In the cases administered with I¹³¹, its distributing condition and its successive changes were observed. Nextly, distributing condition of serum protein bound iodine was observed in rats, and zone electrophoresis in filterpaper was tried on the mobility of the extracts of their thyroids.
Electrophoresis was conducted with PH 6.7 phospate buffer. In order to observe trashes of protein, portion of protein was stained with Ninhydrin and the rest was observed by radio-autography.
1) Distribution of the radioactive protein bound iodine showed the mobility in which α₂-globulin was central, and appeared as a single stripe. This will indicate the possibility of its bounding with a single protein trash.
No difference was observed between normal, hyperthyroid or malignant struma status.
2) As for the successive mobility ratio of radioactive protein bound iodine, it tended to concentrate to α₂-globulin, by 24 hours.
3) 24 hours after the oral administration of I¹³¹, blood sample was taken, from which serum was separated, washed with trichloride acetic acid and electrophoresis of the precipitate was examined. Remarkable concentration to original point was observed.
4) Serum protein bound iodine in rats showed electrophoresis within the α-globulin.
5) I¹³¹ in the extract of thyroids in rats moved to α-globulin and to albumin and it had great radioactivity.

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Many studies have been reported on the influence of adreno-cortical function in experimental tuberculosis, however, many problems remain. For instance, administration of a large quantity of adreno-cortical hormone seems to give bad results in tuberculosis. In the present study, the authors conducted experiments on adreno-cortical function in tuberculosis by hyper-and hypo-status of the adreno-cortical function.
Guinea pigs with negative tuberculin test were used. Fresh human-type tubercle bacilli of enough quantity, which shall eliminate any individual differences, were given intravenously and complete infection of tuberculosis were obtained. Then, cortisone, choline chloride, Vitamin-B₃ and others, known as effective to adreno-cortical gland, were administered, and the survival period of the test animals and cholesterol in their adreno-cortical glands were examined.
Under the condition of cortisone's administration of large dose (over 0.1mg per day), period of survival was shortened and adreno-cortical cholesterol decreased, as in case of choline administration.
Administration of small quantity of cortisone (0.03mg per day) resulted in remarkably long period of survival and increase of adreno-cortical cholesterol. Under the condition of increase of quantity of adreno-cortical cholesterol, the survival period were lengthened.

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The present paper deals with leprous paralysis of facial muscles, especially, on the rate of occurrence of leprotic paralysis and location of lesions of nerves.
1) Statistics of 138 inpatients at Rakusenen:
Rate of occurrence of paralysis of facial muscles was 53%. No difference was found by sex. Rate of paralysis in the upper half of face was higher than in the lower half.
2) Paralysis of facial muscles was generally assumed to be due to disturbance in the periphery of the responsible nerves, and motor paralysis due to lesion in the trunk of facial nerve might be few.
3) Clinical observation on 41 cases of various types, for motor function and skin sensitivity in the area innervated by the 3rd ramification of N. trigeminus:
In spite of no motor paralysis of M. masseter, lost of skin sensitivity in the area controlled by the 3rd ramification of N. trigeminus was frequently found.
Therefore, paralysis of that area may be caused by lesion of end-apparatus of the nerve or by lesion in the periphery of the 3rd branch.
It is considered that motor paralysis develops from leprosy which starts at skin, spreads deeper and destroys nerves of that part. It is also considered that leprous lesion spreads to peripheral never by hematogenic dissemination. Moreover, it is assumed that ishemic contraction is another possible factor for leprous paralysis of muscle.

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