Two cases of imported malaria which occurred in Okayama prefecture are reported. One was infected with Plasmodium vivax in India, the other with P. falciparum at Nigeria, Africa. The efficacy of some antimalarial drugs in these cases is discussed. One patient was infected with P. falciparum, despite taking the medicine Daraprim^® regularly. The efficacy of Daraprim^® for suppressive cure in Nigeria is doutful.
The therapy of chloroquine-resistance tropical malaria is also discussed.

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Methods of measuring the activity of the total alternative complement pathway, properdin and Factor B with rabbit red blood cells(RaRBC) were examined. The following results were obtained.
1) 0.03M EGTA-GVB permitted activation of the alternative complement pathway without activation of the classical complement pathway.
2) RaRBC were hemolysed by C4/C2 depleted serum as well as by normal serum. RaRBC were not hemolysed by inulin or zymosan treated serum.
3) The activity of the total alternative complement pathway was measured with 50% hemolysis of RaRBC in EGTA-GVB, designated as ACH50.
4) The activity of properdin or Factor B was measured with RaRBC and normal fresh human serum deficient in properdin(RP) or deficient in Factor B(RB).

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Hemolytic activity of the total alternative complement pathway(ACH50), properdin activity(P activity) and Factor B activity(B activity) were measured in 64 systemic lupus erythematosus(SLE) patients using rabbit red blood cells. The following results were obtained.
1) ACH50, P activity and B activity were significantly lower in SLE patients than in normal subjects.
2) ACH50 correlated with CH50, C3, Factor B, B activity, C5 and P activity. P activity correlated only with ACH50. B activity correlated with ACH50, CH50, C3 and Factor B.
3) CH50, C4, C3, Factor B correlated with each other.
4) The degree of ACH50 reduction was less than that of CH50 reduction in the active stage of SLE.
These findings suggest that the alternative complement pathway was activated mainly by the C3b positive feedback mechanism possibly due to triggering by immune complexes in vivo. The alternative complement pathway might play a part in defence mechanisms instead of decrease in the classical complement pathway in the active stage of SLE.

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Homovanillic acid (HVA), a major metabolite of dopamine, and 5-hydroxyindoleacetic acid (5HIAA), a major metabolite of serotonin, were measured in the lumbar CSF of 7 patients with Huntington's chorea, one patient with senile chorea, 5 patients with a clinical diagnosis of dentatorubropallidoluysian atrophy (DRPLA), 2 patients with essential myoclonus, 8 patients with Parkinson's disease and 10 normal subjects as controls. HVA levels in patients with DRPLA and Parkinson's disease were significantly lower than that of the controls. HVA levels were not altered in Huntington's chorea. One patient with senile chorea showed low HVA level. 5HIAA levels in Parkinson's disease were significantly lower than that of the controls. Two patients with essential myoclonus showed low 5HIAA levels. These results suggest that dopaminergic neurons in the central nervous system (CNS) might be impaired in DRPLA and Parkinson's disease, and that serotonergic neurons in the CNS might also be impaired in Parkinson's disease.

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It has been reported that substance P influences plasma glucagon concentrations; some investigators reported elevation of glucagon but the results are conflicting. This might be due to the differences in the species of experimental animal, dose of administered substance P, study system (in vivo or in vitro), and other experimental conditions. In this study, various doses of substance P were infused into the superior pancreaticoduodenal artery of anesthetized mongrel dogs for 30 min. Plasma glucagon and insulin concentrations in the superior pancreaticoduodenal (pancreatic) vein were measured by radioimmunoassay. For measuring plasma glucagon, 30K antibodies were used.
Substance P (100 ng/kg body weight/min) infusion brought about mild hypoglycemia. A rapid and significant increase of plasma glucagon level was observed shortly after substance P administration, then plasma glucagon concentrations decreased transiently during the next 10 to 20 min. Gradual increase to a high plateau level followed after discontinuation of the drug. A small transient decrease of plasma insulin level was seen at the beginning of the experiment. Blood pressure decreased during substance P infusion. Impedance in pancreatic tissue was markedly lowered. The lowered impedance reflects increased blood flow in the tissue. Administration of 25 or 50 ng/kg/min of substance P induced mild lowering of blood glucose and plasma insulin, but increase of plasma glucagon. The infusion of substance P at a dose of 5 ng/kg/min for 30 min did not cause any changes in blood glucose, plasma glucagon or insulin levels. But, after discontinuation of the drug, the plasma glucagon level gradually rose to a significantly high level. Blood pressure was not affected, but impedance in pancreatic tissue showed a gradual, marked decrease. During substance P infusion at a dose of 0.5 ng/kg/min, blood parameters did not vary. After ceasing the infusion, the plasma glucagon level gradually increased.
In conclusion, substance P was thought to stimulate dose-related glucagon secretion not only by a neurogenic circulatory action, but also by a direct action on pancreatic alpha cells. The increase in glucagon concentration in the later part of the experiments might be caused by vaso-circulatory changes and other hormonal pharmacological actions of substance P.

