Changing stroke rehab and research worldwide now.Time is Brain! trillions and trillions of neurons that DIE each day because there are NO effective hyperacute therapies besides tPA(only 12% effective). I have 523 posts on hyperacute therapy, enough for researchers to spend decades proving them out. These are my personal ideas and blog on stroke rehabilitation and stroke research. Do not attempt any of these without checking with your medical provider. Unless you join me in agitating, when you need these therapies they won't be there.

What this blog is for:

My blog is not to help survivors recover, it is to have the 10 million yearly stroke survivors light fires underneath their doctors, stroke hospitals and stroke researchers to get stroke solved. 100% recovery. The stroke medical world is completely failing at that goal, they don't even have it as a goal. Shortly after getting out of the hospital and getting NO information on the process or protocols of stroke rehabilitation and recovery I started searching on the internet and found that no other survivor received useful information. This is an attempt to cover all stroke rehabilitation information that should be readily available to survivors so they can talk with informed knowledge to their medical staff. It lays out what needs to be done to get stroke survivors closer to 100% recovery. It's quite disgusting that this information is not available from every stroke association and doctors group.

Saturday, January 6, 2018

A Novel Short Isoform of Cytosolic PSD-95 Interactor (Cypin) Regulates Neuronal Development

We need dendritic branching post stroke so go ask your doctor what researchers they are working with to bring this research to translational intervention. Doing nothing should result in being fired.
https://link.springer.com/article/10.1007/s12035-017-0849-z
  • Mihir V. Patel
  • Przemyslaw Swiatkowski
  • Munjin Kwon
  • Ana R. Rodriguez
  • Keith Campagno
  • Bonnie L. Firestein
  • Mihir V. Patel
    • 1
    • 2
  • Przemyslaw Swiatkowski
    • 1
    • 3
  • Munjin Kwon
    • 1
    • 3
  • Ana R. Rodriguez
    • 1
    • 4
  • Keith Campagno
    • 1
  • Bonnie L. Firestein
    • 1
  1. 1.Department of Cell Biology and NeuroscienceRutgers University (USA)PiscatawayUSA
  2. 2.Graduate Program in NeurosciencesRutgers University (USA)New BrunswickUSA
  3. 3.Graduate Program in Molecular BiosciencesRutgers University (USA)New BrunswickUSA
  4. 4.Graduate Program in Biomedical EngineeringRutgers University (USA)New BrunswickUSA
Article
First Online: 02 January 2018

Abstract

The guanine deaminase cypin (cytosolic PSD-95 interactor) binds to PSD-95 (postsynaptic density protein 95) and regulates dendrite branching by promoting microtubule polymerization. Here, we identify a novel short isoform of cypin, termed cypinS, which is expressed in mouse and human, but not rat, tissues. Cypin and cypinS mRNA and protein levels peak at P7 and P14 in the mouse brain, suggesting a role for these isoforms during development. Interestingly, although cypinS lacks guanine deaminase activity, overexpression of cypinS increases dendrite branching. This increase occurs further away from soma than do increases resulting from overexpression of cypin. In contrast, overexpression of cypin, but not cypinS, decreases dendritic spine density and maturity. This suggests that changes to spines, but not to dendrites, may be dependent on guanine deaminase activity. Furthermore, overexpression of either cypin or cypinS increases miniature excitatory postsynaptic current (mEPSC) frequency, pointing to a presynaptic role for both isoforms. Interestingly, overexpression of cypinS results in a significantly greater increase in frequency than does overexpression of cypin. Thus, cypin and cypinS play distinct roles in neuronal development.

Keywords

Cypin Neuron Dendrite Dendritic spine Morphology Electrophysiology Cell culture 
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