From: ironjustice on
Alzheimer Disease Plaques Seen with Conventional MRI in Animal Model
for the First Time
- MRI and advanced computer analysis bring us closer to early
identification of Alzheimer's -

Chicago, July 27, 2008 – For the first time, scientists have captured
images of brain lesions similar to those found in Alzheimer's disease
using clinical-grade MRI in an animal model of the disease, according
to research reported today at the Alzheimer's Association's 2008
International Conference on Alzheimer's Disease (ICAD 2008), in
Chicago.

These lesions, known as amyloid plaques, have been "imaged" previously
using very high power MRI scanners that are only used on animals, and
also with PET scans combined with specialized marker chemicals. This
is the first time images of plaques were captured with conventional,
clinical strength MRI.

John Ronald, a Ph.D. candidate in Medical Biophysics, along with Brian
Rutt, PhD, and colleagues at the Robarts Research Institute and
University of Western Ontario, London, Ontario, Canada, used clinical
strength MRI scanners to take brain images from rabbits that had been
fed a high cholesterol diet for more than two years. These animals
form amyloid plaques in their brains.

According to the researchers, the MRI scans revealed distinct signal
voids – black spots – in several brain areas including the
hippocampus, which is very important for memory. Autopsy examination
revealed that the void areas reflected the presence of small clusters
of amyloid plaques. Each cluster had high levels of iron, which the
researchers say caused the MRI signal voids; these signal voids were
not found in animals fed a normal diet.

http://www.alz.org/icad/_icad_release_072708_3pm_mri.asp


-----------------------------

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Tom


Jesus Was A Vegetarian!
http://tinyurl.com/2r2nkh


Man Is A Herbivore!
http://tinyurl.com/4rq595


DEAD PEOPLE WALKING
http://tinyurl.com/zk9fk



From: jay on
> ... rabbits that had been fed a high cholesterol diet for more
> than two years. These animals form amyloid plaques in their brains.

7-Ketocholesterol is one of the major forms of oxidized cholesterol
found in vivo. While 7-Ketocholesterol activates AhR-mediated
pathways, Persistent Organic Pollutants (ie TCDD, a potent dioxin) are
even stronger activators.

7-ketocholesterol is an endogenous modulator for the arylhydrocarbon
receptor.
We have identified 7-ketocholesterol (7-KC) as an endogenous modulator
that inhibits transactivation by the arylhydrocarbon receptor (AhR)
through competitive binding against xenobiotic ligands. 7-KC binds AhR
and displaces labeled dioxin (2,3,7,8-tetrachlorodibenzo(p)dioxin
(TCDD)). IC(50) is 5 x 10(-7) m in vivo and 7 x 10(-6) m in vitro.
These figures are consistent with its concentration in human blood
plasma and tissues. Association with 7-KC prevents AhR binding to DNA.
7-KC blocks the TCDD-mediated transactivation of stably expressed
reporter gene constructs in T47-D cells as well as the expression of
the endogenous CYP 1A1 gene in HepG2 cells and in primary porcine
aortic endothelial cells. Injection of 7-KC to rats blocks the
induction of CYP 1A1 messenger RNA and protein in endothelial cells
from myocardial blood vessels. The differential sensitivity of
mammalian species to toxic effects of AhR ligands, especially dioxin
(TCDD), correlates with the expression of 7-hydroxycholesterol
dehydrogenase, which synthesizes 7-KC from 7-hydroxycholesterol. The
documented involvement of AhR ligands in cardiovascular diseases
through lipid peroxidation and endothelium dysfunction can now be
examined in the context of displacement of this protective modulator.
PMID: 11042205
From: ironjustice on
On Aug 10, 9:04 pm, jay <jaym1...(a)hotmail.com> wrote: snip <<
I see you didn't mention anything about iron ..

