Smoke Em If You Got Em
ironjustice
in for nicotinamide as these 'nutritionists' tell you.
People in families predisposed to alzheimers' don't 'get' alzheimers
if they smoke .. those in the family who DON'T smoke .. DO .. get
alzheimers'.
-------
Vitamin B3 Reduces Alzheimer's Symptoms, Lesions: Clinical Trial On
Nicotinamide Effect In Alzheimer's Patients
ScienceDaily (Nov. 5, 2008) — An over-the-counter vitamin in high
doses prevented memory loss in mice with Alzheimer's disease, and UC
Irvine scientists now are conducting a clinical trial to determine its
effect in humans.
Nicotinamide, a form of vitamin B3, lowered levels of a protein called
phosphorylated tau that leads to the development of tangles, one of
two brain lesions associated with Alzheimer's disease. The vitamin
also strengthened scaffolding along which information travels in brain
cells, helping to keep neurons alive and further preventing symptoms
in mice genetically wired to develop Alzheimer's.
"Nicotinamide has a very robust effect on neurons," said Kim Green,
UCI scientist and lead author of the study. "Nicotinamide prevents
loss of cognition in mice with Alzheimer's disease, and the beauty of
it is we already are moving forward with a clinical trial."
The study appears online Nov. 5 in the Journal of Neuroscience.
Nicotinamide is a water-soluble vitamin sold in health food stores. It
generally is safe but can be toxic in very high doses. Clinical trials
have shown it benefits people with diabetes complications and has anti-
inflammatory properties that may help people with skin conditions.
Nicotinamide belongs to a class of compounds called HDAC inhibitors,
which have been shown to protect the central nervous system in rodent
models of Parkinson's and Huntington's diseases and amyotrophic
lateral sclerosis. Clinical trials are underway to learn whether HDAC
inhibitors help ALS and Huntington's patients.
In the nicotinamide study, Green and his colleague, Frank LaFerla,
added the vitamin to drinking water fed to mice. They tested the
rodents' short-term and long-term memory over time using water-maze
and object-recognition tasks and found that treated Alzheimer's mice
performed at the same level as normal mice, while untreated
Alzheimer's mice experienced memory loss.
The nicotinamide, in fact, slightly enhanced cognitive abilities in
normal mice. "This suggests that not only is it good for Alzheimer's
disease, but if normal people take it, some aspects of their memory
might improve," said LaFerla, UCI neurobiology and behavior professor.
Scientists also found that the nicotinamide-treated animals had
dramatically lower levels of the tau protein that leads to the
Alzheimer's tangle lesion. The vitamin did not affect levels of the
protein beta amyloid, which clumps in the brain to form plaques, the
second type of Alzheimer's lesion.
Nicotinamide, they found, led to an increase in proteins that
strengthen microtubules, the scaffolding within brain cells along
which information travels. When this scaffolding breaks down, the
brain cells can die. Neuronal death leads to dementia experienced by
Alzheimer's patients.
"Microtubules are like highways inside cells. What we're doing with
nicotinamide is making a wider, more stable highway," Green said. "In
Alzheimer's disease, this highway breaks down. We are preventing that
from happening."
Who loves ya.
Tom
Jesus Was A Vegetarian!
http://tinyurl.com/634q5a
Man Is A Herbivore!
http://tinyurl.com/4rq595
DEAD PEOPLE WALKING
http://tinyurl.com/zk9fk
Taka
> Sooo .. there isn't as much loonacy in the theory of nicotine standing
> in for nicotinamide as these 'nutritionists' tell you.
>
> People in families predisposed to alzheimers' don't 'get' alzheimers
> if they smoke .. those in the family who DON'T smoke .. DO .. get
> alzheimers'.
Or you can just drink beer ! It's full of B vitamins including
nicotinamide. The malts & yeast combination in it is a VitB bomb ...
Now why are novadays people so deficient in B vitamins that they have
to smoke and drink beer ??? Are more B vitamins needed in the modern
world full of PUFAs, lack of sleep and stress ? To combat and
detoxify the lipid peroxides ...
Taka
clams_casino
>Sooo .. there isn't as much loonacy in the theory of nicotine standing
>in for nicotinamide as these 'nutritionists' tell you.
>
>People in families predisposed to alzheimers' don't 'get' alzheimers
>if they smoke .. those in the family who DON'T smoke .. DO .. get
>alzheimers'.
>-------
>
>
The reason is so obvious - smokers typically don't live long enough to
develop Alzheimer's.
Along that line, smoking greatly helps social security funding.
Smokers pay in all their lives, but for the most part, don't get back
anywhere near what they contribute.
ironjustice
Smokers pay in all their lives, but for the most part, don't get back
anywhere near what they contribute.
<<
Now it's a matter of who is 'better off' .. though .. ?
The incidence of elderly abuse in nursing homes has hit a new level ..
What I've seen of old age .. it ain't all that pretty ..
I'm up to about twelve packs a day ..
Just joking ..
ironjustice
Are more B vitamins needed in the modern
world full of PUFAs, lack of sleep and stress ? To combat and
detoxify the lipid peroxides ... <<
BY what .. virtue .. ?
What quality do they have to do that .. ?
Do they say anything about the B vitamins doing that .. AS .. the
'mode of operation' / combat and detoxify the lipid peroxides ?
"Nicotinamide belongs to a class of compounds called HDAC inhibitors"
Who loves ya.
Tom
Jesus Was A Vegetarian!
http://tinyurl.com/634q5a
Man Is A Herbivore!
http://tinyurl.com/4rq595
DEAD PEOPLE WALKING
http://tinyurl.com/zk9fk
>
> Taka
ironjustice
"Nicotinamide belongs to a class of compounds called HDAC inhibitors"
<<
Any significance that the problem with Friedreich ataxia is the
increased iron.
When given this HDAC inhibitor the Friedreich ataxia mouse seems to
be .. cured .. ?
HDAC inhibitors correct frataxin deficiency in a Friedreich ataxia
mouse model.
PLoS ONE (2008) 3: e1958.
M Rai, E SORAGNI, K Jenssen, R Burnett, D Herman, G Coppola, DH
Geschwind, JM Gottesfeld, M Pandolfo
BACKGROUND:
Friedreich ataxia, an autosomal recessive neurodegenerative and
cardiac disease, is caused by abnormally low levels of frataxin, an
essential mitochondrial protein. All Friedreich ataxia patients carry
a GAATTC repeat expansion in the first intron of the frataxin gene,
either in the homozygous state or in compound heterozygosity with
other loss-of-function mutations. The GAA expansion inhibits frataxin
expression through a heterochromatin-mediated repression mechanism.
Histone modifications that are characteristic of silenced genes in
heterochromatic regions occur at expanded alleles in cells from
Friedreich ataxia patients, including increased trimethylation of
histone H3 at lysine 9 and hypoacetylation of histones H3 and H4.
METHODOLOGY/PRINCIPAL FINDINGS:
By chromatin immunoprecipitation, we detected the same heterochromatin
marks in homozygous mice carrying a (GAA)(230) repeat in the first
intron of the mouse frataxin gene (KIKI mice). These animals have
decreased frataxin levels and, by microarray analysis, show
significant gene expression changes in several tissues. We treated
KIKI mice with a novel histone deacetylase inhibitor, compound 106,
which substantially increases frataxin mRNA levels in cells from
Friedreich ataxia individuals. Treatment increased histone H3 and H4
acetylation in chromatin near the GAA repeat and restored wild-type
frataxin levels in the nervous system and heart, as determined by
quantitative RT-PCR and semiquantitative western blot analysis. No
toxicity was observed. Furthermore, most of the differentially
expressed genes in KIKI mice reverted towards wild-type levels.
CONCLUSIONS/SIGNIFICANCE:
Lack of acute toxicity, normalization of frataxin levels and of the
transcription profile changes resulting from frataxin deficiency
provide strong support to a possible efficacy of this or related
compounds in reverting the pathological process in Friedreich ataxia,
a so far incurable neurodegenerative disease.
---------------------
Iron decreases erythropoietin.
Iron overload has been shown IN .. Friedreich's Ataxia .. one might
wonder if reduction of iron would NOW .. kickstart ..
everything .. ? .. just like in ..
leukemia .. ? .. somewhat like the choke on your .. ride .. ?
"Persistent and significant increase in frataxin levels"
Friedreich's ataxia: clinical pilot trial with recombinant human
erythropoietin.
Ann Neurol. 2007 Aug 13;
Boesch S, Sturm B, Hering S, Goldenberg H, Poewe W,
Scheiber-Mojdehkar B.
Department of Neurology, Innsbruck Medical University, Innsbruck,
Austria.
To determine the role of recombinant human erythropoietin as a
possible treatment option in Friedreich's ataxia, we performed an
open-
label clinical pilot study.
Primary outcome measure was the change of frataxin levels at week 8
versus baseline.
Twelve Friedreich's ataxia patients received 5,000 units recombinant
human erythropoietin three times weekly subcutaneously.
Frataxin levels were measured in isolated lymphocytes by enzyme-linked
immunosorbent assay.
In addition, urinary 8-hydroxydeoxyguanosine and serum peroxides, were
measured.
Treatment with recombinant human erythropoietin showed a persistent
and
significant increase in frataxin levels after 8 weeks (p < 0.01).
All patients showed a reduction of oxidative stress markers. Ann
Neurol
2007.
PMID: 17702040
Who loves ya.
Tom
Jesus Was A Vegetarian!
http://tinyurl.com/634q5a
Man Is A Herbivore!
http://tinyurl.com/4rq595
DEAD PEOPLE WALKING
http://tinyurl.com/zk9fk
> On Nov 6, 7:15 am, Taka <taka0...@gmail.com> wrote:
> Are more B vitamins needed in the modern
> world full of PUFAs, lack of sleep and stress ? To combat and
> detoxify the lipid peroxides ... <<
>
> BY what .. virtue .. ?
>
> What quality do they have to do that .. ?
>
> Do they say anything about the B vitamins doing that .. AS .. the
> 'mode of operation' / combat and detoxify the lipid peroxides ?
>
> "Nicotinamide belongs to a class of compounds called HDAC inhibitors"
>
> Who loves ya.
> Tom
>
> Jesus Was A Vegetarian!http://tinyurl.com/634q5a
>
> Man Is A Herbivore!http://tinyurl.com/4rq595
>
> DEAD PEOPLE WALKINGhttp://tinyurl.com/zk9fk
>
>
>
>
>
> > Taka- Hide quoted text -
>
> - Show quoted text -
anon...@nowhere.you.know
in for nicotinamide as these 'nutritionists' tell you.
People in families predisposed to alzheimers' don't 'get' alzheimers
if they smoke .. those in the family who DON'T smoke .. DO .. get
alzheimers'.
-------
Vitamin B3 Reduces Alzheimer's Symptoms, Lesions: Clinical Trial On"
What a hoot, all the mistakes amateurs often make in one post. Let us
see if the poster can extradite himself from this one.
ironjustice
What part of you ain't welcome on my threads don't you understand
there .. aspartame .. boy .. ?
---------
Vitamin B3 Reduces Alzheimer's Symptoms, Lesions: Clinical Trial On
Who loves ya.
Tom
John Hasenkam
research re smokers and Alz confers a slight advantage but is easily
outweighed by other health risks.
--
http://healthycuriousity.blogspot.com/
"ironjustice" <teamt...@hotmail.com> wrote in message
news:fd17d3c3-4f77-4cf6...@l33g2000pri.googlegroups.com...
ironjustice
Ridiculous, smokers have a much greater risk for vascular dementia.
The
research re smokers and Alz confers a slight advantage but is easily
outweighed by other health risks. <<
What makes you think this 'Alzheimers' they treated ISN'T vascular
dementia .. ?
Nicotinamide is also called niacin or niacinamide ..
It is used for .. ? .. vascular problems ..
Sooo .. it is coincidence this vitamin is used to treat vascular
problems which cause vascular dementia which **closely** resembles
Alzheimers' .. AND the vitamin is NOW shown to inhibit ..
Alzheimers' ..
Coincidences .. abound ..
http://www.pubmedcentral.nih.gov/articlerender.fcgi?artid=1898481
Niacin in Vascular Disorders and Hyperlipemia
Reviewed by J R A Mitchell
------------
Who loves ya.
Tom
Jesus Was A Vegetarian!
http://tinyurl.com/634q5a
Man Is A Herbivore!
http://tinyurl.com/4rq595
DEAD PEOPLE WALKING
http://tinyurl.com/zk9fk
>
> --http://healthycuriousity.blogspot.com/"ironjustice" <teamtan...@hotmail.com> wrote in message
ironjustice
What makes you think this 'Alzheimers' they treated ISN'T vascular
dementia .. ? <<
"Nicotinamide lowered levels of phosphorylated tau"
"Neither measurement can discriminate entirely"
"It is concluded that neither measurement of phospho-tau, tau nor
A1-42 in CSF can discriminate entirely between dementia and
cognitively non-disturbed controls or between dementia of different
aetiologies"
Cerebrospinal Fluid Phospho-Tau, Total Tau and -Amyloid1-42 in the
Differentiation between Alzheimer's Disease and Vascular Dementia
Katarina Näggaa, Johan Gottfriesb, Kaj Blennowc,d, Jan Marcussona
aDepartment of Geriatric Medicine, Linköping University Hospital,
Linköping,
bMedicinal Chemistry, AstraZeneca R&D, Mölndal,
cDepartment of Clinical Neuroscience, Section of Experimental
Neuroscience, University of Göteborg, Sahlgrenska University Hospital,
Mölndal, and
dThe Medical Research Council, Sweden
Dement Geriatr Cogn Disord 2002;14:183-190 (DOI: 10.1159/000066023)
Abstract
The two most frequently examined biomarkers in the diagnosis of
dementia are cerebrospinal fluid (CSF) tau and -amyloid1-42 (A1-42).
An assay for tau phosphorylated at threonine 181 (phospho-tau) has
recently been developed.
We studied these three markers in patients with possible Alzheimer's
disease (AD; n = 23), probable AD (n = 50), AD with relevant
cerebrovascular disease (AD with CVD; n = 14), possible vascular
dementia (VaD; n = 39), probable VaD (n = 36), cognitively impaired (n
= 13) and 27 neurologically healthy controls.
Compared with the controls, tau levels were significantly increased in
possible AD, probable AD, AD with CVD and probable VaD. A1-42 was
decreased in all dementia groups compared with the controls.
In contrast, phospho-tau levels were increased only in probable AD
compared with the controls.
From the results of the present study, it is concluded that neither
measurement of phospho-tau, tau nor A1-42 in CSF can discriminate
entirely between dementia and cognitively non-disturbed controls or
between dementia of different aetiologies in the clinical diagnostic
procedure.
Copyright © 2002 S. Karger AG, Basel
--------------------------------------------------------------------------------
Author Contacts
Katarina Nägga, MD
Department of Geriatric Medicine
Linköping University Hospital
S-581 85 Linköping (Sweden)
Tel. +46 13 224093, Fax +46 13 227389, E-Mail Katarin...@lio.se
Vol. 14, No. 4, 2002
--------------------------------------------------------------------------------
anon...@nowhere.you.know
there .. aspartame .. boy .. ?"
Ah shucks, there you went and done it, called me sweet.
You still don't see how completely in the dark you are in your mistakes
on this one, and many many before it.
What part of you ain't welcome on my threads don't you understand
there .. aspartame .. boy .. ?
What an amateur doesn't know is no barrier to them.
ironjustice
What part of you ain't welcome on my threads don't you understand
there .. aspartame .. boy .. ?
anon...@nowhere.you.know
John Hasenkam
dementia .. ?
These are two different conditions. If they were treating "dementias" they
would say so, not "Alzheimers". Please explain why smokers have very high
rates of vascular problems.
--
http://healthycuriousity.blogspot.com/
"ironjustice" <ironj...@cashette.com> wrote in message
news:d0a951d1-020d-4a82...@a17g2000prm.googlegroups.com...
ironjustice
These are two different conditions. If they were treating "dementias"
they
would say so, not "Alzheimers". Please explain why smokers have very
high
rates of vascular problems. <<
Increased red blood cell production and lack of antioxidants.
Erythrocytosis causes kidney disease and kidney disease leads to
cognitive impairment.
Kidney Transplantation Can Improve Mental Performance, University of
Pittsburgh Study Finds
11/7/2008
NEW YORK (Reuters Health) - People with kidney disease often suffer
from cognitive impairment, but kidney transplantation can improve
their mental performance, research presented Thursday at the Society
of Nephrology's annual meeting in Philadelphia confirms.
--------------------------------
(The FASEB Journal. 2007;21:741.8)
© 2007 FASEB This Article
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Articles by Ogunshola, O.
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Articles by Ogunshola, O.
Articles by Gassmann, M.
--------------------------------------------------------------------------------
Chronic excessive erythrocytosis increases susceptibility to vascular
damage
Omolara Ogunshola and Max Gassmann
Institute of Veterinary Physiology, University of Zurich,
Winterthurerstrasse 260, Zurich, CH8057, Switzerland
ABSTRACT
Excessive erythrocytosis causes severely increased blood viscosity,
which may have significant detrimental effects on endothelial cells
and vascular endothelial function. Although our erythropoietin-
overexpressing transgenic mouse line (which has a hematocrit of 0.8–
0.9) has no significant increase in brain vascular permeability at 4–5
months of age under normoxic or acute hypoxic conditions, the brain
vascular endothelial cells appeared activated with increased luminal
protrusions reminiscent of ongoing inflammatory processes. Consistent
with this, we detected increased levels of ICAM-1 and von Willebrand
factor, markers of endothelial activation and damage, in brain tissue.
Current data shows that by 9–11 months of age these mice have
significantly increased serum levels of IL-6 and VCAM-1 expression.
Further nuclear NFkB levels are augmented and JNK and ERK/MAPK
pathways are also upregulated. In addition P53 levels are induced and
Bcl-XL levels decreased indicating activated cell death pathways. As
these mice die prematurely we propose that chronic excessive
erythrocytosis results in inflammation and endothelial damage
increasing susceptibility to vascular disease.
Supported by SNF grant 3100AO-112216.
Who loves ya.
Tom
Jesus Was A Vegetarian!
http://tinyurl.com/634q5a
Man Is A Herbivore!
http://tinyurl.com/4rq595
DEAD PEOPLE WALKING
http://tinyurl.com/zk9fk
>
> --http://healthycuriousity.blogspot.com/"ironjustice" <ironjust...@cashette.com> wrote in message
>
> news:d0a951d1-020d-4a82...@a17g2000prm.googlegroups.com...
> On Nov 6, 10:48 pm, "John Hasenkam" <jo...@goawayplease.com> wrote:
> Ridiculous, smokers have a much greater risk for vascular dementia.
> The
> research re smokers and Alz confers a slight advantage but is easily
> outweighed by other health risks. <<
>
> What makes you think this 'Alzheimers' they treated ISN'T vascular
> dementia .. ?
>
> Nicotinamide is also called niacin or niacinamide ..
>
> It is used for .. ? .. vascular problems ..
>
> Sooo .. it is coincidence this vitamin is used to treat vascular
> problems which cause vascular dementia which **closely** resembles
> Alzheimers' .. AND the vitamin is NOW shown to inhibit ..
> Alzheimers' ..
>
> Coincidences .. abound ..
>
> http://www.pubmedcentral.nih.gov/articlerender.fcgi?artid=1898481
>
> Niacin in Vascular Disorders and Hyperlipemia
> Reviewed by J R A Mitchell
> ------------
> Who loves ya.
> Tom
>
> > DEAD PEOPLE WALKINGhttp://tinyurl.com/zk9fk- Hide quoted text -
anon...@nowhere.you.know
Debs
Debs
ironjustice
What part of you ain't welcome on my threads don't you
understand .. ?
---------
Abstract
--------------------------------------------------------------------------------
Katarina Nägga, MD
Department of Geriatric Medicine
Linköping University Hospital
S-581 85 Linköping (Sweden)
Tel. +46 13 224093, Fax +46 13 227389, E-Mail Katarina.Na...@lio.se
Vol. 14, No. 4, 2002
--------------------------------------------------------------------------------
ironjustice
nicotinamide. <<
Orrr .. two pieces of my special bread .. Texas toast .. or in a
sandwich .. or as a side to your soup .. etc ..
It is enriched with vegetable lecithin to allow those B vitamins to be
absorbed at a very high rate ..
If one were to use hemp flour one might think then .. since hemp is
supposed to contain all that is required for life .. then a few pieces
of this bread .. enriched with vegetable lecithin would / could keep
one alive as a staple food .. all by itself ..
That's theory though ..
Any other requirements would be accomplished by breathing ..
Who loves ya.
