Since electronic techniques became utilized for statistical analysis of bioelectric phenomena, attempts to analyze the electromyographic waveforms have been performed by many investigators.
The purpose of this paper is to descrive the auther' s method and to report the results of its physiological and clinical applications.
To analyze surface EMG in stationary state, recording was carried out during static contraction of skeletal muscles (M. deltoides, M. quadriceps femoris). Adopting analog correlator and short range spectrum analyzer, auto-correlograms and power spectra were obtained. The results were as follows.
1) In normal subjects its frequency components occupied the whole analyzed range (15-180 c/s), although main components exsisted below 120 c/s. The power spectra showed the dominant rhythm of about 80-90 c/s.
2) In order to examine the instantaneous effect of weight load various grade of load (0.9-5.0 kg) were given. As the load was increased, the rhythmicities of EMG became exaggrated. In power spectra the faster components about 60 or 80 c/s became dominant.
3) The effect of fatigue on EMG were examined by sustained weight loading (0-5 min.). When sustained weight load continued, the lower components of rhythm (below 40 c/s) became dominant.
4) In hemiparetic patients due to brain stokes the lower components were dominant on paretic muscles. And, its main cause was deduced to be the results from disturbances of phasic control mechanism by central nervous system.

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Electron microscopic observations were made on human breasts with mastopathic lesions (10 cases), and normal breasts (4 cases) as a control. The following results were obtained :
1. In sclerosing adenosis, shapes of the cells, nuclei and glandular lumina were irreglular as compared with those of normal duct epithelial cells. Fine filaments in the cytoplasm were rather increased and connected with desmosomes. Myoepithelial cells were increased in number,
2. In blunt duct adenosis, cells and nuclei were flat and the margins of both sides of the nuclei were uneven. Secretory vacuoles were especially abundunt. Clustered small vesicles were recognized in the myoepithelial cells.
3. In apocrine metaplasia, rough-surfaced endoplasmic reticulim was slightly well developed. The interior of apocrine projection was electron-lucent and contained a few small vacuoles. Basal infoldings were, often seen. Clustered small vacuoles were often in the myoepithelial cells.
4. In duct papillomatosis, the following findings were seen frequently. These were increase of nucleocytoplasmic ratio, uneven nuclear membranes, heterogeneous karyoplasm, decrease in number of ribosomes, dilatation of.cisternae of the endoplasmic reticulum and protrusion of the outer membrane of the nuclear envelope in the apical cells of the papilloma, less development of Golgi apparatus, increase in amount of fine filaments in the cytoplasm, less developed cellular attachment and tendency of infolding of the basement membranes.
5. Clear cells and dark cells were found both in normal and mastopathic breasts. Clear cells were seen both on the luminal layer and upon the basement membranes. Most of the dark cells seemed to be degenerative, but some which seemed not to be degenerated were also seen.

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Cancers, fibrocystic diases and fibroadenomas of the breast were studied biochemically with respect to the activities of phosphohexose isomerase, aldolase, isocitric dehydrogenase, leucine aminopeptidase, glutamic oxaloacetic transaminase and glutamic pyruvic transaminase.
Activities of all the enzymes were higher in mammary cancer tissue than in normal mammary tissues.
Difference of activities on histological type in mammary cancer were not significant, and fibrocystic diseases also showed no changes.
As to enzyme in serum of patients with breast cancer, aldolase and leucine aminopeptidase were relatively increased in activity, but other enzymes varied withen normal range
Effects of regional perfusion with anticancer drugs in cancer tissue were shown as fall of activity in case of leucine aminopeptidase.

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The effects of anticancer agents, amino acids and chelating agents on the distribution and excretion of ⁵⁹FeCl₃, on the catalase activity of liver and blood in Ehrlich ascites cancer bearing-mice were examined with the following results.
1. In ascites cancer cells intraperitoneally implanted mice, the time course of the changes of ⁵⁹Fe distribution were examined. At 24 hours after the ⁵⁹Fe administration, its concentration in the kidney was decreased in many cases with no changes in the other organs. Liver catalase activity was decreased about half in cancer bearing-mice compared with the normal.
2. In subcutaneously implanted mice, the time course of the changes of ⁵⁹Fe distribution were examined. Blood ⁵⁹Fe concentration was decreased at 120 hours after the administration without any changes in the other organs.
3. The effects of continual administration of anticancer agents to cancer-bearing mice were examined. In Mitomycin C treated group, ⁵⁹Fe concentration was decreased in blood and its concentration was increased in liver along with an inhibiting effect on ascites retention. Depressed liver catalase activity was returned to normal levels in this group. In Toyomycin treated group, ⁵⁹Fe distribution did not change in all organs, but liver catalase activity was returned to the normal and ascites retention was inhibited in this group. After the administration of Merphyrin, ⁵⁹Fe distribution in liver and spleen was decreased in normal mice, but same changes were not seen in cancer bearing-mice. Nitromin did not affect both ⁵⁹Fe distribution in organs and ascites retention. In cortisol acetate treated group, the ascites retention was inhibited in larger dose, but ⁵⁹Fe distribution was not changed.
4. Anticancer agents, amino acids and chelating agents were administered intraperitoneally with ⁵⁹Fe to cancer bearing-mice and its effect on ⁵⁹Fe distribution was examined. ⁵⁹Fe distribution was not changed in many organs with one or two exception.
5. At 1 hour after the intraperitoneal injection of ⁵⁹Fe, ascites was removed and the distribution of ⁵⁹Fe in cancer cells was examined. Its concentration was 5. 2% of injected dose per ml, but this grade was decreased to 0. 78% after the washing of cancer cells. Using above washed cancer cells the incorporation of ⁵⁹Fe into subcellular fraction was examined. Nuclear fraction had the highest concentration, followed by supernatant, microsomal and mitochondrial fractions in the descending order.

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1. some of Habu-bitten patients was produced extensive myonecrosis, which left behind functional disorder. And obliterative changes was elicited in arteries passing the necrotized muscle. It is therefore considered that this extensive and severe myonecrosis would have resulted from ischemia due to the obliterative arterial lesion, which must have been produced by direct invasion of the arterial wall by Habu venom.
This experiment was carried out to see whether Habu venom would effectively produce arterial lesion.
2. When 2mg. per 0. 1ml. of Habu venom was injected near the femoral artery of guinea pigs, the arterial lesions were histologically observed. The results were as follows, i) adventitial and perivascular hemorrhages, exudation of blood plasmas and necrosis of tissues in the injected area, ii) swelling, -degeneration, detachment from internal elastic menbrane and loss of the endothelial cells in intima, exudations of leucocytes into subendothelial spaces, subendothelial hemorrhages, iii) development of thrombus in the arterial cavities.
3. Degenerative arterial lesions as mentioned above were found till 2 or 4 days after the injection of Habu venom, and then intimal cellular thickening to be considered as regenerative change wae gradually produced in the intimal layers.
4. On the basis of these finding it is evident that the necrotic and obliterative arterial lesions are primarily caused by Habu venom.

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