Subjective workload measurement of the transition from a conventional operative microscope to a Robotic Digital Microscope. A pilot study.

•Evaluate the subjective workload for transition of an experienced neurosurgeon from a conventional operative microscope /OPMI/ to a Robotic Digital Microscope /RDM/.•Show a single center initial experience of the use an exoscope.•The exoscope improves ergonomics.

A directional Wnt/beta-catenin-Sox2-proneural pathway regulates the transition from proliferation to differentiation in the Xenopus retina.

Progenitor cells in the central nervous system must leave the cell cycle to become neurons and glia, but the signals that coordinate this transition remain largely unknown. We previously found that Wnt signaling, acting through Sox2, promotes neural competence in the Xenopus retina by activating proneural gene expression. We now report that Wnt and Sox2 inhibit neural differentiation through Notch activation.

[Examination of behavioral reaction in hyperactive children with attention deficit syndrome using software-hardware systems Binatest and SVET].

The problem of instrumental examination of children with socially important psychoneurological disorders (attention deficit syndrome and hyperactivity) is considered.

Frizzled 5 signaling governs the neural potential of progenitors in the developing Xenopus retina.

Progenitors in the developing central nervous system acquire neural potential and proliferate to expand the pool of precursors competent to undergo neuronal differentiation. The formation and maintenance of neural-competent precursors are regulated by SoxB1 transcription factors, and evidence that their expression is regionally regulated suggests that specific signals regulate neural potential in subdomains of the developing nervous system. We show that the frizzled (Fz) transmembrane receptor Xfz5 selectively governs neural potential in the developing Xenopus retina by regulating the expression of Sox2.

Prion protein fate governed by metal binding.

The conversion of the normal cellular prion protein to an abnormal isoform is considered to be causal to the prion diseases or transmissible spongiform encephalopathies. The prion protein is a copper binding protein but under some conditions may bind other metals. In particular, the binding of manganese has been suggested to convert the prion protein (PrP) to a protease resistant isoform.