Learning from Physics Education Research: Lessons for Economics Education

We believe that economists have much to learn from educational research practices and related pedagogical innovations in other disciplines, in particular physics education. In this paper we identify three key features of physics education research that distinguish it from economics education research - (1) the intentional grounding of physics education research in learning science principles, (2) a shared conceptual research framework focused on how students learn physics concepts, and (3) a cumulative process of knowledge-building in the discipline - and describe their influence on new teaching pedagogies, instructional activities, and curricular design in physics education. In addition, we highlight four specific examples of successful pedagogical innovations drawn from physics education - context-rich problems, concept tests, just-in-time teaching, and interactive lecture demonstrations - and illustrate how these practices can be adapted for economic education.Comment: 19 pages, 3 figures, submitted to Journal of Economic Education, also available from Social Science Research Network <http://ssrn.com/abstract=1151430

Axon fasciculation and differences in midline kinetics between pioneer and follower axons within commissural fascicles

Early neuronal scaffold development studies suggest that initial neurons and their axons serve as guides for later neurons and their processes. Although this arrangement might aid axon navigation, the specific consequence(s) of such interactions are unknown in vivo. We follow forebrain commissure formation in living zebrafish embryos using timelapse fluorescence microscopy to examine quantitatively commissural axon kinetics at the midline: a place where axon interactions might be important. Although it is commonly accepted that commissural axons slow down at the midline, our data show this is only true for leader axons. Follower axons do not show this behavior. However, when the leading axon is ablated, follower axons change their midline kinetics and behave as leaders. Similarly, contralateral leader axons change their midline kinetics when they grow along the opposite leading axon across the midline. These data suggest a simple model where the level of growth cone exposure to midline cues and presence of other axons as a substrate shape the midline kinetics of commissural axons

Learning from physics education research: Lessons for economics education

We believe that economists have much to learn from educational research practices and related pedagogical innovations in other disciplines, in particular physics education. In this paper we identify three key features of physics education research that distinguish it from economics education research - (1) the intentional grounding of physics education research in learning science principles, (2) a shared conceptual research framework focused on how students learn physics concepts, and (3) a cumulative process of knowledge-building in the discipline - and describe their influence on new teaching pedagogies, instructional activities, and curricular design in physics education. In addition, we highlight four specific examples of successful pedagogical innovations drawn from physics education - context-rich problems, concept tests, just-in-time teaching, and interactive lecture demonstrations - and illustrate how these practices can be adapted for economic education.economic education; physics education research (PER); research-based teaching; preconceptions; metacognition; transfer; context-rich problems; peer instruction; just-in-time teaching; interactive lecture demonstration

Semantic and dialogue processing in the VERBMOBIL spoken dialogue translation system

In this paper we sketch the role of semantic and dialogue processing in the Verbmobil spoken dialogue translation system. A full demonstration system is currently under development although a "mini\u27; demonstration system has been implemented

Dexamethasone leads to Zn2+ accumulation and increased unbound Zn2+ in C2C12 muscle and 3T3-L1 adipose cells

Skeletal muscle atrophy is associated with increases in circulating glucocorticoid levels and insulin resistance. Zinc accumulates in atrophic muscle, but the relationship between atrophy, insulin resistance, and Zn2+ homeostasis remains unclear. In this study, the effect of the glucocorticoid dexamethasone (DEX) on insulin and Zn2+ homeostasis was explored. Treatment of differentiated C2C12 skeletal myotubes and 3T3-L1 adipocytes with DEX significantly increased mRNA expression of the metal-binding proteins Mt1 and 2 and altered energy storage as shown by the increased size of lipid droplets in 3T3-L1 cells. In C2C12 cells the total cellular Zn2+ was higher after DEX treatment, and in both C2C12 and 3T3-L1 adipocytes, free unbound Zn2+ was increased. Insulin treatment led to a gradual increase in free Zn2+ in C2C12 cells, and no significant change in DEX-treated cells such that concentrations were similar 10 min after insulin treatment. These data demonstrate that DEX disturbs Zn2+ homeostasis in muscle and fat cells. Further study of the molecular pathways involved to identify novel therapeutic targets for treatment of skeletal muscle atrophy is warranted. © 2023 The Authors. Journal of Cellular Biochemistry published by Wiley Periodicals LLC

Mig6 haploinsufficiency protects mice against streptozotocin-induced diabetes

AIMS/HYPOTHESIS: EGF and gastrin co-administration reverses type 1 diabetes in rodent models. However, the failure of this to translate into a clinical treatment suggests that EGF-mediated tissue repair is a complicated process and warrants further investigation. Thus, we aimed to determine whether EGF receptor (EGFR) feedback inhibition by mitogen-inducible gene 6 protein (MIG6) limits the effectiveness of EGF therapy and promotes type 1 diabetes development. METHODS: We treated Mig6 (also known as Errfi1) haploinsufficient mice (Mig6 (+/-)) and their wild-type littermates (Mig6 (+/+)) with multiple low doses of streptozotocin (STZ), and monitored diabetes development via glucose homeostasis tests and histological analyses. We also investigated MIG6-mediated cytokine-induced desensitisation of EGFR signalling and the DNA damage repair response in 832/13 INS-1 beta cells. RESULTS: Whereas STZ-treated Mig6 (+/+) mice became diabetic, STZ-treated Mig6 (+/-) mice remained glucose tolerant. In addition, STZ-treated Mig6 (+/-) mice exhibited preserved circulating insulin levels following a glucose challenge. As insulin sensitivity was similar between Mig6 (+/-) and Mig6 (+/+) mice, the preserved glucose tolerance in STZ-treated Mig6 (+/-) mice probably results from preserved beta cell function. This is supported by elevated Pdx1 and Irs2 mRNA levels in islets isolated from STZ-treated Mig6 (+/-) mice. Conversely, MIG6 overexpression in isolated islets compromises glucose-stimulated insulin secretion. Studies in 832/13 cells suggested that cytokine-induced MIG6 hinders EGFR activation and inhibits DNA damage repair. STZ-treated Mig6 (+/-) mice also have increased beta cell mass recovery. CONCLUSIONS/INTERPRETATION: Reducing Mig6 expression promotes beta cell repair and abates the development of experimental diabetes, suggesting that MIG6 may be a novel therapeutic target for preserving beta cell