[Localization and nature of retinal A-antigen].
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Biomedical subjects
Publications and source records attributed to S Takano.
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The authors reported 4 cases with preoperative diabetes insipidus (DI) following the rupture of cerebral aneurysms. In addition, the incidence of preoperative DI and the mechanisms as the cause of DI in cases with the ruptured cerebral aneurysms were also discussed. In the 114 cases underwent clipping of the ruptured cerebral aneurysms more than 14 days after the bleed, only 4 cases (3.5%) developed DI preoperatively. The time period between last subarachnoid hemorrhage and the onset of DI ranged from 23 to 35 days. This delayed onset of DI after subarachnoid hemorrhage was different from previous reports. A few of mechanisms had been suggested through which DI could be brought about in cases with cerebral aneurysm. That is; direct compression to the hypothalamo-hypophysial system by a giant aneurysm. compression and destruction of the hypothalamus by a hematoma or hemorrhage, ischemic changes in the hypothalamo-hypophysial system caused by vasospasm. In the present 4 cases, no had giant aneurysms. Although CT scan revealed subarachnoid clot in all cases, it did not show apparent hypothalamic lesion except case 1 who had small hematoma in the region of the basal frontal interhemispheric fissure. Symptomatic vasospasm was recognized in 3 cases. However, one of them had mild vasospasm restricting in M1 portion and case 3 was free of any vasospasm. Furthermore, the time period from the identification of vasospasm until the onset of DI ranged from 2 to 3 weeks. These results suggest that another mechanism in addition to a hemorrhage, hematoma and/or vasospasm may exist.(ABSTRACT TRUNCATED AT 250 WORDS)
The antitumor effect of a new synthetic cord factor analogue, 6, 6'-Di-O-dacanoyl-alpha, alpha-trehalose (SS 554), was examined in vivo and in vitro. Remarkable life prolongation effects were observed after the intraperitoneal administration of SS554 at a dosage of 150 mg/kg in mice implanted with Ehrlich ascitic tumor cells. Using in vitro tests, the growth of various tumor cell lines i.e. Meth-A, EL-4, RL male-1, X5563, Raji and Jurkat were inhibited by SS554 at a 25 mcg/ml concentration. The mechanism of the direct antitumor activity of SS554 was studied using these tumor cell lines and bacterial cells. After treatment with SS554 at a 50 mcg/ml dose for 30 minutes, tumor cells and bacterial protoplasts but not intact bacterial cells were destroyed, indicating that SS554 causes the lysis of the membranes of these cells.
The changes of colonic epithelial ornithine decarboxylase (ODC) activity and DNA synthesis following intrarectal administration of a tumor-promoting agent, 12-O-tetradecanoylphorbol-13-acetate (TPA), or various bile acids to male noninbred rats were studied. A single instillation of TPA, at a dose as low as 16 nmol, led to a significant (about 10-fold) increase in colonic ODC activity. Peak ODC activity was observed at 4 hr, and the enzyme activity returned to the control level about 24 hr after intrarectal TPA. This pattern was almost the same as that observed after sodium deoxycholate treatment. TPA showed more potent induction of ODC activity than deoxycholate, although the maximal induction was greater in the case of deoxycholate treatment. Both TPA and deoxycholate stimulated DNA synthesis at 2 days after intrarectal instillation, after an initial depression at 4-12 hr. A structure-activity study of 26 bile acids revealed that 5 beta-cholanoic acid with alpha-hydroxy groups in two of the 3 alpha, 7 alpha, 12 alpha positions and 5 beta-cholanoic acid with a 3 alpha-hydroxy group induced colonic ODC activity significantly, while the 3 alpha, 6 alpha-dihydroxy acid did not. Replacement of hydroxy groups by keto groups or a change from alpha to beta configuration decreased the ODC-inducing activities. Tri-substituted 5 beta-cholanoic acid derivatives, whether hydroxy or keto, did not stimulate ODC. These data indicate that a specific bile acid structure with a definite spatial relationship of the hydroxy groups is required for induction of colonic ODC activity.
The effect of hyperoxic or hypoxic inhalation on blood lipid levels and on the development of atherosclerosis was studied in young male WHHL rabbits. They were exposed to ordinary room air containing different concentrations of oxygen: 6 animals were exposed to 40% oxygen (hyperoxia group) or 5-10% oxygen (hypoxia group) for 5 h a day, 5 days a week for 8 weeks. Four control rabbits inhaled ordinary room air. The following results were obtained. (1) The severity of aortic lesions significantly decreased in the hyperoxia group and increased in the hypoxia group, when these two groups were compared. However, both hypoxic and hyperoxic groups did not statistically differ from the control. (2) Plasma cholesterol levels were not changed either by hyperoxic or hypoxic inhalation. (3) Plasma triglyceride levels were elevated only in the hypoxia group, with significant differences from the values in both control and hyperoxia groups. (4) There was no significant correlation between mean plasma lipid level and severity of aortic lesions. From these results, we conclude that hyperoxic or hypoxic inhalation respectively regresses or aggravates the development of atherosclerotic lesions, not by an indirect action on blood lipid concentrations but by a direct action on the vascular wall.
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A low-molecular-weight factor (less than 1000) which impairs the capacity of normal mice to resist Listeria infection has been isolated from the ascitic fluid of tumor-bearing mice. The factor showed potent suppressive activity when as little as 0.2 ml of 1:10(5) dilution of the factor was given iv to mice. The factor impaired stage 2 (72 hr after infection) of Listeria elimination in the liver when circulating monocytes migrate from the blood to the liver to begin eliminating the bacteria, but not stage 1 (within 24 hr after infection) when Listeria elimination depends on resident liver macrophages. The factor also inhibited macrophage accumulation in the peritoneum of mice after ip injection of phytohemagglutinin and macrophage chemotaxis in vitro. The factor was heat labile and lost its suppressive activity after being heated at 56 degrees C for 30 min. The factor was detectable in the ascitic fluid rather late after tumor implantation and its production was closely related to tumor growth.
