VII INTERNAL FACTORS 637 



Extracts of necrotic tissues also promote wound-healing (Arey, 1936; Palla- 

 dina and Gudina, 1953; Engley et al., 1955; see also Chapter 8), and other 

 regenerative growths (Fedotov, 1946; Levander, 1949; Teir, 1952; Weiss, 1952). 

 Extraction-procedures in fact liberate such promotors from any cells (Loof- 

 bourow, 1948); extracts of most cells promote growth and regeneration (Laser, 

 1933; Efimov, 1943; Kerr and Werners, 1944; Margoliash and Doljansky, 1950; 

 Engley et al., 1955)- Regeneration-promoting extracts ("trephones") from leu- 

 cocytes (Carrel, 1922; Khruschev, 1946) may have a more specific significance, 

 since these cells are very active in the demolition-stage (Menkin, 1950). The 

 extracts of tissues of embryos in general are probably more potent promotors 

 than those from adults (Weiss, 1952, 1955) though weight for weight some adult 

 tissues yield equally potent material (Laser, 1933; Margoliash and Doljansky, 

 1950). Embryo-extracts accelerate wound-healing (Arey, 1936) and probably 

 regeneration in Amphibia (Morosow, 1935). 



The wound-factor of Amphibia promotes the movement of cells to form a 

 blastema, and in planarians also wounding stimulates the immigration of neo- 

 blasts (Goldsmith, 1940; Wolff and Dubois, 1947, 1948). Curiously, irradiation- 

 damage does not attract these cells, though an irradiated region traps neoblasts 

 attracted into it by a normal type of trauma on the far side. In Annelids nutritive 

 cells as well as neoblasts are attracted to the site of injury (Liebmann, 1946). In 

 compensatory hypertrophy there is no cell-migration, and cell-proliferation is 

 the first effect, on the orbital gland of the rat, of necrotic products from the homol- 

 ogous gland (Teir, 1952). 



It is uncertain if the wound-factor is always so evanescent as it appears to be 

 in Amphibia but certainly this or other promotors are produced locally in subse- 

 quent stages (Nettleship, i943;Neuman, 1946; Balazs and Holmgren, 1949, 1950; 

 Auerbach, 1952; Engley et al., 1955). The regressive processes in general probably 

 release more of this wound-factor; thus although infection delays regeneration 

 (Du Nouy, 1936; Paulain, 1938) it probably produces more wound-factor, since 

 regeneration is more rapid once it does begin (Du Noiiy, 1936). A promotor factor 

 escapes into the circulation (Auerbach and Doljansky, 1945; Engley et al., 1955) 

 and affects regenerates elsewhere (Nettleship, 1943). It may be transfused to affect 

 regeneration in another individual (Engley et at., 1955) and it persists long enough 

 to affect later regenerates (Nettleship, 1943; Needham, 1949b). Each injection of 

 serum from a partially hepatectomised individual causes a burst of mitoses in the 

 liver of a recipient (Friedrich-Freksa and Zaki, 1955). The mutual stimulation of 

 regeneration among the limbs of Crustacea etc., may be due to such a circulating 

 factor, and similarly the improvement of regeneration on repeated evocation 

 (Korschelt, 1927; Chranova, 1938; Needham, 1949b). A temporary depression, 

 at the second and third evocation (Fig. 4 see p. 609), may be due to the inhibitor 

 factor, which presumably diminishes progressively through the subsequent evo- 

 cations. 



A failure to detect any acceleration of regeneration due to active regeneration 

 elsewhere (Taffel et al., 1951) might be due to subsequent neutralisation of the 

 effect of the promotor by this inhibitor, which is produced later in the regenera- 

 tion-cycle (Balazs and Holmgren, 1949, 1950; Auerbach, 1952; Steinberg, 1954). 



-Literature p. 641) 



