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PROCEEDINGS 


OF THE 


SOCIETY FOR 


EXPERIMENTAL BIOLOGY AND MEDICINE 


VOLUME IX 


IQII-IQI2 


EDITED BY THE SECRETARY 


, NEW YORK 


Igi2 


PRESS OF 
THE NEW ERA PRINTING COMPANY 
LANCASTER. PA. 


CONTENTS: 


PAGE 

SCIENTIFIC PROCEEDINGS (45th-49th meetings) : 
Communications of the forty fifth meeting, October 18, I911 . 6 I 
Communications of the forty sixth meeting, December 20, 1911 . Soy Bt) 


Communications of the forth seventh meeting, February 21, 1912 . 35 
Communications of the forty eighth meeting, April 17, 1912 . SAL 


Communications of the forty ninth meeting, May 15, 1912 . 2 yy 
Recapitulation of the names of the authors and of the titles of the 
communications . < 2 : : : : 6 - 125 
EXECUTIVE PROCEEDINGS (45-49th meetings) . 3 ; 5 Iss 
REGISTER OF NAMES AND ADDRESSES OF THE MEMBERS . ° ° 5 Lis 9/ 
LisT OF OFFICERS . : 5 : c c c . ° - 145 


CLASSIFIED List OF MEMBERS z R 3 3 ‘: c A ek Ag 
INDEX OF THE SCIENTIFIC PROCEEDINGS . 6 5 5 6 oy 15E 


SCIENTIFIC PROCBEDINGS. 
1 (610) 
Experimental pernicious anemia. 
By HERMAN M. ADLER. 
[From the Laboratory of the Danvers State Hospital.] 


These experiments were performed on rabbits; fourteen rabbits 
in all were employed. Olive oil was fed in varying doses. Two 
feedings of 10 c.c. of olive oil per kilo of body weight sufficed to 
kill after 5 days. 6 c.c. per kilo weight killed in six days when 
fed daily. 5 c.c. per kilo weight did not kill but produced secondary 
anemia with blood crises presenting the picture of pernicious 
anemia—blood count 4 to 5,000,000, Hb. 50 per cent. or less, 
achromia, irregularity in size and shape, polychromatophilia, 
stipling, blasts. 

Eight rabbits were thus subjected to chronic poisoning with 
olive oil. Of these, three had previously been daily fed (for about 
a year) 0.3 gram quinine. Three rabbits had been treated for 
three months with intravenous injection of 0.01 gram quinine 
daily. The remaining two received daily feedings of olive oil 
without previous treatment. In all of these rabbits the blood 
picture of secondary anemia developed within a few days. In 
four the blood picture of pernicious anemia developed in from 2-3 
months. The anemia was not constant but varied considerably. 
The weight curve approximately followed the appearance of the 
blood; dropping sharply as the anemia became apparent, rising 
as the anemia improved. Five of these rabbits showed marked 
impairment of nutrition during the entire course, the younger 
ones being decidedly stunted in their development. The three 
rabbits that had been fed quinine per os showed less severe 
disturbances and none of them have thus far (after 1% years) 


shown the picture of pernicious anemia. The weight and blood 
I 


2 ScIENTIFIC PROCEEDINGS. 


conditions improved markedly when the feeding of oil was sus- 
pended. 

Calcium lactate, lime water, Fowler’s solution and tincture of 
ferric chloride were fed at different times with the olive oil without, 
however, appreciably diminishing the effect of the oil. The action 
of the olive oil depends upon its content of triolein (oleic acid). 
Pure oleic acid was fed to a rabbit and found to be no more toxic 
than olive oil. 

A noteworthy phenomenon in the chronically poisoned rabbits 
was a swelling of the heels, evidently hematomata, which came 
on suddenly in all of the rabbits, furthermore a crusted suppurating 
skin lesion which appeared on the inner surfaces of the ears of six 
out of eight of the rabbits. 

The post mortem examination of the rabbits which died after 
only a few doses showed practically nothing except a slight con- 
gestion of the small intestine. In the autopsies on rabbits which 
had received many doses general absence of fatty deposits together 
with fatty changes in liver, heart and kidneys and an atrophic 
condition of the spleen and lymphoid apparatus were noted. 

From this and from the appearances observed in human beings 
suffering from pernicious anemia, it is fair to assume that the 
lymphoid tissue, particularly of the intestine, is chiefly concerned 
in handling the fat absorbed from the food by the intestine. 


2 (611) _ 
The influence of age on the symptoms following 
thyro-parathyroidectomy. 


By SUTHERLAND SIMPSON. 


[From the Physiological Laboratory, Medical College, Cornell 
University, Ithaca, N. Y.] 


With regard to the question as to whether the thryoid and 
parathyroid glands become less and less essential to the organism 
as age advances there is some difference of opinion. Vincent 
and Jolly! found that in the various species of animals which they 
used (cats, dogs, foxes, monkeys, rats, guinea-pigs, rabbits), the 
symptoms following thyroidectomy and parathyroidectomy were 


1 Vincent and Jolly, Jour. of Physiology, 1904, xxxii, p. 80. 


SYMPTOMS FOLLOWING THYRO-PARATHYROIDECTOMY 3 


not influenced, to any extent, by age or sex. In the case of dogs 
the writer can corroborate this statement, but it appears to be 
otherwise in the sheep, as the following account of experiments on 
this animal will show. 

In the course of another investigation? the thyroids were com- 
pletely removed from eighteen lambs, from seven to eight months 
old, and twelve adult sheep, without, in the course of the six 
months which intervened between the operation and their slaugh- 
ter, any apparent ill effects. There was no falling out of the wool, 
nor any of the other symptoms of myxcedema supposed to be 
associated with complete thyroidectomy, and several of the adults 
gave birth to full-time, and to all appearance, perfectly normal 
lambs. 

From three of these lambs, at the age of two months, the thy- 
roids were removed, the two external parathyroids being left behind, 
and from two others at the same age (also born of thyroidectomized 
mothers) all the thyroid and parathyroid tissue was taken away. 
The latter, in the course of ten and nineteen days respectively, 
developed typical and acute parathyroid tetany. In one, the first 
fit was fatal in less than an hour from the onset, the rectal tem- 
perature being 112° F. one minute after death, and in the other, 
which was killed during the fit, the thermometer reached 108.7° F. 
immediately before death. 

The three from which the thyroids alone were removed de- 
veloped into typical cretins. 

In these three, about one year after the first operation, the two 
remaining external parathyroids were removed. As a result of 
this there followed what appeared to be some gastro-intestinal 
disturbance, and on three or four occasions, several weeks apart, 
each lasting about a week, some stiffness of the limbs, but nothing 
of the nature of acute tetany with rise of temperature, increased 
respiration, etc., which was so marked in the other two. These 
three sheep are still alive more than four months after the second 
operation. 

In addition to the three above mentioned, other two adult 
sheep, aged two and seven years respectively, have had the com- 


2 Simpson and Hunter, Quart. Jour. Exper. Physiol., 1911, iv, p. 340. 


4 SCIENTIFIC PROCEEDINGS. 


plete operation of thyro-parathyroidectomy performed on them 
and no noticeable symptoms have followed. 

In the sheep therefore it would appear that both the thyroid 
and parathyroid glands are much more important organs in the 
young than in the adult animal, and consequently that they be- 
come functionally less active as age advances. 

In relation to the influence of the parathyroids on calcium 
metabolism it is interesting to note that the two young lambs 
which showed acute parathyroid tetany were fed almost entirely 
on milk, rich in calcium salts, while the three which had the 
external parathyroids removed when they were about fourteen 
months old, and the other two parathyroidectomized adults, lived 
on a purely herbivorous diet in which potassium salts predominate. 
It may be, however, that in the young animal, where bone is being 
rapidly formed, the ratio between the demand for calcium and the 
supply is even greater than in the adult, although in the latter a 
far smaller quantity is being ingested. 

In the case of the adult sheep the results of thyro-parathyroi- 
dectomy are in agreement with those of MacCallum! who from a 
similar operation found that ‘Practically no effect whatever was 
produced in these five sheep, although in at least three of them 
ample time elapsed for the development of symptoms.” The 
other two died early of pneumonia, due probably to the administra- 
tion of ether. 


3, (612) 
Peculiarity in the mode of entrance of the optic nerve into the 
eyeball in some rodents. 


By J. A. BADERTSCHER. 


| From the Physiological Laboratory, Medical College, Cornell 
University, Ithaca, N. Y.] 


In the majority of animals the optic nerve enters the eyeball 
as a round compact bundle of nerve fibers and the optic disc is 
circular in outline or nearly so. While removing the eyes from 
the woodchuck and prairie dog for histological material, I observed 
that here there was an exception to the general rule in that the 


1 MacCallum, Johns Hopkins Hosp. Bull., 1907, xviii, p. 335- 


ENTRANCE OF Optic NERVE INTO EYEBALL IN RODENTS. 5 


optic nerve became transformed into a band flattened antero- 
posteriorly before it entered the eyeball, and that the disc was 
linear instead of circular in outline. In these animals the disc 
consists of a long slender band, bending slightly dorsally in the 
center and gently widening at theends. The absence of rods and 
cones along this band indicates that it is a true blind spot. As far 
as the investigation has been carried on, this form of optic disc 
was found to reach its greatest development in the prairie dog and 
has only been observed in members of the family Sciuride. Fur- 
ther investigation is necessary to show whether this peculiarity 
is limited to species of this family. 

Johnson! has pointed out the presence of an elongated disc in 
the squirrel and marmot, but he makes no statement regarding 
the mode of entrance of the optic nerve into the bulbus oculi. 
As stated above, the optic nerve spreads out in an antero-posterior 
direction shortly after it enters the orbit and penetrates the coats 
of the eye in the region marked by the optic disc. In the wood- 
chuck and prairie dog the flattened portion of the optic nerve 
is slightly concave on both the dorsal and ventral sides, and the 
latter is marked by a slight groove extending along the long axis 
of the nerve midway between the ends of the disc. The optic 
nerve from a short distance within the orbit to the chiasma has the 
usual cylindrical outline. This tendency of the nerve to bifurcate 
is also seen in the squirrel and chipmunk but it has not developed 
to the same extent as in the animals above mentioned. 

In the rabbit’s eye the optic nerve enters the eyeball as a 
cylindrical bundle of nerve fibers, from which one might expect 
the optic disc to be circular in outline, but this is not the case 
as has been observed by Johnson and figured by Haab.2. The optic 
papilla is nearly circular but instead of the fibers radiating from it 
to the different parts of the retina they divide into two nearly 
equal portions which run in opposite directions toward the equator 
of the eyeball. From these two bands the fibers spread out to the 
different parts of the retina. The expansion of the optic nerve 
on the inside of the bulbus oculi of the rabbit, in contrast to its 
spreading out on the outside of the bulbus in some forms of the 


1 Johnson, Phil. Trans. Roy. Soc., 1901, 194 B, p. 30. 
2 Haab, cited by Fuchs, ‘‘ Physiologisches Praktikum fiir Mediziner,”’ p. 227. 


6 ScIENTIFIC PROCEEDINGS. 


family Sciuride may suggest an intermediate stage in the process 
of evolution between the latter group and those higher mammals 
in which the fibers radiate to all parts of the retina from a circular 
optic disc. However, an extended investigation is necessary be- 
fore any conclusion can be arrived at with regard to the possible 
taxonomic value of this character. 

Experiments to trace the fibers of the optic tract are now in 
progress. As the optic nerve is spread out near the eyeball, it is a 
simple operation to cut either the inner or outer half for a study of 
the degeneration of its fibers. 

So far I am not in a position to offer any opinion regarding 
the physiological significance of this peculiarity. 

Note.—In the case of the squirrel and European marmot this 
peculiarity in the optic nerve is mentioned in Cuvier’s ‘‘ Lecons 
d’Anatomie Comparée,’’ Tome 3B, p. 430. 


4 (613) 


Biological and toxicological studies upon Penicillium 
puberulum Bainier. 


By C. L. ALSBERG and O. F. BLACK. 
[From the Bureau of Plant Industry, Washington, D. C.] 


This species when grown upon Raulin’s solution, in pure cul- 
ture, produces a new organic acid which has been termed penicillic 
acid. This acid gives a brownish-red solution when treated with 
a dilute solution of ferric-chloride. With ammonia it gives a deep 
red color. From the analyses, molecular weight determinations 
and other data, it seems probable that this acid belongs to the 
same general class of compounds as are found in lichens, and 
termed lichen acids. Like them, it is slightly bitter and irritating. 
Pharmacologically, it is moderately toxic, having an antiseptic 
action and being a protoplasmic poison. It is not astonishing to 
find substances of this class in fungi, since lichens are symbiotic 
forms, composed of fungi and alge. The finding of this type 
of substances in the pure culture of a fungus makes it probable 
that in lichens, lichen acids are the product of the fungus meta- 
bolism, and not of that of the alge. 


HyPERTROPHY PRODUCED BY ADRENALIN IN RABBITS. a 


5 (614) 


The influence of the salts of calcium and potassium on the 
degree of hypertrophy produced by adrenalin 
injections in rabbits. 


By HUGH A. STEWART. 


[From the Depariment of Pathology, College of Physicians and 
Surgeons, Columbia University, New York.] 


A series of experiments was conducted with a view to deter- 
mine whether the antagonism between calcium and adrenalin, as 
recently described by Meltzer and Auer, Schrank and others, holds 
good also as regards the hypertrophy of the heart which adrenalin 
produces when injected intravenously into rabbits. 

The method of investigation was as follows: One lot of rabbits 
was given every second day 0.2 c.c. of adrenalin chloride (1 in 
1,000) in 2 c.c. of physiological salt solution. Throughout the 
whole series, twenty-four injections were given. A second lot 
received the same amount of adrenalin in 2 c.c. of a 10 per cente 
solution of calcium chloride for the same length of time. Still a 
third lot was given 0.2 c.c. of adrenalin (1 in 1,000) in 2 c.c. of 
physiological salt solution every second day for twenty-four 
injections. The animals of this lot, however, were kept on a 
diet of carrots and potatoes only, the object being to give a diet 
containing a minimal amount of calcium. A fourth lot received 
the same amount of adrenalin in 2 c.c. of a 2 per cent. solution of 
potassium chloride. 

As a result of these experiments, data were obtained which 
justified the following conclusions: 

I. That calcium does not inhibit or prevent the hypertrophy 
of the heart produced by adrenalin. 

II. That on a diet poor in calcium, the degree of hypertrophy 
is insignificant. From this it would seem that a certain percent- 
age of calcium in the tissues is necessary in order that injections 
of adrenalin will produce hypertrophy. 

III. The addition of potassium to adrenalin increases slightly 
the degree of hypertrophy. 


8 SCIENTIFIC PROCEEDINGS. 


6 (615) 
Color inheritance in Fundulus hybrids. 
By FRANK W. BANCROFT. 
[From the Rockfeller Institute for Medical Research.] 


In the hybrids of Fundulus heteroclitus and Fundulus majalis 
it was found that, in general, wherever the color characters were 
not concerned with the rate of development, the F. heteroclitus 
characters were dominant over those of F. majalis. These 
dominant characters were: 

1. Red yolk chromatophores large and abundant. 

2. Black yolk chromatophores large and usually polygonal in 
shape. 

3. An early first crop of head chromatophores is present, in 
addition to a later crop which is found in both pure species and 
both hybrids. 

4. There is a row of red chromatophores on the lateral line 
shortly before and immediately after hatching. As soon as the 
fish hatch the red chromatophores begin to fade, and within 
a few days disappear entirely. 

On the other hand, when the characters were concerned with 
the rate of development, the Mendelian dominance was partly 
or entirely obscured. These characters were: 

5. In F. heteroclitus there are no or very few black chromato- 
phores on the lateral line at hatching; but they increase rapidly 
during the first few days after hatching. In F. majalis there are 
50 or 60 black lateral line chromatophores at hatching. The 
hybrids are intermediate. 

6. In F. heteroclitus when the yolk chromatophores first appear 
they are uniformly distributed over the whole yolk; while in 
F. majalis they are confined to the hemisphere containing the 
embryo. The hybrids are intermediate. 

7. Both with respect to time, and with respect to the stage 
of development of the embryo the yolk chromatophores appear 
first in F. heteroclitus, next in the F. heteroclitus egg hybrid, next 
in the F. majalis egg hybrid, and last in the pure F. majalis. 

An apparent case of blended inheritance in the time of the 


SEMI-CIRCULAR CANALS OF EAR To Motor System. 9 


first appearance of head pigment was found to be really a case 
of the combination of two crops of head chromatophores, one of 
which did not develop in the recessive species F. majalis. 


7 (616) 


A note on the relation of the semi-circular canals of the ear 
to the motor system. 


By J. GORDON WILSON and F. H. PIKE. 


[From the Laboratories of the University of Chicago and Northwestern 
University.] 


The work on the semi-circular canals was undertaken with 
the object of studying: (1) The results of stimulation of the 
end organ of the vestibular nerve; (2) the immediate and remote 
results of destruction of the labyrinth or of the eighth nerve on 
one or both sides; (3) the effect of removal of various parts of 
the brain on phenomena which have been observed to follow 
stimulation or destruction of the labyrinth, and (4) the paths of 
nervous connection between the labyrinth and the eye muscles — 
the optico-acoustic path. Later it is the intention to study 
anatomically the degenerative processes occurring in various parts 
of the central nervous system after destruction of the labyrinth 
or eighth nerve. 

Method.—The mastoid bone is exposed by a skin incision and 
the separation of the muscles from their attachment at the linea 
nuchz superioris and the anterior inferior border of the pars 
mastoidea. A trephine opening is made through the outer table 
and diploe of the mastoid bone. The hard portion of the otic 
bone, in which the semi-circular canals are imbedded, can be 
removed with a mastoid gouge and the labyrinth destroyed without 
direct anatomical injury to the cochlea. Dogs, cats and tortoises 
were used. The results here given apply to dogs, unless other- 
wise stated. 

Results —Immediately following recovery from the anesthetic 
after removal of one labyrinth, there is marked torsion, particu- 
larly of the anterior part of the body, of the animal toward the 
injured side. The animal is unable to walk and falls over toward 


10 ScIENTIFIC PROCEEDINGS. 


the injured side on attempting to stand. It may roll completely 
over on the floor. There is a quick movement of the eyes toward 
the sound side and a slow return to the injured side. The un- 
steadiness of gait and the nystagmus are transient. Marked 
torsion of the head is permanent (two years). 

Stimulation of the labyrinth, under moderate anesthesia, by 
putting hot water in the trephine opening before destruction of 
the semi-circular canals, causes slow marked deviation of both 
eyes to the opposite (unstimulated) side. Ice in the trephine hole 
causes the eyes to deviate to the same (stimulated) side. On 
electrical stimulation, the zinc terminal of a battery causes devia- 
tion to the opposite side; the carbon terminal, to the same side. 

The deviation of the eyes on stimulation of the labyrinth may 
be obtained after total removal of the cerebrum, the optic thala- 
mus, the anterior portion of the anterior corpora quadrigemina 
and the cerebellum. ‘The torsion of the head in tortoises following 
destruction of one labyrinth is as marked after decerebration as 
before. There are no apparent ‘‘shock’’ phenomena in these 
reflexes after decerebration. 

The nystagmus is not due to irritation of the wound, but to 
the action of the opposite uninjured labyrinth. Nystagmus fol- 
lowing extirpation of the second labyrinth is much less marked, 
and more fleeting than after extirpation of the first, and is re- 
versed in direction, 7. e., the quick movement is to the injured side. 

There is no torsion of the body nor any rolling movements 
after extirpation of both labyrinths at the same operation, nor 
when the second labyrinth is destroyed after an interval. The 
animal becomes very ataxic and is unable to grasp food if both 
labyrinths are removed at the same time. 

Complete or partial removal of the cerebellum one or two 
weeks previous to removal of one labyrinth has no effect upon the 
onset and course of labyrinthine nystagmus. Eye movements 
following injury to the cerebellum are jerky, irregular, and quick 
in all directions. Labyrinthine nystagmus is slow in one direction 
and quick in the opposite direction. The eye movements following 
cerebellar extirpation greatly outlast those of labyrinthine origin, 
and the labyrinthine movements may be superposed on those 
following cerebellar removal. 


EXPERIMENTAL NEPHRITES IN GUINEA-PIGS. II 


Removal of one or both occipital lobes of the cerebrum does 
not abolish labyrinthine nystagmus. True labyrinthine nystag- 
mus has never been observed after complete decerebration, al- 
though the slow deviation of the eye persists. The slow compo- 
nent of nystagmus is of labyrinthine origin. The quick component 
is probably of cerebral origin. 

The results suggest that the vestibular mechanism is con- 
nected far more closely with the phylogenetically older motor 
system (von Monakow) than with the phylogenetically newer 
system. 


8 (617) 


‘Experimental nephritis in guinea-pigs by subcutaneous 
injections of chromates. 


By W. OPHULS. 


[From the Pathological Laboratory of Cooper Medical College and 
Stanford University.] 


After having determined that 1 centigram of bichromate of 
potash is very nearly a lethal dose for guinea pigs of from 500- 
750 gm., forty guinea pigs were used in an effort to produce, if 
possible, lasting anatomic lesions in the kidneys by repeated in- 
jections. Great difficulty was encountered in continuing larger 
doses on account of the extensive necroses produced at the site 
of injection. In the end it was found that a }-+ per cent. solu- 
tion of chromate of potash to which an equal amount of carbonate 
of soda had been added was most satisfactory, although still 
quite irritating. As our experience has taught us that sublethal 
doses are most effective in experiments of this character, injections 
of one or one half centigram were used in one half of the experi- 
ments and the doses crowded as closely as the animals would 
tolerate; in other series smaller doses down to a quarter of a 
milligram were employed and continued for long periods (in one 
case for nearly two years). The immediate effect of the injection 
of large doses in the guinea pig is the production of an albuminuria 
which is usually quite limited in amount and the appearance in 
the sediment of desquamated cells from the uriniferous tubules, 
much more rarely of casts. The kidneys in the acute intoxication 


12 SCIENTIFIC PROCEEDINGS. 


are very markedly hyperemic, there is more or less fatty degenera- 
tion and well marked necrosis and desquamation of the epithelium, 
later cast formation also occurs. The glomeruli are hyperemic, 
do not show any distinct histologic lesions. Hemorrhages from 
them were not observed. The lesions are hardly severe enough to 
account for the early death of the animals. I have become rather 
strongly persuaded that the chromates cause death in guinea pigs 
not primarily by their action upon the kidneys, but in a different 
way, although nothing definite could be ascertained in this regard. 

Results with Injections of One Half Centigram.—Several guinea 
pigs died from the first or second dose. Four lived from five 
months to 153 months. The immediate reaction from each dose 
was well marked and it was impossible to give the doses very 
frequently; the highest was 12 doses in five months. One of these 
animals receiving five doses in seven months showed merely cystic 
dilation of some glomeruli similar to that which was observed in 
controls; in one, apart from well marked epithelial lesions, there 
was a slight diffuse interstitial process; the other two showed 
definite small areas of collapse of degenerated tubules but with 
very little evidence of new formation of connective tissue between 
them. 

Results with Injections of One Quarter of a Centigram.—Few 
animals died after the first injections; the immediate reaction on 
the part of the kidneys in most instances was very slight and the 
doses could be repeated more frequently. Some of these animals 
lived for one year or more, one for nearly two years. All showed 
more or less well marked epithelial lesions with formation of casts, 
very few interstitial lesions of a character which was not en- 
Countered in the controls also. In these few there were small 
areas of collapse of degenerated tubules and very little new formed 
connective tissue between them. 

Experiments with smaller doses even when very frequently 
repeated and continued for long periods were entirely negative so 
far as the kidneys were concerned. 

Hearts and bloodvessels remained normal in all animals. 

The conclusion seems justified that it is impossible to produce 


1See Ophiils, ‘‘ Occurrence of spontaneous lesions in kidneys and livers of 
rabbits and guinea pigs,’’ Proc. Soc. for Exp. Biol. and Medicine, 1911, viii, 75. 


EXPERIMENTAL NEPHRITIS IN RABBITS. 13 


severe lasting renal lesions in guinea pigs with chromates, prob- 
ably because in these animals the chromates are too toxic in 
a general way and too slightly effective on the kidneys locally. 


9 (618) 


Experimental nephritis in rabbits by subcutaneous 
injections of chromates. 


By W. OPHULS. 


[From the Pathological Laboratory of Cooper Medical College and 
Stanford University.] 


Rabbits are relatively more susceptible to the action of chro- 
mates than guinea pigs. Animals of from 2,000-2,500 gm. in 
weight sometimes die after the injection of two centigrams of 
bichromate of potash. The acute renal lesions produced by large 
sublethal doses are much more marked than those found in guinea 
pigs under similar conditions. There is marked albuminuria, 
much degeneration, necrosis and desquamation of the epithelium 
and abundant formation of casts of different kinds. The extreme 
lesions which may develop after a while as a result of crowding 
of large doses were described by me in 1908,! but they do not 
necessarily follow even repeated administration of large doses. 

Fifty animals were experimented upon. The dosage varied 
between two centigrams and two milligrams. Some of the 
animals were kept alive for a year or more. So far as epithelial 
lesions are concerned the experiences are similar to those in guinea 
pigs, except that the epithelial lesions became more severe and 
seemed to continue longer after the last injection. Very marked 
interstitial lesions were observed at times, but they resemble 
those observed spontaneously? so closely and occurred so irregu- 
larly, sometimes soon, sometimes late after the administration 
of various doses and sometimes not at all, that any definite con- 
clusion of their relation to the injections could not be arrived at. 

Hearts and bloodvessels remained normal in all animals. 


1 Ophiils, ‘‘ Some interesting points in regard to experimental chronic nephritis,” 
Journ. Med. Res., 1908, xviii, 49. 
2 Ophiils, 7. c. 


14 SCIENTIFIC PHOCEEDINGS. 


10 (619) 
A dominant sex-limited character. 


By T. H. MORGAN. 
[From the Department of Zodlogy, Columbia University.] 


A new mutant of the fruit fly, Drosophila, characterized by 
abnormal arrangement of the black bands on the abdomen, 
proves to be dominant to the normal arrangement of the bands, 
and since the factor for the character is coupled with femaleness 
it may be assumed to be contained in the X-chromosome. Abnor- 
mal @ by normal o gives abnormal males and females. These 
inbred produce in the next, or F2, generation 50 per cent. abnormal 
@, 25 per cent. abnormal o& and 25 per cent. normal o’. No 
normal females appear in this generation. Thus the zxormal 
character is sex-limited in relation to the abnormal. 

The reciprocal cross, viz., normal @ by abnormal & gives 
abnormal females and normal males. These inbred produce in 
the next, or F2, generation, 25 per cent. abnormal 9, 25 per cent. 
normal 9, 25 per cent. normal o’, and 25 per cent. abnormal 
od. The explanation is as follows: 

Abnormal 9 = Ab. X — Ab. X. 
Normal o& =N.X ———. 
Fi 219° NAb. CXUN: x: 


co Ab. X — 
Fe Ab. X Ab. X = Ab. Q. 
Ab. X N. X =Ab. 9, 
Ab. X = Ab. ot. 
N. X =N. GC. 


It will be seen that the abnormal factor is contained in X, 
hence sex-limited inheritance. The explanation of the recip- 
rocal cross will be clear from this example. 

Five other cases of sex-limited inheritance have been found 
in Drosophila, viz., miniature wings, rudimentary wings, black 
color, bright red eye and orange eye. All of these are recessive 
characters, and ex hypothesi are also present or absent from X. 
By crossing a red-eyed, abnormal type with a white-eyed, normal 


1 Since the abnormal character overlaps the normal some difficulty is found in 
classifying the Fe generation. 


A DOMINANT SEX-LIMITED CHARACTER. 15 


type two points are established: first, that the same chromosome 
X may carry both a recessive (absence) and a dominant character 
at the same time, and second, that a strong ‘‘association”’ or 
coupling of characters exists. Thus, when an abnormal red-eyed 
@ is paired with a normal white-eyed male the offspring are ab- 
normal red-eyed males and females. These inbred have given 
in the second generation: 


Abnormaliredt a) Orie ctarciecoMoisicl ne ccersielevereverctclorevereraiece 18 
Abnormallredia dice sciersrsctersiete sae he ciaesevatoersierevsuace ee 6 
ADOT Male MILE Cy state leseveretsler a cr erst Sualrel slo ollove) et otious ats ok ° 
Nori alee Teds Bl Ole aieyrsve nicicts s.ciovereve ciate siohenelveu w\she is 18° 
Normale Leda s Otis eicvacrsparerstersicse: cs ltvslele.e.¢ e1s. sie o ein'e.s 6 
IN OLMIal ee WHIteTCyie a isicitel ets ore Sie fn ic evcloineciaceverays os 14 


A strong tendency for the grandparental combination to 
reappear in the F2 generation is manifest. 

The reciprocal cross, viz., abnormal red-eyed o& by normal 
white-eyed @Q gives abnormal red-eyed females and normal 
white-eyed males. These inbred have produced: 


IN Ornate WCC Oe rere ernsict eins s cianot alc ons ezeCeusicy eletete.eve.e) eyes 47 
IN OLA le WOILEN Cilerserctaciiere sist tetalctocrevsiere ec erelorryecie 55 
Abnormaliwhites Qi ierec.s storckec. o1atstore ore) stele, clea avareyevareress ° 
Abnormal: white: ‘Cues sinssccisroce cusietoretetersiois: sierele m eieisicne 4 
IN Ori alee retains Cie sreterst aisle secslvcivleserereets cleiorsielcislolsieners 34 
Normale rede le cretavess cars ciczetn civlcteles ells iere eieleies ovis 19 
Abnormealiredon Qi es viaccvaretoraie.sraetessveleia ateieiaelauciawerss AI 
A DnOKmal rede «iterate cater ie eoteteterarcrovietel nis ealere eTaeteke 48 


Here also the normal and white combination reappear, while 
the abnormal and white are scarcely represented. 


I (620) 
Trypanosomiasis in monkeys (Macacus rhesus) in captivity. 


By B. T. TERRY. 


[From the Laboratories of the Rockefeller Institute for Medical 
Research, New York City.] 

In the blood of an experimental monkey (Macacus rhesus), 
Dr. Richard Lamar found on October 28, 1911, an actively motile 
trypanosome. This discovery led to my examining the blood of 
all of the monkeys at the Rockefeller Institute. 

In examining 130 monkeys, 28 were found infected with 
trypanosomes. The infected monkeys had been used for experi- 
ments between July 17 and October 6. Six monkeys used on or 
before July 17 were negative, and 80 others, some normal, the 
rest used after October 6, were also negative. 

With but one exception, all of the monkeys examined belonged 
to the Macacus rhesus species. 

The trypanosomes found in the 28 monkeys were apparently 
of the same kind. They have been successfully inoculated into 
one monkey (Macacus rhesus), six mice, two rats, one guinea pig, 
and one young rabbit. In none of these animals has a rich infec- 
tion been seen. The two rats were infected on the 8th day, the 
six mice between the 9th and the 52d day, the guinea pig and 
rabbit on the 16th day, and the monkey between the 16th and the 
24th day. The trypanosomes do not appear to be very patho- 
genic. 

The micronucleus is usually at the extreme posterior end of 
the parasite, is strikingly large, measures Iw or more in diameter, 
and often projects on either side of the parasite. The nucleus is 
oval, measures 124 to 224y in its long diameter, and is situated 
near the juncture of the anterior 14 and the posterior 24 of the 
body. The flagellum is very long, the free part measuring 10 to 
12l4u. The entire length of the parasites thus far measured has 
varied between 25 and 28y, the breadth between 2 and 2)4uy. 

If the future shows that the trypanosomes here described 

17 


18 SCIENTIFIC PROCEEDINGS (46). 


belong to a new species, I propose for them the name Trypanosoma 
rhesit. 


2 (621) 


On the question of immunization against transplantable cancer 
by injection of an animal’s own tissues. 


By R. A. LAMBERT. 


[From the Department of Pathology, College of Physicians and 
Surgeons, Columbia University.| 


That the injection of a suitable quantity of homologous tissue 
induces in susceptible mice a certain degree of resistance to the 
inoculation of their transplantable cancers is a well-established 
fact. There appeared recently a paper by Woglom! in which 
experiments were described showing that autogenous tissue 
(spleen) injected subcutaneously was also capable of inducing this 
immunity. Woglom’s work has been questioned by Apolant? who 
repeated the experiments with negative results. Apolant main- 
tains further that the spleen of a mouse does not afford sufficient 
tissue for immunization, and that the question as to the possibility 
of immunizing with an animal’s own tissues is still an open one. 

In the experiments herewith reported, blood has been used as 
the immunizing agent. The quantity of defibrinated blood neces- 
sary for immunizing young mice was shown by Bashford to be 
about .3 c.c. In order to eliminate, however, the possibility of 
insufficient dosage, it was considered desirable to use at least .5 
c.c. As Woglom stated in his paper, mice cannot be bled 
this amount plus the loss attending the bleeding without caus- 
ing death. Interval bleedings from the jugulars were there- 
fore resorted to. In nearly all of the experiments two bleedings 
only, on successive days, were necessary. About ten drops of 
blood in citrate solution were taken each time. The corpuscles 
were preserved in the ice box and injected subcutaneously on the 
day after the last bleeding. Ten mice were treated in this way; 
ten controls were injected with a similar quantity of homologous 
blood; ten normal mice were set aside as controls on the two 


1 Jour. Exp. Med., January, 1910, p. 29. 
2 Zeit. f. Immunitatsforschung, July, 1911. 


IMMUNIZATION AGAINST TRANSPLANTABLE CANCER. 19 


treated groups. The mice were all young and thrifty; average 
weight, 18 grams. The three series were inoculated with carci- 
noma tendayslater. The record of the tumors resulting from these 
inoculations shows a definite immunity in the series treated with 
homologous blood, but practically no difference between the 
normal controls and those receiving injections of their own blood. 

These findings, then, indicate that immunity against trans- 
plantable cancer in mice is, at least, not regularly induced by 
injections of an animal’s own tissues. A larger series would prob- 
ably be necessary to determine the existence of individual varia- 
tions in the reaction of animals to such injections.! 


3 (622) 
Another case of sex-limited heredity in poultry. 
By C. B. DAVENPORT. 


[From the Carnegie Institution of Washington.] 


To the four or five described cases of sex-limited heredity 
in poultry another is added. 

The Jungle-fowl and its derivative, the Brown Leghorn, have 
the hackle and saddle feathered ‘‘laced’”’ with red. The upper 
wing coverts of the cock are also red, forming the ‘“‘wing bar.” 
In the Dark Brahma, on the other hand, the red is not formed on 
the hackle and saddle and is nearly absent on the wing bar of the 
male, so that the red is replaced by white. 

If, now, a male Dark Brahma be crossed with a female Brown 
Leghorn, or if the cross be made in the opposite direction, all sons 
are white-laced; but the wing bar is red. Thus, in these sons 
the white lacing is dominant but the white wing bar appears to 
be recessive. The most important point, however, is that the 
sons derived from the reciprocal crosses are practically indis- 
tinguishable. 

With the daughters this is by no means the case. When the 
father is white-laced, the daughter is also; but if the father is red- 

1A second set of experiments has been done which shows a slightly larger per- 
centage of resistant animals among those immunized with autogenous tissue than 


among the normal controls. The difference, however, is not sufficiently striking to 
influence the conclusion drawn from the first experiments. 


20 SCIENTIFIC PROCEEDINGS (46). 


laced the daughter is likewise; 7. e., the daughter's lacing comes 
from the father’s side of the house only. 

The explanation is simple on the assumption that the lacing 
is linked with the sex-chromosome, following the scheme of trans- 
mission of the sex-chromosome as worked out by Stevens, Wilson 
and Morgan. While the male of poultry must have two somatic 
sex-chromosomes the female has only one. Therefore, while all 
sperm possess a sex-chromosome, only half of the eggs do. In 
the fertilized egg or zygote that has only one sex-chromosome, this 
is derived from the father and the zygote becomes a daughter. 
Hence the daughter “‘inherits’”’ from the father only. 

The hybrids have been bred together and a second generation 
has been obtained. When the hybrid male is mated to a white- 
laced hybrid female all the sons are white-laced while half the 
daughters are white-laced and half red-laced. But when the 
hybrid male is mated to a red-laced female half of the sons are 
white-laced and half red-laced while half of the daughters are 
white-laced and half red-laced as in the reciprocal mating. This 
result accords with the hypothesis. 


4 (623) 
The gastric and pancreatic secretions of the newborn: 


By ALFRED F. HESS. 


[From the Department of Health, New York City.] 

I have been able by means of a simple duodenal catheter to 
obtain for the first time access to the duodenum in the living 
infant. This has enabled me to investigate the secretion of the 
upper part of the smallintestine. This catheter is, in brief, merely 
a Nelaton soft rubber catheter No. 14 (F). That I actually do 
reach the intestine is proved by X ray photographs which I show. 

The present report concerns solely newborn infants, which had 
never obtained any nourishment. I have found some interesting 
conditions not only as concerns intestinal secretions but also 
regarding the secretion of the gastric juice. It is noteworthy 
that there have been no previous investigations in this regard; 
in fact I have been able to find note of only one test of the gastric 
secretion of the newborn before it has been given food. 


GASTRIC AND PANCREATIC SECRETIONS OF THE NEWBORN. 21 


I found that in almost all cases hydrochloric acid is present in 
the stomach of these newborn infants whether they are examined 
one half hour or twenty hours after birth. The hydrochloric acid 
varies from 1% cu. cm. to about 7 cu. cm., and is not in direct 
proportion to the age of the child. This hydrochloric acid is not 
stimulated merely by the passage of the tube, for it was obtained 
within a minute or two after the catheter was introduced. It, 
therefore, must have another origin. I believe that it is a reflex 
due to the sucking of the tube. The longer the catheter is kept 
in the stomach the more juice is obtained; in one hour 14 cu. cm. 
was obtained; in an hour and 50 minutes 17 cu.cm. This gastric 
juice has an acidity on an average of about 50. Pepsin and rennet 
were also present in considerable amount. 

These facts show that the infant at birth is prepared to digest 
food. The large amount of hydrochloric acid may be present in 
order to digest the high percentage of proteid of the colostrum and 
it may also serve the purpose of a bactericide, for we have found 
it to possess high bactericidal power. 

The duodenum also was entered by means of the catheter. 
It can be entered almost as easily and quickly as the stomach in the 
newborn infant, and the contents aspirated. It was found that 
in the newborn infant there is very little to be aspirated from the 
duodenum compared to older infants. In spite of the fact that a 
large amount of hydrochloric acid is present, this does not seem 
to stimulate to a proportional degree the flow of the duodenal 
secretion. However, I have been able by this method to find 
protease, lipase, and amylase in the duodenum before any food 
was ingested, and, therefore, can state that the hydrochloric acid 
is sufficient hormone to stimulate these ferments. Amylase was 
found with least regularity. Frequently no secretion at all was 
obtained. In all about 35 tests were undertaken. 

It is of special interest to note that bile was not found in these 
tests. It was expected that this would be quite otherwise, as the 
meconium is rich in bile, and we know that bile is found in the 
gall bladder of the fetus by the fourth month. I have not tested 
for the presence of the bile salts. Many other problems suggest 
themselves for investigation by this method; with some of these 

Jam at present occupied. 


22 SCIENTIFIC PROCEEDINGS (46). 


5 (624) 


Nitrogen and sodium chloride excretion in experimental 
uranium nephritis.! 


By HERMAN 0. MOSENTHAL. 


[From the Departments of Biological Chemistry and Medicine, 
College of Physicians and Surgeons, Columbia University, 
New York.] 


A series of experiments were performed upon dogs with the 
object of determining the effects on the output of nitrogen and 
sodium chloride in nephritis produced by the subcutaneous injec- 
tion of uranium nitrate. These dogs were fed the usual standard 
diets, also diets containing much meat, as well as food to which 
considerable amounts of urea and sodium chloride had been added. 

The results of these experiments appear to justify the following 
conclusions regarding uranium nephritis. 

1. The nitrogen secreted by the small intestine, as determined 
by the Thiry fistula method, is somewhat diminished. 

2. The fecal nitrogen remains approximately unchanged. 

3. The urinary nitrogen is not diminished even when the diet 
demands an excretion of one gram of urinary nitrogen per kilo 
of body weight of the dog. 

4. In some cases the urinary nitrogen is increased. The source 
of this excess of nitrogen is problematical. It may be due to 
protein destruction of the body tissues caused by the same toxic 
agent as the nephritis. If this be true, the ‘‘rest’’ nitrogen of 
the blood serum should be higher than normal. Experimental 
attempts have been made to ascertain the facts in this connection 
but have not been pushed far enough to warrant a definite state- 
ment. 

5. The sodium chloride excretion in the urine keeps pace with 
the intake even when considerable quantities are added to the 
food. 

6. The above statements have held true for dogs after the 
first as well as after several large single injections of the drug at 
long intervals. One animal was tested after he had received as 
many as seven injections. 


1 Under the auspices of the Edward N. Gibbs Memorial Prize Fund. 


Seat oF ACTION IN TETANY AFTER PARATHYROIDECTOMY. 23 


6 (625) 
The seat of action in tetany after parathyroidectomy. 


By W. G. MACCALLUM. 


[From the Department of Pathology of the College of Physicians and 
Surgeons, Columbia University.] 


Both the immediate cause and seat of tetany are still obscure. 
It has been suggested, though never proven, that a poison must 
circulate in the blood to cause the tetanic twitchings. It has also 
been suggested that these twitchings may result from a lack of 
calcium in the circulating fluids. It has been shown that tetany 
does not appear in a limb to which the nerves have been cut. It is 
conceivable that this is due to the fact that no impulses reach 
that limb from the spinal cord. The present experiments show 
that if the nerves be cut during tetany, their electrical excitability 
remains the same as that of the intact nerves on the opposite 
side. Further, it is shown that if the nerves be cut before the 
development of tetany, they become hyperexcitable to an extent 
which equals that of the intact nerve on the opposite side, although 
they are quite separate from the spinal cord. Since degeneration 
occurs within two or three days, such observations must be made 
with due regard to this fact. The peculiar character of this rise 
in the excitability is seen in the figures obtained for the cathode 
and anode opening shocks to which the nerves become especially 
excitable. In complete anemia or after the death of the animal 
there is a period of about one half hour during which this char- 
acteristic rise in the excitability of the nerve to the cathode and 
anode opening shocks appears. Nevertheless, the excitability of 
the nerves is, throughout this period, very much lowered and the 
curve is in no way comparable, therefore, to that in tetany. 

Transfusion of the blood of an animal in tetany into the vessels 
of a normal animal has not succeeded in produeing a characteristic 
tetany nor even a marked change in the excitability of the nerve. 

This is probably partly due to inadequate technique and partly 
to the action of the normal dog’s parathyroids. If the leg of a 
normal dog be isolated, with the exception of the nerves which 


24 SCIENTIFIC PROCEEDINGS (46). 


remain in intact connection with the spinal cord, and if the vessels 
be anastomosed with those of a dog in tetany, so that the peripheral 
portions of the normal leg are bathed with tetany blood, the nerves 
of that leg assume the characteristic hyperexcitability of tetany, 
and twitchings may even occur. Reéstablishment of the con- 
nection with the normal circulation brings back the excitability 
to normal. 

From these experiments, it may be concluded that the hyper- 
excitability is peripheral and is dependent upon some change in 
the character of the blood. Experiments with curare, to deter- 
mine whether or not this is an affection of the nerves alone, have 
not yet been completed, although one has the general impression 
that the excitability of the muscles themselves is increased over 
normal. The value of the experiments is thought to lie particu- 
larly in the opportunity which is offered for the study of tetany 
blood modified in various ways and used as the fluid for perfusing 
an isolated extremity. 


