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The clinical efficacy of intravenous fibrinolytic treatment using a moderate dose of urokinase (UK) on acute myocardial infarction (AMI) has not been well evaluated in randomized trials.
In order to assess the efficacy of UK, a prospective randomized study was undertaken, aimed mainly at evaluating coronary myocardial blood flow in the infarcted myocardium using Tl-201 myocardial scintigraphy. 166 patients (131 male and 35 female, mean age 61.1 years) with AMI classified in Killip I or II who were admitted to the CCU within 24 hours of the onset of symptoms were devided into two groups; 76 patients treated with UK (UK group) and 90 patients treated with conventional therapy without UK (control group). Intravenous UK 72, 000 IU was injected over 10 minutes and UK 528, 000 IU was subsequently given by drip infusion over the following 12 (n=36) or 24 hours (n=40). There was no significant difference between the two groups with regard to the patients'background.
Tl-201 uptake of infarcted myocardium in the UK group (n=17) significantly increased in the first week compared with that on the day of admission (p<0.005) and a further significant increase was observed in the fourth week (p<0.05). In the control group (n=10) Tl-201 uptake did not change in the first week and then increased significantly in the fourth week (p<0.05). Coronary angiography and left ventriculography (43 cases in the UK group and 32 cases in the control group) performed in the convalescent stage of AMI showed: 1) similar prevalence of patency of the infarct related artery (UK group: 72.1%, control group: 75.0%), 2) more prominent collateral circulation in the UK group (62.9% vs 41.4%), 3) significantly better perfusion of infarcted myocardium by coronary antegrade flow and/or collateral flow in the UK group (70.0% vs 46.9%, p<0.05), 4) a trend towards reduction of severe asynergy in the infarcted regional wall of the left ventricle in the UK group (16.3% vs 34.4%).
The mortality rate of patients with first AMI in the UK group (n=66) was significantly lower than that in the control group (n=68) (4.5% vs 14.7%, p<0.05), and a similar trend was also found in patients with prior infarction (UK: n=10, 0% vs control: n=22, 1 3.6%). Cardiac rupture diagnosed on autopsy was less frequent in the UK group (n=2) than in the control group (n=7).
In conclusion, systemic fibrinolytic treatment by a moderate dose infusion of UK has some beneficial effects on AMI due to an improvement of microcirculation in the border zone.

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The effects of electrical stimulation on epiphyseal growth were studied. The epiphyseal cartilage of the proximal tibia of New Zealand white rabbits was stimulated by direct current for 2 weeks. A constant direct current of 5μA was supPlied by an electrical stimulation system buried under the subcutaneus tissue. Contralateral tibia with dummy electrodes served as control. The results were as follows: The height of the epiphyseal plate near the electrodes was slightly increased by traumatic reaction to the electrodes in the control group. However, in the stimulation group, the height was more remarkably increased than in the control group. The height of the epiphyseal plate was 0.6±0.2mm in the control grouP, and 1.0±0.4mm in the stimulation group, showing a statistical difference. The mineral appositional rate, determined by tetracycline labels, was 3.0±0.8μm/day in the control group and 4.6±0.4μm/day in the stimulation group. It was observed that the turnover of the epiphyseal plate was accelerated in the stimulation group, but no other abnormal findings were observed by electron microscopy. In conclusion, it is clear that growth of the epiphyseal cartilage is accelerated by direct current.

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Chondromalacia patellae is one of the common causes of patellofemoral disorders in young subjects. It frequently occurs in patients with lateral subluxation of the patella. However, the etiology of this disease is still obscure. The purpose of this study was to elucidate the histological changes of articular cartilage and bone in chondromalacia patellae. Lateral subluxations of the patellae were produced experimentally in forty New Zealand white rabbits.
The mean tilting angle of the patellae was 14.2 degrees just after surgery, 10.7 degrees after 6 weeks, and 7.1 degrees after 12 weeks respectively. Contact pressure was lower on the medial facets than on the lateral facets and both facets of the controls. Macroscopic changes on the patellar cartilage did not appear until 12 weeks postoperatively. On the other hand, histological changes such as vascular invasion of the calcified layer, irregularity of tidemark and a decrease in the number of chondrocytes in the deep layer of the cartilage were observed on the medial facet about 4 weeks postoperatively. The degeneration of chondrocytes and matrix gradually progressed from the deep layer to the superficial layer. Twelve weeks after, a depressed area was shown in the medial facet macroscopically. Repairing process was substantiated such as the proliferation of synovial tissue, the cluster formation of chondrocytes and the recurrence of the tidemark about 30 weeks postoperatively.
From the results mentioned above, it is suggested that cartilaginous and bony degeneration were caused by a decrease in contact pressure on the articular cartilage. The histological features of the chondromalacia patellae would be eventually developed by degenerative changes and restorative reaction.

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Three hundred and ninty-two consecutive patients with acute myocardial infarction (AMI) were studied to delineate the clinical features of ventricular tachycardia (VT) (three or more VPC). The incidence of VT in AMI was 23.5% and was higher in inferior AMI (29.8%) than in anterior AMI (19.3%) (p<0.05). The incidence of ventricular fibrillation (VF) and mortality were higher in the VT group than in the non-VT group. VT was most frequent on the first day after the onset of AMI. However, another peak of the occurrence of VT was observed in the 4th week after AMI in the anterior AMI group, but not in the inferior AMI group. The late-onset VT had a rapid heart rate during the VT attack (209±42 vs 170±62 beats/min, p<0.05) which frequently developed to VF (20.9 vs 8.4%, p<0.05). This was associated with severe heart failure and indicated a poor prognosis (mortality; 75.0 vs 24.2%, p<0.01), when compared with VT that occurred in the early period after the onset of AMI. The effectiveness of the thump-version for the termination of VT was 60.9%. Lidocaine was effective at 57.1%.