Tom
Jesus Was A Vegetarian!
http://tinyurl.com/634q5a
Man Is A Herbivore!
http://tinyurl.com/4rq595
DEAD PEOPLE WALKING
http://tinyurl.com/zk9fk
The malts & yeast combination in it is a VitB bomb ...
ironjustice
Are more B vitamins needed in the modern
world full of PUFAs, lack of sleep and stress ? To combat and
detoxify the lipid peroxides ...
'mode of operation' / combat and detoxify the lipid peroxides ? <<
It may .. because it protects from metal toxicity which DOES cause
these peroxides you talk about.
B vitamins have been in controversy for awhile. Some argue "on paper B
vitamins are not antioxidants" .. others argue "in evidence based
medicine B vitamins are antioxidants" .. one argument being since they
don't add or remove an electron they are technically not antioxidants
and the other argument being they are **metal** chelators .. all of
them.
This plant study seems to give some type of credence to the metal
binding / toxicity .. thesis / theory ..
"Nicotinamide and nicotinic acid increased the defence against heavy
metals"
Increased metal tolerance in Salix by nicotinamide and nicotinic acid
Anna B. Ohlssona, , , Tommy Landbergb, Torkel Berglunda and Maria
Gregerb
aDepartment of Biotechnology, Royal Institute of Technology (KTH),
AlbaNova University Center, SE-106 91 Stockholm, Sweden bDepartment of
Botany, Stockholm University, SE-106 91 Stockholm, Sweden
Received 11 October 2007. Available online 22 April 2008.
Abstract
We have earlier shown that nicotinamide (NIC) and nicotinic acid (NiA)
can induce defence-related metabolism in plant cells; e.g. increase
the level of glutathione. Here we investigated if NIC and NiA could
increase the metal tolerance in metal sensitive clones of Salix
viminalis and whether this would be mediated via increased glutathione
level.
Salix clones, sensitive or tolerant to zinc (Zn), copper (Cu) and
cadmium (Cd) were grown in the presence of heavy metals (Cd, Cu or Zn)
or NIC and NiA as well as in combination.
In addition, the influence of N-acetyl-cystein (NAC) and l-2-
oxothiazolidine 4-carboxylate (OTC), stimulators of reduced
glutathione (GSH) biosynthesis, and the glutathione biosynthesis
inhibitor buthionine sulfoximine (BSO) was analysed. Tolerance was
measured as effects on root and shoot dry weight, and the glutathione
and metal concentrations in the tissues were analysed.
Results showed that NIC and NiA decreased the toxic effects of Cd, Cu
and Zn on growth significantly in sensitive clones, but also to some
extent in tolerant clones. However, the glutathione level and metal
concentration did not change by NIC or NiA addition.
Treatment with NAC, OTC or BSO did not per se influence the
sensitivity to Cd, although the glutathione level increased in the
presence of NAC and OTC and decreased in response to BSO.
The results suggest that NIC and NiA increased the defence against
heavy metals but not via glutathione formation per se.
Keywords: Glutathione; Heavy metal defence; Nicotinamide; Nicotinic
acid; Salix viminalis; Toxicity
Abbreviations: BSO, l-buthionine (S,R)-sulfoximine; GSH, glutathione;
NAC, N-acetyl-cystein; NIC, nicotinamide; NiA, nicotinic acid; OTC,
l-2-oxothiazolidine 4-carboxylate; PARP, poly(ADP-ribose)polymerase;
PC, phytochelatin; ROS, reactive oxygen species
doi:10.1016/j.plaphy.2008.04.004
Copyright © 2008 Elsevier Masson SAS All rights reserved.
Research article
Who loves ya.
Tom
Jesus Was A Vegetarian!
http://tinyurl.com/634q5a
Man Is A Herbivore!
http://tinyurl.com/4rq595
DEAD PEOPLE WALKING
http://tinyurl.com/zk9fk
> On Nov 6, 7:15 am, Taka <taka0...@gmail.com> wrote:
> Are more B vitamins needed in the modern
> world full of PUFAs, lack of sleep and stress ? To combat and
> detoxify the lipid peroxides ... <<
>
> BY what .. virtue .. ?
>
> What quality do they have to do that .. ?
>
> Do they say anything about the B vitamins doing that .. AS .. the
> 'mode of operation' / combat and detoxify the lipid peroxides ?
>
> "Nicotinamide belongs to a class of compounds called HDAC inhibitors"
>
> Who loves ya.
> Tom
>
> Jesus Was A Vegetarian!http://tinyurl.com/634q5a
>
> Man Is A Herbivore!http://tinyurl.com/4rq595
>
> DEAD PEOPLE WALKINGhttp://tinyurl.com/zk9fk
>
>
>
>
>
> > Taka- Hide quoted text -
anon...@nowhere.you.know
"Nicotinamide - one of two forms of vit b3
So let us ask again, is tobacco a good source of vit b3? Keeping in
mind the subject line and the original post.
ironjustice
You've been told a number of times to stay off my threads ..
Stay off my threads ..
anon...@nowhere.you.know
"Nicotinamide - one of two forms of vit b3
So let us ask again, is tobacco a good source of vit b3? Keeping in
The response:
"Stay off my threads .."
As soon as your false notions are corrected and there is absolutely no
chance someone will be hurt by them. With the kind of foot in mouth
silly mistakes seen in this thread someone needs to come behind and
clean up the mess.
ironjustice
You've been told a number of times to stay off my threads ..
Stay off my threads ..
You have for a number of years morphed into different disguises to
hawk your aspartame wares .. haven't ya ...
Been called a whack by EVERYONE it seems .. obviously with good ..
reason ..
Take all those .. whacko .. conclusions your theories AND personality
AND weird .. fkg .. hat .. somewhere OTHER than **my** threads ..
whacko ..
Go update your blogs ..
Your .. busy .. busy .. beautiful .. wonderful .. blogs ..
Understand .. ?
What you do is PROVE your theory ..
Do like Betty did ..
PROVE it ..
Try homeopathy ..
OD .. see if you get .. something ..
What will you .. get .. there .. smart guy ..
Some type of .. illness .. ?
Heh .. heh ..
Stay off my threads ..
ironjustice
Sooo .. there isn't as much loonacy in the theory of nicotine
standing
in for nicotinamide as these 'nutritionists' tell you. <<
"α7 nicotinic acetylcholine receptor (α7 nAChR)"
This .. coincidentally .. is the same receptor being TARGETED in
alzheimers or lack thereof.
"Activation of α7 nAChR may provide a new therapeutic pathway"
"Reduced by nicotine treatment"
"Inhibition of a7 nAChR in the cells exposed to high ferrous iron"
AJRCMB Articles in Press.
Published on April 12, 2007 as doi:10.1165/rcmb.2006-0240OC
ABSTRACT
New evidence indicates that neural mechanisms can downregulate
acute inflammation.
In these studies, we tested the potential role of the α7 nicotinic
acetylcholine receptor (α7 nAChR) in a rodent model of
acid-induced acute lung injury.
We first determined that the α7 nAChR was expressed by
alveolar macrophages and lung epithelial cells.
Then, using an acid-induced acute lung injury mouse model,
we found that nicotine, choline, and PNU-282987
(a specific α7 nAChR agonist) decreased excess lung water
and lung vascular permeability, and reduced protein
concentration in the bronchoalveolar lavage(BAL).
Deficiency of α7 nAChR resulted in a 2-fold increase in
excess lung water and lung vascular permeability.
The reduction of proinflammatory cytokines (MIP-2 and
TNF-α) in the BAL with nicotine probably resulted from
the suppression of NF-κB activation in alveolar macrophages.
The beneficial effect of nicotine was also tested in
rat model of acid-induced acute lung injury in which BAL
protein and RAGE, a marker of type I cell injury, were
reduced by nicotine treatment.
These results indicate that activation of α7 nAChR may
provide a new therapeutic pathway for the treatment of
acute lung injury.
---------------
Oxidative stress might be a mechanism connected with the
decreased α7 nicotinic receptor influenced by high-concentration
of fluoride in SH-SY5Y neuroblastoma cells
QIN GAO ; LIU Yan-Jie ; GUAN Zhi-Zhong ;
Abstract
The possible mechanism concerning decreased α7
nicotinic acetylcholine receptor (nAChR) influenced
by fluorosis was investigated.
SH-SY5Y cells were exposed to fluoride within the
range of 0.05-5 μM, or ferrous iron (1-100 pM), a free
radical inducer.
The levels of α7 nAChR expression, lipid peroxidation
and protein oxidation were detected.
The results showed that both high-concentrations of fluoride
and ferrous iron induced increased levels of lipid peroxidation
and protein oxidation in SH-SY5Y cells with
concentration-dependent manners.
In addition, inhibition of a7 nAChR at protein level was observed
in the cells exposed to high amounts of fluoride or ferrous iron.
Furthermore, a declined value of Bmax in [125I]α-bungarotoxin
binding sites was found in the cells treated with the
high-concentration of fluoride.
Interestingly, antioxidants (vitamin E and glutathione) can attenuate
the inhibition of the receptor induced by fluoride.
These findings suggest that oxidative stress resulted from fluorosis
might directly induce the deficit of a7 nAChR.
Revue / Journal Title
Toxicology in vitro ISSN 0887-2333 CODEN TIVIEQ
Source / Source
2008, vol. 22, no4, pp. 837-843 [7 page(s) (article)]
Langue / Language
Anglais
Editeur / Publisher
Elsevier Science, Oxford, ROYAUME-UNI (1987) (Revue)
Mots-clés d'auteur / Author Keywords
Fluoride ; Ferrous iron ; α7 Nicotinic receptor ; Oxidative stress ;
SH-SY5Y cells ;
Localisation / Location
INIST-CNRS, Cote INIST : 21203, 35400017375834.0020
-----------------
Who loves ya.
Tom
Jesus Was A Vegetarian!
http://tinyurl.com/2r2nkh
Man Is A Herbivore!
http://tinyurl.com/a3cc3
DEAD PEOPLE WALKING
http://tinyurl.com/zk9fk
>
> People in families predisposed to alzheimers' don't 'get' alzheimers
> if they smoke .. those in the family who DON'T smoke .. DO .. get
> alzheimers'.
> -------
> Vitamin B3 Reduces Alzheimer's Symptoms, Lesions: Clinical Trial On
> Nicotinamide Effect In Alzheimer's Patients
> ScienceDaily (Nov. 5, 2008) -- An over-the-counter vitamin in high
ironjustice
nicotinamide. The malts & yeast combination in it is a VitB bomb ...
<<
I'm not sure if there is really any difference between non-alcoholic
beer and alcoholic beer but .. I've always held .. non-alcoholic beer
should theoretically be very good for you ..
"Consumption of non-alcoholic beer produces a decrease in oxidative
stress that can have a beneficial impact on cardiovascular risk."
Topic: Consumption of Alcohol-Free Beer May Lower Oxidative Stress
Keywords: OXIDATIVE STRESS - Alcohol-Free Beer
Reference: "Effects of alcohol-free beer on lipid profile and
parameters of oxidative stress and inflammation in elderly women,"
Alvarez JR, Codoner-Franch P. et al, Nutrition, 2008 Oct; [Epub ahead
of print]. (Address: Spanish Society of Dietetics and Food Science,
Madrid, Spain).
Summary: In a study involving 29 nuns aged 58 to 73 years, results
indicate that regular consumption of alcohol-free beer may be
associated with decreased oxidative stress. The nuns received 500 mL/
day of alcohol-free beer, with meals, for a period of 45 days. At
intervention end, antibody titers to oxidized low-density lipoprotein
were significantly lower, and thiobarbituric acid-reactive substances
(-18%) and plasma carbonyl group content (-21%) were decreased,
compared with baseline. Additionally, increases in alpha-tocopherol
levels (+9%) and erythrocytic glutathione levels (+29%) were observed.
Thus, the authors of this study conclude, "Consumption of non-
alcoholic beer produces a decrease in oxidative stress that can have a
beneficial impact on cardiovascular risk."
Who loves ya.
Tom
Jesus Was A Vegetarian!
http://tinyurl.com/634q5a
Man Is A Herbivore!
http://tinyurl.com/4rq595
DEAD PEOPLE WALKING
http://tinyurl.com/zk9fk
> Now why are novadays people so deficient in B vitamins that they have
> tosmokeand drink beer ??? Are more B vitamins needed in the modern
anon...@nowhere.you.know
hawk your aspartame wares .. haven't ya ..."
Getting more paranoid are we? Not me, I have not posted on that product
to the best of my knowledge. Nor have I posted false information
confusing a toxin from tobacco as being a form of vit b3; among other
silly foot in mouth tricks you do on a regular basis. Do you smoke too?
Just because you are paranoid does not mean someone will not be coming
behind you to clean up your mess.
ironjustice
You've been told a number of times to stay off my threads ..
Stay off my threads ..
You have for a number of years morphed into different disguises to
hawk your aspartame wares .. haven't ya ...
anon...@nowhere.you.know
You have for a number of years morphed into different disguises to
hawk your aspartame wares .. haven't ya ...
Been called a whack by EVERYONE it seems .. obviously with good ..
reason .."
Oh dear, the paranoia is more advanced then we first suspected. Prove I
am the person you think resides under your bed.
Confusion is one primary symptom of low iron, along with other cognitive
and mental disorders.
Just because you are paranoid does not mean someone will not come along
after to clean up your messes so others will not be hurt.
ironjustice
You've been told a number of times to stay off my threads .. aspartame
boy ..
Stay off my threads ..
Been called a whack by EVERYONE it seems .. obviously with good ..
reason ..
Take all those .. whacko .. conclusions your theories AND personality
AND weird .. fkg .. hat .. somewhere OTHER than **my** threads ..
whacko ..
Go update your blogs ..
Who loves ya.
anon...@nowhere.you.know
after to clean up your messes so others will not be hurt.
Hmmmm, wonder if tobacco helps with low iron, ya know, all that vit b3
in it and all.
ironjustice
anon...@nowhere.you.know
b3. Do you by any chance partake of that toxic substance?
Here comes de broom.
ironjustice
ironjustice
other argument being they are **metal** chelators <<
"Metal chelating properties of nicotine"
Both the d-(+) and l-(-) Enantiomers of Nicotine Inhibit Abeta
Aggregation and
Cytotoxicity.
Moore SA, Huckerby TN, Gibson GL, Fullwood NJ, Turnbull S, Tabner BJ,
El-Agnaf
OM, Allsop D.
Department of Biological Sciences and Magnetic Resonance Laboratory,
University
of Lancaster, Lancaster LA1 4YQ, U.K.
The underlying cause of Alzheimer's disease is thought to be the
aggregation of
monomeric beta-amyloid (Abeta), through a series of toxic oligomers,
which
forms the mature amyloid fibrils that accumulate at the center of
senile
plaques.
It has been reported that l-(-)-nicotine prevents Abeta aggregation
and toxicity, and inhibits senile plaque formation.
Previous NMR studies have suggested that this could be due to
the specific binding of l-(-)-nicotine to histidine residues (His(6),
His(13),
and His(14)) in the peptide.
Here, we have looked at the effects of both of the l-(-) and d-(+)
optical
enantiomers of nicotine on the aggregation and cytotoxicity of
Abeta(1-40). Surprisingly, both enantiomers inhibited aggregation of
the peptide and
reduced the toxic effectsof the peptide on cells.
In NMR studies with Abeta(1-40), both enantiomers of nicotine were
seen to interact with the three histidine residues.
Overall, our data indicate that nicotine can delay Abeta fibril
formation and maintain a population of less toxic Abeta species.
This effect cannot be due to a highly specific binding interaction
between nicotine and Abeta, as previously thought, but could be due
instead to weaker, relatively nonspecific binding, or to the
antioxidant or metal chelating properties of nicotine. d-(+)-Nicotine,
being biologically much less active than l-(-)-nicotine, might be a
useful
therapeutic agent.
PMID: 14730987
ironjustice
other argument being they are **metal** chelators "Metal chelating
properties of nicotine" <<
Iron: a new target for pharmacological intervention in
neurodegenerative diseases.
Semin Pediatr Neurol. 2006 Sep;13(3):186-97.
Whitnall M, Richardson DR.
Iron Metabolism and Chelation Program, Department of Pathology,
University of Sydney, Sydney, New South Wales, Australia.
Iron (Fe) is an essential element that is imperative for the redox-
driven processes of oxygen transport, electron transport, and DNA
synthesis.
However, in the absence of appropriate storage or chelation, excess-
free Fe readily participates in the formation of toxic-free radicals,
inducing oxidative stress and apoptosis.
A growing body of evidence suggests that Fe may play some role in
neurodegenerative diseases such as Huntington disease, Alzheimer's
disease, Parkinson's disease, and particularly Friedreich's ataxia.
This review examines the role of Fe in the pathology of these
conditions and the potential use of Fe chelators as therapeutic agents
for the treatment of neurodegenerative disorders.
Consideration is given to the features that comprise a clinically
successful Fe chelator, with focus on the development of ligands such
as desferrioxamine, clioquinol, pyridoxal isonicotinoyl hydrazone, and
other novel aroylhydrazones.
PMID: 17101458
Who loves ya.
Tom
anon...@nowhere.you.know
driven processes of oxygen transport, electron transport, and DNA
synthesis.
However, in the absence of appropriate storage or chelation, excess-
free Fe readily participates in the formation of toxic-free radicals,
inducing oxidative stress and apoptosis.
A growing body of evidence suggests that Fe may play some role in"
Just so, when the normal activity of the human body to control iron is
distorted such can happen. The prime question then becomes what causes
this distortion so the resulting iron levels can be avoided. We need
the cause not the result which is the iron levels.
One is at a loss to see the cause in using tobacco, unless the vit b3
some claim it has is the problem? Why then would one follow the subject
line and use tobacco?
anon...@nowhere.you.know
So is it a form of vit b3 or not? Farmers used to feed horses tobacco
because nicotine is a toxic substance which would kill intestinal worms.
anon...@nowhere.you.know
ironjustice
Been called a whack by EVERYONE it seems .. obviously with good ..
reason ..
Take all those .. whacko .. conclusions your theories AND personality
AND weird .. fkg .. hat .. somewhere OTHER than **my** threads ..
whacko ..
Go update your blogs ..
Iron: a new target for pharmacological intervention in
neurodegenerative diseases.
Semin Pediatr Neurol. 2006 Sep;13(3):186-97.
Whitnall M, Richardson DR.
Iron Metabolism and Chelation Program, Department of Pathology,
University of Sydney, Sydney, New South Wales, Australia.
Iron (Fe) is an essential element that is imperative for the redox-
driven processes of oxygen transport, electron transport, and DNA
synthesis.
However, in the absence of appropriate storage or chelation, excess-
free Fe readily participates in the formation of toxic-free radicals,
inducing oxidative stress and apoptosis.
A growing body of evidence suggests that Fe may play some role in
ironjustice
PMID: 17101458
ironjustice
Been called a whack by EVERYONE it seems .. obviously with good ..
reason ..
Take all those .. whacko .. conclusions your theories AND personality
AND weird .. fkg .. hat .. somewhere OTHER than **my** threads ..
whacko ..
Go update your blogs ..
Iron: a new target for pharmacological intervention in
PMID: 17101458
anon...@nowhere.you.know
not well clean up this mess.
ironj...@aol.com
ironj...@aol.com
using an acid-induced acute lung injury mouse model,
we found that nicotine, choline, and PNU-282987
(a specific α7 nAChR agonist) decreased excess lung water
and lung vascular permeability, <<
It seems to me .. the words nicot - ine .. and chol - ine .. are
coming up alot .. and they both seem to be capable of doing the same
thing .. increasing .. bliss ..
Now .. would could the decrease of CONSUMPTION / destruction OF ..
chol - ine BE the .. 'need' FOR .. nicot - ine .. and the like .. ? ..
IE: gambling .. sex addiction .. etc .. / DOPE - amine .. ?
http://www.sciencenews.org/articles/20050625/timeline.asp
A new vitamin that is essential for liver function and that may play
an important role in controlling diabetes was described at the
meeting
of the American and Canadian Medical Associations by one of its
discoverers, Dr. C.H. Best of Toronto, codiscoverer of insulin, the
life-saving remedy for diabetes.
The new vitamin has a real name, choline, instead of a letter, as do
most other members of the vitamin family. It is found in many foods,
but the best sources are meat, egg yolk, and yeast.
Dr. M. Hershey and Miss M.E. Huntsman, of the University of Toronto,
were responsible for many of the fundamental observations that led up
to the discovery of the significance of choline, Dr. Best stated.
Lack of this vitamin causes the serious condition of fatty liver, Dr.
Best said. When the liver becomes fatty, it fails to make sugar or
handle bile or do many of the things it should do, he explained.
The vitamin was discovered in the course of insulin investigations.
Dogs that had no pancreas, the insulin-secreting organ, failed to
live
for more than a few months, even when given insulin injections. When
they were fed minced pancreas, in addition to the insulin, they lived
for years.