7 (626) 


Curves from a case of transient complete heart block, showing 
constantly varying ventricular complexes. 


By ALFRED E. COHN. 


[From the First Medical Division, Mount Sinai Hospital, 
New York.]| 


The patient from whom the curves were taken has been under 
observation since August, 1910. He was at that time suffering 
from cardiac decompensation. It was clear from the physical 
examination that he had a valvular defect. Combined arterial 
and venous curves were made. These showed that for short 
periods every impulse from the auricles was answered by a ven- 
tricular contraction, while at others the ventricular contractions 
responded to every second beat of the auricles. Curves were 
taken in February and March, 1911. These were volume curves 
from the jugular vein and radial artery and likewise curves of the 
cardiac action current, registered with an Edelmann string- 
galvanometer. At first the ventricles responded to every second 


CuRVES FROM A CASE OF TRANSIENT HEART BLOCK. 25 


auricular beat, but somewhat later there was complete dissociation 
between the two pairs of cavities. Before the patient left the 
hospital, the relation between the auricles and ventricles was 
normal. Electric curves were taken on December 19, 1911, when 
the ventricles responded to every auricular contraction. 

The curves which are of interest date from the period of com- 
plete auriculo-ventricular dissociation. Each ventricular complex 
is represented by R-, S-, and 7J-waves. They vary from each 
other in that, when the R- is large, the S-wave is small; and that 
when the S-wave is large, the R-wave is small. The R-wave 
gradually increases in size and then gradually diminishes, when 
the S-wave gradually increases in size and as gradually diminishes. 
If the apexes of succeeding R- and S-waves, 7. e., the significant 
wave in each complex were joined, a waved line would result. So 
diagrammatic a sequence as this did not occur frequently, but 
there was a tendency to approximate to this description. Some- 
times the transition from complexes of one type to those of another 
was abrupt. The time between the complexes was almost equal, 
except at points of transition, when it was reduced. 

It is concluded from the variation in the shape of the complexes, 
that they are responses to stimuli arising at levels in the heart 
varying from some supraventricular position to the apex. The 
explanation of the shortened time at points of transition is difficult. 
No hypothesis yet suggested is satisfactory. The fact that there 
was merely a temporary and not a permanent dissociation may be 
a significant factor, although the P-—R interval associated with the 
transitions is not of uniform length. (P is the wave representing 
auricular systole.) 


8 (627) 
Further observations on the tolerance of gases by the 
circulatory apparatus. 
By J. P. ATKINSON and C. B. FITZPATRICK. 


[From the Department of Health, City of New York.] 


In the New York Medical Journal of November 26 and at the 
New Haven meeting of December, 1910, we gave observations on 
the quantities of gas (air) tolerated and the apparent relation of 


26 SCIENTIFIC PROCEEDINGS (46). 


the adrenals to this tolerance. We have further determined that 
section of the cord between the fifth and sixth cervical vertebrz 
interferes with this tolerance of gas (air). After the removal of 
the adrenals from two dogs carbon dioxide was tolerated up to 942 
c.c. in one case and 952 c.c. in the other, in 1 hour and 23 minutes. 

Two dogs were injected with nitrogen... One received 32 c.c. 
in six minutes with marked depressions; the animal lived. Pant- 
ing occurred. The other received 272 c.c. within 22 minutes 
and died; panting was not noticed. The lungs were collapsed at 
autopsy. 

The tolerance of oxygen was tested on two dogs. One received 
150 c.c. slowly and survived. The other received 312 c.c. in 234% 
minutes and died. During the oxygen experiments, panting 
occurred. The lungs were practically normal. 

The tolerance of hydrogen was tested in two dogs. In one 184 
c.c. in 8 c.c. volumes were injected in 1344 minutes. Each injec- 
tion caused a moderate depression. 60 c.c. were given in 20 c.c. 
volumes in 3/4 minutes, and 20 c.c. in 5 c.c. volumes. The large 
volumes caused great depression and almost death. In the other 
dog 90 c.c. were injected in 7 minutes in 8 c.c. volumes without 
harmful results. 

Sulphuretted hydrogen was used to study elimination on two 
dogs. Three c.c. saturated H:S water were injected into the 
femoral vein. The breath almost immediately blackened lead 
acetate. Twenty-five minutes after tying and clamping off the 
adrenals 3 c.c. more of saturated H.S water was injected and a 
similar result was obtained. 100 c.c. of H2S water introduced 
into the rectum did not give the reaction at the mouth in 25 
minutes. In the other dog 30 c.c. of HS water were injected into 
the duodenum. In 8 minutes it was detected at the mouth. 


1In every case morphin sulphate was given before etherization of the dog. 
Each dog was killed and autopsied after the experiment. 


THE DESTRUCTION OF ADRENALIN BY SPINAL FLUID. 27 


9 (628) 
The destruction of adrenalin by spinal fluid. 


By S. J. MELTZER. 


[From the Department of Physiology and Pharmacology of the 
Rockefeller Institute.] 


Soon after the discovery of the profound effect of adrenal 
extract upon blood-pressure the question arose as to the fate of 
this extract in the blood. The rise of the blood-pressure after 
an intravenous injection of adrenin passes off in a few minutes 
and none of the adrenin is found to persist in the blood, no matter 
how large the injected dose has been. The quite natural explana- 
tion of this phenomenon was, that the blood destroys adrenin. 
But Oliver and Schafer found that in a mixture of adrenin and 
blood, even after standing for 22 hours, the adrenin remained un- 
affected. It has been confirmed since by several investigators, 
that neither blood nor serum is capable of destroying adrenal ex- 
tract. I shall not discuss for the present the problem of the fate 
of adrenin in the body in general. I wish only to report the dis- 
covery of the fact that there is at least one body fluid which is 
capable of destroying adrenin and that is spinal fluid. The obser- 
vation was made by mixing human spinal fluid with adrenalin. 
The spinal fluids were obtained in the first place from a number of 
cases of poliomyelitis of the Rockefeller Hospital and from two 
cases of tuberculous meningitis, obtained for me by Dr. Flexner. 
But this destructive action is not specific to these diseases. I 
found it to be possessed by spinal fluids from cases of resolving 
pneumonia, gastro-enteritis and eczema, obtained through the 
kindness of Dr. Wollstein. Evidently it is a physiologic property 
of normal spinal fluids, although there seems to be a difference in 
degree of action between some pathologic cases; for instance the 
spinal fluid from poliomyelitis seems to destroy adrenalin definitely 
more readily than that from tuberculous meningitis. This fact 
might attain a practical significance. The presence of adrenalin 
was studied by its dilating action upon the frog’s pupil (the so-called 
Meltzer-Ehrmann reaction) and its action upon blood-pressure. 


28 SCIENTIFIC PROCEEDINGS (46). 


The tracings speak for themselves. The mixture of adrenalin 
with spinal fluid in proportion of 1:20 when kept on ice caused a 
considerable rise of blood-pressure by a dose of 0.5 c.c., while 
when this mixture was incubated for an hour in the thermostat 
at 37° C. even 4 times the dose caused no change in blood- 
pressure. 
10 (629) 
Glucuronic acid determination (Tollens) in duodenal 
obstruction.1 


By JOHN WILLIAM DRAPER AND FREDERICK 
W. SCHLUTZ. 


While the liver generally plays a subordinate part in the syn- 
thesis of glucuronic acid, it would seem from the experiments of 
Pohl (1), that upon the incorporation of chloral-hydrate or 
camphor, the conjugation of these substances with glucuronic 
acid does take place largely in that organ. 

We have been interested in seeking a measure of the functional 
activity of the liver before and after experimental duodenal ob- 
struction. By giving a dog camphor and determining the output 
of camphor-glucuronic acid, both before and after obstruction, 
we hoped to measure at least in a relative way any impairment in 
liver function which may follow this intestinal lesion. 

The experiments were carried out on dogs—the operative 
portion under complete ether anesthesia. The animals were fed 
for fully a week on an exclusive meat diet in order to free the urine 
as much as possible from pentoses. 

For the glucuronic acid determinations we employed one of the 
two methods described by C. Tollens (2, 3), viz., distillation of 
the glucuronic acid lacton with dilute hydrochloric acid, and pre- 
cipitation of the resulting furfurol with phlorglucin. This method 
seems open to less objection that most of the other quantitative 
methods which have been proposed. In the hope of further 
determining the accuracy of our results, we are now experimenting 
with the CO, method described by Tollens. 


1Studies from the Laboratory of the Department of Physiology, University 
of Minnesota, Minneapolis, and from the Laboratory of Surgical Chemistry and 
Physiology, Rochester, Minnesota. 


Guiucuronic AcID DETERMINATION. 29 


The experiments here reported were carried out as follows: 
The glucuronic acid excreted during one or two 24-hour periods 
was determined and used as a normal. According to Tollens, 
the variations in the daily quantities of glucuronic acid are very 
slight, if the diet is uniform. 

From 2 to 5 gm. of commercial camphor dissolved in olive oil 
were given subcutaneously and the camphor-glucuronic acid 
excretion in the urine determined for three to four 24-hour periods. 
The duodenum was then obstructed by cross section and infolding 
at a point just aboral to the greater pancreatic duct. From 12 to 
24 hours after obstruction, determined by the first indication of 
marked clinical symptoms, the same dose of camphor was again 
given and the camphor-glucuronic output determined in 24-hour 
periods until death ensued. 

Including a report made by Draper (4) on one dog, we have 
completed experiments on three dogs. The results, expressed in 
per cent. of recovered camphor-glucuronic acid, are as follows: 
From Dog No 30, before obstruction, 41.76 per cent. of a theoret- 
ical total was recovered. From Dog No. 124, 44.00 per cent., 
and from Dog No. 128, 43.47 per cent. After obstruction, from 
Dog No. 30 was recovered 27.19 per cent. of a theoretical 
total; from Dog No. 124, 19.29 per cent. and from Dog No. 128, 
18.05 per cent. Somewhat less than one half the camphor given 
during the normal period was recovered in the urine as camphor- 
glucuronic acid. What becomes of the balance is a matter of 
conjecture. The results obtained by Schlutz (5) in an earlier 
study differ from the above but this can probably be accounted for 
by the inferiority and uncertainty of the polarimetric method. 
This was at the time considered the method of choice. 

The histological examination of the livers, hearts, spleens and 
kidneys of the animals cited in this report was negative except for 
a moderate capillary dilatation in a few of the sections. The 
nitrogen metabolism remained unchanged in Nos. 30 and 124. 
It was not determined in No. 128. 

The above results from their uniformity suggest accuracy for 
the method so far as it goes and the marked decrease after opera- 
tion implies possible diminution of certain liver functions after 
duodenal obstruction. 


30 SCIENTIFIC PROCEEDINGS (46). 


BIBLIOGRAPHY. 
. Posy, J. Arch. f. Exp: Pathol., <I, p.07- 
. TOLLENS, C. Zeitschrift f. Physiol. Chemie, LXI, p. 95. 
. TOLLENS, C. Zeitschrift f. Physiol. Chemie, LXIV, p. 39. 
. Draper, J. W. Jour. A. M. A., Vol. LVII, 1911, pp. 1338-1343. 
. SCHLUTZ, F. W. Zeitschrift f. Kinderheilkunde, Band I, Heft II, p. 197, 1910. 


nb WN 


II (630) 


The convulsant effect of the removal of the heart upon frogs 
which had injections of morphin. A demonstration. 


By T. 8. GITHENS and S. J. MELTZER. 


[From the Department of Physiology and Pharmacology of the 
Rockefeller Institute.| 


Last April it was reported from this laboratory that (1) sub- 
stances which are capable of causing a definite biological reaction 
in frogs cause the characteristic reaction also when injected after 
the removal of the heart, and (2) that some substances, like 
morphin and acid fuchsin, appear to be even more effective in 
cardiectomized than in normal frogs. The first phenomenon was 
explained by the theory that distribution in frogs deprived of the 
cardio-vascular circulation is accomplished by a peripheral mechan- 
ism, namely, by the tissue spaces, which present a connected 
system throughout the body. The second phenomenon was in- 
terpreted by the hypothesis that the fresh blood in the cardio- 
vascular mechanism continually antagonizes the convulsant action 
of such substances as morphin and acid fuchsin. The study of the 
last mentioned hypothesis and the underlying phenomenon has 
been hampered by the fact that the distribution by the peripherai 
mechanism is necessarily a slow one and since, at the warmer 
seasons, frogs survive cardiectomy only a short time, it happens 
that the animals die before the convulsant effect could make its 
appearance. We have therefore tried to study the hypothesis by 
the reversed method, that is, morphin injected first and the heart 
removed later. This was carried out in several series, the doses 
varying from 0.1 to 0.5 mg. of morphin per gram frog, and the 
intervals between the injection and the subsequent removal of the 
heart varying from a few minutes to 4 hours. We shall not enter 


CoNvuLSANT EFFECT OF REMOVAL OF HEART. a1 


upon details: we shall merely state that the result was strikingly 
positive. While the morphin frogs, which were kept with hearts 
intact, remained normal, all the frogs which received proper doses 
of morphin and had their hearts removed at different intervals, 
developed tetanic convulsions, which in many cases had to be char- 
acterized as very violent. With doses of 0.25 mg. per gram frog, con- 
vulsions developed in practically every case, no matter how soon 
or how late the heart was removed. After intervals of 60 minutes 
and longer the result was positive practically with every dose 
between 0.2 and 0.5 mg. per gram frog. (The essential points 
were demonstrated before the Society.) 


12 (631) 
Intravascular foreign bodies. 


By C. C. GUTHRIE and A. H. RYAN. 


[From the Laboratory of Physiology and Pharmacology, 
University of Pittsburgh.] 


Experiments were performed by introducing sterilized (1) 
untreated, (2) oiled silk, and (3) human hair into arteries and 
veins and observing the results. Twelve common carotid arteries 
and twelve external jugular veins were employed. The number 
of silk strands varied from the smallest single strands used in 
blood vessel suture to twenty-four such strands. Where a 
number were used they were threaded into suitably large needles 
and were not twisted. Cambric needles were used. 

The experiments were performed by exposing the vessels of 
anesthetized dogs, transversely piercing the vessel with the 
needle as near the mid-line as possible, drawing the ligatures 
through and loosely tying the free ends together. Three weeks 
later specimens were taken and examined. 

In no instance was there occlusion of the lumen nor was 
there any evidence to indicate that the vessels would have sub- 
sequently become occluded through thrombus formation. In 
general the ligatures were found dividing the lumen and coated 
with a substance closely resembling the intima in gross appear- 
ance. 


32 SCIENTIFIC PROCEEDINGS (46). 


In the case of one artery and one vein, an ordinary occluding 
ligature was first tied about the vessel, after which a transverse 
suture was introduced about one centimeter on each side of the 
ligature. The results in these cases did not materially differ 
from those observed on the non-occluded vessels. No marked 
differences were observed with different kinds or sizes of sutures. 

Microscopical results, particularly as regards the character 
of the deposit on the foreign surfaces and the presence or absence 
of intimal covering, will be reported later. 


13 (632) 
On tumor-immunity in rats (with demonstrations). 


By RICHARD WEIL. 


[From the Department of Experimental Therapeutics, Cornell 
University Medical School, New York City.] 


It is the intention of the present paper to summarize briefly 
experiments bearing on the problem of the acquired immunity 
of rats to the implantation of tumors. In rats, as indeed in 
practically all the other species of animals in which similar exper- 
iments have been practicable, it has been found that the absorp- 
tion of an implanted tumor is succeeded by a period during which 
the animal is refractory to further implantations. The same 
refractory condition can be induced by the injection of tumor 
autolysates (Levin), or by the injection of suspensions of normal 
tissue, or even of blood. The relative specificity and effective- 
ness of these procedures vary in their details; the underlying 
principle has been thought to be the same throughout. 

In a series of experiments with the Flexner-Jobling rat tumor, 
I have observed certain phenomena which seem in a measure 
to support the belief that the mechanism of immunity to the 
tumor is identical in its biological manifestations with that found 
in infectious disease, and is therefore mediated by immune sub- 
stances carried by the serum. These observations may be 
summarized as follows: 

1. Inoculation of the Flexner-Jobling adeno-carcinoma into 
normals rats is not followed by any macroscopic evidence of 


On Tumor Immunity In Rats. 33 


inflammation or reaction, if the grafts are made from a small, 
non-necrotic tumor. 

2. Rats specifically immunized to the Flexner-Jobling adeno- 
carcinoma respond to an implantation by an intense local in- 
flammatory reaction, often with necrosis. 

3. Animals bearing necrotic tumors present this reaction on 
reinoculation. 

4. After removal of the necrotic tumor, the animal still reacts 
to reimplantation by local inflammation. 

These phenomena seem analogous to those instances of local 
anaphylaxis known as the “ Arthus’’ phenomenon in rabbits, and 
to the local allergetic reactions described in human beings by 
Pirquet. Until the possibility of a reaction to a complicating 
infection of the tumor can be excluded (as suggested by Apolant 
of Yamanouchi’s experiments), this interpretation must be con- 
sidered provisional. 

In the sarcomata of rats, it has not been possible to elicit 
these phenomena. 


SCIENTIFIC PROCEEDINGS. 


ABSTRACTS OF THE COMMUNICATIONS. 
Forty seventh meeting. 


The Laboratory of Natural History, College of the City of New York. 
February 21, 1912. President Morgan in the chair. 


24 (633) 
The fermentation of carbohydrates and other organic media 
by streptococci. 
By C. E. A. WINSLOW. 


[From the Department of Public Health, American Museum of 
Natural History, New York.| 


The study of the fermentative powers of the streptococci has 
been carried out in England by merely noting the change of 
color in litmus media. In this country, Palmer and the writer, 
Broadhurst and Hilliard have used the more exact methods of 
titrating inoculated tubes and uninoculated controls, using 
phenolphthalein as an indicator and plotting the quantitative 
results obtained. The line of demarcation between fermenting 
and non-fermenting forms is drawn at the intermodal point 
between the peaks of the curve. A comparison of several hun- 
dred results obtained by English and American methods shows 
that the English method gives a uniformly higher proportion 
of fermenters, suggesting that a number of strains producing a 
very slight amount of acid and properly classed as non-fermenters, 
are recorded as positive by the English method. 

A study of the correlations between action on different organic 
media shows that those substances tested may be arranged in a 
definite order of availability, such that a positive reaction in one 
medium usually implies that all those earlier in the series will be 
fermented, while failure to act on a given substance almost always 
implies that substances later in the series will not be fermented 
either. Among the streptococci dextrose comes first in order of 
availability, then the disaccharides, lactose and saccharose, and 
the glucoside, salicin (which easily yields a simple sugar). The 

35 


36 SCIENTIFIC PROCEEDINGS (47). 


starch-like body inulin and the alcohol mannit come next and 
the trisaccharide raffinose is least available of all. This order 
corresponds to the size of the molecule, whereas in the B. coli 
group, the configuration of the molecule is the main thing, the 
aldehydic sugars being acted upon very readily, and the ketonic 
sugars less readily. The bacillus of the colon group which can 
utilize the ketonic disaccharide can almost always utilize the 
ketonic trisaccharide raffinose as well. 


25 (634) 
The comparative resistance of spores and vegetative cells of 
bacteria towards calcium hypochlorite. 
By C. M. HILLIARD. 


[From the College of the City of New York.] 


At least three distinct grades of resistance to the disinfectant 
action of calcium hypochlorite may be recognized among the 
bacteria. They are respectively ordinary vegetative cells, acid- 
fast organisms, having a fatty composition, and the true spore 
cells. The present study is concerned only with the vegetative 
cell and the spore. Subsequent work will be done with the 
tubercle bacillus as representing the acid-fast group. 

Pure cultures of B. coli, B. prodigiosus, B. subtilis (spore 
former) and B. anthracis (spore former) were grown in broth for a 
time sufficient for spores to appear in large numbers in the two 
latter cultures. A few drops were then transferred to dilution 
bottles, the initial number present was determined, and the 
calcium hypochlorite of known strength was added in carefully 
weighed amount. Agar plates were made at intervals and 
the reduction determined. 

The results of the work to date may be summarized as follows: 

1. The sterilizing action of calcium hypochlorite in water is 
very rapid at first, the maximum reduction being nearly complete 
in three hours. 

2. Of the organisms studied, B. subtilis is most resistant, 
followed by B. anthracis, and then by the non-spore formers, 
B. coli and B. prodigiosus. 

3. At least 1.5 parts of available chlorin to 1,000,000 parts 


GRAFTED AND MULTIPLE EMBRYOS. 37 


of water is necessary to get 99 per cent. reduction with a spore 
former in six hours, while 0.5 part to 1,000,000 is sufficient 
for this degree of reduction with non-spore formers. 

4. Sixteen parts of available chlorin per million of water does 
not effect complete killing of B. subtilis; 1.5 parts brings about com- 
plete sterilization with B. coli and B. prodigiosus. 


26 (635) 
Studies on barium feeding. 
By C. L. ALSBERG and O. F. BLACK. 


[From the Office of Drug Plant, Poisonous Plant, Physiological 
and Fermentation Investigations, Bureau of Plant Industry, 
Department of Agriculture, Washington, D. C.| 

Half-grown rats fed for some months on a mixed diet to which 
BaSO, was added remained in good health and did not store up 
measurable traces of barium in their tissues. However, when 
instead of a mixed diet one poor in calcium was fed, other condi- 
tions being the same, a few milligrams of barium were stored 
in the tissue of each animal. It is therefore evident that under 
special conditions even very insoluble substances may be absorbed 
to some extent. 

27 (636) 
The production of grafted and multiple embryos. 
By A. J. GOLDFARB. 
[From the College of the City of New York.| 

After removing the fertilization membranes of sea urchin 
eggs (Arbacea) and allowing them to develop to the desired stage, 
the eggs were placed in an alkaline (NaOH) sea water and centri- 
fuged in narrow bore tubes. In this way large numbers of eggs 
were agglutinated, and developed into double, triple, etc., blas- 
tule, gastrule and plutei. In ten to forty per cent. the eggs and 
blastomeres were more or less completely fused, forming giant 
blastule, composed of three, four or more eggs. 

In the first group parallel development took place, resulting 
in double, triple, etc., embryos, many of which were subsequently 
separated by the antagonistic sweep of the cilia. In the second 
group, the eggs were more intimately united to form a common 


38 SCIENTIFIC PROCEEDINGS (47). 


blastoccele, common gut, or common body, within which the 
independent organs may or may not unite. When the embryos 
fuse slowly the contained organs appear to be antagonistic, for 
one is often absorbed completely, or the interaction results in a 
united but very atypic gut, skeleton, body, etc. The details of 
these changes are exceedingly interesting, but can be given only 
in the fuller publication. 
28 (637) 
The production of typical monstrosities by various means. 
By A. J. GOLDFARB. 


[From the College of the City of New York.] 


Typical abnormalities have been produced by subjecting de- 
veloping eggs to the action of certain salts, such as lithium chloride, 
and the implication, if not the conclusion has been made that a 
certain specificity obtained between these salts and the resulting 
abnormality. Herbst for example produced definite atypic gas- 
trule, by subjecting sea urchin eggs to lithium chloride in sea 
water. Stockard produced definite atypic conditions of the eye 
and brain formation in Fundulus. 

That the same results may be obtained in other ways seems to 
demonstrate that the extra-gastrulate condition of the sea urchin, 
for example, is due not so much to any specific action of the 
lithium chloride, as to a factor common to each of the following. 
Extra-gastrulate embryos were produced in fairly large numbers 
by such anesthetics as chlorotone and alcohol, by changing the 
concentration of the sea water in opposite directions, either by 
dilution or by concentration of the sea water, by the action of 
carbon dioxide and lastly various sugar solutions. 

Similarly other well-defined atypic blastule, gastrule or plutei, 
though not always produced by each of these solutions, were 
found in many of them, thus giving color to the view that a 
disturbance once set up results in a typical reaction conditioned 
not so much by the nature of the disturbance as by the mechanism 
(the egg) involved. 


PERCENTAGE OF WATER IN THE BRAIN OF THE DOG-FISH. 39 


29 (638) 
The percentage of water in the brain of the dog-fish. 
By G. G. SCOTT. 


[From the Department of Physiology, Columbia Unvwersity, and 
Biological Laboratory of the U. S. Bureau of Fisheries, 
Woods Hole, Mass.] 


Donaldson (’10) has shown that in the albino rat between 
birth and maturity the percentage of water in the brain diminishes 
from 87.8 per cent. to 77.5 per cent. He calls attention to the 
fact that the human brain at birth contains a greater percentage 
of water than at maturity and from the investigations of Koch 
and Weisbach he obtains as the percentage of water in the human 
encephalon to be: Birth 88.3 per cent.; 2 yrs. 81.1 per cent.; 5 
yrs. 79.2 per cent.; 25 yrs. 77.0 per cent. He concludes that 
probably in all mammals we will find the same range in percentage 
of water, that the loss in water occurs in the same manner but that 
the time required for each successive step is determined by the 
intensity of the growth process characteristic of each period. The 
present writer determined the percentage of water of the brains 
of 17 spiny dog-fish (Squalus acanthias) and 97 smooth dog-fish 
(Mustelus canis). The smooth dog-fish ranged in size from very 
small tolarge. There is no such reduction in the percentage of water 
as found by Donaldson and others in the case of the mammalian 
brain. The average percentage of water in all the Mustelus brains 
examined was 78.5 per cent. There was very little difference 
between this and that obtained for the very young or the old. 
There is an indication of a slight fall of about 2-3 per cent. between 
birth and maturity. The great reduction (7. e., about 7 per cent.) 
occurs in mammals during the period when the central nervous 
system is growing most rapidly. Both the rat and man during 
this short post-birth period pass from a helpless state to one of 
activity. The rat is born helpless and blind, etc. The dog-fish 
is an active free-swimming organism at birth. The present writer 
would conclude then that the differences in reduction of water in 
the two cases is that the nervous (and body) changes which occur 
in the mammal are post-embryonic and extra-utero. Inthe dog- 
fish they take place in utero. Determinations from brains of late 
embryonic stages can only settle this hypothesis. 


40 SCIENTIFIC PROCEEDINGS (47). 


30 (639) 
The advantage for certain experiments zz vitro of suspending 
trypanosomes in serum. 


By B. T. TERRY. 


[From the Laboratories of the Rockefeller Institute for Medical 
Research, New York, and from the George Speyer House, 
Frankfort a/M, Germany.] 

The amount of trypanocidal substance contained in a given 
solution is sometimes estimated in vitro by determining the degree 
to which the solution may be diluted before it ceases to immobilize 
the parasites. 

For want of a better diluent, trypanosomes have usually been 
suspended in physiological salt solution (with or without the addi- 
tion of citrate), although salt solution not infrequently immobilized 
the parasites in 30 to 60 minutes. 

In I910, the writer made observations which caused him to 
substitute serum for the salt solution he had previously employed 
in suspending T. brucei. Serum (when not bound by the medica- 
ment under investigation) had the following advantages: 

1. The motility of the control parasites was greatly prolonged. 
This enabled the observations to be continued over a longer time. 

2. The motility of the control parasites was accelerated. This 
enhanced the delicacy of the tests im vitro by rendering more 
striking the contrast between the poisoned and the non-poisoned 
trypanosomes. 

It was found, moreover, that poisons not infrequently im- 
mobilized more quickly trypanosomes suspended in serum than 
they did those suspended in salt solution. This also seemed to 
give serum a slight advantage over salt solution as a medium in 
which to suspend trypanosomes. 

Rabbit, ox, horse, goat, sheep, pig, chicken, rat, and mouse 
sera were tested and were found to be efficient in prolonging the 
motility of trypanosomes. 

It soon became easy to keep on hand a large supply of serum, 
for experiment showed that cattle serum, filtered through a Berke- 
feld filter, bottled aseptically, and preserved in the ice-box, retained 
its activity for many months. 


THE ACTION OF ATOXYL, AI 


That the motility of trypanosomes is preserved longer in serum 
than in salt solution was noted years ago and has recently been 
emphasized by Schern,! but the writer is not aware that anyone 
has previously recommended suspending trypanosomes in serum 
for experiments 7” vitro. 

31 (640) 
The action of atoxyl. 
By B. T. TERRY. 


[From the Laboratories of the Rockefeller Institute for Medical 
Research, New York. 


The action of atoxyl is paradoxical. Jn vivo it is effective 
against certain parasites, 7m vitro it has little or no action. Ehrlich 
believes that the medicament must be reduced in the body before 
it becomes active. This view has been strengthened by Levaditi 
and Yamanouchi who have shown that emulsions of liver, muscle, 
and lung, when incubated with atoxyl, transform this medicament 
into a toxic substance. Levaditi apparently believes that the 
transforming agent is in the liver and other organs, while Yaman- 
ouchi concludes that it is in the red blood cells only. My results 
confirm much of the experimental work of Levaditi and Yaman- 
ouchi, but lead to a conclusion that, in its entirety, is apparently 
held by neither of these investigators. 

In my experiments, both liver and blood when incubated with 
atoxyl (10 per cent.) at 37 degrees for 3 hours, transformed this 
medicament into a toxic substance. 

The transforming agent in liver had characteristics, however, 
which in some respects were quite different from those of the 
active agent in blood. 

The active agent in liver was soluble in salt solution, was filter- 
able through collodium, and was quite resistant. Liver emulsion 
ground with sand in a mortar, or heated to 100 degrees for 10 m., 
lost little or none of its activity. The addition of blood to liver 
emulsion before incubation with atoxyl increased its activity, but 
liver emulsion washed thoroughly to free it of red blood corpuscles 
was inactive, probably because of the solubility of the transforming 
agent. 

From the blood the active agent was apparently not extract- 


1“ Arbeiten aus dem kaiserlichen Gesundheitsamte,”’ Berlin, 1911, xxxviii, 338. 


42 SCIENTIFIC PROCEEDINGS (47). 


able by salt solution. Moreover, it was very easily destroyed, 
soon losing all or nearly all of its activity if the blood was 
laked (e. g., by the addition of distilled water or saponin, by 
prolonged shaking at 37 degrees, or by grinding in a mortar with 
sand and salt solution, or with sand and serum). It was almost 
completely destroyed by heating to 100 degrees for 10 minutes. 

Conclusion.—Atoxyl is probably transformed into a trypano- 
cidal substance in the living body both by the blood and by the 
liver (other organs were not tested). In tests in vitro the trans- 
forming agent in liver may be readily distinguished from the 
active agent in blood. 

32 (641) 
Parturient paresis and eclampsia. Similarities between these 
two diseases. 


By DANIEL J. HEALY and JOSEPH H. KASTLE. 


[From the Laboratory of the Kentucky Agricultural Experiment 
Station.| 


In June, 1907, the attention of one of us (Healy) was called by 
Dr. M. A. Scovell, Director of the Kentucky Agricultural Experi- 
ment Station, to parturient paresis in the dairy cow. Dr. Scovell’s 
intention was to have, if possible, the etiology cleared up. 

It proved impossible to take up the problem until one year 
ago, and as our studies progressed, the similarity between par- 
turient paresis and eclampsia became more and more evident. 
They are both intoxications which occur suddenly just before, 
during or immediately after labor. They are characterized by the 
same clinical features, namely, suddenness of onset, loss of con- 
sciousness, coma and similar febrile conditions. In both, the 
urinalyses are the most important clinical features, and the 
urinalyses in these two conditions are similar, namely, a dis- 
turbance of the nitrogen distribution among the compounds con- 
taining nitrogen, an increase of the ammonia excreted, the presence 
of albumen, and microscopically the presence of hyaline, granular 
and epithelial casts and blood cells. 

The finer pathological changes occurring in parturient paresis 
have not been established, and as none of our cases died, we have 
not had the opportunity of studying these changes. However, we 


PARTURIENT PARESIS AND ECLAMPSIA. 43 


have had ample opportunity to study the finer pathological changes 
in three guinea pigs which died in five, six and seven days under 
the influence of the toxin of parturient paresis. We have also 
observed these changes in another guinea pig, which received a 
smaller dose of the toxin, the dose not being sufficient to cause 
death in ten days and therefore he was chloroformed. The patho- 
logical findings in these guinea pigs correspond in every way to 
the characteristic lesions of eclampsia, namely, there was hemor- 
rhagic necrosis of the liver, acute parenchymatous nephritis with 
interstitial hemorrhages, degeneration of the cells of the adrenal 
cortex, with interstitial hemorrhages, and destruction of the 
medullary portion. These experiments were fully controlled in 
every detail by means of guinea pigs injected with normal salt 
solution, fresh milk, fresh normal colostrum and fresh, normal, 
cow’s urine. The control pigs all remaining alive and well at the 
present time, with the exception of the normal urine pig, which 
was chloroformed at the end of seven days and on post mortem 
found normal. 

The modern treatment of parturient paresis is most remarkable 
in its result. The mortality has been reduced from 60 per cent. 
to less than I per cent. It was introduced by J. Schmidt, of 
Kolding, Denmark, and was based upon the theory that the disease 
was due to bacterial invasion of the udder. The treatment con- 
sists of acute dilatation of the udder by means of oxygen or 
sterile air. 

That the disease is due to a toxin elaborated in the udder as 
the result of its own metabolism preceding normal milk production, 
there can be no reasonable doubt, and that the success of the 
modern treatment is due to preventing, by means of pressure, the 
absorption of this toxin, seems most highly probable. 

We are of the opinion that eclampsia is due to a similar toxin, 
elaborated by the breast in a similar manner, and would strongly 
recommend, as the most promising treatment, dilatation of the 
breasts with oxygen or sterile air, or forcible compression of them 
by means of a properly applied bandage, after they have been 
emptied by means of the breast pump, and at the same time using 
whatever medical measures may be indicated. 

We, ourselves, shall thoroughly test this method of treatment 
as soon as the opportunity occurs. 


44 SCIENTIFIC PROCEEDINGS (47). 


33 (642) 
The toxic character of the colostrum in parturient paresis. 
By JOSEPH H. KASTLE and DANIEL J. HEALY. 


[From the Laboratory of the Kentucky Agricultural Experiment 
Station.] 


Parturient paresis is preéminently a disease of plethoric heavy 
milking breeds of cows, and of those individuals which give the 
greatest yield of milk. Among the prime and immediate causes 
of the disease are parturition, a permanent or transient plethoric 
condition of the blood vessels, with corresponding increase of 
pressure on the nerve centers of the brain. The phenomenal 
trophic and secreting activity of the udder of the heavy milker 
and intense physiological activity of the mammary glands resulting 
in the sudden rise and absorption into the circulation of leuco- 
maines or toxic alkaloids of the cells of the mammz. These ac- 
cording to Law! are the principal causes operating to bring on an 
attack of this disease. In the present state of our knowledge it is 
of little moment whether we call the substances, other than milk, 
resulting from the sudden disintegrative changes in the udder at 
or about the time of parturition, leucomaines, alkaloids, toxins, 
or what not. It seems reasonably certain, however, that there is 
no gland of the size and physiological activity of the udder of a 
heavy milking cow, but what must contribute very largely and 
sometimes malignantly to the internal secretions of the animal. 

The question, therefore, immediately before us in the study of 
parturient paresis and of eclampsia in the woman is to determine 
experimentally whether the udder and the breast, respectively, do 
under these acutely toxic conditions actually secrete poisonous 
substances, which if not quickly eliminated or prevented from 
entering the circulation might be held responsible for these 
diseases. 

It therefore occurred to one of us, Kastle,? to test the conduct 

1“‘Text-book of Veterinary Medicine,” 2d ed. (1905), Vol. 3, pp. 301-317 
Ithaca, N. Y. 

2On the day after our three papers on parturient paresis and eclampsia were 
mailed to the editor of the Journal of Infectious Diseases, Chicago, viz., on February 


13, 1912, Dr. Surface called our attention to an abstract by Helfer of a paper by 
Hoyois in the Berliner Tierarztliche Wochenschrift, October 5, 1911, No. 40, pp. 727- 


CHARACTER OF COLOSTRUM IN PARTURIENT PARESIS. 45 


of the first fresh colostrum of the cow obtained during an attack 
of parturient paresis, upon the lower animals. We have not yet 
been able to obtain a case of eclampsia. Accordingly eighteen 
experiments have been carried out on guinea pigs. These experi- 
ments have included a few other substances besides the first 
colostrum of a cow suffering from parturient paresis, by way of 
comparison, and these of course serve as controls on our other 
results. Up to the present, therefore, the following substances 
have been tested on the guinea pig, and in all instances were given 
intraperitoneally, by hypodermic injection, using 10 c.c. or in 
some cases less, viz., the first, fresh colostrum of the normal cow, 
fresh milk from a high-class dairy herd, the first urine of a cow 
suffering from parturient paresis, the urine of a healthy cow, 
normal salt solution, and aqueous solutions of the residue from 
colostrum and milk left after precipitating the same with dilute 
acetic acid and finally the first, fresh colostrum of a cow, obtained 
during an attack of parturient paresis. Briefly the following 
results have been obtained. 

The normal salt solution, the urine of the healthy cow, and the 
fresh milk from the healthy herd produce no bad effects when 
injected intraperitoneally into guinea pigs. The first fresh colos- 
trum of the normal cow produced diarrhea in the guinea pigs from 
which they speedily recovered and these pigs are now alive and 
well. The dried residue obtained by evaporating the filtrates from 
normal colostrum after precipitating with dilute acetic acid and 
neutralizing produced no effect. 

Three female guinea pigs received 10 c.c. each, of the first, 
fresh colostrum of a cow in an attack of parturient paresis. (1) 
The whole colostrum, (2) skimmed colostrum, (3) colostrum 
cream. Pig 1 had no diarrhea, but died on the sixth day. On 
post-mortem this pig showed acute parenchymatous nephritis 
with interstitial hemorrhages, acute parenchymatous hepatitis 
with interstitial hemorrhages, acute degeneration of the cells of 
the adrenal cortex with complete destruction of the medullary 
728, the original of which appeared in the Annales de Med. Vet. de Bruxelles, July, 
Aug., Sept., 1910, in which according to Hoyois the colostrum in cases of parturient 
paresis, on intraperitoneal injection in doses of 10 to 20 grams, caused paralyzing 


symptoms in rabbits and guinea pigs, with subsequent death at the end of seven to 
twelve days. 


46 SCIENTIFIC PROCEEDINGS (47). 


cells, and interstitial hemorrhages. No evidence of tuberculosis. 
Cultures from the liver, kidney and spleen showed no micro- 
organisms. No peritonitis. The pig was not pregnant. 

Pig 2 seemed well after the injection; had no diarrhea. Died 
at the end of five days. On post-mortem showed acute paren- 
chymatous nephritis, with interstitial hemorrhage, acute paren- 
chymatous hepatitis, with interstitial hemorrhage, and marked 
peripheral necrosis. Acute degeneration of the cells of the adrenal 
cortex, with complete destruction of the medullary cells and inter- 
stitial hemorrhages. No evidence of tuberculosis. The pig 
was in the very early stages of pregnancy. Cultures from the 
liver, spleen and kidneys negative. No peritonitis. 

Pig 3 seemed well after injection and had nodiarrhea. Aborted 
during first twelve hours after injection, fetus five and five tenths 
cm.in length. Died in six days. The post-mortem showed acute 
parenchymatous nephritis, with interstitial hemorrahges; acute 
parenchymatous hepatitis, with areas of complete necrosis and 
interstitial hemorrhages. Some degeneration of the cells of the 
adrenal cortex with complete destruction of the medullary portion, 
and interstitial hemorrhages. Acute lobar pneumonia of the left 
lung. No tuberculosis. Pig no longer pregnant. Cultures from 
the liver, kidney and spleen negative. Cultures from the pneu- 
monic lung contained a diplococcus. No peritonitis except over 
upper and anterior surfaces of the liver. 

A healthy male guinea pig received Io c.c. of the first, fresh, 
clear urine of a cow ill with parturient paresis. This pig showed 
no discomfort and no diarrhea. It developed a very marked 
diuresis however, passing at least 200 c.c. of urine in 24 hours. 
This urine contained a small amount of albumin and no sugar. 
This pig recovered from the diuresis and seemed well, and was 
chloroformed on the 13th day. On post-mortem this pig showed 
parenchymatous nephritis with some interstitial hemorrhage, a 
rather extensive necrosis of the liver cells, but without hemorrhage, 
and also localized areas of necrosis in the adrenals. 

It is evident from these results that normal salt solution, fresh 
milk, and the urine of a healthy cow cause no disturbances in 
healthy guinea pigs. The colostrum of the normal cow invariably 
produced a diarrhea when injected into the peritoneal cavity of 


CHARACTER OF COLOSTRUM IN PARTURIENT PARESIS. 47 


healthy guinea pigs. In this connection it is of interest to note 
that it has long been known that human colostrum acts as a mild 
cathartic on the suckling (Williams, ‘‘ Obstetrics,’’ 1908, 351-352). 
Otherwise no bad effects followed the administration of the normal 
colostrum of the cow to healthy guinea pigs. It will be seen from 
our results that death invariably resulted in guinea pigs from the 
intraperitoneal injection of the first, fresh colostrum of a cow in an 
attack of parturient paresis, and that the post-mortem examination 
of the organs of pigs that had died from this cause showed the 
same pathologic degenerations and changes that are shown by 
the organs of women who have died of eclampsia. Unfortunately 
but little is known regarding the micropathology of the cow in 
parturient paresis. We have shown, however, that cows recover- 
ing from an attack of this disease invariably show a nephritis 
which may, as the result of repeated attacks, become chronic. 

Our results with the colostrum of a cow suffering from par- 
turient paresis certainly go to show the presence therein of some 
substance or substances toxic to guinea pigs, and certainly point 
to the udder and the mammary glands as the place of origin of the 
toxins or internal secretions producing parturient paresis and 
eclampsia respectively. The fact that the urine of the cow with 
parturient paresis causes such a profound diuresis in the guinea 
pig, points to the presence of toxic substances even in the urine 
of animals so affected. A conclusion which is sustained by the 
results of the post-mortem examination on this particular case. 
We hope in the near future to attempt the isolation of the par- 
ticular substance or substances in the colostrum or the udder, 
responsible for parturient paresis or at any rate, its more careful 
study and nearer identification. We would, therefore, reserve the 
right to continue these investigations along the lines indicated 
above with the object of throwing further light on the nature of 
the toxine contained in the colostrum of cows suffering from 
parturient paresis and also the possible occurrence of such a 
toxine in the colostrum of women suffering from eclampsia, and 
with the still further object of arriving, if possible, at the precise 
conditions under which these toxins are elaborated in the udder 
and mammary glands. 


48 SCIENTIFIC PROCEEDINGS (47). 


34 (643) 
The internal secretion of the mamme as a factor in the onset 
of labor. 


By DANIEL J. HEALY and JOSEPH H. KASTLE. 


[From the Laboratory of the Kentucky Agricultural Experiment 
Station.| 


The importance of the internal secretions has come to be well 
recognized in modern physiology and medicine. Among other 
interesting observations in this field may be mentioned the fact 
that Miss Lane-Claypon and Starling (Proc. Roy. Soc., 1906, 
B. 505) have shown that the stimulus to the hypertrophy and 
lacteal activity of the mammary glands, in pregnant animals, 
comes not from the ovaries, or the placenta or the uterus, but 
from the fetus itself. In connection with our studies on the toxic 
nature of the colostrum of the cow, ill with parturient paresis, we 
have succeeded in showing that the colostrum both of the normal 
cow and that of the cow ill with parturient paresis contain a sub- 
stance, or substances, which have the power to bring on abortion 
in pregnant guinea pigs; and that neither normal salt solution 
(0.85 per cent. NaCl) nor the fresh milk of a healthy dairy herd 
have the power to bring on premature labor. It has also been 
shown that boiling for a short time does not destroy the power of 
the normal colostrum of the cow to accomplish premature labor 
in pregnant guinea pigs. 

