metabolic bone diseases / oxidative stress

And what exactly are we to make of this, how does it relate
to any body of theory, to what practical use is it, and to
what goal can it be useful? Without this information it is
but another random abstract plucked from the web, one among
thousands of such.

Quoted message said:

Subject: Re: metabolic bone diseases / oxidative stress

Toxicology. 2004 Apr 15;197(2):92-9. Links

[In Process Citation]

Isomura H, Fujie K, Shibata K, Inoue N, Iizuka T, Takebe G,
Takahashi K, Nishihira J, Izumi H, Sakamoto W.

Department of Biochemistry, School of Dentistry, Hokkaido
University, North 13 West 7 Kita-ku, Hokkaido, Sapporo
060, Japan.

Osteoporosis is associated with many etiological causes such
as nutrition, cytokines, hormones, and aging. Recently,
reactive oxygen species (ROS) are considered to be
responsible for the aging process and osteoporosis. We
investigated the relationship between ROS and bone
metabolism in young female and postmenopausal rats, by using
dietary iron overload and several indices including bone
metabolic markers, oxidative stress and antioxidant markers,
and cytokines. Postmenopausal rats exhibited significant
decreases in serum alkaline phosphatase activity and the
level of osteocalcin as bone formation markers compared with
young female rats; however, urinary excretion of
deoxypyridinoline, a bone resorption marker, did not change.
On the other hand, a 5% iron lactate diet for 4 weeks in
postmenopausal rats led to significantly increased excretion
of urinary deoxypyridinoline and 8-hydroxy-2'-deoxyguanosine
(8-OHdG) but not serum alkaline phosphatase activity.
Interestingly, the diet induced significant increases of
serum osteopontin and TGF-beta1, augumenting osteoclast-
mediated bone resorption through the RANK/RANKL pathway [J.
Clin. Invest. 112 (2003) 181]. TGF-beta1 showed a negative
correlation with serum glutathione peroxidase (GPx) activity
( [Formula: see text], [Formula: see text] ), but a positive
correlation with the serum iron level ( [Formula: see text],
[Formula: see text] ). Taken together, these results suggest
for the first time that oxidative stress could be involved
in the pathogenesis of metabolic bone diseases such as
osteoporosis as demonstrated by analysis of the relationship
between bone metabolism and oxidative stress.

PMID: 15003320 [PubMed - in process]

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

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pages.ivillage.commanisaherbivoreOpen ↗ DEAD
PEOPLE WALKING
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And what exactly are we to make of this, how does it relate
to any body of theory, to what practical use is it, and to
what goal can it be useful? Without this information it is
but another random abstract plucked from the web, one among
thousands of such.

Quoted message said:

Subject: Re: metabolic bone diseases / oxidative stress
From: [email hidden]
Date: 3/11/2004 7:34 AM Mountain Standard Time
Message-id: <[email hidden]>

And what exactly are we to make of this, how does it relate
to any body of theory, to what practical use is it, and to
what goal can it be useful? Without this information it is
but another random abstract plucked from the web, one among
thousands of such.

What part of .. abuse .. don't you understand .. jrkff ..

Quoted message said:

Subject: Re: metabolic bone diseases / oxidative stress

Toxicology. 2004 Apr 15;197(2):92-9. Links

[In Process Citation]

Isomura H, Fujie K, Shibata K, Inoue N, Iizuka T, Takebe G,
Takahashi K, Nishihira J, Izumi H, Sakamoto W.

Department of Biochemistry, School of Dentistry, Hokkaido
University, North 13 West 7 Kita-ku, Hokkaido, Sapporo
060, Japan.

