1. The conditions for inducement of spindle bursts were studied, in correlation with the hippocampal EEG, using the midpontine pretrigeminal transected preparation.
2. The slow and fast components of hippocampal EEG were demonstrated to be enhanced or depressed independently.
3. Stimulation of the central cut end of the left vagus (the right vagus intact) induced spindle bursts in the motor cortex, together with enhancement of the hippocampal fast component. This effect was observed after bilateral cervical sympathetic trunk section, but disappeared after contralateral vagotomy.
Stimulation of the peripheral cut end of the vagus caused a marked fall in blood pressure, but neither spindle bursts nor enhancement of the hippocampal fast component.
4. Transient clamping of the abdominal aorta induced few spindle bursts during the recovery phase of blood pressure. Clamping of the common carotid induced spindle bursts also. In both cases the hippocampal slow component diminished and no enhancement of the fast component was observed.
5. Small doses of pentobarbital induced many spindle bursts accompanied by enhancement of the hippocampal fast component, and abolition of the hippocampal slow component.
6. During hyperventilation the transient enhancement of the hippocampa: fast component were observed concomitantly with the spindle appearance, but the slow component showed no consistent change (either enhanced or remained the same level).
7. Low frequency stimulation of the mesencephalic reticular formation induced spindle bursts if the hippocampal fast component was enhanced alone, but no spindle bursts were induced if both the slow and fast components were enhanced.
8. These observations suggest a humoral factor for spindle inducement, and also indicate a close relationship between the spindle-inducing mechanism and production of the hippocampal fast component.

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Influences of the neurohypophysial preparations on the thyroid activities were investigated in the thyroxine treated SM mice. The experiments were carried out 4 days after the injection of carrier free ¹³¹I. Both Pitressin and synthetic lysine vasopressin in doses larger than 10mU and 20mU per mouse respectively significantly increased the blood ¹³¹I concentration at 2 hours interval. The stimulation was also observed in the hypophysectomized mice, indicating the direct actions of the hormone on the thyroids. Smaller dose of Pitressin, less than 2mU, and synthetic lysine vasopressin, less than 4mU, depressed the blood ¹³¹I level comparing the saline-injected control mice. The suppressive effect was also seen in the hypophysectomized mice, though the extent was less than in the intact ones. Exogenous vasopressin did not modify the decay curve of the blood radioactivity after the administration of ¹³¹I labelled L-thyroxine, showing no influence of vasopressin on the distribution of L-thyroxine in the mice. The biological half life of L-thyroxine in the thyroxine treated mice was 5 hours 20 minutes. Synthetic oxytocin, either in a large or small dose, did not influence the blood ¹³¹I concentrations. Treatment of the neurohypophysial preparations with thioglycollate resulted in the loss of both stimulative and inhibitory effects on the thyroids of synthetic lysine vasopressin, but not abolish the stimulative effect of Pitressin, indicating an active contaminant or contaminants in Pitressin. They were also effective in the hypophysectomized mice. A possibility that this contaminant could be MSH was suggested.

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The effects of sonication and other agents on the calcium-binding and the relaxing activity of microsomes were studied and the following results were obtained.
1. Sonication of microsomes destroyed the membraneous structure and enhanced the calcium-binding activity, whereas scarcely affected the relaxing activity of them.
The heat treatment and ultraviolet irradiation produced the inhibitory effects on the calcium-binding and the relaxing activity.
2. In the presence of oxalate, at the concentration of 0.001mM calcium the microsomes was able to bind calcium and the calculated value of the capacity of the microsomes for binding calcium was about 2.5 μM/mg protein.
3. The addition of caffeine or nicotine scarcely inhibited the calciumbinding activity of the microsomes, whereas the addition of salyrgan, deoxycholate or ethylenediaminetetraacetate markedly did. By the addition of 2, 4, -dinitrophenol, furthermore, the calcium-binding rate was decreased.
4. Inosinetriphosphate, uridinetriphosphate or adenosinediphosphate could be replaced with adenosinetriphosphate for the calcium-binding of the microsomes. Furthermore, KF did not inhibit the calcium-binding activity in the presence of adenosinetriphosphate, whereas markedly did in the presence of adenosinediphosphate.

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The reflection photoelectric plethysmograph has been modified to record volume changes in the different vascular layers in the human skin. It was found that pulse amplitude of the skin measured with this device increased as the pressure applied on the skin increased and it became maximum under a pressure of 50-70 mmHg. Three different and significant plethysmographic traces were identified during the Valsalva maneuver by compressing the skin surface with pressures of 0-20 mmHg, 30-50 mmHg and 50-120 mmHg respectively. There was a great difference between the plethysmographic traces of the finger and those of the ear lobe under a pressure of 30 mmHg. However, it was almost impossible to find any difference under a pressure of 80 mmHg. These plethysmographic traces corresponded with the arterial blood pressure changes recorded sphygmomanometrically. This may prove to be a useful device for continuous recording of the blood pressure in man.

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Adrenal atrophy produced by adenohypophysectomy was the same in extent as that after total hypophysectomy. In adenohypophysectomized rats the corticosterone levels in the adrenal gland and blood plasma and the adrenal ascorbic acid concentration were decreased to the same levels as those found in totally hypophysectomized ones. Administration of epinephrine into adenohypophysectomized rats did not cause any increase in the corticosterone levels nor depletion in the adrenal ascorbic acid concentration.