In this abstract of our paper on this subject we have only space 
for the details of one experiment, which are as follows: 

Experiment 15.—A healthy guinea pig in the 5th to the 7th 
week of pregnancy received by intraperitoneal injection 10 c.c. of 
sterile, normal salt solution (0.85 per cent. NaCl). The injection 
caused no discomfort and at the end of five days she had not 
aborted. She then received by intraperitoneal injection I0 c.c. 
of fresh milk, from a healthy dairy herd. This was heated to 
38° C. before the injection. The pig showed no discomfort and 
had not aborted at the end of four days. She then received, by 
intraperitoneal injection, 8 c.c. of the first, fresh, whole colostrum 
of a normal cow (second calf). This colostrum was heated to 
38° C. before the injection. Following this last injection this 


INTERNAL SECRETION OF MAMMZ. 49 


pig aborted in 60 hours, giving premature birth to two fetuses, 
each 6.5 cm. in length, and 60 hours after this she aborted a 
second time, giving premature birth to one fetus 7 cm. long. 

It is evident from these results that the colostrum of the normal 
cow contains a substance, or substances, capable of causing a 
premature onset of labor in pregnant guinea pigs. This substance 
is also present in the colostrum of cows ill with parturient paresis. 
It resists boiling and is probably of the nature of a hormone. Our 
results bring to light a new and hitherto unrecognized correlation 
between the mammary glands and the uterus. According to 
Lane-Claypon and Starling the fetus through its internal secre- 
tions stimulates the hypertrophy and lacteal activity of the mam- 
mary gland. It is evident from our experiments that the internal 
secretions of the mammary gland stimulate the pregnant female 
to labor and the birth of the offspring. 


35 (644) 
Some vaso-reacting substances in blood serum. 
By J. P. ATKINSON and C. B. FITZPATRICK. 
[From the Department of Health Laboratories, New York City.] 


These observations supplement our previous articles on serum 
digestive processes. All the reactions were obtained by the 
kymograph, the pressure in the carotid of the normal dog being 
recorded with a mercury manometer. The injections were made 
into the femoral vein. The normal sera (horse and rabbit) give 
a slight rise, whether freshly drawn or after standing for some 
weeks as far as we have observed. 

The whole serum of a horse which had been injected with 800 
c.c. of strong diphtheria toxin gave no reaction with the serum 
drawn the first three days after the injection. The serum of the 
4th, 5th, and 6th day each gave depressions, when given in 8 c.c. 
volumes. 

Another series of sera from the same horse, bled 6 weeks later 
gave well-marked depressions, with the sera drawn on the 3d, 4th; 
5th, 6th, 7th, 8th and oth day after the toxin injection. 

Several specimens of refined antidiphtheria sera, some of which 
had given rise to rashes in humans, gave well-marked depressions, 


50 SCIENTIFIC PROCEEDINGS (47). 


These depressions are not caused by the injection of minute quan- 
tities of ammonium sulphate per se. A recent, whole, anti- 
pneumococcus serum, which produced rashes in humans, gave in 
a young dog well-marked depressions and after the total injection 
of 35 c.c. given in 7 c.c. volumes, there was a rise, 13 minutes after 
which the dog died. This depressor substance practically dis- 
appeared after four days standing in the ice-box. 

We have noticed a similar rise after the injection of numerous 
6 c.c. doses of beef extracts, each of which had produced marked 
depressions; we have however been unable to kill a dog with these 
injections. These observations would seem to indicate that the 
amount of depression per se within moderate limitations is not 
so important as the recoil or loss of recoil. 

Three c.c. of nutrient peptone broth gave no depression. The 
blood sera of a rabbit, which had 5 days previously been injected 
with nutrient peptone broth gave splendid depressions in 6 c.c. 
volumes. 

The blood sera of rabbits, which had been 5 days previously 
injected with heated, sterilized, cultures of the typhoid bacillus, 
pneumococcus, and streptococcus, gave remarkable depressions 
in 4 c.c. volumes. 

The injection of 21% c.c. of the serum of a rabbit which died 
4% hours after having received 1,000 m.1.d. of tetanus toxin intra- 
venously, gave a decided depression. 

The injection of 214 c.c. of the serum of a rabbit which had 3 
hours previously received 1,000 m.].d. of diphtheria toxin, intra- 
venously, gave a depression. The depressor substance of both 
of these sera practically disappeared, after standing 6 days in 
the ice-box. 

Adrenalin chloride prevents the depression caused by the 
tetanus depressor serum. 

Twelve m.|.d. and 15 m.1.d. of diphtheria toxin gave no reaction 
when injected into the dog intravenously, 3 c.c. of broth containing 
210 m.|.d. of diphtheria toxin gave a well-marked depression when 
injected intravenously into a dog which had been sensitized 24 
hours previously with 100 m.1.d. of diphtheria toxin. 

The blood serum of rabbits injected with 3 m.|.d. of diphtheria 
and tetanus toxins, drawn 4 days after the injections, gave marked 
depressions. 


Some Vaso—REacTING SUBSTANCES IN BLoop SERUM. 51 


Contaminated sera cause depressions. 

An antimeningococcus serum, which had produced rashes in 
humans caused well-marked depressions in 614 c.c. doses. 

Serum of a diphtheria antitoxin horse, which was recovering 
from an attack of indigestion gave a slight depression. This serum 
was secured through the courtesy of Dr. Banzhaf. 

These observations have extended over a period of 214 years. 

Note.—We have already reported depressions from the injec- 
tion of the sera of tuberculous rabbits and from the injection of 
tuberculins as well as from the injection of the sera of animals in- 
oculated subdurally with normal and hydrophobic brain tissue 
emulsion. 


36 (645) 


A study by the Meyer method of the effect of blood serum and 
certain inorganic salts on surviving arteries. 


By E. A. PARK and J. C. JANEWAY. 


[Department of Medicine, Columbia University.] 


The method employed is an adaptation of the Meyer ox 
carotid method. Instead of strips from the carotid, rings from 
the mesenteric or hepatic arteries of the ox strung in pairs were 
used, and from the coronary arteries as controls. Adrenalin, 
even in every dilute solution, constricts the former, while it 
causes the coronary to dilate, whether it be added to Ringer- 
Locke fluid, or to the ox blood serum. This method, then, 
based on the contrary effects produced by adrenalin on two 
kinds of arteries, each possessing a different reactive property 
to adrenalin, should be ideal for the detection of adrenalin and 
the separation of it from the confusion with other substances in 
the blood serum exerting a constrictor or dilator action. Ox 
blood serum as opposed to adrenalin produces a constriction of 
both coronary and mesenteric or hepatic arteries. Thus it 
essentially differs in its action from adrenalin. There is, then, 
so far as surviving arteries are concerned, a vasoconstrictor 
property of ox blood serum, not to be explained by the presence 
of adrenalin. 

The constriction produced by ox blood serum on ox arteries 


52 SCIENTIFIC PROCEEDINGS (47). 


occurs abruptly after a latent period of only a few seconds and 
is comparable in its intensity to that produced by adrenalin on 
the mesenteric or hepatic arteries. The duration is at least four 
hours, the limit of our means for recording it. Passing oxygen 
through it weakens this constricting property, as does time, 
1. €., allowing it to stand one or two days at room temperature. 
Adrenalin added to blood serum even at the height of a contrac- 
tion further increases it in the case of hepatic and mesenteric 
arteries, but produces an especially marked relaxation in the 
case of the coronary artery. Adrenalin added to fresh ox blood 
to make a proportion of one to 800,000, we have identified thirty- 
six hours later; and when added to make a proportion of one to 
100,000 after seven hours’ oxygenation under a pressure of more 
than 100 millimeters mercury at incubator temperature. 

Sodium chloride in dilution less than .o1 produces a marked 
constriction of the above-named arteries as compared with 
Ringer-Locke fluid. The latent period is longer than that of 
adrenalin or ox blood serum, the ascent more gradual; moreover 
the height of the curve seems to vary inversely to the sodium 
chloride water ratio to a point .005, below which we have not 
investigated. At .013 sodium chloride the strips of artery appar- 
ently die. The relations of calcium and potassium to tonus have 
not been taken up yet. Barium chloride produces a vasocon- 
striction which exceeds that produced by adrenalin, or, so far 
as our experience goes, any other substance. The curve produced 
by it tends to be irregular, frequently assuming a staircase 
character. 


37 (646) 
The influence of the sugar concentration of the blood on the 
protein metabolism in phlorhizin diabetes. 


By A. I. RINGER. 


[From the Department of Physiological Chemistry 
of the University of Pennsylvania.] 
According to Rubner, the protein metabolism of a normal 
starving animal is composed of two fractions: 
I. Wear and tear quota. 


PROTEIN METABOLISM IN PHLORHIZIN DIABETES. 53 


II. Dynamogenetic quota. 

The first fraction represents the protein metabolized in the life 
processes of the cells. The second fraction represents the protein 
burnt for the purpose of maintaining the temperature of the body. 

Landergren, however, presents considerable evidence to show 
that the ‘“‘dynamogenetic quota’’ of Rubner is really the result 
of two distinct processes: 

I. The protein that is metabolized for the increased pro- 
duction of sugar, in cases where sugar is absent from the diet and 
the glycogen supply becomes low. 

II. For the maintenance of body temperature. 

It is a well-known fact, that in phlorhizin diabetes, the pro- 
tein catabolism rises enormously; in some cases as high as five 
times the starvation requirements. Because of the renal origin 
of the glycosuria, there is a constant tendency for the concen- 
tration of the sugar in the blood to fall. The following experi- 
ment was performed in order to test what part, if any, the con- 
centration of the sugar in the blood plays in the regulation of the 
protein metabolism. 

A dog was phlorhizinized in the usual manner, and the D:N 
ratio established. Seventy-five grams of glucose dissolved in 
water and divided into six doses were given per os on the fourth 
day of the glycosuria. 150 grams were given on the sixth day. 

The results are here tabulated: 


Dog No. IT. 
. Total 
Date. Period. |Weight.| wy. |Total Sugar.| D:N. Remarks. 
February, 

1912 
Tat III. | 17.53 | 14.40 52.08 3.62 
16 IV. | 17.24| 9.32 | 103.10 11.06 |75 gm. of glucose given per os. 
17 V. | 16.86] 14.00 50.95 3.64 
18 Wil |) 16:60) 7 18a e272 07, 17.71 |150 gm. of glucose given per os. 
19 VI 16:2'55)) 7278 56.29 7.23 
20 Animal died under anesthesia, while a sample of blood was being with- 


drawn from the carotid artery. 


From the D : N ratio on the third and fifth days, we may assume 
that the phlorhizin intoxication was complete and that the protein 
burnt on the fourth, sixth and seventh days yielded 3.6 gm. of 
glucose for every gram of nitrogen. 


54 SCIENTIFIC PROCEEDINGS (47). 


The amount of glucose eliminated on the fourth day was 103.1 
gm. By subtracting 33.55 gm., which originated from the 
protein (9.32 X 3.6), we find that 69.5 gm. of the 75 gm. of 
glucose fed, were eliminated unburnt. By applying similar 
calculations to the results obtained on the sixth and seventh days, 
we find that the protein metabolized during the sixth day yielded 
(7.18 X 3.6) 23.85 gm. of glucose, and during the seventh day 
(7.78 X 3.6) 28.01 gm. The total amount of glucose eliminated 
during these two days was 183.46gm. By subtracting the glucose 
that was derived from the protein, we find that 131.6 gm. of the 
150 gm. of glucose ingested were eliminated unburnt. 

The nitrogen metabolism was diminished by a little more than 
5 gm. on the fourth day and was reduced almost fifty per cent. 
on the sixth and seventh days. If the increase in the protein 
metabolism in phlorhizin diabetes were due to dynamogenetic 
reasons only, the burning of 5.5 gm. of glucose on the fourth 
day could not have spared the combustion of 31.8 gm. of protein. 
Nor could the burning of 18.4 gm. of glucose on the sixth and 
seventh days have spared as much as 81 gm. of protein. 

From this experiment it is apparent that in phlorhizin diabetes, 
extra protein is catabolized in order to maintain the glucose 
concentration of the blood which, perhaps for some physico- 
chemical reason, is essential to the processes of life. The intro- 
duction of glucose into the system, although very little of it is 
burnt, spares that amount of protein. 

It is also noteworthy in this experiment that the 150 gm. of 
glucose given within 12 hours were not eliminated completely 
during the first 24 hours, but were carried over to a great extent 
to the second 24 hours. 


38 (647) 
The influence of glutaric acid on phlorhizin diabetes. 
By A. I. RINGER. 


[From the Department of Physiological Chemistry of the University 
of Pennsylvania, Philadelphia, Pa.] 

Baer and Blum found that the subcutaneous injection of Io 

gm. of glutaric acid had the power of greatly reducing the amount 


ProTeIN METABOLISM IN PHLORHIZIN DIABETES. 55 


of sugar and nitrogen in the urine of phlorhizinized dogs. The 
degree of reduction in the nitrogen elimination in most of their 
dogs is so marked (less than I gm. per 24 hours for dogs weighing 
5-4 to 10.0 kilos!) that a repetition of this experiment seemed 
desirable. 

Thanks to the kindness of Prof. Graham Lusk, I received 
100 gm. of glutaric acid, which was prepared by Kahlbaum, and 
which enabled me to carry out the following research: 

Dogs were phlorhizinized in the usual manner, and after estab- 
lishing the D : N ratio, they received, subcutaneously, 10 gm. of 
glutaric acid dissolved in water and neutralized by means of 
NaHCO;. The glutaric acid was administered in three equal 
doses during the course of the day. 


Dog No. 5. 
Weight. Total N. |Total Sugar. DN. Remarks. 
12.7 18.02 60.96 3.38 
12.2) 21.07 70.32 3-33 Io gm. glutaric acid. 
II.9 19.75 66.24 3-35 
Dog No. 7. 

13.87 16.92 63.05 3-72 

17.86 65-54 3.67 Io gm. glutaric acid. 


These results show that the glutaric acid, contrary to the 
findings of Baer and Blum, has no influence whatsoever either on 
the sugar or on the nitrogen elimination. 

Another experiment was performed on a normal starving 
animal. It received 10 gm. of glutaric acid without showing any 
effect on the nitrogen elimination. 

Baer and Blum report that a good many compounds containing 
two carboxyl groups possess the power of reducing the sugar and 
nitrogen elimination. Experiments are in progress to verify their 
contention. 


56 SCIENTIFIC PROCEEDINGS (47). 


39 (648) 


Influence of anemia and hyperemia on the growth of sarcoma 
in the white rat. 


By M. J. SITTENFIELD. 


[From the Department of Pathology of Columbia University, 
College of Physicians and Surgeons.| 


From previous experimentation, it becomes evident that cer- 
tain physiological and pathological factors on the part of the 
organism, as starvation, pregnancy, the feeding of various salts, 
racial differences, and so on, exert a decided influence upon the 
growth of transplanted tumor tissue. Moreschi in his experiments 
in 1909 concluded that under-feeding and starvation of the animal 
predisposes to retardation of the transplanted mouse carcinoma. 
Cluett, Mercier, and others have shown that during pregnancy 
the progress of the growth of the tumor which may be at a stand- 
still shortly before the ending of pregnancy, is very much lessened, 
and after labor and during lactation may even recede, 1. e., that 
the growth of one tissue exerts an unfavorable influence upon the 
artificially transplanted tissue growth of another. 

Negré, Borrell’s pupil, was able to control the percentage of 
takes by increasing or diminishing the salt contents of the fluids 
and tissues of the body. This proves conclusively that the sub- 
cutaneously transplanted tumor is dependent upon a great many, 
as yet unknown, conditions of the host, and also upon its metabolic 
changes. 

The present experiments were undertaken with a view to study- 
ing the effect of tumor growth in a locally induced anemic and 
hyperemic condition in the white rat. The lower extremity of 
the rat was rendered partially anemic by ligation of the femoral 
artery at the saphenous opening, and a few hours subsequent, 
it was observed that the extremity became slightly paler than the 
opposite one, though there was no evident lack of circulation; 
and twenty-four, forty-eight, and seventy-two hours after this 
induced anemia, Ehrlich’s rat sarcoma was inoculated sub- 
cutaneously into the leg. This experiment was performed on 
forty animals; of these thirty-three survived four to ten weeks, 


GROWTH OF SARCOMA IN THE WHITE Rat. 57 


and in only six animals, or eighteen per cent., did the tumor grow, 
and then only to a small size. The same number of controls were 
inoculated with seventy per cent takes. 

To study to what extent anemia was present in these animals, 
several animals were killed, the blood washed out of both extremi- 
ties by salt solution, subsequently injected with bismuth, and 
skiagraphed. These show that there is a marked difference be- 
tween the vascular supply of the anemic leg, compared to the 
normal one. 

Another set of experiments was performed to study the effect 
of passive hyperemia of the leg, induced either by rubber ligature, 
or by a bandage of adhesive plaster strips. A few hours after- 
wards, the leg became slightly swollen, grayish red, and the 
arteries still pulsating. This was continued for five to eight days, 
caution having been taken not to permit edema. Twenty-four 
hours after the onset of the hyperemia, twenty-five animals were 
subcutaneously inoculated in the leg with Ehrlich’s rat sarcoma, 
and here the takes were ninety-six per cent.; and the tumor grew 
more rapidly and to a larger size than in the control animals, in 
which the takes were sixty per cent. 

It is noteworthy that the anemic animals were subsequently 
inoculated subcutaneously and in only two out of twenty-nine 
did a growth result. It would seem, therefore, that these animals 
possessed an acquired immunity, probably from the absorption of 
substances from the first inoculation. 

From these experiments it becomes apparent that partial 
anemia and passive hyperemia of the leg exert different influences 
upon the growth of the transplanted tumor, similar to the dif- 
ference noted by Moreschi in his experiments of over and under 
feeding of his animals. 

Goldman, in his experiments, has shown that the blood supply 
and the new formation of blood vessels are essential factors in the 
growth of a cancer cell. 

Carl Levin, Bashford, and Gierke, have pointed out that the 
fibro-plastic and angeoplastic reaction on the part of the host are 
the deciding factors in the growth of a transplanted tumor cell, 
and it shall be the aim of subsequent experiments to further study 
the relation of the angeoplastic reaction on the part of the host 
in the anemic and hyperemic condition. 


58 SCIENTIFIC PROCEEDINGS (47). 


40 (649) 
Tho elimination and toxicity of caffein in nephrectomized 
rabbits. 


By W. SALANT and J. B. RIEGER. 


[Presented by permission of the Secretary of Agriculture.] 


In experiments on the elimination of caffein in rabbits and 
guinea pigs carried out by the writers! in this laboratory recently 
it was found that much larger amounts of caffein were recovered 
from the gastro-intestinal canal when these animals were fed oats 
than when carrots were given. Since greater quantities of urine 
are secreted ona diet of carrots than on one of oats, it seemed 
probable that the excretory function of the gastro-intestinal canal 
might be stimulated to greater activity in order to compensate for 
the diminished diuresis when oats were fed. The elimination of caf- 
fein into the gastro-intestinal canal after the removal of both kid- 
neys ought to be greater, therefore, than in normal animals. 

In experiments which were performed with caffein which was 
given subcutaneously to rabbits after double nephrectomy, the fol- 
lowing results were obtained: The amounts recovered at the end 
of about 22 hours from the contents of the stomach and intestines 
varied between 7.7 per cent. and 11.78 per cent., which is two to 
three times greater than was found in normal rabbits, much larger 
amounts being present in the intestines than in the stomach. In 
one rabbit which died seven hours after caffein was injected sub- 
cutaneously, about 103 per cent. were recovered from the intestines 
and about half this amount was obtained from the contents of the 
stomach. 

The total amount of caffein eliminated in nephrectomized 
rabbits in about 22 hours was approximately equal to that elimi- 
nated by the gastro-intestinal canal and kidneys combined of normal 
rabbits during an equal period of time, thus showing that the 
stomach and intestines acquire much greater power of elimination 
after the kidney is removed. 

Observations were also made on the toxicity of caffein in nephrec- 
tomized rabbits. The results obtained showed that the resistance 


1 Bull. 157, Bur. of Chemistry. 


Toxicity OF CAFFEIN IN NEPHRECTOMIZED RABBITS. 59 


is not less than in normal rabbits. In fact, it showed rather 
a tendency to greater resistance after the kidneys had been re- 
moved. Thus 100-150 milligrams of caffein per kilo failed to 
produce symptoms in nephrectomized rabbits. As was shown by 
the writers elsewhere,! 15 omilligrams per kilo injected subcuta- 
neously into normal rabbits are usually toxic. A dose of 200 mil- 
ligrams per kilo proved fatal to one rabbit, but two others survived 
with the manifestation of symptoms. It is interesting to recall 
in this connection that similar results were obtained several years 
ago by Meltzer and Salant? in experiments with strychnin in 
nephrectomized rabbits. 


41 (650) 
A quantitative study of the pupil dilatation caused by adrenalin. 
By DON R. JOSEPH. 


[From the Department of Physiology and Pharmacology of the 
Rockefeller Institute for Medical Research.] 


In the normal rabbit, adrenalin given subcutaneously has no 
effect on the pupil; if given intravenously in fairly large doses 
there may be a dilatation lasting less thana minute. S.J. Meltzer 
and C. M. Auer have shown that after removal of a superior 
cervical sympathetic ganglion in rabbits, the pupil of the corre- 
sponding side dilates maximally upon the administration of 
adrenalin either subcutaneously, intravenously or by instillation. 
Their experiments were carried out from the qualitative point of 
view, that is, fairly large doses of adrenalin were used and a 
wide, long-lasting dilatation of the pupil on the gangliectomized 
side resulted. 

I have recently made a quantitative study of the effects of 
intravenous injections of adrenalin on the pupil after removal 
of a superior cervical ganglion in rabbits. The object was to 
determine the minimal dose that will give a dilatation, and also 
the amount and duration of the dilatation produced by larger 
doses. The doses of adrenalin used per kilo animal, expressed in 
c.c. of the 1/1,000 commercial adrenalin solution, were 1/50, 1/30, 
1/20, 1/10 and 2/10 c.c. 


1Bull. 148, Bur. of Chemistry. 
2 Jour. Exp. Med., 1901, Vol. 5, p. 643. 


60 SCIENTIFIC PROCEEDINGS (47). 


The results, stated briefly, are as follows: The average pupil- 
dilatation in six experiments with 1/50 c.c. of adrenalin per kilo 
animal was 1.62 mm., with a beginning recovery from dilatation 
in four minutes, and a complete recovery in ten minutes. 

In six experiments with 1/30 c.c. there was an average dilata- 
tion of 2.25 mm.; recovery began in eight minutes and was com- 
plete in twenty-eight minutes. 

In thirteen experiments with 1/20 c.c., there was an average 
dilatation of 3.61 mm.; recovery began in six minutes and was 
complete in thirty-seven minutes. 

In eight experiments with 1/Io0 c.c., there was an average 
dilatation of 3.87 mm.; recovery began in ten minutes and was 
complete in forty-nine minutes. 

Finally, in eight experiments the dosage was 2/10 c.c. Here 
the average dilatation was 4.25 mm.; recovery began in twenty- 
five minutes, and was practically complete in an average of one 
hundred and eight minutes. 

In other words, 1/50 c.c. of adrenalin per kilo animal was prac- 
tically the minimum amount that could be relied upon to give a 
definite dilatation; as the dosage of adrenalin was increased, the 
dilatation also became greater, remained at its maximum for a 
longer time, and the return to a normal diameter was slower. 


42 (651) 
Intermittent and continuous lights of equal intensity as stimuli. 


By G. H. PARKER and B. M. PATTEN. 


[From the Zoélogical Laboratory of the Museum of Comparative 
Zoology at Harvard College.| 


It is generally assumed that white lights of equal intensity 
give equal stimulation. We have attempted to ascertain whether 
there is any observable physiological difference between the action 
of continuous white light and intermittent white light of equal 
intensity. From a common source of light two beams were con- 
ducted over separate paths of equal length to a common observa- 
tion point. One beam passed through a narrow slit and was thus 
reduced to a continuous stream of light of low intensity. The 


Licuts oF Equa INTENSITY AS STIMULI. 61 


other beam was reduced by being passed through a revolving 
sector-wheel, thus giving rise to a succession of flashes and dark 
intervals which fused indistinguishably in the eye, producing the 
appearance of a continuous flow of light of low intensity. By 
adjusting the sector aperture and comparing the lights in a pho- 
tometer, the two lights could be made physiologically equal. On 
measuring the physical intensities of the two physiologically 
balanced lights by means of a radiomicrometer, the intermittent 
light was found to be about 6 per cent. stronger than the continu- 
ous light. When the two lights were made equal from the stand- 
point of their physical intensity and were compared in a photo- 
meter, the continuous light appeared much brighter than the 
intermittent one. From these results we conclude that inter- 
mittent white light is a measurably less efficient stimulus than 
continuous white light of the same intensity, and that in this 
respect the action of the retina, like that of the photographic plate, 
affords an exception to the Bunsen-Roscoe law. The reduced 
efficiency of intermittent light is probably the result of chemical 
induction dependent upon the frequent interruptions of the light. 
The sector wheel (episcotister) is therefore an unreliable means for 
reducing the intensity of light. 


43 (652) 
Preliminary communication on the cytolytic action of ox-blood 
serum upon sea-urchin eggs, and its inhibition by proteins. 


By T. BRAILSFORD ROBERTSON. 


[From the Herzstein Research Laboratory and the Rudolph Spreckels 
Physiological Laboratory of the University of California.] 

1. It has been shown by Loeb! that the eggs of sea urchins 
(Strongylocentrotus purpuratus and Strongylocentrotus franciscanus) 
may be fertilized by the blood-sera of mammalia, provided the 
eggs be previously sensitized by a brief immersion in a solution of 
SrClz which is approximately isotonic with sea water. 

2. I find that if ox-serum be rendered sufficiently potent by 
dilution (cf. below) the formation of a fertilization-membrane by 


1J. Loeb, Arch. f. d. ges. Physiol., 118, 36, 1907; 122, 196, 1908; 124, 37, 1908; 
“Die chemische Entwicklungserregung des Tierischen Eies,’’ Berlin, 1909, p. 185. 


62 SCIENTIFIC PROCEEDINGS (47). 


the action of the serum is succeeded by cytolysis or may even be 
accompanied by marked agglutination of the eggs, thus confirming 
Loeb’s view that the formation of a fertilization membrane is 
essentially a phenomenon of incipient cytolysis. 

3. The cytolytic (and fertilizing) action of ox serum (rendered 
isotonic to sea water) upon sensitized sea-urchin eggs is enhanced 
by dilution with sea water, a maximum potency being attained at 
a dilution of about 1/16. 

4. I find that the increase in the cytolytic activity of serum 
which accompanies dilution is attributable to the fact that the 
proteins in serum in some degree inhibit membrane-formation. 
The inhibitory effect of the proteins becomes negligible if these 
are sufficiently diluted. If a protein (e. g., gelatin or ovomucoid) 
be added to diluted serum its cytolytic activity is greatly di- 
minished or even abolished. 

5. The inhibiting action of proteins upon cytolysis is due to 
the fact that they penetrate the outer membranes of the cells 
either with difficulty or not at all, so that by their osmotic tension 
they prevent the taking up of water by the cells. This is well 
illustrated by the fact that the order of efficiency of different pro- 
teins (the mixed proteins of serum, gelatin, ‘‘insoluble’’ serum 
globulin, casein and ovomucoid) is the reverse order of their 
ability to pass through the pores of a porcelain filter. The follow- 
ing table shows the concentrations of the various proteins inves- 
tigated which were observed to permit or inhibit the formation of 
spherical membranes after treatment of the eggs with 50 c.c. of 
sea water containing 214 c.c. of N/1o butyric acid for 244 minutes 
and then transferring them to 50 c.c. of the protein solution in 


sea water: 
Highest Observed Concentration Lowest Observed Concentration 


which Permits the Formation which Prevents the Forma- 
of a Spherical Membrane tion of a*Spherical Mem- 
within 1% Hours. brane within 1% Hours. 
Protein. Per Cent. Per Cent. 
The mixed serum proteins............. er) 7.4 
Gelatin. 6 vers. fom ceicteeclcks ee ilies 1.0 2.0 
“Tnsoluble”’ serum globulin............ 0.3 0.6 
Caseiniec s.r nc 5 ee Gee meme ple nee 0.25 0.5 
Ovomucoid:* 2 chase eccmeee eee 0.125 0.25 


6. It will be observed that the power of the mixed proteins of 
serum to inhibit membrane-formation is very strikingly inferior 


ACTION OF Ox-—BLOOD SERUM UPON SEA-URCHIN Eccs. 63 


to that of the other proteins investigated. On the other hand the 
CO.- or “insoluble ’’ globulin of serum, when isolated and dis- 
solved in sea water, is no less potent than other proteins in in- 
hibiting membrane-formation. A 0.3 per cent. solution of the 
‘insoluble ’’ serum globulin very noticeably inhibits membrane- 
formation, and yet a 3.7 per cent. solution of the mixed proteins 
of serum, containing 0.33 per cent. of the CO:-globulin, under the 
conditions enumerated above only inhibits membrane-formation 
to a barely perceptible extent. These facts would appear to lend 
confirmation to the view advanced by Hardy! and myself? that 
the various proteins in sera are not present therein in the free 
condition, but bound together in a molecular complex. 


44 (653) 


Preliminary note.— The action of various agents upon the 
secretion of milk. 


By ISAAC OTT, M.D., and JOHN C. SCOTT, M.D. 


In these experiments we used the lactating goat, obtaining 
the milk by aspiration with a water bottle. We found, as Macken- 
zie has noted, an increased secretion from venous injections of 
extracts of the mammary gland. The boiled gland was also active. 
The pineal body, corpus luteum, and infundibulin were active 
after a previous dose of atropin. Atropin and antipyrin greatly 
decreased the secretion. Pilocarpin and digitalin augmented the 
secretion. Pilocarpin in large doses was active after a preliminary 
dose of atropin. Albumoses, peptones, and glucose increased the 
secretion. Sodium, potassium and calcium chloride increased the 
secretion. Eserine, muscarine, and nicotine did not augment the 
secretion. 1/1000 of a drop of infundibulin increased the flow of 
milk, and 1/100 of a drop caused a marked increase. Infundibulin 
is a 20 per cent. extract of the infundibular part of the pituitary 
body. 


1W. B. Hardy, Journ. of Physiol., 33, 251, 1905 (Appendix). 
27. Brailsford Robertson, Univ. of Calif. Publ. Physiol., 4, 25, 1911; ‘“‘Die 
physikalische Chemie der Proteine,’’ Dresden, 1912, pp. 126-133. 


64 SCIENTIFIC PROCEEDINGS (47). 


45 (654) 
Preliminary note on the pineal gland and the corpus luteum. 


By ISAAC OTT, M.D., and JOHN C. SCOTT, M.D. 


In a series of experiments we have found the pineal gland to 
have a marked diuretic action, previously noted by Eyster. At 
the time of each injection per jugular the volume of the kidney 
increases considerably, whilst, after a temporary fall, the pressure 
in the carotid shows some increase. About one half of one per 
cent. of glucose appears in the urine after the injection of pineal 
extract and after the use of corpus luteum. 

Corpus luteum does not markedly change the pulse rate, but 
lowers blood-pressure 20-40 millimeters of mercury, and then it 
rises above normal for a short time. The intestinal peristalsis is 
markedly increased by corpus luteum. 

In the pregnant uterus, corpus luteum increased the contrac- 
tions. 


46 (655) 
The spleen and chronic constipation. 


By ISAAC OTT, M.D., and JOHN C. SCOTT, M.D. 


In the Medical Bulletin, 1897, one of us (Ott) stated, the spleen 
of all the animal extracts has the most marked effect on peristalsis. 
It produces the largest peristaltic waves. When the spleen was 
removed then peristalsis decreased. If now spleen extract was 
injected, then peristalsis was restored to a considerable extent 
above normal. 

In 1908, Zuelzer (Dohrn, Marxer and Zuelzer, “‘ Specifische 
Aufregung der darm Peristaltik, etc.,” Berliner Klinische Wochen- 
schrift, 1908, No. 48) with others confirmed the preceding results. 
He prepared an extract of the spleen, called ‘‘ hormonal,” for intra- 
venous and intramuscular injection in man for the cure of chronic 
constipation. He reports marked success in this condition. This 
statement has been confirmed by Saar, Henle, Unger and several 
others. 


THE SPLEEN AND CuHronic CoNnSTIPATION. 65 


We have tried the action of the Zuelzer extract of the spleen 
by the Magnus method. This consists in immersion of an excised 
segment of the intestine from an etherized animal in Ringer’s 
solution through which oxygen is bubbling. The intestine is 
attached to a heart-lever and the contractions registered. The 
spleen extract showed a marked action. In another method a 
balloon was inserted into the small intestine of an etherized animal 
and the contractions registered by Albrecht’s piston recorder. 
This method also exhibited an increase of contractions in the 
intestine. But they are not so marked as when a watery filtered 
infusion of the spleen was used. 


47 (656) 
The sequence of the protozoan fauna of hay infusions. 


By LORANDE LOSS WOODRUFF. 
[Sheffield Biological Laboratory, Yale University.| 


1. In hay infusions, seeded with representative forms of the 
chief groups of Protozoa, there is a definite sequence of appearance 
of the dominant types at the surface of the infusion, 7. e., Monad, 
Colpoda, Hypotrichida, Parameecium, Vorticella and Ameceba. 

2. The sequence of maximum numbers and of disappearance 
is identical with that of appearance, except that apparently the 
position of Amoeba advances successively from the last (sixth) 
place to the fifth place and then to the fourth place. 

3. A definite sequence of forms is not apparent at the middle 
or bottom of the infusions. 

4. The middle of the infusions is tenanted chiefly by a free- 
swimming population brought there by an overcrowding at the 
top or bottom. 

5. All of the protozoan forms considered (except Amceba) are 
chiefly surface dwellers and it is evident that when they pass their 
greatest development at the surface this maximum is seldom ap- 
proached again, and their cycle is practically over. 

6. The major rise and fall in numbers at the surface are usually 
about equally rapid, though the final disappearance of an organism 
may be long deferred. 


66 SCIENTIFIC PROCEEDINGS (47). 


7. The appearance of any of the protozoan forms under con- 
sideration, excepting Amceba, in appreciable numbers at the bot- 
tom is most often coincident with, or immediately subsequent to, 
its surface maximum, and portends its more or less rapid elimina- 
tion as an important factor in the life of the infusion. 

8. Numerous abnormal individuals and cysts are frequently 
to be found at the bottom in great abundance immediately after 
the surface maximum. 

9. Emphasis is put upon the strictly biological interrelations 
(e. g., those involving food and specific excretion products) of 
the various forms as the most important determining factors in 
the observed sequence. 


48 (657) 
The experimental demonstration of the identity of so-called 
Brill’s disease to typhus fever. 


By J. F. ANDERSON and J. GOLDBERGER. 


[From the Hygienic Laboratory.] 


The rhesus monkey is susceptible to infection by inoculation 
with the blood from a case of “‘ Brill’s disease.” One attack of 
the disease in the monkey induces a definite immunity to a sub- 
sequent infection with virulent blood of the same strain. Monkeys 
recovered from an infection with ‘‘ Brill’s disease’’ have been 
found to be immune to a subsequent infection with virulent blood 
from a case of Mexican typhus fever. Monkeys recovered from 
an infection with Mexican typhus fever have been found to be 
immune to a subsequent infection with “‘ Brill’s disease.” 

From the above results we conclude that the disease described 
by Brill is identical with the typhus fever of Mexico, and inasmuch 
as the New York strain is undoubtedly of European origin, we may 
also conclude that the typhus of Europe and the tabardillo of 
Mexico are identical. If this conclusion is correct, typhus fever 
has been present in New York City for a number of years and, 
according to verbal reports made to us, has occurred in other large 
cities of the United States. These results make the clinical recog- 
nition and study of typhus fever of increased importance and 
necessitate the exercise of appropriate prophylactic measures. 


IDENTITY OF BrRILLS DISEASE WITH TYPHOID FEVER. 67 


It is not intended to exaggerate the menace of this disease to 
the public health. Nevertheless, although the disease in New 
York City has apparently been mild and has shown little tendency 
to spread, it is apparently on the increase there and the possibility 
should be borne in mind that it may acquire virulence and epi- 
demic prevalence. 


49 (658) 
The relation of the parathyroid glands to electrical 
hyperirritability. 


By HERBERT B. WILCOX. 


[From the Laboratory of Clinical Pathology of the College of 
Physicians and Surgeons, N. Y. C.] 


The following observations were undertaken for the purpose 
of obtaining information as to the relation between parathyroid 
lesion and infantile tetany and of the value of the galvanic reaction 
as a diagnostic sign of the disease. 

In all 25 operations were done on 18 dogs, tests being carried 
on during August and September, 1910, and from March, 1gI11, to 
the present time. 

Information was sought on the following points: 

1. The limits of response to be expected in peripheral galvanic 
stimulation of the normal dog. 

2. The influence of age upon this galvanic response. 

3. The comparability of electrical response in the dog to that 
of man. 

4. The incidence of electrical hyperirritability and tetany 
following injury to or removal of I, 2, 3 or all of the parathyroid 
glands. 

5. The time of appearance of these evidences after operation. 

6. The length of time by which the electrical evidences precede 
the physical signs of tetany in their appearance. 

7. The constant or varying qualities of the changes of response 
to electrical stimulation. 

8. The frequency of the presence of the electrical evidences of 
tetany when all other signs are absent. 


68 SCIENTIFIC PROCEEDINGS (47). 


9. The predisposition to more sudden and severe electrical 
irritability, when further parathyroid loss is suffered, by animals 
previously subjected to parathyroid injury. 

10. The influence of gestation on the galvanic response of 
parathyropriva animals. 

Technique.—Ether anesthesia. 

Three procedures or a combination of the first two were fol- 
lowed. 

1. The parathyroid gland or glands were exposed, lifted on the 
point of a needle and excised or crushed. 

2. A thyroparathyroidectomy of one side was done. 

3. A complete thyroparathyroidectomy was done on both 
sides and thyroid extract given to the dog. 

For the galvanic tests the peroneal nerve-muscle group was 
used. The negative electrode was placed on the upper abdomen, 
the positive over the peroneal nerve as it passes around the head 
of the fibula. The instrument employed supplied a galvanic cur- 
rent from dry cells and was provided with a rheostat, polarity 
switch and balanced milliampere-meter measuring from .2 to 10 
milliamperes. 

Findings.— 

1. In normal adult dogs K.C. is usually less than 2 m.a. and 
may vary between I m.a.and3m.a. A.C. is usual at from 3 to 5 
m.a. It is seldon less than three and often greater than 5 m.a. 
A.O. is rarely obtained at less than 5 m.a. K.O. is never below 
5 m.a. 

2. Young puppies are less susceptible to galvanic stimulation 
than grown dogs. K.C. and A.C. alone are obtained at less than 
5 m.a. Frequently K.C. alone is obtained and not often below 
2 eae 

3. Comparison of the findings on normal and parathyropriva 
dogs with over 300 observations on normal children and children 
having tetany shows that galvanic response is very similar in the 
two classes. 

4. Of 4 dogs with one parathyroid gland removed, none de- 
veloped frank! tetany. Two showed mild anodal hyperirritability 


1 By frank tetany is meant the development of tremors, muscular or laryngeal 
spasms, convulsions or paralyses. 


RELATION OF PARATHYROID GLANDS TO HYPERIRRITABILITY. 69 


during a period of to days following operation. One showed mod- 
erate anodal hyperirritability during a period of 7 days following 
operation. One showed no electrical change during 11 days after 
operation. The removal of one parathyroid resulted in only 
moderate lowering of the anodal reactions. 

Of 8 dogs with 2 parathyroids removed none developed 
frank tetany. Twoshowed marked electrical hyperirritability to 
K.C., A.C., A.O. and K.O. during 25 days following operation. 
Two showed marked anodal irritability during 13 days and 10 
months respectively after operation. Four showed very slight 
anodal irritability during periods of from 1 to 4 weeks after opera- 
tion. Electrical irritability of varying degree follows injury to 
or removal of 2 parathyroid glands. 

Of 2 dogs with 3 parathyroids removed neither developed 
frank tetany. Both gave prompt and marked anodal irritability 
with occasional low response to K.O. Observations were con- 
tinued for 36 days after operation. 

Of 4 dogs subjected to complete thyroparathyroidectomy at 
one operation, two gave complete hyperirritability on day follow- 
ing operation and developed tetany two days later. One de- 
veloped marked anodal irritability with tetany the following day. 
One, for 46 days, showed neither electrical nor other symptoms of 
tetany. 

Of 7 dogs having part of their parathyroid tissue removed at 
one time, and the remainder later, 5 developed prompt and com- 
plete electrical change and frank tetany. One showed no hyper- 
irritability but died of tetany in six days after operation. One 
showed complete galvanic reactions but died on the sixth day 
without other signs of tetany. Prompt and complete hyper- 
irritability, followed in from one to two days by severe tetany, 
resulted in the removal of all parathyroid glands. 

5. Electrical change was noted in from 5 to 48 hours after 
operation. The promptness and severity of its development de- 
pended to a considerable degree upon the amount of parathyroid 
tissue removed. 

6. In all dogs developing frank tetany the electrical diagnosis 
was established from I to 3 days before other symptoms appeared. 
Lesions which failed to produce tetany were usually accompanied 


70 SCIENTIFIC PROCEEDINGS (47). 


by electrical change. Marked hyperirritability was present in 
one case for II months without other symptoms of tetany. 

7. Sixteen dogs at some time during their periods of observa- 
tion gave response to all forms of current at less than 5 m.a. 
Seven dogs with all parathyroids absent were constantly low in 
all reactions. Five dogs, 2 with all glands removed, 3 with 2 
removed, I with 3 removed, were constantly low in all but K.O. 
Four dogs, 3 with 2 glands removed, I with 3 removed, gave con- 
stantly varying reactions. 

In one instance there was constant low K.C., high K.O. and 
great variation in the anodal tests. 

As a rule the electrical change is sufficiently constant to make 
the test a valuable one. Variations are, however, to be expected. 

8. Eight dogs, 2 with 1 gland, 4 with 2 glands, 2 with 3 glands 
removed showed marked and complete electrical hyperirritability 
without other symptoms of tetany. Parathyroid injury sufficient 
to produce hyperirritability does not necessarily result in frank 
tetany. 

g. Eight dogs were subjected to parathyroid injury and later 
to further loss of glands. In each instance the electrical changes 
following second operation were more rapid in development and 
more severe than those noted after the first operation. 

10. While under observation 2 parathyropriva dogs littered 
normally and 1 aborted at about 1 month. None developed 
tetany during gestation or lactation. There was moderate in- 
creased irritability during gestation which became more marked 
during lactation. No electrical change occurred in the animal 
which aborted. 


a 


SCIENTIFIC. PROCEEDINGS: 


ABSTRACTS OF THE COMMUNICATIONS. 
Forty eighth meeting. 


Cornell University Medical College. April 17, 1912. President 
Ewing in the chair. 


50 (659) 
The influence of alcoholism on the offspring. 
By CHARLES R. STOCKARD. 


[Department of Anatomy, Cornell University Medical College, 
N. Y. City.] 


Two years ago I showed that almost all known gross deformities 
of the brain could be produced by treating developing fish embryos 
with alcohol and a number of anesthetics. 

Since that time these experiments have been extended to birds 
andmammals. The workof Feré with hen’s eggs has been repeated 
and his results confirmed. When these eggs are subjected to the 
fumes of alcohol the shell is penetrated and the developing embryo 
is affected. The rate of development is reduced and a large num- 
ber of monstrosities occur. 