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Immunoreactive glucagon (using 30K antibodies) and insulin concentrations in the superior pancreaticoduodenal (pancreatic) vein of anesthetized mongrel dogs were measured after administration of 2-bromo-α-ergocryptine (CB154), γ-aminobutyric acid (GABA), and γ-hydroxybutyric acid (GHB) into the superior pancreaticoduodenal artery.
A bolus administration of CB154 (200 μg/kg) induced a hyperglycemic response with biphagic increases in plasma glucagon and insulin levels. Blood pressure was lowered after a transient slight elevation. Impedance in pancreatic tissue was markedly increased after an initial rapid decrease. The lowered impedance reflects increased blood flow in the tissue. CB154 (50 μg/kg) administration brought about hyperglycemia and mild hyperglucagonemia. However, the plasma insulin level did not vary. After premedication with pimozide (1 mg/kg, intramuscularly), CB154 (200 μg/kg) administration caused a mild gradual increase of blood glucose, mild increase of plasma glucagon and significant decrease of plasma insulin concentrations. The premedication had no effect on blood pressure changes. Impedance in pancreatic tissue was slightly increased after a mild transient decrease.
GABA (5 mg/kg) infusion for 30 min induced mild hyperglycemia, biphasic increase of pancreatic plasma glucagon and biphasic decrease of pancreatic plasma insulin concentrations. Blood pressure rose slightly, then gradually fell after a few minutes. Impedance in pancreatic tissue increased slowly. With a GABA (1 mg/kg) infusion for 5 min, the pancreatic plasma glucagon level gradually rose, and the plasma insulin level fell. During a GABA infusion at a dose of 0.1 mg/kg for 5 min, the plasma glucagon level increased slightly, but the plasma insulin level did not vary.
A GHB (500 mg/kg for 2 min) infusion brought about a mild transient hyperglycemia. Although there was an initial decrease in the glucagon concentration, the amount of secreted glucagon seemed unchanged since the volume of blood flow in pancreatic tissue increased markedly during this period. The biphasic increase in glucagon concentration followed. Plasma insulin concentrations decreased significantly. GHB administration at a dose of 100 mg/kg for 2 min had similar effects on insulin and glucagon secretion, and did not cause any change in blood glucose level. The changes in plasma glucagon and insulin levels during 5 min infusion of GHB (100 mg/kg) were tested in more detail. The level of glucagon decreased slightly followed by a gradual increase after a few minutes. The plasma insulin level decreased significantly. GHB (10 mg/kg) infusion for 5 min resulted in no change of plasma glucagon concentration and a mild decrease in plasma insulin concentration.

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A new method is described for quantitative determination of insulin antibodies. In this method, the insulin binding capacity of non-iodinated insulin is determined. Diluted serum containing insulin antibodies was saturated by native insulin. Bound insulin in the incubated serum was fractionated by polyethyleneglycol(PEG). After the precipitated bound insulin was acidified, insulin antibodies were separated by PEG again and immunoreactive insulin in the supernatant was measured. The titer of insulin antibodies is expressed as microunits of insulin antibodies per milliliter of serum. The determination is not influenced by free or antibody bound serum insulin. The co-efficient of variation of insulin antibody titers was 7.04%. There was a significant correlation (r=0.846, p<0.001) in serum antibody titers between our method and that of Welborn, but more sensitive results were obtained by our procedure. In patients with high bound insulin titers, reasonably accurate determinations were demonstrated. Acidification of samples was able to be performed at lower pH and longer reaction time was available. Another advantage of this method is that the changes in the titer of insulin antibodies in individual patients can be followed accuratly, because in other methods identical purity of hot insulin is not always available for each test. The diagnostic tool provided by this new method proved useful for diabetic patients being treated with insulin.