However, chemical studies of the pancreas showed that in addition to
producing insulin and a digestive ferment, this organ contained
choline, and that it was the choline in the diet of minced pancreas
that kept the dogs alive after they had lost their own pancreases.
--------------------------------------------------------------------------------
"Lecithin may therefore be the method of choice for
accelerating acetylcholine synthesis"
Lancet. 1977 Jul 9;2(8028):68-9. Related Articles, Links
Lecithin consumption raises serum-free-choline levels.
Wurtman RJ, Hirsch MJ, Growdon JH.
Consumption of choline by rats sequentially increases serum-choline,
brain-choline, and brain-acetylcholine concentrations. In man
consumption of choline increases in levels in the serum and
cerebrospinal fluid; its administration is an effective way of
treating tardive dyskinesia.
We found that oral lecithin is considerably more
effective in raising human serum-choline levels than an equivalent
quantity of choline chloride. 30 minutes after ingestion of choline
chloride (2-3 g free base), serum-choline levels rose by 86% and
returned to normal values within 4 hours; 1 hour after lecithin
ingestion, these levels rose by 265% and remained significantly
raised for 12 hours.
Lecithin may therefore be the method of choice for
accelerating acetylcholine synthesis by increasing the availability
of choline, its precursor in the blood.
PMID: 69151 [PubMed - indexed for MEDLINE]
--------------------------------------------------------------------------------
http://www.medicalnewstoday.com/medicalnews.php?newsid=72010
New Study Indicates That People May Need More Dietary Choline Than
Previously Thought
Article Date: 30 May 2007 - 9:00 PDT
A new study published in the May issue of the American Journal of
Clinical Nutrition indicates that the current recommended Adequate
Intake (AI) for choline may, in fact, be inadequate for some people.1
Choline is an essential nutrient for normal functioning of all cells,
including those involved with liver metabolism, brain and nerve
function, memory, and the transportation of nutrients throughout the
body.
In this depletion-repletion study, 57 adult subjects (26 men, 16
premenopausal women and 15 postmenopausal women) were fed a diet
containing 550 mg of choline for 10 days, then fed less than 50 mg a
day of choline for up to 42 days.
* When deprived of the nutrient, 77 percent of men, 80 percent of
postmenopausal women and 44 percent of premenopausal women developed
fatty liver or muscle damage.
* Six men (23 percent) developed these signs while consuming the
initial 550 mg of daily choline, even though 550 mg is the current AI
for men.
* Nineteen percent of the subjects required as high as 825 mg of
daily choline to prevent or reverse the organ dysfunction associated
with
the low-choline diet, an amount significantly higher than the current
AI.
* For all participants, blood homocysteine levels increased during
choline depletion. Other studies have associated high homocysteine
levels with heart disease.
"These study results clearly indicate that some adults, notably men
and post-menopausal women, need more choline than is recommended by
the current AI," says study co-author Kerry-Ann da Costa, PhD, a
research assistant professor at the University of North Carolina at
Chapel Hill. "We hope these findings will aid the Institute of
Medicine in refining the Dietary Reference Intake (DRI) of this
nutrient."
This study is the most complete study of choline requirements to date
and is the first to include women. Its division of participants into
two groups - one receiving dietary supplementation of folic acid and
one not - also determined that susceptibility to choline deficiency
was not altered by folic acid supplementation.
Closing the Choline Gap
Additional research on the population demonstrated that choline
intake
is far below the current AI, a concern that intakes may be too low to
meet the needs of many individuals.
* Research conducted at Iowa State University found that only 10
percent or less of older children, men, women and pregnant women in
America get the AI of choline each day.2
* A separate study presented this month at the National Nutrient Data
Bank Conference found that choline intake decreases with age and that
adults ages 71 and older consume an average of about 264 milligrams
per day - roughly half of the AI for choline.3
Eggs, beef liver, chicken liver and wheat germ are considered
excellent sources of choline. Two eggs contain 280 milligrams of
choline, half the recommended daily supply.
"Eggs are a practical food that can help people get the choline they
need, along with several other nutrients, at just 75 calories an
egg,"
says registered dietitian Maye Musk. "Choline is actually found in
the
yolk of the egg, so people who consistently only eat egg whites may
be
missing out on a key nutrient opportunity."
Why Choline Matters
The importance of dietary choline has been well-established.
* A 2004 study in the American Journal of Epidemiology linked poor
dietary choline to adverse outcomes during pregnancy, including a
four-
fold increased risk of having a baby with a neural tube defect. 4 * A
research review published in the Annual Reviews of Nutrition suggests
that choline plays an important role in normal fetal development,
particularly during the stages that involve knowledge acquirement and
life-long memory function. 5
###
For more information, on the benefits of choline for pregnant women,
visit http://www.pregnancyfoodguide.org/ or http://www.enc-online.org/.
About the American Egg Board (AEB)
AEB is the U.S. egg producer's link to the consumer in communicating
the value of 'the incredible edible egg' and is funded from a
national
legislative checkoff on all egg production from companies with
greater
than 75,000 layers in the continental United States. The board
consists of 18 members and 18 alternates from all regions of the
country who are appointed by the Secretary of Agriculture. The AEB
staff carries out the programs under the board direction. AEB is
located in Park Ridge, Ill. Visit http://www.aeb.org/ for more
information.
About the Egg Nutrition Center (ENC)
ENC was established in 1979 for the purpose of providing commercial
egg producers and processors, health promotion agencies, and
consumers
with a resource for scientifically accurate information on egg
nutrition and the role of eggs in the health and nutrition of the
American diet. The center exists under a cooperative agreement
between
the American Egg Board (AEB) and United Egg Producers (UEP). ENC is
located in Washington, DC. Visit http://www.enc-online.org/ for more
information.
1 Fischer LM, et al. Sex and menopausal status influence human
dietary
requirements for the nutrient choline. Am J Clin Nutr 2007;
85:1275-85.
2 Jensen HH, et al. Choline in the diets of the US population:
NHANES,
2003-2004, Iowa State University (presented at Experimental Biology
2007, Washington DC)
3 Keast DR, Food sources of choline in the diets of US older adults:
NHANES, 1999-2004." (presented at the 31st National Nutrient Databank
Conference, Washington DC) Food sources of choline in the diets of US
older adults: NHANES, 1999-2004.
4Shaw GM, et al. Periconceptional dietary intake of choline and
betaine and neural tube defects in offspring. Am J Epid 2004; 160(2):
102-109.
5Zeisel SH. Choline:critical role during fetal development and
dietary
requirements in adults. Annu Rev Nutr, 2006; 26:229-50.
Contact: Egg Nutrition Media Hotline
Edelman Public Relations
----------------------------------
ironjustice
On Nov 8, 5:50 pm, ironjustice <ironjust...@cashette.com> wrote:
Then,
using an acid-induced acute lung injury mouse model, we found that
decreased excess lung water and lung vascular permeability, <<
"Decreased excess lung water "
THAT latest article seems to confirm this one from awhile ago ..
Nicotinic acid reduction of plasma volume loss after thermal trauma.
Science. 1976 Feb 27;191(4229):861-2.
Hilton JG, Wells CH.
Intravenous administration of nicotinic acid to the anesthetized dog
prior to thermal trauma reduced plasma loss at 10 minutes after burn
from 7 milliliters per kilogram to less than 2 millimeters per
kilogram.
During the next 50 minutes plasma loss was the same in treated and
untreated animals.
An additional dose of nicotinic acid 30 minutes after burn prevented
this further loss.
----------------
http://www.pubmedcentral.nih.gov/articlerender.fcgi?artid=1396423
Abstract
Pulmonary extravascular water has been measured as lung thermal volume
(LTV) in a group of nine burned patients.
Transducer-detectable indicators were used to permit frequent
repetition and quick results.
Concurrent recordings were made of cardiac output, pulmonary capillary
wedge pressure and the usual hemodynamic variables.
Moderate elevation of LTV was seen in all, reaching a maximum value
before peripheral edema formation was complete.
Left heart filling pressures were low as plasma albumin
concentration.
Clinical pulmonary edema occurred in one patient treated mostly with
crystalloid solution.
In several, a secondary peak coincided with edema mobilization.
Who loves ya.
Tom
Jesus Was A Vegetarian!
http://tinyurl.com/634q5a
Man Is A Herbivore!
http://tinyurl.com/4rq595
DEAD PEOPLE WALKING
http://tinyurl.com/zk9fk
>
> visithttp://www.pregnancyfoodguide.org/orhttp://www.enc-online.org/.
>
> About the American Egg Board (AEB)
>
> AEB is the U.S. egg producer's link to the consumer in communicating
> the value of 'the incredible edible egg' and is funded from a
> national
> legislative checkoff on all egg production from companies with
> greater
> than 75,000 layers in the continental United States. The board
> consists of 18 members and 18 alternates from all regions of the
> country who are appointed by the Secretary of Agriculture. The AEB
> staff carries out the programs under the board direction. AEB is
> located in Park Ridge, Ill. Visithttp://www.aeb.org/for more
> information.
>
> About the Egg Nutrition Center (ENC)
>
> ENC was established in 1979 for the purpose of providing commercial
> egg producers and processors, health promotion agencies, and
> consumers
> with a resource for scientifically accurate information on egg
> nutrition and the role of eggs in the health and nutrition of the
> American diet. The center exists under a cooperative agreement
> between
> the American Egg Board (AEB) and United Egg Producers (UEP). ENC is
> located in Washington, DC. Visithttp://www.enc-online.org/for more
anon...@nowhere.you.know
"Nicotinic acid" A form of vit b3
The two are very different substances, you keep confusing them because
of the similar spelling. Foot in mouth disease, a typical mistake an
amateur makes.
De broom, he is a cleaning so others they done not get hurt.
ironjustice
Nicotinamide belongs to a class of compounds called HDAC inhibitors,
which have been shown to protect the central nervous system in rodent
sclerosis. <<
Excess iron in neurons is involved in Parkinson's disease
October 28, 2008
http://www.inserm.fr/en/presse/communiques/hirsch_281008.html
Limiting excess iron in dopaminergic neurons (1) may protect against
Parkinson's disease. This is the conclusion of studies carried out by
Etienne Hirsch, CNRS research director and his team of researchers in
Inserm-UPMC/Université Pierre-et-Marie-Curie Mixed Unit 67 "Neurologie
et Thérapeutique Expérimentale" and published in the journal PNAS.
They showed that affected rodents over-express DMT1, responsible for
iron uptake by neurons. This causes iron accumulation and the death of
the neurons. The researchers therefore inhibited the activity of this
transporter in order to evaluate the consequences on the disease.
Mutant mice were twice less affected by the disease than controls.
Parkinson's disease represents the second neurodegenerative disorder
after Alzheimer's disease in France. It is caused by the degeneration
of dopaminergic neurons in a precise area of the brain called the
substantia nigra. Affected patients therefore develop tremors and
stiffness and their movements are slowed.
The causes of the disease are still poorly understood. However,
examination of the brains of patients who died with the disease have
shown that the degenerating neurons contain a very high iron content
compared to normal levels. Iron is essential for the correct
functioning of the body, but at high concentrations it damages cell
components. "Iron accumulation causes oxidative stress which destroys
lipids and proteins in particular and causes cell death. We therefore
suspected that an iron excess may be involved in the degeneration of
neurons in affected patients," pointed out Etienne Hirsch, director of
the Inserm-Université Pierre et Marie Curie unit.
To clarify this point, the researchers tried to understand how iron
accumulated to such high levels in diseased cells. They rapidly
orientated their research towards DMT1, which is responsible for
neuronal iron uptake. The first stage of their work consisted in
chemically inducing Parkinson's disease in mice in order to observe
the possible consequences on the expression of these transporters.
They noted that their numbers doubled in affected mice in only one to
two days after the injection. In parallel, there was a very large
increase in the iron concentration of nerve cells, causing a
predictable oxidative stress followed by neuronal death after five
days.
After obtaining this result, the researchers wanted to observe the
effect caused by inhibition of this transporter in rodents. They
therefore studied mice in which the activity of DMT1 was greatly
impaired and subjected these rodents to a toxin causing Parkinson's
disease. These rodents resisted the disease much better than control
mice. They were two times less affected, suggesting that the damage to
the transporter protected them from the effect of the toxin. "These
results are quite conclusive. We have shown that by inhibiting the
activity of DMT1, we protected rodents from the disease," concluded
Etienne Hirsch.
Footnotes:
(1) Dopaminergic neurons synthetize dopamine, a brain
neurotransmitter. Researchers have shown that there is a relation
between dopamine deficiency and neurological disorders surh as
Parkinson's disease.
------------
Source
Divalent metal transporter 1 (DMT1) contributes to neurodegeneration
in animal models of Parkinson's disease
Julio Salazara,b,c, Natalia Menac, Stephane Hunota,b, Annick
Prigenta,b, Daniel Alvarez-Fischera,b, Miguel Arredondoc, Charles
Duyckaertsa,b, Veronique Sazdovitcha,b, Lin Zhaod, Laura M. Garrickd,
Marco T. Nun˜ ezc, Michael D. Garrickd, Rita Raisman-Vozaria,b, and
Etienne C. Hirscha,b
PNAS, October 27 th
a Neurologie et Thérapeutique Expérimentale, Institut National de la
Santé et de la Recherche Médicale, Unité Mixte de Recherche S679, 47
Boulevard de l'Hôpital, 75013 Paris, France;
b Unité Mixte de Recherche S679, Université Pierre-et-Marie-Curie -
Université Paris 6, Boulevard de l'Hôpital, 75013 Paris, France;
c Millennium Institute for Cell Dynamics and Biotechnology and
Department of Biology, Faculty of Sciences, Universidad de Chile, Las
Encinas 3370, Santiago, Chile;
d Department of Biochemistry, University at Buffalo, State University
of New York, 140 Farber Hall, 3435 Main Street, Buffalo, NY 14214.
Researcher contact
Etienne Hirsch
Inserm Unit 679
Université Pierre-et-Marie-Curie "Neurologie et Thérapeutique
Expérimentale"
Phone: 01 42 16 22 02
etienne...@upmc.fr
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
> Sooo .. there isn't as much loonacy in the theory of nicotine standing
> in for nicotinamide as these 'nutritionists' tell you.
>
> People in families predisposed to alzheimers' don't 'get' alzheimers
> if they smoke .. those in the family who DON'T smoke .. DO .. get
> alzheimers'.
> -------
> Vitamin B3 Reduces Alzheimer's Symptoms, Lesions: Clinical Trial On
> Nicotinamide Effect In Alzheimer's Patients
> ScienceDaily (Nov. 5, 2008) — An over-the-counter vitamin in high
> doses prevented memory loss in mice with Alzheimer's disease, and UC
> Irvine scientists now are conducting a clinical trial to determine its
> effect in humans.
>
> Nicotinamide, a form of vitamin B3, lowered levels of a protein called
> phosphorylated tau that leads to the development of tangles, one of
> two brain lesions associated with Alzheimer's disease. The vitamin
> also strengthened scaffolding along which information travels in brain
> cells, helping to keep neurons alive and further preventing symptoms
> in mice genetically wired to develop Alzheimer's.
>
> "Nicotinamide has a very robust effect on neurons," said Kim Green,
> UCI scientist and lead author of the study. "Nicotinamide prevents
> loss of cognition in mice with Alzheimer's disease, and the beauty of
> it is we already are moving forward with a clinical trial."
>
> The study appears online Nov. 5 in the Journal of Neuroscience.
>
> Nicotinamide is a water-soluble vitamin sold in health food stores. It
> generally is safe but can be toxic in very high doses. Clinical trials
> have shown it benefits people with diabetes complications and has anti-
> inflammatory properties that may help people with skin conditions.
>
> Nicotinamide belongs to a class of compounds called HDAC inhibitors,
> which have been shown to protect the central nervous system in rodent
> models ofParkinson'sand Huntington's diseases and amyotrophic
> Who loves ya.
> Tom
>
ironj...@aol.com
we found that nicotine, choline, and PNU-282987 (a specific á7 nAChR
agonist)
decreased excess lung water and lung vascular permeability, <<
Do you need more choline?
Kirk McKoy / Los Angeles Times
Flintstones Complete’s maker says its choline aids healthy brain
function.
The supplement is touted as beneficial for mood, mental acuity and
heart health. But many get enough in their diets.
By Chris Woolston
November 17, 2008
From arginine to zinc, there's a frighteningly long list of nutrients
that you can't live without. You certainly don't want to fall short of
choline -- a nutrient that the body uses to make cell membranes and
key compounds in the brain.
Choline is found in many foods, including eggs, beef, salmon, wheat
germ and broccoli. That's the good news about essential nutrients:
They tend to show up regularly in foods, which helps explain how
humans managed to survive quite a while before the invention of the
multivitamin.
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But not everyone is willing to take chances on diet alone. Like many
other nutrients, choline is now a commodity in the supplement market.
Touted as an aid for mood, mental sharpness and cardiovascular health,
choline supplements are sold at health food stores everywhere.
GNC sells 100 tablets of 250-milligram choline for about $7. Users are
instructed to take one or two tablets each day. You can buy 60 tablets
of 500-milligram choline from Physician Formulas for about $15.
Physician Formulas also offers choline as one of the main ingredients
(along with ginkgo and ginseng) in Mind Power Rx, a supplement that
supposedly improves alertness and focus. Ninety capsules -- each
containing 25 milligrams of choline -- costs about $30. Choline is
also showing up in multivitamins: Even Flintstones Complete now
includes 38 milligrams of choline per tablet.
The claims: According to the GNC label, its choline supplement
"supports brain, liver and cardiovascular health." The Physician
Formulas website claims that "most people who take a choline
supplement notice having more mental focus and being more alert." The
company also claims that Mind Power Rx will improve memory,
concentration and focus. The Flintstones Vitamins website says that
the choline in Flintstones Complete will "support healthy brain
function."
The bottom line: Choline is undoubtedly a vital nutrient, and anyone
who skimps on it does so at their own peril, says Dr. Steven Zeisel,
professor of nutrition and pediatrics at the University of North
Carolina at Chapel Hill and the director of the UNC Clinical Nutrition
Research Center. But since many people already get plenty of choline
in their diets, the value of supplements is uncertain.
Men should get at least 550 milligrams of choline each day and women
need at least 425 milligrams a day, according to guidelines set by the
National Academy of Sciences. A single egg contains about 130
milligrams, 3 ounces of beef contains about 70 milligrams, a cup of
cooked broccoli contains about 60 milligrams, and a glass of milk
contains about 40 milligrams.
Even people who aren't getting enough choline -- perhaps they avoid
eggs or have a very low-fat diet -- shouldn't expect an instant pick-
me-up from supplements, Zeisel says. "I don't think they would notice
more energy or a better mood."
But for pregnant women, the benefits of extra choline could go far
deeper than a mood lift, says Marie Caudill, an associate professor of
nutritional sciences and genomics at Cornell University in Ithaca,
N.Y. Like folic acid, choline seems to help prevent neural-tube
defects in developing fetuses, and it may also help prevent cleft
palates. There's also intriguing evidence that choline can supercharge
developing brains. When researchers give pregnant rats extra choline,
the pups showed impressive memory skills throughout their entire
lives.
Caudill says it's too early to say if pregnant women who get extra
choline can expect extra-smart children. Still, she says, women who
are pregnant or breast-feeding should try to get plenty of the
nutrient every day. "My first inclination would be to recommend foods
that are high in choline."
Mothers aren't the only ones who might benefit from choline. The
nutrient might also help nourish brain cells in young children, Zeisel
says, although the amount in Flintstones Complete may be too small to
make much difference. High levels of choline in adults may help reduce
homocysteine, a compound that can increase the risk of heart disease.
A shortfall of choline can cause liver damage known as fatty liver.
(On the flip side, exceeding 3,500 milligrams daily -- the highest a
person can consume without risk -- could result in a fishy body odor
and an unsafe drop in blood pressure.)
Despite these potential benefits, Zeisel doesn't believe that
supplements are always in order. "I would try to get my diet in good
shape first," he says. If that's not possible, he says, choline
supplements could be a valuable addition.
Woolston is a freelance writer.
Is there a consumer product you'd like the Healthy Skeptic to examine?
E-mail the details to hea...@latimes.com. Read other Healthy Skeptic
columns at www.latimes.com/ skeptic.
ironjustice
we found that nicotine, choline, and PNU-282987 (a specific á7 nAChR
agonist) decreased excess lung water and lung vascular permeability,
<<
"It can be seen that participants who ate higher choline amounts had,
on average, 22% lower CRP levels, 26% lower interleukin-6 levels, and
6% lower tumor necrosis factor-alpha levels, compared with those who
ate least choline. Similarly, higher betaine consumption was
associated with 10% less homocysteine, 19% less CRP, and 12% less
tumor necrosis factor-alpha in the blood."