Guinea pigs have been put into a state of chronic alcoholism 
by treating them for six days per week with alcohol fumes to 
almost the point of intoxication. Forty full-term matings of 
various combinations have been made with these alcoholic animals. 
Treated males have been paired with normal females (test of 
paternal influence on offspring), treated females paired with normal 
males (maternal influence plus the direct effect on the developing 
embryo) and finally treated males and females were paired. The 
outcome of these matings has been most striking. 

Twenty-five matings gave no result or the embryos were 
aborted early and eaten by the mother. Fifteen matings pro- 
duced in all 25 young, of these two have lived to reach maturity 
and are apparently normal, four are still young but seem normal. 
Of the other 19, eight were stillborn or aborted shortly before 

71 


72 SCIENTIFIC PROCEEDINGS (48). 


term, seven lived for a few days after birth and all died in con- 
vulsions, four were in utero when the mothers were killed and one 
of these was deformed. 

All of the control matings were successful, all of the young lived 
and were vigorous. 


51 (660) 
Growth and maintenance on purely artificial diets. 
By THOMAS B. OSBORNE and LAFAYETTE B. MENDEL. 


[From the Laboratory of the Connecticut Agricultural Experiment 
Station, and the Sheffield Laboratory of Physiological Chemistry 
in Yale University, New Haven, Connecticut.] 


[With the coéperation of the Carnegie Institution of Washington.] 


In earlier reports of the authors’ feeding experiments with 
isolated food substances! attention was directed to the failure to 
induce growth or secure prolonged maintenance of body weight in 
albino rats with any of the food mixtures tried prior to the intro- 
duction of ‘‘protein-free milk’’ as the adjuvant of the dietary 
which furnished the inorganic nutrients together with some of the 
carbohydrate (in the form of lactose). In order to determine 
whether the nutritive success achieved by the use of the protein- 
free milk was due to the peculiar supply of inorganic salts or some 
other ingredient, an artificial mixture of salts was prepared to 
imitate as nearly as possible the proportions of acid and basic 
radicals in the milk product. This mixture, the preparation of 
which will be described in detail in a forthcoming paper, contains: 
Ca 1.97; Mgo.23; Na 2.03; K 2.66; POs 3.33; Cl 4.13; SO; 0.30; 
Fe 0.04; citric acid 3.33; lactose 82.0 per cent. This purely arti- 
ficial product added to purified proteins, starch, sugar and lard 
has already sufficed to meet the needs of rats for maintenance over 
very considerable periods of time, and has, thus far, proved as 
efficient in promoting early growth as the so-called protein-free 
milk used in our former experiments. 


1 Osborne, T. B., and L. B. Mendel, Carnegie Institution of Washington, Pub- 
lication 156, Part II, 1911; and Scéence, 1911, XXXIV, p. 722. 


FEEDING EXPERIMENTS WITH FAT-FREE Foop MIXTURES. 73 


52 (661) 
Feeding experiments with fat-free food mixtures. 


By THOMAS B. OSBORNE and LAFAYETTE B. MENDEL. 


[From the Laboratory of the Connecticut Agricultural Experiment 
Station, and the Sheffield Laboratory of Physiological Chemistry 
in Yale University, New Haven, Connecticut.] 


[With the coéperation of the Carnegie Institution of Washington.] 


The question as to whether fats are, like proteins and carbo- 
hydrates, in some measure indispensable components of the diet 
has never been adequately determined. Stepp! has lately main- 
tained that the so-called ‘‘lipoids,’”’ in distinction from true fats, 
are necessary for adequate nutrition. His experiments were con- 
ducted with mice. Following the methods employed by the 
writers? it has been possible to induce rats to grow at a normal 
rate with food mixtures containing only purified proteins, carbo- 
hydrates and inorganic salts. The problems suggested by the 
possibilities of this method of investigation are obvious. 


53 (662) 


The masking of a Mendelian result by the influence 
of the environment. 


By T. H. MORGAN. 
[From the Department of Zoélogy, Columbia Unwversity.] 


As reported (Oct., 1911) a mutant of Drosophila appeared with 
a dominant sex-linked character, viz., abnormal abdomen. Typica] 
Mendelian ratios are found in the F» offspring if an abundance 
of food and of moisture is present. As the culture grows older 
the flies that emerge later gradually change over to the normal 
type. As a result the Mendelian ratio completely disappears 
from the surface phenomena. That Mendelian inheritance has 
actually occurred, but is temporarily masked, is shown by testing 
the F, flies, when the expected number is found (under wet 

1Stepp, Zeitschrift fiir Biologie, 1911, LVII, p. 135. 


2 Osborne, T. B., and L. B. Mendel, ‘‘Feeding Experiments with Isolated Food- 
Substances,” Carnegie Institution of Washington, Publication 156, 1911. 


74 SCIENTIFIC PROCEEDINGS (48). 


conditions) to transmit the abnormal abdomen. This is best 
demonstrated by linking the factor for abnormal abdomen A with 
another sex-linked factor, such as the 6 factor in the yellow 
mutant, or the ¢ factor in the white mutant, or to both together 
as in the two examples given below. 


GRA? 95 56 3 
GRN 9 ) 4 32 
YRAG@ \GRAQ _}GWNQ 88 49 34 
GWN2 7GWN&~ | GWN& 98 49 19 
YRAS 81 47 7 
YRNG& I 2 25 
GWAo 50 21 9 
GWNo 1 24 24 
WARN 9 GRIN 20) GARANO D7 3 o 
GWAco' 7 YRNG GRN 9 5 49 60 
YRN@? 45 93 61 
YRNO 49 29 30 


The tables show that in the expected classes for abnormal 
abdomen A this character at first appears but later is replaced by 
the normal character V. When the normal flies (of the last sort) 
were tested they were found to transmit abnormality. The other 
classes that are genotypically normal remain so in the next 
generation. Cultures that had produced only abnormal flies for 
nine generations under wet conditions were allowed to dry out 
when all the later-hatched flies became normal. These were then 
placed under moist conditions, and all of their offspring were as 
abnormal as their ancestors had been. 


54 (663) 
Sources of error in serological work. 


By WILFRED H. MANWARING. 
[From the Rockefeller Institute for Medical Research.] 


I have been engaged for some time in attempts to determine 
the approximate chemical nature of certain bactericidal substances 
obtained from horse leucocytes. My earlier attempts to isolate 
and identify these substances were characterized by inconstant 
and inconsistent results. This led to an examination of the 


SourcEs OF ERROR IN SEROLOGICAL Work. 75 


experimental method, with the discovery of certain sources of 
error not usually taken into account in serological work. 

The first source of error is the possibility of there being marked 
changes in the chemical composition of serological substances as a 
result of changes in concentration. The bactericidal substance 
with which I was working is fairly stable. It can be heated to 
60° C. for an hour without loss of bactericidal power and can be 
stored in the ice chest for weeks with but slight deterioration. The 
substance can be passed through a series of chemical manipulations, 
involving such processes as salting-out, dialyzing, evaporating to 
dryness, and redissolving, and can be recovered quantitatively 
from the final product of such manipulations, provided the volume 
of fluid in which it is dissolved is at no time allowed to increase 
much above the original volume from which the substance was 
obtained. If the volume is allowed at any stage to materially 
increase, there is brought about a rapid deterioration of the 
bactericidal substance at that stage, giving a final product without 
bactericidal action. 

The second source of error is the possibility of there being 
marked changes in the specific properties of serological substances 
as a result of variations in the amount of sodium chloride with 
which they are mixed. The purified bactericidal substance from 
horse leucocytes, dissolved in distilled water, has about half the 
bactericidal power of the initial crude product. If dissolved in 
physiological saline solution, instead of in distilled water, it is 
without bactericidal power. 


55 (664) 


The relation of the virulence of the tubercle bacillus to its 
persistence in the circulation. 


By ALFRED F. HESS. 
[From the Research Laboratory, Department of Health, New York 
City.] 
It seems as if the tubercle bacillus offered an exceptional oppor- 
tunity to study the question presented in the title of this study. 


As is well known, one type of the bacillus, namely, the human 
type, is non virulent for the rabbit, whereas the bovine type causes 


76 SCIENTIFIC PROCEEDINGS (48). 


a general tuberculosis in this animal. Accordingly experiments 
were instituted in the following manner: four rabbits were injected 
for each test, two with a human type of bacillus, the other two 
with the bovine type, in each case 1/100 mg. and 1 mg. of a culture 
being injected into the ear vein. These four animals were bled 
one half hour, one hour, two hours, and three hours after injection, 
5 cu. cm. being caught in a solution of sodium citrate. There were 
thus eight specimens taken from the two rabbits inoculated with 
the human tubercle bacillus, and eight from the two inoculated 
with the bovine bacillus. These sixteen specimens were injected 
into as many guinea-pigs, and after six weeks these animals were 
examined for tuberculosis. 

In all, six experiments of this description were successfully 
carried out, using twenty-four rabbits and 112 pigs. In the 
tuberculosis test, 44 of the pigs injected with ‘‘bovine blood”’ 
survived, 26 of these, that is, 69 per cent., were found tuberculous. 
Of 45 of those injected with the human virus 7 developed tuber- 
culosis, that is, about 1814 per cent. In almost all of these experi- 
ments the bovine bacillus was found more frequently in the 
circulation than the human type of bacillus. This was not the 
case to any great extent in two of the experiments, where the 
bovine strain was not of marked virulence. 

The conclusion is, therefore, that a certain parallelism exists 
between the virulence of the tubercle bacillus and its persistence 
in the circulation of the rabbit. The more virulent bovine organism 
remains in the circulation more constantly and for a longer period 
than the less virulent human type. The cause of this difference 
is being studied at present. Perhaps we can generalize from this 
fact in the case of other microérganisms. 


56 (665) 
On indican in the blood of uremic patients. 
By NELLIS B. FOSTER. 

[From the medical service of the New York Hospital and the Labora- 
tory of Biological Chemistry, Columbia University, at the 
College of Physicians and Surgeons, New York.] 

A demonstration of the constant presence in uremic blood of an 
abnormal aromatic body such as indican would be highly signifi- 


On INDICAN IN THE BLoop oF UREMIC PATIENTS. 77 


cant since this would be suggestive of the nature of the abnormal 
metabolism. Hence a recent report! to the effect that indican is 
present in the blood in uremia invited confirmation, and especially 
as the amounts present are stated to be sufficient to give the 
ordinary blue color with chloroform when only 10 c.c. of serum 
are used for the test. Considering the total volume of blood this 
would mean an enormous concentration. 

The method for detecting indican employed by Obermayer, 
was, in brief, to separate all of the proteins from the serum by 
means of alcohol, which after filtration is evaporated on the steam 
bath. The residue from the alcohol filtrate is taken up in water, 
freed of salts with lead acetate and the latter in turn removed by 
sodium phosphate. A water clear filtrate is the final result which 
is tested by the usual method employed for urine with Obermayer’s 
reagent. 

In repeating Obermayer’s experiments the method above 
mentioned was used, also the separation of the proteins was con- 
ducted by means of phosphotungstic and hydrochloric acids and 
in a third series a method was used which is based on that of Rona 
for the precipitation of colloids in blood, by means of kaolin. 
The clinical material consisted of ten typical cases of uremia, all 
of the convulsive type. It was noted that indican could not be 
detected in fresh serum when I0 c.c. was used for tests; with 
larger amounts, 25 c.c., a questionable coloration of the chloroform 
resulted in one instance. If instead of using fresh serum or blood, 
the material be allowed to stand twenty-four to thirty-six hours 
many of the uremic bloods then gave a fairly definite reaction. 
When the kaolin method of separation of proteins is employed, 
however, no indican could be detected even though the equivalents 
of as much as 50 c.c. of blood be used for the test. 


1 Obermayer and Popper, Zeitschr. f. Klin. Med., 1911, 72, pp. 333-72. 


78 SCIENTIFIC PROCEEDINGS (48). 


57 (666) 
The inhibitory action of adrenalin in muscle-pancreas mixtures. 


By ALWIN M. PAPPENHEIMER, M.D. 


[From the Department of Pathology, College of Physicians and 
Surgeons, New York City.] 


Much evidence has accumulated since Blum’s discovery of 
adrenalin glycosuria in 1901, to indicate an antagonistic action 
between the adrenal and the pancreas in carbohydrate metabolism. 
The more intimate nature of this antagonism is still obscure. 
Bayer in a recent article has suggested three possible modes of 
interaction: 

1. The action of the internal secretion of the pancreas may be 
directly inhibited by the adrenalin, or 

2. The secretion of the pancreatic hormone may be prevented, 
either directly or through reflex nervous influence, or 

3. The adrenalin, through its vaso-constrictory action, may 
close up the channels of exit through which the internal secretion 
of the pancreas reaches the circulation. 

At the suggestion of Professor MacCallum, the attempt was 
made to demonstrate this antagonistic action between adrenal and 
pancreas in vitro, where the problem is simplified by the exclusion 
of secretory or vaso-motor influences. The technique used was, 
with slight modifications, that described by Cohnheim in 1906 
for the demonstration of the activating effect of pancreas extract 
upon the glycolytic ferment of muscle. The finely hashed muscle 
of cats was extracted in iced sodium oxalate solution, the excess of 
oxalate precipitated with calcium chloride, and glucose added in 
known amount. Duplicate flasks of muscle extract alone, of 
muscle extract plus pancreas, and of muscle extract plus pancreas 
plus adrenal gland extract or adrenalin in varying dilutions up to I 
in I10,000, were incubated overnight at 37° under toluol. Sugar 
determinations were made with Benedict’s solution from samples 
taken before and after incubation. 

It was found that the addition of adrenalin to muscle-pancreas 
mixtures prepared in this way, gave a higher sugar content than 
the controls. This effect was obtained definitely in 9 out of 10 


INHIBITORY ACTION OF ADRENALIN. 79 


experiments. In 6 of the 10 positive experiments, there was an 
actual increase in the amount of reducing substance during the 
course of the experiment. 


The results may be summarized as follows: 
Average Loss of Re- 


Mixture. ducing Substance. 
Muscle-extract alone): i). wie oo cre lciniels suns. shoreuacerela) ovsteWleleserohe — 0.096 gm. in 100 c.c. 
WEUSCIEU DANCKEAS) ie. cy aielarete shea cin cicae a slelolc eveis.clai selene aiellelieTeuee\'« — 0.225 gm. in 100 c.c. 
Miurscle-pancreas-adrenalin. c ci5c6 is sie erase fe wlelpier sieves. oinvey hel eres +0.01 gm. in 100 c.c. 


These experiments then show that the antagonistic action between 
adrenalin and pancreas, as schematized by Falta, Eppinger and 
Rudinger, may be demonstrated in vitro independently of any 
possible nervous influence. King in 1910 showed that a similar 
retarding influence upon the disappearance of reducing substance 
in muscle pancreas mixtures was exerted by thyroid extract. 

The question as to whether there occurs in this reaction, a 
true glycolysis, or as Levene and Meyer hold, merely a condensa- 
tion of the sugar molecule, is left untouched by these experiments. 
The antagonistic action of adrenalin and pancreas in regard to the 
disappearance of reducing substance in muscle extracts seems to 
be clearly demonstrated. 


58 (667) 
The characteristic course of the rise of blood pressure caused 
by an intraspinal injection of adrenalin. 


By J. AUER and S. J. MELTZER. 


[From the Department of Physiology and Pharmacology of the 
Rockefeller Institute.] 


An intravenous injection of adrenalin causes a rapid steep rise 
of the blood pressure with a gradual fall. An intramuscular in- 
jection produces a similar effect. A subcutaneous injection either 
produces practically no effect or it causes a very slow rise which 
rarely exceeds fifteen millimeters. In recent years adrenalin was 
injected into the spinal canal in conjunction with some local 
anesthetic. The question as to the nature of the effect of these 
injections upon the blood pressure has to our knowledge never yet 
been investigated. On the basis of the generally accepted assump- 
tion that the absorption from the spinal canal into the circulation 


80 SCIENTIFIC PROCEEDINGS (48). 


is not very prompt we might expect that the intraspinal injection 
of adrenalin will have no stronger effect upon the blood pressure 
than that of a subcutaneous injection. We studied this question 
experimentally and may say at the outset that our results did 
not bear out this anticipation. Our experiments were made 
on six monkeys, using each monkey two or three times. The 
amount injected was either I c.c. or 1.5 c.c. of the commercial 
adrenalin. Most of the injections were made in the lumbar 
region; but in a few instances the adrenalin was injected in the 
thoracic region in the fifth intervertebral space. During the 
experiments the animals were under fairly profound anesthesia 
and we are unable to state whether the injection had any other 
effect besides the change in the blood pressure. But it is impor- 
tant to point out that even doses of 1.5 c.c. of adrenalin had no 
recognizable after-effects upon the animal. 

The action upon the blood pressure was in most cases very 
characteristic. The pressure would begin to rise slowly but 
steadily, so that in a few minutes it would reach a maximum 
varying between 150 and 190 millimeters, and would then com- 
mence to go very gradually down. As a rule the entire course 
of the rise lasted longer than in intravenous injections, in some 
instances even longer than half an hour. The fall of blood 
pressure occurred so slowly at times that the original level was 
not reached during the entire time of observation, a fact which 
might be of considerable practical importance. 

Twenty-one injections were given to these six monkeys at 
intervals; of these thirteen gave the typical rise described. In 
six cases the rise was preceded by a moderate fall (9-52 mm.) 
of short duration (14-4 minutes) and in one case this fall was 
the only effect of the injection. In the seven instances the injec- 
tion brought on a rise similar to that of an intravenous injection 
but of longer duration. It is possible that in these cases part 
of the injection entered indeed into a vein. 


VomitTInG MovEMENTS IN AN EVISCERATED ANIMAL. 81 


59 (668) 


Demonstration of vomiting movements in an eviscerated 
animal under the influence of digitalis. 


By C. EGGLESTON and R. A. HATCHER. 
[Laboratory of Pharmacology of Cornell University Medical College.] 


It is commonly accepted that apomorphine produces emesis 
through its action on the center in the medulla concerned in 
emesis, but that digitalis produces emesis through its irritant 
action on the stomach. 

We had some evidence that digitalis produced vomiting 
through its central action and decided to carry out as many experi- 
ments as possible of those which had been made in establishing 
the seat of action of apomorphine, but substituting digitalis, and in 
the course of the investigation we utilized a method which has 
not been described hitherto, and which consists in the removal 
of the gastro-intestinal tract from the esophagus to the anus, 
after tying the vessels which supply the tract, and injecting 
digitalis intravenously after an appropriate interval of time, 
varying from a few minutes to an hour and a half. 

We have produced vomiting movements in about fifty per 
cent. of the experiments so made, and nausea in all but one of the 
others, and barring those experiments where the depression from 
the operation seemed to indicate that nausea could not be induced, 
the percentage of successful experiments is still higher. 

Using apomorphine intramuscularly, we have been able to 
produce vomiting movements in nine out of ten such experiments 
on the dog. 


60 (669) 
The variations of pressure in the pulmonary artery. 
By CARL J. WIGGERS. 


[From the Physiological Laboratory, Cornell University Medical 
College, New York City.]} 


The systolic and diastolic pressures existing in the pulmonary 
artery of naturally breathing dogs have not been heretofore 
investigated. By means of a sensitive pulse pressure instrument 


82 SCIENTIFIC PROCEEDINGS (48). 


capable of standardization against maximal and minimal valves,! 
it has been possible to fill this gap in the physiology of the 
circulation. The operative technic was so adapted that (1) 
normal intrathoracic pressure relations during inspiration and 
expiration were obtained when the records were taken, (2) arti- 
ficial pressure changes in the intrathoracic cannula and manom- 
eter tubes were obviated, (3) clot formation was minimized and 
recognized when present, (4) only a small portion of the pul- 
monary circuit was occluded, and (5) the systemic and right 
auricle pressures corresponded to that habitually found in animals. 

The results of 13 such experiments showed that, during 
quiet normal breathing the systolic and diastolic pressures fell 
during inspiration and rose during expiration. The systolic 
pressure averaged 43.3 mm. in expiration and 31.7 mm. in 
inspiration, the diastolic pressure 20 mm. in inspiration and 
11.9 mm. in expiration. In experiments where the heart rate 
ranged from 180 to 25 per minute, it was found that the diastolic 
pressure decreases as the heart rate is reduced. The same holds 
true for the systolic pressure between heart rates ranging from 
from 180 to 100 or 80 (the latter figure varying in different ani- 
mals). When the heart becomes still slower the systolic pressure 
again increases. 

During temporary apnea vagi, the maximal pressure dropped 
40 to 32 percent., the minimal pressure increased 10-25 per cent. 
over that occurring during natural breathing, showing that respi- 
ratory movements determine to a pronounced extent the ex- 
treme pressures in the pulmonary artery. 


61 (670) 
The results of ligation of the pulmonary and cutaneous arteries 
in the frog. 
By T. S. GITHENS. 
[From the Department of Physiology and Pharmacology of the 
Rockefeller Institute for Medical Research.] 


The frog possesses, in the lungs and the skin, two organs for 
the purpose of respiratory exchange, and it has long been estab- 


1 Wiggers, Journ. Exp. Med., XV, 1912, Dp. 174. 


RESULTS OF LIGATION IN THE FRoG. 83 


lished that the skin respiration suffices for his needs at low tem- 
perature. 

I have attempted to produce asphyxia in frogs by ligating 
the vessels which carry blood to the lungs and to the skin. It 
may be well to mention here certain anatomical data. The 
truncus arteriosus rises from the heart of the frog and divides 
into a right and left branch which each give off three branches, 
the carotid, the aorta and the pulmocutaneous. The last divides 
into two, one of which goes to the lungs and the other, the cutaneous, 
supplies the skin of the entire trunk. A large branch from the 
carotid makes a free anastomosis with the cutaneous artery. 

At temperatures below 20° C. the frog requires very little 
gas exchange and I found that ligation of the pulmocutaneous and 
anastomosis was not sufficient to produce asphyxia, although it 
deprives the frog of the lungs and most of the skin, leaving only 
the mucous membrane of the mouth and the skin of the legs 
for respiratory purposes. If in addition the mouth was excluded, 
by ligation of the carotid arteries, thus leaving only the skin of the 
legs, the frogs died in 2-3 days. If the lungs and entire skin were 
excluded by ligating the pulmocutaneous and the iliac arteries 
death occurred in about 36 hours in spite of the respiratory ex- 
change through the mucous membrane of the mouth. Frogs in 
which the respiration of the lungs and mouth was absolutely 
prevented by keeping them under water, but in which the entire 
skin was available, lived indefinitely at this temperature. 

With an increase of temperature to 28° frogs in which the 
cutaneous respiration was entirely excluded by ligation of the 
cutaneous and iliac arteries were still able to live indefinitely. 
If the lungs and skin of the body were excluded by ligation of the 
pulmocutaneous and anastomosing arteries, death occurred in 
about 24 hours, and if the skin of the legs was also excluded by 
ligation of the iliac arteries, in about 12 hours. If the pulmonary 
and buccal respiration was prevented by keeping frogs under 
water, no asphyxia was noted during the five hours of the experi- 
ment, but frogs in which the cutaneous arteries were tied and 
which were kept under water died within 3 hours. 

At a temperature of 34°, asphyxia could be caused by excluding 
the cutaneous respiration. Frogs in which the cutaneous and 


84 SCIENTIFIC PROCEEDINGS (48). 


anastomosing branches were ligated lived only about 8 hours. 
If the lungs and most of the skin were excluded by tying the 
pulmocutaneous and anastomosing arteries, the frogs lived about 
6 hours and if the mouth also were excluded by sewing this and the 
nostrils shut and tying the cutaneous arteries, they lived about 
4% hours. Control frogs kept at this temperature, showed no 
deviation from normal excepting slight over-excitability. 

These results show with how little gas exchange frogs can 
live and also the large factor of safety with which their respiration 
is normally provided. Auer and Meltzer have recently shown 
that dogs could live with a supply of oxygen only one tenth of 
that which they normally consumed. 

The results also show the great increase in the requisite gas 
exchange with rise of temperature and the inability of the skin 
respiration of the frog to support life at even moderately high 
temperatures, at which the lungs and mouth alone are still sufficient. 


62 (671) 
Variations in the response of different arteries to blood 
serum and plasma, 


By HUGH A. STEWART and SAMUEL C. HARVEY. 


Recent work by Brodie, Sollmann, and O’Connor has shown 
that the blood contains substances acting on the vasomotor 
apparatus other than suprarenin. Even before the work of these 
investigators it had been noticed by Stevens and Lee that the 
use of defibrinated blood for the perfusion of isolated organs 
was often unsatisfactory because of the gradual diminution in 
outflow. This was not investigated thoroughly until 1900 by 
Brodie. He observed that the injection of blood serum into the 
jugular vein of a cat caused an immediate fall in blood pressure. 
The cat’s own serum was as efficient in this respect as the serum 
of any other animal. The cat, however, is the only animal which 
responds in this manner, for Brodie’s experiments were negative 
on the dog and rabbit. The mechanism in this case appears to 
be a reflex inhibition of the vasomotor center from excitation of 
the pulmonary branches of the vagus. The importance of Brodie’s 
work lies in the fact that he was the first to show that plasma and 


RESPONSE OF ARTERIES TO BLOOD SERUM AND PLASMA. 85 


serum are not identical in their physiological activities, for, 
whereas the effect just described is produced by serum, plasma 
is entirely inactive. The process of clotting liberates some 
substance to which this action is to be attributed. 

It was probably these experiments of Brodie which guided 
O’Connor in the analysis of the constrictor effect produced by 
blood serum on the hind limbs of the frog. He was able to show 
that the constriction produced by serum is not entirely due to its 
suprarenin content. Another substance comes into play which 
causes constriction and which is present only in the serum. 

We have investigated the vasomotor effect of plasma and 
serum in different vessels of the body, especially in regard to their 
mode of action. 

The methods we employed were the perfusion of the organ 
with Ringer’s solution in a moist atmosphere at the temperature 
of the body and under a constant pressure. The outflow from 
the vein was recorded with a signal magnet writing on a smoked 
paper. Two c.c. of serum or hirudin plasma were injected close 
to the canula inserted in the artery. 

Effect of serum.—The typical effect when injected into the 
vessels of the limb is to produce an immediate diminution in the 
rate of outflow. This usually lasts for from five to ten seconds, 
when it gradually begins to return to normal. The original rate 
of flow is regained in about five minutes. 

A similar result is obtained when the heart is perfused. 

Entirely different is the effect which is produced when 2 c.c. 
of serum are injected into the vessels of the perfused kidney. 
Instead of a vasoconstriction there is produced a pronounced 
vasodilatation. 

We have first to determine whether the dilatory effect on the 
kidney and the constrictor effect on the limb vessels are due to 
the same substance. It can readily be shown that two substances 
are operating. If the serum is boiled and filtered through a 
Berkfeldt filter and injected we now get no dilatation of the 
kidney vessels, but instead a constriction. 

As before, the effect of boiled serum is to produce a constriction 
of the limb vessels. 

Precipitation of the protein constituents of serum by alcohol 


86 SCIENTIFIC PROCEEDINGS (48). 


and the injection of the dried filtrate dissolved in Ringer’s solution 
retains the constrictor substance, but it contains no vasodilator 
for the kidney vessels. 

We are, therefore, led to the conclusion that serum contains a 
constrictor substance which acts on the limb vessels, the kidney 
vessels and the coronaries. In addition there is also present a 
dilator substance acting specifically on the renal vessels. The 
dilator substance is a proteid, the constrictor substance is not. 
The perfused kidney after the injection of serum is subject to the 
action of both a dilator and a constrictor substance. The dilator 
is the more powerful and masks the action of the constrictor. The 
constrictor substance becomes manifest after removal of the 
dilator by boiling or by precipitation by alcohol. 

Is the constrictor substance described above the suprarenin 
quotient of serum? Suprarenin, as is well known, causes con- 
striction by stimulation of the sympathetic nerve fibers. If we 
add apocodeine hydrochloride to the perfusion fluid we can para- 
lyze the sympathetics and in this way render the preparation 
insensitive to the strongest solutions of suprarenin. If, however, 
we inject serum there is still produced almost as great a diminution 
in the rate of outflow as before. We have thus evidenced that 
the constrictor substance is not suprarenin, and further, that it 
is a body which acts directly on the muscle coats. 

In regard to the dilator substance acting on the kidney we 
have found that it still causes an increased outflow after the 
injection of serum when the perfusion fluid contains apocodeine. 

Effect of plasma.—Plasma differs markedly in its action. If 
hirudin plasma is injected into the vessels of the limb it produces a 
much less constriction than does the corresponding amount of 
serum. This result is dependent only upon the amount of supra- 
renin it contains, for when the sympathetics are paralyzed the 
injection of serum produces no change in the rate of outflow. 

On the kidney vessels, however, plasma produces an even 
greater dilatation than does serum. 

The conclusions which we have been able to draw from these 
experiments are as follows. 

1. That in both plasma and serum there is present a substance 
which causes dilatation of the renal vessels. This substance is a 
proteid. 


RESPONSE OF ARTERIES TO BLOOD SERUM AND PLASMA. 87 


2. That the process of clotting liberates a vasoconstrictor 
substance which acts on the coronaries, the renal vessels and the 
limb vessels. It acts directly on the muscle coat and it is not a 
proteid body. 


63 (672) 
General physiological properties of diaphragm muscle. 
By FREDERIC 8. LEE and A. E. GUENTHER. 
[From the Department of Physiology, Columbia Unwversity.] 


Strips of the diaphragm of the cat, both curarized and non- 
curarized, have been excised after death and experimented with 
in moist chambers at room temperature. Their great resistance is 
demonstrated by the facts that they remain irritable two to three 
times longer than, and do several times the amount of work done 
by, a leg muscle, such as the extensor longus digitorum. Moreover, 
the diaphragm is not paralyzed by curare until long after the leg 
muscles have ceased to act. A most striking phenomenon is the 
tendency of the diaphragm strips to yield rhythmic twitches. This 
is much more pronounced than with the control leg muscles. It 
may be made manifest by the action of solutions of certain electro- 
lytes, where the twitches are irregular in extent and duration; and 
by weak faradic currents, which insure more regular responses. 
With 40 to 100 faradic stimuli in the second, the twitches occur 
at a rate of from 2 to 4. They are much more marked in non- 
curarized muscle. When irregularities due to the stimulated 
current are excluded, the following factors may possibly interact 
in the production of the rhythmic responses: (1) There may be 
present the Wedenski effect; (2) the weak stimulus may affect 
from time to time different groups of fibers within the muscle, the 
irritability of the groups varying; (3) polarizing factors may be 
present. The relations of these and other possible factors are 
not yet established. A strip of diaphragm muscle as a whole has 
a decided power of rhythmical response, but it is not yet certain 
whether this power is possessed by the individual muscle fibers. 


88 SCIENTIFIC PROCEEDINGS (48). 


64 (673) 
The stimulation of nerve-endings in muscle and the theory of 
receptive substances. 


By MARY WHITALL WORTHINGTON.! 
[Physiological Laboratory of the Johns Hopkins University.) 


Langley has shown that the stimulating action of nicotine 
upon muscle is prevented by curare and that this antagonism is 
exhibited also in muscles in which the nerve fibers have been 
removed by degeneration. This and other facts have led him to 
formulate the hypothesis of special receptive substances present 
in the muscle upon which these drugs and other chemical stimuli 
exert their action, and furthermore he ventures the generalization, 
in contradiction of the usual belief, that ‘‘in no case do chemical 
substances have a special action on nerve-endings.”’ 

The series of experiments here reported were made at the 
suggestion of Dr. J. W. Warren to test the above hypothesis. The 
gastrocnemius muscle of the frog was used and its reactions were 
studied after immersion in solutions of sodium sulphocyanide and 
potassium sulphocyanide. The following results were obtained. 

1. Action of potassium sulphocyanide.—This salt was used in 
hypertonic solutions (2 per cent. KCNS made up in a Ringer’s 
mixture) and in isotonic solutions (1 per cent. KCNS in water). 
In both cases solutions of this salt caused an immediate rapid 
primary contraction followed by a prolonged contracture. This 
effect was not removed by the action of curare nor by the de- 
generation of the motor nerve fibers. It was obtained also by 
the action of other potassium salts, e. g., potassium chloride—and 
must be considered as an instance of the “‘ potassium contraction” 
described by other authors. The potassium ions may act upon 
the supposed receptive substance, but evidently their effect does 
not depend upon the presence of the nerve terminals. 

2. Action of sodium sulphocyanide—This salt was used also in 
hypertonic and isotonic solutions as in the case of the potassium 
sulphocyanide. In hypertonic (2 per cent.) solutions it caused a 
large primary contraction followed by a condition of contracture 
and by frequent isolated or grouped twitches of a codrdinated or 

1 Deceased. Presented by W. H. Howell. 


STIMULATION OF NERVE-ENDINGS IN MUSCLE. 89 


fibrillar character. In isotonic solutions the primary contraction 
was lacking, but fibrillar twitches occurred, although less fre- 
quently than in the hypertonic solutions. Hypertonic solutions 
(2 per cent.) of sodium chloride failed to give anything more than 
a small increase in tone. The marked primary contraction as well 
as the isolated twitches observed in the hypertonic solutions of 
sodium sulphocyanide were entirely lacking in the muscles of 
curarized frogs or in frogs in which nerve degeneration had been 
effected by cutting out a portion of the sciatic nerve. In the 
latter experiments observations were made upon frogs at varying 
intervals from 3 to 51 days after section of the nerve. It is 
noteworthy that the falling out of the contraction caused by the 
sodium sulphocyanide was observed as early as seven days after 
section and at a time when a response could still be obtained from 
the muscle by electrical stimulation of the peripheral end of the 
nerve. So, also, in the case of curare it was found that the sodium 
sulphocyanide contraction might be abolished even when the 
curarization of the animal was incomplete. Two per cent. solu- 
tions of sodium sulphocyanide have no stimulating action upon 
the sciatic nerve when immersed in the solution. 

Conclusion.—The stimulating action of sodium sulphocyanide is 
not simply a sodium effect. The fact that its action is abolished 
by curare may be explained in accordance with Langley’s hypothe- 
sis of receptive substances, but the fact that its action is readily 
removed by de-nervating the muscle is in contradiction to the 
generalization made by Langley in regard to the improbability of 
a special action of chemical substances upon the nerve endings 
in muscle. 

Since hypertonic solutions of the sodium sulphocyanide do 
not stimulate the motor fibers in the sciatic nerve, their action in 
stimulating the muscle can be explained only on the assumption 
that they stimulate the nerve endings, if one bears in mind that 
this stimulating action falls out after the nerve fibers in the muscle 
begin to degenerate, as well as after administration of curare. 
It is noteworthy that the stimulating effect of this sodium sulpho- 
cyanide upon the nerve-terminals disappears in the incipient 
stages of the degeneration following section of the motor nerves. 


go SCIENTIFIC PROCEEDINGS (48). 


65 (674) 


On the isolation of odcytase, the fertilizing and cytolyzing 
substance in mammalian blood-sera. (Preliminary 
report.) 


By T. BRAILSFORD ROBERTSON. 


[From the Rudolph Spreckels Physiological Laboratory of the 
Unwersity of California.] 


It has been observed by Loeb that the eggs of sea-urchins 
(Strongylocentrotus purpuratus) may be induced to form fertiliza- 
tion-membranes by immersing them in mammalian blood-sera 
which have been rendered isotonic with sea-water by the addition of 
NaCl. Occasionally, if the serum be especially potent, simple im- 
mersion of the eggs in the serum suffices to bring about this result, 
but asarule previous treatment of the eggs with a sensitizing agent 
(SrClz or CaCl) is required. Prolonged action of the serum upon 
sensitized eggs results in the cytolysis of the eggs. Very potent 
sera usually cause agglutination of the eggs as well, especially of 
sensitized eggs. 

I have isolated from ox-serum a fraction which is extremely 
potent in fertilizing, cytolyzing, and agglutinating sea-urchin eggs. 

To 860 c.c. of fresh, whipped, and centrifugalized ox-serum, 
which had been rendered isotonic with sea-water by the addition 
of 244M NaCl solution, I added 400 c.c. of 7 per cent. BaCle. A 
thick cloud was produced. This mixture after standing for an 
hour in a warm place until its temperature rose to 37° C. was 
centrifugalized. The entire precipitate, consisting of BaCOs, 
BaSQ,, and the barium compound of the fertilizing agent and, 
possibly, of other substances, settled in the form of a cake at the 
bottom of the centrifuge-tubes. This precipitate was thoroughly 
drained and then suspended several times in 2 per cent. BaCle 
and re-centrifuged in order to free it from adherent serum. It 
was then stirred up for an hour in 100 c.c. of N/1o HCl and the 
insoluble residue (probably barium sulphate) was centrifuged out. 
To the clear fluid thus obtained were added 10 c.c. of 10 per cent. 
NazSO, in order to free it from barium. This mixture was allowed 
to stand for some hours at 50° and then centrifuged. The clear 


ON THE ISOLATION OF OOCYTASE. gI 


yellowish fluid thus obtained yielded no precipitate or opalescence 
upon the further addition of Na,SO, and was therefore free from 
barium. To this fluid were added 4 volumes of acetone. A light 
flocculent precipitate was formed at once which settled readily. 
This was collected upon a hardened filter, washed in alcohol and 
ether, and dried for 314% days over H2SO, at 36° C. 

The substance thus obtained does not dissolve in sea-water. 
It dissolves readily in N/10 HCl and remains in solution upon 
neutralization. To this solution sufficient 244M NaCl was 
added to render it isotonic with sea-water and the solution (0.5 
per cent.) thus obtained was diluted to 1, %,... , etc., by the 
addition of sea water. On adding sea water, the mixture becomes 
very opalescent but the substance is not precipitated. 

Eggs of Strongylocentrotus purpuratus which have not under- 
gone previous sensitization are fertilized and agglutinated by 
solutions of this substance in dilutions of from 1 part in 200 to I 
part in 800. Eggs which have been sensitized by immersion for 
4 minutes in M/2 CaCl are fertilized and agglutinated by dilutions 
of from I part in 200 to I part in 1,600. Eggs which have been 
sensitized by immersion for 4 minutes in M/2 SrCl: are agglutinated 
by dilutions of from I part in 200 to I part in 25,000. The 
sensitizing action of SrCle and CaCl, is clearly seen to reside in 
their power to precipitate the fertilizing agent upon the egg. 

Since this substance is thermostable, withstanding 18 hours’ 
exposure to a temperature of 50° without destruction, and there 
is some reason for suspecting that it is not present as such in 
circulating blood but is discharged from white corpuscles in shed 
blood, it would appear to present many analogies to the cytases or 
cell-liquefying substances found by Metchnikoff in white cor- 
puscles. Accordingly, I propose that it be called ‘‘Odcytase.” 


92 SCIENTIFIC PROCEEDINGS (48). 


66 (675) 
The food factor in hibernation. (Preliminary communication.) 


By SUTHERLAND SIMPSON. 


[From the Physiological Laboratory, Medical College, Cornell 
Unwwersity, Ithaca, N. Y.] 


In those animals that hibernate the condition is generally 
believed to be brought about mainly by a low external temperature; 
when the winter cold sets in the animal retires to its burrow or nest 
and remains dormant until spring. Some, on the other hand, hold 
that a diminished food supply is the chief, or at any rate, an im- 
portant cause of hibernation, and my experience with a colony of 
woodchucks (Marmotta monax) during the past winter would ap- 
pear to support the latter view. 

About the middle of September, 1911, eighteen woodchucks, 
which had been caught in box traps in the neighborhood of Ithaca, 
and were uninjured, were placed in eight artificial burrows about 
five feet below the surface of the ground, the object being to study, 
amongst other things, changes in the nervous system during 
hibernation. The burrows, which were packed with dry straw, 
opened into a central court into which food (clover, corn, apples, 
carrots, etc.) was placed every second day, and it was expected 
that when the animals began to hibernate the food would cease 
to be consumed. 

In this locality I was told that woodchucks are rarely seen in 
the open fields later than the first or second week of October, and 
as the food still continued to disappear after that time, the burrows 
were opened up and the animals caught and examined to find out 
their condition, on the following dates.—Oct. 13, Nov. 11 and 27, 
Dec. 18 and 26. They were found to be quite active on all these 
occasions, with rectal temperatures somewhere in the neighbor- 
hood of 100° F. 

The weather up till the end of December had been unusually 
mild for this climate, and this might possibly have had some 
influence in maintaining the wakeful condition, but from the 
beginning of January till the end of March the winter was exces- 
sively cold, the air temperature being often below zero fahrenheit, 


Tue Foop Factor IN HIBERNATION. 93 


and on two occasions 16° below. Notwithstanding this low 
temperature the food was still eaten by the woodchucks. 

No food was supplied from Jan. 20 till Feb. 14 when the animals 
were again examined in the burrows. On that day their tracks 
in the snow were abundant. Six were found to be in a semitorpid 
condition, but they did not show the deep narcosis of true hiberna- 
tion; the others were very active and combative, one having a 
rectal temperature of 99° F. Although no food had been placed 
in the inclosure for three weeks, it is still possible that they had 
some stored in their burrows, or that they ate the straw. 

The six which showed some degree of torpor were removed to 
the laboratory, kept overnight outside the building in a large box 
amongst straw, and the next day, under ether anesthesia, a 
small lesion was made in the spinal cord of each. On the day 
following they were completely awake and active, and remained 
so until killed at various intervals after the operation. Food was 
supplied to these as well as to those left behind in the burrows 
from Feb. 14 onwards; they were inspected at short intervals from 
that date till the end of March and never showed any tendency 
to hibernate. The rectal temperature ranged from about 95° F. 
to 101° F. 

These animals were not artificially protected from the weather 
in any way; the only circumstance in which their condition dif- 
fered from that of their fellows in the open fields was that food 
was furnished them. The behavior of this colony would seem to 
point to the fact, therefore, that the absence of food supply is 
an important factor in determining the onset of hibernation. 


67 (676) 
A rapid method of producing a hemolytic serum. 
By FREDERICK P. GAY and J. G. FITZGERALD. 
[From the Department of Pathology and Bacteriology, University of 
California.] 


Fornet and Miiller! were first to suggest the intensive method 
of immunizing animals by giving large doses of serum for pro- 


1Fornet and Miiller, Zestschrsft fiir biologtsche Technik und Methodik, Strassburg, 
1908, vol. I, p. 201. 


94 SCIENTIFIC PROCEEDINGS (48). 


ducing precipitins intra-peritoneally on successive days. Such a 
method apparently gave rise to a potent precipitating serum and 
they claim equally successful results in producing hemolysins. 
These results as regards hemolysins were not confirmed in a later 
communication by Bonhoff and Tsuzuki.1 

We have found that one can obtain uniformly a sufficiently 
potent hemolytic serum for fixation tests by immunizing rabbits 
with washed sheep blood in a dose of one to two cubic centimeters 
administered intravenously on three successive days. The hemo. 
lytic titer of such a serum four days after the third injection is 
usually 1 to 2,000. In other words, it is possible to produce a 
thoroughly reliable hemolytic serum in one week by this method. 

Further details of this intensive method of immunizing to 
produce hemolytic sera and also its use in producing precipitins, 
bacteriolysins, agglutinins, and antitoxins will form the basis of 
a more extensive communication to be published in the Patho- 
logical series of the University of California Publications. 


68 (677) 


Note on the effect of the internal secretions upon the secre- 
tion of epinephrin. 


By ISAAC OTT and JOHN C. ScorT. 


