636 STUDIES IN GENERAL PHYSIOLOGY 



might say the change in the character of the contact causes 

 an increase in the cell-divisions. This is still more obvious 

 where whole organs are produced or regenerated. In one of 

 my former papers I pointed out a very definite chemical dif- 

 ference between embryonic tissue and muscle tissue. 1 The 

 former is more immune against K ions and more sensitive 

 toward Ca ions. It has long been noticed, especially by 

 botanists, that young tissue contains comparatively more K 

 than old tissue. I am inclined to assume that this accounts 

 for the fact that young tissue contains more water or has a 

 greater degree of turgidity than old tissue. An increase in 

 K allows the protoplasm to take up more water, an increase 

 in Ca has the opposite effect. 2 Ion effects and the effects of 

 certain enzymes of liquefaction or solidification are often 

 similar, or may at least support each other. It is not impos- 

 sible that the increase in cell-divisions among the cells of 

 the margin of the wound may be due to the different charac- 

 ter of the contact to which these cells are exposed during or 

 after the lesion, inasmuch as this different contact sets free 

 or throws into activity certain enzymes which do not act as 

 long as these cells are in their natural surroundings, e. g., as 

 long as they are in contact with other cells. 



In returning after this digression to our main subject we 

 must mention that the nature of the contact is not the only 

 means by which solid elements in living tissues may be 

 liquefied. Five years ago I proved that lack of oxygen 

 liquefies the cell walls in the blastomeres of a teleost egg 

 (Ctenolabrus), 3 and Budgett showed in my laboratory that 

 lack of oxygen produces the same phenomenon in Infusoria. 4 

 This case may find its explanation through the well-known 

 experiment of Pasteur on the effect of oxygen on yeast cells. 

 With plenty of oxygen the yeast cells multiply abundantly, 



i Part II, p. 559. 2 p ar t II, p. 510. a p ar t I, p. 370. 



* BUDGETT, American Journal of Physiology, Vol. I (1898), p. 210. 