How about the Middle Ages .. there .. buddy ..
-------------------

Each cluster had high levels of iron, which the
researchers say caused the MRI signal voids; these signal voids were
not found in animals fed a normal diet.


http://www.alz.org/icad/_icad_release_072708_3pm_mri.asp


-----------------------------


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



> > ... rabbits that had been fed a high cholesterol diet for more
> > than two years. These animals form amyloid plaques in their brains.
>
> 7-Ketocholesterol is one of the major forms of oxidized cholesterol
> found in vivo. While 7-Ketocholesterol activates AhR-mediated
> pathways, Persistent Organic Pollutants (ie TCDD, a potent dioxin) are
> even stronger activators.
>
> 7-ketocholesterol is an endogenous modulator for the arylhydrocarbon
> receptor.
> We have identified 7-ketocholesterol (7-KC) as an endogenous modulator
> that inhibits transactivation by the arylhydrocarbon receptor (AhR)
> through competitive binding against xenobiotic ligands. 7-KC binds AhR
> and displaces labeled dioxin (2,3,7,8-tetrachlorodibenzo(p)dioxin
> (TCDD)). IC(50) is 5 x 10(-7) m in vivo and 7 x 10(-6) m in vitro.
> These figures are consistent with its concentration in human blood
> plasma and tissues. Association with 7-KC prevents AhR binding to DNA.
> 7-KC blocks the TCDD-mediated transactivation of stably expressed
> reporter gene constructs in T47-D cells as well as the expression of
> the endogenous CYP 1A1 gene in HepG2 cells and in primary porcine
> aortic endothelial cells. Injection of 7-KC to rats blocks the
> induction of CYP 1A1 messenger RNA and protein in endothelial cells
> from myocardial blood vessels. The differential sensitivity of
> mammalian species to toxic effects of AhR ligands, especially dioxin
> (TCDD), correlates with the expression of 7-hydroxycholesterol
> dehydrogenase, which synthesizes 7-KC from 7-hydroxycholesterol. The
> documented involvement of AhR ligands in cardiovascular diseases
> through lipid peroxidation and endothelium dysfunction can now be
> examined in the context of displacement of this protective modulator.
> PMID: 11042205

From: jay on
> > While 7-Ketocholesterol activates AhR-mediated
> > pathways, Persistent Organic Pollutants (ie TCDD,
> > a potent dioxin) are even stronger activators.
>
> How about the Middle Ages .. there .. buddy ..

The Ah-R mediated pathways are also activated by compounds generated
by combustion of matter found in Middle Ages and before.

Role of aryl hydrocarbon receptor-mediated induction of the CYP1
enzymes in environmental toxicity and cancer.
The mammalian CYP1A1, CYP1A2, and CYP1B1 genes (encoding cytochromes
P450 1A1, 1A2, and 1B1, respectively) are regulated by the aromatic
hydrocarbon receptor (AHR). The CYP1 enzymes are responsible for both
metabolically activating and detoxifying numerous polycyclic aromatic
hydrocarbons (PAHs) and aromatic amines present in combustion
products... PMID: 15028720


Wiki - PAHs: Natural crude oil and coal deposits contain significant
amounts of PAHs, arising from chemical conversion of natural product
molecules, such as steroids, to aromatic hydrocarbons.
Formed by incomplete combustion of carbon-containing fuels such as
wood, coal, diesel, fat, tobacco, or incense.


Wiki - Some heterocyclic amines (HCAs) found in cooked meat are known
carcinogens. Research has shown that cooking certain meats at high
temperatures creates chemicals that are not present in uncooked meats.
For example, heterocyclic amines are the carcinogenic chemicals formed
from the cooking of muscle meats such as beef, pork, fowl, and fish.
HCAs form when amino acids and creatine (a chemical found in muscles)
react at high cooking temperatures. Researchers have identified 17
different HCAs resulting from the cooking of muscle meats that may
pose human cancer risk. NCI's Division of Cancer Epidemiology and
Genetics found a link between individuals with stomach cancer and the
consumption of cooked meat, and other studies for colorectal,
pancreatic, and breast cancer is associated with high intakes of well-
done, fried, or barbecued meats.
From: jay on
> I see you didn't mention anything about iron ..

Activation of Aryl Hydrocarbon Receptor Mediated Pathways increases
cellular production of iron-utilizing detoxification enzymes (CYP1A1,
CPY1A2, CYP1B, etc).
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