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The significance of insulin antibodies in determining diabetic control was examined in 56 patients treated with insulin. Diurnal changes in blood glucose, serum free insulin and bound insulin concentrations were measured. C-peptide concentrations before and after meals were measured as an index of residual insulin secretion. The control of blood glucose was estimated by the calculation of M-value (Schrichtkrull). The SD/mean of serum free insulin in patients with high insulin antibody titers was significantly lowered. This finding suggests that insulin antibodies have a buffer action of stabilization of serum free insulin. The buffer action of the insulin antibodies was affected by quantitative changes of bound insulin concentrations, which were accompanied by concomitant changes in free insulin concentrations within physiological limits. The capacity of the buffer action of insulin antibodies seems to be determined not only by the titer of insulin antibodies, but also by quantitative changes in free and bound insulin concentrations. In patients with antibodies of high buffer action, diurnal blood glucose levels were stable. Insulin antibodies seem to have a stabilizing action of blood glucose levels. Thus, insulin antibodies are thought to be an important factor in the control of blood glucose.
In insulin-treated diabetics, serum free insulin levels in patients with obesity or liver dysfunction were as high as in non-insulin treated diabetics with these disorders.

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Rates of clinical tumor growth were studied in 47 patients with 50 primary advanced gastric cancers (Borrmann type; 1:9, 2:27, and 3:14 lesions).
Long term serial changes in tumor size on X-ray films were evaluated retrospectively. Three lesions studied in this series showed fairly constant and simple exponential growth. For 46 tumors, the mean volume doubling time (VDT) was 8.7±2.6 months (5-17 months). These gastric cancers seemed to be moderately growing. Four tumors had VDTs of 26 to 34 months and might be slow growing.
One lesion with mainly submucasal progression might not be rapid growing.
Prediction of the size of missed lesions on X-ray films provides early detection of “gastritis-like-stomach cancers”.

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The relation between morphologic changes of human basophils and IgE receptors on cells from patients with bronchial asthma was studied during the reaginic hypersensitivity reaction. Peripheral blood basophils were separated and reacted with rabbit IgG anti-human IgE antiserum. Goat anti-rabbit IgG antiserum was then derivatized to carboxylate-modified latex particles, 0.254 μm in diameter, (immunolatex) and this was used as a probe to detect IgE receptors on basophil surface. Using this probe, significantly more IgE receptors were detected on the basophils from patients with atopic asthma (with high serum IgE levels) than from normal subjects and patients with intractable asthma (with normal IgE levels).
Moreover, the density of the IgE receptors was much higher on pear-shaped basophils than on spherical basophils.
These pear-shaped basophils are believed to be in the degranulating state during the reaginic reaction.
The distribution of immunolatex particles on the basophil surface was either diffuse or displayed patch and cap formation. Patch and cap formation was more common in pear-shaped cells and patients with atopic asthma.
These phenomena were temperature-dependent.
These results support the view that the pear-shaped form is the functionally active form of basophils in reaginic hypersensitivity.

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Experiments were carried out on the rat liver metallothionein induced by X-ray irradiation. The following results were obtained. 1) The metallothionein content of liver cells increased for a certain time after X-ray irradiation. SOD activity showed an upward trend in accordance with the increasing metallothionein. 2) The increase in metallothionein content induced kept in certain level with the time course after irradiation. 3) This metallothionein contains Zn²⁺, and also has the ability to bind Cd²⁺. 4) The SDS-PAGE pattern indicated that this metallothionein consists of two subunits having molecular weights of 11, 000 and 9, 000 respectivily. Also this metallothionein showed the same electrophoretic properties as that of Zn²⁺-induced metallothionein.

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Monoamine and acetylcholine in rat heart were studied embrylogically. The following results were obtained.
Monoamine was present in the heart in monoaminergic nerves which appeared in the atrium of the 14 day old fetus and in the ventriculum 3 days after birth. The distribution of monoamine in 7-14 day old rat hearts was similar, and that of 35 day old rats was identical to that of adult rats.
Cholinergic nerves appeared in the atrium and ventriculum of the 20 day old fetus. Its distribution in 7-14 day old rats was similar, and that of 35 day rats was identical to taht of adult rats.
Both nerves were already distributed at birth in the sinoatrial node and the atrioventricular node. The distribution in 35 day rats was identical to that of adult rats. Ordinary heart muscle cells also showed less positive cholinesterase activity than specific heart muscle cells at birth.

