It is natural (hat wc will still need a piuiongcd development of plant 

 physiology before \\c can establish the fundamental premises of a fully valid 

 theory of the ontogenesis of the plant organism. Krenkc's theory represents the 

 Hrst steps in this extremely important area. Some of his propositions are very 

 questionable or obscure. Thus, it is difficult to agree with his reduction of the 

 development of the organism to a struggle between aging and rejuvenescence, 

 and hence with his reduction of the concept of vital capacity to the concept of 

 maturity. The development of the organism proceeds in time and gives rise 

 to extensive age-associated changes, but this development is certainly immeasur- 

 ably richer in its differentiation, adaptation, and change in its interactions widi 

 external conditions than the inherent age-associated changes. Hence the vital 

 potential of the organism also is not the consequence of its age alone, although 

 it is indeed dependent on it to a considerable degree. Also questionable is his 

 statement that the mechanism of aging differs in the resting and in the dividing 

 cell. The tempos of aging may actually be different in them, but we cannot 

 agree \\ith the view that rapidly dividing tissue ages most rapidly of all. Thus, 

 the vigorously dividing cells of the malpighian layer of the cutaneous epidermis, 

 the intestinal epithelium, and the hemocytoblasts of the bone marrow in the 

 higher \ertebrates retain their viability to the greatest extent. The rate of 

 division of cells is by no means always proportional to the rapidity of their 

 differentiation. 



In any case, N. P. Krenke's theory must be recognized as a serious attempt 

 to develop a general theory of ontogenesis with respect to the peculiar conditions 

 in the plant organism. 



Proceeding from her ideas about the hemato-encephalic and histo-hematic 

 barriers, L. S. Shtern (1935-1940) stressed the great importance of the age- 

 associated consolidation of the colloids of these barriers and the resultant lower- 

 ing of their permeability with the onset of old age. Both in the studies by her 

 school and in a number of other investigations we find some evidence in support 

 of such a reduction of permeabiHty. Thus far, it is difficult for us to ascertain 

 the actual significance of these still relatively unstudied changes in the total 

 complex picture of aging of the organism as a whole. 



O. B. Lepeshinskaya (1935-1953) regards aging as the consequence of the 

 age-associated condensation of the colloids of the cell membranes. Age- 

 associated condensation of the "superficial cortex" of the cytoplasm may be 

 regarded as having been established in a number of cases. In addition to this, 

 we must bear in mind the fact that the uninterrupted flow of the metabolism 

 "sweeps away," after a few days or even hours, the molecules and their colloidal 

 aggregates and does not give time for the appearance of hysteresis of the colloids 

 (and especially of the proteins) in a pure form in the living protoplasm. Hence 

 the condensation of the protoplasmic colloids is a consequence of the qualitative 

 changes in protein metabolism with age. 



A number of studies by V. A. Negovskiy and his pupils (1939-1954) have 

 not dealt with the struggle against premature aging but rather with premature 

 human death, occuring at a time when it is still possible for man, by making 



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