100 j:\z)ui:s 



to non-coajrulahle forms of nitroficn was as follows: Normal spleen, 

 noii-coagulable iiitrojren, 5.7 per cent, of the total; sta^e of marked 

 pycnosis, without rhexis or lysis, 7.4 per cent.; stage of karyorrhexis 

 and early karyolysis, 26.5 per cent.; stage of complete karyolysis, 30.3 

 per cent. That is, when nuclear structures in the spleen have lost 

 their staining properties entirely througli autolysis, about 72 per cent, 

 of the nuclein nitrogen, 50 per cent, of the insoluljle i)hosphorus com- 

 pounds, and 70 i)er cent, of the coagulnlilc nitrogen, are .still intact, 

 and about two-tliii-ds of the lecitliiu remains in comijlex organic com- 

 binatif)ns. 



Liver Degenerations, — The relation of tlie disintegration observed 

 in phosphorus-poisoiiiiKj and acutf i/dloir alrophu to the experimental 

 autolysis of the liver has been tlie objeet of much study. Salkowski 

 origiiuilly pointed out that the same jn-oducts were found in the blood, 

 urine, and liver tissue in acute yellow atrophy as are produced in 

 autolysis. Jacoby -^ found that the livers of dogs, taken just as the 

 animals Avere dying of phosphorus-poisoning, contained free leucine 

 and tyrosine; also, he found that the rate of autolysis of such livers 

 after removal from the body was much greater than in normal livers. 

 The oxidizing ferments (aldehydase) are not destroyed by the proc- 

 ess. He found that addition of minute amounts of phosphorus to 

 liver enzymes did not increase their proteolytic power; nevertheless, 

 he seems inclined to assume that in phosphorus-poisoning alteration 

 in the autolytic "enzymes is an important factor in the liver degen- 

 eration. It would seem much more probable that phosphorus is a 

 poison that kills cells and does not destroy their antolytic enzymes, 

 hence favoring autolysis. The liver degeneration following chloro- 

 form poisoning may, perhaps, be explained in a similar way, the cells 

 behaving exactly as bacteria would do under the same conditions. 

 Taylor * has analyzed several livers in degenerative conditions for 

 amino-acids and found them only in one liver, which showed necrosis 

 ])robably due to chloroform poisoning, ami wliich was from a case 

 clinically resembling acute yellow atrophy. Here he obtained 4 gm. 

 of leucine, 2.2 gm. of tyrosine, and 2.3 gm. of arginine nitrate. 

 AValdvogel and Tintcmann,"' in phosphorus livers, found an increase 

 in ])i-()tagon, jecoi'in, fatty aeids, cholesterol, and neutral fat. while 

 lecithin was decreased. Wakeman " found arginine, histidine, and ly- 

 sine decreased in jiliospliorus livei's in pi'oj)oi1 ion to the total nitro- 

 <ren, indicating that the ])i'otein-spli1t ing enzyme in this condition 

 eitlu'r i)icks out certain varieties of pi'oteins lirst, or removes the 

 nitrogen-rich constituents most rapidly.' 



•■i Z«-it. f. plivsiol. Cli.'iM.. l!i(l() I lid I. 171. 

 4 Univ. of ("'alif. I'lililic. ( patliol.) , 1!)(»4 (1). 4:i. 

 oCent. f. Path., l!t()4 (15). <)7. 

 n Ik'il. kliii. Wocli.. l!t()4 (41), lOtn. 



7 ( 'on^idcialilc tjiiant it ics of ainiiio-aciils of \arioiis sorts liavi' lu'cii isolattnl 

 from llii' li\rr in ariilc yellow atropliy and chlorofoiiii iiccidsi: liy Wolls (.lo\ir. 



