Urinary estrogens have been assayed chiefly with the Kober hydroquinone colorimetry or sulfuric acid fluorimetry. However, it is difficult to determine accurately small amounts of estrogens such as in urines from males, oophorectomized women or menopausal women. In this study, male urinary estrogens were determined by a modification of the method reported by Kambegawa and some experimental studies were made on male urines. 200ml aliquot of 24-hour urine is hydrolyzed by the 3-step hydrolysis, added with estrone-6, 7³H, 17β-estradiol-6, 7³H and estriol-6, 7³H, and extracted with ether, followed by alkaline washes, methylation by a supersonic wave mixer, thin layer and column chromatography, liquid scintillation spectrometry and the Ittrich fluorometry. Results of experimental studies and estimation of urinary estrogens in males are as follows: 1) After the 3-step hydrolysis, 54.5% of the urinary estrogens were collected as the glucuronide, 30% in the solvolyzed fraction and 15.5% as the hot acid hydrolyzate. 2) The methylation of estrogens was achieved 10-20% better by the use of the supersonic wave mixer than by a magnetic stirrer. 3) Calculating efficiency of the Packard Tri-carb liquid scintillation spectrometer was tested in varieties of the estrogen concentrations using the dilution and the external standardization methods. There was noted no influence of the estrogen concentrations on the counting efficiency in the determination ranges. 4) In the range of 2×10^-3-1.0μg, a linear relationship on the standard curve was obtained applying the Allen's correction, when fluorometry was conditioned with the excitation light wave length of 510mμ and the fluorescence wave lengths of 530, 550 and 570mμ for each of the three estrogen-methyl ethers. 5) Urinary estrogens were determined in 15 normal males. In 5 subjects (2-13 years old) the values were: E₁: 1.06±1.09; E₂: 0.64±0.54; E₃: 0.76±0.68 and the total E: 2.46±1.99μg/24hr. In 5 men (22-38 years old), E₁: 5.02±1.57; E₂: 2.58±0.21; E₃: 4.11±1.82 and the total E: 11.72±2.97μg/24hr. In 5 men (46-72 years old), E₁: 3.81±0.31; E₁: 1.71±0.48; E₃: 3.51±0.94 and the total E: 9.03±1.33μg/24hr. 6) Urinary estrogens were also determined in patients with a variety of clinical syndromes.

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Recently, considerable interest has been directed to electrical stimulation of the bladder as a means of management of the incompetent detrusor muscle due to neurogenic dysfunction. Rokujo, one of our colleagues, reported the results of electrical stimulation of the bladder in dogs with upper motor neuron lesion (acute and chronic stages) and also in dogs with acute lower motor neuron lesion. This paper is concerned with the results in dogs with chronic lower motor neuron lesions. 35 female mongrel dogs were subjected to transection of the conus medullaris at the level of the 6-7th lumbar vertebra, and were followed over 5 weeks to 17 months. In dogs with chronic lower motor neuron lesions, the bladder pressure above 40cm. of water could be obtained by using a stimulus of 30 pulses per second, 3 millisecond, and 10-15 volts with a pair of electrodes buried in the detrusor muscle near the uretero-vesical junction, and pressure response remained for 7 months, and then gradually reduced after 8 months.
In most cases, despite a good rise in intravesical pressure, bladder emptying was incomplete mainly because of the urethral contraction encountered in detrusor stimulation. Mechanism of the urethral contraction was analysed by 1) measurement of so called urethral resistence and intraurethral pressure, 2) pick-up of the spread-current, 3) stimulation of urethral muscle, and 4) stimulation of the pudendal nerves. It became apparent that the urethral contraction are due to stimulation of the unsevered pudendal nerves. In many dogs, after bilateral pudendal neurectomy, the bladder could be satisfactorily emptied by electrical stimulation. And in some cases showing poor electrical micturition even after pudendal neurectomy, longitudinal incision of the urethral muscle layer was necessary to produce a good urinary stream. No vesicoureteral reflux was observed.

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The sensitivity of the eccrine sweat gland to adrenaline and noradrenaline was examined in 70 patients with adrenal, renal and essential hypertension according to the Wada-Takagaki's method. The results were summarized as follows:
1) In aldosteronism, the sensitivity varied over a very wide range. These abnormally elevated or suppressed sensitivities of the eccrine sweat gland approached the normal range after the extirpation of the adrenal tumor or the subtotal adrenalectomy.
2) In Cushing's syndrome, the sensitivity was in normal range or slightly elevated. The postoperative data on the sensitivity also approached the normal range.
3) Patients with pheochromocytoma showed remarkably low sensitivity in the majority of the cases. The sensitivity rapidly elevated after the extirpation of the tumor.
4) The sensitivity of the eccrine sweat gland in renal hypertension was in normal range or slightly elevated.
5) The sensitivity in essential hypertension varied over a wide range.
6) It is probable that these changes in the catecholamine sensitivity of the eccrine sweat gland represtent a part of phenomena of the general change in the catecholamine sensitivity of the whole body.

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