It is difficult to evaluate morphologically the degree of lesions of the brain stem which is directly related with death because the secondary hemorrhages can be observed at times which would testify that there have been some hindrances of circulation in the corresponding section. The author has studied on various illnesses where secondary hemorrhages of the brain stem had occured and their causes.
Carefull study on some 43 cases with or without secondary hemorrhages of the brain stem had been conducted. The result showed that 70% had secondary hemorrhages of the brain stem. Their causes of deaths showed that 89% died of head injuries with secondary hemorrhages of the brain stem, 50% died of poisoning and 40% of acute heart attack with similar condition.
The causes of secondary hemorrhages of the brain stem can be explained to be the deformation of the brain stem and the nosologic significance of the angioarchitecture. Further, the deformation of the brain stem result for its downward herniation brought about by space-occupying intracranial lesions and brain swelling. However, according to the author's cases, the causes can be divided into 6 types.
There are the arterial and venous congestion types of secondary hemorrhages of the brain stem.

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Report 1
The clinico-statistical observations are made of a large group of patients with the socalled whiplash injuries and their results summarized as follows:
1) The subjects used in this study were a total of 28, 362 patients, seen in our clinic during the past 5 years, of whom 1, 187 (or 4.19%) were of traffic accident.
2) The most frequent site of injury was the cervical region, accounting for 47% of the cases studied.
3) According to our classification, 578 of the entire 611 patients, treated as so-called whiplash injuries during the last 3 years, were found in sprain type of the cervical spine (with associated damage to muscles and ligaments), only a very few in fracture and dislocation types.
4) Recovery from injuries was attained within a month or two in the great majority of the cases, but repuired 6 months or more not infrequently in those of above 40 years presumably because of the injuries superinduced onto preexisting aging processes.
5) Residual complaints and symptoms mostly included heavy head, tender shoulders and tenderness over the trapezius muscle.
6) Therapeutic outcome was definitely more favorable with immobilization in plaster cast than without it.
7) The course of the disease was also investigated and it was considered that those symptoms, worsending after a certain interval, were mainly due to the associated disorder of the soft supporting tissues.
Report 2
The study described in Report 1 showed that the application of immobilization was reasonably effective in recovery from the so-called whiplash injuries. However, the true nature and pathology of the injuries are still obscure and there not infrequently are instances in which symptoms make an appearance not simultaneously with bu behind the trauma.
In the present study an experiment simulant of actual automotive accident was therefore conducted utilizing apparatus devised by the author, in which rabbits were shocked form behind (at an impinging velocity of 20 km/h) and were then examined for their cervical spine roentogenologically as well as for the cervical spinal cord and its surrounding tissues both macroscopically and microscopically. The results thus obtained are summarized as follows:
1) In not a single instance there was any definite X-ray evidence of damage to the bone.
2) Following the experimental injury there were extradural hemorrhage, subarachnoid hemorrhage, swelling of the dura mater, periradicular hemorrhage, extravasation surrounding the vertebral artery, and subarachnoid and extradural edema noted in both of the groups A (without immobilization) and B (with immobilization) .
These change varied in their degree and extent with time, the hemorrhages and edema attaining to their maximum in 24 hours and tending to subside thereafter.
3) At the 2nd day of receiving shock 3 animals exhibeted paresis like symptoms in the left forelegs, which disappeared afterwards. These symptoms were inferred to be due to hemorrhage and edema from the fact that they occurred at the height of the latter manifestations.
4) The predominant macroscopic change just after the injuries was extradural hemorrhage; extravasated blood tended, with the elapse of time, to be centered around the arch of vertebrae, especially intervertebral foramina, and was observable until the 7th days.
The predilecting site of hemorrhage in ventral to the spinal column and appears to be closely related to the presence of congestion of or bleeding from the venous plexus at the posterior edhe of the vertebral body and of damage to the periosteum. It seems that the blood extravasated moves downwards with time through the vertebral canal or foramina to be gradually absorbed.
5) Histological examination showed evidence for the persistence of the extradural, periradicular and periarterial hemorrhage more longer than 7 days in all of the cases studied. Intramedullary hemorrhage was noted in none.