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An epileptogenic cortical focus was induced by the topical application of cobalt powder to the sensori-motor cortex, then guanidino compounds in the cobalt focus were analysed by HPLC. An extraordinally high peak was observed in the epileptogenic focus 24 hours after the cobalt application. α-Guanidinoglutaric acid (GGA), which is synthesized from glutamic acid and S-methylisothiourea sulfate, was confirmed by GC/MS as a dimethylpyrimidyl derivative of GGA.
An unknown substance was isolated from the cobalt focus and identified as GGA by the same GC/MS technique as in the case of an authentic sample. GGA was present in the normal cat cortex in amounts of 1n mol/g. GGA increased after cobalt application, and reached a maximum after 24 hours. The abnormal GGA recovered to the normal level about 40 days after the application by which time the cobalt focus had disappeared. Other guanidino compounds, that is taurocyamine, guanidinosuccinic acid, guanidinoacetic acid, β-guanidinopropionic acid, creatinine, γ-guanidinobutyric acid, arginine, and methylguanidine, except for guanidine tended to decrease in the cobalt focus. Taurocyamine and α-guanidinobutyric acid were still decreased 40 days after the cobalt application.
Spike and wave complex was induced after topical application of 0.2M GGA to the sensori-motor cortex, and a burst continued for one hour.

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A few reports have so far been presented on the scanning electron microscopy of herpesviruses. This study attempted to reveal first, whether herpesvirus particles could be detected on the cell surface of infected cells by scanning electron microscopy; second, the morphology and the dynamic aspect of the particles if they were seen; third, the ultrastructural changes of cell surface membranes after infection with the viruses; and fourth, the differences in morphological appearances among various herpesviruses.
In vitro cultured cells infected with five human herpesviruses were examined by scanning electron microscopy and the following observations were made:
1) Particles 170-200 nm in diameter were detected on the surface of cells infected with type 1 and type 2 herpes simplex virus (HSV-1 and -2), human cytomegalovirus (HCMV) and varicella-zostervirus (VZV), but not on EB virus (EBV) associated lymphoblastoid cell lines.
2) FL cells infected with HSV-1 and HSV-2 at an MOI of 10-20 were observed time sequentially. Particles of 170-200 nm began to appear at 6 hr and increased in number thereafter. At and after 24 hr the entire surface of most infected cells was covered with the particles. These observations were confirmed by transmission electron microscopic (TEM) examination of similar samples.
3) On the surface of HSV-2 infected cells, a group of projections resembling a cauliflower was occasionally observed.
4) Besides 170-200 nm particles, larger particles of variable size were found on the surface of human embryonal fibroblasts infected with HCMV, while smaller particles were seen on that of Vero cells infected with VZV. TEM observation of cells infected with both viruses revealed that larger particles of HCMV corresponded to dense bodies and smaller particles of VZV to aberrant forms devoid of capsids.

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Convulsions were induced in 80% of CBA mice by throwing stimulation six from eight weeks after birth, and continued for more than one year. The procedure for causing a CBA mouse convulsion was as follows: the mouse was rolled over suddenly by throwing stimulation and set in tonic flexion. After a few seconds of clonic convulsion, tonic extension followed, and opisthotonus was observed in this stage. After a convulsion, the mouse rose, seemed stunned for a few seconds, then recovered to a normal state. This convulsive process took about 10-15 seconds for the whole procedure. Urinary incontinence was observed.
Bilateral sporadic spikes of about 100-150μV were induced in the resting stage of stimulated CBA mice, but the EEG was not abnormal in normal untreated mice.
Dopamine (DA) in the cortex and brainstem of the CBA mouse at the pre-convulsive stage was significantly decreased compared with the resting stage, and these changes recovered during the convulsion stage. DA in the cerebellum was also significantly decreased one hour after convulsion. Norepinephrine (NE) of CBA cortex was significantly decreased before, during, and one hour after, a convulsion, compared with the resting stage. 5-Hydroxytryptamine (5-HT) in the CBA brainstem was significantly decreased compared with the resting stage, and this change recovered to the normal level one hour after a convulsion.
DA and 5 HT of the cortex of CBA mice, which convulsions had induced for more than one year, were significantly decreased compared with untreated CBA mice of the same age. There was no difference in the monoamines of CBA mouse brain between females and males.

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