Osteoporosis is associated with many etiological causes such
as nutrition, cytokines, hormones, and aging. Recently,
reactive oxygen species (ROS) are considered to be
responsible for the aging process and osteoporosis. We
investigated the relationship between ROS and bone
metabolism in young female and postmenopausal rats, by using
dietary iron overload and several indices including bone
metabolic markers, oxidative stress and antioxidant markers,
and cytokines. Postmenopausal rats exhibited significant
decreases in serum alkaline phosphatase activity and the
level of osteocalcin as bone formation markers compared with
young female rats; however, urinary excretion of
deoxypyridinoline, a bone resorption marker, did not change.
On the other hand, a 5% iron lactate diet for 4 weeks in
postmenopausal rats led to significantly increased excretion
of urinary deoxypyridinoline and 8-hydroxy-2'-deoxyguanosine
(8-OHdG) but not serum alkaline phosphatase activity.
Interestingly, the diet induced significant increases of
serum osteopontin and TGF-beta1, augumenting osteoclast-
mediated bone resorption through the RANK/RANKL pathway [J.
Clin. Invest. 112 (2003) 181]. TGF-beta1 showed a negative
correlation with serum glutathione peroxidase (GPx) activity
( [Formula: see text], [Formula: see text] ), but a positive
correlation with the serum iron level ( [Formula: see text],
[Formula: see text] ). Taken together, these results suggest
for the first time that oxidative stress could be involved
in the pathogenesis of metabolic bone diseases such as
osteoporosis as demonstrated by analysis of the relationship
between bone metabolism and oxidative stress.

PMID: 15003320 [PubMed - in process]

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

Who loves ya. Tom Jesus Was A Vegetarian!
jesuswasavegetarian.7h.comjesuswasavegetarian.7h.comOpen ↗ Man Is A Herbivore!
pages.ivillage.commanisaherbivoreOpen ↗ DEAD
PEOPLE WALKING
pages.ivillage.comdeadpeoplewalkingOpen ↗

Quoted message said:

Subject: Re: metabolic bone diseases / oxidative stress
From: [email hidden]
Date: 3/11/2004 7:34 AM Mountain Standard Time
Message-id: <[email hidden]>

And what exactly are we to make of this, how does it relate
to any body of theory, to what practical use is it, and to
what goal can it be useful? Without this information it is
but another random abstract plucked from the web, one among
thousands of such.

What part of .. abuse .. don't you understand .. jrkff ..

Quoted message said:

Subject: Re: metabolic bone diseases / oxidative stress

Toxicology. 2004 Apr 15;197(2):92-9. Links

[In Process Citation]

Isomura H, Fujie K, Shibata K, Inoue N, Iizuka T, Takebe G,
Takahashi K, Nishihira J, Izumi H, Sakamoto W.

Department of Biochemistry, School of Dentistry, Hokkaido
University, North 13 West 7 Kita-ku, Hokkaido, Sapporo
060, Japan.

Osteoporosis is associated with many etiological causes such
as nutrition, cytokines, hormones, and aging. Recently,
reactive oxygen species (ROS) are considered to be
responsible for the aging process and osteoporosis. We
investigated the relationship between ROS and bone
metabolism in young female and postmenopausal rats, by using
dietary iron overload and several indices including bone
metabolic markers, oxidative stress and antioxidant markers,
and cytokines. Postmenopausal rats exhibited significant
decreases in serum alkaline phosphatase activity and the
level of osteocalcin as bone formation markers compared with
young female rats; however, urinary excretion of
deoxypyridinoline, a bone resorption marker, did not change.
On the other hand, a 5% iron lactate diet for 4 weeks in
postmenopausal rats led to significantly increased excretion
of urinary deoxypyridinoline and 8-hydroxy-2'-deoxyguanosine
(8-OHdG) but not serum alkaline phosphatase activity.
Interestingly, the diet induced significant increases of
serum osteopontin and TGF-beta1, augumenting osteoclast-
mediated bone resorption through the RANK/RANKL pathway [J.
Clin. Invest. 112 (2003) 181]. TGF-beta1 showed a negative
correlation with serum glutathione peroxidase (GPx) activity
( [Formula: see text], [Formula: see text] ), but a positive
correlation with the serum iron level ( [Formula: see text],
[Formula: see text] ). Taken together, these results suggest
for the first time that oxidative stress could be involved
in the pathogenesis of metabolic bone diseases such as
osteoporosis as demonstrated by analysis of the relationship
between bone metabolism and oxidative stress.