Drilling Down into the Mediterranean Diet
Summarized by Robert W. Griffith, MD
2/29/2008
Summary
A study of healthy adults in Greece shows that their consumption of
two substances, choline and betaine, are linked to the level of
inflammatory markers (e.g. CRP) in the blood; a higher intake is
associated with lower inflammatory markers, which themselves are
possible precursors of cardiovascular disease.
Introduction
Since the realization that people living in Mediterranean countries
had a decreased risk of coronary artery disease compared with northern
Europeans and North Americans, the search has been on for the factor
or factors responsible. Not surprisingly, nutritional factors have
been in the forefront of the search. Recently, the antioxidant
resveratrol has become a favorite candidate for a protective effect -
news that's been welcomed by wine lovers, although the amounts of the
compound in wine are very, very small.
However, other candidates are emerging for the role of leading factor
in the Mediterranean diet. Greek researchers have just published a
study of dietary choline and betaine intake in the American Journal of
Clinical Nutrition. These substances have been reported to affect the
homocysteine level, itself a factor for cardiovascular disease. As
they are both plentiful in the Mediterranean diet, the researchers
decided to examine the links between their intake and the levels of
low-grade inflammation in the body.
What was done
The ATTICA study was done on healthy adults between 18 and 89 years
old living in the province of Attica, Greece. Over 3,000 inhabitants
agreed to participate. They were all interviewed to ascertain their
health status, and were given a semi-quantitative food-frequency
questionnaire, using pictures to represent different portion sizes.
Daily choline and betaine intakes were calculated from food-
composition tables.
Fasting blood samples were taken and analyzed for the following
inflammatory markers: C-reactive protein (CRP), interleukin-6,
homocysteine, and tumor necrosis factor-alpha. In addition, fasting
glucose and total cholesterol was determined.
The socio-economic data collected included average income, education
levels, smoking status, and physical activity level. Height, weight,
and blood pressure were recorded, and the body mass index (BMI)
calculated.
For the purpose of analysis, the participants were allocated to three
different categories (or tertiles) according to their daily choline
intake: less than 250 mg, 250-310 mg, and more than 310 mg daily.
Similar tertiles were created for betaine: less than 260 mg, 260-350
mg, and more than 350 mg daily.
What the results showed
There were roughly 1,500 men and 1,500 women making up a total
collective of 3,000 people. Their average age was 40; the average BMI
was 26 (i.e. slightly overweight, not obese). The major sources of
choline in their diets were: beef, potatoes, whole milk, fish,
legumes, broccoli, eggs, and poultry. For betaine, the major sources
were: spinach, 'vegetable pie', pasta, white bread, pizza, whole-wheat
bread, and seafood.
The participants with higher choline levels ate more servings of
fruit, vegetables, legumes, and red meat. Those with higher betaine
levels were older, more active, and, as for choline, ate more fruit,
vegetables, legumes and red meat. Gender, alcohol use, BMI,
socioeconomic status, and the presence of diabetes or high blood
pressure were not different with different choline or betaine
intakes.
The average inflammatory markers levels found in the different
tertiles for choline and betaine are given in the tables below:
Markers Choline Tertiles
Low Mid High
Homocysteine (micromol/L) 11.8 11.5 10.9
CRP (mg/L) 2.30 1.82 1.69*
Interleukin-6 (mg/dL) 1.68 1.40 1.11*
Tumor necrosis factor-a (mg/dL) 6.37 6.35 5.99*
Markers Choline Tertiles
Low Mid High
Homocysteine (micromol/L) 12.7 11.5 10.2*
CRP (mg/L) 2.13 1.92 1.61
Interleukin-6 (mg/dL) 1.61 1.44 1.42
Tumor necrosis factor-a (mg/dL) 6.80 6.00 5.99*
* = significant difference between low and high values
It can be seen that participants who ate higher choline amounts had,
on average, 22% lower CRP levels, 26% lower interleukin-6 levels, and
6% lower tumor necrosis factor-alpha levels, compared with those who
ate least choline. Similarly, higher betaine consumption was
associated with 10% less homocysteine, 19% less CRP, and 12% less
tumor necrosis factor-alpha in the blood.
When subgroups were formed that combined the choline and betaine
intakes, it was found that a high intake of both choline and betaine
was linked to lower concentrations of all the investigated
inflammatory markers.
What these findings may mean
This study shows an association between choline and betaine intakes
and the inflammation process in healthy Greek adults, who presumably
consumed a Mediterranean-type diet. The authors of the study point out
that, whatever the mechanism underlying the findings, the magnitude of
the differences between the inflammatory markers in the low and high
tertiles is similar to those found in subjects following the
Mediterranean diet.
These inflammatory markers are believed to be important factors in the
initiation of cardiovascular disease. It's possible that they
represent the path whereby the Mediterranean diet is successful in
warding off such disease. The next step (apart from confirming these
results) will be to see if there are beneficial clinical effects of
prolonged consumption of choline and betaine supplements.
In the USA, the average choline intake is similar to that in Greece.
But the average betaine intake in Greece is substantially higher than
that in the USA. Betaine is usually found in plants, and the native
Greeks tend to eat more vegetables and fruits than Americans. Maybe
this is enough to nudge people towards a more vegetarian diet . . .
Source
Detopoulou P, Panagiotakos DB, Antonopoulou S, et al. Dietary choline
and betaine intakes in relation to concentrations of inflammatory
markers in healthy adults: the ATTICA study.
Copyright © 2008 HealthandAge.com. All rights reserved.
Who loves ya.
Tom
ironjustice
"Nicotinamide lowered levels of phosphorylated tau" <<
"The lower number of tangles in the super aged appears to be the
critical difference in maintaining memory skills"
"Tangles consist of a protein called tau "
'Super' Aged Brains Reveal First Secrets Of Sharp Memory In Old Age
ScienceDaily (Nov. 17, 2008) — Maybe you have an 85-year-old
grandfather who still whips through the newspaper crossword puzzle
every morning or a 94-year-old aunt who never forgets a name or a
face. They don't seem to suffer the ravages of memory that beset most
people as they age.
Researchers at Northwestern University's Feinberg School of Medicine
wondered if the brains of the elderly with still laser sharp memory --
called "super aged" -- were somehow different than everyone else's.
So, instead of the usual approach in which scientists explore what
goes wrong in a brain when older people lose their memory, they
investigated what goes right in an aging brain that stays nimble.
Now they have a preliminary answer. Scientists examined the brains of
five deceased people considered super aged because of their high
performance on memory tests when they were more than 80 years old and
compared them to the brains of elderly, non-demented individuals.
Researchers found the super aged brains had many fewer fiber-like
tangles than the brains of those who had aged normally. The tangles
consist of a protein called tau that accumulates inside brain cells
and is thought to eventually kill the cells. Tangles are found in
moderate numbers in the brains of elderly and increase substantially
in the brains of Alzheimer's disease patients.
"This new finding in super aged brains is very exciting," said Changiz
Geula, principal investigator of the study and a research professor of
neurology at the Cognitive Neurology and Alzheimer's Disease Center at
Northwestern's Feinberg School. "It was always assumed that the
accumulation of these tangles is a progressive phenomenon through the
aging process. But we are seeing that some individuals are immune to
tangle formation and that the presence of these tangles seems to
influence cognitive performance." Individuals who have few tangles
perform at superior levels, while those who have more tangles appear
to be normal for their age, Geula noted.
The number of plaques in the brains of the super aged was similar to
that in the brains of the normally aging group. The plaque is an
aggregation of protein called amyloid that becomes deposited outside
the brain cell and disrupts communication between neurons. Like
tangles, plaques also are found in modest numbers in the brains of
aged individuals and show a dramatic increase in number in Alzheimer's
disease.
Geula said the lower number of tangles in the super aged appears to be
the critical difference in maintaining memory skills.
Some of the super aged in the study performed memory tasks at the
level of people who were about 50 years old. For example, after being
told a story, they were able to remember it immediately after and
still accurately recall its details 30 minutes later. They also
remembered a list of 15 words and recalled these words equally well
when tested after 30 minutes.
Geula said new research will focus on what makes cells in super aged
brains more resistant to tangle formation. "We want to see what
protects the brains of these individuals against the ravages that
cause memory loss," he said. " Understanding the specific genetic and
molecular characteristics of the brains that makes them resistant,
someday may lead to the ability to protect average brains from memory
loss. "
Geula's research is part of a larger super aging study at
Northwestern's Cognitive Neurology and Alzheimer's Disease Center
(CNADC). The study's goal is to identify high functioning individuals
over 80 and investigate what factors are important to maintain this
ability into old age. A number of super aged individuals have been
identified and are being followed up annually with tests of cognitive
abilities. Recruitment continues for the study.
Geula will present his findings November 16, at the Society for
Neuroscience annual meeting in Washington, D.C.
Other Feinberg School collaborators on the study are Marsel Mesulam,
M.D., CNADC director and the Ruth and Evelyn Dunbar Professor of
Psychiatry and Behavioral Sciences; Sandra Weintraub, professor of
psychiatry and behavioral sciences; Emily Rogalski, research assistant
professor of medicine.
--------------------------------------------------------------------------------
Adapted from materials provided by Northwestern University, via
EurekAlert!, a service of AAAS.
------------
Who loves ya.
Tom
Jesus Was A Vegetarian!
http://tinyurl.com/634q5a
Man Is A Herbivore!
http://tinyurl.com/4rq595
DEAD PEOPLE WALKING
http://tinyurl.com/zk9fk
>
> "Neither measurement can discriminate entirely"
>
> "It is concluded that neither measurement of phospho-tau,taunor
> A1-42 in CSF can discriminate entirely between dementia and
> cognitively non-disturbed controls or between dementia of different
> aetiologies"
>
> Cerebrospinal Fluid Phospho-Tau, TotalTauand -Amyloid1-42 in the
> Differentiation between Alzheimer's Disease and Vascular Dementia
> Katarina Näggaa, Johan Gottfriesb, Kaj Blennowc,d, Jan Marcussona
>
> aDepartment of Geriatric Medicine, Linköping University Hospital,
> Linköping,
> bMedicinal Chemistry, AstraZeneca R&D, Mölndal,
> cDepartment of Clinical Neuroscience, Section of Experimental
> Neuroscience, University of Göteborg, Sahlgrenska University Hospital,
> Mölndal, and
> dThe Medical Research Council, Sweden
>
> Dement Geriatr Cogn Disord 2002;14:183-190 (DOI: 10.1159/000066023)
>
> Abstract
>
> The two most frequently examined biomarkers in the diagnosis of
> dementia are cerebrospinal fluid (CSF)tauand -amyloid1-42 (A1-42).
> An assay fortauphosphorylated at threonine 181 (phospho-tau) has
> recently been developed.
> We studied these three markers in patients with possible Alzheimer's
> disease (AD; n = 23), probable AD (n = 50), AD with relevant
> cerebrovascular disease (AD with CVD; n = 14), possible vascular
> dementia (VaD; n = 39), probable VaD (n = 36), cognitively impaired (n
> = 13) and 27 neurologically healthy controls.
> Compared with the controls,taulevels were significantly increased in
> possible AD, probable AD, AD with CVD and probable VaD. A1-42 was
> decreased in all dementia groups compared with the controls.
> In contrast, phospho-taulevels were increased only in probable AD
> compared with the controls.
> From the results of the present study, it is concluded that neither
> measurement of phospho-tau,taunor A1-42 in CSF can discriminate
> entirely between dementia and cognitively non-disturbed controls or
> between dementia of different aetiologies in the clinical diagnostic
> procedure.
>
> Copyright © 2002 S. Karger AG, Basel
>
> --------------------------------------------------------------------------------
>
> Author Contacts
>
> Katarina Nägga, MD
> Department of Geriatric Medicine
> Linköping University Hospital
> S-581 85 Linköping (Sweden)
> Tel. +46 13 224093, Fax +46 13 227389, E-Mail Katarina.Na...@lio.se
> Vol. 14, No. 4, 2002
> --------------------------------------------------------------------------------
ironj...@aol.com
alive after they had lost their own pancreases <<
"Choline, a precursor to acetylcholine, increases serum glucose and
insulin levels"
Intraperitoneal administration of choline increases serum glucose in
rat: involvement of the sympathoadrenal system.
Horm Metab Res. 2002 Jun ;34 (6):341-7 12173076 (P,S,G,E,B)
Y O Ilcol, M S Gurun, Y Taga, I H Ulus
Department of Biochemistry Marmara University Medical School,
Istanbul, Turkey.
Intraperitoneal injection of choline (40, 80 or 120 mg/kg) produced a
dose-dependent increase in serum glucose and choline levels in rats.
The increases in serum glucose and choline were associated with an
increase of serum insulin as well as plasma levels of epinephrine and
norepinephrine.
The increases in serum glucose and plasma catecholamine concentrations
induced by choline (120 mg/kg) were blocked by pretreatment with the
ganglionic nicotinic receptor antagonist hexamethonium (15 mg/kg), but
were not affected by pretreatment with atropine (5 mg/kg).
The choline-induced rise in serum insulin was blocked by pretreatment
with atropine and with hexamethonium each.
The increase in serum glucose evoked by choline (120 mg/kg) was
blocked by alpha-adrenoceptor blockade and bilateral adrenalectomy
each.
Blockade of beta-adrenoceptor by propranolol or chemical sympathectomy
by 6-hydroxydopamine failed to alter the hyperglycemic response to
choline.
These results show that choline, a precursor of the neurotransmitter
acetylcholine, increases serum glucose and insulin levels.
The effect of choline on serum insulin is mediated by both muscarinic
and nicotinic acetylcholine receptors, whereas the effect of choline
on serum glucose is mediated solely by nicotinic receptors.
The stimulation of adrenal medullary catecholamine release and
subsequent activation of alpha-adrenoceptors apparently mediates the
hyperglycemic effect of choline.
Who loves ya.
Tom
Jesus Was A Vegetarian!
http://tinyurl.com/2r2nkh
Man Is A Herbivore!
http://tinyurl.com/a3cc3
DEAD PEOPLE WALKING
http://tinyurl.com/zk9fk
> On Nov 8, 5:50 pm, ironjustice <ironjust...@cashette.com> wrote: Then,
> using an acid-induced acute lung injury mouse model,
> we found that nicotine,choline, and PNU-282987
> (a specific á7 nAChR agonist) decreased excess lung water
> and lung vascular permeability, <<
>
> It seems to me .. the words nicot - ine .. and chol - ine .. are
> coming up alot .. and they both seem to be capable of doing the same
> thing .. increasing .. bliss ..
>
> Now .. would could the decrease of CONSUMPTION / destruction OF ..
> chol - ine BE the .. 'need' FOR .. nicot - ine .. and the like .. ? ..
> IE: gambling .. sex addiction .. etc .. / DOPE - amine .. ?
>
> http://www.sciencenews.org/articles/20050625/timeline.asp
>
> A new vitamin that is essential for liver function and that may play
> an important role in controlling diabetes was described at the
> meeting
> of the American and Canadian Medical Associations by one of its
> discoverers, Dr. C.H. Best of Toronto, codiscoverer of insulin, the
> life-saving remedy for diabetes.
> The new vitamin has a real name,choline, instead of a letter, as do
> most other members of the vitamin family. It is found in many foods,
> but the best sources are meat, egg yolk, and yeast.
>
> Dr. M. Hershey and Miss M.E. Huntsman, of the University of Toronto,
> were responsible for many of the fundamental observations that led up
> to the discovery of the significance ofcholine, Dr. Best stated.
>
> Lack of this vitamin causes the serious condition of fatty liver, Dr.
> Best said. When the liver becomes fatty, it fails to make sugar or
> handle bile or do many of the things it should do, he explained.
>
> The vitamin was discovered in the course of insulin investigations.
> Dogs that had nopancreas, the insulin-secreting organ, failed to
> live
> for more than a few months, even when given insulin injections. When
> they were fed mincedpancreas, in addition to the insulin, they lived
> for years.
>
> However, chemical studies of thepancreasshowed that in addition to
> producing insulin and a digestive ferment, this organ containedcholine, and that it was thecholinein the diet of mincedpancreas
> that kept the dogs alive after they had lost their own pancreases.
>
> --------------------------------------------------------------------------------
>
> "Lecithin may therefore be the method of choice for
> accelerating acetylcholine synthesis"
>
> Lancet. 1977 Jul 9;2(8028):68-9. Related Articles, Links
>
> Lecithin consumption raises serum-free-cholinelevels.
>
> Wurtman RJ, Hirsch MJ, Growdon JH.
>
> Consumption ofcholineby rats sequentially increases serum-choline,
> brain-choline, and brain-acetylcholine concentrations. In man
> consumption ofcholineincreases in levels in the serum and
> cerebrospinal fluid; its administration is an effective way of
> treating tardive dyskinesia.
> We found that oral lecithin is considerably more
> effective in raising human serum-cholinelevels than an equivalent
> quantity ofcholinechloride. 30 minutes after ingestion ofcholine
> chloride (2-3 g free base), serum-cholinelevels rose by 86% and
> returned to normal values within 4 hours; 1 hour after lecithin
> ingestion, these levels rose by 265% and remained significantly
> raised for 12 hours.
> Lecithin may therefore be the method of choice for
> accelerating acetylcholine synthesis by increasing the availability
> ofcholine, its precursor in the blood.
>
> PMID: 69151 [PubMed - indexed for MEDLINE]
>
> --------------------------------------------------------------------------------
>
> http://www.medicalnewstoday.com/medicalnews.php?newsid=72010
>
> New Study Indicates That People May Need More DietaryCholineThan
> Previously Thought
>
> Article Date: 30 May 2007 - 9:00 PDT
>
> A new study published in the May issue of the American Journal of
> Clinical Nutrition indicates that the current recommended Adequate
> Intake (AI) forcholinemay, in fact, be inadequate for some people.1Cholineis an essential nutrient for normal functioning of all cells,
> including those involved with liver metabolism, brain and nerve
> function, memory, and the transportation of nutrients throughout the
> body.
>
> In this depletion-repletion study, 57 adult subjects (26 men, 16
> premenopausal women and 15 postmenopausal women) were fed a diet
> containing 550 mg ofcholinefor 10 days, then fed less than 50 mg a
> day ofcholinefor up to 42 days.
>
> * When deprived of the nutrient, 77 percent of men, 80 percent of
> postmenopausal women and 44 percent of premenopausal women developed
> fatty liver or muscle damage.
>
> * Six men (23 percent) developed these signs while consuming the
> initial 550 mg of dailycholine, even though 550 mg is the current AI
> for men.
>
> * Nineteen percent of the subjects required as high as 825 mg of
> dailycholineto prevent or reverse the organ dysfunction associated
> with
> the low-cholinediet, an amount significantly higher than the current
> AI.
>
> * For all participants, blood homocysteine levels increased duringcholinedepletion. Other studies have associated high homocysteine
> levels with heart disease.
>
> "These study results clearly indicate that some adults, notably men
> and post-menopausal women, need morecholinethan is recommended by
> the current AI," says study co-author Kerry-Ann da Costa, PhD, a
> research assistant professor at the University of North Carolina at
> Chapel Hill. "We hope these findings will aid the Institute of
> Medicine in refining the Dietary Reference Intake (DRI) of this
> nutrient."
>
> This study is the most complete study ofcholinerequirements to date
> and is the first to include women. Its division of participants into
> two groups - one receiving dietary supplementation of folic acid and
> one not - also determined that susceptibility tocholinedeficiency
> was not altered by folic acid supplementation.
>
> Closing theCholineGap
>
> Additional research on the population demonstrated thatcholine
> intake
> is far below the current AI, a concern that intakes may be too low to
> meet the needs of many individuals.
>
> * Research conducted at Iowa State University found that only 10
> percent or less of older children, men, women and pregnant women in
> America get the AI ofcholineeach day.2
>
> * A separate study presented this month at the National Nutrient Data
> Bank Conference found thatcholineintake decreases with age and that
> adults ages 71 and older consume an average of about 264 milligrams
> per day - roughly half of the AI forcholine.3
>
> Eggs, beef liver, chicken liver and wheat germ are considered
> excellent sources ofcholine. Two eggs contain 280 milligrams ofcholine, half the recommended daily supply.
>
> "Eggs are a practical food that can help people get thecholinethey
> need, along with several other nutrients, at just 75 calories an
> egg,"
> says registered dietitian Maye Musk. "Cholineis actually found in
> the
> yolk of the egg, so people who consistently only eat egg whites may
> be
> missing out on a key nutrient opportunity."
>
> WhyCholineMatters
>
> The importance of dietarycholinehas been well-established.
