LDL receptor activity of cultured arterial smooth muscle cells from genetically hyperlipidemic rabbits (WHHL-rabbit).
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Biomedical subjects
Publications and source records attributed to S Takano.
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A 13-year-old girl with Prader-Willi syndrome was admitted to our hospital with an 18-month history of anal bleeding and mucus discharge on defecation. Physical examination revealed obesity, hypogonadism, hypotonia and hypomentia. On digital examination, a nodular mass was palpated on the right wall of the ampulla recti, which was suspected to be carcinoma on a barium enema study. Proctoscopic examination revealed a large, irregular ulceration with white slough at the base, surrounded by the nodular and lumpy mucosa. The lesion was excised by the abdomino-anal pull-through method. The resected specimen showed a lesion of large, shallow, irregular ulcer, 5.0 x 2.2 cm in size. Microscopic examination revealed obliterated lamina propria by fibroblasts and muscle fibers derived from the muscularis mucosae, and misplaced cystic dilated glands in the submucosa at the margin of the ulcer. The gross and microscopic appearances are identical to those of "solitary ulcer of the rectum" described by Madigan and others, and similar to those of "colitis cystica profunda" described by Goodall and others. According to these findings, this lesion was diagnosed as solitary ulcer of the rectum. In the present report, the relationship between solitary ulcer of the rectum and colitis cystica profunda was discussed.
This study was performed to investigate the prophylactic effect of disopyramide phosphate on ventricular fibrillation in acute myocardial infarction. Lidocaine and disopyramide phosphate were compared in terms of their effects on the lowered ventricular fibrillation threshold in experimental myocardial infarction produced by coronary ligation in dogs. The following results were obtained: 1) The effect of lidocaine i.v. + infusion appeared promptly and the ventricular fibrillation threshold exceeded control levels from 45 min onwards (p less than 0.01). 2) The i.m. injection of lidocaine was effective in a dose of 10 mg/Kg. The minimally effective blood level was 1.7 mcg/ml. 3) Disopyramide phosphate 5 mg/Kg i.v. produced a tendency towards recovery from 15 min onwards. After 30 min, the ventricular fibrillation threshold was significantly higher than control (p less than 0.01). 4) Disopyramide phosphate 5 mg/Kg i.m. was initially effective after 45 min. The effect was significant from 1 hour and 30 min onwards, compared with control (p less than 0.01). The minimally effective blood level was 2.4 mcg/ml. 5) Disopyramide phosphate 2 mg/Kg i.m. produced a tendency towards recovery but the difference from the control was not significant. 6) In equivalent i.m. doses, disopyramide phosphate tended to be more potent than lidocaine in increasing the ventricular fibrillation threshold. 7) In the aforementioned doses, disopyramide phosphate did not cause any marked changes in PQ interval or QT time in ECG. These results suggest that the intramuscular injection of disopyramide phosphate is a hopeful clinical treatment to prevent ventricular fibrillation in the very early stages of acute myocardial infarction.
The present study was attempted to determine difference in effects of vinblastine and vincristine on ADP-induced aggregation of dog platelets. Vinblastine manifested biphasic influence depending upon concentrations, i.e., in low concentrations (0.2-20 micrograms/ml) it promoted the aggregation, and in a high concentration (100 micrograms/ml) it inhibited the aggregation with increasing incubation time. Vincristine in any concentrations, however, neither promoted nor inhibited the aggregation. In scanning electron micrographs, platelets were gradually damaged as revealed by their surface appearances with increasing incubation time in the presence of vinblastine (100 micrograms/ml). There existed a parallel relationship between the inhibition of the aggregation by vinblastine and the increase in number of severely damaged platelets. However, there was no such a parallel relationship between them in the presence of vincristine.
S antigen was isolated from human and bovine retinas and purified by two chromatographic steps. Its purity was controlled by SDS-electrophoresis and immunodiffusion. Seven Cynomolgus monkeys received a single subcutaneous immunization with either 50 or 100 micrograms of human S antigen (5 animals) or 100 micrograms of bovine S antigen (2 animals) with complete Freund's adjuvant. All the monkeys had bilateral uveoretinitis and anti-"S" antibodies were found in their serum. The time course of the disease was followed clinically during one year and pathologic features were described at various time intervals. The disease includes prominent retinal vasculitis and granulomatous chorio-retinitis, with a chronic course, and leads after many months to almost complete destruction of the retina, with persistence of inflammatory infiltrates and pigment of cell migration.
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The features of regional wall motion abnormalities of the left ventricle were analysed in 11 patients of congestive cardiomyopathy (CCM) in comparison with 22 patients of progressive muscular dystrophy (DMD) of Duchenne type who showed an abnormal motion of the left ventricle by echocardiography. Real time two-dimensional echocardiographic study demonstrated the following results: I) In CCM, (1) only 2 or less of 11 cases preserved a normal motion in each left ventricular segment, and the depression of wall motion of the left ventricle were thought to be generalized; (2) there were 9 cases with segmental wall motion abnormalities and 3 of them demonstrated ventricular aneurysms, and (3) the localizations of the segmental abnormalities varied in each case, and there was no apparent accumulation to any segments. II) In DMD, (1) all the cases showed depressed motions and 8 of them demonstrated a ventricular aneurysm in the posterior wall of the left ventricle (LVPW), (2) while, there was no case showing ventricular aneurysm in the segments other than LVPW, and about one third of all cases showed normal motion in those segments. From these results, we concluded as follows: 1) Although the depression of a wall motion of the left ventricle was generalized in CCM, this was not always uniform and the segmental abnormalities of a wall motion were frequently observed. The localization of the most severely disturbed segment varied in each case. 2) On the other hand, in DMD, the wall motion was disturbed more frequently and more severely in LVPW than in other ventricular segments.