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Localization of S-antigen was studied by a direct enzyme-labeled immunohistochemical method with light and electron microscopes. IgG was prepared from rabbits which were sensitized by swine retinal S-antigen and the IgG was conjugated with horseradish peroxidase (HRP). This HRP-labeled IgG was directly applied to normal rabbit retina and the retina was processed to make slides for light and electron microscopic examinations. In light microscopic findings, a clear-cut positive response was noted in the outer segment of photoreceptor cells which was similar to that of Wacker's observation, and a weak response was observed in the inner segment of the photoreceptor cells and the outer nuclear layer. In electron microscopic findings, immunoprecipitates, which were represented by electron-dense particles, were observed on both sides of the disk membrane of the outer segment with evenly distributed particles on both outer and inner surfaces, showing a pattern symmetric to that of the membrane. These immunoprecipitates were also noted in the plasma membrane of the outer segment but there they did not show a pattern similar to that of the disk membrane. A small amount of pinpoint-shaped immunoprecipitates were also noted in the cytoplasm of the inner segment and the connecting cilia. The immunoprecipitates were observed to gradually decrease in number with the phagocytosis of the outer segment by the retinal pigment epithelium, and they finally disappeared as fragments which were completely phagocytized. These findings may suggest a renewal process of S-antigen and a rationalization of this theory was discussed.
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The prevalence of mitral valve prolapse (MVP) was examined in 16 patients with right ventricular pressure overload with a peak systolic pressure ranged from 60 to 204 mmHg (Group 1; 9 cases of primary pulmonary hypertension and 7 cases of pulmonary valve stenosis), and the clinical and echocardiographic data were compared to those of 12 patients with idiopathic MVP (Group 2) and 10 healthy persons (Group 3). MVP was defined when either or both of the mitral valve leaflets protruded into the left atrium beyond the plane of the mitral ring, and "gap" was defined as positive when one of the leaflets of the mitral valve slipped 3 mm or more without prolapse toward the left atrium than the other leaflet. Eccentricity of the left ventricle was obtained from the cross-sectional view of the left ventricle at the mid-ventricular level: the ratio of the internal diameter (S) passing through the mid-point of the interventricular septum (IVS) and perpendicular to the IVS divided by the longest internal diameter (L) parallel to the IVS, at end-diastole (S/L(d] and at end-systole (S/L(s], respectively. The following results were obtained. MVP was found in seven cases of 16 patients (43.8%) of Group 1. Two cases had positive "gap" (12.5%). Eccentricity of the left ventricle in Group 1 (S/L(d) 0.81 +/- 0.12, S/L(s) 0.78 +/- 0.15) was more marked than that of Group 2 (S/L(d) 0.98 +/- 0.09, S/L(s) 1.02 +/- 0.06) or of Group 3 (S/L(d) 1.03 +/- 0.08, S/L(s) 1.00 +/- 0.04) (p less than 0.001 in each).(ABSTRACT TRUNCATED AT 250 WORDS)
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Solid tumors produced in mice by Ehrlich ascites cancer cells were completely regressed by treatment with the copolymer of polyriboinosinic acid-polyribocytidylic acid (poly (I):(C)) when 200 microgram of this compound was intravenously injected 3 times a week for 3-4 weeks, starting 7-8 days after transplantation of the tumor. Although the first injection of poly (I):(C) caused hyporeactivity to re-induction of IFN, the subsequent 6 doses stimulated the formation of IFN at 3685 units/ml on average after each injection, strongly suggesting that IFN plays a role in the antitumoral effect of poly (I):(C).
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We have investigated reproducible and quantitative thrombus formation in rat mesenteric arterioles using electrical stimulation under an inverted microscope. In vivo thrombi were formed in arterioles of 30-40 micrometers diameter by electrical stimulation using a tungsten electrode with a tip of 5 micrometers diameter. A "threshold" response was defined as one in which platelets adhered to the injured site of vascular wall and formed a white body which flowed away intermittently. The thrombus formations were classified into three stages: stage I, thrombi covering up less than 20% of the vessel lumen; stage II, when 20% to 40% of the lumen was covered; or state III, when more than 40% was covered. This preparation was demonstrated to be valuable for testing the potency of anti-thrombotic drugs if we performed the experiment within 2 hr after removing the mesentery from the peritoneal cavity which exposed it to air. PGl2, t a dose of 0.5 micrograms/100 g intravenously administered, inhibited the growth of the thrombus at stage II and III. PGE1, PGD2 and PGE2 had no effect at the same dose on these stages. The threshold response was significantly suppressed by both PGI2 and PGE1 at doses of 5 micrograms/100 g.
Effects of locally applied prostaglandins on platelet thrombus formation in the mesenteric arterioles of rats were studied in vivo. Prostaglandin (PG) I2 and PGE1, which were reported to be powerful inhibitors of blood platelet aggregation, prevented the thrombus formation, whereas PGE2, which was reported, in low concentrations, to enhance platelet aggregation, showed a tendency to promote the thrombus formation. PGA1, PGA2 or PGF2 alpha had no effect. PGD2 had a very weak inhibitory effect. As prostaglandins tested had no effect on the diameter of mesenteric arterioles, it is assumed that the effectiveness of PGI2 and PGE1 in preventing thrombus formation is due mainly to their powerful inhibiting effects on platelet aggregation.