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Iron Binding Drug For Limb Wounds
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ironjustice
May 21, 2013, 2:17:05 PM5/21/13
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Drug That Binds Iron Could Be a Godsend For Stubborn Limb Wounds
Aug 22, 2009
Deferoxamine, a drug already FDA-approved for the treatment of
disorders related to excess iron in the blood, may help doctors heal
stubborn leg and foot wounds in people with diabetes. Scientists at
the Stanford University School of Medicine and the Albert Einstein
College of Medicine found that with deferoxamine, small cuts in
diabetic mice healed 10 days faster than they did in untreated mice:
13 days as opposed to 23 days. If deferoxamine works similarly on
humans, it could significantly speed the healing of diabetic wounds.
Diabetic wounds heal slowly because the body doesn't do a good job of
creating new blood vessels to reconnect the damaged tissue to the
oxygen-bearing bloodstream. Previously, scientists didn't know why
these new connections didn't take place. Now, based on the Stanford/
Einstein study, they believe that the high-glucose environment of
diabetic tissue prevents the production of a necessary vessel-building
factor known as VEGF.
VEGF, or vascular endothelial growth factor, is a protein that prompts
new blood vessel formation. Fibroblasts, the cells that heal wounds,
ramp up the production of VEGF when oxygen levels drop. To study how
this was going wrong in diabetic tissue, the researchers grew some
fibroblasts in high-glucose environments and others in low-glucose
environments. The low-glucose fibroblasts increased VEGF production by
200 percent, versus only 20 percent in the high-glucose group. And
mice treated with deferoxamine produced almost threefold more VEGF
than untreated mice.
The researchers found that glucose interferes with the production of
VEGF by creating free radicals, which oxidize iron. The oxidized iron
interacts with other molecules to form hydroxyl radicals, which then
damage DNA.
For the production of VEGF to occur, two things must happen. First,
DNA must bind with a protein called HIF-1a, a sort of cellular sensor
that sounds an alert when oxygen is low. That interaction allows the
DNA to produce the growth factor, which then allows the creation of
new blood vessels.
But to work efficiently, HIF-1a also needs to bind with a molecule
called p300. In high-glucose environments, HIF-1a binds with p300 only
half as well as normal. The result is a drastic reduction in
fibroblasts' ability to heal damaged tissue.
Because deferoxamine binds to and removes iron from cells, the
Stanford/Einstein researchers hypothesized that it could prevent the
DNA damage that ultimately resulted from the oxidized iron that is
created in a high-glucose environment. And in fact, the drug did bring
the binding of p300 and HIF-1a back to normal levels.
Scientists are already experimenting with ways to use deferoxamine in
the treatment of diabetic wounds. Although the drug is commonly
injected when used for iron overload, the Stanford/Einstein team is
developing a dissolvable sheet that could be placed directly on a
wound to deliver deferoxamine as a medication.
Who loves ya.
Tom
Jesus Was A Vegetarian!
http://tinyurl.com/2r2nkh
Man Is A Herbivore!
http://tinyurl.com/4rq595
DEAD PEOPLE WALKING
http://tinyurl.com/zk9fk
Aug 22, 2009
Deferoxamine, a drug already FDA-approved for the treatment of
disorders related to excess iron in the blood, may help doctors heal
stubborn leg and foot wounds in people with diabetes. Scientists at
the Stanford University School of Medicine and the Albert Einstein
College of Medicine found that with deferoxamine, small cuts in
diabetic mice healed 10 days faster than they did in untreated mice:
13 days as opposed to 23 days. If deferoxamine works similarly on
humans, it could significantly speed the healing of diabetic wounds.
Diabetic wounds heal slowly because the body doesn't do a good job of
creating new blood vessels to reconnect the damaged tissue to the
oxygen-bearing bloodstream. Previously, scientists didn't know why
these new connections didn't take place. Now, based on the Stanford/
Einstein study, they believe that the high-glucose environment of
diabetic tissue prevents the production of a necessary vessel-building
factor known as VEGF.
