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Dear all,
For those of you who are interested, the following are some of the replies
I've received so far (I've deliberately left out those which give personal
details of people I've been advised to contact). Many thanks to all those
who relied, it's much appreciated. Also, my apologies if I have not replied
to everyone personally - it gets confusing when I access my mail from more
than one computer!
Kaf
****************************************
The bone growth specification is depended to some
complex molecules such as IGFs (Internal Growth
Factors), TGFs (Transforming Growth Factors), etc.
which are secreted in a very slight amounts. The
amount of this moleculs and the end organ responses
have a genetic basis. There are plenty of theories
which try to describe the mechanisms but as far as I
know, the exact mechanism is not agreed. The answer of
your second question is the same. I recommend you
referring to the Immunology and Biochemistry
references.
**************************************************
I'm no expert in the bone growth field. But I can tell you from a
remodeling point of view, the right and left legs may be the same size
because they see the exact same mechanical loading. In other words, if the
right leg was a foot longer than the left, the loading seen would be very
different. The bones may remodel so the load bearing is evenly distributed
between the two legs.
I would be interested in any other responses you get. Good luck!!
************************************************** *
The answer to your second question hints at the answer to the first.
Symmetry is not perfect, for one --- it is close. the question becomes,
"why are the lengths so similar?" The reason for length symmetry is
simple: the loading (properly, stress, i.e., force per unit area) is
nearly
equal. The molecules themselves contain no information about bone
length (as the genome contains none). Osteoblasts (where the molecule
of interest resides) remodel bone to maintain stress at a certain level,
called the "set point." If the bone was of a small diameter, stress
(given
a 700-kg animal) would be high, and the osteoblasts would remodel the
bone, adding tissue to increase the cross-sectional area, reducing
stress to
"normal."
If the bone possesed a huge diameter (and so a large cross sectional
area),
stress would be very low, and so the o-blasts would remove tissue until
the stress reached "normal" levels. The o-blasts don't measure area,
they
probably are sparked into action when the molecule of interest (or those
in
the pathway) transduces the stress signal. If you change the
molecule(s) at
work in the osteoblasts, you change the set point. Mammal limb bone in
general has about the same set point. Vertebrate limb bones aren't too
different, altogether. So:
The horse is symmetrical because the loading is symmetrical.
Although running around the track might seem enough to generate a bias,
with the associated cyclic stress, that signal is probably lost in the
noise of
just standing (shifting balance) and walking around. To make an
asymmetry,
it might be useful to load an animal with a cantilever on one side ---
although
the behavioral response to that might negate your signal there, too.
Think of this: astro/cosmo-naughts suffer loss of bone tissue as the
osteoblasts remodel the bone --- as the stress levels in microgravity
are almost
nothing without constant exercise. The molecules are not subjected to
the
stress fields, the o-blasts "feel" that stress is too low, and so
metabolize bone in
an attempt to get the stress back to where it should be --- with
disastrous results
for the human. Now, if someone could find a way to activate the stress
transducing
molecule during zero-G, then you might have something. The cool part is
that the
feedback loop between bone shape and the stress fields of normal loading
ensures
that the bone shapes maintain. In other words, the o-blast stress
triggerring mechanism
is global, but it responds locally to local stresses, both during early
development and
during later growth, and during adulthood. One probably does not want
to mess
with the set point of human bone for work in space, because that would
trigger nasty
remodeling all over. And imagine what would happen if the molecule(s)
of interest
failed to respond (or responded too well) to stress, because of a
pathology?
One could see lots of bone loss, or see massive accumulations of bone.
Good luck with this --- the subject is fascinating.
************************************************** ****
Kaf Barriball BSc (Hons)
Equine Biomechanics Research Student
De Montfort University
Caythorpe Court
Caythorpe
Grantham
Lincolnshire
NG32 3EP
tel: 01400 275673
email:kathryn.barriball@students.dmu.ac.uk
OR: kaf.barriball@virgin.net
fax: 01400 272722
---------------------------------------------------------------
To unsubscribe send SIGNOFF BIOMCH-L to LISTSERV@nic.surfnet.nl
For information and archives: http://isb.ri.ccf.org/biomch-l
---------------------------------------------------------------
For those of you who are interested, the following are some of the replies
I've received so far (I've deliberately left out those which give personal
details of people I've been advised to contact). Many thanks to all those
who relied, it's much appreciated. Also, my apologies if I have not replied
to everyone personally - it gets confusing when I access my mail from more
than one computer!
