Increasing Student Cognitive Engagement in the Math Classroom Through Sustained Professional Development

We share the case of one teacher engaged in professional development (PD) designed to improve collective argumentation. We present an analysis of two lessons in her classroom, one before and one after her engagement with the professional development. Findings show that the classrooms differ across both teacher support for collective argumentation (requesting ideas and elaboration vs. requesting/acts and methods), and student contributions Oustifications vs. procedures and facts)

Connecting Teachers’ Buy-Into Professional Development with Classroom Habits and Practices

While professional development (PD) provides an opportunity for teachers to cultivate skills that are consistent with best practices in the field, it is their buy-into the PD that ultimately determines the effectiveness of the PD. We examined how teacher buy-in affected the classroom habits and practice of four elementary teachers who took part in a district wide PD. Using baseline and first-year implementation video recordings, in conjunction with frameworks for discourse analysis, cognitive demand, and tools built specifically to measure PD implementation, we found that varying combinations of teachers\u27 beliefs served as a mitigating factor for PD implementation

Depleting hypothalamic somatostatinergic neurons recapitulates diabetic phenotypes in mouse brain, bone marrow, adipose and retina.

Aims/hypothesisHypothalamic inflammation and sympathetic nervous system hyperactivity are hallmark features of the metabolic syndrome and type 2 diabetes. Hypothalamic inflammation may aggravate metabolic and immunological pathologies due to extensive sympathetic activation of peripheral tissues. Loss of somatostatinergic (SST) neurons may contribute to enhanced hypothalamic inflammation.MethodsThe present data show that leptin receptor-deficient (db/db) mice exhibit reduced hypothalamic SST neurons, particularly in the periventricular nucleus. We model this finding, using adeno-associated virus delivery of diphtheria toxin subunit A (DTA) driven by an SST-cre system to deplete these neurons in Sstcre/gfp mice (SST-DTA).ResultsSST-DTA mice exhibit enhanced hypothalamic c-Fos expression and brain inflammation as demonstrated by microglial and astrocytic activation. Bone marrow from SST-DTA mice undergoes skewed haematopoiesis, generating excess granulocyte-monocyte progenitors and increased proinflammatory (C-C chemokine receptor type 2; CCR2hi) monocytes. SST-DTA mice exhibited a 'diabetic retinopathy-like' phenotype: reduced visual function by optokinetic response (0.4 vs 0.25 cycles/degree; SST-DTA vs control mice); delayed electroretinogram oscillatory potentials; and increased percentages of retinal monocytes. Finally, mesenteric visceral adipose tissue from SST-DTA mice was resistant to catecholamine-induced lipolysis, displaying 50% reduction in isoprenaline (isoproterenol)-induced lipolysis compared with control littermates. Importantly, hyperglycaemia was not observed in SST-DTA mice.Conclusions/interpretationThe isolated reduction in hypothalamic SST neurons was able to recapitulate several hallmark features of type 2 diabetes in disease-relevant tissues