VEGF, or vascular endothelial growth factor, is a protein that prompts
new blood vessel formation. Fibroblasts, the cells that heal wounds,
ramp up the production of VEGF when oxygen levels drop. To study how
this was going wrong in diabetic tissue, the researchers grew some
fibroblasts in high-glucose environments and others in low-glucose
environments. The low-glucose fibroblasts increased VEGF production by
200 percent, versus only 20 percent in the high-glucose group. And
mice treated with deferoxamine produced almost threefold more VEGF
than untreated mice.
The researchers found that glucose interferes with the production of
VEGF by creating free radicals, which oxidize iron. The oxidized iron
interacts with other molecules to form hydroxyl radicals, which then
damage DNA.
For the production of VEGF to occur, two things must happen. First,
DNA must bind with a protein called HIF-1a, a sort of cellular sensor
that sounds an alert when oxygen is low. That interaction allows the
DNA to produce the growth factor, which then allows the creation of
new blood vessels.
But to work efficiently, HIF-1a also needs to bind with a molecule
called p300. In high-glucose environments, HIF-1a binds with p300 only
half as well as normal. The result is a drastic reduction in
fibroblasts' ability to heal damaged tissue.
Because deferoxamine binds to and removes iron from cells, the
Stanford/Einstein researchers hypothesized that it could prevent the
DNA damage that ultimately resulted from the oxidized iron that is
created in a high-glucose environment. And in fact, the drug did bring
the binding of p300 and HIF-1a back to normal levels.
Scientists are already experimenting with ways to use deferoxamine in
the treatment of diabetic wounds. Although the drug is commonly
injected when used for iron overload, the Stanford/Einstein team is
developing a dissolvable sheet that could be placed directly on a
wound to deliver deferoxamine as a medication.
Who loves ya.
Tom
Jesus Was A Vegetarian!
http://tinyurl.com/2r2nkh
Man Is A Herbivore!
http://tinyurl.com/4rq595
DEAD PEOPLE WALKING
http://tinyurl.com/zk9fk
GysdeJongh
May 21, 2013, 4:15:17 PM5/21/13
to
ironjustice wrote:
> Drug That Binds Iron Could Be a Godsend For Stubborn Limb Wounds
> Aug 22, 2009
>
> Deferoxamine, a drug already FDA-approved for the treatment of
> disorders related to excess iron in the blood, may help doctors heal
> stubborn leg and foot wounds in people with diabetes. Scientists at
> the Stanford University School of Medicine and the Albert Einstein
> College of Medicine found that with deferoxamine, small cuts in
> diabetic mice healed 10 days faster than they did in untreated mice:
> 13 days as opposed to 23 days. If deferoxamine works similarly on
> humans, it could significantly speed the healing of diabetic wounds.
<http://diabeteshealth.com/read/2009/08/22/6327/>
> Drug That Binds Iron Could Be a Godsend For Stubborn Limb Wounds
> Aug 22, 2009
>
> Deferoxamine, a drug already FDA-approved for the treatment of
> disorders related to excess iron in the blood, may help doctors heal
> stubborn leg and foot wounds in people with diabetes. Scientists at
> the Stanford University School of Medicine and the Albert Einstein
> College of Medicine found that with deferoxamine, small cuts in
> diabetic mice healed 10 days faster than they did in untreated mice:
> 13 days as opposed to 23 days. If deferoxamine works similarly on
> humans, it could significantly speed the healing of diabetic wounds.
Drug That Binds Iron Could Be a Godsend For Stubborn Limb Wounds
Aug 22, 2009
Selective pick-up of increased iron by deferoxamine-coupled cellulose
abrogates the iron-driven induction of matrix-degrading metalloproteinase 1
and lipid peroxidation in human dermal fibroblasts in vitro: a new dressing
concept.
PMID: 11407968
John H. Gohde
May 22, 2013, 5:33:17 PM5/22/13
to
What Diabetes?
What Iron?
What justice?
What Science Bull, ... and I do NOT mind saying so. :)
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