To elucidate the morphogenesis of cellulofibrous intimal thickening of the arteries which is regarded as a primary form of arteriosclerosis, the left common carotid arteries of rabbits and guinea-pigs were invested with various materials and by methods.
In the invested segments of the arteries, it would be expected that the medial muscle cells are degenerated by cut of the vasa vasorum and the local hemodynamics are changed by means of constriction and or fixation.
1) On both edges of the invested segment marked intimal thickenings were always revealed, on the contrary in the central part of the segment in which medial muscle cells predominantly disappeared the thickening seldom occured. Whenever the arteries were invested by tube having a small window in the midportion, on the surrounding area of the window the intimas also thickened.
In these portions medial muscle cells would be relatively injured by oxygen deficiency and hemodynamic stress would be most effectively acted on the vessel wall.
2) When the arteries were loosely tubed, medial changes were moderate and diffuse slight intimal thickening was observed over all invested segment.
3) By means of bending and constriction of the arterial wall the intima proliferated in certain portions.
4) Increase of permeability at thickened intimas were proved by the intravenous injection of trypan blue, carbon particles and fluorescent fibrinogen which had been injected.
5) It was clarified that the muscle cells in the intima were drived from the medial muscle cells and endothelial cells.
6) Both some degree of the malnutrition of the arterial wall and mechanical in juries of the arterial wall by hemodynamics were emphasized as causative factors on the morphogenesis of the arteriosclerosis. These two factors induced increase of vascular permeability and stagnation of tissue fluid in the arterial wall. Consequently cells consisting of the arterial wall reacted on plasma protein which is insudated and stagnated in the wall, and then proliferated. Also, regenerative proliferation of the cells occured.
The proliferation of the cells followed cellulofibrous intimal thickening of the artery, namely arteiosclerosis.

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1. Out of 2000 cases of autopsy, performed in the First Department of Pathology, School of Medicine, Gunma University duiring the 9 years' period from April 1959 through June 1968, 71 had metastatic cerebro-meningeal tumor. This accounts for 3.6% of the total autopsy cases, and 14.6% of malignant tumor cases (excluding leukemic cases) which underwent total dissection inclusive of craniotomy.
2. Classification of the metastatic cerebro-meningeal tumors by their primarily affected-organs shows that bronchial cancer ranks the first, accounting for nearly a half of the total. And the rate of metastasis of bronchial cancer into the cerebro-meninges is 40.7%.
3. As for the localization of the metastatic foci in the meninges (dura mater and pia mater) and brain parenchyma, 12 out of the 71 cases showed the foci in the brain, 5 in the pia mater, 21 in the dura mater, and 3 in the brain and meninges.
4. Macroscopically, metastatic cerebro-meningeal tumors can be classified into 1) nodular metastasis in the brain parenchyma (type I), 2) multiple nodular metastasis in the brain parenchyma (type II), 3) diffuse meningeale carcinomatosis (type III), 4) nodular metastasis in the dura mater (type IV), and 5) infiltrative metastasis in the dura mater (type V).
5. There is no significant histological difference between the metastatic cerebro-meningeal tumors and their primary tumors. Cases with metastatic foci in the brain parenchyma are characterized by loop-like stroma with rich vascularity and tendency of papillary proliferation of tumor cells.
6. The boundary between the normal and metastatic tissues is distinct in many cases on the histological level. The boundary tissues exhibits degeneration of parechyma, gliocytic reaction and formation of vascular net work. This histological reactive zone is generally narrow.
7. In some cases which has the metastatic focus in the hemisphere, the white matter is markedly swollen. Histopathologically, the lesion consists of generalized rarefaction and diminution of myelin sheath fibers in the white matter of the hemisphere, but subcortical U-fibers, corpus callowsum and capsulla interna are relatively well preserved.
8. Axon fibers show stronger resistance than myelin sheath fibers. Dark stained atrophied nuclei are prominent in oligodendroglia in the foci. In general phagocytes are not involved in disintegration of the foci. Astrocytes are proliferated, exhibiting protoplasmic or plum cell form, their protoplasmic processes are swollenlike pseudopodia, or fragmented presenting a picture of clasmatodendrosis.
9. In cases of protracted clinical course, severe swelling of axon fibers, and apperance of “epitheliale Zellen”, so called by Zülch, which are devoid of cytoplasmic processes, are noticeable.
In addition there are spongiosis of white matter and its active distegration with marked proliferation of phagocytes, all of which make complication modification of the basic picture. 10. When degeneration is mild, rarefaction of parenchymal fiber structure is often emphasized in the perivascular region; but when it is severe, imbibition of protein fluid from the adventitia into the parenchyma is observed.
11. The degenerative lesion extending though the whitr matter of the metastatic hemisphere is considered, from its distribution and histopathologic features, to be edematic.
As for its genesis, blood flow disturbance and stagnant anoxia of the venous system produced by pressure of developing tumors, and disturbance in permiability of blood-brain-barrier caused by noxious factor resulting from necrotic destruction of tumor tissue are considered to be the principal causes.
12. When edematic lesion is severe, it is not only seen in the white matter but also found extending to the deep cortical layer and basal nuclei as well as to subcortical U-fibers and capsula interna.

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With a test method devised by Matumoto et al., which was applied of the putting method in the golf, the fitness of an individual subject for the action requiring fine control was intended to measured. The following results were obtained.
1) The average score of the first tests to all subjects was 38.0. The one of male subjects was slightly higher than that of female ones.
2) The curve of learning effect on the individual subject ascended with zigzag course and reached plateau after 4050 times tests (training), but the height of the plateau differed quite large on different subject.
3) There was little difference between the curves of learning effect of male and female.
4) There was also little difference between the curves of learning effect of the subject with and without experience of the golf, except the phase at the beginning.
5) When the learning effect to each time of the test was compared on the subject who carried out the test one time every day and one time every week, the former was higher than the latter.

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