One? of us was the first to show that the adrenal secretion 
relaxed and inhibited the rhythmic contractions of the intestine. 
Hoskins has shown that a dilution of 1-400 millions of epinephrin 
inhibits the rhythmic contractions. It thus becomes the most 
sensitive test for the presence of epinephrin. We tested its pres- 
ence by the Magnus method. We injected a few grains of the 
filtered solution of the different glands into the jugular of the 
narcotized cat, and drew off, as Cannon has done, some blood from 
the vena cava above the openings of the adrenal veins, and de- 
fibrinated it. Normal blood defibrinated was then applied to 
a segment of the intestine of a narcotized rabbit and its rhythmic 
movements recorded. Then the blood, after the injection of the 
glandular filtrate, was applied to the same intestine and its move- 


1 Bonhoff and Tsuzuki, Zeitschrift fiir Immunitatsforschung., IV, page 180. 
2 Medical Bulletin, 1897, p. 376. 


SECRETIONS UPON THE SECRETION OF EPINEPHRIN. 95 


ments registered. It was found that the injection of iodothyrin, 
parathyroid, infundibulin, thymus and pineal caused a distinct 
fall in tonus and inhibition of rhythmic contractions, showing 
the presence of epinephrin beyond normal in the blood. Normal 
blood of the cat never produces this effect, but stimulates 
tonus and rhythmic contraction. We have been careful to 
exclude albumen in these glandular tests, as the foreign albumen 
in the antithyroid serum of Mébius and in the diphtheritic anti- 
toxic serum in 2 drop doses increases the amount of epinephrin in 
the blood. As cholin also produces an epinephrin reaction we 
can only be certain that iodothyrin and infundibulin stimulate 
the adrenals. 


69 (678) 
Standardization of the Wassermann reaction. Attempts to 
prepare a standard antigen and antibody. 


By J. G. FITZGERALD and J. B. LEATHES. 


[From the Department of Pathological Chemistry, Univ. of Toronto, 
and Department of Pathology and Bacteriology, Univ. of 
California.] 


For some time past we have endeavored to determine more 
exactly the nature of the Wassermann reaction. This led us first 
to an investigation of the antigen. In this connection Noguchi, 
and we ourselves, have shown the importance of the substances 
contained in the acetone precipitate. Incidentally, we have found 
that an antigen containing these substances (lipoids) is available 
for use after a period of two years. The exact steps in the pro- 
duction of this antigen differ in certain details from methods here- 
tofore published. The method will appear, shortly, elsewhere. 
The next step in the work was an effort to produce an antibody 
to this relatively stable antigen. Three attempts have been made 
and all were unsuccessful. No evidence of antibody formation 
could be shown by means of the reaction of fixation or the precipitin 
reaction. These lipoid substances were found not to act as antigens. 

Had the production of an antibody been possible, the stand- 
ardization of the Wassermann reaction could have been accom- 
plished. This was the ultimate object of the work. No method 


96 SCIENTIFIC PROCEEDINGS (48). 


has been devised that permits of the “‘lipotropic’”’ content of 
syphilitic sera being determined by quantitative methods by com- 
paring them with such a standard serum as we have tried un- 
successfully to produce. Noguchi has shown that one can deter- 
mine the absolute amount of a given syphilitic serum that will 
give complete fixation with a fixed amount of antigen, under 
certain conditions, at any given time. 

In addition, for purposes of comparison at different times it 
would be necessary to have a standard antigen and a standard 
antibody (a “synthetic syphilitic’? serum) both of relatively 
constant potency. These things are at present impossible. Quan- 
titative standardization of the Wassermann reaction is, therefore, 
not feasible in the present state of our knowledge. 


SCIENTIFIC PROCEEDINGS. 


ABSTRACTS OF THE COMMUNICATIONS. 
Forty-ninth meeting. 


University and Bellevue Hospital Medical College. May 15, 1912. 
President Ewing in the chair. 


70 (679) 
The effect of chemicals on the division rate of protozoa. 


By GARY N. CALKINS. 
[From the Department of Zoélogy, Columbia University.] 


These experiments have been carried out during the past year 
for the purpose of finding out whether the products of nucleo- 
proteid breakdown have any effect upon the division rate of free- 
living cells, the ultimate aim being to get some light on the con- 
trolling factors of cell division. 

Two ciliated protozoa were used. One, Actinobolus radians 
Stein, lives exclusively on a diet of Halteria grandinella, another 
ciliate. The other, Blepharisma undulans Stein, lives on bacteria. 
Four control lines of each have been watched, fed, and the number 
of divisions recorded daily, and curves based upon the averaged 
division rates for five day periods, give the fluctuations in vitality 
of the organisms as measured by the division rates. Periods of 
depression, and of decreasing and increasing vitality have been 
clearly marked. Individuals for experimentation were in all 
cases sister cells of the control lines of the same dates. 

The chemicals used included various amino acids, nucleins, 
and their derivatives, for many of which I am indebted to Dr. 
Levene and Dr. Walter Jones. In each experiment four strengths 
of chemical were used after empirical determination of the lethal 
dose. The number of divisions of all four lines were averaged 

97 


98 SCIENTIFIC PROCEEDINGS (49). 


for five-day periods for comparison with the controls of the same 
periods, and all experiments were continued for at least ten days. 

The results show that amino acids and their derivatives have 
but slight effect on the division rate at any period of vitality. The 
purins and their derivatives have but a slight effect on the division 
rate when vitality is very low or very high, but a marked effect of 
increasing the rate when vitality is decreasing (allantoin) or 
increasing (hypoxanthin, xanthin). 


71 (680) 
The first onflow and diastolic waves in the venous pulse. 


By E. M. EWING. 


[From the Department of Physiology of the University and Bellevue 
Hospital Medical College.| 


Simultaneous records of the contractions of the auricle and 
ventricle, intraventricular pressure, arterial pulse, and the pulse 
of the superior vena cava were made. 

Previous investigators have not agreed as to the time relations 
of the 3d positive (Mackenzie’s ‘‘v’’) wave, some placing its 
appearance during ventricular systole, and others believing that it 
occurs in diastole. This confusion has arisen from the fact that 
Mackenzie’s ‘‘v’’ wave in reality consists of two positive waves 
which are separate both in time and origin. (Bard described two 
such waves, but was not definite concerning the time relations.) 

The first of these waves has been called the “‘onflow’’ wave, and 
the second, the ‘‘diastolic’’ wave. They are preceded, of course, 
by the auricular and systolic (‘‘c’’) waves. 

In a series of some fifty dogs, the onflow wave has always 
appeared just at the end of auricular relaxation, and therefore, 
during the first half of ventricular systole. The wave is terminated 
at the very beginning of ventricular diastole. The origin of the 
wave cannot be ascribed to the passive auricle, nor to the ventricle, 
the base of which is still moving downward, and which would 
tend, therefore, to produce a negative, rather than a positive 
wave. The wave must simply represent the increased pressure 


DiasToLic WAVES IN THE VENOUS PULSE. 99 


resulting from the onflowing blood, which can now no longer enter 
the completely relaxed auricle, and must necessarily “back up”’ 
into the great veins. The instant ventricular relaxation com- 
mences, the base of the ventricle pushes up against the column of 
blood in the auricle and veins, and thus produces a still greater 
pressure—i. e., the diastolic rise. In all of the experiments this 
diastolic rise has occurred synchronous with the beginning of 
ventricular relaxation, before the closure of the semilunar valves. 
The auricle, of course, is still passive. 

The diastolic rise continues until the ventricle has relaxed 
sufficiently to allow the a-v valves to open, when the increased 
pressure in the auricle is terminated by the rapid outrush of 
blood. The resulting diastolic fall then continues until the end of 
ventricular relaxation, or, in other words, until the ventricle 
ceases to enlarge and receive the onflowing blood. The blood 
which cannot enter the ventricle, ‘backs up”’ into the auricle and 
veins, and thus produces the 2d onflow wave (Hirschfelder’s ‘“‘h’’), 
in a manner similar to that in which the Ist onflow wave was 
originated. 

The reason for the non-appearance of the Ist onflow wave in 
many jugular pulse tracings is that it is partially or completely 
fused with the diastolic wave. (The point of separation is indi- 
cated by a notch in many of Mackenzie’s records.) The ‘‘a,’’ ‘‘s,”’ 
and ‘‘d”’ waves are essentially impact waves, and therefore travel 
faster than the onflow wave, which is dependent, for its rate of 
propagation, upon the rapidity of the onflow of blood from the 
periphery. The onflow wave appears just after the ‘‘s’”’ wave in 
the lower part of the sup. vena cava, but by the time the effect of 
the “backing up”’ of blood has been felt in the veins of the neck, 
the onflow wave has been overtaken and obscured by the “d”’ 
wave. 

The above conclusion is supported by figures from several 
experiments, showing that the onflow wave appeared in the jugular 
vein .05 second later than in the venacava. The relative positions 
of the “a,” “s,” and ‘“‘d’”’ waves do not vary in the different 
regions. 


100 SCIENTIFIC PROCEEDINGS (49). 


72 (681) 


On the action of the infundibular portion of the hypophysis 
upon vasodilators. 


By J. AUER and 8. J. MELTZER. 


[From the Department of Physiology and Pharmacology of the 
Rockefeller Institute.| 


By the investigations of Oliver and Schafer, Howell and others, 
it has been established that by intravenous injections of an extract 
of the infundibular portion of the hypophysis a rise of blood 
pressure is produced, which, however is usually not as strong as 
the one produced by an injection of adrenalin. It is now generally 
assumed that, like adrenalin, the rise is produced by a stimulation 
of the constricting mechanism. On the basis of the hypothesis, 
that the hypophysis may raise the blood pressure not by a stimula- 
tion of the constricting, but by a depression of the vasodilating 
mechanism, we studied the effect of stimulation of the depressor 
nerve in rabbits soon after an intravenous injection of an extract 
of the hypophysis. We used for this purpose the pituitrin of 
Parke, Davis & Co., which is made up from the infundibular portion 
of the hypophysis. In some of the experiments the pituitrin 
was heated for the purpose of driving off the chloretone. In some 
of the experiments both vagi were cut to eliminate the inhibitory 
action through these nerves. 

We may state briefly that in every experiment the irritability 
of the depressor nerve was either abolished or considerably reduced 
for a few minutes after the injection of the pituitrin. This was 
definite even before the rise which follows the injection began to 
develop and also during an insignificant rise. The larger the 
injected dose of pituitrin, the longer did the reduction of the irrita- 
bility of the depressor nerve last. In 12 or 16 minutes, however, 
the irritability, as a rule, returned to normal. On repeating the 
injections, the reducing effect upon the irritability of the depressor 
became less and less pronounced. 

We may recall here the fact, observed by Oliver and Schafer 
and others, that during the rise of blood pressure from adrenalin, 
stimulation of the depressor nerve is ineffective. But this applies 


ON THE REDUCTION OF TOXICITY OF STRYCHNIN. IOI 


only to the strong rise which sets in, as is known, immediately 
after injection of that substance. With the onset of the descent 
of pressure the depressor action of the depressor nerve becomes 
more and more effective. Here the inefficiency of the stimulation 
of the depressor may be due merely to the inability of the de- 
pressor nerve to overcome the high pressure. It is different, 
however, with the action of the hypophysis. Here the rise of 
blood pressure develops as a rule, gradually and sometimes it is 
even preceded by a fall. Furthermore in some instances the rise 
is comparatively insignificant. Nevertheless in all these condi- 
tions there is definite evidence of a striking reduction of the 
irritability of the depressor. We are therefore, for the present, 
inclined to look upon the discovered reduction of the irritability of 
the depressor nerve as a confirmation of our hypothesis that the 
infundibular portion of the hypophysis reduces the irritability 
of vasodilators. We may mention that studies upon the vaso- 
motor effects of stimulations of the central end of the vagus nerve 
in dogs, which we,shall not discuss here in detail, seem to furnish 
a further confirmation of this view. As to the locality where the 
hypophysis develops its action, whether upon the central or periph- 
eral mechanisms or upon both, we shall not discuss at present. 


73 (682) 


On the reduction of toxicity of strychnin by the simultaneous 
administration of large quantities of fluid. 


By I. 8. KLEINER and 8S. J. MELTZER. 


[From the Department of Physiology and Pharmacology of the 
Rockefeller Institute for Medical Research.| 


In the course of some experiments on adrenalin glycosuria in 
which the simultaneous injection of blood, serum or lymph with 
adrenalin was studied, it became manifest that the significance 
of the factor of dilution had to be previously established. It was 
thought that the study of the effect of dilution upon strychnin 
poisoning would throw some light upon this. The definite and 
instructive results which were obtained will be stated here very 
briefly. 


102 SCIENTIFIC PROCEEDINGS (49). 


Controls.—Six rabbits received subcutaneously 0.45 mg. strych- 
nin per kilogram body weight. All six had convulsions, with fatal 
termination in three. Nine animals received 0.5 mg. per kilo; 
all had convulsions, terminating fatally in four. In 15 controls, 
then, a dose of 0.5 mg. strychnin or less per kilo body weight 
brought on convulsions in every one and a fatal termination in 7; 
in other words 0.5 mg. strychnin proved to be toxic in 100 per 
cent. and fatal in 47 per cent. 

Strychnin diluted in too c.c. of normal saline-—Ten rabbits 
received subcutaneously doses of strychnin varying between 0.7 
and 0.84 mg. per kilo body weight diluted in 100 c.c. of 0.9 per 
cent. sodium chlorid. Of these only two had convulsions, one of 
which died. In other words, strychnin in great dilution is con- 
siderably less toxic; doses which exceed the minimal fatal dose 
proved to be toxic only in 20 per cent. and fatal in 10 per cent. 

Strychnin and saline injected in separate places.—In a series of 
eleven rabbits each received subcutaneously 0.5 mg. strychnin per 
kilo body weight at one point shortly after having been injected 
with 100 c.c. of 0.9 per cent. sodium chlorid at another place. Of 
these only three had convulsions and only one died. In other 
words, when 100 c.c. of saline was injected in another part of the 
body, a dose of 0.5 mg. per kilo of body weight, which in controls 
proved toxic in 100 per cent. and fatal in 47 per cent., was toxic 
only in 27 per cent. and fatal in 9 per cent. 

Strychnin subcutaneously and water given by mouth—Eight 
rabbits received 0.5 mg. strychnin per kilo body weight sub- 
cutaneously shortly after 100 to 150 c.c. of water had been given 
by mouth. Of these animals only two had convulsions and none 
died, that is, in these cases 0.5 mg. strychnin proved to be toxic 
only in 25 per cent. and caused no fatalities. Twelve animals 
were given strychnin subcutaneously, in doses varying between 
0.52 and 0.56 mg. per kilo body weight, receiving at the same time 
100 c.c. of water by mouth. Of these animals four had convulsions 
and none died. In other words even doses which definitely exceed 
the sure toxic dose of 0.5 mg. per kilo, proved toxic only in 33 
per cent. with no fatalities at all, when at the same time, a com- 
paratively large quantity of water was given by mouth. 

These experiments seem to demonstrate conclusively that the 


INFLUENCE OF INFUNDIBULAR HYPOPHYSIS UPON PUPIL. 103 


toxicity of strychnin is definitely reduced not only when it is 
administered in great dilution, but also when saline or water is 
administered nearly simultaneously in other parts of the body, 
thus, perhaps, diluting the poison within the circulation. These 
results are of general theoretical interest and have obviously 
also a practical bearing, neither of which we shall discuss here. 


74 (683) 


The influence of the infundibular portion of the hypophysis 
upon the pupil. 


By S. J. MELTZER. 


[From the Department of Physiology and Pharmacology of the 
Rockefeller Institute.] 


The action of the extract of the hypophysis is similar to that 
of adrenal extract in the first place by the influence which both 
exert upon blood pressure. There seems to be also some similarity 
in their action upon the uterus and intestines. With regard to 
the action of hypophysis upon the frog’s pupil which, as is well 
known, becomes definitely dilated by adrenalin, opinions differ. 
While Cramer and others report a dilatation, Kepinow and Gottlieb 
recently stated that in their hands the extract of the hypophysis 
caused a constriction of the frog’s pupil. In my own observations 
upon the enucleated bulbi from Rana pipiens, heated and un- 
heated pituwitrin (Parke Davis & Co., prepared from the infun- 
dibular portion of the hypophysis) im most instances caused a dilata- 
tion of the pupil. The extent of the dilatation varied greatly in 
various eyes and was never as striking as is observed under the 
influence of adrenalin. Ina smaller number no dilatation of the 
pupils took place; but in no instance have I observed a miosis follow- 
ing the bathing of the bulbt in pituitrin. 

A very striking test is the action of adrenalin on the pupil of 
mammals (rabbit or cats) on the side on which the superior cervical 
ganglion had been removed 24 hours or longer. If a sufficient 
dose was used, that pupil showed a maximal dilatation which may 
last for hours, while the pupil on the normal side remains un- 
changed. I have studied this test with pituitrin. In six rabbits 


104 SCIENTIFIC PROCEEDINGS (49). 


in whom one superior cervical ganglion had been removed, either 
on the right or on the left side, I have injected at various times 
various doses of pituitrin—1I c.c., 2 c.c. and 3 c.c.—through the 
marginal ear vein. At no time did a dilatation of the pupil on the 
operated side follow these injections, neither soon nor late. Both 
pupils, however, and especially that of the eye on the operated side, 
showed a constriction of short duration immediately after the in- 
jection. 

Here we meet, then, with a definite difference between the 
action of adrenalin and pituitrin which, in some cases, might 
assist in the identification of the nature of the blood-raising prin- 
ciple found to be present in some fluids. 


75 (684) 


Observations on the relation of carbon dioxide and oxygen to 
the development of certain amphibian embryos. 


By A. M. BANTA. 


[From the Station for Experimental Evolution, Cold Spring Harbor, 
Long Island, New York.] 


The following observations were made during the past two 
seasons upon material kept for other purposes.! 

Eggs of all the species mentioned below were placed when 
fresh or in early cleavage in artesian water containing 1.32 per 
cent. of CO., the amount normal to large open ponds here being 
only about 0.04 per cent. 

Ambystoma punctatum.—Development was at the normal rate 
with no mortality of embryos traceable to the CO, in the water. 
The larve likewise lived fairly well, though in many cases not so 
well in the CO, water as in pond water. 

Spelerpes bilineatus—Cleavage and later development were 
probably at the normal rate, but there was a large mortality 
percentage in standing or running artesian water. The mortality 
was less in standing water from ponds but thoroughly oxygenated 
water comparatively free from CO: was necessary to get the 
highest percentage of developing embryos. 


1 Observations on Spelerpes, Rana pipiens (?), and Rana sylvatica were made 
on material kept in collaboration with Dr. R. A. Gortner, of this station. 


DEVELOPMENT OF CERTAIN AMPHIBIAN EMBRYOS. 105 


Bufo lentiginosus.—Only a small percentage developed at all 
and none beyond early cleavage. 

Hyla versicolor and Hyla pickeringii—A few went through 
cleavage but none beyond. 

Rana pipiens (?).—Mortality was very large during early 
stages but perhaps 5 per cent. developed until the embryos were 
considerably differentiated and about 3 mm. in length. None 
developed further. In two of the ponds observed all the eggs and 
embryos of this species died much as those placed in CO2 water 
in the laboratory. These were ponds practically without aquatic 
plants and containing great quantities of decaying leaves and 
other plant debris and therefore doubtless had much CO, in the 
water. 

Rana sylvatica—The development was apparently at the 
normal rate. In many cases the larve hatched, but though 
active for a day or two and clinging to the jelly mass and sides 
of the jars in the usual fashion took no food and developed no 
further. All died within a few days. In other jars where con- 
siderable masses of the eggs were placed and where large numbers 
died before hatching the larve in the interior of the masses and 
thus least exposed to the CO: water survived longest. 

Often the eggs of the inner portions of the egg masses of Rana 
sylvatica and Ambystoma tigrinum (all of which were otherwise 
developing normally) show a retarded development, progressively 
the more so the farther the eggs are from the periphery of the mass, 
due to insufficient oxygen. In one egg mass of Ambystoma the 
exterior embryos of the mass were 10.2 to 11 mm. long and almost 
ready to hatch, while at the other extreme those deepest within 
the mass were only 3.6 mm. long and still in the late neural groove 
stage. In most cases in the ponds where the Ambystoma eggs 
are laid, as well as in jars in the laboratory, a portion of the 
interior of the masses die before hatching. In one pond near 
the laboratory protected from wind and containing very quiet 
and poorly oxygenated water perhaps 90 to 95 per cent. of the 
eggs die each year. That insufficient oxygen is the cause was indi- 
cated by the low percentage mortality in a few masses left almost 
entirely exposed to the air by the lowering of the level of the pond. 
These conditions were imitated in the laboratory with the result 


106 ScIENTIFIC PROCEEDINGS (49). 


that in some cases 60 to 100 per cent. of the eggs of egg masses 
kept in a depth of 12 to 18 inches of quiet, poorly oxygenated 
water died, while in similar adjoining vessels eggs less than half 
submerged developed almost without exception. 


76 (685) 
Direct observation of cell division in mammalian tissue. 


By ROBERT A. LAMBERT. 


[From the Department of Pathology, College of Physicians and 
Surgeons, Columbia University.] 


Connective tissue cells of the rat cultivated outside the body 
in rat plasma for as long as seventy-six days formed the material 
for observation. For maintaining activity for such a period, the 
pieces of tissue were transferred to fresh plasma at intervals of 
five to ten days. Measures employed by Carrel for rejuvenating 
the cells in old cultures were found to be unnecessary. 

We have found that the process of karyokinetic division may 
be followed in the living cells. The earlier phases often escape 
notice. The later phases, however, may be observed with ease 
even with the lower powers of the microscope. In actively 
growing cultures the time required for the entire process is from 
forty to sixty minutes. The time elapsing between the divergence 
of the masses of daughter chromosomes to complete division of the 
cytoplasm averages about ten minutes. In slowly growing cul- 
tures the process may be retarded. A half hour to an hour after 
division is required for the daughter cells to develop the form and 
staining qualities of the resting cell. These time periods relate to 
observations made on cells at 35-37°C. At lower temperatures 
(25-30°) the process is slower. 

Cells containing numerous fat droplets have been seen to 
divide as rapidly as cells free from fat. 

Amitotic division has not been observed. 

Cells after division have been followed and further division 
noted. The size reached by these daughter cells was approxi- 
mately that of the parent cells. This observation affords proof 
that true growth takes place in cells cultivated in vitro. 


EFFECT OF DRYING UPON THE VIABILITY OF BACTERIA, 107 


77 (686) 
The effect of drying upon the viability of bacteria. 


By C. E. A. WINSLOW and F. ABRAMSON. 


[College of the City of New York.| 


The curve of viability, measuring the rate of decrease among 
bacteria exposed to an unfavorable environment, has been deter- 
mined for many conditions. Drying is known to cause a rapid 
elimination, but no exact quantitative determinations have been 
made. In the experiments here reported, colon bacilli were used. 
One cubic centimeter of a 48-hour broth culture was mixed with 
21% grams of sea sand spread out in an ordinary Petri dish. 
Duplicate dishes prepared in this way were covered with porous 
earthenware tops and kept for various periods of time from four 
hours to ten days. At the end of each period nine cubic centi- 
meters of sterile water were added to the sand in one of the dishes 
and well mixed by careful agitation. Portions of this water were 
then plated in duplicate on agar in the usual manner. 

The results of eight series of tests are shown in the table 
below expressed in percentages of the original number of bacteria 
present. The original numbers in different series varied from 
4,150,000 to 117,300,000 per gram of sand, and the final number 
remaining after ten days in Series II and III were 20,700 and 
18,900 per gram, respectively. The average temperature and 
humidity of the room in which the plates were kept is shown for 
the last five series at the bottom of the table. 


PERCENTAGE OF ORIGINAL NUMBER SURVIVING. 


Series. 


Period 
Ele uts ie I. lil. IV. V. VI. VII. VII. 
es 76.45 
52 57.18 
6 75.90 79.82 
7 57-56 37.46 57-76 
8 67.23 59.30 69.03 
10 44.48 41.38 
24 85 85 85 
48 .16 -16 “15 
120 -08 .06 .06 
166 -04 .04 .04 
216 .02 02 
240 .02 .02 
Average temperature....... 69° 69° 70° 69° 69° 


Average relative humidity ...| 090% 72% 60% 90% 12% 


108 SCIENTIFIC PROCEEDINGS (49). 


The results are quite concordant when the dryness of the 
atmosphere is taken into consideration. Series VI showed a more 
rapid reduction than the others during the first 7 hours and the 
relative humidity was 60 per cent. Then came Series V and VIII 
with a relative humidity of 72 per cent., while in Series IV and 
VII with an atmospheric humidity of 90 per cent., nearly 70 per 
cent. of the bacteria were alive after 8 hours. - 

The general rate of reduction was directly proportional to the 
time, during the first 24 hours, and then fell off more and more 
gradually. As a rule, intestinal bacteria in any foreign medium, 
colon bacilli in water, for example, decrease rapidly at first and 
more and more slowly as time goes on, following almost a parabolic 
curve. Most die at first, but a few persist for a long time. In 
its general relations the curve for drying is similar. 99 per cent. 
of the bacteria are gone after 24 hours while 2 out of 10,000 persist 
after 10 days. The curve for the first 24 hours is however here 
practically a straight line. 50 per cent. perished after 10 hours, 
and 99 per cent. after 24 hours. This is to be explained by the 
fact that during this period the bacteria were not exposed to con- 
stant conditions, since the originally moist sand was becoming 
progressively dryer. Determinations made by weighing at inter- 
vals duplicate samples prepared just like those which were in- 
oculated with the bacteria showed that nine tenths of the moisture 
in the sand was gone after 10 hours and practically all of it was 
gone after 24 hours (with an atmospheric humidity of 80 per cent.). 
With a constant unfavorable environment, the reduction of 
bacteria proceeds at a decreasing rate. With an environment 
growing more and more unfavorable we might expect an approxi- 
mately even rate of reduction such as is indicated here. 

So far as the absolute reduction is concerned, it appears that 
drying is highly inimical to the bacteria studied. A uniform 
reduction of 99 per cent. is indicated after 24 hours. It takes 
over a week to reach such a point when colon bacilli and similar 
intestinal forms are stored in water. 


DETERMINATION OF AMINO-ACID NITROGEN IN URINE. 109 


78 (687) 
Determination of the amino-acid nitrogen in the urine. 


By 8. R. BENEDICT and J. R. MURLIN. 
[From the Cornell University Medical College.] 


Since the abandonment of the Pfaundler method for deter- 
mination of the amino-acid nitrogen of the urine, the only direct 
methods proposed which have met with any favor, are the gaso- 
metric method of D. D. Van Slyke and the titration method of 
Henriques and Sérensen. In our hands the Van Slyke method as 
originally described! has not proved entirely satisfactory, (1) be- 
cause of the difficulty of removing all the ammonia after conversion 
of urea, and (2) because poly-peptids and other condensation 
products of amino-acids, e. g., hippuric acid, are estimated as well 
as free amino-acid nitrogen. The method, therefore, probably 
gives results which are too high. 

The Henriques and Sérensen method as improved by the 
authors themselves? likewise presents some difficulties. For ex- 
ample, as objected by de Jager and since admitted by Henriques 
and S6rensen, in the presence of large quantities of ammonia the 
total titration is less than the sum of the ammonia N and amino- 
acid N done separately. It is therefore necessary first to remove 
the ammonia. Henriques and Sdérensen recommend for this the 
method of Krieger and Reich slightly modified. This is essentially 
the method well known in this country by Shaffer’s name. Since 
the method is based on distillation under diminished pressure, it is 
not adapted to rapid determinations in a series of urines simul- 
taneously. Besides, as used by Henriques and Sérensen, we have 
not been able to obtain as high ammonia figures as by the Folin 
method. Use of the latter method for removal of ammonia, while 
perfectly satisfactory for small samples of urine (10 or 20 c.c.) is 
not satisfactory for a sample large enough to give a titration for 
amino-acid nitrogen (40-50 c.c.). 

Another objection to the Henriques and Sérensen procedure 
is the difficulty of titration with phenolphthalein in a barium 
filtrate because of interference of carbon dioxide. 


1 Proc. Soc. Exp. BIOL. AND MED., 1910, VII, p. 47. 
2 Zeitschr. f. physiol. Chemie, 1909, LXIV, p. 120. 


110 SCIENTIFIC PROCEEDINGS (49). 


These various difficulties have led us to return to the precipita- 
tion of ammonia by means of phosphotungstic acid. Gumlich! 
showed originally that the proper conditions for removal of am- 
monia by 10 per cent. phosphotongstic acid are a strongly acid 
urine and sedimentation for 24 hours. We have satisfied ourselves 
that this strength of phosphotungstic acid does not precipitate 
the mono-amino acids in the concentration usually found in urines. 
Instead, however, of removing the urea from the phosphotungstic 
filtrate and the determination of amino-acid nitrogen by difference, 
as in the original Schéndorff-Pfaundler method, or the modifica- 
tions of it by Krieger and Schmidt, Van Leersum, and others, 
we remove the phosphotungstic acid by means of tribasic lead 
acetate and litharge, and titrate for mono-amino acids in the 
filtrate (after removal of lead) according to the procedure of 
Henriques and Sérensen. The filtrate is water-clear and free of 
any constituents which can interfere with the formalin titration. 


COMPARISON OF THE HENRIQUES AND SORENSEN METHOD WITH MopiIFIED METHOD. 


Urine No. H. ands. Modified Method. 
Case 1. Pernicious Urine No. 1 0.215 gm. NH,N 0.015 gm. NH,N 
vomiting. Urine No. 2 0.434 gm. NH,N 0.048 gm. NH,N 
Urine No. 4 0.268 gm. NH,N 0.025 gm. NH,N 
Urine No. — 0.245 gm. NH,N 0.023 gm. NH,N 
Case 2. Eclampsia. Urine No. 0.397 gm. NH,N 0.120 gm. NH,N 


3 
Urine No. 7 0.157 gm. NH,N 0.035 gm. NH,N 
Urine No. 8 0.375 gm. NH,N 0.148 gm. NH,N 
Urine No. 11 0.210 gm. NH,N 0.155 gm. NH,N 


All the urines contained a large amount of ammonia. It 
would seem from this comparison that the Henriques and Sérensen 
method like the Van Slyke method gives results (especially on 
pathological urines) even after the supposed removal of ammonia 
which may be quite misleading. 

The following are a few of the results obtained with pure sub- 
stances. 


A. Pure Solutions: 
I. 20 c.c. N/20 leucine, purity tested by Kjeldahl and 
formol titration, added to 5 c.c. N/10 NHiCl < 200 c.c.; 
45 c.c. of final filtrate, titration 2.4, theory 2.28. 


1 Zeitschr. f. physiol. Chemie, 1893, XVII, p. 13. 


PICROLONATES OF THE MoNoAMINO ACIDS. III 


2. 20 c.c. leucine + NH,Cl < 180 c.c.; 50 c.c. final filtrate, 
titration 2.7, theory 2.77. 

3. Mixture of urea, (NH4)2SOu, uric acid, alanin, glycocoll, 
glutamic acid (all tested substances), containing 0.144 
gm. amino-acid nitrogen, yielded by new method 0.132, 
0.148, 0.143 gm. 


B. Pure Substances added to urines. 
I. 200 c.c. normal urine; 100 c.c. final filtrate, titration 
9.6 c.c. N/10 NaOH. 
200 c.c. normal urine + 20 c.c. N/20 leucin; 100 c.c. fil- 
trate, titration 11.8 NaOH 
Difference 2.2 c.c., theory 2.5 c.c. 
2. 200 c.c. urine of puerperient woman; 100 c.c. filtrate, 
titration 9.7 N/10 NaOH. 
200 c.c. urine of puerperient woman + 20 c.c. N/Io 
alanin, titration 14.7 N/1o NaOH. 
Difference 5.0 c.c. N/10 NaOH, theory 5.0 c.c. 


79 (688) 
Picrolonates of the monoamino acids.! 


By P. A. LEVENE and DONALD D. VAN SLYKE. 
[From the Rockefeller Institute for Medical Research, New York.] 


Picrolonic acid, used by Steudel to precipitate the hexone bases, 
and later shown by Mayeda to form salts with the aromatic amino 
acids tryptophane and phenylalanine, also forms crystalline salts 
of normal composition with the other monoamino acids obtained on 
hydrolysis of proteins. The salts are made by dissolving molecular 
proportions of amino acid and picrolonic acid in a minimum 
amount of boiling water. The picrolonates crystallize from the 
cooling solutions, usually while they are stillwarm. In cold water 
many of them are very insoluble. In alcohol they are all more 
soluble than in water. Following is a list of the amino acids of 


1 After this title had been sent to the secretary an article by Abderhalden and 
Weil appeared describing picrolonates of glycocoll; d-alanine, and dl-leucine (Zischr. 
physiol. Chem., 78, 150). They were formed in alcoholic solution, which yielded 
products of abnormal composition in the cases of glycocoll and alanine. 


112 SCIENTIFIC PROCEEDINGS (49). 


which picrolonates were prepared, after each being given the solu- 
bility of the picrolonate in grams per 100 c.c. of water at 20°-23°, 
and the melting point. The picrolonates are arranged in order of 
solubility. Dl-phenyl-alanine, 0.12, 212° (decomp.); Tyrosine, 
0.29, blackens at 260°; 1-phenyl-alanine, 0.34, 208°; dl-leucine, 
0.53, indefinite above 140°; /-leucine, 0.55, indefinite at about 150°; 
d-isoleucine, 0.58, 170°; dl-valine, 0.81, indefinite above 150°; 
dl-serine, 0.98, decomposed 265°; glycocoll, 0.99, 214°; dl-alanine, 
1.01, 216°; d-valine, 1.20, 180°; d-alanine, 1.61, 214°; dl-aspartic 
acid, 1.69, blackens at 130°; dl-glutaminic acid, 2.37, 194°. 
Nearly all the picrolonates decompose more or less on melting, 
and the melting points are not sharp. L-Phenyl-alanine picrolo- 
nate is much more soluble in alcohol than the racemic salt, and can 
be separated from most of the racemic substance by solution in 
alcohol. The optically active compound has a sp. rotation in 
absolute alcohol of + 30°. The specific rotation of d-isoleucine 
picrolonate in alcohol is + 33.3°. Phenyl-alanine can be sepa- 
rated from glutaminic or aspartic acid by dissolving the mixture 
with enough picrolonic acid to combine with the phenyl-alanine 
only. The picrolonate of the latter crystallizes pure. It is prob- 
able that other amino acids can be separated by similar use of 
picrolonic acid. The pyrrollidine acids, proline and oxyproline, 
do not readily yield picrolonates when treated as described above. 


80 (689) 


An improved apparatus for gasometric determination of amino 
nitrogen. 


By DONALD D. VAN SLYKE. 


[From the Rockefeller Institute for Medical Research, New York.] 


The apparatus differs from that reported at the meeting of this 
society in December, 1909, in that: (1) The desamidizing bottle 
with stopper holding the 10 c.c. burette and tubes is replaced by a 
bulb into which the tubes and burette are sealed; (2) the Hempel 
absorption pipette is modified so that it can be suspended from 
hooks; (3) both absorption pipette and desamidizing bulb are so 
arranged that they can be shaken by a motor. The apparatus, 


NaTuRE OF AMINO Groups IN NATIVE AMINO PROTEINS. I13 


without losing any of the accuracy of the original, is much more 
convenient because it can be used an indefinite number of times 
without disconnecting the parts, and the shaking by hand is 
replaced by the less laborious and more efficient motor. The latter 
also increases the rapidity, so that with one apparatus a deter- 
mination can be made every seven or eight minutes. 


81 (690) 
The nature of the free amino groups in the native proteins. 
By DONALD D. VAN SLYKE and F. J. BIRCHARD. 
[From the Rockefeller Institute for Medical Research, New York.] . 


The fact that at least some proteins contain a small but definite 
proportion of their nitrogen in the form of free amino groups ca- 
pable of reacting with nitrous acid has been proven by one of us. 
Levites and Skraup failed to obtain lysine from proteins which 
had been treated with nitrous acid before hydrolysis. This 
indicates that the w-NH:2 group of lysine, NH2-(CHe)4-CHe2(NH2)- 
COOH, may be free in the protein molecule. As lysine is peculiar 
among the amino acids in possessing an w-NHp group, it appeared 
possible that this might be responsible for all or most of the 
amino nitrogen determined. We have, therefore, determined the 
free amino nitrogen in ten proteins in which the lysine has already 
been quantitatively determined in either our laboratory or in 
Osborne’s. 


Per Cent. of Total N in 


Protein. Lysine. ¥Y% Lysine N. | Free Amino N. 
Ox-hemoglobin............. 12.0 (Van Slyke) 6.0 5.6 
Lab) Oy she Yeates Sito iNIOiiatec Ceceeneceec 11.4 (Van Slyke) 7 as} 
FVEMOCY ATM ya) ray clelet + «feifatsiaevere 8.5 (Van Slyke) 4.25 4.3 
(CEG) tn reste caotechirhenertro OCR cRree 6.9 (Osborne) 3.45 3.4 
Gelapinicr charactors sreletevetetniese*s 6.3 (Van Slyke) 3.15 3.1 
ESF SAL DUM peyier ot al ctlerleve eels foiiet 2 4.0 (Osborne) 2.0 2.4 
EVA OStIIIE tyne Gracey ele scar ecere ley teens 3.8 (Van Slyke) 1.9 T.2 
FLIES Bea b pb ORTOP ere 0.0 (Osborne) 0.0 0.3 

Albumoses from Witte Pepton. 
Heteroalbumose............ 10.3 elis 6.3 
Protoalbumosey. cece s i tkise + 9.6 4.8 6.6 


Without exception the free amino N of the native proteins 


114 SCIENTIFIC PROCEEDINGS (49). 


equals within a fraction of a per cent. that of the w-group of the 
lysine. It appears that the w-group of lysine constitutes prac- 
tically all of the free amino nitrogen of the native proteins deter- 
minable with nitrous acid. The albumoses show appreciably more 
free amino nitrogen, which is to be expected from the fact that 
the protein molecule is partially broken down in their preparation. 


82 (691) 
An experimental study of anti-anaphylaxis. 
By R. WEIL and A. F. Coca. 


[From the Laboratories of Experimental Therapeutics and Experi- 
mental Pathology, Cornell University Medical School, 
New York City.] 


If a guinea-pig be given a single injection of a foreign proteid, 
it becomes, after the lapse of 10 to 14 days, actively sensitized 
to that proteid, in such wise that the reinjection of the same, in 
doses far too small to cause any symptoms in a normal animal, 
produces almost immediate death with convulsions. If, however, 
such a sensitized pig, after the sensitizing injection, be given a 
second dose, too small to induce its death, it immediately passes 
into a condition of anti-anaphylaxis, in which it is refractory to 
the foreign proteid in question, and may manifest no symptoms 
even after the injection of doses toxic to normal animals. This 
refractory stage lasts for weeks or months. In the same way, 
an animal may be passively sensitized by the introduction into 
its veins or peritoneum of the serum of another animal, which has 
been previously immunized or sensitized to a foreign proteid; in 
this case, too, the injection of a relatively small, 7. e., sublethal, 
dose of the same proteid into the passively sensitized animal 
produces a condition of anti-anaphylaxis. 

By no experimental device hitherto employed has it been 
possible to alter this condition of anti-anaphylaxis. The theories 
offered to explain it are numerous. Friedemann, in his general 
review of anaphylaxis, in I9II, cites three hypotheses, those of 
Gay and Southard, of Besredka, and of Friedberger, all of which 
he proves to be untenable, and offers three other possible explana- 


An EXPERIMENTAL STUDY OF ANTI-ANAPHYLAXIS. 115 


tions. He concludes that anti-anaphylaxis presents a ‘‘most 
interesting, novel, and as yet unexplained phenomenon.” 

The following experiments appear to us to throw much light 
on the problem. Guinea-pigs have been actively sensitized, by 
injection, to a foreign proteid; after the lapse of about two weeks, 
they have been rendered anti-anaphylactic by the intra-peritoneal 
injection of a sublethal dose of this proteid. (That anti-ana- 
phylaxis had actually been so induced was demonstrated by the 
injection of relatively enormous doses of the proteid into controls 
similarly treated, without toxic effect.) The anti-anaphylactic 
animals have then been re-sensitized. This re-sensitization is ac- 
complished by bleeding to death another guinea-pig, sensitized to 
the identical proteid, and then injecting his serum, in amounts of 
from 2 to 5’ c.c., into the veins of the anti-anaphylactic animal. 
After the lapse of less than 24 hours, the re-sensitized pig has been 
tested by an intravenous injection of the foreign proteid. In each 
and every case, the pig, upon undergoing this test, has manifested 
the typical symptoms of anaphylaxis, with immediate death. In 
other words, such a pig acts exactly like a normal pig, which has 
been passively sensitized by the introduction of serum from an 
anaphylactic pig. 

If instead of a sensitized pig, one makes use of the serum from 
a pig highly immunized by means of repeated injections, re- 
sensitization of the anti-anaphylactic animal is accomplished in 
the same manner. 

If an actively anti-anaphylactic pig be passively re-sensitized 
with the serum of a rabbit immunized to the same foreign proteid, 
he too becomes hypersensitive, and is killed by a subsequent dose 
of this proteid. 

The same experiments can be performed in the case of animals 
rendered anti-anaphylactic after passive sensitization. If, during 
the refractory period, say two days after the anti-anaphylactizing 
dose, they are re-sensitized to the same foreign proteid by the 
reintroduction of an immunized rabbit’s serum, they may be killed 
in the typical manner by the re-injection of the proteid. The only 
difference between passive anaphylaxis as primarily and as 
secondarily induced, is that in the latter somewhat larger doses 
are required to re-sensitize. The cause of this difference is being 
investigated and will form the subject of a later report. 


116 SCIENTIFIC PROCEEDINGS (49). 


These experiments in anti-anaphylaxis were originally per- 
formed with horse serum. In order to avoid any possible source 
of error, however, due to the complex character of this material 
they were repeated with a solution of crystalline egg albumen 
which had been four times re-crystallized, and the same results 
were obtained. 

It appears from these experiments that anti-anaphylaxis is a 
condition in which an animal becomes refractory to the toxic 
effects of a foreign proteid simply through the exhaustion from his 
blood of those bodies which induce the reaction. The proof 
hereof lies in the fact that the simple re-introduction of these bodies 
with the blood of another sensitized animal restores him at once 
to his original condition of anaphylaxis. The bodies which induce 
the reaction are, so far as we know, two: first, the ‘‘anaphylactic 
anti-bodies,’’ which resemble in character, and may be identical 
with, the amboceptors; second, the complement substances of 
the blood. 

It is unlikely that the complement is the substance herein at 
fault, inasmuch as Friedemann states, as the complement is 
rapidly restored to its normal amount in anti-anaphylactic pigs, 
whereas the condition of anti-anaphylaxis persists. We have 
tested whether the complement plays an important réle by two 
sets of experiments. In the first place, the animals have been 
simultaneously sensitized by hypodermic injection to two different 
forms of foreign proteid, namely horse serum and egg albumen. 
They have then been rendered anti-anaphylactic to one of these. 
Immediately, thereafter, it has been found that their sensitiveness 
to the other albumen is little, if at all, impaired. This indicates 
that the complement cannot be deficient. In the second type of 
experiments, the pigs, having been made anti-anaphylactic to egg 
albumen, have been given an intra-venous injection of 5 c.c. of 
normal guinea-pig serum, which would, of course, suffice to supply 
any defect of complement. When now re-injected with egg albu- 
men, they fail to evidence any sensitiveness. This indicates, 
therefore, that something other than complement, necessary to 
the anaphylactic reaction, has been removed from the blood in 
anti-anaphylaxis. It seems to us, therefore, that animals are 
anti-anaphylactic simply through the absence of the appropriate 


An EXPERIMENTAL STUDY OF ANTI-ANAPHYLAXIS. riz, 


anti-bodies from the serum. If these are supplied, an animal 
passes directly into the anaphylactic condition again, and this 
reversal could conceivably be repeatedly renewed. 


