To clarify the clinical significance of the exercise test in acute myocardial infarction (AMI), the relationship between the results of exercise test and the clinical features was studied. The low level treadmill exercise test (maximum exercise time was 1080 seconds and the maximum oxygen consumption was 7 METs) were performed in 111 patients within 2 months after the onset of AMI. The exercise time, the endpoint of the exercise test, the exercise-induced ST-segment deviation and ventricular premature beats (VPC) were evaluated from the exercise tests. Among the clinical features, age, sex, the severity in the acute period (Killip's classification and Forrester's hemodynamic subset), the findings in cardioangiography (the number of diseased coronary arteries, left ventricular ejection fraction and abnormal wall motion in the left ventricle) and short term prognosis after AMI were evaluated. The prognosis was judged as poor when cardiac death, congestive heart failure, postinfarction angina, the decrease of exercise tolerance and reattack of AMI occurred, or when an aorto-coronary bypass graft or percutaneous transluminal coronary angioplasty was performed.
The exercise time was shorter in patients over the age of 60 years (578 ± 360 seconds) than in younger patients (818 ± 296 seconds), and also in females (487 ± 392 seconds) than in males (767 ±± 319 seconds). The patients classed as Forrester's hemodynamic subset IV had shorter exercise time than the others. But, there was no relationship between the exercise time and Killip's classification. Low left ventricular ejection fraction (55% or less) was associated with short exercise time and the apperance of exercise-induced VPC. But the number of diseased coronary artery and abnormal wall motion in the left ventricle were not related to the exercise test. The patients with high exercise tolerance (4.2 METs or more) in the AMI recovery period showed better prognosis than those with low exercise tolerance within one year after AMI (96% vs 50%, p<0.0001, respectively).
In conclusion, the low level exercise test in AMI was influenced by age, sex and cardiac function, and it was useful in evaluating the short term prognosis after AMI.

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1-Methyl-4-phenyl-1, 2, 3, 6-tetrahydropyridine (MPTP) induces parkinsonisms in humans, monkeys, and some animals. MPTP is metabolized to 1-methyl-4-phenylpyridine (MPP⁺), which is a primary neurotoxin, by monoamine oxidase B. MPP⁺ destroys nigro-striatal dopaminergic neurons, but the mechanism of the neurotoxic effects of MPP⁺ is not known. In this study, the effects of MPP⁺ on O^-₂ generation by neutrophils was examined. Neutrophils possess several functional and antigenic similarities to glial cells. Therefore, the O^-₂ generating system of neutrophils might be useful in studying the mechanism of MPP⁺ neurotoxicity related to active oxygen species.
1) MPP⁺ did not affect myristic acid (MA), and elaidic acid stimulated O^-₂ generation and H₂O₂ generation by the glucose-glucose oxidase system, suggesting that MPP⁺ did not react with O^-₂ or H₂O₂ itself.
2) When fatty acid-activated neutrophils were treated with a neutral detergent, Renex 30, and then NADPH was added, the O-2 generation by these permeabilized cells was inhibited by MPP⁺.
3) Kinetic study revealed that MPP⁺ was a noncompetitive inhibitor of the NADPH oxidase in plasma membranes isolated from MA-activated pig neutrophils.
These results did not support the hypothesis that the action of MPP⁺ is related to acitve oxygen species. The results suggest that MPP⁺ does not penetrate through the plasma membrane, and interacts with the inner domain of NADPH oxidase in the neutrophil plasma membranes. MPP⁺ inhibits NADPH oxidase, a hydrophobic flavoprotein, such as monoamine oxidase, NADH dehydrogenase and a-ketoglutarate dehydrogenase.