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To know the relationship between positive ventricular late potentials (LP) and occurrence of ventricular tachycardia (VT), signal-averaged electrocardiogram (SAECG) was recorded in 214 patients with myocardial infarction (MI). According to the time course of SAECG recording after the onset of MI, the subjects were divided into three groups; acute MI (AMI) group (onset-2nd week, n=148), recent MI (RMI) group (3rd-6th week, n=19) and old MI (OMI) group (7th week or later, n=47). The incidence of positive LP in each group was 22.3%, 36.8% and 12.8%, respectively. VT was observed in 51.5% (AMI), 71.4% (RMI) and 83.3% (OMI) in LP positive patients, and these proportions were significantly higher than those (25.2%, 0% and 9.8%) in LP negative patients. Sensitivity, specificity and predictive accuracy of positive LP to predict occurrence of VT were 37.0%, 84.3% and 69.7% in AMI, 100%, 85.7% and 89.5% in RMI and 55.6%, 97.4% and 89.5% in OMI, respectively. Incidence of positive LP in the patients with inferior infarction (23.9%) or with combination of inferior and anterior infarction (60.0%) were significantly higher than those in patients with anterior infarction alone (13.9%). Significantly higher peak-CPK value (4333±2580 IU/L) in the patients with positive LP compared to those with negative LP (2438±2023 IU/L) suggests that patients with positive LP have an infarction of larger size. In conclusion, non-invasive LP detection using signal averaging technique was useful in prediction of occurrence of VT in patients with MI in any phase.

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In 17 compensated liver cirrhosis and 8 chronic hepatitis cases (no histories of cardiac or pulmonary disease), wedged hepatic venous pressure (WHVP), hemodynamics, and pulmonary function were measured and their clinical significance and interrelations evaluated. Both diseases were comparatively analyzed.
WHVP was determined by wedging a catheter from the right femoral vein into the right hepatic vein. Hemodynamics was measured with a Swan-Ganz catheter. Spirography, flow-volume curve, closing-volume curve and pulmonary diffusion capacity were measured and aortic blood gas analyzed to assess pulmonary function. Esophageal endoscopy was used to diagnose the presence or absence of esophageal varices.
The results showed that the group of liver cirrhosis patients featured elevated WHVP and a hyperhemodynamic pattern and a positive correlation between WHVP on the one hand and cardiac index and right left ventricle stroke work indexes on the other; there was a negative correlation between WHVP and the systemic vascular resistance and pulmonary vascular resistance indexes. The results showed an increase in oxygen consumption in the group of patients with esophageal varices. In all chronic hepatitis cases, findings were normal. Pulmonary function was characterized by abnormal %VC, PaO₂, and pulmonary diffusion capacity in both groups along with abnormal PaCO₂ in the liver cirrhosis group; no significant differences were noted between the two groups.
These results indicate that liver cirrhosis elevates intarahepatic pressure, affecting systemic hemodynamics and resulting in a circulatory distribution disorder, leading to right and left ventricle overload and a decline in potential cardiac function. The results also indicated that mild pulmonary function disorder can occur as early in a state of chronic hepatitis.

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Histopathological changes in alcoholic liver disease are characterized by Mallory body, fatty liver, and peculiar fibrosis such as pericentral fibrosis, pericellular fibrosis, stellate fibrosis originating from Glisson's sheath, and swelling of the liver cells. However, the mechanism of fibrosis remains unknown.
The author tried to demonstrate, by the immunohistochemical method, fibronectin (FN), collagen type I, III, IV (IC, IIIC, IVC), factor XIIIa, and factor VIII related antigen (VIII RAg), all of which are related to the process of wound healing, in order to clarify the mechanism of fibrosis in alcoholic liver disease.
With the progress of fibrosis, FN was demonstrated in the sinusoidal wall, as well as the portal areas and around the central veins. IC and IIIC were positive in the fibrotic area extending into the lobules and pericellular fibrosis. IVC was similar to FN and was positive in the sinusoidal wall. Scattered XIIIa positivity was recognized in the fibrotic areas, especially in the foci of active fibrosis. VIII RAg was positive in the capillary vessels invading the lobules through the limiting plates. The distribution of these proteins in the fibrotic area in alcoholic liver disease closely resembled that in the wound healing process.
It is concluded that fibrosis occurring in the periportal area is essentially the same as in the wound healing process and the mechanism of fibrosis in alcoholic liver disease is thought to be active fibroplasia.

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In period of April, 1982 to March, 1987 for 5 years, fifty-four patients with superficial bladder tumors were treated at the Department of Urology, Nippon Medical School. There were 42 males and 12 females with age ranged from 28 to 85 years old. All patient underwent TUR-Bt (trans urethral resection-bladder tumor) as an initial treatment. The rather long term follow-up study after initial treatment was 47 months in average.
Recurrence rate at 2 years after TUR-Bt was 30%. The risk factors of recurrence were analysed in connection with sex, age, tumor number, histological grade and stage, and infiltration pattern.
In conclusion, significantly higher recurrence rate were observed in G2 than G1 and G3, and in pT1b rather than pTa and pT1a. Other factors were not distinctly correlated with incidence of recurrence.

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[in Japanese]

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[in Japanese]

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