16
THOMAS S. ARGYRIS
1962b) has shown that a very light shave will not induce hair growth,
even though epidermal proliferation occurs. Also, Ford (quoted in T. S.
Argyris and B. F. Argyris, 1962b) claims that tattooing of rat skin does
not lead to growth of resting hair follicles, although surely there is
epidermal damage. It may be that in order to stimulate hair growth a
critical amount of epidermal damage must occur. Thus, although the
stimulation of hair growth is quite specific, the degree of specificity is
unknown and deserves further investigation.
Finally, we raise the question if damage to skin epithelium stimulates
connective tissue growth. Bullough and Laurence (1960b) have shown
that plucking resting hair follicles, which initiates both epidermal and
hair follicle growth (Chase, 1954), does not increase the mitotic activity
of the connective tissue in the subcutis; therefore, connective tissue
proliferation induced by damage is probably also tissue-specific.
Recently, preliminary experiments by us suggest that the growthpromoting effect of damage in other organs is also somewhat specific.
If one damages the mouse kidney by inserting a needle into it, there is
an increased mitotic activity up to 500 /x around the area of damage
(Argyris, 1966b; Argyris and Trimble, 1964b). If the damage extends
only into the kidney cortex, the mitotic response is limited to the cortex.
This is true even if the damage is only 50-100 jx from the medulla. Yet
cortical areas 100-500 ^ away from the damage show an increased mitotic
activity. Conversely, if one inserts a needle through the hilus of the
kidney, limiting the damage to the medulla, only the medulla shows an
increase in mitotic activity. Damaging the cortex and medulla results in
an increased mitotic activity in both of them. These experiments suggest
that damage-induced growth in the kidney may be specific to a considerable extent.
We may conclude that the evidence strongly suggests that damageinduced growth is considerably more specific than it was thought to be
previously. Whether or not it is generally tissue-specific, as Bullough
(1962, 1964, 1965) suggests, remains to be proven.
Another important problem, which may be conveniently considered
along with the question of specificity of damage-induced growth, is
whether damage to an organ results in proliferative effects that are
systemic. We have recently demonstrated that, in the mouse, damage to
one kidney stimulates mitotic activity in the contralateral kidney
(Argyris and Trimble, 1964b).
If multiple needle insertions are made in one kidney there is an increase
in the cortical mitotic activity of the contralateral kidney (Table I).
THOMAS S. ARGYRIS
1962b) has shown that a very light shave will not induce hair growth,
even though epidermal proliferation occurs. Also, Ford (quoted in T. S.
Argyris and B. F. Argyris, 1962b) claims that tattooing of rat skin does
not lead to growth of resting hair follicles, although surely there is
epidermal damage. It may be that in order to stimulate hair growth a
critical amount of epidermal damage must occur. Thus, although the
stimulation of hair growth is quite specific, the degree of specificity is
unknown and deserves further investigation.
Finally, we raise the question if damage to skin epithelium stimulates
connective tissue growth. Bullough and Laurence (1960b) have shown
that plucking resting hair follicles, which initiates both epidermal and
hair follicle growth (Chase, 1954), does not increase the mitotic activity
of the connective tissue in the subcutis; therefore, connective tissue
proliferation induced by damage is probably also tissue-specific.
Recently, preliminary experiments by us suggest that the growthpromoting effect of damage in other organs is also somewhat specific.
If one damages the mouse kidney by inserting a needle into it, there is
an increased mitotic activity up to 500 /x around the area of damage
(Argyris, 1966b; Argyris and Trimble, 1964b). If the damage extends
only into the kidney cortex, the mitotic response is limited to the cortex.
This is true even if the damage is only 50-100 jx from the medulla. Yet
cortical areas 100-500 ^ away from the damage show an increased mitotic
activity. Conversely, if one inserts a needle through the hilus of the
kidney, limiting the damage to the medulla, only the medulla shows an
increase in mitotic activity. Damaging the cortex and medulla results in
an increased mitotic activity in both of them. These experiments suggest
that damage-induced growth in the kidney may be specific to a considerable extent.
We may conclude that the evidence strongly suggests that damageinduced growth is considerably more specific than it was thought to be
previously. Whether or not it is generally tissue-specific, as Bullough
(1962, 1964, 1965) suggests, remains to be proven.
Another important problem, which may be conveniently considered
along with the question of specificity of damage-induced growth, is
whether damage to an organ results in proliferative effects that are
systemic. We have recently demonstrated that, in the mouse, damage to
one kidney stimulates mitotic activity in the contralateral kidney
(Argyris and Trimble, 1964b).
If multiple needle insertions are made in one kidney there is an increase
in the cortical mitotic activity of the contralateral kidney (Table I).