PMID: 15003320 [PubMed - in process]

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

Who loves ya. Tom Jesus Was A Vegetarian!
jesuswasavegetarian.7h.comjesuswasavegetarian.7h.comOpen ↗ Man Is A Herbivore!
pages.ivillage.commanisaherbivoreOpen ↗ DEAD
PEOPLE WALKING
pages.ivillage.comdeadpeoplewalkingOpen ↗

"What part of .. abuse .. don't you understand .. jrkff .."

"Abuse" is in the mind of the reader, one thinks. If one
thinks posting abstracts which might suggest some connection
to something not declared is abuse, then so be it. If one
thinks personal attack on a ng abuse, then so be it. If one
think using criptic variations of vulgar name calling an
abuse, then so be it. If one thinks an atempt to make all
sides known so an informed opinion can be formed, so be it.
If one finds one cornered and blocked in strident attempts
at agenda promotion, bhen so be it. However, after all is
said and done we are still left with the burning question:

And what exactly are we to make of this, how does it relate
to any body of theory, to what practical use is it, and to
what goal can it be useful? Without this information it is
but another random abstract plucked from the web, one among
thousands of such.

Der Sur: i hav imperical evidance thet u preduce a pane in
the rectul cevity.

<[email hidden]> wrote in message -"]news:[email hidden]-
net.com...

Quoted message said:

"What part of .. abuse .. don't you understand ..
jrkff .."

"Abuse" is in the mind of the reader, one thinks. If one
thinks posting abstracts which might suggest some
connection to something not declared is abuse, then so be
it. If one thinks personal attack on a ng abuse, then so
be it. If one think using criptic variations of vulgar
name calling an abuse, then so be it. If one thinks an
atempt to make all sides known so an informed opinion can
be formed, so be it. If one finds one cornered and blocked
in strident attempts at agenda promotion, bhen so be it.
However, after all is said and done we are still left with
the burning question:

And what exactly are we to make of this, how does it
relate to any body of theory, to what practical use is it,
and to what goal can it be useful? Without this
information it is but another random abstract plucked from
the web, one among thousands of such.

[email hidden] [email hidden] [email hidden] Once
upon a time, our fellow [email hidden] rambled on about
"Re: metabolic bone diseases / oxidative stress." Our
champion De-Medicalizing in sci.med.nutrition retorts,
thusly ...

Quoted message said:

And what exactly are we to make of this

I have twit filtered doe, but you guys, who are responding
to him, are comprising about 75% of the posts on this ng.
The other 25% of the posts are Fat Farm threads.

Just thought that you might want to know. 🙂

[email hidden] [email hidden] [email hidden] Once
upon a time, our fellow Mike V rambled on about "Re:
metabolic bone diseases / oxidative stress." Our champion
De-Medicalizing in sci.med.nutrition retorts, thusly ...

Quoted message said:

i hav imperical evidance thet u preduce a pane in the
rectul cevity.

I second that motion.

"John 'the Man'" <[email hidden]> wrote in message
"]news:[email hidden]...

Quoted message said:

[email hidden] [email hidden] [email hidden] Once
upon a time, our fellow [email hidden] rambled on
about "Re: metabolic bone diseases / oxidative stress."
Our champion De-Medicalizing in sci.med.nutrition retorts,
thusly ...

Quoted message said:

And what exactly are we to make of this

I have twit filtered doe, but you guys, who are responding
to him, are comprising about 75% of the posts on this ng.
The other 25% of the posts are Fat Farm threads.

Just thought that you might want to know. 🙂

Sorry about that :o)

I've given up on him now !

MB