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HST virus which was isolated in 1950 from the roshida ascites tumor by Hamazaki and his associates is a pantropic virus which creates a unique inflammatory granulation in mice. When virus of an acute infections disease was inoculated on embryonated eggs, not only the egg membrane but also the chick embryo were infected more or less, and when the number of virus increased the chick embryo died, terminating the development of the egg. However, the tumor inducing virus which represents the Rous virus does not cause heavy disturbances in the embryo and it is well known that chick hatched from this egg can long maintain health unless it is subjected to a provocative factor. HST virus is no exception to this example and though it is inoculated on an embryonated egg it does not cause any serious disturbance on the embryo. The tissue changes of the chorio allantois infected by the "Virus were the focal proliferation and necrosis of ectodermal epithelium, the proliferation of the mesenchymal cells of the mesodermal layer adjacent to these foci, accompaning infiltration of lymphoid cells and leukocytes with edema, especially eosinophilic leukocytes. By these tissue changes a terrace-shaped thickening of the membrane was the result. In the viscera of the chick embryo a special change in the liver was seen, i. e., along the edge of the liver greyish white nodules submacroscopic to miliary in size appeared. The principal pathologic change of the foci is the coagulation necrosis of the liver parenchyma and only a slight infiltration about the periphery of the foci was observed. Moreover, proliferation of mesenchymal cells occurred next to the walls of the large blood vessels of the liver (principally, the portal veins) and with the added infiltration of a small number of lymphoid cells and leukocytes sharply defined nodular foci were formed. Though this was a rare instnace, similar pathologic changes were seen also in the walls of the blood vessels of the cerebrum stem of the embryo and along the periphery local gliosis was observed.

Histopathological investigations were carried out on five fatal cases of a type of polyneuritis of unknown etiology diagnosed as Landry-Guillain-Barre syndrome, which endemically occurred in children in the regions surrounding the Inland Sea of Japan. The most characteristic pathologic feature in the nervous system was pronounced patchy degenerative changes with slight or moderate degree of inflammatory cell response of focal type in the peripheral and cranial nerves, predominantly in the nerve fibers of the spinal and cranial roots. In the spinal cord, medulla, pons, and in some portions of the cerebrum and cerebellum, engorgement of the small blood vessels as well as edema and the less predominant scattered degenerative changes of ganglioncells and nerve fibers with extremely slight degree of glial response and sparse perivascular cell collections were encountered. The cerebrospinal meninges displayed edema and congestion of the pial blood vessels with focal collections of a small number of lymphocytes and/or monocytes. No advanced involvement of the anterior horn of the spinal cord in a strict sense of anterior poliomyelitis was, however, recognized. These changes may lead the histopathologic diagnosis of the present disease to infectious encephalomyelo-polyradiculoneuritis or a type of infectious polyneuritis. The main histopathologic changes in the visceral organs were a moderate degree of engorgement of the small blood vessels, degeneration of parencymatous organs such as the liver and kidney, hyperplasia or follicular atrophy of the lymphatic tissues, interalveolar pneumonia, focal myositis, and slight degree of round cell infiltrations in the interstitial tissues of the other viscera, such as the liver, heart, and gastrointestinal canal. Based upon the observations on the histopathological changes as well as clinical manifestations, discussions were made on the pathogenesis and etiologic factor of the present endemic disease with critique on the literatures.

For the purpose of obtaining the dibasic acid indirect bilirubin in a pure state from the dried canine cholecystic bile, an optimal developing solvent was selected by paper partition chromatography as a preliminary experiment, and it was isolated on cellulose column as an applied experiment. 1. The dibasic acid indirect bilirubin was separable at the starting point in a pure state by paper chromatography under development with the top layer of a n-butanol, acetic acid, water mixture (4:1:5). 2. The dibasic acid indirect bilirubin formed a fixed band at the upper starting place on cellulose column under development with the top layer of a n-butanol, acetic acid, water mixture (4:1:5), and no other substance could be detected there. 3. The dibasic acid indirect bilirubin existing in the fixed band could be eluted out into chloroform with a 1% acetic acid solution. An orange yellow powder was obtained from the eluate by evaporating the solvent in vacuo. 4. Thus separated orange yellow powder agreed well with the crystalline bilirubin in the solubility into organic or inorganic solvents and in the spectrochemical characteristics as well as in the chemical properties.

Two forms of the direct bilirubin separated from the dried canine cholecystic bile were subjected to paper chromatography and emission or infra-red spectroscopy, and the following results were obtained: 1. The two forms of the direct bilirubin contain plenty of bile acid or its salt, and benzidine- and ninhydrine-positive substances together with various inorganic elements were also detected. 2. The ester-form bilirubin had carboxyl radical by infrared spectroscopy. But it will not be easily concluded that an existence of carboxyl radical will owe to free carboxyl radical of the dibasic acid bilirubin by the reason why an existence of plenty of bile acid in the sample may inhibit the characteristic absorption of ester. 3. It may be suggested that the two forms of the direct bilirubin combine with bile acid or its salt, and that the affinity between them is stronger in the salt-form bilirubin. 4. It seems probable that properties of the salt-form and ester-form bilirubins are not influenced by an existence of bile acid or its salt, and further by acornbination with it.

Blood cells of schizophrenics differ in many points from those of normal subjects. First of all the shape of them is flat and thin. This tendency is more marked in old group than in new group; the volume is small; flat corpuscles are more numerous in them in the normal; and the blood resistance against diluted saline solution is stronger than that of the normal. It has long since been known that the rate of corpuscle sedimentation is being accelerated in schizophrenics. A simple physical cause that blood corpuscles are flat and numerous can explain this phenomenon. It is said that there is an antisphering substance among the factors controlling the thickness and roundness of blood corpuscles. Yet it has not been determined whether this substance on the surface of the blood of schizophrenics is large or small. Blood corpuscles are said to lose their peculiar disc-shape and to be completely destroyed at the pH of 9.2 when the antisphering substance is removed from the surface of blood corpuscles. The lower the pH is the better is the absorption of this substance on the surface of blood corpuscles; and it seems that the more this substance attaches itself to blood corpuscles the greater is the degree of flatness and in this connection it is interesting to note that the pH of schizophrenic blood is low in low in general. On the other hand, however, sphericity is increased at the time when the acidity of blood is increased due to a sudden movement of acidic substances immediately after ECT. Again in the case of coma of insulin treatment, blood tends to be alkaline and even then an increase in the sphericity of corpuscles is indicated. Consequently it seems tnat the roundness of blood corpuscles is not solely dependent upon antisphering substance and pH.