Kaf
****************************************
The bone growth specification is depended to some
complex molecules such as IGFs (Internal Growth
Factors), TGFs (Transforming Growth Factors), etc.
which are secreted in a very slight amounts. The
amount of this moleculs and the end organ responses
have a genetic basis. There are plenty of theories
which try to describe the mechanisms but as far as I
know, the exact mechanism is not agreed. The answer of
your second question is the same. I recommend you
referring to the Immunology and Biochemistry
references.
**************************************************
I'm no expert in the bone growth field. But I can tell you from a
remodeling point of view, the right and left legs may be the same size
because they see the exact same mechanical loading. In other words, if the
right leg was a foot longer than the left, the loading seen would be very
different. The bones may remodel so the load bearing is evenly distributed
between the two legs.
I would be interested in any other responses you get. Good luck!!
************************************************** *
The answer to your second question hints at the answer to the first.
Symmetry is not perfect, for one --- it is close. the question becomes,
"why are the lengths so similar?" The reason for length symmetry is
simple: the loading (properly, stress, i.e., force per unit area) is
nearly
equal. The molecules themselves contain no information about bone
length (as the genome contains none). Osteoblasts (where the molecule
of interest resides) remodel bone to maintain stress at a certain level,
called the "set point." If the bone was of a small diameter, stress
(given
a 700-kg animal) would be high, and the osteoblasts would remodel the
bone, adding tissue to increase the cross-sectional area, reducing
stress to
"normal."
If the bone possesed a huge diameter (and so a large cross sectional
area),
stress would be very low, and so the o-blasts would remove tissue until
the stress reached "normal" levels. The o-blasts don't measure area,
they
probably are sparked into action when the molecule of interest (or those
in
the pathway) transduces the stress signal. If you change the
molecule(s) at
work in the osteoblasts, you change the set point. Mammal limb bone in
general has about the same set point. Vertebrate limb bones aren't too
different, altogether. So:
The horse is symmetrical because the loading is symmetrical.
Although running around the track might seem enough to generate a bias,
with the associated cyclic stress, that signal is probably lost in the
noise of
just standing (shifting balance) and walking around. To make an
asymmetry,
it might be useful to load an animal with a cantilever on one side ---
although
the behavioral response to that might negate your signal there, too.
Think of this: astro/cosmo-naughts suffer loss of bone tissue as the
osteoblasts remodel the bone --- as the stress levels in microgravity
are almost
nothing without constant exercise. The molecules are not subjected to
the
stress fields, the o-blasts "feel" that stress is too low, and so
metabolize bone in
an attempt to get the stress back to where it should be --- with
disastrous results
for the human. Now, if someone could find a way to activate the stress
transducing
molecule during zero-G, then you might have something. The cool part is
that the
feedback loop between bone shape and the stress fields of normal loading
ensures
that the bone shapes maintain. In other words, the o-blast stress
triggerring mechanism
is global, but it responds locally to local stresses, both during early
development and
during later growth, and during adulthood. One probably does not want
to mess
with the set point of human bone for work in space, because that would
trigger nasty
remodeling all over. And imagine what would happen if the molecule(s)
of interest
failed to respond (or responded too well) to stress, because of a
pathology?
One could see lots of bone loss, or see massive accumulations of bone.
Good luck with this --- the subject is fascinating.
************************************************** ****
Kaf Barriball BSc (Hons)
Equine Biomechanics Research Student
De Montfort University
Caythorpe Court
Caythorpe
Grantham
Lincolnshire
NG32 3EP
tel: 01400 275673
email:kathryn.barriball@students.dmu.ac.uk
OR: kaf.barriball@virgin.net
fax: 01400 272722
---------------------------------------------------------------
To unsubscribe send SIGNOFF BIOMCH-L to LISTSERV@nic.surfnet.nl
For information and archives: http://isb.ri.ccf.org/biomch-l
---------------------------------------------------------------