Microbiological and thin-layer chromatographic identification of aminoglycoside antibiotics in animal body.
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Biomedical subjects
Publications and source records attributed to H Yoshimura.
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A typical lot of Kanemi rice oil ingested by patients with yusho (PCB poisoning) and the blood, liver and adipose tissue of the patients were analyzed for individual congeners of polychlorinated biphenyls (PCBs) and polychlorinated dibenzofurans (PCDFs) by gas chromatography and gas chromatography-mass spectrometry. The individual congeners identified were assayed for biological properties such as accumulation ability in the liver of monkeys and rats, inducing activities of benzo[a]pyrene 3-hydroxylase, benzphetamine demethylase and DT diaphorase in rats, and gravimetric changes of the thymus and liver in rats. Among the seven PCB congeners detected in yusho patients, 2, 3, 4, 5, 3', 4'-hexa-CB seems to be the most related compound to yusho by its strong effects on induction of the liver enzymes, and on atrophy of the thymus and hypertrophy of the liver in rats. PCDF congeners identified in the patients showed severe toxicity in rats than this PCB, exhibiting stronger enzyme induction and gravimetric changes of the tissues even at very low doses of 1-10 micrograms/kg. These PCDFs, especially 2, 3, 4, 7, 8-penta-CDF, were also very accumulative in the liver. Therefore, they are considered as the most important etiologic agents for current symptoms of yusho.
1. 8 alpha, 9 alpha-Epoxyhexahydrocannabinol (8 alpha, 9 alpha-EHHC) was formed from delta 8-tetrahydrocannabinol (delta 8-THC) by mouse liver microsomal preparation in the presence of an NADPH-generating system. 2. The epoxide was identified by t.l.c., g.l.c. and g.l.c.-mass spectrometry and, together with 11-hydroxy-delta 8-THC (11-OH-delta 8-THC), was determined by g.l.c. 3. When delta 8-THC was incubated with mouse liver microsomal preparation, 8 alpha, 9 alpha-EHHC and 11-OH-delta 8-THC was formed to the extents of 14% and 23%, respectively, of the added delta 8-THC.
The present study was conducted to investigate the effect of neonatal gonadal hormone treatments on the rat's emotionality in adult life. Female Sprague-Dawley rats treated subcutaneously on the day of birth with 100 micrograms of 17 beta-estradiol (E) or 1000 micrograms of testosterone propionate [TP] or 1000 micrograms of dihydrotestosterone[DHT] were tested in the open-field apparatus on 5 consecutive days at 6 months of age. All TP-treated rats and 6 out of 11 E-treated rats exhibited the persistent estrus on the vaginal smears, while DHT-treated rats and control rats did not show such changes in estrus cycle. Highly significant difference in either ambulation and defecation scores was found between persistent estrus and normal estrus cycle rats in E-treated group: persistent estrus rats showed higher ambulation and lower defecation than normal estrus cycle rats. As compared with the control level TP-treated persistent estrus rats showed a lower defecation score. These findings indicate that persistent estrus rats induced by E or TP are in the state of low emotionality. A possible relationship between the emotionality and the induction of mammary carcinomas was discussed.
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A 33 year-old woman was admitted with chief complaint of abdominal pain and high fever. A barium-enema showed serration and a tumor was seen in the proximal ascending colon. At laparotomy, a localized tumor about 5 cm in diameter was located in the proximal portion of the ascending colon. The operation was made according to the ileoceal resection. On the macroscopic examination of the resected specimen, a small hole penetrating into the subserosa of the ascending colon was noticed and a tumor measuring approximately 3 x 1.2 x 1 cm was located under the hole. A female worm, Trichuris trichiura, was found to be harbored in the adjacent site of the lesion. Histopathologic examination revealed granulomatous tissue reaction due to penetrating of Trichuris trichiura. The patient is in good health now 20 months after operation.