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Using cardiotocogram and umbilical arterial gas analysis, the presence or absence and variations of umbilical cord coiling were examined with relation to the incidence of variable deceleration (V.D.) and neonatal asphyxia. The results obtained were as follows.
1) The incidence of V.D. with cord coiling was higher than that without cord coiling (p<0.005). The incidence of severe V.D. with cord coiling was also higher than that without cord coiling (p<0.005).
2) The mean Apgar scores of cases with cord coiling were lower than that without cord coiling (p<0.02).
3) On the umbilical arterial gas analysis, the mean pH of cases with cord coiling was lower than that without cord coiling (p<0.05). And the mean pCO₂ of cases with cord coiling was higher than that without cord coiling (p<0.005). So neonate with cord coiling showed a tendency towards respiratory acidosis in comparison with that without cord coiling.
4) The incidence of neonatal asphyxia with cord coiling was 16.0% (Apgar score≤7), 20.0% (pH<7.20) and that without cord coiling was 8.8%, 13.2%, respectively. Although there was no statistically significant difference, a tendency was observed towards a higher rate of neonatal asphyxia with cord coiling.
5) The incidence of neonatal asphyxia with severe V.D. was 44.4% (Apgar score≤7), 36.1% (pH<7.20) and that without severe V.D. was 5.7%, 8.6%, respectively. There was a statistically significant difference (p<0.005, p<0.005). In addition, the incidence of neonatal asphyxia with repeated V.D. was 35.3% (Apgar score≤7), 44.1% (pH<7.20) and without repeated V.D. was 3.8%, 6.5%, respectively. There was a statistically significant difference (p<0.005, p<0.005).
6) There was a statistically significant change in the incidence of repeated V.D. with cord coiling and without cord coiling (p<0.005). And especially, with tight cord coiling, there was a significant increase in the incidence of repeated V.D. (p<0.05), or in the insidence of severe V.D. (p<0.05). Moreover, the incidence of neonatal asphyxia with tight cord coiling was 62.5% (Apgar score≤7), 62.5% (pH<7.20). There was a statistically significant increase in comparison with the control (p<0.005, p<0.005).

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In our study, we investigated the clinical features of sicca syndrome in the presence and absence of rheumatoid arthritis. Twenty patients with sicca syndrome alone and 22 patients with sicca syndrome accompanied by rheumatoid arthritis were examined.
The average onset age of the sicca syndrome alone is 12 years younger than the syndrome associated with rheumatoid arthritis. Moreover, rheumatoid arthritis tended to antecede the clinical onset of the sicca syndrome in the latter group.
Relevant to the clinical investigative data, frequent lower values of CH 50 and positive reactions to the anti-nuclear antibody were noted in the sicca syndrome alone group. In this group, a lowering of cell-mediated immunity and a decrease in lysozyme density in lacrimal fluid were also noted.
Relevant to the clinical manifestation, a high frequency of recurrence of parotitis, purpura and lymphadenopathy was also noted.
Related to the joint findings, 45% of the patients with sicca syndrome alone disclosed clinical evidence for arthritis, however, no significant radiographic findings were observed.
It is clear that there were distinct differences in clinical figures in both groups, while continuity of the clinical figures between them was also confirmed. When we take the known pathological and molecular genetic findings into consideration, it may be assumed that the differences in the clinical figures between these two entities could result from the difference of the causative mechanism of the conditions. Furthermore, we may safely say that the sicca syndrome alone may reflect the essential pathophysiologic figure of this particular syndrome.

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Proliferative changes of the glomerular mesangium of the kidney are generally considered to be a progressive inflammatory process of glomerulonephritis. There are several reports on experimental glomerulonephritis induced by snake venom which is known to cause demonstrable mesangiolytic changes in the glomerulus.
The author investigated the sequential morphological changes of the renal glomerulus by light and electron microscopy after administration of 1.0 mg/kg of Habu (Trimeresurus flavoviridis) snake venom to 56 guinea-pigs via tail vein injection. In addition, an analysis of proliferated cells in the glomerulus was attempted by applying the immunostaining method for the antibody to BrdU as the marker of the dividing cells.
Various degrees of mesangiolytic changes of the glomerulus were induced after Habu venom injection. In this model, however, the majority of mesangiolytic changes were mild. Subsequent segmental nodular proliferation of the mesangial cells was observed in mesangiolytic areas. Mitotic figures appeared from 24 hours to 7 days after the venom injection, as shown by BrdU staining. New capillary lumens were formed among the proliferated cells of the postmesangiolytic segment 4 to 5 days after the venom injection. Formation of capillary lumens and reconstruction of the glomerular loops had been gradually established through the time course. The histological structure of the glomeruli returned almost to normal 15 weeks after the venom injection, with occasional features of remolded-healing, although a small number of glomeruli still showed persisted mild segmental mesangial proliferation as well as mild increase of PAM-positive substance in the mesangial area.
These results suggest that mesangial proliferation is related to the reconstruction of the glomerulus rather than the progression of the glomerular lesions, at least in this model. The author postulates that the mesangial cell has the functional ability to repair the injured glomerular structure.
The application of the BrdU immunostaining method turns out to be a useful tool for analyzing the relationship between cell mitosis and cell proliferation.
In the guinea-pig, the Habu-snake venom induced mesangiolytic lesions are milder than those in the rabbit and the rat and the degree of subsequent mesangial proliferative changes is less prominent.

