1. A new method of determining the glutamic decarboxylase activity of the brain with the use of glutamic acid-1-¹⁴C has been devised by the author and its feasibility is discussed from various angles.
2. The erro in the determination of radioactivity of the experimental materials by this method is extremely small.
3. It is thounght that there occurs no accumulation of ¹⁴CO₂ during the determination of radioactivity by this method.
4. Since the self absorption by the material during the determination of its radioactivity is considerably high, a care should be excercised on a proper thickness of the material.
5. The incubation should be carried out under anaerobic condition in the experiment by this method.
6. The optimal pH for the system of this experiment is 6.6.
7. The amount of the substrate to be added to the system should be 5 mg.
8. The incubation period of this experiment is set at two hours.
9. By applying this method on rabbit organs it has been proven that the activity of glutamic decarboxylase can be determined.

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The activity of glutamic decarboxylase was measured with the use of cerebral cortices in human idiopathic epilpsy and in experimental epilespy of ep (epileptogenic) mice, of rabbits with local anaphylaxis of the brain and of vitamin B₆ deficiency mice and the folowing results were obtained.
1. While there can be recognized no significant defference in the activity of glutamic decarboxylase in non-focal cerebral cortex of human idiopathic epilepsy from that in the control (non-epileptic brain), the glutamic decarboxylase activity in the focal cortex of the human idiopathic epilepsy is markedly lower than that in the non-focal area.
2. The activity of glutamic decarboxylase in the cerebral cortex of adult ep mice is considerably decreased, but in the immature ep-mice that had not yet experienced convulsion its activity is rather accelerated.
3. The glutamic decarboxylase activity in the cerebral cortex of the rabbit with a local anaphylaxis is not significantly different from that in the normal control rabbit.
4. The activity of glutamic decarboxyase in the brain of vitamin B₆ deficient mice is markedly lower than that in the normal mice brain.

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With the brain extracted from the anesthetized mice or the mice with experimental convulsion, the glutamic decarboxylase activities of the brain were measured and the following results were obtained.
1. Anesthesia by ether or phenobarbital does not affect the glutamic decarboxylase activity of the brain.
2. Anesthesia by metrazol shows a slight decrease in the glutamic decarboxylase activity but it is not significant.
On the other hand, the glutamic decarboxylase activity is decreased in the brain of the animal given electroshock.

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The author studied the effects of high hydrostatic pressure on respiration of liver tissue of frog (Rana nigromaculata).
The results were obtained as follows.
1) After exposure to 300 kg/cm² the oxygen consumption of liver tissue were accelerated and inhibited by 400-1500 kg/cm² in proportion to the strength of applied pressure.
2) The oxygen consumption of liver tissue in the presence of citrate, acetate and glycerophosphate was accelerated at various hydrostatic pressures.
3) The oxygen consumption of liver tissue in the presence of succinate, glucose and pyruvate was inhibited at various hydrostatic pressure.
4) At relatively low pressure (300 kg/cm²), succinic dehydrogenase activity increased, but at moderate high pressure (500-800 kg/cm²) and very high pressure (1000-1500 kg/cm²), it was decreased.
5) The effects of high hydrostatic pressure on the inhibitor of succinic dehydrogenase activity was discussed.

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Although there are many reports by various investigators concerning to the urinary steroids of schizophrenics, the general agreement is not established yet for the normal value.
Prior to the study on urinary steroids of schizophrenics, the author determined the normal values for urinary steroids and also investigated the fluctuation and correlation of free and conjugated forms of urinary 17-hydroxycorticosteroid.
The urine specimens were colloected from 18 male and 18 female persons (ranging 18-47 year old of age, the avarage age 26 year old). Measurement was performed on total neutral 17-ketosteroid, total 17-hydroxycorticosteroid and free and conjugated forms of the later. 17-ketosteroid was measured by the modified Koch & Holtorff's method and 17-hydroxycorticosteroid was carried out by Silber-Porter's method.
The results obtained were as follows. (Every value shows mean and standard error.)
1) Daily excretion of total 17-ketosteroid was 8.3±0.6 mg/day for male and 5.8±0.4 mg/day for female. The difference between both sexes is thought to be significant from the statistical viewpoint.
2) Daily excretion of 17-hydroxycorticosteroid of male were 6.6±0.4 mg/day as total amount, 1.0±0.1 mg/day as free form and 5.7±0.3 mg/day as conjugated form; that of female were 6.2±0.9 mg/day, as total, 0.8±0.2 mg/day as free form, and 5.4±0.7 mg/day as conjugated form. These obtained values are higher than that of other workers in this country. The difference between sexes is seemed to be insignificant. There was no case on both sexes which had lower ratio than 3.0 in conjugated form/free form and also than 75% in conjugated form/total amount.

