310 Papers from the Department of Marine Biology. 



pressure, the peripheral endothelial cells to continue their further 

 differentiation into definitive endothelium. 



As to the endothelial strands of hemoblast-like cells, I incline to 

 an interpretation in accord with the idea that slightly differentiated 

 endothelium anywhere carries the capacity of producing hemoblasts. 

 In a footnote (p. 407) Emmel describes similar strands in the aorta 

 and the proximal portion of the left umbilical artery in the 12-mm. pig 

 embryo which contained the encapsulated cluster, and in a second 

 12-mm. embryo, and suggests that they may be associated with the 

 fusion of the two original dorsal aortse. 



If one wishes to adhere to an interpretation of these proliferation 

 products of the aortic endothelium in terms of a toxin, one might locate 

 the source of the toxic substance in the mesonephros, where degenera- 

 tive processes are initiated in the anterior portion; but such a view is 

 again contradicted by the observation that endothelial desquamation 

 products are practically lacking in the glomerular capillaries, though 

 occasionally present near the aortic mouth of the afferent arteriole. 

 The view that we are dealing with a normal hemogenic process related 

 to a relatively undifferentiated condition of endothelium such as would 

 seem to be requisite in the ventral portion of the abdominal aorta, to 

 permit of the shifting of the celiac, superior mesenteric, and inferior 

 mesenteric arteries by almost any reasonably conceivable process, seems 

 to fit all the facts better than the idea of a toxic influence dependent 

 upon a tissue degeneration in redundant atrophying blood-vessels. 



In a second paper ("Concerning certain cellular elements in the 

 ccelomic cavities and mesenchyma of the mammalian embryo," Amer. 

 Jour. Anat., vol. 20, 1, 1916, pp. 73-125), Emmel describes the origin 

 of "macrophages" from the pericardial and peritioneal mesothelium; 

 he describes and illustrates also certain free cell-masses in the peri- 

 cardial cavity comparable with my illustration (fig. 21) in the mongoose 

 embryo. The causal factor is again assumed to be a toxic substance, 

 in this case liberated in part by degenerating erythrocytes in the ccelom. 

 But it would seem quite as reasonable to regard this formation of 

 macrophages in the embryo as a normal incident in the life of the 

 embryo. 



In conclusion, I believe that a careful consideration of all the facts 

 relative to Emmers observations and my own, upon which there is 

 essential agreement, more amply justifies the conclusion that young, 

 relatively undifferentiated endothelium and mesothelium may any- 

 where in the embryo normally produce hemoblasts (and macrophages), 

 than that such activity demands the operation of a pathologic factor 

 in the form of a dilute, slow-acting toxin. 



