2IO GROWTH PRINCIPLES AND THEORY 2 



The Weiss-Kavanau model underlies objections of which the authors are by no 

 means unaware, and which concern I. the basic assumptions, and II. the mathe- 

 matical procedure in elaborating the model. 



/. The following assumptions are at present unverified : 



/. The assumption that "generative mass" in the absence of inhibition by differentiation 

 or "antitemplates" grows exponentially does not account for the growth of microorganisms 

 (p. i6if.). There appears to be no difference as to differentiation or antitemplates between 

 rod-like and spherical microorganisms; but only the first grow exponentially, while the 

 second show a sigmoid growth curve. This shows that even in the simplest case of single 

 cells there are growth-limiting factors different from those assumed in the model. This 

 objection is not overruled by the fact that growth of populations, i.e. multiplication of 

 unicellular organisms (and of organisms in general : Malthus' law) is exponential in the 

 absence of limiting factors; for the homology is between individual organisms, unicellular 

 or multicellular, rather than between a multicellular individual and a population of 

 mutually independent cells. On the other hand, the growth curve of many higher organisms 

 (Type I) is empirically similar to that of spherical microorganisms. This suggests that the 

 mechanism producing the characteristic course of growth, although different in the 

 underlying biochemical processes, is isomorphic in its fundamental structure (surface- 

 volume relations after Bertalanffy's theory). 



2. "Generative" and "differentiated mass" and the transition from the first to the latter 

 cannot, at present, be defined quantitatively. The relations between differentiation and 

 loss of growth potential are obscure and differentiation as estimated by histological, 

 cytological, biochemical, etc. standards is no measure of the loss of the ability to repro- 

 duce (p. 141). 



3. The template hypothesis is well supported with respect to nucleoproteins (Watson- 

 Crick model of DNA and its more recent developments). However, the mechanism of 

 protein synthesis is unknown even though a number of template models were proposed. 

 Thus a hypothesis is introduced which, in its own field, i.e. the biochemistry of organic 

 syntheses, so far is not proved. 



4. Similar considerations apply to the "antitemplate" hypothesis. There is some 

 supporting evidence (see below) but also this factor cannot be inserted in the model as a 

 proved mechanism of growth limitation. 



The basic assumption in the model is that catalysts or "templates" responsible for 

 growth {e.g. nucleoproteins, proteins, myoproteins, etc.), being high-molecular compounds, 

 are restricted to the cell while growth-inhibiting factors produced by them, being smaller 

 molecules, are freely diffusible and hence can act in the feedback loop. The experimental 

 evidence for this hypothesis is reviewed by Weiss (1955b) and discussed by Ebert (1954). 

 The following facts are presented in support of the theory : 



{a) The phenomenon of compensatory growth after removal of part of the organ. This, 

 as can be shown by experiments in prefunctional stages {e.g. compensatory hyperplasia 

 of the embryonic chick metanephros when the mesonephros is still functioning), is not 

 necessarily due to functional overload imposed upon the remaining rest of the organ, 

 but rather is an expression of an "equilibrium of the organs" {cf. p. 229ff.). One possible 

 (although not the only) explanation is by way of a decrease of specific growth-inhibiting 

 compounds whose concentration is lowered by removal of part of the organ producing 

 them, with consequent compensatory spurt of growth in the rest. 



{b) Supposing specific growth-regulating compounds, implants, cell extracts, etc. 

 should have different effects, depending on the ratio between "templates" and "anti- 

 templates". If the implanted cells survive, this may lead to an increase of "templates" 

 or building blocks thereof, with a resulting increase of growth of the host. It may also lead 

 to an increase of "antitemplates" produced by these cells and hence growth rate of the 

 host would decrease. Disintegrated cells, on the other hand, may add to the pool of 

 "templates" and/or trap circulating "antitemplates" with the effect of a spurt of growth. 

 Transmission of organ-specific influences has been shown in various experiments : a. En- 