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Observations were made on the cutaneo-respiratory reflex in rabbits by pneumograms and electromyograms (EMG).
A single tactile stimulation delivered to the inner side of the earlobe accelerated the depth and rate of respiration. When a relatively intense stimulation was delivered, the pneumogram shifted towards the inspiratory side. EMG changes were observed with stimulation hardly strsong enough to produce any changes in the pneumogram. An increase in the unit discharge frequency and recruitment of both inspiratory and expiratory neuromascular units were observed by a single tactile stimulation. Such stimulation brought out not only a reduction in the length of the discharging phase of both inspiratory and expiratory neurons, but also a reduction in that of the resting phase in the respiratory cycle.
Clasping the earlobe with a clip elicited an augmentative on-effect in the pneumogram and EMG. This effect was of exactly the same nature as that yielded by a single tactile stimulation. This initial on-effect, however, was followed by reduction of the depth and rate of respiration. Corresponding to this depression, decrease in the frequency of unit-discharge and recruitment of both inspiratory and expiratory neurons were observed in the EMG, and prolongation of the resting phase of the discharge was observed in the respiratory cycle. These depressive effect probably are produced by the pressure stimulation which is of spatio-temporally constant intensity delivered by clasping with a clip. By removal of the clip, an augmentative off-effect, which is the same as the on-effect, was seen.
As the pressure stimulation was delivered by cutaneous clipping, pain stimulation which produce the “ first pain ” may have combined to cause the on-and off-effects. On the other hand, the inhibitory response following the on-effect may have been caused not only by the afferent impulses of pressure receptors but also by those which evoke the “ second (slow) pain”.
Both of these augmentative and inhibitory cutaneo-respiratory responses decreased considerably by bilaterally sectioning the lung vagi in the neck. Thus, the cutaneo-respiratory reflex appears to be regulated by the vagal respiratory reflex.

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1. The dependence of the heme-heme interaction of human adult hemoglobin on the species and strength of the evironmental salts was studied. In a series of several neutral salt solution, the magnitude of the interaction was dependent not only upon the ionic strength but also upon the species of the environmental salt. In the latter of the two factors, the charge of the constituent cation appears to have a primary importance. All these results confirm our previous observations.
2. Similar salt effects were also verified in potassium phosphate buffer (pH 6.9). The magnitude of the effect was roughly comparable to that of the divalent cation neutral salts.
3. An attempt was made to graphically estimate the intrinsic constants of the first asd fourth oxygen association (κ₁1 and κ₄) by human adult hemoglobin. The κ₄ value was 170 to 250 times as great as the κ₁ in sodium chloride (μ=1.0), whereas the enhancement was only 14 to 25 fold in no salt medium.
4. Oxygenation of hemoglobin was accompanied with a hyperchromicity and a slight blue shift in the medium ultraviolet range. These changes were completely reversible. The derived ultraviolet difference spectrum (oxy vs. deoxy subtraction) showed three difference peaks around 238, 275, and 290mμ. A linear correlation was shown between the degree of oxygenation and the magnitude of the ultraviolet spectral change.
5. Deoxygenation of bovine oxy-hemoglobin induced a remarkable reduction in the alkali resistance.
6. Discussions were made of a probable correlation of the alterations in the ultraviolet absorption and the alkali denaturation with a configurational change of hemoglobin molecule upon the oxygenation.

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The cross circulation technique was applied for perfusing the innervated hindlimb and kidney preparation for analysing the reflex response in the systemic blood pressure and the respiratory movement, when dimethylaminopropyl-tetrahydro-azaazepino-phenothiazine (RPP 201), andromedotoxin, veratridine, bradykinin and kallikrein were injected into the femoral artery of hindlimb preparation.
The pressor reflex response was constantly observed by use of RPP 201, andromedotoxin and veratridine but the depressor, or the pressor or the combined reflex was obtained by use of bradykinin and kallikrein. The depressor reflex induced by bradykinin disappeared when the skin of leg was removed, while the pressor reflex was reversed to the depressor one by preceding injection of sodium salicylate into the femoral artery. The pressor reflex with respiratory excitation induced by RPP 201 was also blocked by sodium. salicylate. The afferent fibers in the sciatic nerve were principally responsible to the reflex, and anticholinergic, antiadrenergic, antihistamic, antiserotonic, neuromusclar blocking and ganglion blocking agents did not block the reflex but procaine did it. Authors conclude that the depressor reflex response is probably induced by the excitation of afferent fiber from the skin while the pressor one is originated from the muscle, joint and other parts than the skin, and that sodium salicylate blocks peripherally these nociceptive or pseudoaffective reflex responses, especially originated from the muscle and joint but not from the skin.

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1. Effects of strychnine upon the pontine reticular inhibition to lumbar extensor motoneurons were examined by using the monosynaptic reflex test as well as the intracellular potential recording from motoneurons of the cat.
2. The inhibition elicited by single pulse stimulation of the pontine reticular formation was eliminated by strychnization in the same dosis with that for blocking the direct inhibition. The elimination of inhibition usually made the facilitatory component, having been hidden by the inhibition, predominant.
3. Under heavy strychnization which evoked strychnine tetanus, it was observed on ventral root and intracellular potentials that, when repetitive stimulation of the pontine reticular formation was applied with appropriate strength and frequency, the strychnine tetanus could be completely stopped during the stimulation. The appropriate parameters of stimulation were those for eliciting the sufficient and continuous smooth depolarization in motoneurons.
4. The mechanism of stopping the strychnine tetanus was discussed in concern with the accommodation of motoneurons to the elicited sustained depolarization.

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