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Determining the normal value, the author measured the daily excretions of total urinary 17-ketosteroid (17-KS) and total, free and conjugated forms of urinary 17-hydroxycorticosteroid (17-OHCS) of schizophrenics. The measuring methcds used were those which described in Part I. The urine specimens were collected from 51 cases, including male and female (ranging 16-58 year old of age, the average age 29 year old), which consist of acute, chronic and lobotomized schizophrenic groups.
The following results were obtained.
1) Acute Schizophrenic group: Total urinary 17-KS was 5.8±0.5 mg/day for male and 4.4±0.5 mg/day for female; lower than normal value also that of chronic or lobotomized group. Total urinary 17-OHCS was 9.0±0.9 mg/day for male and 7.9±2.2 mg/day for female. This means elevation in total 17 OHCS than normal value, chronic or lobotomized group. Above all, free form 17-OHCS was 2.9±0.6 mg/day for male and 2.0±0.5 mg/day for female, which showed 2-3 times higher amount than normal, but not much difference to chronic or lobotomized group. Conjugated 17-OHCS was 6.2±0.6 mg/day for male and 5.9±1.9 mg/day for female; almost equal to normal value and higher than chronic or lobotomized groups.
2) Chronic Schizophrenic group: Total urinary 17-KS was 7.3±0.6 mg/day for male and 5.5±1.3 mg/day for female; higher than acute group and lower than normal or lobotomized group. Total urinary 17-OHCS was 6.6±0.7 mg/day for male and 5.2±1.1 mg/day for female; the values were almost same as normal. Free form was 2.6±0.3 mg/day for male and 2.1±0.6 mg/day for female; 2 times or more higher than normal but not much difference to other groups of schizophrenics. Conjugated form was 3.9±0.5 mg/day for male and 3.0±0.7 mg/day for female; lower than normal and other groups of schizophrenics.
3) Lobotomized Schizophrenic group: Total urinary 17-KS was 8.7±1.5 mg/day; higher than normal and other groups of schizophrenics. Total urinary 17-OHCS was 6.8±1.3 mg/day; almost equal to normal. Free form was 3.0±0.6 mg/day; elevated than normal but not much increase than other groups. Conjugated form was 3.9±0.7 mg/day: decreased than normal.
4) From the results of this study, it can be hardly recognized the correlation between the fluctuations of 17-KS and 17-OHCS on the different groups of schizophrenics. From the viewpoint of fluctuation of 17-OHCS which is thought to reflect the adrenal function, the steroid pattern showed slight tendencies to hyper-function, hypo-function and normal function in acute, chronic and lobotmoized schizophrenics respectively. The characteristic change on urinary steroids of schizophrenics was the increased excretion of free form of 17-OHCS; this lowered the ratio of conjugated form/free form and the percentage of conjugated form/total.
The author put the consideration on process of schizophrenics from the view point of homecstasis and the effect of biologically active 17-OHCS to mental phenomena.

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Experiments were performed to examine the disturibution of Cornin on the organs in the rabbit.
1) Cornin was demonstrable in all segments of digestive tract. Relatively little Cornin was found in extracts of oesophagus and considerable amounts of Cornin in stomach. The intestine contained large amounts of Cornin.
2) All parts of the central nervous system contained Cornin. The large amounts were found in the hypothalamus and corpus quadrigeminus, whereas extracts of the telencephalon showed little.
3) In adition to the digestive tract, other smooth muscle organs such as uterus, urinary bladder contained Cornin, although only in minute amounts. Other organs contained little amounts of Cornin.

