Use the labels in the right column to find what you want. Or you can go thru them one by one, there are only 12345 posts. Searching is done in the search box in upper left corner. I blog on anything to do with stroke.DO NOT DO ANYTHING SUGGESTED HERE AS I AM NOT MEDICALLY TRAINED, YOUR DOCTOR IS, LISTEN TO THEM. BUT I BET THEY DON'T KNOW HOW TO GET YOU 100% RECOVERED. I DON'T EITHER, BUT HAVE PLENTY OF QUESTIONS FOR YOUR DOCTOR TO ANSWER.
Deans' stroke musings
Changing stroke rehab and research worldwide now.Time is Brain!Just think of all thetrillions and trillions of neuronsthateach daybecause there areeffective hyperacute therapies besides tPA(only 12% effective). I have 493 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:
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's quite disgusting that this information is not available from every stroke association and doctors group. My back ground story is here:http://oc1dean.blogspot.com/2010/11/my-background-story_8.html
Tuesday, March 14, 2017
Stroke alters behavior of human skin-derived neural progenitors after transplantation adjacent to neurogenic area in rat brain
of human induced pluripotent stem cells (iPSCs) can ameliorate
behavioral deficits in animal models of stroke. How the ischemic lesion
affects the survival of the transplanted cells, their proliferation,
migration, differentiation, and function is only partly understood.
Here we have assessed the
influence of the stroke-induced injury on grafts of human skin
iPSCs-derived long-term neuroepithelial-like stem cells using
transplantation into the rostral migratory stream (RMS), adjacent to the
neurogenic subventricular zone, in adult rats as a model system.
We show that the occurrence of
an ischemic lesion, induced by middle cerebral artery occlusion, in the
striatum close to the transplant does not alter the survival,
proliferation, or generation of neuroblasts or mature neurons or
astrocytes from the grafted progenitors. In contrast, the migration and
axonal projection patterns of the transplanted cells are markedly
influenced. In the intact brain, the grafted cells send many fibers to
the main olfactory bulb through the RMS and a few of them migrate in the
same direction, reaching the first one third of this pathway. In the
stroke-injured brain, on the other hand, the grafted cells only migrate
toward the ischemic lesion and virtually no axonal outgrowth is observed
in the RMS.
Our findings indicate that
signals released from the stroke-injured area regulate the migration of
and fiber outgrowth from grafted human skin-derived neural progenitors
and overcome the influence on these cellular properties exerted by the
neurogenic area/RMS in the intact brain.
transplantation of induced pluripotent stem cells (iPSCs) or their
derivatives, generated by reprogramming human somatic cells, can reverse
behavioral deficits in experimental stroke models (for references, see ).
Improvements were detected early after transplantation, indicating that
they were not due to neuronal replacement but to other mechanisms such
as modulation of inflammation, and promotion of plastic responses and
neovascularization. However, we recently showed that human iPSC-derived
long-term neuroepithelial-like stem cells (lt-NESCs) transplanted into
stroke-injured cortex can differentiate to form functional cortical
neurons, which receive afferent inputs from appropriate brain areas and
respond to mechanical stimulation of nose and paw .
It remains to be demonstrated, though, that this incorporation into
host neural circuitry contributes to the long-term functional recovery
fundamental question, also in a clinical-therapeutical perspective, is
how the stroke-induced injury affects the survival, proliferation,
migration, neuronal differentiation, integration and function of the
grafted human iPSC-derived cells. Implantation of the cells in the
rostral migratory stream (RMS), close to one of the main neurogenic
areas in the brain, the subventricular zone (SVZ), seems to be a useful
model system to address these issues. In the SVZ, neural stem/progenitor
cells form new neurons that travel, via the RMS, toward the main
olfactory bulb (MOB) ,
where they integrate as interneurons in the granule and periglomerular
cell layers. Several cues have been identified which take part in this
process [4, 5, 6]
and may regulate the behavior also of cells transplanted close to the
SVZ into the adult rodent brain. For example, differentiated neurons
from a human teratocarcinoma send their axons through the RMS and in
association with ipsilateral and contralateral white matter pathways .
When implanting human skin-derived iPSCs close to the SVZ in adult
intact brains, most of the grafted cells migrate via the RMS. In
contrast, oligodendrocytes implanted do not migrate along the RMS but
follow the white matter pathways along the corpus callosum and internal
Whether the occurrence of an ischemic lesion affects the migration,
axonal outgrowth or other properties of human iPSCs implanted close to
the SVZ is unknown.
we have explored the role of the ischemic injury for the behavior of
human iPSC-derived lt-NESCs after transplantation into the RMS, adjacent
to the neurogenic SVZ, in intact and stroke-damaged rats. We
demonstrate that the stroke-induced lesion markedly alters the patterns
of axonal outgrowth and migration of the grafted cells, whereas
survival, proliferation, and generation of neuroblasts, mature neurons
or astrocytes are unaffected.