CONCLUSIONS. 


1. Guinea-pigs which have been rendered actively anaphylactic 
by a preliminary injection of foreign proteid (horse serum, egg 
albumen), and have then been made anti-anaphylactic by the 
injection of a sub-lethal dose of this proteid, may be immediately 
re-sensitized by the introduction of serum from a pig sensitized, 
or one immunized to the same proteid. Death is then produced, 
with typical anaphylactic symptoms by the intravenous injection 
of an amount of this proteid which to normal pigs is non-toxic. 

2. Actively anti-anaphylactic pigs may be re-sentitized with 
serum derived from a rabbit immunized against the same proteid. 

3. Passively sensitized pigs, rendered anti-anaphylactic by 
the usual methods, can be re-sensitized by the re-introduction of 
an immune serum. 

4. A pig simultaneously sensitized to two different foreign pro- 
teids, may be rendered anti-anaphylactic to one of these by the 
usual methods, while its sensitiveness to the other remains un- 
impaired. This demonstrates that anti-anaphylaxis cannot be 
due to exhaustion of complement, since complement is amply 
present. 

5. The introduction of normal guinea-pig’s serum into an 
anti-anaphylactic animal fails to re-sensitize. Some factor other 
than complement, therefore, must be introduced in re-sensitization. 

6. The absence of available anaphylactic antibodies appears 
to be the cause of the refractory condition known as anti-ana- 
phylaxis, and re-sensitization is due to their re-introduction. 


83 (692) 
The toxicity of foreign leucocytes. 
By WILFRED H. MANWARING. 
[From the Rockefeller Institute for Medical Research.] 


The injection of from 0.7 c.c. to I.0 c.c. of rabbit leucocytes 
into the cerebral meninges of dogs is apparently invariably fatal. 


118 SCIENTIFIC PROCEEDINGS (49). 


The animals show no immediate symptoms; but about two hours 
later there is beginning incodrdination, rigidity and respiratory 
distress, increasing to collapse about the fourth hour, and death 
about the sixth. An occasional dog survives till the twenty-fourth 
hour. Autopsy usually shows extensive local hemorrhagic, inflam- 
matory and necrotic changes. 

Horse leucocytes similarly injected produce symptoms of the 
same general nature, though less severe. About two thirds of the 
dogs injected with horse leucocytes recover. A reinjection of 
these dogs, however, or the injection of dogs whose meninges 
have been previously injured by tubercle bacilli, is almost in- 
variably fatal. 

The injection of 0.5 c.c. of rabbit leucocytes into the spinal 
meninges of monkeys produces slight symptoms from which most 
of the monkeys recover. Larger amounts are usually fatal. 

Horse leucocytes are less toxic for monkeys, producing few if 
any symptoms, even when injected in 1.0 c.c. doses. The toxicity 
of both leucocytes however increases on repeated injection, the 
third injection often being fatal. Autopsy in such cases often 
shows edema of the lungs as the apparent immediate cause of 
death. 

These tests have a bearing on the possible therapeutic uses of 
leucocytes in meningeal infections. 


84 (693) 
The occurrence, and the significance, of tyrosinase in the re- 
productive organs of certain amphibians. 


By ROSS AIKEN GORTNER. 


[From the Laboratory of Biological Chemistry of the Station for 
Experimental Evolution, The Carnegie Institution of Washington.] 


Tyrosinase—the enzyme which oxidizes tyrosin to produce a 
black, insoluble, pigment-like compound—has been shown by 
Phisalix (C. R. Soc. Biol., 50, p. 793, 1898) to occur in the skin of 
the European frog, Rana esculenta. Gessard, later (ibid., 56, p. 285, 
1904), shows that the same enzyme occurs in the skin of the toad, 
Bufo vulgaris, and in the frog, Rana temporaria. In discussing the 


TYROSINASE IN REPRODUCTIVE ORGANS OF AMPHIBIANS. I1Q 


importance of the tyrosinase Phisalix says: “It is probable that the 
oxidase presides over the oxidations within the organism . . . and 
plays the réle of fixing oxygen in cutaneous respiration.”’ If such 
is the case, and the production of the pigment in the skin is only a 
secondary reaction, or the elimination of a byproduct, the study of 
this enzyme becomes of much greater importance than merely as a 
pigment-producer. 

In every instance where the mechanism of melanin formation 
has been elucidated, it has been found that pigmentation is due 
to the interaction of tyrosinase and a chromogen. It therefore 
seemed probable that the enzyme might be present in the ovaries 
of those amphibians which deposit pigmented eggs, and might be 
responsible for the pigment formation. I have found that tyrosin- 
ase is present in the ovaries of the green frog, Rana clamata, and 
the wood frog, Rana sylvatica. Owing to the greater ease in 
securing material of various ages most of the tests were carried 
out using material from the green frog. Im every instance the 
intensity, and the rapidity of the development of the tyrosinase test 
was in inverse proportion to the amount of pigment present in the 
eggs. Ovaries which were immature, and contained no pigmented 
eggs, gave a positive tyrosinase test in a very few hours, partially 
pigmented ovaries required in some instances as much as 96 hours 
to produce a positive test, while the ovaries which contained ripe 
eggs failed to give any indication of the presence of the enzyme in 
168 hours. All solutions were kept sterile by the addition of a few 
drops of chloroform. When partially pigmented ovaries were 
used the “blank”’ (no tyrosin added) usually showed considerable 
darkening, which, however, did not appear in a boiled check, show- 
ing that a chromogen was also present. It would, therefore, 
appear that the pigmentation of the eggs of the frog is due to an 
oxidation induced by tyrosinase, and that as the pigmentation 
progresses the amount of tyrosinase decreases, until there is no 
perceptible amount of the enzyme present in the unfertilized 
eggs which are fully ripe. 

The tadpoles at the moment of liberation from the egg contain 
tyrosinase, as do also the larve of the salamander, Ambystoma 
punctatum. Inasmuch as the ripe unfertilized ova do not seem to 
contain tyrosinase, it seemed probable that the enzyme might be 


120 SCIENTIFIC PROCEEDINGS (49). 


added through the sperm, and on testing the testes of adult green 
frogs during the breeding season, I found tyrosinase to be present, 
although the coloration was slow to develop (72 hrs.). It is 
possible that all of the tyrosinase in the ovary was used up in the 
production of the egg pigment, and that the oxidase for the tad- 
pole is introduced by the male. It is well known that oxidative 
processes proceed much more rapidly after fertilization and perhaps 
we may find that in other instances this is due to the entrance 
of an oxidase with the sperm. Evidences of oxidase action have 
been found in all of the fertilized amphibian eggs that I have 
examined, including eggs which contain no pigment.! It is also 
possible that the ‘“‘poisonous complex,’’ to which Loeb (Arch. 
Entwick. Organ., 31, p. 658) ascribes the death of the unfertilized 
egg, is destroyed by the entrance of an oxidase (perhaps a specific 
oxidase) with the sperm. 


85 (694) 
On two different types of melanin. 


By ROSS AIKEN GORTNER. 


[From the Laboratory of Biological Chemistry of the Station for 
Experimental Evolution, The Carnegie Institution of Washington.] 


In investigating the nature of the melanin molecule, I have 
found that the pigment which is present in black wool is readily 
soluble in dilute sodium hydroxide, and that it is apparently a 
protein. To pigments of this nature I have given the name of 
melano-protein to distinguish them from both the unpigmented 
proteins and those other melanins, the nature of whose molecule 
is as yet unknown. The melano-protein which I have obtained 
from black wool contains no ash, showing that ash is not a part 
of this pigment, and also proving that this melanin does not contain 
iron. In some of the preparations of pigment from black wool 
where less precautions were taken to insure the absence of all 
contaminating mineral matter, a low percentage of ash was ob- 


1In collaboration with Dr. Banta, of this station, I have recently had occasion 
to test fertilized eggs of Rana sylvatica, Rana pipiens, Ambystoma punctatum, and 
Spelerpes bilineatus. 


PEDIGREE RACE OF PARAMECIUM WITHOUT CONJUGATION. 121 


tained (0.10 per cent.—o.20 per cent.) but this ash appeared as 
white particles and was probably silica. 

When I undertook to prepare a melanin from black rabbit hair 
and black feathers I found that the pigment was very insoluble in 
dilute (0.2 per cent.) sodium hydrate, and it was only after long 
boiling, in some instances nearly a week, that solution was effected. 
Of course this procedure altered the nature of the melanin molecule, 
but the fact that was of chief interest was that the resulting product 
contained between 2 per cent. and 3 per cent. of ash and that this 
ash was chiefly iron oxide. I have recently observed that there 
are probably at least two pigments in the darker colors of horse 
hair, one of these being a melano-protein with a very low ash 
content, and the other containing approximately 3 per cent. of 
ash which 1s chiefly tron oxide. 

These pigments have been prepared in such a manner as to 
preclude any iron entering through contamination, and inasmuch 
as other pigments, prepared by exactly the same process, contain no 
iron, or at most only traces, we must conclude that im some in- 
stances melanins may contain tron as a part of the molecule, but 
that all melanins do not contain iron. Perhaps in this instance 
the oxidase acted on the hemoglobin, or some other iron complex, 
instead of oxidizing a protein containing no iron. 


86 (695) 


A five-year pedigreed race of Paramecium without 
conjugation. 


By LORANDE LOSS WOODRUFF. 
[From the Sheffield Biological Laboratory, Yale University.] 


The unicellular organisms afford a natural means of approach 
to the problem of fertilization, and the study of data, from 
a long series of careful experimental studies on these forms by 
various investigators, has pointed to the conclusion that the most 
important function of conjugation in the life history of the Protozoa 
is a satisfying of an inherent periodic physiological need of living 
matter, resulting in a renewal of the vigor of the cell. This 
“dynamic” view of fertilization has gradually assumed a com- 


122 SCIENTIFIC PROCEEDINGS (49). 


manding position, though it is neither contradictory nor con- 
firmatory of the view that fertilization, resulting in amphimixis, 
is concerned in some way with the phenomenon of variation, or 
that it may be a process which enables certain forms to withstand 
changed environmental conditions. 

The present paper briefly outlines the results which have been 
obtained to date from an intensive study of a pedigreed race of 
Paramecium aurelia with reference to the problem of protoplasmic 
senescence and the function of conjugation. I have previously 
published! the results obtained to September, 1910, and the reader 
is referred to earlier papers for further details of the culture and 
for a general discussion of the various phases of the work. 

This culture was started on May 1, 1907, with a ‘‘wild”’ 
Paramecium aurelia which was isolated from a laboratory aqua- 
rium. This individual was placed in about five drops of culture 
medium on a glass slide having a central ground concavity, and 
when the animal by division had formed four individuals, each 
of these was isolated on a separate slide to form the four lines, Ia, 
Ib, Ic, and Id, of this culture, Paramecium 1. The pedigreed 
culture has been maintained by a specimen isolated from each 
of these lines practically every day up to the present time, thus 
precluding the possibility of conjugation occurring and facilitating 
an accurate record of the number of generations attained. A 
culture medium consisting of infusions of hay and fresh grass 
was employed during the first nine months of the work, but there- 
after infusions of nearly any materials which might be found in 
ponds, swamps, etc., have been used. The medium has invariably 
been boiled to render the introduction of ‘‘wild’”’ individuals 
into the culture absolutely impossible. 

This race of Paramecium has attained so far, (May 1, 1912) 
3,029 generations during the five years it has been under daily 
observation. The number of generations attained during each 
of the first five years of its existence is as follows: first year 452, 
second year 690, third year 613, fourth year 612, and fifth year 
662. The mean rate of division for the entire period is over three 
divisions in forty-eight hours. Periods of marked physiological 
depression have not occurred—such variations in the rate of 


1 Archiv fiir Protistenkunde, Bd. 21, 4. 


INFLUENCE OF TARTRATES UPON PHLORHIZIN DIABETES. 123 


reproduction as have appeared being either normal rhythms or 
the effects of environmental changes of temperature and culture 
medium. The organisms of the present generation are in as 
normal morphological and physiological condition as the original 
“‘wild”’ individual isolated to initiate the culture. 

This study has demonstrated that, under favorable environ- 
mental conditions, the protoplasm of the cell originally isolated 
possessed (at least) the potentiality to produce similar cells to 
the number represented by 2 raised to the 3,029th power, or 
a volume of protoplasm approximately equal to 10° times the 
volume of the Earth. I believe this result proves beyond ques- 
tion that the protoplasm of a single cell may be self-sufficient to 
reproduce itself indefinitely, under favorable environmental 
conditions, without recourse to conjugation and clearly indicates 
that senescence and the need of fertilization are not primary at- 
tributes of living matter. 


87 (696) 
The influence of tartrates upon phlorhizin diabetes. 


By FRANK P. UNDERHILL. 


[From the Sheffield Laboratory of Physiological Chemistry, Yale 
University, New Haven, Conn.] 


A recent communication of Baer and Blum (Archiv fiir Exper- 
imentelle Pathologie und Pharmakologie, 1911, 65, p. 1) shows 
that the subcutaneous administration of a number of organic com- 
pounds, containing two carboxyl groups, exercises a remarkable 
inhibitory influence upon the elimination of urinary nitrogen and 
dextrose in dogs with phlorhizin diabetes. Among the substances 
possessing this property may be mentioned glutaric and tartaric 
acids. 

In an endeavor to explain the mechanism of the unique influ- 
ence exerted by these compounds investigations have been carried 
out with tartrates upon both dogs and rabbits under conditions 
similar to those established by Baer and Blum. We have been 
able to corroborate the findings of Baer and Blum with respect 
to the action of tartrates although Ringer (Proc. Soc. Exp. BIOL. 


124 SCIENTIFIC PROCEEDINGS (49). 


AND MED., 1912, 9, p. 54) failed to obtain the reported results 
with glutaric acid. 

Our interpretation of the diminution of the urinary constituents 
is, however, entirely different from that offered by Baer and Blum. 
Tartrates subcutaneously injected cause a prompt disintegration 
of the cellular elements of the kidney tubules, leading to partial 
or complete loss of secretory activity, and in many cases to anuria. 
Hence, in phlorhizin diabetes urinary nitrogen and sugar are not 
eliminated to an appreciable extent. 


RECAPIEULATION "OF THE NAMES: .OF 
Pie AULHORS ANDI OP THE TITLES 
OF THE COMMUNICATIONS. 


VOLUME IX. 
Abramson, F. 
686. See Winslow, C. E. A. 
Adler, H. M. 
610. Experimental pernicious anemia. 
Alsberg, C. L. [with O. F. Black.] 
613. Biochemical and toxicological studies upon Penicil- 
cium Bainier. 
635. Studies on barium feeding. 
Anderson, J. F. [with J. Goldberger.] 
657. The experimental demonstration of the identity of 
so-called Brill’s disease to typhus fever. 
Atkinson, J. P. [with C. B. Fitzpatrick.] 
627. Further observations on the tolerance of gases by 
the circulatory apparatus. 
644. Some vaso reacting substances in blood serum. 
Auer, J. [with S. J. Meltzer.] 
667. A characteristic course of the rise of blood pressure 
caused by an intra-spinal injection of adrenalin. 
681. The effect of the infundibular portion of the hy- 
pophysis upon vaso-dilators. 
Badertscher, J. A. 
612. Peculiarity of the mode of entrance of the optic 
nerve into the eyeball of some rodents. 
Bancroft, F. W. 
615. Color inheritance in Fundulus hybrids. 
Banta, A. M. 
684. The relation of oxygen and carbon dioxide to the 
development of certain amphibian embryos. 
125 


126 SCIENTIFIC PROCEEDINGS (49). 


Benedict, S. R. [with J. R. Murlin.] 
687. Determination of the amino-acid nitrogen in the 
urine. 
Birchard, F. J. 
690. See Van Slyke, D. D. 
Black, O. F. 
613, 635. See Alsberg, C. L. 
Calkins, G. N. 
679. The effect of chemicals on the division rate of 
protozoa. 
Coca, A. F. [with R. Weil.] 
691. Observations on anaphylaxis. 
Cohn, A. E. 
626. Curves from a case of complete heart block. 
Davenport, C. B. 
622. A case of sex-limited heredity in poultry. 
Draper, J. W. [with F. W. Schlutz.] 
629. Glucuronic acid determination in duodenal obstruc- 
tion. 
Eggleston, C. [with R. A. Hatcher.] 
668. Demonstration of vomiting movements in an 
eviscerated animal under the influence of digitalis. 
Ewing, E. M. 
680. The first onflow and diastolic waves in the venous 
pulse. 
Fitzgerald, J. G. 
676. See Gay, F. P. 
678. [with J. B. Leathes.] 
Standardization of the Wasserman reaction. 
Fitzpatrick, C. B. 
627, 644. See Atkinson, J. P. 
Foster, N. B. 
665. On indican in the blood of uremic patients. 
Gay, F. P. [with J. G. Fitzgerald.| 
676. A rapid method of producing hemolytic serum. 
Githens, T. S. [with S. J. Meltzer.] 
630. The convulsant effect of removal of the heart on 
morphinized frogs. 


NAMES OF AUTHORS. 127 


670. The results of ligation of the pulmonary arteries in 
the frog. 
Goldfarb, A. J. 
636. The production of grafted and multiple embryos. 
637. The production of typical monstrosities. 
Goldberger, J. 
657. See Anderson, J. F. 
Gortner, R. A. 
693. On two different types of melanins. 
694. The occurrence and significance of tyrosinase in the 
reproductive organs of certain amphibians. 
Guenther, A. E. 
672. See Lee, F. S. 
Guthrie, C. C. [with A. H. Ryan.] 
631. Intravascular foreign bodies. 
Hatcher, R. A. 
668. See Eggleston, C. 
Harvey, S. 
671. See Stewart, H. A. 
Healy, D. J. [with J. N. Kastle.] 
641. Parturient paresis and eclampsia. 
642. The toxic character of colostrum in parturient 
paresis. 
643. The internal secretion of the mammae as a factor in 
labor. 
Hess, A. F. 
663. The relation of the virulence of the tubercle bacillus 
to its persistence in the circulation. 
Janeway, T. C. 
645. See Park, E. A. 
Joseph, D. R. 
650. A quantitative study of the pupil dilatation caused 
by adrenalin. 
Kastle, J. N. 
641, 642, 643. See Healy, D. J. 
Kleiner, I. S. [with S. J. Meltzer.] 
682. The reduction of toxicity of strychnine by the 
administration of large quantities of fluid. 


128 SCIENTIFIC PROCEEDINGS (49). 


Lambert, R. A. 
621. Immunization against transplanted cancer. 
685. Cell division in mammalian tissue. 
Leathes, J. B. 
678. See Fitzgerald, J. G. 
Lee, F. S. [with A. E. Guenther.] 
672. Properties of diaphragm muscle. 
Levene, P. A. [with D. D. Van Slyke.] 
688. Picrolonates of mono amino acids. 
MacCallum, W. G. 
625. The seat of action in tetany after parathyroid- 
ectomy. 
Manwaring, W. H. 
663. Sources of error in serological work. 
692. The toxicity of foreign leucocytes. 
Meltzer, S. J. 
628. The destruction of adrenalin by spinal fluid. 
683. The influence of the infundibular portion of the 
hypophysis on the pupil. 
630. See Githens, J. S. 
667, 681. See Auer, J. 
682. See Kleiner, I. S. 
Mendel, L. B. 
660, 661. See Osborne, T. B. 
Morgan, T. H. 
619. A dominant sex limited character. 
662. The masking of a Mendelian result by the influence 
of the environment. 
Mosenthal, H. O. 
624. Nitrogen and sodium chloride excretion in uranium 
nephritis. 
Murlin, J. R. 
687. See Benedict, S. R. 
Ophuls, W. 
617,618. Experimental nephritis produced by chromates. 
Osborne, T. B. [with L. B. Mendel.] 
660. Growth and maintenance on purely artificial diets. 
661. Feeding experiments with fat-free food mixtures. 


Names oF AUTHORS. 129 


Ott, Isaac [with J. B. Scott.] 
653. The action of various agents on the secretion of milk. 
654. The pineal gland and the corpus luteum. 
655. The spleen and chronic constipation. 
677. The effect of internal secretions on the secretion of 
epinephrin. 
Pappenheimer, A. M. 
666. The inhibitory action of adrenalin in muscle- 
pancreas mixtures. 
Park, E. A. [with T. C. Janeway.] 
645. A study of the Meyer strip method for the reaction 
of arteries to adrenalin. 
Parker, G. H. [with B. M. Patten.] 
651. Intermittent and continuous lights as stimuli. 
Patten, B. M. 
651. See G. H. Parker. 
Pike, F. H. 
616. See Wilson, J. G. 
Rieger, J. B. 
649. See Salant, W. 
Ringer, A. I. 
646. Studies in phlorhizin diabetes. 
647. The influence of glutaric acid on phlorhizin diabetes. 
Ryan, A. H. 
631. See Guthrie, C. C. 
Robertson, T. B. 
652. The cytolytic action of ox blood on sea urchin eggs. 
674. On the isolation of odcytase, from mammalian blood 
serum. 
Salant, W. [with J. B. Rieger.] 
649. The elimination of caffeine in nephrectomized 
rabbits. 
Schlutz, F. W. 
629. See Draper, J. W. 
Scott, G. G. 
638. The percentage of water in the brain of the smooth 
dog-fish. 
Scott, J. C. 
653, 654, 655, 667. See Ott, Isaac. 


130 SCIENTIFIC PROCEEDINGS (49). 


Simpson, Sutherland. 
611. The influence of age on the symptoms following 
thyro-parathyroidectomy. 
675. The food factor in hibernation. 
Sittenfeld, M. J. 
648. Influence of anemia and hyperemia on the growth 
of sarcoma. 
Stewart, H. A. 
614. Influence of salts on hypertrophy produced by 
adrenalin. 
671. [with S. Harvey.] Variations in the response of 
different arteries to blood serum. 
Stockard, C. R. 
659. Influence of alcoholism on the offspring. 
Terry, B. T. 
620. Trypanasomiasis in monkeys. 
639. The advantage of certain experiments in vitro of 
suspending trypanasomes in serum. 
640. The action of atoxyl. 
Underhill, F. 
696. The influence of tartrates upon phlorhizin diabetes. 
Van Slyke, D. D. 
688. See Levene, P. A. 
689. Improved method for determination of amino acid 
nitrogen. 
690. [with F. J. Birchard.] The nature of the free amino 
nitrogen group in proteins. 
Weil, Richard. 
632. Tumor immunity in rats. 
691. [with A. F. Coca.] An experimental study of anti- 
anaphylaxis. 
Wilcox, H. B. 
658. The relation of the parathyroid glands to electrical 
conductivity. 
Wiggers, C. J. 
669. Variations in pulmonary blood pressure. 
Wilson, J. Gordon [with F. H. Pike.] 
616. A note on the relation of the semicircular canals 
of the ear to the nervous system. 


NaMEs OF AUTHORS. 131 


Winslow, C. E. A. 
633. The fermentation of carbohydrate media by strepto- 
cocci. 
686. [with F. Abramson.] The effect of drying on the 
viability of bacteria. 
Woodruff, L. L. 
656. The sequence of the protozoan fauna in hay in- 
fusions. 
695. A five year pedigree culture of paramecium without 
conjugation. 
Worthington, Mary Whitall. 
673. The stimulation of nerve endings in muscle and the 
theory of receptive substances. 


EXECUIIVE PROCEEDINGS: 


Forty fifth meeting. 

Columbia University, October 18, 1911. President Morgan in 
the chair. 

Members present: H. M. Adler, I. Adler, Alsberg, Auer, Ban- 
croft, Calkins, Field, Jackson, Joseph, Levene, Levin, Meltzer, 
Morgan, Pappenheimer, Senior, Simpson, Stewart, Wallace, H. B. 
Williams. 

Forty sixth meeting. 

The Rockefeller Institute for Medical Research, December 20, 
rg11. President Morgan in the chair. 

Members present: Atkinson, Auer, Cohn, Davenport, Emerson, 
Eisenbrey, Field, Foster, Famulener, Fitzpatrick, Gies, Goldfarb, 
Hess, Jacobs, Janeway, Joseph, Lambert, Lee, Levin, Loeb, 
MacCallum, Manwaring, Meltzer, Morgan, Mosenthal, Norris, 
Ottenberg, Pappenheimer, Rous, Steinhardt, Swift, Terry, Wal- 
lace, Weil. 

Members elected: A. M. Banta, E. C. Dickson, E. M. Ewing, 
J. G. Fitzgerald, R. A. Gortner, A. E. Guenther, W. de B. Mac- 
Nider, B. S. Oppenheimer, F. H. Pike. 


Forty seventh meeting. 

College of the City of New York, February 21, 1912. President 
Morgan in the chair. 

Members present: Alsberg, Atkinson, Bancroft, Fitzpatrick, 
Githens, Goldfarb, Guenther, Janeway, Joseph, Karsner, Kast, 
Kleiner, Lambert, Lee, Longcope, Lusk, Mandel, Meltzer, Morgan, 
McCrudden, Parker, Pike, Ringer, Senior, Stewart, Storey, Terry, 
Wallace, Winslow. 

Members elected: E. E. Butterfield, A. F. Coca, George Draper, 
G. Canby Robinson, H. Wastenays, C. J. Wiggers. 

Officers elected: President, James Ewing; Vice-president, P. A. 
Levene: Treasurer, Charles Norris; Secretary, George B. Wallace. 

133 


134 SCIENTIFIC PROCEEDINGS (49). 


Resolution adopted: Resolved, that groups of members be 
allowed by special vote of the society to form local branches of the 
society: that such local branches be designated by local names, 
e. g., ‘‘The San Francisco Branch of the Society for Experimental 
Biology and Medicine;”” and have power to hold meetings inde- 
pendently of the meetings of the society as a whole; that the 
expenses of such local meetings be borne by the local branches; 
that the members of such local branches have power to arrange 
their own programs and to publish their scientific papers in the 
proceedings of the society; and that only members of the society 
as a whole and who shall have been duly proposed to the council 
and elected in the manner provided for by the constitution be 
members of the local branches. 


Forty eighth meeting. 


Cornell Unwersity Medical College, April 17, 1912. President 
Ewing in the chair. 

Members present: Auer, Bancroft, Benedict, Butterfield, Cohn, 
Ewing, Field, Fitzpatrick, Foster, Githens, Guenther, Hatcher, 
Kleiner, Lee, Levine, Longscope, Lusk, Manwaring, McCrudden, 
Meltzer, Mendel, Morgan, Murlin, Norris, Pappenheimer, Robin- 
son, Steinhardt, Stewart, Stockard, Swift, Terry, Van Slyke, 
Wallace, Wiggers, H. B. Williams. 

Members elected: J. H. Austin, H. E. Jordan, C. C. Lieb, F. W. 
Schlutz. 

Resignation accepted: V. C. Vaughan. 

Resolution adopted: Resolved, that abstracts of communica- 
tions to be published in the Proceedings of the meeting at which 
they are presented must be delivered to the secretary not later 
than two days after the meeting; Otherwise they shall be published 
in the Proceedings of a subsequent meeting. 


Forty ninth meeting. 


University and Bellevue Hospital Medical College, May 15, 
1912. President Ewing in the chatr. 
Members present: Auer, Bancroft, Banzhaf, Benedict, Birchard, 


EXECUTIVE PROCEEDINGS 135 


Butterfield, Calkins, Coca, J. W. Draper, Emerson, James Ewing, 
E. M. Ewing, Githens, Goldfarb, Harris, Hatcher, Jackson, 
Kleiner, Lambert, Lieb, J. A. Mandel, McCrudden, Murlin, 
Norris, Pike, Rous, Terry, Wallace, Weil, Wiggers, H. B. Williams, 
Winslow. 

Members elected: M. T. Burrows, E. F. DuBois. 


REGISTER OF NAMES AND ADDRESSES 
OF Tir MEMBERS OF TH SOCIETY 
HORT EXPERIMENTAL: BIOLOGY 
AND MEDICINE. 


ABBOUE ALEXANDER’ Cac oi 5 vsje-s hoeiciereda Ow vie eiete University of Pennsylvania. 
ABEL Ee OHNGe isc leicoriins sistas otelscecsc trosene Johns Hopkins University. 
IAT AINE Ss ote GEOR Give cr carat ckerchoveteron tes oust a) etalon Sishea McGill University, Montreal. 
ADI Ry ELE RMAND Milas cis icine ste sie Danvers Insane Hospital, Hathorne, Mass. 
IADEERSMLSAVA Corrine sistent Sororecices ie ats New York Polyclinic Medical School. 
ALSBERG, CARL...... U. S. Department of Agriculture, Washington, D. C. 
ANDERSON, JOHNF......... U.S. Public Health and Marine-Hospital Service, 
Hygienic Laboratory, Washington, D. C. 
ATKINSON SAME Eye ay sie itis on < Department of Health, New York City. 
AUDR:, SOHN: cs ore ons Seidl cite Rockefeller Institute for Medical Research. 
ASUSTIN Salpeter cceas sicfeielag-ouslelorel cb sitinitete Ghae are are University of Pennsylvania. 
BANGRORT (bey Wieriece cose: Rockefeller Institute for Medical Research. 


Banta, A. M...Carnegie Institution, Station for Experimental Evolution, Cold 
Spring Harbor, Long Island, N. Y. 


BANZHAF, EDWIN J............. Department of Health, New York City. 
IBARDEPN es CHAREES: Riis sielals cicreiseleie has eases University of Wisconsin. 
IBBEBEH SUGASn iy sani lareccrsscyelicovaoxc seers oie Cornell University Medical College. 
BENEDICT, FRANCIS G...Nutrition Laboratory, Carnegie Institution, Boston. 
IBENEDICU SE OTANED Ye IX e) alot ioien « Cornell University Medical College. 
SENSIS Wore Econ: Rar) ots eusteyaye o2ehs hie) 4) S aie oe elersicyoal bie evalepayy = University of Chicago. 
Berc, WILLIAM N.....U. S. Department of Agriculture, Washington, D. C. 
BERGHE Ys DAVID dds cosa eo ecins @araie canoes University of Pennsylvania. 
BIRGHARD) slau eet ciecie «ctor Rockefeller Institute for Medical Research. 
PSRODIE Marg Gs ag ateee locos ay ste, i oeseva ek oie soos lenedatey Seite euacei es age University of Toronto. 
BROOKS re EUARYOW Ac reine ania cier vobe aia orotic ue Satake New York University. 
BUNTING WGaE Emme mitre aute karan ane ects siansie sone University of Wisconsin. 
BURROWS) AVS yD istey acre sctatereaietelegnare erste Cornell University Medical College. 
BURTON OPUDZ A RUSSED Lt srsvastelocerentie toile aie oon. gueipiiel ents Columbia University. 
IB UMTERRIEED seb cg | yee/al ciel s:s e161 Rockefeller Institute for Medical Research. 
EV UXALONGgEs ey Edettay teh cy sha isleler sais oloregsre sus ye ees Cornell University Medical College. 
(CAVGING Wnt Ge ARVs W Nistetias se tates je peieyosoiete co lorekekalecs’ cncisleveueiste Columbia University. 
GANNON VVALRER abet cee aro rie, Aa coarse ter cictouey hsv ane lalovenavabe Harvard University. 
CARTON Aa latent Bai ofl ova oral Shel enotara hevasleuoressteeuaces University of Chicago. 
GARRET) (AVEXISE cit rvicicta piste oiers Rockefeller Institute for Medical Research. 


137 


138 SociETY FOR EXPERIMENTAL BioLocy AND MEDICINE. 


CHITTENDEN; Re Hic cchaseo ct Ree eee ee Yale University. 
CuowEs MG! He Ae sea a eee er ee CEE ae University of Buffalo. 
COCA VASOR AA at hats sen enter aree eee Cornell University Medical College. 
CoBaN; /ALERED HES... one. oee Rockefeller Institute for Medical Research. 
Coben}, jb. Pal eben ae oer Cee eee University of Wisconsin. 
Gove RUPUSHE Ry eee Uae ee Rockefeller Institute for Medical Research. 
COLLINS, KATHARINE R...............State Board of Health, Atlanta, Ga. 
CONKLIN; EDWIN) Gy. yeccu en See ee eee Princeton University. 
CooKE;: J. Wilitaake eee Sad eee Re eee Tulane University. 
COUNCIEMAN, \WILLTAM) nL rieinaan ee cnn ee ener Harvard University. 
CRAMPTON, C. WARD............ Department of Education, New York City. 
GRAMPTON, HIENR Yes See cule ee ee ee Columbia University. 
CRAWFORD; ATBERTIC ties oe Cee Leland Stanford University. 
GrmpiiGEORGE Wee core ee Western Reserve University, Cleveland. 
CUNNINGHAM IRIGHARDBEI- ane oe eee EEE eer Columbia University. 
CUSHING; TIARVEV.Wianaenciaates et ee bere Johns Hopkins University. 
CUSHNY, “ARTHURERG aes ane ose mira University College, London. 
DAKIN SEL ID Aa hero Be Beene crs ee 819 Madison Avenue, New York City. 
DAVENPORT, CHARLES B............. Carnegie Institution, Station for Experi- 
mental Evolution, Cold Spring Harbor, Long Island, N. Y. 
DICKSON; JE. 1G. aware ie eee ee Ries Stanford University Medical School. 
DOCHEZ, WAGIR: 3 okt cyysccee heaters Rockefeller Institute for Medical Research. 
IDONALDSON HEIL yeni eerie Wistar Institute of Anatomy, Philadelphia. 
DRAPER, (GEORGE reo eerie te Rockefeller Institute for Medical Research. 
DRAPERY Ys Witinia a ohicsta o caret ere oie ee eee Re eee New York University. 
DU BOSvE Mb cas tetas ee aa Ieee Cornell University Medical College. 
DUNHAM, [EDWARD KG .,cocrconiactsarhineioecianacet eine New York University. 
DUVAL; (CHARLES Witla. acct pbynn ahah ee eee EE nya er Tulane University. 
EDMUNDS (© aWiaweistactre eee ble kek teres tedster eine CIEE University of Michigan. 
EDSALE DAVID Mc Ghee ees: Washington University, St. Louis. 
ESTSENBREYS As Bic oie eee aere University of Pennsylvania. 
IBUSBERG) | 'CHAREES/ JAC. 2a anon teamiochten aie ert artor Mount Sinai Hospital. 
ISUSERYIVWILETAM S| Lerten ane eae ene Cornell University Medical College. 
EMERSON, HUAVEN). eiicicis cara ee cic suet of teens eee Columbia University. 
ERUANGER:, JOSEPH): ee a oon eee Washington University, St. Louis. 
ECWING; EIS eh)3  iaparoe ste ciciaes da chen ease eee a een New York University. 
EWING; JAMES ARS arcana aaa aias Cornell University Medical College. 
HAMULENER Ge Wearikich aie cee Department of Health, New York City. 
FIRED; CYRUSIWiteeont orien rebar Bellevue Hospital, New York City. 
FISCHER) | MARTIN sElsaeos eccrine ein ee ere es University of Cincinnati. 
FUTZGERALD) (JAG rt ee a oe ile erence eee RCN University of California. 
BitZPATRICKConB yan ee aie Department of Health, New York City. 


HGEX NER: SSOIMONe eee nese Rockefeller Institute for Medical Research. 


Rott oF MEMBERSHIP. 139 


HUOURNON ys LHOMAS yererc-c cists ycsieee cess Mercy Hospital, Pittsfield, Mass. 
OLIN OUT OR as hat cyavaterolensics aka Suey seanciame claleraaisng alods, Sel Oearahs Harvard University. 
ORD  VWILETAM EA Winds forty: bck a soe eee emis Johns Hopkins University. 
ROSTER INEELIS) Bi tctoicnece, caesd).ts sbanetorocrehet secure hotel oral ones Columbia University. 
FROST Wirsllete re tscie Sarco U. S. Public Health and Marine-Hospital Service, 
Hygienic Laboratory, Washington, D. C. 
GAGERS Ci STUART ae creo jcovsecisicies Soe tha, Shodeparele oe Sire Brooklyn Botanic Garden. 
GAVARIREDDRICKs PAs a ttugel Soni oimiace Seton to see University of California. 
GIBSONSCROBERTIND 5. cyte noe ohare ian ololoasrelerne University of Minnesota. 
GIES MAVVIEL TANI ie tauesel danas crete latovaia en wiles apeherorevels: svereve siete Columbia University 
GITHENS MESS 4s wei aera ae Rockefeller Institute for Medical Research. 
(GAS PR eg OT TOm Oct rs ohne cred ce tsicler a his sister siaveine'e bee University of Michigan. 
GOMDRAR BHAA Mose veyal ci claye vedere nbah oa falls tedcetna, w pieraiese te City College of New York. 
(GORDNERARGE AM irate = cyeieivars s Carnegie Institution, Station for Experimental 
Evolution, Cold Spring Harbor, Long Island, N. Y. 
(GUENTHE ReRAS Ist acto titer usc eit clevata ais crsiletercds lobia cere basis Columbia University. 
(Giumehwon, (ClUCsS Shon erg caso cL Mas AC CRITE ero Oe University of Pittsburg. 
LEUNGOS NNiNG WWeopogogsooue U. S. Public Health and Marine-Hospital Service, 
Hygienic Laboratory, Washington, D. C. 
FVAUSTED ie VWVALELAMUS ra tein ertictcacea doctesrie craieie tise Johns Hopkins University. 
IFVARRIS ISNA Chbirr tildes ier roaer Arlington Chemical Co., Yonkers, N. Y. 
FUARRISON EIR OSS Gia nhis cvcctapch iets fh Lenape on nie le terestcne eae a ioce alors Yale University. 
FIAT CHER ROBERT Airs ois c.c.cteocrope sake este Cornell University Medical College. 
EVAR AT ROHUN KASHI eye referees < sietelsters Wistar Institute of Anatomy, Philadelphia. 
UAW ASICEITISUP ESS cl 35 4% ai cite) vahesays sondage sowie Seecateieereny oe ahecas University of Illinois. 
PARTON G MIS UD VIG ta70h5 si 0.5: 3c lofevs, ole ore etay = intel ol tei eeoctore che University of Chicago. 
EIESS WALERED I Haera nici cer fart acie erae Department of Health, New York City. 
UES WEES TsD se Aoea WV ioe lahat sti assy oe siee teh abe cucicdeserst ayer wearsisce niet University of Michigan. 
FATS Sep pT Palas ren tafay Ns. 2 hepato s sectors lata aloreesee eats Columbia University. 
LOWELL me WALL TAM OT nie cree eiaiacieis ek elotecetce« Johns Hopkins University. 
ELOWIAND SOHN veyaicea ce caters lernicrecist rerio Washington University, St. Louis. 
TUBER Gr CARI crini. tia oa oideraoo ae cites aise: University of Michigan. 
ERUNT REID ec ioeioarce ce ates U. S. Public Health and Marine-Hospital Service, 
Hygienic Laboratory, Washington, D. C. 
ELUNTERS ANDREW cuericlincroae memerdate sere Cornell University, Ithaca, N. Y. 
PAGKSON WH OUMES) Ger Sin dt Lect ecole cisc ides beeen New York University. 
PACOBSWINVALTER Acct: .c/scil ac ate 5: Rockefeller Institute for Medical Research. 
ANEW AYA ODORD MCs. ata. a aterttd aoa ah laa Columbia University. 
JENNINGS ibd Sap piper tee cc fede te yeteicievchehetonstanchstevahe Johns Hopkins University. 
JOBLING SJ AMESEWerery in aoe sae cineca. Michael Reese Hospital, Chicago, II. 
JONES VALTER a aeee iia nec citsirk ads nv cmscnenete ekg Johns Hopkins University. 
NORDAN EOD WINTON destinies tartan ane civ ear ealted University of Chicago. 
WORDAN TED Ere cuice amelie a tat ee aie eat University of Virginia. 


NOSEEH) DONUR stea seen ace asc Rockefeller Institute for Medical Research, 


140 SoclETY FOR EXPERIMENTAL BioLoGy AND MEDICINE. 


IKARSNERS (Bie fle 3 ohice re Satan en ee Harvard University. 
KASTYILUDWIGY os teecec er nore re New York Postgraduate Medical School. 
IKASTEE, JOSEPH) Tie. sa eee ce ee Kentucky Agricultural Experiment Station, 
Lexington, Ky. 
IKEEINER; | UCRS. Chikara eae eaters Rockefeller Institute for Medical Research. 
K01Z,; (OSKAR Mavceu t Series Oe ae ee University of Pittsburgh. 
IUAMAR, RICHARD "Vasel.- aaerae naee Rockefeller Institute for Medical Research. 
LAMBERT. “WR: All Ret iatant 5 secieerane aa ee aa eas Columbia University. 
LEATHES, J dB. S ask ae dnccn se Cee ee tee el eaee ne University of Toronto. 
LEE FREDERIC:S O20 tac eee ee ao ee eee Columbia University. 
LEVENE, AE Ato watoncore pare Rockefeller Institute for Medical Research. 
LEVIN, ISAAC Hie 5h0 sneha ee ere Columbia University. 
ILEWIS, CPAUL PAL cttne ce dita tere iter tei te Phipps Institute, Philadelphia. 
LIBR; Go Ca yn doe ROT eek ORS Ee Columbia University. 
LILLIE, GE RANKAR See Seether: came eee seb e ee University of Chicago. 
EWI, SRACPH SY Peis cole tal lerdal ie eae University of Pennsylvania. 
IOEB; JACQUES. he pete tee Rockefeller Institute for Medical Research. 
MOERS EO 4S ces ee ee ee Barnard Cancer Hospital, St. Louis. 
OE VENHART, ARTHUR'S: 22 ee el ieee en eieeiaaoee University of Wisconsin. 
LOMBARD; / WARREN, Pen as nto nora e Cenee me University of Michigan. 
MONGCOPE AWE... Naas ctesertehnccccn ee Lie eacene Columbia University. 
UUSK; (GRAHAM 2.5.2 tetas eis eae Cornell University Medical College. 
LP (0). Ral Onn! RN inet RAG Ga Acari aits's Gabo alo to dds St. Louis University. 
Macarrum, (At BS o.h) Jsccs cee ane eee eee University of Toronto. 
MACCATEUM: WaG. 2. 2ett Sore cee Hie Columbia University. 
MACDOUGATANDS dhe see eee Carnegie Institution, Washington, D. C. 
MACLEOD een Rociewc cere ae tees Western Reserve University, Cleveland. 
MAGCNEAL WARD) J scoca-eece cece New York Post-Graduate Medical School. 
IMAGNIDER?SW23DEUB sc urs. aes ee ee ele eremiare University of North Carolina. 
IMIGELENDON; Ye Bijccae eee elton Cornell University Medical College. 
IMCCRUDDEN] Es Vie eae eee Rockefeller Institute for Medical Research. 
MALE, JFRANKEIN on chiles ienelen ee eieseee Johns Hopkins University. 
INVANDEL, ARTHUR IR: 3 4c¢ os a crrcee hee ea eee New York University. 
MANDEL; JOHN Anco caacmtes terion eelcar ceieree New York University. 
MANWARING, W. H............. Rockefeller Institute for Medical Research. 
MAYER: ALFRED/G...\0- |. 5s Marine Laboratory of the Carnegie Institution, 
Tortugas, Fla. 
MEIGS “EDWARD Baossooe ee LOE eee Wistar Institute of Anatomy. 
MELTZER, 19.9] ernastcen eer oe Rockefeller Institute for Medical Research. 
MENDEL; (LAFAYETTE (Bc otto eee re pees ee rit Yale University. 
MEYER, ADOUPHS.. face bottsctsek Como eeu Johns Hopkins University. 
MEYER GUSTAVE M............ Rockefeller Institute for Medical Research. 