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In order to elucidate the molecular mechanism of the heterogeneity of rat hemoglobin, hemoglobin components in adult rat hemolysate were isolated and differences in the primary structures of their constituent globins were determined. The results obtained were as follows :
1) Crystalline hemoglobin prepared from the hemolysate of an adult male Wistar rat was separated into nine hemoglobin components by means of DEAE-cellulose column chromatography, each giving a single band on polyacrylamide gel electrophoresis.
2) Of these hemoglobins, six major components, designated DE-I, II, IV, V, VI and VII, were further subjected to reverse-phase HPLC to yield their respective constituent a and β globins.
3) Peptide mapping and NH₂-terminal amino acid sequence analysis of the β globins confirmed that DE-I and II hemoglobins possessed the previously known IIIβ globin, while DE-IV, V, VI and VII hemoglobins contained the previously known 11β globin.
4) The mechanism underlying the heterogeneity of rat hemoglobin was discussed on the basis of these findings.

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The purpose of this study is to clarify the causative mechanism as well as the clinical significance of myocardial ischemic attacks in patients suffering from angina pectoris.
The subjects were 127 patients upon whom 24-hour Holter electrocardiographic monitoring was performed. The patients were classified into the four types of angina pectoris: exertional angina (56 cases, EA), exertional and rest angina (28 cases, ERA), and rest angina (4 cases, RA), all of which show ST-segment depression during ischemic attacks; and variant angina (39 cases, VA) which shows ST-segment elevation. The Holter electrocardiographic findings were classified into the four above-mentioned types and were analyzed.
The frequency of symptomatic ischemic attacks in descending order was EA, ERA, RA and VA, while the frequency of asymptomatic ischemic attacks was in the reverse order. EA was significantly higher than the other three types of angina. In the daytime, however, the frequency of ischemic attacks in descending order was EA, ERA, RA and symptomatic and asymptomatic ischemic attacks was in the same order. The peak occurrence of hourly ischemic attacks was at 10:00 am and 1:00 pm in the case of EA, 7:00 am in the case of ERA, 2:00 am in the case of RA and 5:00 am in the case of VA. The magnitude and duration of ischemic attacks and maximal heart rates during attacks were greater in symptomatic ischemic attacks than in asymptomatic ischemic attacks in each type of angina pectoris.The maximal heart rates during symptomatic ischemic attacks were in descending order, EA, ERA, RA and VA. On the other hand, the maximal heart rates during attacks recorded on a Holter electrocardiograph were lower than those during induced attacks on treadmill exercise testing, and the difference in rates was significant in both EA and VA. In patients with angina pectoris showing ST-segment depression during attacks, no relation was observed between the magnitude and duration of ST-segment depression and the severity of coronary artery lesions.
In conclusion, it may be stated that the situation and the mechanism of the occurrence of the myocardial ischemic attacks varied based on the types of angina pectoris. Moreover, it was clarified that the mechanism of ischemic attacks was different between spontaneous and exercise induced attacks as the threshold of the occurrence of the former group was lower than that of the latter group. Therefore, it was concluded that the circadian alternation of the increased coronary vascular tonus is one of main causes of the spontaneous ischemic attacks.

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Glucose-induced insulin secretion in rat pancreas islets was studied by means of the modified perifusion technique. The biphasic insulin increase after 0.3% glucose application consisted of a rapid response (the first phase response) and a delayed one (the second phase response). The former was brought about by shortening the 0.3% glucose application time to one and a half minutes and the latter by treatment with 1μg/ml of synthetic somatostatin. It was proposed that the rapid response depended mainly on D-cell activity and the delayed response depended on B-cell function.

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