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For the purpose of determining the distribution of mercury in various organs in mercury poisoning, above all, whether mercury is combined with tissue protein or not, the radio isotope mercury, Hg²⁰³(NO₃)₂ in the dose of 6, 000, 000 c. p. m./1.0 kg body weight (0.13 mg/kg of mercury) was injected into the dorsal muscle of guinea pigs, and the distribution of isotopic mercury was estimated in kidney, liver, spleen, heart, brain, blood cells, serum and blood plasma both before and after dialysis after 24 hours of the injection. As the result the following conclusion was drawn.
1. Some of the isotope, Hg²⁰³(NO₃)₂, so injected into guinea pigs, has been found combined with organ protein and blood protein in a non-dialyzable state, while the other portion exists free without combining with protein in a dialyzable state.
2. The mercury combined with protein (the percentage calculated as radio-activity of the material after dialysis/radio-activity of the material before dialysis) differs considerably between the organs and the blood. The ratio of mercury combined with protein is found in the descending order of heart>kidney>liver>spleen, revealing all of those combined with more than 70 per cent of mercury to organ protein in a non-dialyzable state.
On the contrary, in the brain mercury combined with the protein is found to be 67 per cent, revealing a lower rate of mercury combined with protein. In comparing the mercury combined with protein in blood, the percentage of mercury combined with blood cells and that of blood plasma is 49 per cent in the former, while it is 55 per cent in the latter. Although the latter shows a higher rate, the mercury combined with protein in blood cells and blood plasma is lower than that in other organs. Furthermore, even by the salting-out method the mercury combined with protein to various tissue has been found 76.7 per cent in kidney, 73.9 per cent in liver, 61.9 per cent in brain, and 50.0 per cent in blood serum, showing the results approximately same as those obtained by dialysis.
3. In comparing the mercury distribution combined with tissue protein per 1.0 mg dry tissue weight, it has been found in the descending order of kidney>blood plasma>blood serum>liver>spleen>heart>blood cells>brain, indicating mercury combined with protein is extremely minimal in the brain and blood. Mercury shows a marked quantity of the tissue protein of kidney, amounting to 27-fold that of blood plasma, 39-fold that of liver, 47-fold that of spleen, 156-fold that heart, 244-fold that of blood cells, and 407-fold that of brain.
In addition, when the quantity of mercury combined with protein in blood is compared as per 1.0 mg of dry protein weight, the ratio is blood cells: blood plasma equals to 19, while blood cells: blood serum equals to 1:7, respectively.
4. In blood and principal organs the total amount of mercury combined with tissue protein as against the total amount of the mercury injected has been found to be in the descending order of kidney>liver>blood plasma>blood cells>spleen>heart>brain. Twenty-four hours after the injection of Hg²⁰³(NO₃)₂, of mercury injected, 32 per cent of it is distributed in the kidney, 4.4 per cent in the liver, 1.1 per cent in blood plasma, 0.6 per cent in blood cells. 0.2 per cent in spleen, 0.07 per cent in heart, and 0.06 per cent in the brain.
5. From these results it has been clarified that more than 67 per cent of mercury in organs combines with tissue protein and mercury has an extremely strong gathering to the tissue protein of kidney.

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This experiment was conducted in order to elucidate the distribution of mercury combined with protein in the intracellular granules in the case of mercury poisoning, one of the most important heavy-metal industrial poisonings that occur quite frequently. For this purpose, radio isotope Hg²⁰³(NO₃)₂ was injected at varying concentration into the dorsal muscle of guinea pigs, and the distribution of mercury combined with protein in the intracellular granules of kidney and liver was studied. The results of observations were as follows.
1. Injected mercury has been found combined with protein of all cell fractions such as nucleus, mitochondria, microsomes, and soluble protein in kidney and liver.
2. Twenty-four hours after the injection of 6, 000, 000 c. p. m./kg of Hg²⁰³(NO₃)₂ (0.13 mg/kg of mercury), the radio activity of mercury combined with protein per 1.0 mg. of the intracellular granules of the kidney in dry weight is distributed in the descending order of soluble protein>microsomes>mitochondria>nucleus.
The distribution of mercury combined with protein in the liver cell fractions proves to be in the descending order of soluble protein>nucleus>microsomes>mitochondria.
3. A lesser dose of the radio active mereury injected, rather than a larger dose of it, showes a higher activity of mercury combined with protein per 1.0 mg of kidney soluble protein in dry weight against the activity of mercury injected. In contrast to this, in the nucleus, mitochondria, and microsomes the distribution of the activity of mercury combined with protein per 1.0 mg of dry weight hardly differ irrespective of the does of mercury injectd.
4. The changes in the order on the distribution of the radioactive mercury combined with protein in the intracellular granules of the kidney and the liver can not be observed by injection of 12, 000, 000 c. p. m./kg of Hg²⁰³(No₃)₂, (0.26 mg/kg of mercury) and 1, 200, 000 c. p. m./kg of Hg²⁰³(NO₃)₂, (0.026 mg/kg of mercury).

