18
THOMAS S. ARGYRIS
stances involved in liver and kidney compensatory hypertrophy might
be able to stimulate hair growth, but they cannot be concentrated in
sufficient amounts at any one point in the skin to do so. Others have
shown (Paschkis, 1958) that liver regeneration can affect the mitotic
activity of some organs, but this is minimal. Clearly, much more work is
needed in this area.
IV. The Mechanism of Initiation of Damage-Induced Growth
A. The Biological Basis for the Mechanism of the
Initiation of Damage-Induced Growth
1. The Local Loss of Mass as the Stimulus for Damage-Induced
Growth
The foremost student of growth control, who believes that the loss of
mass initiates growth in wound healing, is Bullough (1962, 1964, 1965).
The critical experiment that Bullough and his colleagues have done to
show that it is the loss of mass following damage which initiates mitotic
activity is as follows. Using a fine dental drill, Bullough and Laurence
(1960a) have removed a 3-mm square piece of the epidermis and superficial dermis on one side of a mouse ear. They then have studied the
pattern of mitotic activity in the epidermis adjacent to the wound and in
the epidermis on the side opposite to the one from which the epidermis
has been removed. Figure 8 shows the pattern of mitotic activity
expected, depending on whether growth is initiated by the release of a
stimulating substance or by the loss of an inhibitor. The lower diagram in
Fig. 8 shows that if the loss of an inhibitor is responsible for the stimulation of epidermal mitotic activity, the increase in mitotic activity in the
epidermis on the side opposite to the one wounded should have a single
broad peak, extending about the width of the area removed. The reason
for this is that the inhibitor, which is presumably produced by the
epidermis and permeates the entire ear skin, is lost, or drastically reduced,
in the area of damage, owing to the fact that the epidermis producing the
inhibitor in this area has been removed. In this experiment, the epidermis
that is within 1 mm from the wound, and, therefore, the epidermis that is
within range to respond to changes in the level of an inhibitor (see
Section II,B,1), is the epidermis surrounding the wound, and the epidermis directly opposite the wound. The latter, because the thickness of
the mouse ear, is less than 1 mm. Thus there should be a single broad
peak of mitotic activity in the epidermis opposite the wound. On the
THOMAS S. ARGYRIS
stances involved in liver and kidney compensatory hypertrophy might
be able to stimulate hair growth, but they cannot be concentrated in
sufficient amounts at any one point in the skin to do so. Others have
shown (Paschkis, 1958) that liver regeneration can affect the mitotic
activity of some organs, but this is minimal. Clearly, much more work is
needed in this area.
IV. The Mechanism of Initiation of Damage-Induced Growth
A. The Biological Basis for the Mechanism of the
Initiation of Damage-Induced Growth
1. The Local Loss of Mass as the Stimulus for Damage-Induced
Growth
The foremost student of growth control, who believes that the loss of
mass initiates growth in wound healing, is Bullough (1962, 1964, 1965).
The critical experiment that Bullough and his colleagues have done to
show that it is the loss of mass following damage which initiates mitotic
activity is as follows. Using a fine dental drill, Bullough and Laurence
(1960a) have removed a 3-mm square piece of the epidermis and superficial dermis on one side of a mouse ear. They then have studied the
pattern of mitotic activity in the epidermis adjacent to the wound and in
the epidermis on the side opposite to the one from which the epidermis
has been removed. Figure 8 shows the pattern of mitotic activity
expected, depending on whether growth is initiated by the release of a
stimulating substance or by the loss of an inhibitor. The lower diagram in
Fig. 8 shows that if the loss of an inhibitor is responsible for the stimulation of epidermal mitotic activity, the increase in mitotic activity in the
epidermis on the side opposite to the one wounded should have a single
broad peak, extending about the width of the area removed. The reason
for this is that the inhibitor, which is presumably produced by the
epidermis and permeates the entire ear skin, is lost, or drastically reduced,
in the area of damage, owing to the fact that the epidermis producing the
inhibitor in this area has been removed. In this experiment, the epidermis
that is within 1 mm from the wound, and, therefore, the epidermis that is
within range to respond to changes in the level of an inhibitor (see
Section II,B,1), is the epidermis surrounding the wound, and the epidermis directly opposite the wound. The latter, because the thickness of
the mouse ear, is less than 1 mm. Thus there should be a single broad
peak of mitotic activity in the epidermis opposite the wound. On the