University of Tübingen

About: University of Tübingen is a education organization based out in Tübingen, Germany. It is known for research contribution in the topics: Population & Immune system. The organization has 40555 authors who have published 84108 publications receiving 3015320 citations. The organization is also known as: Eberhard Karls University & Eberhard-Karls-Universität Tübingen.

Professional Competence of Teachers: Effects on Instructional Quality and Student Development

Abstract: This study investigates teachers’ pedagogical content knowledge, professional beliefs, work-related motivation, and self-regulation as aspects of their professional competence. Specifically, it examines how these aspects impact instruction and, in turn, student outcomes. In a nationally representative sample of 194 German secondary school mathematics classes, multiple measures were used to assess teacher competence, instructional quality, and students’ achievement and motivation. The effect of teachers’ professional competence on student outcomes was estimated in a 1-year repeated-measures design. Two-level structural equation models revealed positive effects of teachers’ pedagogical content knowledge, enthusiasm for teaching, and self-regulatory skills on instructional quality, which in turn affected student outcomes. In contrast, teachers’ general academic ability did not affect their instruction. The multidimensional model of teachers’ professional competence introduced in this article seems suited to stimulate further research on the personal indicators of teacher quality.

Aβ42‐driven cerebral amyloidosis in transgenic mice reveals early and robust pathology

Abstract: We have generated a novel transgenic mouse model on a C57BL/6J genetic background that coexpresses KM670/671NL mutated amyloid precursor protein and L166P mutated presenilin 1 under the control of a neuron-specific Thy1 promoter element (APPPS1 mice). Cerebral amyloidosis starts at 6–8 weeks and the ratio of human amyloid (A)β42 to Aβ40 is 1.5 and 5 in pre-depositing and amyloid-depositing mice, respectively. Consistent with this ratio, extensive congophilic parenchymal amyloid but minimal amyloid angiopathy is observed. Amyloid-associated pathologies include dystrophic synaptic boutons, hyperphosphorylated tau-positive neuritic structures and robust gliosis, with neocortical microglia number increasing threefold from 1 to 8 months of age. Global neocortical neuron loss is not apparent up to 8 months of age, but local neuron loss in the dentate gyrus is observed. Because of the early onset of amyloid lesions, the defined genetic background of the model and the facile breeding characteristics, APPPS1 mice are well suited for studying therapeutic strategies and the pathomechanism of amyloidosis by cross-breeding to other genetically engineered mouse models.

Mechanism of calcium gating in small-conductance calcium-activated potassium channels

Abstract: The slow afterhyperpolarization that follows an action potential is generated by the activation of small-conductance calcium-activated potassium channels (SK channels) The slow afterhyperpolarization limits the firing frequency of repetitive action potentials (spike-frequency adaptation) and is essential for normal neurotransmission SK channels are voltage-independent and activated by submicromolar concentrations of intracellular calcium They are high-affinity calcium sensors that transduce fluctuations in intracellular calcium concentrations into changes in membrane potential Here we study the mechanism of calcium gating and find that SK channels are not gated by calcium binding directly to the channel alpha-subunits Instead, the functional SK channels are heteromeric complexes with calmodulin, which is constitutively associated with the alpha-subunits in a calcium-independent manner Our data support a model in which calcium gating of SK channels is mediated by binding of calcium to calmodulin and subsequent conformational alterations in the channel protein