MORGAN, ‘THOMAS His < ca3s hereon eis oe See Columbia University. 


Rott oF MEMBERSHIP. I4I 


MORSE yA xii art icteric tosvsieis & Riccio vs esters tee siete eistadaserepars Trinity College. 
IMOSENTHAT) HERMAN) Of 5 250 ciicrerae a isisicial chasers eis Slossiovaxene Columbia University. 
AVION Fel OHM Reo wte 3} ria Use) ain orale’ sPatay stan Cornell University Medical College. 
Murpny, Joun B........ Northwestern University Medical School, Chicago. 
INeGUcHT; HHIDBYO: }.%.5..5055... Rockefeller Institute for Medical Research. 
INORRISSEGHARIES Sez cris trerstoies Gites oh Bellevue Hospital, New York City. 
INOVVAD DREDERICKS Gin s asic, octesyvin tis hlatcielcaeniele crketes University of Michigan. 
DERTED HORST opryeciine cremireaiere cies Sage Institute of Pathology, New York. 
OPHULS:) WILLIAM) co). aciciene © oe oe Cooper Medical College, San Francisco. 
OPIEVEUGENB Lacs dae sere sired anise eetelel sts Washington University, St. Louis. 
OPPENHEIMER eB Ose cece secs o ciate elete bre oe Pipe ial Columbia University. 
OSBORNE, THOMAS B.......... Connecticut Agricultural Experiment Station, 
New Haven, Conn. 
(OTSA CHA facusvorsrstets tne tsca eee ats Medico-Chirurgical College, Philadelphia. 
OTTENBURG HY Ohetntastet acts steers 4 bys SAS Cee e len oes Mount Sinai Hospital. 
PAPPENHEUMER  ADAVIN/E Mss ms suis’. ses sig ne ter aavaierecs« ofelele) « Columbia University. 
ARICA ENV TETEDAME Edo xofatayss oo sieine cers ipl smite etsieiei pees ep eels New York University. 
PARKER a GHORGE/ Els te taiectopeits. a ch claude tans iareteietolars ciate pistoral Harvard University. 
PEARCE, RICHARD IM, chy ctcradc anne cir ssicine eure « University of Pennsylvania. 
PEARL, RAYMOND..... Maine Agricultural Experiment Station, Orono, Maine. 
IPRARE A IIRIAN Zee Aaa tk cry bat set oleaeainal oie ate te Orecaio ne ele Harvard University. 
PUKE iw Eds suo cies elie ‘arate neheisua sptsiesar ab eseeavslotops aba «Stecs, seekedars Columbia University. 
IR OR DERG WTIGIOLA MG, Urea 5s tar oval oar a-aieile colar cr overs Tosmeateieverate stelors Harvard University. 
PRATT OSE PHN EL sairareyers tes otsiete cess oo hrctapar mwa ai avetarbiniers clerecn ts Harvard University. 
IVAVIENE Dp INUAZV GK: besetscus. cic a ave ainierlonneitte eiorche oe caereie University of Wisconsin. 
REICHERT WEDWARD (Lire sicc 4. esletleacine Jee sree University of Pennsylvania. 
RICHARDS WATERED) Nisispaic sic) olcfei sia ties ereisieusterets, ors University of Pennsylvania. 
IRTINGRRM ASM eper temas Sr vist pic: cetenevaretesevevenesteieus aeues University of Pennsylvania. 
ROBERTSONF dy BRATESHORD cs elsinaie sescie a ole arate: University of California. 
Rosinson, G. CANBY......,..... Rockefeller Institute for Medical Research. 
ROSENAU se VILE TONG) ie faci haaweGreaaue eG ec mietetass oe vate aise Harvard University. 
IVOSENBEOOM aA COB. cians sense sin cotta aie were ters Sake ear Columbia University. 
IROUSPREVTON aeiG aac sone yaar Rockefeller Institute for Medical Research. 
SACHS HORNS Deri ia st aati io en oo aaa Washington University, St. Louis. 
SALANT, WILLIAM....... U. S. Department of Agriculture, Washington, D. C. 
SGHIU DZ MH pe tieetievareictclic oisienetetla ove niles wisi ani avave tickers University of Minnesota. 
SCHULTZ Wiawblenr. bracelet scdisne ies, '0 6 U. S. Public Health and Marine-Hospital 
Service, Hygienic Laboratory, Washington, D. C. 
SGHWYZERA IRIDZio ata ee less eels oles St. Francis Hospital, New York City. 
SENIOR clon) ebaeen ecdetatare aint iissakctbve, beletelatelaleieierev’ chs New York University. 
SHABEER) EHUUIP “Avec cits slcccuin ns sdgeeaece Washington University, St. Louis, 


SWARM DE AG OMe, setapileinctele a sce scoters Philippine Medical School, Manila, P. I. 


142 SocieTy FOR EXxFERIMENTAL BioLocy AND MEDICINE. 


SHERMAN; HENRY: (Gio 52s ban ete eee Ee Columbia University. 
SIMON; (CHARLES) Ey titan... cts Coe een Oe eee Baltimore Medical College. 
SIMPSON; ISUTHERLANDE Ee eel nee eee iaeeee Cornell University, Ithaca, N. Y. 
SMITH, THEOBALD Ss 5220 Ceca ne Geen Ee GEEe Harvard University. 
SOLEMAN, (hORAUD A Eee ee ee rere Western Reserve University, Cleveland. 
SOUTHARD) BoE nidac set en chee Ee Eee Harvard University. 
STEINBARDT SE DNASE Een mente Department of Health, New York City. 
STEWART, GEORGE Nit os enaecaeonee Western Reserve University, Cleveland. 
STEWART, [HUGHVAS.. 36.53.05 e oe Cee eee Columbia University. 
STILES;) PERCY, iG: heer t nee eee Massachusetts Institute of Technology. 
STOCKARD) (CHAS: GRE pia icnenlen nee iotaeiee Cornell University Medical College. 
STOOKEY, LYMAN B.......... University of Southern California, Los Angeles. 
STOREY; THOMAS As) 42: Soke ch each oon een City College of New York. 
STRONG; RICHARD! Picasa ete eee U. S. Bureau of Science, Manila, 
SWEET, EDWINA. oso eis ie ee aes University of Pennsylvania, 
SWiIRT Hi pees nae eet Rockefeller Institute for Medical Research. 
SYMMERS; (DOUGLAS cote cutter ie ot en MORE New York University. 
TRAYLOR, WAWONZO BE itaacing Sc teidacl eerie University of Pennsylvania. 
TEAGUE, OSCAR 322. <5: U. S. Department of the Interior, Bureau of Science, 
Manila. 
(DERRY, Bitlice pie cetera Rockefeller Institute for Medical Research. 
Topp; JOHNIL:. 27. shiowiaense com a eee McGill University, Montreal. 
TORREY, (JOHN (Cohjcee poke seen one Cornell University Medical College. 
TYZZER, EG Bssan eve cote tote eee ee CR CTE Harvard University. 
UNDERHILL; -FRANK“SD.Acan taness aki nace eae ee eeeee Yale University. 
VAN SLYKE, DONALD D.......... Rockefeller Institute for Medical Research. 
WADSWORTH, PAUGUSTUSID: Ee ete naa Ser one eee Columbia University. 
WATTAGE, GEORGE BLE eerie nereerleee ere. ek Lterore New York University. 
WARTHIN, ALDRED (Ss. easton Ren Ree iene pee University of Michigan. 
WASTENAYS PH pe ein aaaene Rockefeller Institute for Medical Research. 
WEIL, (RICHARD 4.5.4.-68 hea Re renee Cornell University Medical College. 
WELCH, WILETAMIET.R fat taur. eet rae ee ise at Ce Johns Hopkins University. 
WEEUS; Hi: GIDEON: Joe oc oe reecies One Pe OR EEE Cee University of Chicago. 
WIGGERS} Cr Jigs cess ee eee eneeeeeee Cornell University Medical College. 
WiIETETANIS AININIAGA ae rey ereeee Department of Health, New York City. 
WILETAMS, Boe eee cys se nian aca eee eee ere Columbia University. 
WILLIAMS, HERBERT Uist a. open eer cee eee University of Buffalo. 
WILSON, "EDMUND Bataan aera een ee eaiee Columbia University. 
WINSLOW, {CAB SAU a ooher ena eerie metien City College of New York. 
WOLBACH,.S:) BURT Aone me bisite nen Cae Harvard University. 


WOLF ICHARLESI G3. ee eon onee Eee Cambridge, England. 


Rott oF MEMBERSHIP. 143 


WOODS IEIRANCIS! © cise Ge aipetet dicta elon 6 lola suave) sbe.inioietelsialiecste Columbia University. 
WOODRUEEWLORANDE! LOSSiaae asic stoi cisdarencleiersinrcishersiss chale Yale University. 
SATSUSINIAOHIDE As tr titosieeaitte csere ctteaes bots cna cleo ioe mwislers University of Japan. 
WERKES a IROBERDN Wc aees cet aya ln eaten er oee ieee etal coos Harvard University. 
ZINSSER PM ELANS ay sceveie is toicle ee isis sisi orate sieleteehouste Miers Leland Stanford University. 


Total number of members at the close of the academic year, I9I1I-'12: 239. 


ORFICERS-* 


1903-I9I13. 

I903-"04 1904-'05 
Presidents ce. misiciars os » Meltzer Meltzer 
Vice-President.......... Park Ewing 
WUD raraMeys eieys eke icterscuster « Lusk Lusk 
PPTCASIINET << ais: «j\evets ter eyeyeres6 Calkins Calkins 
SEAN aida oobeooenc Gies Gies 

1908-09 1909-10 
President) a. sineteretare lel e Lee Lee 
Vice-President.......... Morgan’ Gies 
PULCASUE Cl cpeecyane steettciser chs Lusk Lusk 
SCCHCCAIY: cians « crscers aperenes Gies Opie 


1905-06 
Wilson 
Dunham 
Lusk 
Calkins 
Gies 


IQIO—’II 
Morgan 
Gies 
Lusk 
Opie 


1 Council—The Past Presidents and the Officers. 


145 


1906-07 
Flexner 
Dunham 


Calkins 
Gies 


IQII—'I2 
Morgan 
Levene 
Lusk 
Wallace 


1907-08 
Flexner 
Morgan 


Calkins 
Gies 


1912-13 
Ewing 
Levene 
Norris 
Wallace 


CLASSIFIED LIST .OF MEMBERS OF THE 
SOCIETY POR EXPERIVIENTAL 
BIOLOGY AND MEDICINE. 


Resident (Greater New York). 


Bellevue Hospital.—Cyrus W. Field, Charles Norris. 

Columbia University.—Russell Burton-Opitz, Gary N. Calkins, Henry E. 
Crampton, Richard H. Cunningham, Haven Emerson, Nellis B. Foster, William 
J. Gies, A. E. Guenther, Philip H. Hiss, Theodore C. Janeway, R. A. Lambert, 
Frederic S. Lee, Isaac Levin, C. C. Lieb, W. F. Longcope, W. G. MacCallum, 
Thomas H. Morgan, H. O. Mosenthal, Alwin M. Pappenheimer, B. S. Oppen- 
heimer, F. H. Pike, Jacob Rosenbloom, Henry C. Sherman, Hugh A. Stewart, 
Augustus B. Wadsworth, Edmund B. Wilson, Francis C. Wood. 

Cornell University Medical College-—S. P. Beebe, Stanley R. Benedict, 
M. T. Burrows, B. H. Buxton, A. F. Coca, E. F. DuBois, William J. Elser, 
James Ewing, Robert A. Hatcher, Graham Lusk, J. F. McClendon, John R. 
Murlin, Chas. R. Stockard, John C. Torrey, Richard Weil, C. J. Wiggers. 

Mt. Sinai Hospital—Charles A. Elsberg, R. Ottenberg. 

New York City College-—A. J. Goldfarb, Thomas A. Storey, C. E. A. 
Winslow. 

New York City Departments. Education.—C. Ward Crampton. Health. 
—James P. Atkinson, Edwin J. Banzhaf, L. W. Famulener, C. B. Fitzpatrick, 
Alfred F. Hess, Edna Steinhardt, Anna W. Williams. 

New York Polyclinic Medical School.—Isaac Adler. 

New York Post-Graduate Medical School—Ludwig Kast, W. J. MacNeal. 

New York University—Harlow Brooks, J. W. Draper, Edward K. Dun- 
ham, E. M. Ewing, Holmes C. Jackson, Arthur R. Mandel, John A. Mandel, 
William H. Park, H. D. Senior, Douglas Symmers, George B. Wallace. 

Rockefeller Institute for Medical Research.—John Auer, F. W. Bancroft, 
F. J. Birchard, E. E. Butterfield, Alexis Carrel, A. E. Cohn, Rufus Cole, A. R. 
Dochez, George Draper, Simon Flexner, T. S. Githens, Walter A. Jacobs, Don 
R. Joseph, I. S. Kleiner, Richard V. Lamar, P. A. Levene, Jacques Loeb, W. 
H. Manwaring, S. J. Meltzer, Gustave M. Meyer, F. M. McCrudden, Hideyo 
Noguchi, G. Canby Robinson, Peyton Rous, H. F. Swift, B. T. Terry, Donald 
D. Van Slyke, H. Wastenays. 

Sage Institute of Pathology.—Horst Oertel. 

St. Francis Hospital—Fritz Schwyzer. 

Brooklyn Botanic Garden.—C. Stuart Gager. 


819 Madison Avenue.—H. D. Dakin. 
147 


148 SCIENTIFIC PROCEEDINGS (49). 


Non-Resident. 


Baltimore Medical College-—Charles E. Simon. 

Carnegie Institution of Washington—Francis G. Benedict (Nutrition 
Laboratory, Boston), A. M. Banta, Charles B. Davenport, R. A. Gortner (Station 
for Experimental Evolution, Cold Spring Harbor, N. Y.), D. T. MacDougal 
(Washington), Alfred G. Mayer (Marine Laboratory, Tortugas, Fla.). 

Connecticut Agricultural Experiment Station (New Haven).—Thomas B. 
Osborne. 

Georgia State Board of Health (Atlanta).—Katharine R. Collins. 

Kentucky Agricultural Experiment Station (Lexington).—J. H. Kastle. 

Maine Agricultural Experiment Station (Orono).—Raymond Pearl. 

Massachusetts Institute of Technology.—Percy G. Stiles. 

Medico- Chirurgical College (Philadelphia).—Isaac Ott. 

Mercy Hospital (Pittsfield, Mass.)—Thomas Flournoy. 

Michael Reese Hospital ( Chicago).—James W. Jobling. 

Northwestern University Medical School ( Chicago).—J. B. Murphy. 

Philippine Medical School (Manila).—A. O. Shaklee. 

Trinity College ( Hartford) —Max W. Morse. 

Yonkers, N. Y.—Isaac F. Harris. 

U. S. Departments. Agriculture (Washington, D. C.).—Carl L. Alsberg, 
William N. Berg, William Salant; Interior (Philippine Islands, Bureau of 
Science, Manila).—Richard P. Strong, Oscar Teague. Tvreasury (Public Health 
and Marine- Hospital Service)—John F. Anderson, W. H. Frost, Wm. H. Hale, 
Reid Hunt and W. H. Schultz, Washington, D. C. 

Universities.— Buffalo—G. H. A. Clowes, Herbert U. Williams. Cah- 
fornia.—F. P. Gay, J. G. Fitzgerald, T. Brailsford Robertson. Chicago.— 
R. R. Bensley, A. J. Carlson, Ludvig Hektoen, Edwin O. Jordan, Frank R. 
Lillie, H. Gideon Wells. Cincinnati—Martin H. Fischer. Cornell—Andrew 
Hunter, Sutherland Simpson. Harvard.—Herman M. Adler, Walter B. Cannon, 
W. T. Councilman, Otto Folin, H. T. Karnser, G. H. Parker, Franz Pfaff, 
W. T. Porter, Joseph H. Partt, M. J. Rosenau, Theobald Smith, E. E. Southard, 
E. E. Tyzzer, S. Burt Wolbach, Robert M. Yerkes. Jilinois.—Philip B. Hawk. 
Japan.—Naohidé Yatsu. Johns Hopkins.—John J. Abel, Harvey W. Cushing, 
W. W. Ford, W. S. Halsted, William H. Howell, S. H. Jennings, Walter Jones, 
F. P. Mall, Adolph Meyer, William H. Welch. Leland Stanford.—A. C. Craw- 
ford, E. C. Dickson, W. Ophiils, Hans Zinsser.— McGill (Montreal).—J. George 
Adami, John L. Todd. Michigan.—W. Edmunds, Otto C. Glaser, A. W. 
Hewlett, Carl G. Huber, Warren P. Lombard, Frederick G. Novy, Aldred 
S. Warthin. Minnesota.—Robert B. Gibson, F. W. Schlutz. North Carolina. 
—W. de B. MacNider. Pennsylvania.—J. H. Austin, Alexander C. Abbott, 
D. H. Bergey, A. B. Eisenbrey, Ralph S. Lillie, Richard M. Pearce, Edward T. 
Reichert, Alfred N. Richards, A. I. Ringer, J. Edwin Sweet, A. E. Taylor. 
Pitisburgh.—C. C. Guthrie, Oskar Klotz. Princeton—Edwin G. Conklin. 
Southern California (Los Angeles)—Lyman B. Stookey. St. Louis.—E. P. 


CrassIFIED List oF MEMBERS. 149 


Lyon. Toronto.—T. G. Brodie, J. B. Leathes, A. B. Macallum. Tulane.— 
Charles W. Duval, J. V. Cooke. Virginia. —H. E. Jordan. Washington (St. 
Loutis).—David L. Edsall, John Howland, Joseph Erlanger, Eugene L. Opie, 
Ernst Sachs, Philip A. Shaffer. Wisconsin.—Charles R. Bardene, C. H. Bunt- 
ing, L. J. Cole, Arthur S. Loevenhart, Mazyck P. Ravenel. Western Reserve 
(Cleveland).—George W. Crile, J. J. R. Macleod, Torald Sollmann, G. N. 
Stewart. Yale—R. H. Chittenden, Ross G. Harrison, Lafayette B. Mendel, 
Frank P. Underhill, Lorande Loss Woodruff. 

University College (London).—Arthur R. Cushny. 

Phipps Institute (Philadelphia).—Paul A. Lewis. 

Wistar Institute of Anatomy (Philadelphia)—H. H. Donaldson, Shinkishi 
Hatai, E. B. Meigs. 

Barnard Skin and Cancer Hospital (St. Louis).—Leo Loeb. 

Cambridge, England.—C. G. L. Wolf. 


INDEX 


OF THE 


SCIENTIFIC PROCEEDINGS: 


[THE NUMERALS IN THIS INDEX CORRESPOND WITH THE NUMERALS IN 


PARENTHESIS ABOVE THE TITLES OF THE ABSTRACTS. 


PAGES 


ARE NOT INDICATED.] 


Adrenalin, cardiac hypertrophy pro- 
duced by, 614; destruction of by 
spinal fluid, 628; reaction of arteries 
to, 645; pupil dilatation caused by, 
650; inhibitory action in muscle- 
pancreas mixtures, 666; rise in blood 
from intra-spinal injections, 667. 

Age, influence of, on symptoms of, 
thyroparathyroidectomy, 611. 

Alcoholism, influence of on offspring, 
659. 

Amino acids, in urine, 687; picrolonates 
of, 688; determination of, 689; 
nature of in proteins, 690. 

Amphibians, tyrosinase in, 693. 

Anemia, experimental pernicious, 610; 
influence of on growth of sarcoma, 
648. 

Anti-anaphylaxis, experimental study 
on, 691. 

Arteries, response of to blood serum, 
671; ligation of pulmonary, 670; 
pressure in pulmonary, 669. 

Atoxyl, action of, 640. 


Bacteria, resistance to calcium hypo- 
chlorite, 634; effect of drying on, 
686. 

Barium, studies on feeding with, 635. 

Blood serum, vaso reacting substances 
in, 644; response of different arteries 


to, 671; occurrence of odcytase in, 
674. 

Blood pressure, rise from adrenalin, 
667; pulmonary, 669. 

Brain of smooth dog-fish, water in, 638. 

Brill’s disease, identity to typhus 
fever, 657. 


Caffein, elimination and toxicity of, 
649. 

Calcium, influence of on hypertrophy 
caused by adrenalin, 614; hypo- 
chlorite, resistance of bacteria to, 634. 

Cancer, immunization against, 621. 

Carbohydrates, fermentation by bac- 
teria, 633. 

Carbon dioxide, relation to develop- 
ment of embryos, 684. 

Cell division in mammalian tissue, 685. 

Character, a dominant sex limited, 
619. 

Chemicals, effect of on division of 
protozoa, 679. 
Chloride excretion 

phritis, 624. 

Chromates, nephritis produced by, 
617, 618. 

Circulatory apparatus, 
gases by, 627. 

Colostrum, toxic character of, 642. 

Constipation, relation to spleen, 655. 


in uranium ne- 


tolerance for 


151 


152 


Corpus luteum, 654. 
Cytolytic action of ox-blood, 652. 


Diaphragm muscle, properties of, 672. 
Diets, growth on artificial, 660. 
Digitalis, vomiting from, 668. 

Dog fish, water in brain of, 638. 
Drying, effect on bacteria, 686. 


ScIENTIFIC PROCEEDINGS (49). 


Immunity, tumor, 632. 


Immunization against transplanted 
cancer, 621. 

Indican, in the blood of uremic patients, 
665. 


Inheritance, in fundulus, 615. 
Intravascular foreign bodies, 631. 


Duodenal obstruction, glycuronic acid | Labor, relation of internal secretion of 


in, 629. 


Ear, semicircular canals of, 616. 

Eclampsia, 641. 

Embryos, relation of oxygen and 
carbon dioxide to, 684. 

Epinephrin, effect of on internal secre- 
tions, 677. 


Fat-free foods, feeding experiments | 


with, 661. 
Fermentation of carbohydrates, 633. 


Food, feeding experiments with fat- 
free mixtures, 661; factor in hiber- 
nation, 675. 

Fundulus, color inheritance in, 615. 


Gases, tolerance of by circulatory 
apparatus, 627. 

Gastric secretion in new born, 623. 

Glutaric acid, in phlorhizin diabetes, 
647. 

Glycuronic acid, in duodenal obstruc- 
tion, 629. 

Growth on artificial diets, 660. 


Hemolytic serum, production of, 676, 

Heart, hypertrophy from adrenalin. 
614; block, 626; convulsant effect of 
removal of, in morphinized frogs, 
630. 

Heredity, sex-limited in poultry, 622. 

Hibernation, food factor in, 675. 

Hyperemia, influence of on growth of 
sarcoma, 648. 

Hypophysis, effect on vaso-dilators, 
681; on the pupil, 683. 


mamme to, 643. 
Larve, production of grafted and 
multiple, 636. 
Leucocytes, toxicity of foreign, 692. 
Lights as stimuli, 651. 


Mamma, internal secretion of, 643. 

Melanins, two types of, 694. 

Mendelian result, masking of by en- 
vironment, 662. 

Meyer strip method, for detection of 
adrenalin, 645. 


| Milk, secretion of, 653. 


Monkeys, trypanasomiasis in, 620. 

Monstrosities, production of, 637. 

Morphinized frogs, effect of removal 
of heart on, 630. 

Muscle, properties of diaphragm, 672; 
stimulation of nerve endings in, 673. 


Nephrectonized rabbits, toxicity and 
elimination of caffeine in, 649. 

Nephritis, experimental uranium, 617, 
618. 

Nerve endings in muscle, stimulation 
of, 673. 

Nitrogen excretion in uranium ne- 
phritis, 649. 


Odcytase, isolation of, 674. 

Optic nerve, mode of entrance of, 612. 

Oxygen, relation of to development of 
embryos, 684. 


Pancreatic secretion in the new born, 
623. 
Paramecium, five year culture of, 695. 


INDEX. 


Parathyroid gland, relation to electrical 
conductivity, 658. 

Parathyroidectomy, influence of age on 
symptoms from, 611; seat of action 
of tetany in, 625. 

Parturient paresis, 641; colostrum in, 
642. 

Penicillium, studies on, 613. 

Phlorhizin diabetes, 646, 647; influence 
of tartrates in, 696. 

Picrolonates of amino-acids, 688. 

Pineal gland, 654. 

Potassium salts, influence of an cardiac 
hypertrophy, 614. 

Proteins, free amino nitrogen groups in, 
690. 

Protozoa, effect of chemicals on division 
rate of, 679. 

Protozoan fauna in hay infusions, 656. 

Pulse, venous, 680. 

Pupil, dilatation caused by adrenalin, 
650; influence of hypophysis on, 683. 


Resistance of bacteria to calcium 
hypochlorite, 634. 


Sarcoma, influence of anemia on growth 
of, 648. 

Secretions, effect of epinephrin on 
internal, 677. 

Semi-circular canals, relation to motor 
system, 616. 

Serological work, errors in, 663. 

Sex-limited, character, a dominant, 
619; heredity in poultry, 622. 

Spinal fluid, destruction of adrenalin 
by, 628. 


153 


Spleen and chronic constipation, 655. 

Streptococci, fermentation of carbo- 
hydrates by, 633. 

Strychnine, reduction of toxicity of by 
fluids, 682. 


Tetany, seat of action of in parathy- 
roidectomy, 625. 

Thyro-parathyroidectomy, influence of 
age on symptoms of, 611. 

Tissue, cell division in mammalian, 
685. 

Tolerance of gases by circulatory sys- 
tem, 627. 

Trypanosomes, suspension of in serum, 
639. 

Trypanasomiasis in monkeys, 620. 

Tubercle bacillus, virulence of, 664. 

Tumor immunity in rats, 632. 

Typhus fever, identity to Brill’s disease, 
657. 

Tyrosinase in reproductive organs of 
amphibians, 693. 


Uranium nephritis, excretion in, 624. 

Uremic patients, indican in blood of, 
665. 

Urine, amino-acid nitrogen in, 687. 


Vaso-dilators, 
upon, 681. 
Vomiting from digitalis, 668. 

Venous pulse waves, 680. 


effect of hypophysis 


Wasserman reaction, standardization 
of, 679. 


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a4 


PROCEEDINGS 


OF THE 


SOCIETY FOR | 


EXPERIMENTAL BIOLOGY AND MEDICINE 


FORTY-FIFTH MEETING 
COLUMBIA UNIVERSITY 
NEW YORK CITY 


OCTOBER 18, IgI1 


VoLuME IX 


No? "1 


NEW YORK 


IQII 


CONTENTS. 
H. M. ADLER: Experimental pernicious anemia. 1 (610). 


SUTHERLAND Simpson : The influence of age on the symptoms following thyro-parathy- 
roidectomy. 2 (611). 


J. A. BADERTSCHER: Peculiarity in the mode of entrance of the optic nerve into the 
eyeball in some rodents. 3 (612). 


C. L. ALsBercG and O. I, Back: Biochemical and toxicological studies upon Peni 
cillium puberlum Bajnier. 4 (613). 


H. A. Stewart: The influence of the salts of calcium and potassium on the degree of 
hypertrophy produced by adrenalin injections in rabbits. 5 (614). 


F, W. Bancrorr: Color inheritance in Fundulus hybrids. 6 (615). 


J. GORDON WILSON and F. H. Pike: A note on the relation of the semicircular canals 
of the ear to the motor system. 7 (616). 


W. OpHis: Experimental nephritis produced in guinea-pigs by subcutaneous injec- 
tions of chromates. 8 (617). 


W. OpHvtis: Experimental nephritis produced in rabbits by subcutaneous injections of 
chromates. 9 (618). 


T. H. Morcan: A dominant sex-limited character. 10 (619). 


The proceedings of the Society for Experimental Biology and Medicine are pub- 
lished as soon as possible after each meeting. Regular meetings of the Society are held 
in New York on the third Wednesdays of October, December, February, April and 
May. A volume of the proceedings consists of the numbers issued during an 
academic year. 

The price per volume, sent postage prepaid, is one dollar. The price of copies 
of the proceedings of any meeting is twenty cents each, postage prepaid. Subscriptions 
are payable in advance. 

Address communications to any of the following members of the Council of the 
Society : 

Past PresipENTS— S. J. Meltzer, Rockefeller Institute for Medical Research ; 
Edmund B. Wilson, Columbia University; Simon Flexner, Rockefeller Institute for 
Medical Research ; Frederic S. Lee, Columbia University. 

PRESIDENT — Thomas H. Morgan, Columbia University. 

VicE-PRESIDENT— Phoebus A. Levene, Rockefeller Institute for Medical 
Research. 

SECRETARY — George B. Wallace, University and Bellevue Hospital Medical 
College. 

TREASURER — Graham Lusk, Cornell University Medical College. 


MANAGING Epiror—The Secretary, 335 E. 26th St., New York City. 


PROCEEDINGS 


OF THE 


SOCIETY FOR 


EXPERIMENTAL BIOLOGY AND MEDICINE 


FORTY-SIXTH MEETING 
ROCKERPELLER INSTITUTE 
NEW YORK CITY 


DECEMBER 20, IogIt 


VOLUME IX 


No. 2 


NEW YORK 


IQII 


CONTENTS. 


B, T. Terry: Trypanasomiasis in monkeys (Macacus rhesus) in captivity. 1 (620). 


R. A. LAMBer?’: On the question of immunization against transplanted cancer by in- 
jections of an animal’s own tissues. 2 (621). 


C. B. DAVENPORT: A case of sex limited heredity in poultry. 3 (622). 

A. F, Hess: The gastric and pancreatic secretions of the new born. 4 (623). 

H. O. MosENTHAL: Nitrogen and sodium chloride excretion in experimental uranium 
nephritis. 5 (624). 

W. G. MacCAL_um: The seat of action in tetany after parathyroidectomy. 6 (625). 

A. E, CoHN: Curves from the case of transient complete heart block. 7 (626). 


J. P. ATKINSON and C. B. FirzpaTrick: Further observations on the tolerance of gases 
by the circulatory apparatus. 8 627). 


S. J. Me_tzer: The destruction of adrenalin by spinal fluid. 9 (628). 


J. W. Draper and F, W. Scuiurz: Glucuronic acid determination (Tollens) in duo- 
denal obstruction. 10 (629). 


T. S. GITHENS and S. J. MeLtzer: The convulsant effect of removal of the heart on 
morphinized frogs. 11 (630). 


C, C. GUTHRIE and A. H, RYAN: Intravascular foreign bodies. 12 (631). 


RIcHARD WEIL: On tumor immunity in rats; with demonstration. 13 (632). 


The proceedings of the Society for Experimental Biology and Medicine are pub- 
lished as soon as possible after each meeting. Regular meetings of the Society are held 
in New York on the third Wednesdays of October, December, February, April and 
May. A volume of the proceedings consists of the numbers issued during an 
academic year. 

The price per volume, sent postage prepaid, is one dollar. The price of copies 
of the proceedings of any meeting is twenty cents each, postage prepaid. Subscriptions 
are payable in advance. 

Address communications to any of the following members of the Council of the 
Society : 

PasT PRESIDENTS— S. J. Meltzer, Rockefeller Institute for Medical Research ; 
Edmund B. Wilson, Columbia University; Simon Flexner, Rockefeller Institute for 
Medical Research ; Frederic S. Lee, Columbia University. 

PRESIDENT — Thomas H. Morgan, Columbia University. 


VicE-PRESIDENT— Phoebus A. Levene, Rockefeller Institute for Medica] 
Research. 


SECRETARY — George B. Wallace, University and Bellevue Hospital Medical 
College. 


TREASURER — Graham Lusk, Cornell University Medical College. 


MANAGING Epiror —The Secretary, 338 E. 26th St., New York City. 


CLASSIFIED LIST OF MEMBERS OF THE SOCIETY FOR 
EXPERIMENTAL BIOLOGY AND MEDICINE. 


Resident (Greater New York). 


Bellevue Hospital.—Cyrus W. Field, Charles Norris, Alwin M. 
Pappenheimer. 


Columbia University. — Russell Burton -Opitz, Gary N. Calkins, 
Henry E. Crampton, Richard H. Cunningham, Haven Emerson, Nellis 
B. Foster, William J. Gies, A. E. Guenther, Philip H. Hiss, Theodore C. Jane- 
way, R. A. Lambert, Frederic S. Lee, Isaac Levin, W. F. Longcope, W. G. 
MacCallum, Thomas H. Morgan, H. O. Mosenthal, B. S. Oppenheimer, R, 
Ottenberg, F. H. Pike, Jacob Rosenbloom, Henry C. Sherman, Hugh A, 
Stewart, Augustus B. Wadsworth, Edmund B. Wilson, Francis C. Wood, 

Cornell University Medical College,—S. P. Beebe, Stanley R. Benedict, 
B. H. Buxton, William J. Elser, James Ewing, Robert A. Hatcher, Graham 
Lusk, J. F. McClendon, John R. Murlin, Chas. R. Stockard, John C. Torrey, 
Richard Weil, H. B. Williams, C. G. L. Wolf. 

Mt. Sinat Hospital.—A. E. Cohn, Charles A. Elsberg. 

New York City College.—A. J. Goldfarb, Thomas A. Storey, C. E. A. 
Winslow. 

New York City Departments. Education.—C. Ward Crampton. 
Flealth.—James P. Atkinson, Edwin J. Banzhaf, L. W. Famulener, C. B. 
Fitzpatrick, Alfred F. Hess, Edna Steinhardt, Anna W. Williams. 

New Vork Polyclinic Medical School.—Isaac Adler. 

New York Post-Graduate Medical School.—Ludwig Kast, W. J. Mac- 
Neal. 

New Vork University. — Harlow Brooks, Edward K. Dunham, E. M. 
Ewing, Holmes C. Jackson, Arthur R. Mandel, John A. Mandel, William 
H. Park, H. D. Senior, Douglas Symmers, George B. Wallace. 

Rockefeller Institute for Medical Research.—John Auer, F. W. Bancroft, 
F. J. Birchard, Alexis Carrel, Rufus Cole, A. R. Dochez, Simon Flexner, 
T. H. Githens, Walter A. Jacobs, Don R. Joseph, I. S. Kleiner, Richard 
V. Lamar, P. A. Levene, Jacques Loeb, W. H. Manwaring, S. J. Meltzer, 
Gustave M. Meyer, F. M. McCrudden, Hideyo Noguchi, R. Ottenberg, 
Peyton Rous, H F. Swift, B. T. Terry, Donald D. Van Slyke. 

Sage Institute of Pathology,— Horst Oertel. 

St. Francis Hospital,—Fritz Schwyzer. 

Central Museum, Brooklyn.—C. Stuart Gager. 


819 Madison Avenue.—H. D. Dakin. 


Non-Resident. 


Baltimore Medical College. —Charles E. Simon. 

Carnegie Institution of Washington.—Francis G. Benedict (Nutrition 
Laboratory, Boston), A. M. Banta, Charles B. Davenport, R. A. Gortner 
(Station for Experimental Evolution, Cold Spring Harbor, N. Y.), D. T. 
MacDougal (Washington), Alfred G. Mayer (Marine Laboratory, Tortugas, 
i7a.). 

Connecticut Agricultural Experiment Station (New Haven).—Thomas 
B. Osborne. 

Geergia State Board of Health (Atlanta).—Katharine R. Collins. 

Maine Agricultural Experiment Station (Orono).— Raymond Fearl. 


Massachusetts Institute of Technology.—Percy G. Stiles. 

Medico-Chirurgical College (Philadelphia).—\saac Ott. 

Mercy Hospital (Pittsfield, Mass.).—Thomas Flournoy. 

Michael Reese Hospital (Chicago).—James W. Jobling. 

Missouri Botanical Garden (St. Louis).—W. Trelease. 

Northwestern University Medical School (Chicago).—J. B. Murphy. 

Philippine Medical School (Manila).—A. O. Shaklee. 

Trinity College ([Tartford ).—Max W. Morse. 

Rochester, Minn.—J. W. Draper. 

Yonkers, NN. Y.—Isaac F. Harris. 

U.S. Departments. Agriculture (Washington, D,C.).—Carl L. Alsberg, 
William N. Berg, William Salant ; /uterior (Philippine Islands, Bureau of 
Science, Manila).—Richard P. Strong, Oscar Teague. Treasury (Public 
Flealth and Marine-Hospital Service).—John F. Anderson, W. H. Frost, 
Wm. H. Hale, Reid Hunt, Joseph H. Kastle and W. H. Schultz, Wash- 
ington, D. C. 

Universitics. Buffalo.—G.H. A. Clowes, Herbert U. Williams. Cad- 
fornia, —¥. P. Gay, F. J. Fitzgerald, T. Brailsford Robertson. Chicago. — 
R. R. Bensley, A. J. Carlson, Ludvig Hektoen, Edwin O. Jordan, Waldemar 
Koch, Frank R. Lillie, Albert P. Mathews, H. Gideon Wells. Cornel/.— 
Andrew Hunter, Sutherland Simpson. H/arvard.—Herman M. Adler, Walter 
R. Brinkerhoff, Walter B. Cannon, W. T. Councilman, Otto Folin, H. T. 
Karsner, G. H. Parker, Franz Pfaff, W. T. Porter, Joseph H. Pratt, M. J. 
Rosenau, Theobald Smith, E. E. Southard, E. E. Tyzzer, S. Burt Wolbach, 
Robert M. Yerkes. ///inois.— Philip B. Hawk. /afan.—Naohidé Yatsu. 
Johns Flopkins.— John J. Abel, Harvey W. Cushing, W. W. Ford, W. S. 
Halsted, William H. Howell, H. S. Jennings, Walter Jones, F. P. Mall, 
Adolph Meyer, William H. Welch. Leland Stanford.—A. C. Crawford, E. 
C. Dickson, W. Ophiils, Hans Zinsser. MacDonald College (Ste. Anne de 
Bellevue, Quebec).—John L. Todd. McGill (Montreal ).—J. George Adami. 
Michigan. —C. W. Edmunds, Otto C. Glaser, A. W. Hewlett, Carl G. 
Huber, Warren P. Lombard, Frederick G. Novy, Victor C. Vaughan, 
Aldred S. Warthin. Mssowrz7.—Robert B. Gibson. orth Carolina.—W. 
de B. MacNider. Pennsylvania. — Alexander C. Abbott, D. H. Bergey, 
A. B. Eisenbrey, Ralph S. Lillie, J. H. Montgomery, Richard M. Pearce, 
Edward T. Reichert, Alfred N. Richards, A. I. Ringer, J. Edwin Sweet, 
A. E. Taylor. Pittsburgh.—C. C. Guthrie, Oskar Klotz. © Princeton.— 
Edwin G. Conklin. Southern California (Los Angeles).—Lyman B. Stookey. 
St.. Louts.—E. P. Lyon. Zoronto.—T. G. Brodie, J. B. Leathes, A. B. 
Macallum. TZulane.—Charles W. Duval, J. V. Cooke. Washington (St. 
Louzs).—David L. Edsall, John Howland, Joseph Erlanger, Eugene L. Opie, 
Ernst Sachs, Philip A. Shaffer. Wisconsin.—Charles R. Bardene, C. H. 
Bunting, Arthur S. Loevenhart, Mazyck P. Ravenel. Western Reserve 
(Cleveland).—George W. Crile, J. J. R. Macleod, Torald Sollmann, G. N. 
Stewart. Yal/e.—R. H. Chittenden, Ross G. Harrison, Yandell Henderson, 
Lafayette B. Mendel, Frank P. Underhill, Lorande Loss Woodruff. 

University College (London).—Arthur R. Cushny. 

Phipps Institute (Philadelphia).—Paul A. Lewis. 

Wistar Institute of Anatomy (Philadelphia).—H. H. Donaldson, Shin- 
kishi Hatai, E. B. Meigs. 

Barnard Skin and Cancer Hospital (St. Louzs).—Leo Loeb. 


Members present at the forty-sixth meeting: 

Atkinson, Auer, Cohn, Davenport, Emerson, Eisenbrey, Field, Foster, 
Famulener, Fitzpatrick, Gies, Goldfarb, Hess, Jacobs, Janeway, Joseph, 
Lambert, Lee, Levin, Loeb, MacCallum, Manwaring, Meltzer, Morgan, 
Mosenthal, Norris, Ottenberg, Pappenheimer, Rous, Steinhardt, Swift, Terry, 
Wallace, Weil. 


Members elected at the forty-sixth meeting: 
A. M. Banta, E. C. Dickson, E. M. Ewing, F. J. Fitzgerald, R. A. Gort- 
ner, A. E. Guenther, W. de B. MacNider, B. S. Oppenheimer, F. H. Pike. 


Dates of the next two regular meetings: 
February 21, 1912— April 17, 1912. 


i 
i 
f 


CLASSIFIED LIST OF MEMBERS OF THE SOCIETY FOR 
EXPERIMENTAL BIOLOGY AND MEDICINE. 


Resident (Greater New York). 


Bellevue Hospital.—Cyrus W. Field, Charles Norris, Alwin M. 
Pappenheimer. 

Columbia University.—Russell Burton-Opitz, Gary N. Calkins, Alfred E. 
Cohn, Henry E. Crampton, Richard H. Cunningham, Haven Emerson, Nellis 
B. Foster, William J. Gies, Philip H. Hiss, Theodore C. Janeway, R. A, Lam- 
bert, Frederic S. Lee, Isaac Levin, W. F. Longcope, W. G. MacCallum, 
Thomas H. Morgan, H. O. Mosenthal, Jacob Rosenbloom, Henry C. Sher- 
man, Hugh A. Stewart, Augustus Db. Wadsworth, Edmund B. Wilson, 
Francis C. Wood. 

Cornell University Medical College.—S. P. Beebe, Stanley R. Benedict, 
B. H. Buxton, William J. Elser, James Ewing, Robert A. Hatcher, Graham 
Lusk, J. F. McClendon, John R. Murlin, Chas. R. Stockard, John C. Torrey, 
Richard Weil, H. B. Williams, C. G. L. Wolf. 

Mt. Sinai Hospital.—Charles A. Elsberg. 

New York City Collegei:—A. J. Goldfarb, Thomas A. Storey, C. E. A. 
Winslow. 

New York City Departments. Education.—C, Ward Crampton. 
Health.—James P. Atkinson, Edwin J. Banzhaf, L. W. Famulener, C. B. 
Fitzpatrick, Alfred F. Hess, Edna Steinhardt, Anna W. Williams. 

New York Polyclinic Medical School.—\saac Adler. 

New York Post-Graduate Medical School.—Ludwig Kast, W. J. Mac- 
Neal. 

New York University.—Harlow Brooks, Edward K. Dunham, Holmes 
C. Jackson, Arthur R. Mandel, John A. Mandel, William H. Park, H. D. 
Senior, Douglas Symmers, George B. Wallace. 

Rockefeller Institute for Medical Research.—John Auer, F. W. Bancroft, 
F. J. Birchard, Alexis Carrel, Rufus Cole, A. R. Dochez, Simon Flexner, 
T. H. Githens, Walter A. Jacobs, Don R. Joseph, I. S. Kleiner, Richard 
VY. Lamar, P. A. Levene, Jacques Loeb, W. H. Manwaring, S. }. Meltzer, 
Gustave M. Meyer, F. M. McCrudden, Hideyo Noguchi, R. Ottenberg, 
Peyton Rous, H. F. Swift, B. T. Terry, Donald D. Van Slyke. 

Sage Institute of Pathology,— Horst Oertel. 

St. Francis Hospital.—F¥ritz Schwyzer. 

Central Museum, Brooklyn.—C. Stuart Gager. 


819 Madison Avenue.—H. D. Dakin. 


Non-Resident. 


