The resistivity index (RI), elasticity index (EI), dicrotic index (DI) and effective arteriolar elastic index (Ea) were investigated by recording finger-tip plethysmograms, in normal pregnancy, puerperium, non-pregnancy and toxemia of pregnancy. The following results were obtained. 1) The RI values in non-pregnancy decreased with increasing age. In normal pregnancy, the RI values also decreased with increasing age. These values were even lower in toxemia of pregnancy. In women over 40 years of age, there was an increase in the incidence of decreased RI and El values and abnormal DI values.
2) In toxemia of pregnancy, especially in those with hypertension and proteinuria, there was a high incidence of decreased RI and El values and abnormal DI values.
3) In toxemia of pregnancy, there was a high incidence of after-effects in patients with abnormal RI, El and DI values.
4) There were a significantly large number of casesjshowing low RI values in the group of toxemia of pregnancy with KW I-IV funduscopic findings.
5) The RI values tended to decrease immediately after delivery. They also tended to decrease gradually during the lying-in period.
6) When 30 mg of progesterone was administered to those cases who showed rigid and anacrotic waves on the 3rd day of lying-in, the waveforms were changed to normal catacrotic and dilated waves.
7) The increase in RI values tended to become greater when lactation ceased and menstruation started.
8) These results show that the RI values in finger-tip plethysmograms are useful in clinical obstetrics, especially in toxemia of pregnancy and vascular dilatation tests before and after delivery.

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Allergy like symptoms of adverse reactions to iodinated contrast media are usually considered to be induced by cellular histamine release or complement activation. But it has not been acceptable to date that these mediators are induced by antigen-antibody reaction. Thus experiments were carried out on the antigenicity of iodine preparations (ICM : iodinated contrast medium, IS : iodine solution). The results obtained were as follows :
1) Antibodies in the rats and rabbits immunized with iodine preparations alone or which those conjugated to bovine serum albumin (BSA), in complete Freund's adjuvant emulsion, were detected by means of a passive hemagglutination test and passive cutaneous anaphylaxis (PCA). Antibodies against ICM and IS were detected and cross antigenicity between ICM and IS was demonstrated.
2) Iodine preparations conjugated to Ascaris suum were incubated with Silicae gel and injected repeatedly into mice and guinea pigs. IgE antibodies against iodine preparations were determined by 48 hour PCA in mice and 8 day PCA in guinea pigs. No specific antibodies were detected in mice. In guinea pigs, high titers of IgE antibodies against IS were demonstrated, but IgE antibody against ICM was not detected.
3) Protein binding capacity of ICM and IS to BSA was studied by a counter current dialyzer, and the ratios were 3.4% and 92.5%, respectively.
4) ICM was injected in the muscle of rats and then radioactivities of I were determined by instrumental neutron activation analysis. Forty-nine cps remained two weeks after the injection while 3.1 cps remained in the control group.
5) IgG levels in sera of reactors (urtica) and nonreactors to ICM were measured by laser nephelometry technique. The IgG levels of reactors were significantly higher than those of nonreactors (chisquare test and binomial test).

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Changes following cerebral infarction were divided into four categories according to the ventricular size visualized on CT scans. Namely, those without the ventricular enlargement were classified as 0, whereas those with the gradual increase in the ventricular size as I, II and III. On the respective group, employing the method of Xenon injection into the intracranial artery, the mean regional cerebral blood flow (mean rCBF), the autoregulation of cerebral circulation and the vascular response to CO₂ inhalation were studied to assist their prognosis determination.
1) In healthy adults over fifty, the ventricular size gradually increased along with aging. Moderate and severe enlargements were observed in 25% of the subjects in the seventh and eighth decades.
2) In the case of the old infarct, the ventricular size classified under 0 category occurred significantly less, in comparison with the healthy subjects in the same age decades, while moderate and severe enlargements occurred much more frequently.
3) In the case of the old infarct, the mean rCBF was decreased as the ventricular enlargement progressed gradually. A significant difference was recognized between 0 and I and also between I and II, but no significant difference was observed between II and III.
4) In the case of the old infarct, the autoregulation of the cerebral blood flow was maintained regardless of the degree of the ventricular enlargements.
5) The cerebral vascular response to 5% CO₂ inhalation was lowered along with the gradual increase in the ventricular size. In particular, those classified under the II and III ventricular enlargements revealed remarkably low values of Δ mean rCBF/Δ PaCO₂.
6) In the case of the old infarct, even in the presence of much severer ventricular enlargement, the autoregulation of the cerebral circulation through neural mechanism was observed. However, the autoregulation through chemical mechanism was severely impaired.
The above results suggest that an improvement in the severer ventricular enlargement is hardly expected from any drug therapy.
Consequently, it is considered essential to prevent ventricular enlargement with proper therapeutic approaches during the acute stage.