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With the purpose to find out the effect of BAL (2.3 Dimercaptopropanol) in mercury poisoning, a group of guinea pigs were divided into two gruops of A group (control) and B group (BAL injection). To A group 1, 200, 000 c. p. m./kg of radio isotope Hg²⁰³(NO₃)₂ (0.026 mg/kg of mercury) was injected into the dorsal muscle, and to B group the same dose of Hg²⁰³(NO₃)₂ was given in the same way and immediately 20 mg/kg of BAL was injected and the same dose for the six consecutive days thereafter. Then, for the period of one week following the injection of Hg²⁰³(NO₃)₂, the excretion of mercury in the urine and stool as well as the distribution of mercury combined with protein in the intracellular granules of kidney after one week of Hg²⁰³(NO₃)₂ injection were observed in order to see the antidotal effect of BAL, and obtained the following results.
1. With the control group, the observations conducted with the lapse of time after Hg²⁰³(NO₃)₂ injection have revealed that the excretion of mercury in the urine is greatest on the second day, the excreted amount being about 21 per cent of the total mercury excreted in the urine in the one week period of observation. This excretion decreases relatively rapidly thereafter, but a transient rise in the quantity of excreted mercury can be observed on the fourth day.
As for the excretion of mercury in stool, it tends to increase from the first day to the fifth day of the observation showing the greatest amount of the excretion on the fifth day and after that it decreases relatively rapidly.
2. In the group injection with BAL, the excretion of mercury in the urine is markedly great on the second day, this amount being as much as about 31 per cent of the total mercury excreted during the one-week period of observation, and it decreases quite rapidly thereafter.
On the other hand, the amount of mercury excreted in the stool increases gradually from the first day to the third day of observation, showing the greatest amount of the excretion on the third day which is two days earlier than that in the control, and it decreases relatively slowly thereafter.
3. In the control group, the sum of the total amounts of mercury excreted in the urine and stool for the period of one week is about 49.8 per cent of the mercury injected, and of this about 35.9 per cent is excreted in the urine and that in the stool about 13.9 per cent, proving that the amouut excreted in the urine to be as much as about 2.6 times that in the stool.
4. In the group injected with BAL, the sum of the total amounts of mercury excreted in the urine and stool for the one-week period is about 82.7 per cent of the mercury injected, and of this about 69.5 per cent is excreted in the urine and about 13.2 per cent in the stool, proving that the amount of mercury excreted in the urine is about 5.3 times that in the stool.
From the findings described in sections 3 and 4, in the group B given BAL, the amount of mercury excreted in the urine during the one-week period is about 69.5 per cent of the injected mercury, whereas that in the stool is about 35.9 per cent in the control A group, proving that the BAL administration has a marked effect on the excretion of mercury in the urine. On the other hand, the amount of mercury excreted in the stool is 13.2 per cent in the B group given BAL as against about 13.9 per cent in the A group, control. This means that there is hardly any effect of BAL on the excretion of mercury in the stool.
5. In the observation of the B group given BAL, the amount of the mercury combined with protein in kidney tissue has been found to decrease markedly after the BAL injection, and the amount of mercury cmbined with protein per 1.0 mg.