>
> * A 2004 study in the American Journal of Epidemiology linked poor
> dietarycholineto adverse outcomes during pregnancy, including a
> four-
> fold increased risk of having a baby with a neural tube defect. 4 * A
> research review published in the Annual Reviews of Nutrition suggests
> thatcholineplays an important role in normal fetal development,
> particularly during the stages that involve knowledge acquirement and
> life-long memory function. 5
>
> ###
>
> For more information, on the benefits ofcholinefor pregnant women,
> visithttp://www.pregnancyfoodguide.org/orhttp://www.enc-online.org/.
>
> About the American Egg Board (AEB)
>
> AEB is the U.S. egg producer's link to the consumer in communicating
> the value of 'the incredible edible egg' and is funded from a
> national
> legislative checkoff on all egg production from companies with
> greater
> than 75,000 layers in the continental United States. The board
> consists of 18 members and 18 alternates from all regions of the
> country who are appointed by the Secretary of Agriculture. The AEB
> staff carries out the programs under the board direction. AEB is
> located in Park Ridge, Ill. Visithttp://www.aeb.org/for more
> information.
>
> About the Egg Nutrition Center (ENC)
>
> ENC was established in 1979 for the purpose of providing commercial
> egg producers and processors, health promotion agencies, and
> consumers
> with a resource for scientifically accurate information on egg
> nutrition and the role of eggs in the health and nutrition of the
> American diet. The center exists under a cooperative agreement
> between
> the American Egg Board (AEB) and United Egg Producers (UEP). ENC is
> located in Washington, DC. Visithttp://www.enc-online.org/for more
> information.
>
> 1 Fischer LM, et al. Sex and menopausal status influence human
> dietary
> requirements for the nutrientcholine. Am J Clin Nutr 2007;
> 85:1275-85.
>
> 2 Jensen HH, et al.Cholinein the diets of the US population:
> NHANES,
> 2003-2004, Iowa State University (presented at Experimental Biology
> 2007, Washington DC)
>
> 3 Keast DR, Food sources ofcholinein the diets of US older adults:
> NHANES, 1999-2004." (presented at the 31st National Nutrient Databank
> Conference, Washington DC) Food sources ofcholinein the diets of US
> older adults: NHANES, 1999-2004.
>
> 4Shaw GM, et al. Periconceptional dietary intake ofcholineand
> betaine and neural tube defects in offspring. Am J Epid 2004; 160(2):
> 102-109.
>
> 5Zeisel SH.Choline:critical role during fetal development and
> dietary
> requirements in adults. Annu Rev Nutr, 2006; 26:229-50.
>
> Contact: Egg Nutrition Media Hotline
> Edelman Public Relations
>
> ----------------------------------
>
> Who loves ya.
> Tom
>
ironj...@aol.com
Sooo .. there isn't as much loonacy in the theory of nicotine
standing
in for nicotinamide as these 'nutritionists' tell you. <<
http://www.cosmosmagazine.com/features/print/2349/nicotine-can-it-save-your-brain
Nicotine: can it save your brain?
Issue 23 of Cosmos, October 2008
by Becky McCall
Is it a scourge on society or a blessing in disguise? Public enemy
number one may soon be a treatment for cognitive diseases.
--------------------------------------------------------------------------------
IT'S RESTLESS NIGHT number three in a row. Four hours of counting the
cracks in the ceiling, then an hour's sleep only to wake herself again
with uncontrollable thrashing around. Most people's muscles are
paralysed during dreams, but Sarah, who suffers from Parkinson's
disease, physically acts hers out.
During the day she's exhausted and depressed about losing control of
her muscles - and her life. But there is one consoling factor: if
Sarah hadn't smoked before her diagnosis, it's likely her disease
would be far worse by now.
A growing body of evidence suggests that smoking helps delay the
progression of Parkinson's disease, and potentially other cognitive
diseases as well. These are statistics that rarely see the light of
day; they are hidden from the public by layers of anti-smoking
campaigns and health warnings.
More than half of Parkinson's patients smoke, as do half of
adolescents with severe Attention Deficit Hyperactivity Disorder
(ADHD). The reasons why they smoke are uncertain, but research is
finding some persuasive clues.
Marcus Munafo is a researcher who specialises in nicotine addiction at
the University of Bristol in the southwest of England. He points to
reams of irrefutable evidence against smoking a deadly cocktail of
toxins (see "Why nicotine is bad for you", p62 and "Why smoking is bad
for you", p63).
"Pure nicotine is a potentially lethal poison," he says, "and as a
constituent of tobacco smoke contributes to the increased risk of
heart disease associated with smoking. In particular, it is known to
raise blood pressure."
But, he adds, it's important to remember that risk is relative and
nicotine per se is not as damaging as it is often perceived to be.
In fact, cigarettes contain almost 3,000 other chemicals that are
considered more dangerous than nicotine. "People equate smoking with
nicotine, saying all nicotine is bad for you. However, most of the
harm from smoking comes from other chemicals."
Munafo admits that the proposed use of nicotine as therapy raises
ethical issues, but points out that the chemical's effects depend on
how it is delivered to the body.
"The addiction potential of pharmaceutical nicotine products such as
patches and gum is quite low, certainly much lower than cigarettes,"
he says. "With appropriate safeguards in place, there are no reasons
to think that nicotine products could not be used safely for
therapeutic purposes beyond their current approved use for smoking
cessation."
STUDIES OF PEOPLE with Alzheimer's, Parkinson's, schizophrenia and
ADHD are raising concerns that by dismissing nicotine alongside
smoking, we risk throwing out the baby with the bathwater.
Some scientists go so far as to say that for many patients suffering
from cognitive diseases, it's more important to avoid the severe
consequences of advanced disease than to fear nicotine dependence.
Most findings have been sourced from studies that record disease
outcomes in smokers and non-smokers, because this is the most
prevalent use of nicotine in our society.
For example, a review of epidemiological studies led by researchers
from the University of Washington, in Seattle, USA, and published in
the journal Behavioural Brain Research in 2000, showed that non-
smokers are twice as likely to develop Parkinson's disease as
smokers.
Another review of 44 previous studies, published in the U.S. journal
Annals of Neurology in 2002, found that smokers have a 60 per cent
lower risk of developing the disease.
At the 2008 Federation of European Neuroscience Societies conference
in Geneva, Switzerland, behavioural pharmacologist Ian Stolerman of
King's College London reported that, in rats, nicotine improves
concentration and quickens responses.
When allowed to concentrate fully, the animals managed to complete a
task accurately 80 per cent of the time, but this figure dropped to 55
per cent when they were distracted by noise and flashing lights.
When nicotine was given to distracted rats, however, their accuracy
rose to 85 per cent. Stolerman believes that - given time to translate
these findings into a clinical therapy - nicotine may help give
dementia patients up to six extra months of independent living.
Clinical findings relating to nicotine use and Alzheimer's disease
vary. But according to a review led by Marina Picciotto of Yale
University in New Haven, Connecticut, and published in the U.S.
journal Frontiers in Bioscience in 2008, the beneficial effects of
nicotine seem to be outweighed by an increase in strokes linked to
smoking.
However, abnormal proteins found at high levels between nerve cells in
the brains of Alzheimer's sufferers (known as amyloid-β and amyloid
plaques) are reduced in both Alzheimer's patients and in other elderly
patients who smoke.
Taken together, these studies indicate that some component of
cigarette smoke may protect against diseases involving nerve
degeneration. In the absence of other effective therapies for these
debilitating diseases, scientists are taking nicotine seriously.
Picciotto, a psychiatric scientist at Yale's School of Medicine, has
been investigating the role of nicotine in cognitive diseases at a
biochemical and at a molecular level.
"In animal studies, if you get the dose and the regimen right, then
nicotine can protect against nearly any cognitive disease model,
whether stroke, Alzheimer's or Parkinson's," she says. "Nicotine has
also been shown to encourage dopamine release from neurones that would
be lost in Parkinson's disease."
Dopamine, a neurotransmitter or chemical messenger in the brain, is
released after nicotine activates nicotinic receptors in the midbrain.
These receptors in turn activate regions responsible for movement and
motivation, as well as addiction behaviour.
"In patients with Parkinson's disease, neurones are lost in these two
regions. So stimulation of any remaining neurones with nicotine could
help prevent further decline," explains Picciotto.
If nicotine does preserve neurones, then diagnosing and treating
patients before neurones are lost is vital; once gone, they cannot be
replaced. Nicotine could potentially slow progression of Parkinson's
disease but is unlikely to reverse it.
Picciotto believes that a clinical study to establish the extent of
nicotine's protective effect in the early stages of the disease is
essential.
At this stage, however, it's almost impossible to predict who will
develop Parkinson's, and by the time it's diagnosed, 60 to 70 per cent
of neurones have already been lost and cannot be regained.
THE POWER OF NICOTINE in the human nervous system has been known since
the early 20th century. Nicotine mimics a neurotransmitter called
acetylcholine, and is a chemical signal sent between nerve cells.
The receptor in the nerve cell's surface, called the nicotinic
acetylcholine receptor, can be open, closed or insensitive. Both
nicotine and acetylcholine affect the entire body, including the
brain, heart and other muscles.
It's the receptors in the brain (see graphic, p64) attracting the
attention of scientists. These receptors are involved in emotion,
concentration and feelings of pleasure due to their high concentration
in the limbic region of the brain, which is associated with emotion
and reward.
But the crux of the matter is this: if nicotine is to be used
therapeutically, then the properties that confer beneficial effects
need to be separated from the addictive ones.
Indeed, all drugs approved for use in humans strive to maximise
efficacy and minimise side effects. It's just that in this case, the
side effects are well known and clearly associated with death and
disease.
The question then arises: should nicotine be sold in its current form,
such as a patch, lozenge or spray, or as a specialised pharmaceutical
product?
It's likely that pharmaceutical products that work on the brain's
nicotinic receptors will be available via prescription in the next few
years; a handful of companies already have products in clinical
trials.
AS DRUG TARGETS, the nicotinic receptors are difficult, because of
both their structure and function. There are an unknown number of
receptor subtypes, but they are all composed of five subunits, called
alpha (α) and beta (β) units.
Studies have shown that different subtypes have particular functions,
and each are related to specific diseases.
Further research into the roles and sensitivities of the many
different subtypes is central to teasing out those that exert a
beneficial effect from those that induce dependence.
As Piciotto explains, "Overwhelming evidence suggests that addiction
relies on activity at the highest affinity nicotinic receptors with
subunits α4 and β2, so it's preferable to avoid activating these
receptors."
Yet developing drugs that target only receptors with a beneficial
effect is akin to trying to remove the ace of diamonds from a house of
cards without causing it to fall.
Still, a number of companies are developing compounds that not only
stimulate these receptors but also make them more likely to be
activated by acetylcholine produced naturally in the body.
Even one of the world's largest cigarette manufacturers, R.J. Reynolds
Tobacco, started a chemicals arm for developing therapeutics based on
the activity of neuronal nicotinic receptors (NNR).
Targacept, now an independent company based in North Carolina, has
shown that the nicotinic receptor subtype known as α7 is a key
regulator of cognitive function. TC-5619, the lead product candidate
in Targacept's α7 NNR program, is currently in clinical trials.
William S. Caldwell, vice president of drug discovery and development
for Targacept, explains that the company discovered and synthesised
completely new compounds that target only those neuronal nicotinic
receptors that regulate the beneficial effects.
"By normalising the activity of under-stimulated NNRs with these novel
substances, therapeutic benefits have been demonstrated in a number of
human clinical studies...[of] age associated memory impairment and mild
cognitive impairment."
He emphasises that the mode of administration is a very important
factor in addiction.
"The abuse liability and dependence potential of nicotine replacement
therapies like the patch or gum are very low when compared to that of
cigarettes due to the slower absorption rate of nicotine from these
products. Since the preferred route of administration for our
selective NNR compounds is by mouth, resulting in slower absorption
[than via inhalation], the abuse potential of our products is
extremely low."
And as Munafo of the University of Bristol points out, most of us
regularly use potentially addictive drugs. "Is nicotine really so
different?" he asks. "Many of us regularly use caffeine or alcohol and
it doesn't have much of an impact on our lives."
Maybe he's right and it all boils down to public perception: a walk
along any modern high street will tell you coffee is trendy, while
shivering in the doorway of a smoke-free public space sucking on a
cigarette is seen as anti-social, unhealthy and very passé.
But according to Amanda Sandford, research manager at British
organisation Action on Smoking and Health, which aims to reduce
smoking, there are compelling reasons for this perception.
"While using nicotine may have a protective effect for a very limited
number of conditions, smoking is responsible for over 5.2 million
deaths a year globally, so the emphasis on getting people to quit
smoking and trying to dissuade children from ever taking it up must
continue," she says.
Yet it seems that - contrary to all common sense - patients with
cognitive diseases who also smoke seem to fare better than their non-
smoking counterparts.
Even more surprising is that an effective means of preventing or
treating some of the world's most challenging diseases could emerge
from public health enemy number one.
--------------------------------------------------------------------------------
Becky McCall is a freelance science writer (and non-smoker) based in
Bristol, England. She also produces webcasts and is presenting a new
British TV series.
Who loves ya.
Tom
Jesus Was A Vegetarian!
http://tinyurl.com/634q5a
Man Is A Herbivore!
http://tinyurl.com/4rq595
ironjustice
"Nicotinamide lowered levels of phosphorylated tau" "The lower number
of tangles in the super aged appears to be the critical difference in
maintaining memory skills"
"Tangles consist of a protein called tau "
<<
ALZHEIMER EFFECT TIED TO CHEMICAL
By WARREN E. LEARY,
Published: October 9, 1992
Researchers say they have the first evidence that two primary
abnormalities seen with Alzheimer's disease, low levels of a chemical
that carries signals between nerve cells and the formation of hard
plaques in the brain, may be directly related to the disorder.
Work with cell cultures suggests that low levels of the brain
transmitter chemical acetylcholine, a common symptom of Alzheimer
patients, contribute to formation of hard deposits of amyloid protein
that also clog the brain tissue of most patients with the disease,
scientists said today.
Researchers at the Massachusetts Institute of Technology and
Massachusetts General Hospital in Boston said the findings, if
confirmed, pointed to a new approach to developing drugs to combat the
disease.
Dr. Richard J. Wurtman of M.I.T., director of the laboratory in which
the work was done, said much of the current research into drugs to
fight Alzheimer's was aimed at finding chemicals that stimulate
acetylcholine production or inhibit its breakdown. Perhaps the ideal
drug, he said in an interview, would be one that stimulated the action
of acetylcholine in its newly discovered role of regulating amyloid
protein production. First Direct Link
"This gives us a real target for drug development," Dr. Wurtman said.
"If we get the right drug, we should be able to reduce symptoms and
actually slow the disease at the same time."
The new work, to be published Friday in the journal Science, is the
first to establish a direct link between two major characteristics of
Alzheimer's disease. Dr. Wurtman said this was also the first time a
neurotransmitter, a chemical that carries messages between brain
cells, had been shown to affect protein metabolism.
"This is a potentially exciting finding that has to be verified in a
living system, such as an animal model," said Dr. Sangram Sisodia, an
Alzheimer researcher at the Johns Hopkins School of Medicine in
Baltimore. Noting that the M.I.T. work was done in cell cultures, Dr.
Sisodia cautioned that it was too early to conclude that there was a
definite connection between the neurotransmitter and deposits of
amyloid plaques in the brain.
"To make the link, you have to go to an animal model to reproduce the
experiment," Dr. Sisodia said. "A promise of the latest work is how it
will help in designing the new experiments."
A principal finding of the new study is acetylcholine's potential role
in the processing of a substance called amyloid precursor protein, the
basic substance from which amyloid plaque deposits originate. The
M.I.T. research indicates this parent protein can be metabolized to
form either protein fragments that break down and are excreted by the
body, or the hard protein plaque that accumulates in the brains of
Alzheimer patients.
The researchers took human kidney cells containing the precursor
protein and added the genetic information that caused them to develop
receptor molecules that respond to acetylcholine. The receptor
molecules on the cells' surface link with acetylcholine and similar
chemicals and this combination triggers protein production by the
cells. 2 Pathways Indicated
In the experiments, the scientists reported, the cells stimulated with
acetylcholine processed four to five times more non-accumulating
protein from the precursor protein than did cells not stimulated with
the neurotransmitter.
Dr. Wurtman said this indicated that there were two pathways for
processing the precursor protein, a "good way" that appeared to be
dominant and resulted in nontoxic, removable protein fragments, and a
"bad way" that resulted in hard, insoluble amyloid plaque. If
acetylcholine is at reduced levels because of Alzheimer's disease, he
theorized, the body takes the "bad" pathway and makes the damaging
amyloid protein.
While it has not been proved that making more of the "good" protein
results in less of the "bad," Dr. Wurtman said there appeared to be a
constant level of precursor protein in the body, indicating that if it
was not metabolized one way, it would be processed by the opposite
pathway. Experiments are under way to see if this is true, he said.
Dr. Roger M. Nitsch of Massachusetts General Hospital and M.I.T., who
did much of the research reported in the Science paper, said that
because few amyloid deposits were found in healthy brains, the
harmless processing pathway of the precursor protein must prevail
under normal conditions.
"This observation showed for the first time that neurotransmission and
amyloid precursor processing are related biochemical events," he
said.
Dr. Gene Cohen, acting director of the National Institute on Aging,
said the work was potentially significant and another example of the
rapid progress researchers were making in understanding Alzheimer's.
An estimated four million Americans suffer from the incurable, memory-
robbing disease and the incidence is rising as the population ages.
"Alzheimer's continues to be one of modern medicine's great mysteries
and we are still trying to find out what causes the disease and how
the disease process unfolds at a fundamental level," Dr. Cohen said in
an interview. "One of the things people have been looking at is the
abnormal processing of amyloid precursor protein, and this latest work
is potentially a big piece of that puzzle." ------------
ironj...@aol.com
nicotine, choline, and PNU-282987 (a specific á7 nAChR agonist)
decreased excess lung water and lung vascular permeability, <<
Research article
Protective efficiacy of taurine against pulmonary edema progression:
experimental study
Orhan Yucel1 , Zeki Ilker Kunak2 , Enis Macit3 , Armagan Gunal4 ,
Alper Gozubuyuk1 , Husamettin Gul4 and Onur Genc1
1Department of Thoracic Surgery, Gulhane Military Medical Academy,
Ankara, Turkey
2Department of Medical CBRN, Gulhane Military Medical Academy, Ankara,
Turkey
3Department of Analytical Toxicology, Gulhane Military Medical
Academy, Ankara, Turkey
4Department of Pathology, Gulhane Military Medical Academy, Ankara,
Turkey
Journal of Cardiothoracic Surgery 2008, 3:57doi:10.1186/1749-8090-3-57
Published: 28 October 2008
Abstract
Re-expansion pulmonary edema (RPE) is an acute, rare and potentially
lethal complication [1,2].
Its beginning is sudden and dramatic.
The mechanism is not yet fully understood [1].
Some authors suggest that it may occur after rapid re-inflation of a
collapsed lung [1].
It was reported by other authors that it may relate to surfactant
depletion or may result from hypoxic capillary damage, leading to
increased capillary permeability [1,3].
In RPE, unilateral lung injury is initiated by cytotoxic oxygen
metabolites and temporally associated with an influx of
polymorphonuclear neutrophils [1].
These toxic oxygen products are the results of re-oxygenation of a
collapsed lung. Treatment of re-expansion pulmonary edema is basically
preventive [4].
© 1999-2008 BioMed Central Ltd unless otherwise stated. Part of
Springer Science+Business Media.
anon...@nowhere.you.know
I'm sorry life has left you so sad and bitter in your old age.
ironjustice
You seem to be a little slow on the uptake ..
Do NOT post to my threads ..
You are a .. loon ..
ironjustice
These are two different conditions. If they were treating "dementias"
they
would say so, not "Alzheimers". <<
It seems it may not .. matter .. WHICH .. specific 'dementia' one
has .. the RESULT of the treatment in them ALL seems to be the
targeting of the acetylcholine in the brain.
"Cholinergic neurotransmission enhancement in cerebrovascular disease"
Vesicular Acetylcholine Transporter (VAChT) in the Brain of
Spontaneously Hypertensive Rats (SHR): Effect of Treatment with an
Acetylcholinesterase Inhibitor.
Tayebati SK, Di Tullio MA, Amenta F
Clin Exp Hypertens 2008 Nov; 30(8):732-743.
The cholinergic marker vesicular acetylcholine transporter (VAChT) was
investigated in different cerebral areas of spontaneously hypertensive
rats (SHR) by immunochemistry (Western blot analysis) and by
immunohistochemistry. SHR were used as an animal model of hypertensive
brain damage. The sensitivity of manipulation of cholinergic system on
VAChT was assessed in rats treated for four weeks with the
acetylcholinesterase (AChE) inhibitor galantamine (3 mg/Kg/day). VAChT
concentrations were increased in the brain of control SHR compared to
age-matched normotensive Wistar-Kyoto rats. This increase probably
represents an up-regulation of VAChT to oppose cholinergic deficits
reported in SHR and is countered by galantamine administration. The
possibility that cholinergic neurotransmission enhancement may
represent a therapeutic strategy in cerebrovascular disease is
discussed.
