Hemopoiesis in the Mongoose Embryo. 307 



EmmeFs interpretation of the cause of the formation of free meso- 

 thelial derivatives appears especially strained. Why may not the 

 mesothelium normally give rise to the cellular elements of the serous 

 fluids as part of its function, by reason of its close genetic relationship 

 to hemogenic mesenchyma and endothelium? At one point Emmel 

 inclines (p. 402) to identify the cells of the cell-clusters of the aorta with 

 macrophages, and he ascribes the cause of their formation to the pres- 

 ence of possible toxins produced by the "atrophying" and "degenerat- 

 ing" ventral aortic vessels in close association with which some of the 

 cell-clusters are found. This conclusion is based upon a number of fun- 

 damental uncertainties. In the mongoose material the cell-clusters 

 consist of typical hemoblasts (mesamoeboids) ; this is in agreement 

 with both Maximow's findings for rabbit and Minot's observations 

 on human and rabbit embryos. The endothelial proliferation products 

 of the embryo need therefore not be confused with macrophages. 

 Moreover, Weidenreich derives the macrophages of Metschnikoff from 

 leucocytes, while Evans avers that macrophages and leucocytes have 

 no direct genetic relationship. On the other hand, many hematolo- 

 gists derive the leucocytes from the common blood mother-cell, the 

 hemoblast, which may have an endothelial origin. A second uncer- 

 tainty involves the manner of the caudal progression of the celiac, 

 the superior mesenteric, and the inferior mesenteric arteries. Evans 

 inclines to explain the process on the basis of an unequal growth 

 between the dorsal and ventral portion of the abdominal aorta, necessi- 

 tating thus a less highly differentiated endothelium ventrally. Degen- 

 eration of certain ventral vessels probably also occurs; but coincident 

 with this atrophy there may be likewise a new origin of vessels in the 

 formation of progressively lower connections with the main ventral 

 stems ; and some of the cell-clusters may be related to the newer vessels, 

 as I believe, rather than to the degenerating vessels, as Emmel believes. 



There appears no valid reason why the endothelium of the yolk-sac 

 vessels and that of the embryonic vessels should function differently; 

 why in the case of the yolk-sac vessels the endothelium should be 

 capable of metamorphosing normally into hemoblasts, while in the 

 intra-embryonic vessels with young endothelium the stimulative factor 

 to metamorphosis should have to be a pathologic one. If endothelial 

 hemogenesis in the yolk-sac increased in activity coincident with the 

 degenerative processes of the sac, Emmel's interpretation might be 

 more confidently accepted; but this is precisely where it fails. Endo- 

 thelial hemogenesis is most active in the yolk-sac of the 10 to 12 mm. 

 embryos when hemopoiesis is at its height in these vessels. Subse- 

 quently it decreases, and by the 25-mm. stage no separating endothelial 

 cells can be found. Moreover, in the small vessels of the pericerebral 

 region endothelial cells may occasionally separate to become intra- 

 vascular elements. In short, wherever only slightly differentiated 



