Fab Lab @ School: Digitale Fertigungstechnologien im Unterricht

Ein Fab Lab ist die moderne Form einer offenen Werkstatt. Interessierten stehen eine Reihe an Design- und Fertigungsmöglichkeiten mit den entsprechenden Geräten (3D-Drucker, Lasercutter, CNC-Fräse, etc.) zur Verfügung, um eigene kreative Ideen umsetzen zu können. Ziel des Projekts "Fab@School" ist es, die digitalen Design- und Fertigungstechnologien eines Fab Labs nachhaltig in die vorschulische und schulische Ausbildung zu integrieren. Gemeinsam mit den Projektpartnern werden Workshops für PädagogInnen und SchülerInnen ausgearbeitet und in einer Pilotphase in ausgewählten Bildungseinrichtungen durchgeführt

"LUSTration" - operative Instrumente gegen den Mythos Fortschritt

Wissenschaftliches Kolloquium vom 27. bis 30. Juni 1996 in Weimar an der Bauhaus-Universität zum Thema: ‚Techno-Fiction. Zur Kritik der technologischen Utopien

Probing the momentum relaxation time of charge carriers in ultrathin semiconductor layers

We report on a terahertz time-domain technique for measuring the momentum relaxation time of charge carriers in ultrathin semiconductor layers. The phase sensitive modulation technique directly provides the relaxation time. Time-resolved THz experiments were performed on n-doped GaAs and show precise agreement with data obtained by electrical characterization. The technique is well suited for studying novel materials where parameters such as the charge carriers' effective mass or the carrier density are not known a priori

Stress-induced TRAILR2 expression overcomes TRAIL resistance in cancer cell spheroids

The influence of 3D microenvironments on apoptosis susceptibility remains poorly understood. Here, we studied the susceptibility of cancer cell spheroids, grown to the size of micrometastases, to tumor necrosis factor-related apoptosis-inducing ligand (TRAIL). Interestingly, pronounced, spatially coordinated response heterogeneities manifest within spheroidal microenvironments: In spheroids grown from genetically identical cells, TRAIL-resistant subpopulations enclose, and protect TRAIL-hypersensitive cells, thereby increasing overall treatment resistance. TRAIL-resistant layers form at the interface of proliferating and quiescent cells and lack both TRAILR1 and TRAILR2 protein expression. In contrast, oxygen, and nutrient deprivation promote high amounts of TRAILR2 expression in TRAIL-hypersensitive cells in inner spheroid layers. COX-II inhibitor celecoxib further enhanced TRAILR2 expression in spheroids, likely resulting from increased ER stress, and thereby re-sensitized TRAIL-resistant cell layers to treatment. Our analyses explain how TRAIL response heterogeneities manifest within well-defined multicellular environments, and how spatial barriers of TRAIL resistance can be minimized and eliminated

Fetal microglial phenotype in vitro carries memory of prior in vivo exposure to inflammation

Objective. Neuroinflammation in utero may result in life-long neurological disabilities. The molecular mechanisms whereby microglia contribute to this response remain incompletely understood. Methods. Lipopolysaccharide (LPS) or saline were administered intravenously to non-anesthetized chronically instrumented near-term fetal sheep to model fetal inflammation in vivo. Microglia were then isolated from in vivo LPS and saline (naïve) exposed animals. To mimic the second hit of neuroinflammation, these microglia were then re-exposed to LPS in vitro. Cytokine responses were measured in vivo and subsequently in vitro in the primary microglia cultures derived from these animals. We sequenced the whole transcriptome of naïve and second hit microglia and profiled their genetic expression to define molecular pathways disrupted during neuroinflammation.Results. In vivo LPS exposure resulted in IL-6 increase in fetal plasma 3 h post LPS exposure. Even though not histologically apparent, microglia acquired a pro-inflammatory phenotype in vivo that was sustained and amplified in vitro upon second hit LPS exposure as measured by IL-1β response in vitro and RNAseq analyses. While NFKB and Jak-Stat inflammatory pathways were up regulated in naïve microglia, heme oxygenase 1 (HMOX1) and Fructose-1,6-bisphosphatase (FBP) genes were uniquely differentially expressed in the second hit microglia. Microglial calreticulin/LRP genes implicated in microglia-neuronal communication relevant for the neuronal development were up regulated in second hit microglia.Discussion. We identified a unique HMOX1down and FBPup phenotype of microglia exposed to the double-hit suggesting interplay of inflammatory and metabolic pathways as a memory of prior inflammatory insult. These findings suggest new therapeutic targets for early postnatal intervention to prevent brain injury