Baltimore Medical College.—-Charles E. Simon. 

Carnegie Institution of Washington.—Francis G. Benedict (Vuérition 
Laboratory, Boston), Charles B. Davenport (Station for Experimental Evolu- 
tion, Cold Spring Hlarbor, N. Y.), D. T. MacDougal (Washington), Alfred 
G. Mayer (Marine Laboratory, Tortugas, Fla.). 

Connecticut Agricultural Experiment Station (New Haven).—Thomas 
B. Osborne. 

Geergia State Board of Health (Atanta).—Katharine R. Collins. 

Maine Agricultural Experiment Station (Orono).— Raymond Fearl. 


Massachusetts Institute of Technology.—Percy G. Stiles. 

Medico-Chirurgical College (Philadelphia).—I\saac Ott. 

Mercy Hospital (Pittsfield, Mass.).—Thomas Flournoy. 

Michael Reese Hospital (Chicago).—James W. Jobling. 

Missouri Botanical Garden (St. Louis).—W. Trelease. 

Northwestern University Medical School (Chicago).—J. B. Murphy. 

Philippine Medical School (Manila).—A. O. Shaklee. 

Trinity College (Hartford).—Max W. Morse. 

Rochester, Minn.—J. W. Draper. 

Yonkers, N. Y.—Isaac F. Harris. 

U. S. Departments. Agriculture (Washington, D.C.).—Car1 L. Alsberg, 
William N. Berg, William Salant ; Jnterzor (Philippine Islands, Bureau oy 
Science, Manila).—Richard P. Strong, Oscar Teague. Treasury (Public 
Health and Marine-Hospital Service).—John F. Anderson, W. H. Frost; 
Wm. H. Hale, Reid Hunt, Joseph H. Kastle and W. H. Schultz, Wash- 
ington, D. C. 

Universitics. Buffalo.—G. H. A. Clowes, Herbert U. Williams. Cadz- 
fornia, —¥. P. Gay, T. Brailsford Robertson. Chicago. —R. R. Bensley, 
A. J. Carlson, Ludvig Hektoen, Edwin O. Jordan, Waldemar Koch, Frank 
R. Lillie, Albert P. Mathews, H. Gideon Wells. Cornme//.—Andrew Hunter, 
Sutherland Simpson. AHarvard.—Herman M. Adler, Walter R. Brinkerhoff, 
Walter B. Cannon, W. T. Councilman, Otto Folin, H. T. Karsner, G. H. 
Parker, Franz Pfaff, W. T. Porter, Joseph H. Pratt, M. J. Rosenau, 
Theobald Smith, E. E. Southard, E. E. Tyzzer, S. Burt Wolbach, Robert M. 
Yerkes. J//inots.—Philip B. Hawk. _Jafan.—Naohidé Yatsu. Johns Hop- 
kins. —John J. Abel, Harvey W. Cushing, W. W. Ford, W. S. Halsted, 
William H. Howell, H. S. Jennings, Walter Jones, F. P. Mall, Adolph 
Meyer, William H. Welch. Leland Stanford. —A. C. Crawford, W. 
Ophiils, Hans Zinsser. MacDonald College (Ste. Anne de Bellevue, Quebec). 
—John L. Todd. McGill (Montreal).—J. George Adami. Michigan.—C. W. 
Edmunds, Otto C. Glaser, A. W. Hewlett, Carl G. Huber, Warren P. 
Lombard, Frederick G. Novy, Victor C. Vaughan, Aldred S. Warthin. 
Missourt.—Robert B. Gibson. /ennusylvania.—Alexander C. Abbott, D. H. 
Bergey, A. B. Eisenbrey, Ralph S. Lillie, J. H. Montgomery, Richard M. 
Pearce, Edward T. Reichert, Alfred N. Richards, A. I. Ringer, J. Edwin 
Sweet, A. E. Taylor. Pittsburgh.—C. C. Guthrie, Oskar Klotz. Princeton.— 
Edwin G. Conklin. Southern California (Los Angeles).—Lyman B. Stookey. 
St. Louts.—E. P. Lyon. Yoronto.—T. G. Brodie, J. B. Leathes, A. B. 
Macallum. TZz/ane.—Charles W. Duval, J. V. Cooke. Washington (St. 
Louis).—David L. Edsall, John Howland, Joseph Erlanger, Eugene L. Opie, 
Ernst Sachs, Philip A. Shaffer. Wzsconsin.—Charles R. Bardene, C. H. 
Bunting, Arthur S. Loevenhart, Mazyck P. Ravenel. Western Reserve 
(Cleveland).—George W. Crile, J. J. R. Macleod, Torald Sollmann, G. N. 
Stewart. YVa/e.—R. H. Chittenden, Ross G. Harrison, Yandell Henderson, 
Lafayette B. Mendel, Frank P. Underhill, Lorande Loss Woodruff, 

University College (London).—Arthur R. Cushny. 

Phipps Institute (Philadelphia).—Paul A. Lewis. 

Wistar Institute of Anatomy-(Philadelphia).—H. H. Donaldson, Shin- 
kishi Hatai, E. B. Meigs. 

Barnard Skin and Cancer Hospital (St. Louis).—Leo Loeb. 


Members present at the forty-fifth meeting: 
H. M. Adler, I. Adler, Alsberg, Auer, Bancroft, Calkins, Field, Jack- 
son, Joseph, Levene, Levin, Meltzer, Morgan, Pappenheimer, Senior, Simp- 
son, Stewart, Wallace, H. B. Williams. 


Dates of the next two regular meetings: 
December 13, 1911 — February 21, 1912. 


PROCEEDINGS 


OF THE 


SOCIETY FOR 


EXPERIMENTAL BIOLOGY AND MEDICINE 


FORTY-SEVENTH MEETING 


COLEEGE;OF THE: CITY OF NEW), YORK 
NEW YORK CITY 


FEBRUARY 21, Ig12 


VoLuUME IX 


No. 3 


NEW YORK 


Igi2 


CONTENTS. 


C, E, A. Winstow: The fermentation of carbohydrate media by streptococci. 24 (633). 

C. M. Hixxiarp (by invitation) : The comparative resistance of spores and vegetative cells of bacteria 
toward calcium hypochloride. 25 (634). 

C. L. AvsperG and O, F. Back: Studies on barium feeding. 26 (635). 

A. J. Go-prars: The production of grafted and multiple larve. 27 (636). 

A. J. Gotprars: The production of typical monstrosities by various methods, 28 (637). 

G. G. Scorr (by invitation): The percentage of water in the brain of the smooth dog-fish. 29 (638)- 

Bot. > 1632) On the advantage for certain experiments in vitro of suspending trypanosomes in serum. 
30 . 

B. T. Terry: The action of atoxyl. 31 (640). 


2) 


Bl fe eeerel and J. H. Kastve: Parturient paresis and eclampsia; similarities in these two diseases. 
32 (641). 
D, J. Heary and J, H. Kasrie: The toxic character of colostrum in parturient paresis, 33 (642). 
D. J. Heaty and J. H. Kasrie: The internal secretion of the mammz asa factor in the onset of 
labor. 34 (643). 
J. P. Arxinson and C, B. Firzparrick: Some vaso-reacting substances in blood serum. 35 (644). 


E. A. Park and T. C. Janeway: A study of the Meyer strip method for the reaction of coronary and 
other arteries to adrenalin and certain salts. 36 (645). 


A. I, Rincer: Studies on phlorhizin diabetes. 37 (646). 

A. 1. Rincer: The influence of glutaric acid on phlorhizin diabetes. 38 (647). 

M. J. SivrENFELD (by invitation); Influence of anemia and hyperemia on the growth of sarcoma in 
rats, 39 (648). 

Ww. ea. J.B. Rrecer: The elimination and toxicity of caffein in nephrectomized rabbits. 
40° ). 

D. R. Josepu: A quantitative study of the pupil dilatation caused by adrenalin. 41 (660). 

G, H. Parker: Intermittent and continuous lights of equal intensity as stimuli. 42 (651). 

T. BraILsFoRD Rosertson: The cytolytic action of ox blood on sea urchin eggs and its inhibition by 
proteins. 43 (652). 

Isaac Orr and J. C. Scorr: The action of various agents on the secretion of milk. 44 (653). 

Isaac Orr and J. C. Scorr: The pineal gland and the corpus luteum. 45 (654). 

Isaac Orr and J. C. Scorr: The spleen and chronic constipation. 46 (655). 

L. L. WooprurF: The sequence of the protozoan fauna in hay infusions. 47 (656). 


J. F. ANpERson and J, GoLpBERGER: The experimental demonstration of the identity of so-called 
Brill’s disease to typhus fever. 48 (657). 


Hersert B. Witcox;: The relation of the parathyroid glands to electrical conductivity. 49 (658). 


The proceedings of the Society for Experimental Biology and Medicine are pub- 
lished as soon as possible after each meeting. Regular meetings of the Society are held 
in New York on the third Wednesdays of October, December, February, April and 
May. A volume of the proceedings consists of the numbers issued during an 
academic year. 

The price per volume, sent postage prepaid, is one dollar. The price of copies 
of the proceedings of any meeting is twenty cents each, postage prepaid. Subscriptions 
are payable in advance. 

Address communications to any of the following members of the Council of the 
Society : 

Past PRESIDENTS— S. J. Meltzer, Rockefeller Institute for Medical Research ; 
Edmund B. Wilson, Columbia University; Simon Flexner, Rockefeller Institute for 
Medical Research; Frederic S. Lee, Columbia University, Thomas H. Morgan, 
Columbia University. 

PRESIDENT — James Ewing, Cornell University Medical College. 

VicE-PRESIDENT— Phoebus A. Levene, Rockefeller Institute for Medical 
Research. 

SECRETARY — George B. Wallace, University and Bellevue Hospital Medical 
College. 

TREASURER — Charles Norris, Bellevue Hospital. 


MANAGING EpiTor —The Secretary, 338 E. 26th St., New York City. 


PROCEEDINGS 


OF THE 


SOCIETY FOR 


EXPERIMENTAL BIOLOGY AND MEDICINE 


FORTY-EIGHTH MEETING 


CORNELL UNIVERSITY MEDICAL COLLEGE 


NEW YORK CITY 


April 17, 1912 


VoLuME IX 


No. 4 


NEW YORK 


IgI2 


CONTENTS. 


Srockarp: The influence of alcoholism on the offspring. 50 (659). 

OszorneE and L. B. Menpev: Growth and maintenance on purely artificial diets, 51 (660). 
Oszorne and L, B. Menpev: Feeding experiments with fat-free food mixtures. 52 (661). 
MorGan: The masking of a Mendelian result by the influence of the environment. 53 (662). 
. H. ManwarinG: Sources of error in serological work. 54 (663). 

. F. Hess: The relation of the virulence of the tubercle bacillus to its persistence in the circulation. 
.B 


pas 
muss 
Be 
aE 

H 


24480 


55 (664). 
. Foster: On indican in the blood of uremic patients. 56 (665). 
A.M. Paprenneimer: The inhibitory action of adrenalin in muscle-pancreas mixtures, 57 (666). 


J. Aver and S. J. Merrzer: A characteristic course of the rise of blood pressure caused by an intra- 
spinal injection of adrenalin. 58 (667). 


C. Eccieston and R, A. HatcHer: Demonstration of vomiting movements in an eviscerated animal 
under the influence of digitalis. 59 (668). 


C. J. Wiccrrs: The variations of pressure in the pulmonary artery. 60 (669). 
T.S. Giruens: The results of ligation of the pulmonary and cutaneous arteries in the frog. 6z (670). 


H. A. Stewart and S Harvey: Variations in the response of different arteries to blood serum and 
plasma. 62(671). 


F, S, Lez and A, E, Gurntuer: General physiological properties of diaphragm muscle. 63 (672). 


Mary WHITALL WorTHINGTON (presented by W. H. Hower): The stimulation of nerve endings 
in muscle, and the theory of receptive substances. 64 (673). 


T. BrartsForp Roxgertson: On the isolation of odcytase, the fertilizing and cytolyzing substance in 
mammalian blood serum. 65 (674). 


SUTHERLAND Simpson: The food factor in hibernation. 66 (675). 
F. P. Gay and J. G. FirzGeratp: A rapid method of producing a haemolytic serum. 67 (676). 


Isaac Orr and J. C. Scorr: The effect of internal secretions on the secretion of epinephrin. 68 
(677). 
J. G. Firzceratp and J. B. Learuers: Standardization of the Wassermann reaction. 69 (678). 


2 > 


The proceedings of the Society for Experimental Biology and Medicine are pub- 
lished as soon as possible after each meeting. Regular meetings of the Society are held 
in New York on the third Wednesdays of October, December, February, April and 
May. A volume of the proceedings consists of the numbers issued during an 
academic year. 

The price per volume, sent postage prepaid, is one dollar. The price of copies 
of the proceedings of any meeting is twenty cents each, postage prepaid. Subscriptions 
are payable in advance. 

Address communications to any of the following members of the Council of the 
Society : 

Past PRESIDENTS— S. J. Meltzer, Rockefeller Institute for Medical Research ; 
Edmund B. Wilson, Columbia University; Simon Flexner, Rockefeller Institute for 
Medical Research; Frederic S. Lee, Columbia University, Thomas H. Morgan, 
Columbia University. 

PRESIDENT — James Ewing, Cornell University Medical College. 

VICE-PRESIDENT — Phoebus A. Levene, Rockefeller Institute for Medical 
Research. 

SECRETARY — George B. Wallace, University and Bellevue Hospital Medical 
College. 

TREASURER — Charles Norris, Bellevue Hospital. 


MANAGING Epiror —The Secretary, 338 E. 26th St., New York City. 


Mh. U. Nn 


PROCEEDINGS | 


OF THE 


SOCIETY FOR: 


EXPERIMENTAL BIOLOGY AND MEDICINE 


FORTY-NINTH MEETING 


UNIVERSITY AND BELLEVUE HOSPITAL 
MEDICAL COLLEGE 


NEW YORK CITY 


MAY 15, 1912 


VoLuME IX 


No. 5 


NEW YORK 


IgI2 


CONTENTS. 


Gary N, CALKINS: The effect of chemicals on the division rate of protozoa. 70(679). 

FE. M. Ewinc: The first onflow and diastolic waves in the venous pulse. 71 (680). 

J. Aver and S. J. MELTZER: The effect of the infundibular portion of the hypophysis 
upon vaso-dilators. 72 (681). 

I. S. KLEINER and S. J. MELTzer: On the reduction of toxicity of strychnine by the 
simultaneous administration of large quantities of fluid. 73 (682). 

S. J. MELTZER: The influence of the infundibular portion of the hypophysis upon the 
pupil. 74 (683). 

A. M. BANTA: Observations on the relation of oxygen and carbon dioxide to the 
development of certain amphibian embryos. 75 (684). 

R. A, LAMBERT: Direct observation of cell division in mammalian tissue. 76 (685). 

C, E. A. WINsLow and F, ABRAMSON: The effect of drying upon the viability of 
bacteria. 77 (686). 

S. R. BENEDICT and J. R. MurLIN: Determination of the amino-acid nitrogen in the 
urine. 78 (687). 

P. A. LEVENE and D, D. VAN SLYKE: Picrolonates of the monoamino-acids. 79 (688). 

D. D. VAN SLYKE: Demonstration of improved method for determination of amino 
nitrogen. 80 (689). 

D. D. VAN SLYKE and F. J. BIRCHARD: The nature of the free amino nitrogen groups 
in the native proteins. 81 (690). 

R. WEIL and A. F. Cuca : An experimental study of anti-anaphylaxis. 82 (691). 

W. F, MANWARING: The toxicity of foreign leucocytes. 83 (692) 

. A. GORTNER : The occurrence and significance of tyrosinase in the reproductive 

organs of certain amphibians. 84 (693). 

. A. GORTNER: On two different types of melanins. 85 (694). 

A On ee eeenta : A five year pedigree culture of paramaecium without conjugation. 
6 (695). 

se at aah : The influence of tartrates upon phlorhizin diabetes. 87 (696). 


The proceedings of the Society for Experimental Biology and Medicine are pub- 
lished as soon as possible after each meeting. Regular meetings of the Society are held 
in New York on the third Wednesdays of October, December, February, April and 
May. A volume of the proceedings consists of the numbers issued during an 
academic year. 

The price per volume, sent postage prepaid, is one dollar. The price of copies 
of the proceedings of any meeting is twenty cents each, postage prepaid. Subscriptions 
are payable in advance. 

Address communications to any of the following members of the Council of the 
Society : 

Past PRESIDENTS— S. J. Meltzer, Rockefeller Institute for Medical Research ; 
Edmund B. Wilson, Columbia University; Simon Flexner, Rockefeller Institute for 
Medical Research; Frederic S. Lee, Columbia University, Thomas H. Morgan, 
Columbia University. 

PRESIDENT — James Ewing, Cornell University Medical College. 

VicE-PRESIDENT— Phoebus A. Levene, Rockefeller Institute for Medical 
Research. 

SECRETARY — George B. Wallace, University and Bellevue Hospital Medical 
College. 


TREASURER — Charles Norris, Bellevue Hospital. 


MANAGING Epiror —The Secretary, 338 E. 26th St., New York City. 


CLASSIFIED LIST OF MEMBERS OF THE SOCIETY FOR 
EXPERIMENTAL BIOLOGY AND MEDICINE. 


Resident (Greater New York). 


Bellevue Hospital.—Cyrus W. Field, Charles Norris. 


Columbia University.—Russell Burton-Opitz, Gary N. Calkins, Henry 
E. Crampton, Richard H. Cunningham, Haven Emerson, Nellis B. Foster, 
William J. Gies, A. E. Guenther, Philip H. Hiss, Theodore C, Janeway, R. 
A. Lambert, Frederic S. Lee, Isaac Levin, C. C. Lieb, W. F. Longcope, W. 
G. MacCallum, Thomas H. Morgan, H. O. Mosenthal, Alwin M. Pappen- 
heimer, B. S. Oppenheimer, F. H. Pike, Jacob Rosenbloom, Henry C. 
Sherman, Hugh A. Stewart, Augustus D. Wadsworth, Edmund B. Wilson, 
Francis C. Wood. 


Cornell University Medical College.—S. P. Beebe, Stanley R. Benedict, 
B. H. Buxton, A. F. Coca, William J. Elser, James Ewing, Robert A. 
Hatcher, Graham Lusk, J. F. McClendon, John R. Murlin, Chas. R. Stock- 
ard, John C. Torrey, Richard Weil, C. J. Wiggers, C. G. L. Wolf. 


Mt. Sinai Hospital.—Charles A. Elsberg, R. Ottenberg. 


New York City College.—A. J. Goldfarb, Thomas A. Storey, C. E. A. 
Winslow. 


New York City Departments. LEducation.—C. Ward Crampton. 
Hlealth.—James P. Atkinson, Edwin J. Banzhaf, L. W. Famulener, C. B. 
Fitzpatrick, Alfred F. Hess, Edna Steinhardt, Anna W. Williams, 


New York Polyclinic Medical School.—Isaac Adler. 

New York Post-Graduate Medical School.—Ludwig Kast, W. J. Mac- 
Neal. ; 

New York University. — Harlow Brooks, J. W. Draper, Edward K. Dun- 
ham, E. M. Ewing, Holmes C. Jackson, Arthur R. Mandel, John A. Mandel, 
William H. Park, H. D. Senior, Douglas Symmers, George B. Wallace. 


Rockefeller Institute for Medical Research.—John Auer, F. W. Bancroft, 
F, J. Birchard, E. E. Butterfield, Alexis Carrel, A. E. Cohn, Rufus Cole, 
A. R. Dochez, George Draper, Simon Flexner, T. H. Githens, Walter A. 
Jacobs, Don R. Joseph, I. S. Kleiner, Richard V. Lamar, P. A. Levene, 
Jacques Loeb, W. H. Manwaring, S. J. Meltzer, Gustave M. Meyer, F. M. 
McCrudden, Hideyo Noguchi, G. Canby Robinson, Peyton Rous, H. F. 
Swift, B. T. Terry, Donald D. Van Slyke, H. Wastenays. 


Sage Institute of Pathology.— Horst Oertel., 
St. Francis Hospital,—¥ ritz Schwyzer. 
Brooklyn Botanic Garden.—C, Stuart Gager. 


$19 Madison Avenue.—H. D. Dakin. 


Non-Resident. 


; Baltimore Medical College.—Charles E. Simon. 

Carnegie Institution of Washington.—Francis G. Benedict (Vutrition 
Laboratory, Boston), A. M. Banta, Charles B. Davenport, R. A. Gortner 
(Station for, Experimental Evolution, Cold Spring Harbor, N. Y.), D. T. 
MacDougal (Washington), Alfred G. Mayer (Marine Laboratory, Tortugas, 
la.). 

Connecticut Agricultural Experiment Station (New Haven).—Thomas 
B. Osborne. 

Georgia State Board of Health ( Atlanta).—Katharine R. Collins. 

Kentucky Agricultural Experiment Station (Lexington).—J. H. Kastle. 

Maine Agricultural Experiment Station (Orono).— Raymond Fearl. 

Massachusetts Institute of Technology.—Percy G. Stiles. 

Medico-Chirurgical College (Philadelphia).—Isaac Ott. 

Mercy Hospital (Pittsfield, Mass.).—Thomas Flournoy. 

Michael Reese Hospital (Chicago).—James W. Jobling. 


Northwestern University Medical School (Chicago).—J. B. Murphy. . 
Philippine Medical School (Manila).—A. O. Shaklee. 

Trinity College (Hartford ).—Max W. Morse. 

Yonkers, N. Y.—Isaac F. Harris. 


U.S. Departments. Agriculture (Washington, D,C.).—CarlL. Alsberg, 


William N. Berg, William Salant; /ntertor (Philippine Islands, Bureau of : 


Science, Manila).—Richard P. Strong, Oscar Teague. Treasury (Public 
Flealth and Marine-Hospital Service).—John F. Anderson, W. H. Frost, 
Wm. H. Hale, Reid Hunt and W. H. Schultz, Washington, D. C. 


Universitics. Buffalo,—G. H. A. Clowes, Herbert U. Williams. Cad- 
fornia. —¥. P. Gay, F. J. Fitzgerald, T. Brailsford Robertson. Chicago. — 
R. R. Bensley, A. J. Carlson, Ludvig Hektoen, Edwin O. Jordan, Frank R. 
Lillie, H. Gideon Wells. Czuctnatéz.—Martin H. Fischer. Corne//.—Andrew 
Hunter, Sutherland Simpson. Harvard.—Herman M. Adler, Walter B. 
Cannon, W. T. Councilman, Otto Folin, H. T. Karsner, G. H. Parker, Franz 
Pfaff, W. ‘I. Porter, Joseph H. Pratt, M. J. Rosenau, Theobald Smith, E. E. 
Southard, E. E. Tyzzer, S. Burt Wolbach, Robert M. Yerkes. J//inois.— 
Philip B. Hawk. /Japan.—Naohidé Yatsu. Johns Hopkins.—John J. Abel, 
Harvey W. Cushing, W. W. Ford, W.S. Halsted, William H. Howell, S. H. 
Jennings, Walter Jones, F. P. Mall, Adolph Meyer, William H. Welch. Le- 
land Stanford.—. C. Crawford, E. C. Dickson, W. Ophiils, Hans Zinsser. 
—AfeGill (Montreal).--J. George Adami, John L. Todd. Jfichigan.—C. 
W. Edmunds, Otto C. Glaser, A. W. Hewlett, Carl G. Huber, Warren P. 
Lombard, Frederick G. Novy, Aldred S. Warthin. Minmnesofa.—Robert B. 
Gibson, F. W. Schlutz. orth Carolina.—W. de B. MacNider. Fennsyl- 
vania,—J.'H. Austin, Alexander C. Abbott, D. H. Bergey, A.B: Eisen- 
brey, Ralph S. Lillie, Richard M. Pearce, Edward,T.° Reichert, Alfred N. 
Richards, A. I. Ringer, J. Edwin Sweet, Av"E. Taylor. Pittsburgh. —C. 
C. Guthrie, Oskar Klotz. . Princefon. — Edwin G. Conklin. Southern Cal- 
Jornta (Los Angeles).—Lyman B. Stookey. S¢. Louwis.—E. P. Lyon. To- 
ronto.—T. G. Brodie, J. B. Leathes, A. B. Macallum. 7zz/ane.—Charles 
W. Duval, J. V. Cooke. Virginta.—H. E. Jordan. Washington (St. 
Louis).—David L. Edsall, John Howland, Joseph Erlanger, Eugene L. 
Opie, Ernst Sachs, Philip A. Shaffer. W2sconsin.—Charles R. Bardene, 
C. H. Bunting, Arthur S. Loevenhart, Mazyck P. Ravenel. Western Re- 
serve (Cleveland).—George W. Crile, J. J. R. Macleod, Torald Sollmann, 
G. N. Stewart. Ya/e.—R. H. Chittenden, Ross G. Harrison, Lafayette B. 
Mendel, Frank P. Underhill, Lorande Loss Woodruff. 


University College (London).—Arthur R. Cushny. 

Phipps Institute (Philadelphia).—Paul A. Lewis. 

Wistar Institute of Anatomy (Philadelphia).—H. H. Donaldson, Shin- 
kishi Hatai, E. B. Meigs. 

Barnard Skin and Cancer Hospital (St. Louts).—Leo Loeb. 


Members present at the forty-ninth meeting: 


Auer, Bancroft, Banzhaf, Benedict, Birchard, Butterfield, Calkins, Coca, 
J. W. Draper, Emerson, James Ewing, E. M. Ewing, Githens, Goldfarb, 
Harris, Hatcher, Jackson, Kleiner, Lambert, Lieb, J. A. Mandel, Mc- 
Crudden, Murlin, Norris, Pike, Rous, Terry, Wallace, Weil, Wiggers, 
H. B. Williams, Winslow. 


Members elected at the forty-ninth meeting: 
M. T. Burrows, E. F. Du Bois. 


Dates of the next two regular meetings: 
October 16, 1912 — December 18, I912. 


CLASSIFIED LIST OF MEMBERS OF THE SOCIETY FOR 
EXPERIMENTAL BIOLOGY AND MEDICINE. 


Resident (Greater New York). 


Bellevue Hospital.—Cyrus W. Field, Charles Norris. 


Columbia University.—Russell Burton-Opitz, Gary N. Calkins, Henry 
E. Crampton, Richard H. Cunningham, Haven Emerson, Nellis B. Foster, 
William J. Gies, A. E. Guenther, Philip H. Hiss, Theodore C. Janeway, R. 
A. Lambert, Frederic S. Lee, Isaac Levin, W. F. Longcope, W. G. Mac- 
Callum, Thomas H. Morgan, H. O. Mosenthal, Alvin M. Pappenheimer, 
B. S. Oppenheimer, F. H. Pike, Jacob Rosenbloom, Henry C. Sherman, 
Hugh A. Stewart, Augustus B. Wadsworth, H. B. Williams, Edmund B. 
Wilson, Francis C. Wood. 


Cornell University Medical College.—S. P. Beebe, Stanley R. Benedict, 
B. H. Buxton, A. F. Coca, William J. Elser, James Ewing, Robert A. 
Hatcher, Graham Lusk, J. F. McClendon, John R. Murlin, Chas. R. Stock- 
ard, John C. Torrey, Richard Weil, C. J. Wiggers, C. G. L. Wolf. 

Mt. Sinai Hospital.—Charles A. Elsberg, Rk. Ottenberg. 

New York City College.—A. J. Goldfarb, Thomas A. Storey, C. E. A: 
Winslow. 

New York City Departments. LEducation.—C. Ward Crampton. 
Hlealth.—James P. Atkinson, Edwin J. Banzhaf, L. W. Famulener, C. B. 
Fitzpatrick, Alfred F. Hess, Edna Steinhardt, Anna W. Williams. 

New York Polyclinic Medical School.—Isaac Adler. 

New York Post-Graduate Medical School.—Ludwig Kast, W. J. Mac- 
Neal. 

New York University. — Harlow Brooks, J. W. Draper, Edward K. Dun- 
ham, E. M. Ewing, Holmes C. Jackson, Arthur R. Mandel, John A. Mandel, 
William H. Park, H. D. Senior, Douglas Symmers, George B. Wallace. 

Rockefeller Institute for Medical Research.—John Auer, F. W. Bancroft, 
F. J. Birchard, E. E. Butterfield, Alexis Carrel, A. E. Cohn, Rufus Cole, 
A. R. Dochez, George Draper, Simon Flexner, T. H. Githens, Walter A. 
Jacobs, Don R. Joseph, I. S. Kleiner, Richard V. Lamar, P. A. Levene, 
Jacques Loeb, W. H. Manwaring, S. J. Meltzer, Gustave M. Meyer, F. M. 
McCrudden, Hideyo Noguchi, G. Canby Robinson, Peyton Rous, H. F. 
Swift, B. T. Terry, Donald D. Van Slyke, H. Wastenays. 

Sage Institute of Pathology.— Horst Oertel. 

St. Francis Hospital.—Fritz Schwyzer. 

Brooklyn Botanic Garden.—C, Stuart Gager. 


$19 Madison Avenue.—H. D. Dakin. 


Non-Resident. 


Baltimore Medical College.—Charles E. Simon. 

Carnegie Institution of Washington.—Francis G. Benedict (Vutrition 
Laboratory, Boston), A. M. Banta, Charles B. Davenport, R. A.‘Gortner 
(Station for Experimental Evolution, Cold Spring Harbor, N. Y.), D. T. 
one (Washington), Alfred G. Mayer (Marine Laboratory, Tortugas, 
fla.). 

Connecticut Agricultural Experiment Station (New Haven).—Thomas 
B. Osborne. 

Georgia State Board of Health (Atlanta).—Katharine R. Collins. 

Kentucky Agricultural Experiment Station (Lexington).—J. H. Kastle. 

Maine Agricultural Experiment Station (Orono).— Raymond Fearl. 

Massachusetts Institute of Technology.—Percy G. Stiles. 

Medico-Chirurgical College (Philadelphia).—Isaac Ott. 

Mercy Flospital (Pittsfield, Mass.).—Thomas Flournoy. 

Michael Reese Hospital (Chicago).—James W. Jobling. 


Northwestern University Medical School (Chicago).—J. B. Murphy. 
Philippine Medical School (Manila).—A. O. Shaklee. 

Trinity College (Hartford ).—Max W. Morse. 

Yonkers, N. Y.—Isaac F. Harris. 


U.S. Departments. Agriculture (Washington, D.C.).—Carl1 L. Alsberg, 
William N. Berg, William Salant ; luterior (Philippine Islands, Bureau of 
Science, Manila).—Richard P. Strong, Oscar Teague. Treasury (Public 
Health and Marine-Hospital Service).—John F. Anderson, W. H. Frost, 
Wm. H. Hale, Reid Hunt and W. H. Schultz, Washington, D. C. 


Universitics. Buffalo.—G. H. A. Clowes, Herbert U. Williams. Cali- 
fornia. —F. P. Gay, F. J. Fitzgerald, T. Brailsford Robertson. Chicago. — 
R. R. Bensley, A. J. Carlson, Ludvig Hektoen, Edwin O. Jordan, Frank R. 
Lillie, H. Gideon Wells. Cincinatéz.—Martin H. Fischer. Corne//.—Andrew 
Hunter; Sutherland Simpson. 4arvard.cHerman M. Adler, Walter B. 
Cannon, W. T. Councilman, Otto Folin, H. T. Karsner, G. H. Parker, Franz 
Pfaff, W. T. Porter, Joseph H. Pratt, M. J. Rosenau, Theobald Smith, E. E. 
Southard, E. E. Tyzzer, S. Burt Wolbach, Robert M. Yerkes. //nois.— 
Philip B. Hawk. /afan.—Naohidé Yatsu. Johns Hopkins.—John J. Abel, 
Harvey W. Cushing, W. W. Ford, W.S. Halsted, William H. Howell, S. H. 
Jennings, Walter Jones, F. P. Mall, Adolph Meyer, William H. Welch. Ze- 
land Stanford.—A. C. Crawford, E. C. Dickson, W. Ophiils, Hans Zinsser. 
—McGill (Montreal).—J. George Adami, John L. Todd. Michigan.—C. 
W. Edmunds, Otto C. Glaser, A. W. Hewlett, Carl G. Huber, Warren P. 
Lombard, Frederick G. Novy, Aldred S. Warthin. J/innesota.—Robert B. 
Gibson, F. W. Schlutz. orth Carolina.—W. de B. MacNider. ennsyl- 
vania.—J. H. Austin, Alexander C. Abbott, D. H. Bergey, A. B. Eisen- 
brey, Ralph S. Lillie, Richard M. Pearce, Edward T. Reichert, Alfred N. 
Richards, A. I. Ringer, J. Edwin Sweet, A. E. Taylor. /ittsburgh. —C. 
C. Guthrie, Oskar Klotz. Primceton. —Edwin G. Conklin. Southern Cal- 
fornia (Los Angeles).—Lyman B. Stookey. S¢. Louis.—E. P. Lyon. To- 
ronto.—T. G. Brodie, J. B. Leathes, A. B. Macallum. 7z/ane.—Charles 
W. Duval, J. V. Cooke. Virginta.—H. E. Jordan. Washington (St. 
Louis).—David L. Edsall, John Howland, Joseph Erlanger, Eugene L. 
Opie, Ernst Sachs, Philip A. Shaffer. Wisconsin.—Charles R. Bardene, 


C. H. Bunting, Arthur S. Loevenhart, Mazyck P. Ravenel. Western Re- , 


serve (Cleveland).—George W. Crile, J. J. R. Macleod, Torald Sollmann, 
G. N. Stewart. Ya/e.—R. H. Chittenden, Ross G. Harrison, Lafayette B. 
Mendel, Frank P. Underhill, Lorande Loss Woodruff. 


University College (London).—Arthur R. Cushny. 

Phipps Institute (Philadelphia).—Paul A. Lewis. 

Wistar Institute of Anatomy (Philadelphia).—H. H. Donaldson, Shin- 
kishi Hatai, E. B. Meigs. 

Barnard Skin and Cancer Hospital (St. Louis).—Leo Loeb. 


Members present at the forty-eighth meeting: 


Auer, Bancroft, Benedict, Butterfield, Cohn, Ewing, Field, Fitzpatrick, 
Foster, Githens, Guenther, Hatcher, Kleiner, Lee, Levine, Longcope, Lusk, 
Manwaring, McCrudden, Meltzer, Mendel, Morgan, Murlin, Norris, Pap- 
penheimer, Robinson, Steinhardt, Stewart, Stockard, Swift, Terry, van 
Slyke, Wallace, Wiggers, Williams. 


Members elected at the forty-eighth meeting: 
J. H. Austin, H. E. Jordan, C. C. Lieb, Frederic W. Schlutz. 


Dates of the next two regular meetings: 
May 15, 1912—October 16, 1912. 


CLASSIFIED LIST OF MEMBERS OF THE SOCIETY FOR 
EXPERIMENTAL BIOLOGY AND MEDICINE. 


Resident (Greater New York). 


Bellevue Hospital.—Cyrus W. Field, Charles Norris. 

Columbia University.—Russell Burton-Opitz, Gary N. Calkins, Alfred E, 
Cohn, Henry E. Crampton, Richard H. Cunningham, Haven Emerson, Nellis 
B. Foster, William J. Gies, A. E. Guenther, Philip H. Hiss, Theodore C. Jane- 
way, R. A. Lambert, Frederic S. Lee, Isaac Levin, W. F. Longcope, W. G. 
MacCallum, Thomas H. Morgan, H. O. Mosenthal, Alwin M. Pappenheimer, 
B. S. Oppenheimer, F. H. Pike, Jacob Rosenbloom, Henry C. Sherman, 
Hugh A. Stewart, Augustus LB. Wadsworth, Edmund B. Wilson, Francis 
C. Wood. 

Cornell University Medical College.—S. P. Beebe, Stanley R. Benedict, 
B. H. Buxton, William J. Elser, James Ewing, Robert A. Hatcher, Graham 
Lusk, J. F. McClendon, John R. Murlin, Chas. R. Stockard, John C. Torrey, 
Richard Weil, H. B. Williams, C. G. L. Wolf. 

Mt. Sinat Hospital.—Charles A. Elsberg. 


New York City College.—A. J. Goldfarb, Thomas A. Storey, C. E. A. 
Winslow. 

New York City Departments. Education.—C. Ward Crampton. 
Health.—James P, Atkinson, Edwin J. Banzhaf, L. W. Famulener, C. B. 
Fitzpatrick, Alfred F. Hess, Edna Steinhardt, Anna W. Williams, 

New York Polyclinic Medical School,—\saac Adler. 

New York Post-Graduate Medical School.—Ludwig Kast, W. J. Mac- 
Neal. 

New York University. — Harlow Brooks, Edward K. Dunham, E. M. 
Ewing, Holmes C. Jackson, Arthur R. Mandel, John A. Mandel, William 
H. Park, H. D. Senior, Douglas Symmers, George B. Wallace. 

Rockefeller Institute for Medical Research.—John Auer, F. W. Bancroft, 
F. J. Birchard, Alexis Carrel, Rufus Cole, A. R. Dochez, Simon Flexner, 
T. H. Githens, Walter A. Jacobs, Don R. Joseph, I. S. Kleiner, Richard 
V. Lamar, P. A. Levene, Jacques Loeb, W. H. Manwaring, S. ). Meltzer, 
Gustave M. Meyer, F. M. McCrudden, Hideyo Noguchi, R. Ottenberg, 
Peyton Rous, H, F. Swift, B. T. Terry, Donald D. Van Slyke. 

Sage Institute of Pathology.— Horst Oertel. 

St. Francis Hospital,—Fritz Schwyzer. 

Central Museum, Brooklyn.—C, Stuart Gager. 


819 Madison Avenue.—H. D. Dakin. 


Non-Resident. 


Baltimore Medical College.—Charles E. Simon. 

Carnegie Institution of Washington.—Francis G. Benedict (Nutrition 
Laboratory, Boston), A. M. Banta, Charles B. Davenport, R. A. Gortner 
(Station for Experimental Evolution, Cold Spring Harbor, N. Y.), D. T. 
CA (Washington), Alfred G. Mayer (Marine Laboratory, Tortugas, 
Fla.). 

Connecticut Agricultural Experiment Station (New Haven).—Thomas 
B, Osborne, 

Georgia State Board of Health ( Atlanta),—Katharine R. Collins. 

Kentucky Agricultural Experiment Station (Lexington).—J. H. Kastle. 

Maine Agricultural Experiment Station (Orono).— Raymond Fear]. 

Massachusetts Institute of Technology.—Percy G. Stiles. 

Medico-Chirurgical College (Philadelphia).—Isaac Ott. 

Mercy Hospital (Pittsfield, Mass.).—Thomas Flournoy. 

Michael Reese Hospital (Chicago).—James W. Jobling. 


Missouri Botanical Garden (St. Louis).—W. Trelease. 

Northwestern University Medical School (Chicago).—J. B. Murphy. 

Philippine Medical School (Manila).—A. O. Shaklee. 

Trinity College (Hartford).—Max W. Morse. 

Rochester, Minn.—J. W. Draper. 

Yonkers, NV. Y.—Isaac F. Harris. ; 

U.S. Departments. Agriculture (Washington, D.C.).—Carl L. Alsberg, 
William N. Berg, William Salant ; Jterior (Philippine Islands, Bureau of 
Sctence, Manila).—Richard P. Strong, Oscar Teague. Treasury (Public 
FHlealth and Marine-Hospital Service).—John F. Anderson, W. H. Frost, 
Wm. H. Hale, Reid Hunt and W. H. Schultz, Washington, D. C. 

Universitics. Buffalo.—G. H. A. Clowes, Herbert U. Williams. Calz- 
Jornia. —¥. P. Gay, F. J. Fitzgerald, T. Brailsford Robertson. Chicago, — 
R. R. Bensley, A. J. Carlson, Ludvig Hektoen, Edwin O. Jordan, Frank R. 
Lillie, H. Gideon Wells. Corned/.—Andrew Hunter, Sutherland Simpson. 
Hlarvard.—Herman M. Adler, Walter B. Cannon, W. T. Councilman, Otto 
Folin, H. T. Karsner, G. H. Parker, Franz Pfaff, W. T. Porter, Joseph H. 
Pratt, M. J. Rosenau, Theobald Smith, E. E. Southard, E. E. Tyzzer, S. Burt 
Wolbach, Robert M. Yerkes. ///inozs.—Philip B. Hawk. Japan.—Naohidé 
Yatsu. /Johus Hopkins. —John J. Abel, Harvey W. Cushing, W. W. Ford, W. 
S. Halsted, William H. Howell, S. H. Jennings, Walter Jones, F. P. Mall, 
Adolph Meyer, William H. Welch. Leland Stanford.—A. C. Crawford, E. 
C. Dickson, W. Ophiils, Hans Zinsser. MacDonald College (Ste. Anne de 
Bellevue, Quebec).—John L. Todd. McGill (Montreal).—J. George Adami. 
Michigan. —C. W. Edmunds, Otto C. Glaser, A. W. Hewlett, Carl G. 
Huber, Warren P. Lombard, Frederick G. Novy, Victor C, Vaughan, 
Aldred S. Warthin. Jfnmnesota.—Robert B. Gibson. North Carolina.—W. 
de B. MacNider. Pennsylvania. — Alexander C. Abbott, D. H. Bergey, 
A. B. Eisenbrey, Ralph S. Lillie, Richard M. Pearce, Edward T. Reichert, 
Alfred N. Richards, A. I. Ringer, J. Edwin Sweet, A. E. Taylor. /%éts- 
burgh. —C. C. Guthrie, Oskar Klotz. Princeton. — Edwin G. Conklin. 
Southern California (Los Angeles).—Lyman B, Stookey. St. Louis.—E. P. 
Lyon. Zoronto.—T. G. Brodie, J. B. Leathes, A. B. Macallum. TZzlane. 
—Charles W. Duval, J. V. Cooke. Washington (St. Louis).—David L. 
Edsall, John Howland, Joseph Erlanger, Eugene L. Opie, Ernst Sachs, Philip 
A. Shaffer. Wisconsiu.—Charles R. Bardene, C. H. Bunting, Arthur S. 
Loevenhart, Mazjck P. Ravenel. Western Reserve (Cleveland).—George 
W, Crile, J. J. R. Macleod, Torald Sollmann, G. N. Stewart. Yale.—R. 
H. Chittenden, Ross G. Harrison, Lafayette B. Mendel, Frank P. Underhill, 
Lorande Loss Woodruff. 


University College (London).—Arthur R. Cushny. 

Phipps Institute (Philadelphia).—Paul A. Lewis. 

Wistar Institute of Anatomy (Philadelphia).—H. H. Donaldson, Shin- 
kishi Hatai, E. B. Meigs. 

Barnard Skin and Cancer Hospital (St. Louis).—Leo Loeb. 


Members present at the forty-seventh meeting: 

Alsberg, Atkinson, Bancroft, Fitzpatrick, Githens, Goldfarb, Guenther, 
Janeway, Joseph, Karsner, Kast, Kleiner, Lambert, Lee, Longcope, Lusk, 
Mandel, Meltzer, Morgan, McCrudden, Parker, Pike, Ringer, Senior, 
Stewart, Storey, Terry, Wallace, Winslow. 


‘Members elected at the forty-seventh meeting: 
E. E. Butterfield, A. F. Coca, George Draper, G. Canby Robinson, 
H. Wastenays, C. J. Wiggers. 


Officers elected at the forty-seventh meeting: 
President, James Ewing; Vice-president, P. A. Levene; Treasurer, 
Charles Norris ; Secretary, George B. Wallace. 


Dates of the next two regular meetings: 
April 17, 1912 — May 15, I912. 


(table fi ‘ah asioe '