ZOOLOGY: H. E. JORDAN 
155 
cytes') by dilute toxins such as are produced by typhoid and tubercle 
bacilli. A more likely interpretation, it seems to me, would attribute 
the presence of the intra-arterial cell mass of the smaller rami to the 
relatively sKghtly differentiated character of the endothelium. The oc- 
clusion of the rami and the degeneration (karyorrhexis) of the cells would 
thus be a secondary effect of the constriction of the regressive atrophy- 
ing vessels. In other words, the intra-arterial cell mass is not the result 
of the action of a toxin; but the occlusion and degeneration (and the 
possible formation of a 'toxic' substance) are all the related common 
sequalae of the shrinking of the atrophying vessel around a previously 
present, normally produced, mass of hemoblasts. 
But the most damaging countervailing evidence to the interpretation 
of endothelial cell-cluster derivatives as the result of a stimulative toxin, 
consists in the fact that in the definitive superior mesenteric artery of 
the 10 mm. pig embryo numerous cell clusters appear, even in the mid- 
dle third of the vessel which is a level that could not be directly affected 
by a possibly later further caudal migration of this artery through 
atrophy of its present connecting aortic root; and which shows not the 
slightest indication of atrophy or degeneration, either of the vessel wall 
or the included blood cells, other than the presence only of hemoblast 
clusters. 
In all the forms studied (pig, mongoose, chick, turtle) the superior 
mesenteric artery also contains both clusters and individual cells in 
process of differentiation into hemoblasts. Moreover, not all the ventral 
rami which ultimately disappear contain clusters or intra-arterial cell 
masses; and occasional clusters are relatively far removed from the 
mouths of any aortic branches. 
If some toxin were correctly held responsible for the endotheHal 
activity in the formation of isolated and aggregated hemoblasts, it 
becomes very difficult to explain its localized effect. The same ob- 
jection holds regarding the clusters in the superior mesenteric (vitelline) 
artery. If the source of the toxic substance is here supposed to be de- 
generating cells of the yolk sac, its influence should be felt far beyond 
this vessel itself, or the ventral portion of only the abdominal segment 
of the dorsal aorta. A certain amount of cell disintegration no doubt 
occurs over wide areas of embryonic vascularised tissue, and numerous 
primitive venous channels also disappear; but, though extensively 
studied by various investigators, no cell clusters have been reported 
except in the ventral portion of the dorsal aorta (and in this paper, in 
the inferior vena cava near the point of fusion of the subcardinal veins), 
levels where a less differentiated endothelium is present as well as re- 
