The differential list of HCBS should be expanded to include SCA7 and SCA8. The elucidation of frequency of HCBS in various SCA subtypes may help prioritize the genetic testing in late-onset dominant ataxia.
A hybrid core–shell material based on carbon nanofibers and a 2D conductive metal–organic framework has been fabricated into a flexible free-standing membrane as an electrode material for supercapacitors.
Co-electrospinning
is a new branch of nanotechnology for producing
composite nanofibers with collective functions and special fiber structures.
Helical fibers in nanoscale have been of increasing interest because
of their unique characteristics. In this work, we report the fabrication
of the helical nanofibers with polyurethane and poly(m-phenylene isophthalamide) by the co-electrospinning system with
an off-centered core–shell spinneret. High-speed photography
and three-dimensional (3D) electric field simulation are carried out
to help in understanding the formation of the helical structures.
The asymmetrical electric field distribution may be a factor affecting
helical fiber formation. We also show that a series of factors such
as the applied voltage, the conductivity of the system, and the composite
ratio have considerable effects on the morphologies of the produced
helical nanofibers. This work can provide a promising technique for
producing nanofibrous nonwovens with helical fiber morphology.
We recommended botulinum toxin as the optimal intervention for multiple sclerosis-related spasticity. Cannabinoids and transcutaneous electric nerve stimulation could also be considered as multiple sclerosis-related spasticity treatments but their safety remained to be verified.
Organ hypertrophy can result from enlargement of individual cells or from cell proliferation or both. Activating mutations in the serine-threonine kinase Raf cause cardiac hypertrophy and contribute to Noonan syndrome in humans. Cardiac-specific expression of activated Raf also causes hypertrophy in Drosophila melanogaster. We found that Yorkie (Yki), a transcriptional coactivator in the Hippo pathway that regulates organ size, is required for Raf-induced cardiac hypertrophy in flies. Although aberrant activation of Yki orthologs stimulates cardiac hyperplasia in mice, cardiac-specific expression of an activated mutant form of Yki in fruit flies caused cardiac hypertrophy without hyperplasia. Knockdown of Yki caused cardiac dilation without loss of cardiomyocytes and prevented Raf-induced cardiac hypertrophy. In flies, Yki-induced cardiac hypertrophy required the TEA domain–containing transcription factor Scalloped, and, in mammalian cells, expression of mouse RafL613V, an activated form of Raf with a Noonan syndrome mutation, increased Yki-induced Scalloped activity. Furthermore, overexpression of Tgi (a Tondu domain–containing Scalloped-binding corepressor) in the fly heart abrogated Yki- or Raf-induced cardiac hypertrophy. Thus, crosstalk between Raf and Yki occurs in the heart and can influence Raf-mediated cardiac hypertrophy.
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