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Observations were carried out on the biochemical properties of “cornin”, as a biological active peptides, extracted from the bovine cornea and its effects on the cell division was studied, and the following results were obtained.
1. Cornin has the maximum absorption band at 210-215 mμ and at 255-265 mμ and the minimum absorbancy at 240 mμ.
2. Cornin in the concentration up to 10^-5 shows a marked inhibitory effect on the cell division, and even at the concentration of 10^-8 it exhibits an effect to retard the cell division.
3. Cornin hardly passes through the fertilization membrane.
4. Both acidic and alkaline hydrolysates of the cornea lose their antimitotic effect already at the concentration of 10^-5.
5. Gelatin and egg albumin, on the other hand, have been found to show no retardation effect on the cell division.
6. The substance P at the concentration of 10^-3 shows the retardation effect on the cell division, but at the concentration of 10^-4 it loses such an effect, while on the contrary, at the concentration of 10^-5 it rather accelerates the cell division.
7. Cornin possesses biochemical properties different from those of the antimitotic substances extracted by Heilbrunn et al.

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Mycological and histopathological characteristics of the yeast phase of an isolated fungus, Histoplasma capsulatum Okayama-56 (Yamato), cultured at 37°C were investigated and the results obtained were as follows:
1. The lethality within 4 weeks in the mice of seven inbred lines given 1.0 mg of the culture intravenously was to be compared as, CF-1=dba-2>> AKR>BALB/c>A>ddT=C57 Br/cd.
2. The minimum lethal dose of CF-1 mice was 1.2 mg by means of intravenous injection.
3. The lethality within 4 weeks of CF-1 mice administered 1.0 mg of the culture intracranially, intravenously, intraperitoneally and by inhalation was 90, 80, 40 and 30 per cent respectively.
4. The most extensive and general pathologic changes were observed in the mice received intravenous injections, and in other cases the lesions produced were more or less localized at the site of invasion. The nature of changes was mostly to be interpreted as productive and granulomatous inflammations of the reticulo-endothelial system.
5. Small form fungi were well distributed in the reticulo-endothelial system and a small number of large form ones were seen in desqumative epithelial cells and in necrotic lesions.
6. The large form organisms were polymorphous being 5 to 20 μ in diameter and budding and chain-formation were infrequently observed. They were not appreciably stained with hematoxylin and eosin, but readily demonstrated by Gridley's stain.
7. The presenting pathologic appearances reached their peak in 2 to 3 weeks and then signs of improvement started to develop.

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An attempt to compare the nature of yeast phase cultures of the two strains and hemagglutination test was made and the findings gained were as follows:
1. In the Japanese strain, the large form fungi werc predominant even on young cultures, and on the contrary, the culture of the American strain was composed of the small form organisms irrespective of the stage of growth.
2. The count of fungi on 3-day cultures attained to (5-6)×10⁶/mg, (9-10)×10⁶/mg in the Japanese and American strains respectively, and decreased gradually with the passage of time.
3. The ratio of viable cells on 3-day culturos was 76 per cent in the former strain and 65 per cent in the latter, and it decreased significantly with the passage of time, especially in the former strain.
4. The lethality of CF-1 mice interavenously inoculated with 1.0 mg of 3-day cultures was found to be 100 per cent in both strains, and when 7-day cultures are applied, no alteration was revealed in the American strain but it was as low as 20 per cent in the Japanese strain. No lethal case was induced by fortnight cultures of either one of the two strains.
5. The pathologic features produced were represented by productive and granulomatous inflammations in the reticulo-endothelial system, and distribution of the small form organism in the reticulo-endothelial cells was more distinguishable in the American strain than in the Japannse one.
6. The characteristic appearance of the experimental infection in mice was disemination of the small form organisms in the reticulo-endothelial system in both strains, but the large form ones were also seen in necrotic lesions of survived mice, and this incidence was more frequent in the Japanese strain.
7. The data obtained from hemagglutination tests suggested that the protein fraction might be common in both strains, and the polysaccharide fraction had somewhat strain-specificity.
The above varieties proved were not always sufficient to differentiate the one from the other as it had been observed in isolated strains in the North America.