Clinical and experimental hypertension (New York, N.Y. : 1993) [Clin
Exp Hypertens]
--------------------------------------------------------------------------------
ironjustice
wrote:acetylcholine <<
Release of acetylcholine by syringin, an active principle of
Eleutherococcus senticosus, to raise insulin secretion in Wistar rats
Neuroscience Letters, Volume 434, Issue 2, 28 March 2008, Pages
195-199
Ko Yu Liu, Yang-Chang Wu, I-Min Liu, Wen Chen Yu, Juei-Tang Cheng
Abstract
The present study is designed to screen the effect of syringin, an
active principle purified from the rhizome and root parts of
Eleutherococcus senticosus (Araliaceae), on the plasma glucose and
investigate the possible mechanisms. Plasma glucose decreased in a
dose-dependent manner 60 min after intravenous injection of syringin
into fasting Wistar rats.
In parallel to the decrease of plasma glucose, increases of plasma
insulin level as well as the plasma C-peptide was also observed in
rats receiving same treatment.
Both the plasma glucose lowering action and the raised plasma levels
of insulin and C-peptide induced by syringin were also inhibited by 4-
diphenylacetoxy-N-methylpiperdine methiodide (4-DAMP), the antagonist
of the muscarinic M3 receptors, but not affected by the ganglionic
nicotinic antagonist, pentolinium or hexamethonium.
Moreover, disruption of synaptic available acetylcholine (ACh) using
an inhibitor of choline uptake, hemicholinium-3, or vesicular
acetylcholine transport, vesamicol, abolished these actions of
syringin.
Also, physostigmine at concentration sufficient to inhibit
acetylcholinesterase enhanced the actions of syringin.
Mediation of ACh release from the nerve terminals to enhance insulin
secretion by syringin can thus be considered.
The results suggest that syringin has an ability to raise the release
of ACh from nerve terminals, which in turn to stimulate muscarinic M3
receptors in pancreatic cells and augment the insulin release to
result in plasma glucose lowering action.
--------------------------------
Release of acetylcholine to raise insulin secretion in Wistar rats by
oleanolic acid, one of the active principles contained in Cornus
officinalis
Jen-Hao Hsua, Yang-Chang Wua, I-Min Liub and Juei-Tang Chengc, ,
aGraduate Institute of Natural Products, Kaohsiung Medical University,
Kaohsiung City, Taiwan, ROC
bDepartment of Pharmacy, Tajen University, Yen-Pou, Ping Tung Shien,
Taiwan, ROC
cDepartment of Pharmacology, College of Medicine, National Cheng Kung
University, Tainan City, Taiwan, ROC
Received 5 April 2006; accepted 11 May 2006. Available online 6 June
2006.
Abstract
The plasma glucose lowering action of fruits of cornus (Cornus
officinalis), the major active constituent of Die-Huang-Wan, has been
documented to mediate acetylcholine (ACh) release, which in turn to
stimulate muscarinic M3 receptors resulting in the enhancement of
insulin secretion in rats with functional pancreatic β-cells.
The present study was conducted to investigate the effect of oleanolic
acid, one of the active principles of cornus fruit, on the release of
insulin in rats.
After an intraperitoneal injection into the fasting Wistar rats for 90
min, oleanolic acid decreased the plasma glucose in a dose-dependent
manner in parallel to an increase of plasma levels of insulin as well
as C-peptide.
Moreover, disruption of synaptic ACh using an inhibitor of choline
uptake, hemicholinium-3, or vesicular acetylcholine transport,
vesamicol, abolished these actions of oleanolic acid.
Also, physostigmine at concentration sufficient to inhibit
acetylcholinesterase enhanced the actions of oleanolic acid.
Both the plasma glucose lowering action and the raised plasma levels
of insulin and C-peptide induced by oleanolic acid were also inhibited
by 4-diphenylacetoxy-N-methylpiperdine methiodide (4-DAMP), but not
affected by the ganglionic nicotinic antagonist, pentolinium or
hexamethonium.
The results suggest that oleanolic acid has an ability to raise the
release of ACh from nerve terminals, which in turn to stimulate
muscarinic M3 receptors in the pancreatic cells and augment the
insulin release to result in plasma glucose lowering action.
Thus, oleanolic acid is one of the active principles responsible for
the increase of plasma insulin produced by cornus fruit in rats.
Keywords: Acetylcholine; Cornus fruit; Muscarinic M3 receptors; Wistar
rats; Oleanolic acid
--------------------------------------------------------------------------------
Who loves ya.
Tom
> --------------------------------------------------------------------------------
> Who loves ya.
> Tom
>
ironjustice
acetylcholine <<
"Nicotine may prove a good preventative or therapeutic modality for AD
patients"
Nicotine leads to improvements in behavioral impairment and an
increase in the nicotine acetylcholine receptor in transgenic mice.
Neurochem Res. 2008 Sep;33(9):1783-8. Epub 2008 Feb 29.
Shim SB, Lee SH, Chae KR, Kim CK, Hwang DY, Kim BG, Jee SW, Lee SH,
Sin JS, Bae CJ, Lee BC, Lee HH, Kim YK.
Team of Laboratory Animal Resources, National Institute of
Toxicological Research, Korea Food and Drug Administration, 194
Tongilro Eunpyung-ku, Seoul, 122-704, Republic of Korea.
Nicotine is the principal psychoactive ingredient in cigarette smoke,
and has been associated with health problems in humans. However, the
pure form of nicotine may prove to be a valuable pharmaceutical agent
for the treatment of AD. However, the beneficial effects of nicotine
remain a matter of much controversy. In order to clarify this issue,
12-month-old transgenic mice, expressing neuron-specific enolase (NSE)-
controlled APPsw, were treated with low, middle, and high doses of
nicotine for 6 months. Herein, we have concluded that the nicotine-
treated groups evidenced improvements in behavior and increases in the
nicotine acetylcholine receptor, nAchRalpha7. These findings provide
experimental evidence that nicotine effects an improvement in impaired
memory, and that this improvement is associated with an increase in
nAchRalpha7. Thus, nicotine may prove a good preventative or
therapeutic modality for AD patients.
Publication Types:
Research Support, Non-U.S. Gov't
PMID: 18307030
ironj...@aol.com
may prove a good preventative or therapeutic modality for AD
patients" <<
Anybody find it curious the drugs given cause an increase in Pufa in
the brain and the use of nicotine causes increase of Pufa in the
brain .. and nicotinamide the drug mentioned IN this thread .. causes
Pufa increase in the brain .. ?
"Nicotinamide is necessary for delta-6 desaturase and enhances the
formation of various PUFAs."
--------------------------------------------------------------------------------
Who loves ya.
Tom
Jesus Was A Vegetarian!
http://tinyurl.com/634q5a
Man Is A Herbivore!
http://tinyurl.com/4rq595
DEAD PEOPLE WALKING
http://tinyurl.com/zk9fk
> On Nov 29, 3:21 pm, ironjustice <teamtan...@hotmail.com> wrote:
> acetylcholine <<
>
> "Nicotinemay prove a good preventative or therapeutic modality for AD
> patients"
>
> Nicotineleads to improvements in behavioral impairment and an
> increase in thenicotineacetylcholine receptor in transgenic mice.
> Neurochem Res. 2008 Sep;33(9):1783-8. Epub 2008 Feb 29.
> Shim SB, Lee SH, Chae KR, Kim CK, Hwang DY, Kim BG, Jee SW, Lee SH,
> Sin JS, Bae CJ, Lee BC, Lee HH, Kim YK.
>
> Team of Laboratory Animal Resources, National Institute of
> Toxicological Research, Korea Food and Drug Administration, 194
> Tongilro Eunpyung-ku, Seoul, 122-704, Republic of Korea.
>
> Nicotineis the principal psychoactive ingredient in cigarettesmoke,
> and has been associated with health problems in humans. However, the
> pure form ofnicotinemay prove to be a valuable pharmaceutical agent
> for the treatment of AD. However, the beneficial effects ofnicotine
> remain a matter of much controversy. In order to clarify this issue,
> 12-month-old transgenic mice, expressing neuron-specific enolase (NSE)-
> controlled APPsw, were treated with low, middle, and high doses ofnicotinefor 6 months. Herein, we have concluded that thenicotine-
> treated groups evidenced improvements in behavior and increases in thenicotineacetylcholine receptor, nAchRalpha7. These findings provide
> experimental evidence thatnicotineeffects an improvement in impaired
> memory, and that this improvement is associated with an increase in
> nAchRalpha7. Thus,nicotinemay prove a good preventative or
> therapeutic modality for AD patients.
>
> Publication Types:
> Research Support, Non-U.S. Gov't
>
> PMID: 18307030
> --------------------------------------------------------------------------------
> Who loves ya.
> Tom
>
ironj...@aol.com
nicotinamide <<
"Nicotinamide Protects against Ethanol-Induced Neurodegeneration"
What connection would there be to the fact lecithin / PUFA is ALSO
efficacious in fetal alcohol syndrome AND it carries the ADDED effect
of .. RECOVERY .. ?
Nicotinamide has been shown to raise PUFA in the brain.
Nicotine stands in for choline remember.
Is it the choline in the lecithin .. causing / allowing FOR an
increase of PUFA in the brain .. ?
Does choline raise PUFA in the brain ..?
------------------------
Nicotinamide Protects against Ethanol-Induced Apoptotic
Neurodegeneration in the Developing Mouse Brain
Alessandro Ieraci1, Daniel G. Herrera1*
1 Department of Psychiatry, Weill Medical College of Cornell
University, New York, New York, United States of America
Background
Exposure to alcohol during brain development may cause a neurological
syndrome called fetal alcohol syndrome (FAS). Ethanol induces
apoptotic neuronal death at specific developmental stages,
particularly during the brain-growth spurt, which occurs from the
beginning of third trimester of gestation and continues for several
years after birth in humans, whilst occuring in the first two
postnatal weeks in mice. Administration of a single dose of ethanol in
7-d postnatal (P7) mice triggers activation of caspase-3 and
widespread apoptotic neuronal death in the forebrain, providing a
possible explanation for the microencephaly observed in human FAS. The
present study was aimed at determining whether nicotinamide may
prevent ethanol-induced neurodegeneration.
Methods and Findings
P7 mice were treated with a single dose of ethanol (5g/kg), and
nicotinamide was administered from 0 h to 8 h after ethanol exposure.
The effects of nicotinamide on ethanol-induced activation of caspase-3
and release of cytochrome-c from the mitochondria were analyzed by
Western blot (n = 4–7/group). Density of Fluoro-Jade B–positive cells
and NeuN-positive cells was determined in the cingulated cortex, CA1
region of the hippocampus, and lateral dorsal nucleus of the thalamus
(n = 5–6/group). Open field, plus maze, and fear conditioning tests
were used to study the behavior in adult mice (n = 31–34/group).
Nicotinamide reduced the activation of caspase-3 (85.14 ± 4.1%) and
the release of cytochrome-c (80.78 ± 4.39%) in postnatal mouse
forebrain, too. Nicotinamide prevented also the ethanol-induced
increase of apoptosis. We demonstrated that ethanol-exposed mice
showed impaired performance in the fear conditioning test and
increased activity in the open field and in the plus maze.
Administration of nicotinamide prevented all these behavioral
abnormalities in ethanol-exposed mice.
Conclusions
Our findings indicate that nicotinamide can prevent some of the
deleterious effects of ethanol on the developing mouse brain when
given shortly after ethanol exposure. These results suggest that
nicotinamide, which has been used in humans for the treatment of
diabetes and bullous pemphigoid, may hold promise as a preventive
therapy of FAS.
Children Prenatally Exposed To Alcohol May Be Identified By Eye Blinks
Article Date: 04 Feb 2008 - 3:00 PST
Eye blinks may help to identify children prenatally exposed to
alcohol
* Not all children prenatally exposed to alcohol show distinctive
facial anomalies usually associated with fetal alcohol syndrome
(FAS).
* New findings indicate that deficits in eyeblink conditioning (EBC)
can identify children with probable FAS.
* EBC may also serve to identify alcohol-exposed children who lack
distinctive FAS features.
While children with fetal alcohol syndrome (FAS) have identifiable
craniofacial abnormalities, children with alcohol-related
neurodevelopmental disorder (ARND) can have significant cognitive
impairments without facial anomalies. An important new study has found
that a deficit in eyeblink conditioning (EBC) can identify children
with probable FAS, and may also serve to identify alcohol-exposed
children who lack distinctive FAS features.
http://www.medicalnewstoday.com/articles/96050.php
--------------------------------------------
Vitamin may help alcohol-damaged babies: study
Thu Mar 1, 2007 2:01PM EST
WASHINGTON (Reuters) - Giving a vitamin called choline to babies
whose
mothers drank too much alcohol while pregnant might help overcome
some
of their resulting deficits, U.S researchers said on Thursday.
Choline, found in peanut butter, iceberg lettuce and soy, among other
foods, affects brain development and may help repair some of the
damage done by alcohol, the team at San Diego State University found.
"These findings have important implications for children exposed to
alcohol prenatally and suggest that dietary interventions implemented
after birth may reduce the severity of some fetal alcohol effects,"
the researchers wrote in their report, published in the journal
Behavioral Neuroscience.
Jennifer Thomas and colleagues tested 170 rats, giving their pregnant
mothers alcohol before they were born and then giving some of the
pups
choline after birth.
As expected, the newborn rats were overactive and had learning
problems. But they improved when given choline.
"Choline is not going to be a panacea for all symptoms of fetal
alcohol spectrum disorders," Thomas cautioned in a statement. "Women
need to be continually reminded of the damaging effects of alcohol on
the developing fetus."
Choline helps brain cells develop, and the body uses it to make
acetylcholine, a neurotransmitter or message-carrying chemical
involved in learning and cognition.
Women are advised to consume 450 mg a day of the vitamin while
pregnant and 550 mg a day while breast feeding.
In the United States, choline is added to some prenatal vitamins,
baby
formulas, children's multivitamins and cereals.
© Reuters 2007. All rights reserved.
--------------------
"Lecithin may therefore be the method of choice for
accelerating acetylcholine synthesis"
Lancet. 1977 Jul 9;2(8028):68-9. Related Articles, Links
Lecithin consumption raises serum-free-choline levels.
Wurtman RJ, Hirsch MJ, Growdon JH.
Consumption of choline by rats sequentially increases serum-choline,
brain-choline, and brain-acetylcholine concentrations. In man
consumption of choline increases in levels in the serum and
cerebrospinal fluid; its administration is an effective way of
treating tardive dyskinesia.
We found that oral lecithin is considerably more
effective in raising human serum-choline levels than an equivalent
quantity of choline chloride. 30 minutes after ingestion of choline
chloride (2-3 g free base), serum-choline levels rose by 86% and
returned to normal values within 4 hours; 1 hour after lecithin
ingestion, these levels rose by 265% and remained significantly
raised for 12 hours.
Lecithin may therefore be the method of choice for
accelerating acetylcholine synthesis by increasing the availability
of choline, its precursor in the blood.
PMID: 69151
Taka
> On Dec 2, 10:04 pm, ironjustice <ironjust...@aol.com> wrote:"Nicotine
> may prove a good preventative or therapeutic modality for AD
> patients" <<
>
> Anybody find it curious the drugs given cause an increase in Pufa in
> the brain and the use of nicotine causes increase of Pufa in the
> brain .. and nicotinamide the drug mentioned IN this thread .. causes
> Pufa increase in the brain .. ?
>
> http://tinyurl.com/5dyaph
>
> "Nicotinamide is necessary for delta-6 desaturase and enhances the
> formation of various PUFAs."
Another bullshit from the "expert" called Undurti N. Das. Actually as
far as the abstract of the cited article is concerned there is no
mention about nicotinamide being necessary for delta-6 desaturase.
They only say that it stimulates 5-LOX. On the other hand the
pyridoxine (VitB6) is know to be co-factor of the desaturases needed
for the LC-PUFA synthesis including the synthesis of the Mead acid in
those who are not overloaded with the "EFAs".
Taka
Pharmacol Toxicol. 1999 Jun;84(6):274-80.
Nicotinic acid and pyridoxine modulate arachidonic acid metabolism in
vitro and ex vivo in man.
Saareks V, Mucha I, Sievi E, Riutta A.
Department of Pharmacological Sciences, University of Tampere,
Finland.
The in vitro effects of nicotinic acid (10-1000 microM), pyridoxine
(0.1-500 microM) and pyridoxal-5'-phosphate (0.1-500 microM) and the
ex vivo effects of nicotinic acid (2500 mg orally during 12 h) and
pyridoxine (600 mg orally daily for seven days) on arachidonic acid
metabolism were investigated in calcium ionophore A23187 (calcimycin)-
stimulated human whole blood. In vitro nicotinic acid stimulated
prostaglandin E2, thromboxane B2 and leukotriene E4 synthesis.
Pyridoxine at all concentrations and pyridoxal-5'-phosphate at the
highest concentration stimulated prostaglandin E2 and thromboxane B2
production, but had no effect on leukotriene E4 synthesis. Nicotinic
acid treatment increased ex vivo prostaglandin E2, thromboxane B2 and
leukotriene E4 synthesis to 185%, 165% and 175% of the initial values,
respectively. In the pyridoxine-treated subjects, ex vivo
prostaglandin E2, thromboxane B2 and leukotriene E4 synthesis was
decreased after seven days to 75%, 65% and 45% of the initial values,
respectively. In the present study the effects of nicotinic acid on
the 5-lipoxygenase pathway in arachidonic acid metabolism were studied
for the first time and the drug was found to stimulate this pathway in
vitro and ex vivo. In vitro pyridoxine and pyridoxal-5'-phosphate had
no effect on the 5-lipoxygenase pathway. The inhibition of leukotriene
synthesis by pyridoxine ex vivo might be of therapeutic importance.
PMID: 10401729
ironj...@aol.com
wrote:nicotinic acetylcholine receptor <<
This means something ..
Brain nicotinic acetylcholine receptor occupancy: effect of smoking a
denicotinized cigarette
Arthur L. Brodya1a2 c1, Mark A. Mandelkerna2a3, Matthew R.
Costelloa1a2, Anna L. Abramsa2, David Scheibala2, Judah Farahia2,
Edythe D. Londona1a4, Richard E. Olmsteada2, Jed E. Rosea5 and Alexey
G. Mukhina5
a1 UCLA Department of Psychiatry and Biobehavioral Sciences, Los
Angeles, CA, USA
a2 Greater Los Angeles VA Healthcare System Positron Emission
Tomography Center, Los Angeles, CA, USA
a3 UCI Department of Physics, Irvine, CA, USA
a4 UCLA Department of Molecular and Medical Pharmacology, Los Angeles,
CA, USA
a5 Duke University School of Medicine, Durham, NC, USA
Abstract
Our group recently reported that smoking a regular cigarette (1.2-1.4
mg nicotine) resulted in 88% occupancy of brain α4β2* nicotinic
acetylcholine receptors (nAChRs). However, this study did not
determine whether nicotine inhalation or the many other
pharmacological and behavioural factors that occur during smoking
resulted in this receptor occupancy. If nicotine is solely responsible
for α4β2* nAChR occupancy from smoking, then (as estimated from our
previous data) smoking a denicotinized (0.05 mg nicotine) or a low-
nicotine (0.6 mg nicotine) cigarette (commonly used for research and
clinical purposes) would result in substantial 23% and 78% α4β2* nAChR
occupancies, respectively, and a plasma nicotine concentration of 0.87
ng/ml would result in 50% α4β2* nAChR occupancy (EC50). Twenty-four
positron emission tomography sessions were performed on tobacco-
dependent smokers, using 2-[F-18]fluoro-A-85380 (2-FA), a radiotracer
that binds to α4β2* nAChRs. 2-FA displacement was determined from
before to 3.1 hours after either: no smoking, smoking a denicotinized
cigarette, or smoking a low-nicotine cigarette. Analysis of this PET
data revealed that smoking a denicotinized and a low-nicotine
cigarette resulted in 26% and 79% α4β2* nAChR occupancies,
respectively, across three regions of interest. The EC50 determined
from this dataset was 0.75 ng/ml. Given the consistency of findings
between our previous study with regular cigarettes and the present
study, nicotine inhalation during smoking appears to be solely
responsible for α4β2* nAChR occupancy, with other factors (if present
at all) having either short-lived or very minor effects. Furthermore,
smoking a denicotinized cigarette resulted in substantial nAChR
occupancy.
