Hello,
I have been thinking about a particular
research question lately, and could not find
any relevant papers on the topic. I hope
someone can suggest some solutions.
The question is - how do continuously
loaded tissues grow? Two good examples
of these tissues exist: (1) the walls of arteries,
and (2) the periosteum surrounding long bones.
Both of these tissues are continuously loaded,
but must grow. My question does not concern
the actual morphological changes occurring during
growth, but the changes that occur in the
molecular load-bearing components of the
tissue. If the tissue is under continuous load,
then how are new load-bearing elements
added? In the arterial tissue, for example,
the load is carried by microfibrils, elastin,
and collagen. (There are some interesting
developmental and evolutionary aspects
of these elements too, which I may raise
in another message.) How are new elements
added while the wall continues to function?
I want to start answering this question
by looking at a very simple mechancial system –
the locomotor system of a scallop. This
consists of two shells that are pulled together
by a single muscle. The shells are connected
by a hinge. The muscle antagonism is elastic
– created by a compressive spring on the inside
of the hinge, and tensile elements on the outside
of the hinge. Most of the energy storage
occurs in the compressive hinge, which is
composed of an elastomer called abductin.
(This is very similar to elastin.)
When a scallop dies, the shells gape open,
but eventually stop, as the collagenous elements
in the muscle are stretched. However, if you cut
the muscle out of the shell, the shells will gape
even farther, showing that the hinge is continuously
loaded. I want to use this simple system to
examine the general question mentioned above.
If anyone is aware of any previous work
on the broad question, or would like to
comment on it, I would appreciate hearing
from you. I will post all replies in about two weeks.
Thank you in advance for your time.
Cheers
M. Edwin DeMont, Ph.D.
email: edemont@stfx.ca
WWW: http://iago.stfx.ca/people/edemont/biomechanics-lab.html
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org: St. Francis Xavier University
adr: Biology Department;;P.O. Box 5000;Antigonish;Nova Scotia;B2G 2W5;Canada
email;internet: edemont@stfx.ca
tel;work: 902-867-5116
tel;fax: 902-867-2389
x-mozilla-cpt: ;0
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I have been thinking about a particular
research question lately, and could not find
any relevant papers on the topic. I hope
someone can suggest some solutions.
The question is - how do continuously
loaded tissues grow? Two good examples
of these tissues exist: (1) the walls of arteries,
and (2) the periosteum surrounding long bones.
Both of these tissues are continuously loaded,
but must grow. My question does not concern
the actual morphological changes occurring during
growth, but the changes that occur in the
molecular load-bearing components of the
tissue. If the tissue is under continuous load,
then how are new load-bearing elements
added? In the arterial tissue, for example,
the load is carried by microfibrils, elastin,
and collagen. (There are some interesting
developmental and evolutionary aspects
of these elements too, which I may raise
in another message.) How are new elements
added while the wall continues to function?
I want to start answering this question
by looking at a very simple mechancial system –
the locomotor system of a scallop. This
consists of two shells that are pulled together
by a single muscle. The shells are connected
by a hinge. The muscle antagonism is elastic
– created by a compressive spring on the inside
of the hinge, and tensile elements on the outside
of the hinge. Most of the energy storage
occurs in the compressive hinge, which is
composed of an elastomer called abductin.
(This is very similar to elastin.)
When a scallop dies, the shells gape open,
but eventually stop, as the collagenous elements
in the muscle are stretched. However, if you cut
the muscle out of the shell, the shells will gape
even farther, showing that the hinge is continuously
loaded. I want to use this simple system to
examine the general question mentioned above.
If anyone is aware of any previous work
on the broad question, or would like to
comment on it, I would appreciate hearing
from you. I will post all replies in about two weeks.
Thank you in advance for your time.
Cheers
M. Edwin DeMont, Ph.D.
email: edemont@stfx.ca
WWW: http://iago.stfx.ca/people/edemont/biomechanics-lab.html
begin: vcard
fn: Edwin DeMont
n: DeMont;Edwin
org: St. Francis Xavier University
adr: Biology Department;;P.O. Box 5000;Antigonish;Nova Scotia;B2G 2W5;Canada
email;internet: edemont@stfx.ca
tel;work: 902-867-5116
tel;fax: 902-867-2389
x-mozilla-cpt: ;0
x-mozilla-html: FALSE
version: 2.1
end: vcard