WILLIAM F. PETERSEN logi 



altered ammonia coefficient, but a reduction in the amount of urine. He concluded that the 

 immediate acidosis was due to cellular irritation, the products of this irritation then effected 

 the oxidative mechanism and an alkalosis resulted — representing an increase in the inter- 

 mediary oxidative metabolism, the products of oxidation of these intermediary products 

 being alkaloidal in character.' The results of Vollmer have been repeatedly confirmed, most 

 recently by Lukacs.^ In a study which Miiller and I^ have just completed we have followed 

 the ionic changes of the lymph during the continuous injection of bacteria and have noted 

 that the calcium-potassium ratio shows diphasic alterations. A primary reduction in the 

 calcium-potassium ratio changes later to an increase. 



An increase in non-protein nitrogen occurs in the serum ,<* here again as a diphasic phe- 

 nomenon. So, too, there is a primary increase in nitrogen elimination, followed by nitrogen 

 retention. Meyer-Bisch has determined a similar change in the sulphur metabolism. ^ The 

 non-protein nitrogen of the liver increases after anaphylactic and protein shock^ and after 

 fatigue. 9 The basal metabolism has been studied by Du Bois.'" 



Immunity Reactions. — Alterations in the antibody titer of the serum after non-specific 

 reactions have occupied the attention of many investigators. That preformed antibodies 

 might be "shed" into the blood stream after various procedures has been long known. Inas- 

 much as it is the cell surface that is involved in the specific processes that are initiated with 

 immunization, the probability that antibodies might be altered in such reactions is obvious. 

 A large number of papers' '"^^ have established that the immunized animal will respond 



' Leimdorfer, A.: Biochem. Zeit., 133, 409. 1922. 



^Lukacs, Jos.: Wien. kl. Wchr., 39, 885. 1926. 



3 Petersen, W. F., and Miiller, E. F. (in press). 



'' Wolpe, G.: Miinch. med. Wchr., 71, 363. 1924. 



s Donath, J., and Heilig, R.: Kl. Wchr., iii, 834. 1924. 



* Jobling, James W., and Petersen, W. F.: loc. cit. 



7 Meyer-Bisch, R.: Zeitschr.f. kl. Med., 94, 237. 1922. 



' Pick, E., and Hashimoto, M.: Arch. f. e.xp. Path, and Pharm., 76, 89. 1914. 



'Weichardt, W., and Scholz, G.: Kl. Wchr., 2, 2305. 1923. 

 "> Barr, D. P., Cecil, R. L., and Du Bois, E. F.: Arch. int. Med., 29, 608. 1922. 

 " Solomonsen and Madsen, quoted by Dieudonne, Med. Kl., 2, 575, 1906. 

 " Obermayer, F., and Pick, E. P.: Wien. Kl. Wchr., 17, 265. 1904. 

 '3 Dieudonne, A.: loc. cit. 



"• Weichardt, W., and Schrader, E.: Miinch. med. Wchr., 66, 289. 1919. 

 '5 Hektoen, L.: Jour. Infect. Dis., 21, 279. 1917. 

 '*Bull, C: Jour. E.xp. Med., 23, 419. 1916. 

 '7 Ling, C. Y.: Arch. Int. Mel., 35, 740. 1925. 



'* Clark, P. F., Zellmer, C. E., and Stone, H. W.: Jonr. Infect. Dis., 31, 215. 1922. 

 '9 Schatz, W. J.: Joiir. Immunol., 11, i. 1926. 



•"Citron, J.: Berl. med. Gess. Discussion, July 14, 1926 (A7. Wchr., s, 1634. 1926). 

 " Fledkseder, R.: Wien. kl. Wchr., 29, 637. 1916. 

 " Hajos, K., and Sternberg, F.: Zeitschr.f. Imm., 34, 218. 1922. 

 ^3 Tsukahara, I.: ibid., 32, 410. 1921. 

 ^•'Furst, T.: Arch. f. Hyg., 89, 161. 1920. 

 ^5 Schultz, M.: Arch. f. Derm, mid Syph., 135, 350. 1921. 

 ^Hermann, S. F.: Jour. Infect. Dis., 23, 457. 1919. 

 27 Khanolkar, V. R.: Jour. Path, and Bad., 27, 181. 1924. 

 '* Prigge, R.: Deut. Arch.f. kl. Med., 192, 216. 1923. "» Rosher, A. B.: Lancet, 2, no. 1924. 



