Use the labels in the right column to find what you want. Or you can go thru them one by one, there are only 29,286 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.
Changing stroke rehab and research worldwide now.Time is Brain!trillions and trillions of neuronsthatDIEeach day because there areNOeffective 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.
Wednesday, June 22, 2022
Protective Effects of Intranasally Administrated Oxytocin-Loaded Nanoparticles on Pentylenetetrazole-Kindling Epilepsy in Terms of Seizure Severity, Memory, Neurogenesis, and Neuronal Damage
With your chance of epileptic seizures post stroke, your doctor is responsible to know EXACTLY how to prevent them. Now we need followup human testing
Approximately 5 percent of people will have a seizure within a few weeks after having a stroke, according to the National Stroke Association.
Be careful out there. Some research points to a 10-40% epilepsy
incidence rate for survivors. What is your doctor doing to ensure you
don't get epilepsy? YOUR DOCTOR'S RESPONSIBILITY!
Pentylenetetrazole
(PTZ)-induced kindling is an animal model for studying human temporal
lobe epilepsy (TLE), which is characterized by alterations of
hippocampal neurons and memory. Although the intranasal (IN)
administration of oxytocin (OT) has limited efficiency, nanoparticles
(NPs) are a promising candidate to deliver OT to the brain. However,
there are very limited data on epilepsy research about oxytocin-loaded
nanoparticles (NP-OTs). The aim of this study is to investigate the
effects of IN administration of chronic NP-OTs on the hippocampus of
PTZ-induced male epileptic rats in terms of seizure severity, memory,
neurogenesis, and neuronal damage. Saline/OT/NP-OTs were administrated
to both control (Ctrl) and PTZ groups intranasally. Consequently, saline
and PTZ were injected, respectively, 25 times every 48 h. Then, seizure
severity (score and latency) was calculated for the PTZ groups. A
spatial working memory evaluation test (SWMET) was performed after the
last injection. Hippocampus histopathology, neurogenesis, and apoptosis
were demonstrated. Serum total antioxidant status (TAS) and total
oxidant status (TOS) levels and the oxidative stress index (OSI) were
measured. We showed that OTs and NP-OTs prevented the kindling
development and had positive effects on seizure severity. SWMET-related
behaviors were also recovered in the PTZ + NP-OT group. A significant
increase of neurogenesis and decrease of apoptosis in the hippocampus of
the PTZ + NP-OT group were observed, while OTs and NP-OTs had
protective effects against PTZ-induced damage to hippocampal neurons.
Our results indicate that the chronic administration of NP-OTs may have
positive effects on hippocampal damage via increasing neurogenesis and
decreasing apoptosis and seizure severity.
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