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Changes in X-ray density corresponding to intracranial hemorrhagic lesions were followed in fourteen patients. In addition, X-ray density of solutions with oxyhemoglobin, CO-hemoglobin and methehemoglobin as well as suspension of blood corpuscles, hemolysate, calcium, sodium, iron, copper, magnesium and phosphate was measured.
The following results were obtained:
1) The average X-ray density of hemorrhagic lesions within 48 hours after intracranial hemorrhage was 73.80 H.N.: 55.81 H.N. between 48 hours and three weeks:49.5 H.N. between three and four weeks:26.81 H.N. over four weeks. In all cases, the intracranial hemorrhage in its acute stage revealed a high X-ray density as compared to the surrounding cerebral tissue. This was helpful for the detection of hemorrhagic lesions.
2) X-ray density of the lesion decreased 1.68 H.N./day after the hemorrhage.
3) Among various constituents of blood, the solution of sodium showed the highest X-ray density, followed by hemoglobin, magnesium, calcium, phosphate, copper and iron.
4) However, when the concentration of each blood constituent was taken into consideration, hemoglobin showed the highest X-ray density, followed by calcium, copper, sodium, magnesium, phosphate and iron.
5) There was no significant difference in X-ray density between the suspension of blood corpuscles and hemolysate. The findings were the same whether hemoglobin was oxyhemoglobin, CO-hemoglobin or methehemoglobin.
6) Oxyhemoglobin showed the highest X-ray density, followed by CO-hemoglobin and methehemoglobin.
These findings suggested that hemoglobin in the intracranial hemorrhagic lesion seems to be a major factor producing a high X-ray density particularly in its acute stage.

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The air tourniquet is routinely used in the surgery of the lower limbs. Circulatory and biochemical changes in the blood were investigated during the use of the tourniquet and after its removal. The blood flow was stopped by tourniquet for 60-120 minutes under general anesthesia with intra-tracheal intubation.
The results obtained were as follows.
Blood pressure and CVP were sharply reduced after the blood flow was restored and the reduction was the largest one minute after the release of the tourniquet.
Blood pressure was normalized 15 minutes after the release of the tourniquet and CVP was significantly lower even 60 minutes after the release of the tourniquet as compared with the control values. It was assumed that there changes were caused by the decrease in the relative circulating blood volume and the reactive hyperemia. The heart rate was slightly elevated one minute after the release of the tourniquet.
The reduction of the cardiac output began 10 minutes after the release of the tourniquet and continued for 30 minutes. The amount of the reduction was statistically significant. This may have been partly due to the influence of accumulated lactic acid.
PaCO₂ was slightly elevated 1 minute after the release of the tourniquet and the levels of lactate and excess lactate were also elevated, which concided with the tendency of pH and base excess. Metabolic acidosis prevailed for 30 minutes after the release of the tourniquet.
There were no variations in PaO₂ following the tourniquet release, nor were there any significant changes in the level of Na, K or Cl. The above findings indicate that the changes in circulation and biochemistry of the blood existed for 30 minutes after the release of the tourniquet.
Consequently, it may be concluded that at least 30 minutes should be allowed before the resumption of the tourniquet.

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A new compound, azelastine, 4-(p-chlorobenzyl)-2-[N-methyl-perhydroazepinyl-(4)]-1-(2H) -phthalazinone hydrochloride, has recently been proved to be an effective antiallergy drug. It is quite different in its chemical structure from hitherto reported antiallergy drugs. In the present investigation, the inhibitory effects of azelastine against the immediate type allergic reactions in the guinea pig or the rat were studied in comparison with those of known antihistamine drugs, clemastine and chlorpheniramine. The results obtained were as follows:
1) The contraction of the small intestine isolated from the intact guinea pig or the rat by adding the histamine, bredykinin, serotonin, acetylcholine were remarkably inhibited by the pretreatment of azelastine.
2) The guinea pigs pretreated orally with a dose of 0.1 mg/kg of azelastine were completely protected from shock, resulting in death by a lethal dose of intravenous injection of histamine (1 mg). When the guinea pigs were pretreated with 1 mg/kg of azelastine 18 hours before the challenging injection of histamine, they were completely protected from shock death, and even if the pretreatment were done 24h before the challenging injection the survival rate of them was 80%.
3) The inhibitory effect of azelastine against the induction of heterologous PCA in the guinea pig and homologous PCA in the rat was rather potent in comparison with that of clemastine or chlorpheniramine.
4) Histamine release from the rat peritoneal mast cells by compound 48/80 or anti-rat IgE serum seemed to be slightly inhibited by the pretreatment with azelastine at the concentration of 10^-8-10^-6 M.
The results indicate that azelastine has a more potent antiallergic effect than such antihista-mine drugs as clemastine or chlorpheniramine.

