden. Wie erfahren und verstehen SchülerInnen bibli-sche Texte und Erzählungen und deren Deutungsmuster heute und wie beziehen sie ihre Lebenswelt mit ein? Wie vollziehen sie visuelle Prozesse der Selbstein-schreibung? Welche semantische bzw. analytisch-reflexive Kompetenz bringen SchülerInnen in Bezug auf zeichenhafte Kommunikation durch Selfies mit und wenden sie an? Für diesen Beitrag werden visuelle Erzeugnisse (Bilder, Texte) von zwei SchülerInnengruppen mit der dokumentarischen Methode analysiert und mit ihren in der unterrichtlichen Präsentation vollzogenen Selbstdeutungen trianguliert, um implizite theologische Denkmuster von SchülerInnen Bilder zu rekonstruieren und zugleich deren Fragen und Leerstellen offenzulegen.

Material transfer is an essential form of intercellular communication to exchange information and resources between cells. Material transfer between neurons and from glia to neurons has been demonstrated to support neuronal survival and activity. Understanding the extent of material transfer in the healthy nervous system is limited. Here we report that in the mouse central nervous system (CNS), neurons receive nuclear and ribosomal material of Sox10-lineage cell (SOL) origin. We show that transfer of SOL-derived material to neurons is region dependent, establishes during postnatal brain maturation, and dynamically responds to LPS-induced neuroinflammation in the adult mouse brain. We identified satellite oligodendrocyte-neuron pairs with loss of plasma membrane integrity between nuclei, suggesting direct material transfer. Together, our findings provide evidence of regionally coordinated transfer of SOL-derived nuclear and ribosomal material to neurons in the mouse CNS, with potential implications for the understanding and modulation of neuronal function and treatment of neurological disorders.

BackgroundOligodendrocytes are a type of glial cells that synthesize the myelin sheath around the axons and are critical for the nerve conduction in the CNS. Oligodendrocyte death and defects are the leading causes of several myelin disorders such as multiple sclerosis, progressive multifocal leukoencephalopathy, periventricular leukomalacia, and several leukodystrophies. Temporal activation of the Sonic Hedgehog (SHH) pathway is critical for the generation of oligodendrocyte progenitors, and their differentiation and maturation in the brain and spinal cord during embryonic development in mammals.MethodsOur protocol utilized adherent cultures of human induced pluripotent stem cells (iPSC) and human embryonic stem cells (hESCs) with a green fluorescent protein (GFP) reporter knocked into one allele of the OLIG2 gene locus, dual SMAD inhibition, and transient partial inhibition of glioma-associated oncogene 1 (GLI1) by the small molecule GANT61 during the formation of the SOX2/PAX6-positive neural stem cells (NSCs). The SHH pathway was later restimulated by a Smoothened agonist purmorphamine to induce the generation of OLIG2 glial precursors. One hundred ninety-two individual oligodendrocyte precursor cells (OPCs) from GANT61 and control group were analyzed by single-cell RNA sequencing (RNA-Seq).ResultsWe demonstrate here that transient and partial inhibition of the SHH pathway transcription factor GLI1 in NSCs by a small molecule inhibitor GANT61 was found to generate OPCs that were more migratory and could differentiate earlier toward myelin-producing oligodendrocytes. Single-cell transcriptomic analysis (RNA-Seq) showed that GANT61-NSC-derived oligodendrocyte precursor cells (OPCs) had differential activation of some of the genes in the cytoskeleton rearrangement pathways that are involved in OPC motility and induction of maturation. At the protein level, this was also associated with higher levels of myelin-specific genes in the GANT61 group compared to controls. GANT61-NSC-derived OPCs were functional and could generate compact myelin in vitro and in vivo after transplantation in myelin-deficient shiverer mice.ConclusionsThis is a small molecule-based in vitro protocol that leads to the faster generation of functional oligodendrocytes. The development of protocols that lead to efficient and faster differentiation of oligodendrocytes from progenitors provides important advances toward the development of autologous neural stem cell-based therapies using human iPSCs.

The mitochondrial translocator protein (TSPO) has been implicated in CNS diseases. Here, we sought to determine the specific role of TSPO in experimental autoimmune encephalomyelitis (EAE), the most studied animal model of multiple sclerosis (MS). To fundamentally elucidate the functions of TSPO, we first developed a viable TSPO knockout mouse. A conditional TSPO knockout mouse was generated by utilizing the Cre-Lox system. We generated a TSPO floxed mouse, and then crossed this mouse with a Cre recombinase expressing mouse driven by the human glial fibrillary acidic protein (hGFAP) promoter. The resultant mouse was a neural linage line specific TSPO knockout. The loss of TSPO in the CNS did not result in overt developmental defects or phenotypes. The TSPO-/- mouse showed a decrease in GFAP expression, correlating with a decrease in astrogliosis in response to neural injury during EAE. This decrease in astrogliosis was also witnessed in the lessening of severity of EAE clinical scoring, indicating an in vivo functional role for TSPO in suppressing EAE. The TSPO-/- mouse could be a useful tool in better understanding the role of TSPO in CNS disease, and our results implicate TSPO as a potential therapeutic target in MS.

The contribution gives insights into a comparative linguistic textbook analysis of two Austrian Catholic Religious Education (RE) textbooks for colleges for higher vocational schools (‘BHS’) and vocational schools for apprentices (‘VocEd’). Gender constructions are still a desideratum in RE textbook research in Austria. Previous gender-oriented analyses mostly used qualitative content analysis or mainly questionnaires. This paper followed the approach of linguistic textbook analysis addressing gender constructions on a linguistic level by comparing both textbooks, asking which and how two selected chapters of Austrian RE textbooks in use construct gender on a linguistic level. A discussion of the main results, considering previous gender sensitive RE research, aimed to develop criteria for prospects of action with teaching materials in the current context of plurality of genders and sexualities in a democratic society. [ABSTRACT FROM AUTHOR]

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Multiple sclerosis (MS) is a chronic autoimmune demyelinating disease with high variability of clinical symptoms. In most cases MS appears as a relapsing-remitting disease course that at a later stage transitions into irreversible progressive decline of neurologic function. The mechanisms underlying MS progression remain poorly understood. Experimental autoimmune encephalomyelitis (EAE) is an animal model of MS. Here we demonstrate that mice that develop mild EAE after immunization with myelin oligodendrocyte glycoprotein 35-55 are prone to undergo clinical progression around 30 days after EAE induction. EAE progression was associated with reduction in CD11c + microglia and dispersed coalescent parenchymal infiltration. We found sex-dependent differences mediated by p38α signaling, a key regulator of inflammation. Selective reduction of CD11c + microglia in female mice with CD11c-promoter driven p38α knockout correlated with increased rate of EAE progression. In protected animals, we found CD11c + microglia forming contacts with astrocyte processes at the glia limitans and immune cells retained within perivascular spaces. Together, our study identified pathological hallmarks of chronic EAE progression and suggests that CD11c + microglia may regulate immune cell parenchymal infiltration in autoimmune demyelination., (Copyright © 2021 The Authors. Published by Elsevier Inc. All rights reserved.)