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Monoamine Oxidase (MAO) [EC. 1. 4. 3. 4. monoamine: O₂ oxidoreductase (deaminating) ] in rat under the several abnormal conditions such as starvation, dehydration or fasting was studied and following results were obtained.
1) During 9 days starvation, rats lost 50% of the body weight. The ratio of organs weight against body weight decreased. Especially in liver, the ratio decreased markedly to about 60% of the control.
2) During 7 days starvation, MAO activity decreased to parallele with the decrease of the organs/body weight ratio and thereafter it increased gradually.
3) Following 9 days starvation, succinic dehydrogenase activity in rat liver increased as same as in case of MAO. On the contrary, remarkable decrease was observed in case of cytochrome oxidase activity.
4) The pattern for MAO, succinic dehydrogenase and cytochrome oxidase activity in liver and brain effected by a 9 days starvation differed notably.
5) The substrate specificity for MAO in rat liver following 9 days starvation was studied. To any substrates tested, MAO activity increased remarkably. When 5-hydroxytryptamine was used as the substrate, MAO activity in brain was approximately 2-fold than that of the control.
6) Michaelis Constants were calculated by the Lineweaver Burk's method. In case of the control, Km value of MAO was 1.0×10^-2M, while 7.1×10^-3M was calculated in case of 9 th day starvation. Feeding following the starvation caused recovery of Km value to the control level.

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Human ceruloplasmin was investigated by immuno-electrophoresis. Results obtained were as follows.
1) Human ceruloplasmin is demonstrated on α₂-globulin band by agar immunoelectrophoresis and cellulose acetate electrophoresis.
2) β-Lipoprotein was also stained by p-phenylenediamine on the plate of agar immunoelectrophoresis. The band obtained by electrophoresis plate treated with β-lipoprotein immunologically was stained by amido black and p-phenylene diamine and had oxidase activity.
3) In a case of Wilson's disease which has no ceruloplasmin in its serum, band stained by p-phenylenediamine was demonstrated on the plate, indicating stained β-lipoprotein. From this standpoint of view, it is inferred that there are several factors to influence on oxidase activity of ceruloplasmin in serum.

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An autopsy case of toxic hepatitis, probably due to rivanol, in a 20 year-old female occurring after the operation of artificial interruption of pregnancy by rivanol Bougie was reported. The cause of this case was Buff ested by the anaphylaxic state of this patient to Rivanol, and further mixed infection due to injury of uterinwall. Histological finding of the liver reviewed marked central necrosis with round cells infiltration, marked fatty degeneration, balloon cells, round cells infiltration at the Glisson's sheath and moderate congestion.

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A case of aplastic anemia with relative hyperplasia of normoblast in the bone marrow, which has been considered to be very rare in the childhood was reported.
This nine year eleven months old boy was admitted to the Showa University Hospital on the July 1 st., 1967 because of epistaxis. He has had history of bruising and buccal bleeding since his six years of age, on and off. Three days prior to the admission, he has had epistaxis suddenly in the morning followed by daily episode. On the June 30, the episode of nasal bleeding strengthened and lasted few hours.
On his past history, chloramphenicol had been given in the occasion of acute upper respiratory infection by his family physician intermittently. Otherwise, no contributable history was taken.
Physical examination on the admission revealed moderatory pale colored skin and epstaxis without any other positive finding. On laboratory studies, he had hypocellular bone marrow with hyperplasia of normoblastic series. The elevated serum iron and normochromic, normocytic anemia with decreased number of white cells and platelet count enabled us to establish the diagnosis of aplastic anemia beside bone marrow finding.
Prednisone was initiated daily followed each tow day administration and partial remission was obtained few months later. Since then, few episodes of similar course had been repeated till complete remission obtained under intermittent administration of steroid hormone.
Patient is still under observation by our out-patient-clinic and doing well for two years six months after establishing the diagnosis.

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