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Sera from 2, 013 persons aged 0-75 years including cord bloods were collected at different areas in Thailand by the Society for Medical Research in South-East Asia, Nippon Medical School in 1977-1981. These sera were examined by the micro cell culture method for determi-nation of diphtheria antitoxin titer using Vero cells.
1) Except Chiang Mai '80-'81, diphtheria antitoxin (> 0.02IU/ml) were found in 81.2% of cord bloods, 67.1, 05 of children at the age of 1-12 months old, 37.9% of 1-2 years old, 55.3 % of 3-4 years old, 58.8% of 5-9 years old, 71.5-78.1, 06 of 10-19 years old, and 90.1% of older than 20 years.
2) Geometrical mean titers of the antitoxin-positive sera were 0.153IU/ml in cord bloods, 0.140-0.141IU/ml at 0-9 years old, 0.193IU/ml at 10-14 years old, 0.180IU/ml at 15-19 years old, and 0.151 IU/ml at older than 20 years.
3) In 68 paired serum samples from mothers and newborns (cord bloods), the antitoxin titer corresponded well each other. Antitoxin level of newborns were retained up to the age of 6 months.
4) Considering the age related antitoxin status of different areas, it was recognized that diphtheria had become common in northern part of Thailand since 1978, and reached the outbreak in Chiang Mai, 1980.
5) Antitoxin status by age were somewhat different in different geografical areas. People in Raming Tea Plantation and a Musur village in Chiang Mai Province had low diphtheria antitoxin level.
6) Antitoxin positive rate and geometrical mean titer of antitoxin-positive sera in Chiang Mai '80-'81 were apparently higher than either of other areas or Chiang Mai '77-'79. This high antitoxin level could be explained by the diphtheria-toxoid immunization and the diphtheria outbreak in Chiang Mai, 1980.
7) Surveys of diphtheria antitoxin in 143 serum samples from children aged 0-14 years showed that the immunization schedule by the Comprehensive Child Care Clinic, Chiang Mai University was efficient to confer the diphtheria immunity. Two shots of the primary immunization increased the antitoxin-positive rate from 16.7% (2/12) to 71.496 (5/7) of newborns. The primary plus the first booster immunization evoked higher than 0.02IU/ml of the antitoxin in 100% of the children. The geometrical mean titer of antitoxin was 6.912IU/ml after one month, and 0.540-1.144IU/ml after 11-64 months of the last booster immunization. Geometrical mean titer of antitoxin after 11 months or more of the first booster (0.438IU/ml) was lower than those after 11 months or more of the second (0.912IU/ml) and the third (2.318IU/ml) booster immunization.8) One hundred and two school-children aged 8-14 years without any record of the imm-unization with diphtheria toxoid in the suburbs of Chiang Mai received one shot of the toxoid during the epidemic of diphtheria in 1980. After one month, 88.2% of the children had the antitoxin in their sera and the geometrical mean titer of the antitoxin was 4.491IU/ml, which decreased to 1.057IU/ml after one year.

