What is your doctor and hospital doing to see if this actually works in humans? Or are they so f*cking lazy because everything in stroke is somebody elses' problem? And your dead brain cells are the result?
http://www.alphagalileo.org/ViewItem.aspx?ItemId=149447&CultureCode=en
Strokes, heart attacks and traumatic brain injuries are separate
diseases with certain shared pathologies that achieve a common end –
cell death and human injury due to hypoxia, or lack of oxygen. In these
diseases, a lack of blood supply to affected tissues begins a signaling
pathway that ultimately halts the production of energy-releasing ATP
molecules – a death sentence for most cells.
By employing derivatives of humanin, a naturally occurring peptide
encoded in the genome of cellular mitochondria, researchers at Ben
Gurion University of the Negev are working to interrupt this process,
buying precious time for tissues whose cellular mechanisms have called
it quits.
"The present findings could provide a new lead compound for the
development of drug therapies for necrosis-related diseases such as
traumatic brain injury, stroke and myocardial infarction - conditions
for which no effective drug-based treatments are currently available
[that work by blocking necrosis]," said Abraham Parola, a professor of
biophysical chemistry at Ben Gurion University of the Negev in
Beer-Sheva, Israel. Parola is presently a visiting professor of
Biophysical Chemistry & Director of Natural Sciences at New York
University Shanghai, and will speak about his lab's finding's this week
at the Biophysical Society's 59th annual meeting in Baltimore, Md.
The humanin derivatives work by counteracting the decrease in ATP
levels caused by necrosis. The researchers tested the effectiveness of
the humanin analogues AGA(C8R)-HNG17 and AGA-HNG by treating neuronal
cells with these peptides prior to exposure to a necrotic agent. The
experiments were a success.
Parola's previous work has dealt with membrane dynamics and the
mechanism of action of anti-angiogenesis drugs, which cause starvation
of malignant tumor growths by preventing the supply of nutrients and
oxygen to the fast growing tissue, in addition to various other
biophysical and molecular medicine and diagnostic topics.
"A recent paper published by our group suggested the involvement of
cardiolipin [a phospholipid in inner mitochondrial membranes] in the
necrotic process," Parola said. "During this work we stumbled along
humanin and were intrigued by its anti-apoptotic effect, and extended it
to anti-necrotic effect."
Parola and his colleagues also performed in vivo studies by
treating mice that had had traumatic brain injuries with an HNG17
analogue, which successfully reduced cranial fluid buildup and lowered
the mice's neuronal severity scores, a metric in which a higher number
corresponds with greater degrees of neurological motor impairment.
As the peptides Parola and his colleagues used are derivatives of
naturally occurring humanin, an ideal treatment might involve a drug
delivery system with the HNG17 as the lead compound, a process aided by
the ability of the peptides to penetrate the cell membrane without the
use of additional reagents.
Future work for Parola and his colleagues includes further
exploration of ischemic activity in liver cirrhosis, as induced by
acetaminophen activity, in addition to searching for a synergistic
effect between humanin and other anti-necrotic agents, such as protease
inhibitors, to increase its clinical potential.
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