SEPTEMBER 27, 1918] 
vestigation into this matter might lead to a 
better insight into the mechanism of the swell- 
ing of gelatine. Whatever the mechanism of 
the change, it remains that always the great- 
est shrinkage subsequent swelling take place 
in axis perpendicular to the largest evap- 
orating surface, regardless of the position of 
that surface. 
Tn all experimentation on the absorbing ca- 
pacity of gelatine it is, then, necessary to see 
that the following conditions prevail: (1) all 
the gelatine has the same original chemical 
composition; (2) the entire history of water- 
content from the time of setting to a jelly to 
the beginning of absorption must be the same 
for all the material; (3) if water loss by. 
evaporation is to take place before absorption, 
then pieces or slabs of the same size and form 
must be used during the process; (4) if the 
increase is determined by the measurement of 
length of one dimension, then all measure- 
ments must be made on similar axes; (5) all 
the gelatine must have been exposed to the 
same temperature conditions. 
TABLE II 
Increase per em. of three dimensions of ree- 
tangular blocks of gelatine (length —0.69 cm., 
height =0.15 cm., breadth = 0.30 em.). Solution 
was made up to contain 33 per cent. of gelatine, 
poured onto a glass plate, allowed to lose water 
until nearly hard, cut into blocks and then allowed 
to absorb water. Ratios are given in brackets be- 
low percentages. Numbers refer to averages of 
two pieces each. 
Total Time | 3 Hrs. | 127 Hrs.| 151 Hrs. 175 Hrs. | 202 Hrs. 
Length..| 0.36 | 0.60 0.65 0.91 1.13 
| (1.0) (1.0) (1.0) (1.0) (1.0) 
Height ..| 1.03 1.39 1.60 1.96 1.96 
1 oy | (ay G7), 2.2). | _.:7) 
Breadth.| 0.30 | 042 0.69 0.88 | 0.88 
| @.8) | 7) | G1) | G0) | 08) 
EpitH BettaMy SHREVE 
DesERT LABORATORY, 
Tucson, ARIZ. 
REASON FOR THE HELPFUL EFFECT OF 
ALCOHOLIC BEVERAGES IN DIABETES, 
STATES OF DEPRESSION, AND CON- 
VALESCENCE 
In diabetes the oxidative processes are de- 
fective, as is indicated by the fact that when 
SCIENCE 
327 
sugar is ingested, it is not oxidized, as is 
normally done, but is exereted. This defective 
oxidation results in the accumulation of cer- 
tain incompletely oxidized substances, acid in 
nature, thus giving rise to a condition of 
acidosis which is thought by many to be the 
cause of coma in the later stages of the dis- 
ease. Neubauer, Benedict and Toérdk,? Allen 
and DuBois have shown that the administra- 
tion of alcohol and alcoholic beverages, such as 
wine and whiskey, facilitates the oxidative 
processes in diabetes, thereby enabling the 
diabetic to burn sugar better with resulting 
decrease in acidosis and sugar excretion. 
The present investigation was carried out 
in an attempt to determine how alcohol favors 
or facilitates oxidation in diabetes. It is 
known that oxidation in the body is increased 
by exercise or work, by the ingestion of food, 
by thyroid feeding, during the excitement 
stage of anesthesia, and in combat, and that 
oxidation is decreased by decreasing the 
amount of work or the amount of food in- 
gested, during deep anesthesia and in phos- 
phorus and chloroform poisoning. We found 
that when oxidation was increased in the ways 
enumerated, there occurred a corresponding 
increase in catalase, an enzyme in the tissues 
and possessing the property of liberating oxy- 
gen from hydrogen peroxide, due to the stimu- 
lation of the liver to an increased output of 
this enzyme into the blood, and that when 
oxidation was decreased, there occurred a cor- 
responding decrease in catalase in the blood 
and tissues due to the decreased output of this 
enzyme from the liver and utilization in the 
tissues. From these results it was concluded 
that catalase is the enzyme in the tissues 
principally responsible for oxidation. Fur- 
thermore, we*® showed that the catalase of the 
1 Neubauer, O., Miinchener med. Wochenschrift, 
1906, LIII., 791. 
2 Benedict and Twérék, Zeitschrift fiir klinische 
Medizin, 1906, LX., 329. 
8 Burge, American Journal of Physiology, 1916, 
XLI., 153; 1917; XLIII., 57, 545, 1917; XLIV., 
290; Scrence, N. S., 1917, XLVI., 440. Burge, 
Kennedy and Neill, American Journal of Physiol- 
ogy, 1917, XLIII., 433. Kennedy and Burge, Arch. 
Int. Med., 1917, XX., 892. 