(Received March 26 2008)
(Reviewed April 28 2008)
(Revised June 23 2008)
(Accepted July 07 2008)
Key Words:Denicotinized cigarette; nicotine; nicotinic acetylcholine
receptors; positron emission tomography; thalamus; tobacco
Correspondence:
c1 Address for correspondence: A. L. Brody, M.D., UCLA Department of
Psychiatry & Biobehavioral Sciences, 300 UCLA Medical Plaza, Suite
2200, Los Angeles, CA 90095, USA. Tel.: 310-268-4778 Fax: 310-206-2802
E-mail: abr...@ucla.edu
The International Journal of Neuropsychopharmacology Cambridge
University Press
Copyright (c) 2008 CINP
doi:10.1017/S146114570800922X
--------------------------------------------------------------------------------
Who loves ya.
Tom
Jesus Was A Vegetarian!
http://tinyurl.com/634q5a
Man Is A Herbivore!
http://tinyurl.com/4rq595
DEAD PEOPLE WALKING
http://tinyurl.com/zk9fk
> On Dec 3, 9:42 am, "ironjust...@aol.com" <ironjust...@aol.com> wrote:
> nicotinamide <<
>
> "Nicotinamide Protects against Ethanol-Induced Neurodegeneration"
>
> What connection would there be to the fact lecithin / PUFA is ALSO
> efficacious in fetal alcohol syndrome AND it carries the ADDED effect
> of .. RECOVERY .. ?
>
> Nicotinamide has been shown to raise PUFA in the brain.
>
> Nicotinestands in for choline remember.
> Western blot (n = 4-7/group). Density of Fluoro-Jade B-positive cells
> and NeuN-positive cells was determined in the cingulated cortex, CA1
> region of the hippocampus, and lateral dorsal nucleus of the thalamus
> (n = 5-6/group). Open field, plus maze, and fear conditioning tests
> were used to study the behavior in adult mice (n = 31-34/group).
> (c) Reuters 2007. All rights reserved.
>
> --------------------
>
> "Lecithin may therefore be the method of choice for
> accelerating acetylcholine synthesis"
>
> Lancet. 1977 Jul 9;2(8028):68-9. Related Articles, Links
>
> Lecithin consumption raises serum-free-choline levels.
>
> Wurtman RJ, Hirsch MJ, Growdon JH.
>
> Consumption of choline by rats sequentially increases serum-choline,
> brain-choline, and brain-acetylcholine concentrations. In man
> consumption of choline increases in levels in the serum and
> cerebrospinal fluid; its administration is an effective way of
> treating tardive dyskinesia.
> We found that oral lecithin is considerably more
> effective in raising human serum-choline levels than an equivalent
> quantity of choline chloride. 30 minutes after ingestion of choline
> chloride (2-3 g free base), serum-choline levels rose by 86% and
> returned to normal values within 4 hours; 1 hour after lecithin
> ingestion, these levels rose by 265% and remained significantly
> raised for 12 hours.
> Lecithin may therefore be the method of choice for
> accelerating acetylcholine synthesis by increasing the availability
> of choline, its precursor in the blood.
>
> PMID: 69151
> Who loves ya.
> Tom
>
ironj...@aol.com
Brain nicotinic acetylcholine receptor occupancy: effect of smoking a
denicotinized cigarette <<
http://archpsyc.ama-assn.org/cgi/content/full/63/8/907
Vol. 63 No. 8, August 2006 Archives
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Cigarette Smoking Saturates Brain 42 Nicotinic Acetylcholine
Receptors
Arthur L. Brody, MD; Mark A. Mandelkern, MD, PhD; Edythe D. London,
PhD; Richard E. Olmstead, PhD; Judah Farahi, PhD; David Scheibal, BS;
Jennifer Jou, BS; Valerie Allen, BS; Emmanuelle Tiongson, BS; Svetlana
I. Chefer, PhD; Andrei O. Koren, PhD; Alexey G. Mukhin, MD, PhD
Arch Gen Psychiatry. 2006;63:907-914.
ABSTRACT
Context 2-[18F]fluoro-3-(2(S)-azetidinylmethoxy) pyridine (2-F-
A-85380, abbreviated as 2-FA) is a recently developed radioligand that
allows for visualization of brain 42* nicotinic acetylcholine
receptors (nAChRs) with positron emission tomography (PET) scanning in
humans.
Objective To determine the effect of cigarette smoking on 42* nAChR
occupancy in tobacco-dependent smokers.
Design Fourteen 2-FA PET scanning sessions were performed. During the
PET scanning sessions, subjects smoked 1 of 5 amounts (none, 1 puff, 3
puffs, 1 full cigarette, or to satiety [2 to 3 cigarettes]).
Setting Academic brain imaging center.
Participants Eleven tobacco-dependent smokers (paid volunteers).
Main Outcome Measure Dose-dependent effect of smoking on occupancy of
42* nAChRs, as measured with 2-FA and PET in nAChR-rich brain
regions.
Results Smoking 0.13 (1 to 2 puffs) of a cigarette resulted in 50%
occupancy of 42* nAChRs for 3.1 hours after smoking. Smoking a full
cigarette (or more) resulted in more than 88% receptor occupancy and
was accompanied by a reduction in cigarette craving. A venous plasma
nicotine concentration of 0.87 ng/mL (roughly 1/25th of the level
achieved in typical daily smokers) was associated with 50% occupancy
of 42* nAChRs.
Conclusions Cigarette smoking in amounts used by typical daily
smokers leads to nearly complete occupancy of 42* nAChRs, indicating
that tobacco-dependent smokers maintain 42* nAChR saturation
throughout the day. Because prolonged binding of nicotine to 42*
nAChRs is associated with desensitization of these receptors, the
extent of receptor occupancy found herein suggests that smoking may
lead to withdrawal alleviation by maintaining nAChRs in the
desensitized state.
--------------------------------------------------------------------------------
Who loves ya.
Tom
Jesus Was A Vegetarian!
http://tinyurl.com/634q5a
Man Is A Herbivore!
http://tinyurl.com/4rq595
DEAD PEOPLE WALKING
http://tinyurl.com/zk9fk
> Arthur L. Brodya1a2 c1, Mark A. Mandelkerna2a3, Matthew R.
> Costelloa1a2, Anna L. Abramsa2, David Scheibala2, Judah Farahia2,
> Edythe D. Londona1a4, Richard E. Olmsteada2, Jed E. Rosea5 and Alexey
> G. Mukhina5
> a1 UCLA Department of Psychiatry and Biobehavioral Sciences, Los
> Angeles, CA, USA
> a2 Greater Los Angeles VA Healthcare System Positron Emission
> Tomography Center, Los Angeles, CA, USA
> a3 UCI Department of Physics, Irvine, CA, USA
> a4 UCLA Department of Molecular and Medical Pharmacology, Los Angeles,
> CA, USA
> a5 Duke University School of Medicine, Durham, NC, USA
> Abstract
> Our group recently reported that smoking a regular cigarette (1.2-1.4
> mgnicotine) resulted in 88% occupancy of brain á4â2* nicotinic
> acetylcholine receptors (nAChRs). However, this study did not
> determine whethernicotineinhalation or the many other
> pharmacological and behavioural factors that occur during smoking
> resulted in this receptor occupancy. Ifnicotineis solely responsible
> for á4â2* nAChR occupancy from smoking, then (as estimated from our
> previous data) smoking a denicotinized (0.05 mgnicotine) or a low-nicotine(0.6 mgnicotine) cigarette (commonly used for research and
> clinical purposes) would result in substantial 23% and 78% á4â2* nAChR
> occupancies, respectively, and a plasmanicotineconcentration of 0.87
> ng/ml would result in 50% á4â2* nAChR occupancy (EC50). Twenty-four
> positron emission tomography sessions were performed on tobacco-
> dependent smokers, using 2-[F-18]fluoro-A-85380 (2-FA), a radiotracer
> that binds to á4â2* nAChRs. 2-FA displacement was determined from
> before to 3.1 hours after either: no smoking, smoking a denicotinized
> cigarette, or smoking a low-nicotinecigarette. Analysis of this PET
> data revealed that smoking a denicotinized and a low-nicotine
> cigarette resulted in 26% and 79% á4â2* nAChR occupancies,
> respectively, across three regions of interest. The EC50 determined
> from this dataset was 0.75 ng/ml. Given the consistency of findings
> between our previous study with regular cigarettes and the present
> study,nicotineinhalation during smoking appears to be solely
> responsible for á4â2* nAChR occupancy, with other factors (if present
> at all) having either short-lived or very minor effects. Furthermore,
> smoking a denicotinized cigarette resulted in substantial nAChR
> occupancy.
>
> (Received March 26 2008)
>
> (Reviewed April 28 2008)
>
> (Revised June 23 2008)
>
> (Accepted July 07 2008)
>
> Key Words:Denicotinized cigarette;nicotine; nicotinic acetylcholine
> receptors; positron emission tomography; thalamus; tobacco
>
> Correspondence:
>
> c1 Address for correspondence: A. L. Brody, M.D., UCLA Department of
> Psychiatry & Biobehavioral Sciences, 300 UCLA Medical Plaza, Suite
> 2200, Los Angeles, CA 90095, USA. Tel.: 310-268-4778 Fax: 310-206-2802
> E-mail: abr...@ucla.edu
> The International Journal of Neuropsychopharmacology Cambridge
> University Press
> Copyright (c) 2008 CINP
> doi:10.1017/S146114570800922X
>
> --------------------------------------------------------------------------------
>
> Who loves ya.
> Tom
>
> Jesus Was A Vegetarian!http://tinyurl.com/634q5a
>
> Man Is A Herbivore!http://tinyurl.com/4rq595
>
> DEAD PEOPLE WALKINGhttp://tinyurl.com/zk9fk
>
>
>
> ...
>
> read more »- Hide quoted text -
>
> - Show quoted text -
ironj...@aol.com
substantial occupancy of brain 42* nAChRs, suggesting significant
occupancy and desensitization of 42* nAChRs in subjects indirectly
exposed to nicotine and pointing to the need for further research to
address this issue. <<
Anybody catch what the PROBLEM is when the receptors ARE fully
saturated all the time .. ?
Desenstization is a bad thing .. ?
If the nicotinic acid is SOOO .. helpful in those with schizophrenia
and ADHD and Parkinsons' and bi-polar .. WHY is it soo . bad .
--------------------------------------------------------------------------------
Who loves ya.
Tom
Jesus Was A Vegetarian!
http://tinyurl.com/634q5a
Man Is A Herbivore!
http://tinyurl.com/4rq595
DEAD PEOPLE WALKING
http://tinyurl.com/zk9fk
> On Dec 3, 12:56 pm, "ironjust...@aol.com" <ironjust...@aol.com>
> wrote:nicotinic acetylcholine receptor <<
>
> This means something ..
>
> Brain nicotinic acetylcholine receptor occupancy: effect of smoking a
> denicotinized cigarette
> Arthur L. Brodya1a2 c1, Mark A. Mandelkerna2a3, Matthew R.
> Costelloa1a2, Anna L. Abramsa2, David Scheibala2, Judah Farahia2,
> Edythe D. Londona1a4, Richard E. Olmsteada2, Jed E. Rosea5 and Alexey
> G. Mukhina5
> a1 UCLA Department of Psychiatry and Biobehavioral Sciences, Los
> Angeles, CA, USA
> a2 Greater Los Angeles VA Healthcare System Positron Emission
> Tomography Center, Los Angeles, CA, USA
> a3 UCI Department of Physics, Irvine, CA, USA
> a4 UCLA Department of Molecular and Medical Pharmacology, Los Angeles,
> CA, USA
> a5 Duke University School of Medicine, Durham, NC, USA
> Abstract
> Our group recently reported that smoking a regular cigarette (1.2-1.4
> mgnicotine) resulted in 88% occupancy of brain á4â2* nicotinic
> acetylcholine receptors (nAChRs). However, this study did not
> determine whethernicotineinhalation or the many other
> pharmacological and behavioural factors that occur during smoking
> resulted in this receptor occupancy. Ifnicotineis solely responsible
> for á4â2* nAChR occupancy from smoking, then (as estimated from our
> previous data) smoking a denicotinized (0.05 mgnicotine) or a low-nicotine(0.6 mgnicotine) cigarette (commonly used for research and
> clinical purposes) would result in substantial 23% and 78% á4â2* nAChR
> occupancies, respectively, and a plasmanicotineconcentration of 0.87
> ng/ml would result in 50% á4â2* nAChR occupancy (EC50). Twenty-four
> positron emission tomography sessions were performed on tobacco-
> dependent smokers, using 2-[F-18]fluoro-A-85380 (2-FA), a radiotracer
> that binds to á4â2* nAChRs. 2-FA displacement was determined from
> before to 3.1 hours after either: no smoking, smoking a denicotinized
> cigarette, or smoking a low-nicotinecigarette. Analysis of this PET
> data revealed that smoking a denicotinized and a low-nicotine
> cigarette resulted in 26% and 79% á4â2* nAChR occupancies,
> respectively, across three regions of interest. The EC50 determined
> from this dataset was 0.75 ng/ml. Given the consistency of findings
> between our previous study with regular cigarettes and the present
> study,nicotineinhalation during smoking appears to be solely
> responsible for á4â2* nAChR occupancy, with other factors (if present
> at all) having either short-lived or very minor effects. Furthermore,
> smoking a denicotinized cigarette resulted in substantial nAChR
> occupancy.
>
> (Received March 26 2008)
>
> (Reviewed April 28 2008)
>
> (Revised June 23 2008)
>
> (Accepted July 07 2008)
>
> Key Words:Denicotinized cigarette;nicotine; nicotinic acetylcholine
> receptors; positron emission tomography; thalamus; tobacco
>
> Correspondence:
>
> c1 Address for correspondence: A. L. Brody, M.D., UCLA Department of
> Psychiatry & Biobehavioral Sciences, 300 UCLA Medical Plaza, Suite
> 2200, Los Angeles, CA 90095, USA. Tel.: 310-268-4778 Fax: 310-206-2802
> E-mail: abr...@ucla.edu
> The International Journal of Neuropsychopharmacology Cambridge
> University Press
> Copyright (c) 2008 CINP
> doi:10.1017/S146114570800922X
>
> --------------------------------------------------------------------------------
>
> Who loves ya.
> Tom
>
> Jesus Was A Vegetarian!http://tinyurl.com/634q5a
>
> Man Is A Herbivore!http://tinyurl.com/4rq595
>
> DEAD PEOPLE WALKINGhttp://tinyurl.com/zk9fk
>
>
>
anon...@nowhere.you.know
ironj...@aol.com
Stay off my threads .. dioxin boy ..
EVERYONE has told you to do that ..
Now how come you figure you don't have to listen to those people who
know better than you .. ?
Because you are .. **nuts** .. dioxin boy ..
You should have told your mother to cut back on the fish ..
Chances are you wouldn't be soooo .. left-handed .. there .. boi ..
Heh .. heh ..
ironjustice
Alzheimer's Drugs Also Treat Behavioral, Psych Problems
Therapy effective at same dosage used to improve cognitive impairment,
study says
WEDNESDAY, Dec. 17 (HealthDay News) -- Drugs used to treat Alzheimer's
patients' cognitive symptoms are also a safe and effective therapy for
behavioral and psychological symptoms such as aggression, wandering
and paranoia, according to U.S. researchers.
They reviewed nine studies that examined the effectiveness of three
popular cholinesterase inhibitors in managing Alzheimer's patients'
behavioral and psychological symptoms, and found the drugs were
effective at the same dosage used to improve cognitive impairment.
The study was published in the December issue of Clinical
Interventions in Aging.
About 90 percent of Alzheimer's patients have behavioral and
psychological symptoms. Cholinesterase inhibitors boost levels of a
brain chemical called acetylcholine, which assists memory, thought and
judgment.
"There is a need for safe alternatives to the antipsychotic drugs
currently used to manage the behavioral and psychological symptoms of
Alzheimer's disease. The results of the studies we analyzed are
encouraging and suggestive that cholinesterase inhibitors are safe and
effective alternatives," review co-author Dr. Malaz Boustani, an
assistant professor of medicine at the Indiana University School of
Medicine, said in a university news release.
"However, [cholinesterase inhibitors] are underutilized and typically
prescribed for less than three months and for less than 10 percent of
patients with Alzheimer's disease. Our findings might provide
clinicians with useful data to justify the appropriate use of these
medications," said Boustani, a researcher at the IU Center for Aging
Research and chief research officer of the Indianapolis Discovery
Network for Dementia.
"This class of medications has already been approved the Food and Drug
Administration to manage symptoms of Alzheimer's type dementia,
although the potential benefits on behavioral symptoms are not
frequently identified by many prescribers," study co-author Noll
Campbell, a clinical pharmacy specialist in geriatric psychiatry with
Wishard Health Services, said in the news release. The use of
cholinesterase inhibitors could reduce "the use of more harmful
medications that are needed to control [dementia-related] behaviors."
More information
The U.S. National Institute on Aging has more about Alzheimer's
medications.
-- Robert Preidt
SOURCE: Indiana University, news release, Dec. 9, 2008
ironjustice
acetylcholine <<
Desensitization of nicotinic acetylcholine receptors as a strategy for
drug development.
J Pharmacol Exp Ther. 2008 Nov 20;
Buccafusco JJ, Beach JW, Terry AV
Medical College of Georgia.
The specific pharmacological response evoked by a nicotinic
acetylcholine receptor (nAChR) agonist is governed by the anatomical
distribution and expression of each receptor subtype, and by the
stoichiometry of subunits comprising each subtype. Contributing to
this complexity is ability of agonists that bind to the orthosteric
site of the receptor to alter the affinity state of the receptor and
induce desensitization; and the observation that, at low doses, some
nAChR antagonists evoke agonist-like nicotinic responses.
Brain concentrations of nicotine rarely increase to the low-mid microM
concentrations that have been reported to evoke direct agonist like
responses such as calcium influx or neurotransmitter release.
Low microg/kg doses of nicotine administered to humans or to non-human
primates to improve cognition and working memory likely result only in
low nM brain concentrations - more in line with the ability of
nicotine to induce receptor desensitization.
Here we review data illustrating that nicotine, its major metabolite
cotinine, and two novel analogs of choline, JWB1-84-1 and JAY2-22-33,
each improve working memory in macaques.
The effectiveness of these four compounds in the task was linearly
related their effectiveness in producing desensitization of the
pressor response to ganglionic stimulation evoked by a nAChR agonist
in rats.
Only nicotine evoked an agonist-like action (increased resting blood
pressure). Therefore it is possible to develop new chemical entities
that have the ability to desensitize nAChRs without an antecedent
agonist action.
Since these "silent desensitizers" are likely acting allosterically,
an additional degree of subtype specificity could be attained.
PMID: 19023041
Who loves ya.
Tom
ironjustice
wrote:acetylcholine <<
Here they wonder HOW the coumarin scopoletin enhances acetylcholine.
Now if one looks closely this coumarin has the SAME results as vitamin
E .. another .. coumarin.
"Seems to regulate the blood pressure: when the blood pressure is
high, it helps to lower it and when it is too low it can help raise
it"
I wonder if vitamin E also raises acetylcholine.
----------------
Effects of the coumarin scopoletin on learning and memory, on release
of acetylcholine from brain synaptosomes and on long-term potentiation
in hippocampus
Ariane Hornick1, Andreas Lieb1, Nguyen P Vo1, Judith Rollinger2,
Hermann Stuppner2 and Helmut Prast1
1Department of Pharmacology and Toxicology, Institute of Pharmacy,
Leopold-Franzens-University of Innsbruck, 6020 Innsbruck, Austria
2Department of Pharmacognosy, Institute of Pharmacy, Leopold-Franzens-
University of Innsbruck, 6020 Innsbruck, Austria
from 14th Scientific Symposium of the Austrian Pharmacological Society
(APHAR)
Innsbruck, Austria. 21–22 November 2008
BMC Pharmacology 2008, 8(Suppl 1):A36doi:10.1186/1471-2210-8-S1-A36
Published: 5 November 2008
First paragraph (this article has no abstract)
Among the chemical class of coumarins several substances have been
described to be effective as cognition enhancers. We have recently
characterized the coumarin scopoletin as a compound which fits a
pharmacophore model of AChE inhibitors and enhances the release of ACh
in rat brain [1]. Now, a comprehensive study was carried out in order
to investigate the effects of scopoletin on learning and memory, on
release of ACh from synaptosomes and on hippocampal long-term
potentiation (LTP) in order to uncover the mechanism of action.