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Studies were made on the antigen-antibody reactions in Ectromelia virus hepatitis and the following results were obtained:
1) Elementary body in the parenchymal cells of the liver was always observed on the third day after the intraperitoneal inoculation of Ectromelia virus, regardless of the amount inoculated. Inclusion body was found in some instances to which a rather larger amount of the virus was inoculated. The changes in chick hemoagglutinin in the blood appeared to be almost similar to those of the elemetary and inclusion bodies.
2) Regardless of the amount of virus inoculated, antivirus complement fixation antibody, which was directly produced by viral infection, and hemoagglutinin inhibitor were noted in an early stage of the infection with their highest titres at 6 th to 10 th days. However, somewhat lower titres of those antibodies in the blood were observed when a larger amount of virus was inoculated.
3) Auto-liver antibody was continuously noted, even rather low titer, during the later stage of the infection (after 21 st day), when a small amount of virus inoculated, and there were marked generalized pathological reactions of the mesenchymal tissue and hyperergic processes such as proliferative demarcation to fibrosis of necrotic parenchymal liver cells. Simultaneously, the auto-liver antibody presented positive cross-reactions with some of soluble infected liver tissue component and liver-phosphatid-antigen (mouse and rabbit).
4) When a small amonnt of virus inoculated the organ-antibodies to soluble infected liver tissue component, which was so-called accompanied substance with infection, were produced in the early stage of infection and had been maintained for a considerable period of time. Changes in the organ-antibodies were almost similar to those of anti-virus antibodies in the early stage and then to those of auto-liver antibodies in the later stage. Heterophile antibody (Paul-Bunnell reaction) was noted in the early stage, while anti-liver phosphatid antibody was noted in the later stage.
5) Changes in γ-globulin were considered to be closely related to the production of antibodies despite the fact that serum protein was affected by infection because of decreased production of albumin in the early stage of infection and also of participation of globulin from unspecific necrosis of parenchymal liver cells.
6) When a small amount of virus inoculated the positive direct-Coomb's antibody, which was an incomplete antibody, appeared in the early stage of the infection. In view from the changes in the positive direct Coomb's antibody, not only such incomplete antibody in specific γ-globulin type but also those factors as adhesion of virus to erythrocytes and influence of affected serum albumin by infection upon surface potential of erythrocytes appeared to play significant roles in the direct Coomb's test.
7) In view from the alternations of the antigen antibody system and histological findings in the viral infection, different mechanisms of antibody production between anti-virus and auto-liver antibodies were postulated.
8) When a large amount of virus inoculated, histological feature of the liver and spleen of the infected mouse was a rapidly progressing unspecific exudative inflammation like Arthus's phenomenon. When a small amount of virus inoculated, a relatively mild hyperergic productive inflammation in which colliquative necrotic foci of parenchymal cells were demarcated by mesenchymal cells and then became nodular was noted.
9) At any rate, an allergic process was observed in the Ectromelia virus infection regardless of the amount of the virus inoculated since that was a feature of the virus as a obligatory parasite.

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Cell reactibilities of various organs during the course of infectious allergy were investigated, and the following results were obtained:
1) When a small amount of Ectromelia virus inoculated to produce subclinical infection, changes in reactibilities such as accelerated reaction of the parenchymal cells of viral hepatitis liver were observed by a phase-contrast microscope under supravital conditions when the autoliver antibody appeared in the blood at the later stage of the infection. This suggested a phenomenon of auto-organ allergy in the cells produced by infection.
2) In view from the attitude towards various antigens, such changes in the reactilities of the parenchymal liver cells during the course of auto-organ allergy were considered to be a part of generalized sensitization at this stage. Therefore, the presence of cell fixed antibody cannot be denied.
3) For the purpose of investigating the biological meaning of the auto-liver antibody its direct influence on the normal parenchymal liver cells under a supravital condition, passive sensitization and homologous liver sensitization were studied, Then it was revealed in every experiment that the auto-liver antibody gave an unfavorable effect on the parenchymal liver cells. Even low titer antibody gave a latent damage as a localizing factor, showing a cytotoxin-like reaction. The higher the titer of the anto-liver antibody, the more severe damage of the liver observed.
4) There was no essential differenee in biological value between two types of auto-liver antibody, the one produced in the process of auto-organ allergy by direct viral infection and the other produced by sensitization by means of homologous liver antigen.
5) Degenerative changes of parenchymal liver cells produced by either addition of antigen to sensitized liver cells or addition of auto-liver antiboty to normal liver cells were mostly due to antigen-antibody reaction in which complement was not always needed. However, in the latter case some exhibited an evidence of latent damage due to cytotoxin-like mechanism.