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It is well recognized that diabetic subjects have a higher incidence of myocardial infarction (MI) than non-diabetic subjects. However, the exact pathogenesis of this finding has not hitherto been described. It has been reported that changes similar to diabetic microangiopathy were found in intramyocardial coronary artery branches (IMCAB). On the other hand, investigations performed in author's laboratory have clarified morphological changes of IMCAB, suggestive of hemodynamic derangement in non-diabetic infarcted hearts, which may indicate the importance of peripheral circulatory disturbance in the development of MI.
In order to discuss the relationship between diabetes mellitus (DM) and MI, histopathological changes of main coronary artery stems (MCAS), IMCAB and myocardium were examined light microscopically in 60 cases and electron microscopically in 10 cases in diabetic autopsied hearts with MI and without MI (30 and 30 cases respectively).
The results obtained are as follows :
1) In diabetics with MI, the findings of MCAS and IMCAB were similar to those previously obtained in non-diabetic patients with MI, and were not specific to DM per se.
2) In diabetics without MI, the MCAS showed severe intimal and medial impairment at the same site as where thrombi had been frequently detected in infarcted heart.
In IMCAB, like those of infarcted hearts, acute changes such as endothelial cell destruction, imbibition of serum components into the subendothelial spaces, and cytolytic changes of medial muscle cells were present, in addition to the remote changes including thickening and fragmentation of subendothelial basement membrane with increase of collagenous fibrils, in spite of the fact that the MCAS remained to be impaired to lesser extent. These acute and old changes of the IMCAB were frequently accompanied with interstitial fibrosis, and justified as the preceding involvement of the MCAS.
In conclusion, these findings obviously suggest the presence of severe repetitive derangement in the intramyocardial peripheral circulation which might be caused by superimposed pathological incidences in DM. The higher incidence of myocardial infarctions in the diabetic subjects may be explained on this theoretical basis.

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Using the method of disc electrophoresis on poly-acrylamide gel, single radial immuno diffusion (SRID) and radio-immunoassay (RIA) method, CSF electro-phoretic pattern and immunoglobulins (lgG, IgA, IgM, IgD, IgE) were analyzed in 142 samples from normal control subjects (15) and patients with neurological diseases, including multiple sclerosis (9), myopathies (22), CVD (58), degenerative diseases (18), brain tumors (14) and infectious diseases (6).
The protein fractions of CSF was compared with those of serum in normal human subjects, and it was shown that CSF contains a high proportion of prealbumin and a low proportion of albumin.
CSF disc electrophoresis in M.S. showed a high proportion of γ-globulin and a low proportion of albumin. In myopathy group, albumin proportion was high, but its origin is unknown.
Mean values of normal CSF immunoglobulins were IgG : 1.7 mg/dl, IgA : 0.2 mg/dl, IgE : 12IU/dl. But CSF IgM and IgD were so little that those could not be detected. Mean values of IgG%, IgA%, IgG (c/s) % and IgA (c/s) % in all neurological disorders, were much more than those levels in control group.
In M.S., both IgG (%) and IgG (c/s)% were elevated. It was suggested that the reason of those high levels is the result of elevation of immunoglobulin IgG produced by brain.
In myopathic diseases, levels of IgG% and IgG (c/s) % were also increased. As the origin of the increase, the latter was suspected of the influence of blood-CSF barrier.
Level of IgM (c/s) % was increased in brain tumor, in cerebral infarcts and in meningitis, but levels in those diseases were only traceable except in metastatic tumor.
IgD could not be detected in CSF.
I could not detect any specific relations between control group and neurological disease group with IgE and IgE (c/s) % in CSF.

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In order to study the relationship between thromboembolism and coagulable capacity, especially coagulation factors, coagulological examinations were performed on 158 patients with establishedd or suspected arteriosclerotic diseases.
Patients with fresh myocardial infarction and aortic arch syndrome were excluded. Of the remainder, 10-30% showed abnormal values for individual clotting factors.
These values exceeded the upper limit of the corresponding normal ones.
In arteriosclerotic patients with suspected thromboembolism, a hypercoagulable state was found to exist both in terms of whole blood clotting capacity (TGT, HTT) and individual coagulation factors. In particular, diabetic patients with vascular disturbances showed. higherr coagulative activity than other groups and the difference was proved to be statistically significant.
A positive correlation with serum total cholesterol was found to be responsible for the cause of high clotting activity levels.

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It is generally said that prostatic cancer is a hormone-dependent tumor which produces acid phosphatase (ACP) and that the amount of ACP parallels the spread of the cancer.
However, since the relationship between sex hormones and the increase in ACP is as yet obscure and the cancer is sometimes hormone-independent, there exists confusion in its treatment.
In order to establish the basic knowledge of treatment for prostatic cancer, we have carried out biochemical and histochemical investigations of ACP activity using established cell lines of human prostatic cancer and examined effects of sex hormones on cell growth.
The established cell lines from human prostatic cancer, such as Duke 145, 8 PC 93, and 19 PC 93, were employed. They were examined for increasing ACP activity and for sensitivity to sex steroid hormones. The results obtained are as follows.

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