This article is part of the supplement: 14th Scientific Symposium of
the Austrian Pharmacological Society (APHAR)
Meeting abstract
© 1999-2008 BioMed Central Ltd unless otherwise stated. Part of
Springer Science+Business Media.
http://www.biomedcentral.com/1471-2210/8/S1/A36/abstract
-------------------------------------------
Phytochemical:
Scopoletin
Synonyms: 7-Hydroxy-6-methoxycoumarin, gelseminic acid, chrysatropic
acid, esculetin-6-methyl ether
Properties: Scopoletin seems to regulate the blood pressure: when the
blood pressure is high, scopoletin helps to lower it and when it is
too low it can help raise it.
Scopoletin has bacteriostatic activity against various species of
bacteria, including Escherichia coli, Staphylococcus aureus,
Streptococcus sp., Klebsiella pneumoniae and Pseudomonas aeruginosa.
Scopoletin has anti-inflammatory activity and can be used to treat
bronchial illnesses and asthma. Scopoletin regulates the hormone
serotonin, which helps to reduce anxiety and depression.
Description: Pure scopoletin is a yellow to beige crystalline powder.
Scopoletin belongs to the group of coumarins (this group also includes
umbelliferone and esculetin).
Distribution: Noni, manaca, passion flower, stevia
Who loves ya.
Tom
anon...@nowhere.you.know
ironjustice
snip <<
Stay off my threads .. dioxin boy ..
Who loves ya.
anon...@nowhere.you.know
then one thing in common with the president elect now.
ironj...@aol.com
anon...@nowhere.you.know
then one thing in common with the president elect now.
Have you sought, like the president elect, to find help for your
addiction?
ironjustice
You know you DO .. look .. left-handed .. and .. act .. left-
handed ..
ARE you left-handed there .. murray .. ?
I suppose a little investigation will bring up your orientation ..
eh .. murray ..
What do you think .. ?
You think you can be .. outed .. ?
Left-handedness in a sample of nine patients with borderline
personality disorder.
Percept Mot Skills. 2004 Dec;99(3 Pt 1):849-52.
Niederhofer H.
Department of Pediatrics, General Hospital of Bolzano, Italy.
helmutniederho...@yahoo.de
Recent literature reports the possibility of right hemisphere
dysfunction in patients with behavioural disorders. 9 subjects
diagnosed as Borderline were studied via parent questionnaire. 5 of 9
patients were reported to use the left hand, more than is reported on
the average in the general population, and more often in complex than
simple and for external (touching food and objects) than for internal
tasks (scratching, rubbing eyes), which suggests a deficit in
cerebral
control of external, goal-oriented hand use. Our results for a small
group are consistent with the former hypothesis of a possible right
hemisphere dysfunction in patients with Borderline disorders.
PMID: 15648479
----------------------------------------------
ironj...@aol.com
iron accumulation <<
Psychological Symptoms Decrease Long-Term Quality of Life After Stroke
Marlene Busko
Information from Industry
Find out about a head-to-head comparison of MS treatment options
Dr. Daniel Mikol discusses the findings from the multicenter REGARD
study.
December 23, 2008 — Depression, anxiety, and fatigue strongly predict
decreased quality of life in patients who survive aneurysmal
subarachnoid hemorrhage (SAH), a new study reports.
In a separate study, the same researchers found that coping strategy
is the most important predictor of psychosocial well-being among
spouses of patients with stroke.
These findings, from J.M. Anne Visser-Meily, MD, from the University
Medical Center Utrecht, in Utrecht, the Netherlands, and colleagues,
are published in the December 18 Online First issue of Stroke.
"The major point is to look beyond physical symptoms and look at
psychological symptoms and personality characteristics to evaluate
quality of life," Dr. Visser-Meily said in a statement. "These
characteristics are important in planning rehabilitation and targeting
an intervention to help improve quality of life."
Psychological Factors Affect Recovery
Decreased quality of life in patients who survive SAH has been linked
to decreased physical abilities, but psychological and personality
factors might also play a role, the researchers write.
To identify the effect that psychological factors have on health-
related quality of life after SAH, they performed a cross-sectional
study of 141 individuals who had survived SAH 2 to 4 years earlier and
were living in the community. The patients were a mean age of 51
years, and 66% were women.
The participants completed a questionnaire based on the Stroke
Specific Quality of Life scale to evaluate health-related quality of
life.
They had a mean total score of 4, indicating a relatively satisfactory
overall quality of life, but this was because of high scores for
physical health and lower scores for emotional and social health.
There were 67% of patients who reported fatigue, 32% who reported
anxiety, and 23% who reported depression.
"Assessment of personality characteristics may be needed to target
interventions for these symptoms and to identify patients at risk for
reduced long-term health-related quality of life," Dr. Visser-Meily
told Medscape Psychiatry.
Patients with a passive coping style would especially benefit from
education and counseling about how to deal with these changes, she
added.
Caregivers' Coping Style Predicts Well-Being
In a separate study, the researchers report that during a 3-year
period after a stroke in their spouse, their partners showed decreases
in psychosocial functioning, and coping was the most important
predictor of well-being.
The patients' spouses had less caregiver burden with time, but they
also had a less harmonious relationship with their spouse; decreased
social interactions; and, after having an initial decline in
depression, showed increased depression.
"Monitoring of all aspects of psychosocial functioning of spouses is
needed, not only in the first period after stroke, but also in the
longer term," Dr. Visser-Meily told Medscape Psychiatry.
"A 'key professional' should assess the caregiver's social and
emotional needs as part of the routine follow-up activities of a
stroke service unit. During rehabilitation, more attention should be
given to programs that focus on empowering spouses and improving their
abilities to develop and maintain a social network," she added.
Few studies have addressed changes in the caregiving experience beyond
the first year after a spouse has had a stroke, she said.
In an earlier study, the researchers identified that a "passive coping
strategy" — that is, not seeking solutions or being proactive, but
rather doing nothing and being depressed — was the most important
predictor of a negative effect on quality of life.
"Coping styles are known to be related to psychosocial well-being of
people who are confronted with a negative or stressful life event,"
said Dr. Visser-Meily.
To assess the changes in psychosocial functioning of spouses and
examine how outcomes were related to coping strategies, the
researchers evaluated 211 spouses of patients with stroke from initial
inpatient rehabilitation of the patient to 3 years later.
The patients and spouses were relatively young (patients' mean age, 56
years; spouses' mean age, 54 years), and the patients were moderately
disabled.
"Using a passive coping strategy was generally associated with
negative outcomes, whereas using active coping strategies and seeking
social support were associated with positive outcomes," the
researchers report.
"Active coping can involve direct interventions, considering different
solutions to the problem, trying to find out everything about the
problem, and making plans," said Dr. Visser-Meily.
Caregiver burden decreased significantly from 2 months after discharge
from the rehabilitation center to 1 year after the stroke and from 1
year to 3 years after the stroke, possibly because of adaptation to
the caregiver role, according to the researchers.
The percentage of spouses with depressive symptoms decreased from 68%
at the start of rehabilitation to 53% at 2 months after rehabilitation
and remained at that high level.
The study authors have disclosed no relevant financial relationships.
Stroke. Published online December 18, 2008.
--------------------------------------------------------------------------------
Marlene Busko is a staff journalist for Medscape Psychiatry. She can
be contacted at mbu...@medscape.net.
Medscape Medical News 2008. © 2008 Medscape
--------------------
"Iron chelation may be useful therapy for stroke"
Activation of c-Jun-N-terminal kinase in a rat model of intracerebral
hemorrhage: The role of iron.
Neurosci Res. 2008 Nov 30.
Wan S, Zhan R, Zheng S, Hua Y, Xi G.
Department of Neurosurgery, First Affiliated Hospital, College of
Medicine, Zhejiang University, Hangzhou, China; Department of
Neurosurgery, University of Michigan, Ann Arbor, MI, USA.
Iron accumulates in the brain and contributes to brain injury after
intracerebral hemorrhage (ICH).
The c-Jun-N-terminal kinase (JNK) signaling pathway mediates cell
death after ischemic stroke, however, the involvement of JNK in ICH
is
not well known.
This study investigated whether the JNK signaling pathway is
activated
by iron after ICH.
Male Sprague-Dawley rats received an infusion of autologous whole
blood (as a model of ICH) or ferrous iron into the right basal
ganglia
and control rats had an infusion of saline.
Some ICH rats were treated with either deferoxamine (DFX), an iron
chelator, or vehicle.
Activation of JNK was measured by Western blot analysis and
immunohistochemistry.
Free iron in cerebrospinal fluid (CSF) and behavioral outcomes
following ICH were also examined.
We found that activated JNK in the brain were increased after ICH,
and
an intracerebral infusion of ferrous iron also upregulated brain
activated JNK.
Free iron accumulated in CSF and systemic administration of DFX after
ICH reduces free iron contents in CSF, suppresses JNK activation and
improves ICH-induced neurological deficits.
Our results demonstrated that the JNK signaling pathway is activated
after ICH and iron may contribute to this activation.
DFX reduces free iron levels and attenuates activation of JNK
suggesting iron chelation may be useful therapy for ICH patients.
PMID: 19100788
anon...@nowhere.you.know
ironjustice
I told you murray ..
You are a little .. pussy ..
Take your dioxin .. bullsht .. AND your dioxin pals .. and .. git ..
anon...@nowhere.you.know
At the start of a new year and now knowing that the toxin in tobacco is
not vitamin b3 you have no longer a reason to continue smoking.
ironjustice
brain iron accumulation <<
Cognitive Impairment in Superficial Siderosis of the Central Nervous
System: A Case Report.
Cerebellum. 2008 Oct 21
Uttner I, Tumani H, Arnim CV, Brettschneider J.
Department of Neurology, University of Ulm, Oberer Eselsberg 45,
89081, Ulm, Germany.
Superficial siderosis is a rare disease characterized by cerebellar
ataxia and sensorineural deafness.
So far, there are only few reports on cognitive dysfunctions
associated with superficial siderosis.
Using a comprehensive psychometric test battery, we describe the
cognitive impairments in a 65-year-old woman fulfilling the clinical
and magnetic resonance imaging criteria of superficial siderosis.
The neuropsychological findings included deterioration of primary and
episodic memory, behavioral and linguistic changes characterized by
social disinhibition, and decreased verbal fluency.
These findings may correspond to the "cerebellar cognitive affective
syndrome" which was suggested to occur in patients with selective
cerebellar lesions. Probable mechanisms leading to the characteristic
cognitive impairment in superficial siderosis are discussed.
PMID: 18937022
ironjustice
brain iron accumulation <<
"Maltol as tobacco smoking inhibitor"
Biotic Type Antioxidants: The Prospective Search Area for Novel ... -
Google Books Resultby E. A. Parfenov, Gennadiĭ Efremovich Zaikov -
2000 - Science - 560 pages
The experimental results confirm that as compared with maltol and
hydroxypyridones, desferal increases the risk of infection
diseases112' 13°. ...
books.google.com/books?isbn=9067643084...
The antioxidant properties of hydroxypyrones allow us to explain and
apply their chemoprotective activity and anticarcinogenic effects.
Besides their ability to inhibit formation of N-nitrosoamines, the
ability of maltol and ethylmaltol to suppress oxidative stress, which
accompanies consumption of alcohol and smoking , is to be considered
as a most valuable property.
Maltol and ethylmaltol as tobacco smoking inhibitors are introduced
in
a 500 mg/day dose into the compositions of chewing gums, caramels or
other food agents, which should be present in the mouth over 10
minutes.
The administration of theser peroaral medicinal forms of maltol
displays an additional advantage, since a chewing gum with maltol is
patented as a dental caries inhibitor.
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
>
> Cognitive Impairment in Superficial Siderosis of the Central Nervous
> System: A Case Report.
> Cerebellum. 2008 Oct 21
> Uttner I, Tumani H, Arnim CV, Brettschneider J.
> Department of Neurology, University of Ulm, Oberer Eselsberg 45,
> 89081, Ulm, Germany.
>
> Superficial siderosis is a rare disease characterized by cerebellar
> ataxia and sensorineural deafness.
> So far, there are only few reports on cognitive dysfunctions
> associated with superficial siderosis.
> Using a comprehensive psychometric test battery, we describe the
> cognitive impairments in a 65-year-old woman fulfilling the clinical
> and magnetic resonance imaging criteria of superficial siderosis.
> The neuropsychological findings included deterioration of primary and
> episodic memory, behavioral and linguistic changes characterized by
> social disinhibition, and decreased verbal fluency.
> These findings may correspond to the "cerebellar cognitive affective
> syndrome" which was suggested to occur in patients with selective
> cerebellar lesions. Probable mechanisms leading to the characteristic
> cognitive impairment in superficial siderosis are discussed.
>
> PMID: 18937022
>
> Who loves ya.
> Tom
>
Ken
ironj...@aol.com
brain iron accumulation "Maltol as tobacco smoking inhibitor" <<
"Maltol remarkably attenuated the neurobehavioral signs and neuronal
loss" <<
"Maltol inhibited iron-mediated lipid peroxidation"
Maltol as an antioxidant : Inhibition of lipid peroxidation and
protection of NADP- isocitrate dehydrogenase from the iron-mediated
inactivation
MURAKAMI Keiko ; ITO Masae ; TANEMURA Yasuko ; YOSHINO Masataka ;
Maltol (3-hydroxy-2-methyl-4-pyrone) inhibited iron-mediated lipid
peroxidation, determined as the formation of thiobarbituric acid-
reactive substances, but dimethylpyrone, an analogue of maltol showed
no effect on the formation of lipid peroxides.
NADP-isocitrate dehydrogenase, a principal enzyme generating reduced
NADP, was protected by maltol but not by dimethylpyrone from the
ferrous ion-mediated inactivation.
Protection of NADP-isocitrate dehydrogenase can enhance the supply of
NADPH required for the regeneration of reduced glutathione for
scavenging reactive oxygen species.
Antioxidant properties of maltol were closely related to the enhanced
oxidation of ferrous ion as a prooxidant, and can be explained by the
electron-deficient nature of 3-hydroxypyrone ring.
Revue / Journal Title
Biomedical research ISSN 0388-6107 CODEN BRESD5
Source / Source
2001, vol. 22, no4, pp. 183-186 [4 page(s) (article)]
Biomedical Research Foundation, Tokyo, JAPON (1980) (Revue)
INIST-CNRS, Cote INIST : 19053, 35400010016716.0010
Copyright 2008 INIST-CNRS. All rights reserved
Toute reproduction ou diffusion même partielle, par quelque procédé
ou
sur tout support que ce soit, ne pourra être faite sans l'accord
préalable écrit de l'INIST-CNRS.
No part of these records may be reproduced of distributed, in any
form
or by any means, without the prior written permission of INIST-CNRS.
Nº notice refdoc (ud4) : 13468314
Who loves ya.
Tom
Jesus Was A Vegetarian!
http://tinyurl.com/634q5a
ironj...@aol.com
On Jan 14, 8:57 am,ironjustice<ironjust...@cashette.com> wrote:
brain iron accumulation "Maltolas tobacco smoking inhibitor"
"Maltol remarkably attenuated the neurobehavioral signs and neuronal
loss" "Maltol inhibited iron-mediated lipid peroxidation"<<
Maltol in soybeans, mung beans, kidney beans, and azuki beans
Inhibitory effects of volatile antioxidants found in various beans on
malonaldehyde formation in horse blood plasma.
Food Chem Toxicol. 2005 Apr;43(4):515-20.
Lee SJ, Lee KG.
Korea Food Research Institute, San 46-1, Backhyun, Bundang-gu,
Sungnam,
Kyonggi-do 463-746, Korea.
The inhibitory effect of aroma extracts isolated from dried soybeans,
mung beans, kidney beans, and azuki beans on malonaldehyde (MA)
formation from horse blood plasma oxidized with Fenton's reagent was
determined by gas chromatography (GC) coupled with nitrogen-
phosphorus
detector (NPD).
Aroma chemicals such as maltol, eugenol, benzyl alcohol, 1-octen-3-ol,
butyrolactone, and 1-methyl-2-pyrrolidone, found in the aroma
extracts
of beans, were also examined for their inhibitory effect on the same
system.
Among the four aroma extracts tested, the aroma extract of soybeans
exhibited the strongest antioxidant activity.
Extracts of soybeans, mung beans, azuki beans, and kidney beans
inhibited MA formation by 58%, 47%, 40%, and 23%, respectively, at
the
level of 400mug/mL, whereas, alpha-tocopherol and BHT inhibited MA
formation by 52% and 70%, respectively, at the same level.
Among the tested aroma chemicals, the antioxidant activity decreased
in the
following order: eugenol>maltol>1-octen-3-ol>benzyl
alcohol>butyrolactone>1-methyl-2-pyrrolidone.
PMID: 15721197
anon...@nowhere.you.know
ironj...@aol.com
I already told you murray ..
YOU have NOOOOOOO .. input in these threads ..
YOU are .. a .. fkg .. looooon .. murray ..
You for some reason BELIEVE you have some .. gift .. from your left
handed buddies I suppose .. that would make someone wish to read what
you put on threads ..
But you are wrong ..
You are a two bit dioxin .. **freak** who couldn't put two medical
studies together to make .. four ..
Understand .. murray .. ?
Who loves ya.
Tom
Jesus Was A Vegetarian!
http://tinyurl.com/2r2nkh
Ken
Juba
> (0)
Ken has been asked several times to stop troll-poking. He has been told
several times that his actions are only making the problem worse. I
warned him that if he didn't stop posting this tripe I would report him
for spamming and post his message IDs here so others could report him as
well. He apparently thinks that no one can stop him. It's time to prove
him wrong.
So, I invite everyone to join me in reporting him for spamming. Just
copy the following to a message and send it off.
-------------------------------------------------------
To:
groups...@google.com, ab...@abuse.earthlink.net
Subject:
Please stop this spammer.
This individual has posted enough substantially identical messages to
qualify as spam. Please make him stop.
-------------------------------------------------------------
Xref: news sci.med.nutrition:284595 alt.support.chronic-pain:330055
misc.health.alternative:634348 alt.support.alzheimers:62363
soc.senior.issues:133371
Path:
news.glorb.com!news2.glorb.com!postnews.google.com!r27g2000vbp.googlegroups.com!not-for-mail
From: Ken <flak...@aol.com>
Newsgroups:
sci.med.nutrition,alt.support.chronic-pain,misc.health.alternative,alt.support.alzheimers,soc.senior.issues
Subject: Re: SpaM sPAm spaM
Date: Sat, 24 Jan 2009 20:06:42 -0800 (PST)
Organization: http://groups.google.com
Lines: 2
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<37ad8063-48dd-40f3...@r27g2000vbp.googlegroups.com>
References:
<0f51fe22-2246-4be9...@g39g2000pri.googlegroups.com>
<497a1bbe$0$31913$1c46...@news.club.cc.cmu.edu>
<7aae1a1f-bd33-4402...@t26g2000prh.googlegroups.com>
NNTP-Posting-Host: 66.245.153.9
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posting-account=fpUx3QoAAADgnytjYurcHomn0oTV40rh
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------------------------------------------
Here is a list of his recent posts that are substantially identical:
(0)
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FOAD Troll
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FOAD Fool
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<2abae6ae-c419-439f...@r37g2000prr.googlegroups.com>
Message-ID:
<8306f0d3-8d75-4d85...@a29g2000pra.googlegroups.com>
--
Juba
www.masterjuba.com
Juba
"Thank you for submitting a report to the EarthLink Network Abuse
Department. Unfortunately, your submission does not contain sufficient
information to determine the nature of your issue. Evidence to Abuse
should always include at least the IP address of the offending party and
a valid timestamp, which includes time, date and timezone. "
Ridiculous, but an effective means of ignoring spam bots. So I replied
with the following:
----------------------------------------------------
The message I sent you contains all of the information you require to
"determine the nature" of my issue.
IP: 66.245.153.9
Date: Sat, 24 Jan 2009 20:06:42 -0800 (PST)
-----------------------------------------------------
And that got this response:
-------------------------------------------------
Thank you for submitting a report to the EarthLink Network Abuse
Department.
Your ticket number is AB0000001350117, which you'll need to reference
if you email us again regarding this issue. We may follow up with
you if we need more information to aid our investigation.
etc.
------------------------------------------------
I warned you Kenny.
--
Juba
www.masterjuba.com
ironjustice
High Miles
> Ken wrote:
>> (0)
>
> Ken has been asked several times to stop troll-poking. He has been told
> several times that his actions are only making the problem worse. I
> warned him that if he didn't stop posting this tripe I would report him
> for spamming and post his message IDs here so others could report him as
> well. He apparently thinks that no one can stop him. It's time to prove
> him wrong.
>
> So, I invite everyone to join me in reporting him for spamming. Just
> copy the following to a message and send it off.
I applaud the abuse of cross posters, and wish there was a way to
clear them off for good.
They need to get a clue that it's ignorant to inflict their messages
on groups that have NO interest in reading their stuff.
High Miles
> The reply I got from Earthlink:
>
Your title should probably be - master abater.
Stop cross posting and you won't have to see complaint posts.