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Bilateral olfactory bulbectomy produced the increased tendency of mouse-killing behavior in nonkiller rats (60% on the 14th day after surgery). Scopolamine hydrobromide (4 and 8 mg/kg, IP) significantly suppressed the killing response in a dose-dependent manner, whereas methylscopolamine nitrate was ineffective. In order to investigate a possible neural mechanisms, choline acetyltransferase (CAT) and acetylcholinesterase (ACh-E) activities were measured in 7 discrete brain areas: cortex, amygdala, hypothalamus, thalamus, tegmentum, hippocampus, and pons plus medulla oblongata. Although the central anticholinergic drug suppressed mouse-killing, no significant difference in either CAT and ACh-E activities was found between the killer and nonkiller rats in any of the brain areas determined in this study. The evidence suggests that the neurochemical findings may not fit the pharmacological findings for supporting a unified cholinergic hypothesis for mouse-killing behavior.
Carbadox and olaquindox were examined for mutagenicities in the repair tests with Bacillus subtilis (rec assay) and Salmonella typhimurium (uvr assay) and in the reverse mutation test (TA100 and TA98 of S. typhimurium). Both compounds were positive in the rec and uvr assays, and were highly mutagenic for strains TA100 and TA98. Carbadox was about 6 times move mutagenic than olaquindox in the absence of S9 mix. When incubated in S9 mix or bacterial cytosol (BC) mix for various times at 37 degree C, carbadox was found to lose its mutagenic activities easier than olaquindox. The mutagenicity of carbadox was almost inactivated at 10 min after incubation with S9 mix, but olaquindox still retained its activities even at 20 min. While carbadox required 20 min to be inactivated in BC mix, olaquindox was not completely inactivated even if incubated for 60 min.
Three separate series of experiments were conducted as follows: isolation housing, bilateral olfactory bulbectomy, and delta 9-tetrahydrocannabinol (THC) administration. All three experimental manipulations produced an increase in the incidence of mouse-killing behavior. In order to elucidate the possible neural mechanisms mediating the killing response, norepinephrine (NE) content was measured in 6 discrete areas of the brain (the cortex, striatum, amygdala, midbrain, hypothalamus, and pons plus medulla oblongata). Following isolation housing, no significant difference in NE levels of any of the brain areas was demonstrated between the aggregated and isolated rats, nor between the killer and nonkiller rats. The rats with olfactory bulbectomy exhibited high NE content in the hypothalamus as compared with the intact or sham-operated rats, but there was no significant difference between the killer and nonkiller rats. After injections of THC, NE content in both the hypothalamus and pons plus medulla oblongata was decreased independent of the manifestation of killing response. The evidence indicates no regional change in brain NE levels specific to the killing response and suggests that brain NE may not participate in the mediation of mouse-killing behavior.
Two series of experiments were performed to differentiate the effects of d-amphetamine on social interactions from those on solitary motor behavior in adult and juvenile squirrel monkeys. In the first experiment, d-amphetamine (3x0.5 mg/kg, PO) induced pronounced stereotyped movements of the head, limbs and torso. When confronted in the colony room with an intruder monkey, the amphetamine-treated resident monkey showed reduced threat and attack behavior. In a separate test for affiliation, amphetamine nearly abolished the affiliative response toward a familiar group member. In a second series of experiments, d-amphetamine (0.3, 1.0 mg/kg, IM) decreased the affiliative behavior of juvenile monkeys towards their mothers; yet, in the presence of an unfamiliar adult male, the detrimental effect of amphetamine on affiliative behavior was prevented. Morphine (0.5, 2.0 mg/kg) increased the affiliative response toward the mother, and chlordiazepoxide (5, 10 mg/kg) was without effect in this situation. These observations suggest that amphetamine impairs a range of social behavior in adult and juvenile monkeys. The general disruption of agonistic and affiliative behaviors due to amphetamine appears to be based on mechanisms which differ from those mediating stereotyped movements. Stimulant-induced changes in social interactions in primates may be linked to disturbed affect.