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For the purpose of clarifying the infection allergy on Ectromelia virus infection, especially auto-allergy which was noted in the later stage of subclinical infection, alternations of membranous electric charge in erythrocyte, which was a host of infected virus and mesenchymal wondering cell, and in parenchymal liver cell were studied by means of cells electrophoresis, and the following results were obtained:
1) Erythrocytes of normal mouse were all negatively charged. Upon Ectromelia virus infection membranous electric charge density of the erythrocytes, which were host of the virus, markedly decreased from the beginning of the infection and then returned to normal level in three days or so. However, in the cases of subclinical infection to which a small amount of virus inoculated, it again decreased around 12 th day and returned to normal in two days or so.
The initial decrease in the membranous electric charge density was considered mainly due to adhesion of the virus and hemagglutinin to the surface membrane of erythrocyte, while the later decrease due to inactivation of specific receptor on the surface of erythroeyte following moving out the virus and also to incomplete antibody attached to the surface of erythrocyte which was able to detect by the direct coombs' test. The influence of break-down products of the liver by the infection was relatively little.
2) There were little changes in the membranous electric charge density at the stage of infection when auto-allergy phenomenon and auto-liver antibody were noted in the blood.
3) During the virus infection, alternations of the membranous electric charge density of parenchymal liver cells were characteristic. At the beginning of the infection the electric charge significantly decreased when the virus atracted te the receptor on the surface membrane of the liver cells and then the virus was ready to move into the cell following inactivation of the receptor. The electric charge rapidly increase when the virus moved into the cells to form elementary body, namely degeneration-necrosis stage.
4) In case of subclinical infection, in which a small amount of virus inoculated, degenerative changes of parenchymal liver cells, as judged by the alternations of suface electric charge, were transient and reversible and recovered to normal shortly.
5) The membranous electric charge of parenchymal liver cells had been almost normal range during the period from the later stage of the infection to the stage of completion of auto-allergy
6) In case of subslinical infection, in which a small amouut of virus inoculated, a slight decrease in the membranous electric charge of parenchymal liver cells was noted around 17 th day.
7) The membranous electric change and velocity of electrophoresis were increased in parenchymal liver cells in subclinical infection around 27th day when the auto-liver antibody titre was rather high. This was due to affected reactibility of the liver cells which had some mild transient reversible degeneration in themselves.
8) The positive direct Coomhs' test component, which appeared in the early stage of the infection, presented close relations with virus, hemoagglutinin and also degenerative substances in the blood seen at the beginning of infection.

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A thourough examination was performed on the 319 cases, passed for more than one year after the release of treatment under the diagnosis of recovery or after the suspension of treatment at Kagato-Cho, Wake-Gun, Okayama in where there were prevalence of mild abortive form of epidemic hepatitis.
1. The cases having subjective symptom were 201 caces (63.0%) and their complaints were mainly the same to those on the course of disease.
2. Hepatomegaly in 77 cases (21.0%) and splenomegaly in 7 cases (2.2%) were ebserved.
3. Cases showing impairment in liver function test were 5.6-10.3% and cases showing a mild hyperbilirubinemia were 10 cases.
4. From the above results, cases required of treatment were 7 (2.2%), cases required of care 36 cases (11.3%). The concept that recovery of epidemic hepatitis was difficults was supported with the above results.
5. In the epidemics patients being required of treatment consisted of the second and third decades.
6. Duriug the last seven years, 1957 to 1963, 67 (21.3%) out of 314 cases of infections hepatitis in the epidemic areas developed into chronic hepatitis.
7. Acute stage of hepatitis at the onset was classified into three forms; typical, abortive and subclinical ones. 40.4% of the typical, 22.7% of the abortive and 36.2% of subclinical form progressed into chronic stage. Attention should be drawn to the high percentage of chronisity from the subclinical form of infectious hepatitis.

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