The responses of male noninbred rat colonic epithelial ornithine decarboxylase (EC 4.1.1.17) (ODC) and S-adenosyl-L-methionine decarboxylase (EC 4.1.1.50) (SAMD) activities following topical administration of N-methyl-N'-nitro-N-nitrosoguanidine (MNNG) or bile salts were studied. A single intrarectal installation of 13 mumol of MNNG resulted in a significant (p < 0.001) 20-fold peak ODC activity after 4 hr, with a prompt return to control levels by 12 hr. Stimulation of SAMD activity was less pronounced but significant (p < 0.01), with a broad 2-fold peak over controls. No significant responses of colonic epithelial enzyme activities were detected following a single intrarectal instillation of N-methyl-N'-nitroguanidine, a noncarcinogenic and nonmutagenic metabolite of MNNG, at a dose equimolar to that of MNNG. Bile salts significantly (p < 0.001) induced ODC with almost the same kinetic pattern as that observed after MNNG administration in the following order: sodium deoxycholate > sodium chenodeoxycholate > sodium cholate. Activations of SAMD were similar for these 3 bile salts. Glycine- or taurine-conjugated deoxycholate showed ODC and SAMD enzyme activations similar to that of nonconjugated deoxycholate. No significant enzyme response was seen after sodium dehydrocholate treatment. Stimulation of activities of both enzymes was directly dependent on bile salt dose. Induced ODC and SAMD activities were principally localized in colonic epithelium. Deoxycholate-stimulated enzyme activities were significantly inhibited by cycloheximide. Enzyme stimulations by active compounds were accompanied by morphological changes such as mucosal cell degeneration, mucus depletion, submucosal congestion, and punctate hemorrhage, followed by submucosal leukocytic cellular infiltration. These data support the concept that initiating and promoting events may be involved in colon carcinogenesis.
Influences of prostaglandin (PG)s on electrophoretic mobilities and aggregation of rabbit platelets were studied. The PGs studied (PGI2, PGE1, PGD2, PGF2 alpha, PGA2 and PGA1) had no effect on platelet electrophoretic mobility. However, both PGE1 and PGI2 in 0.3 and 3.0 muM inhibited ADP-induced aggregation and ADP-induced decrease in the mobility. PGD2 in 0.3 and 3.0, and PGE2 in 30 microM inhibited the aggregation but did not depress the ADP-induced decrease in the mobility. PGF2 alpha, PGA2 and PGA1 had no effect on the decrease in electrophoretic mobility and on the aggregation caused by ADP.
Effects of tiaramide, aspirin an indomethacin were studied on rabbit platelet aggregation in vivo and on platelet electrophoretic mobility. When tiaramide (6 mg/kg), aspirin (30 mg/kg) or indomethacin (1.3 mg/kg) was injected into the ear vein of rabbit during 60 sec, tiaramide only inhibited ADP-induced aggregation, 20 min after the injection. All three drugs prevented collagen-induced aggregation 20 and 120 min after the injection. Tiaramide and aspirin prevented aggregation 24 hours later. The inhibitory effects on the aggregation of tiaramide are presumably independent of prostaglandin synthesis, because malondialdehyde (a metabolite of PGG2) production was not influenced. Tiaramide reduced cyclic AMP levels in platelets after 20 min incubation, despite the ability of this agent to inhibit platelet aggregation. Tiaramide, aspirin and indomethacin per se has no effect on platelet electrophoretic mobility, while tiaramide prevented the decrease in the mobility produced by ADP. Tiaramide and aspirin also depressed the decrease in the mobility produced by collagen.
AmB/NCS combination therapy against cancer was evaluated. Six gastric cancer patients were treated in this manner, and 7 gastric cancer patients treated with NCS alone to serve as the control. AmB sirup was administered orally for 4 days before surgical operation. NCS was given intraveously at the onset of gastric surgery. Lesion tissues and healthy tissues were collected from each patient and the NCS titers were measured by bioassay. It was shown in the majority of the gastric cancer cases that the NCS levels in the lesion tissues were substantially higher than in the surrounding normal tissues, whereas in the gastric cancer patients who received NCS alone, no significant differences were found between the tissues.
The effects of bile from rabbits and deoxycholate on platelat aggregation and platelet morphology were studied. (1) Bile diluted to 1.25%, as well as 0.1% deoxycholate, significantly inhibited ADP-induced aggregation (p less than 0.01). (2) Ring-shaped platelets were observed in preparations treated with bile containing high concentrations of deoxycholate. These platelets lacked the center portion, but maintained the circumferential band of microtubules as revealed by scanning and transmission electron microscopy.
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Two cases of fracture of the penis are reported. Early surgical repair of laceration of the corpus cavernosum brought about excellent results.