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.

Sunday, December 4, 2011

Growth Cone Pathfinding and Filopodial Dynamics Are Mediated Separately by Cdc42 Activation

More on growth cones. My fascination with this topic is due to my probable need to have neurogenesis work for me in order to completely recover. I won't settle for anything less.
http://neuro.cjb.net/content/22/5/1794.short
  1. Michael D. Kim1,
  2. Peter Kolodziej2, and
  3. Akira Chiba1

+ Author Affiliations

  1. 1Department of Cell and Structural Biology, University of Illinois, Urbana, Illinois 61801, and
  2. 2Department of Cell and Developmental Biology, Center for Molecular Neuroscience, Vanderbilt University Medical Center, Nashville, Tennessee 37232

Abstract

Although evidence exists that activation of the Rho family GTPase Cdc42 affects axonal development, its specific roles within a growth cone are not well delineated. To evaluate the model that Cdc42 activation regulates growth cone navigation by promoting filopodial activity, we adopted a live analysis strategy that uses transgenicDrosophila lines in which neurons coexpressed constitutively active Cdc42 (Cdc42V12) and membrane-targeted green fluorescent protein. We found that growth cones that displayed pathfinding defects exhibited little change in their filopodial activity, whereas others without pathfinding defects exhibited an ∼50% increase in their filopodial activity. Moreover, effector loop mutations that were added to the constitutively active Cdc42 (Cdc42V12C40 and Cdc42V12A37) exerted little influence over filopodial activity caused by Cdc42 activation but suppressed the pathfinding defects of the growth cones. Together, these data suggest that Cdc42 controls filopodial activity in axonal growth cones independently of its effects on their pathfinding.

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