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Biomedical subjects

Y Ono

Publications and source records attributed to Y Ono.

At least 1,027 records · Page 57Linked to original sources

Changes of n-hexane metabolites in urine of rats exposed to various concentrations of n-hexane and to its mixture with toluene or MEK.

It is well known that n-hexane produces peripheral neuropathy, and 2,5-hexanedione, one of the metabolites of n-hexane, is thought to be the main causative agent. Recently, the metabolites of n-hexane in urine have been measured by gas chromatography, and 2,5-hexanedione was proved to be useful for the biological monitoring of n-hexane exposure. In the present experiment, we intended to clarify the change of n-hexane metabolites in the urine of rats exposed to various concentrations of n-hexane and to its mixture with toluene of MEK. In the first experiment, five separate groups of five rats each were exposed to 100, 500, 1000, or 3000 ppm of n-hexane, or fresh air respectively in an exposure chamber for 8 h a day. Urinary samples were gathered during exposure, 16, 24, and 40 h after exposure. Half of each sample was analyzed by gas chromatography after hydrolysis with acid and enzymes, and the other half was analyzed without hydrolysis. 2,5-Dimethylfuran, MBK, 2-hexanol, 2,5-hexanedione, and gamma-valerolactone could be identified as n-hexane metabolites in the urine. The main metabolites were 2-hexanol and 2,5-hexanedione. 2-Hexanol was mostly excreted during exposure, while most of the 2,5-hexanedione was excreted after the end of exposure. The amount of metabolites in the urine correlatively increased with the concentration of n-hexane from 100 to 1000 ppm, but the amount of metabolites scarcely increased when the concentration of n-hexane increased from 1000 to 3000 ppm.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗

Antiallergic agents. 2. N-(1H-tetrazol-5-yl)-6-phenyl-2-pyridinecarboxamides.

A new series of N-(1H-tetrazol-5-yl)-6-phenyl-2-pyridinecarboxamides was prepared to determine the effects of substituents on the benzene and pyridine rings on antiallergic activity in the rat passive cutaneous anaphylaxis (PCA) assay after oral administration. One member of this series, N-(1H-tetrazol-5-yl)-4-methyl-6-[4-(methylamino)-phenyl]-2- pyridinecarboxamide (231), has an ED50 value of 0.8 mg/kg po and is 85 times more potent than disodium cromoglycate (DSCG) on intravenous administration. Further evaluation of 231 as a clinically useful antiallergic agent is in progress.

Animals↗

An experimental study of the combined effects of n-hexane and methyl ethyl ketone.

This study was intended to determine whether or not methyl ethyl ketone (MEK) enhances the neurotoxicity of n-hexane at low concentration and after long term exposure. Separate groups of eight rats were exposed to 100 ppm n-hexane, 200 ppm MEK, 100 ppm n-hexane plus 200 ppm MEK, or fresh air in an exposure chamber for 12 hours a day for 24 weeks. The body weight, motor nerve conduction velocity (MCV), distal motor latency (DL), and mixed nerve conduction velocities (MNCVs) were measured before exposure and after four, eight, 12, 16, 20, and 24 weeks' exposure. One rat of each group was histopathologically examined after 24 weeks' exposure. Exposure of 100 ppm n-hexane did not significantly decrease the functions of the peripheral nerve throughout the experiment. Exposure to 200 ppm MEK significantly increased MCV and MNCVs and decreased DL after four weeks' exposure, but at this later stage no significant changes were found throughout the experiment by comparison with the controls. Mixed exposure to 100 ppm n-hexane plus 200 ppm MEK significantly decreased by comparison with the controls. On histopathological examination of the tail nerve, however, no changes were found in any of the exposed groups or the controls. These results suggest that MEK might enhance the neurotoxicity of n-hexane at a low concentration, and mixed exposures to n-hexane and MEK should be avoided.

Animals↗

Prevalence of autonomic disturbances in diabetics as compared with non-diabetics and healthy subjects.

The prevalence of autonomic disturbances in diabetics was investigated using a direct questionnaire. Compared to non-diabetics and healthy subjects, diabetics had a much higher incidence of paresthesia in the limbs (41%) and impotence (66%). These two symptoms proved to be important in diabetic autonomic neuropathy. Other symptoms of autonomic disturbances in diabetics such as postural vertigo, abnormal sweating, diarrhea and constipation, abnormally cold or burning feet, itching, thirst, urinary bladder disturbance and libido decrease in females seemed to be non-specific for diabetic autonomic neuropathy. Paresthesia in the limbs, abnormally cold or burning feet, urine bladder disturbance and impotence were thought to be related to some degree to the duration, severity and complications of diabetes respectively.

Age Factors↗

Antibacterial activity of palmitoyltuberactinamine N and di-beta-lysylcapreomycin IIA.

Palmitoyltuberactinamine N (Pal-Tua N) and di-beta-lysylcapreomycin IIA (di-beta-Lys-Cpm IIA), which are synthetic derivatives of the antituberculous agent tuberactinomycin (Tum) and capreomycin (Cpm) respectively, were tested for anti-bacterial activity. Pal-Tua N inhibited not only tuberactinomycin-resistant Mycobacterium smegmatis but also Escherichia coli, Corynebacterium diphtheriae, Staphylococcus aureus, Streptococcus pyogenes, although it has lost activity against Mycobacterium tuberculosis. Di-beta-Lys-Cpm IIA inhibited the growth of laboratory-derived Tum-resistant M. smegmatis and M. tuberculosis as well as Tum-resistant M. tuberculosis from patients with one exceptional case.

Anti-Bacterial Agents↗

[Intraarterial high-dose adriamycin for patients with skeletal or soft tissue sarcoma].

In this paper, we summerized our experience with intraarterial high-dose adriamycin for thirteen patients with skeletal or soft tissue sarcoma. Eight patients had skeletal sarcoma and five had soft tissue sarcoma. Anticancer agents delivered intermittently an intra-arterial catheter (percutaneous placement by Sledinger technique) over 30 minutes. The compound of 1 mg of vincristine, 3 mg of Carboquone and 600 mg of dextran sulfate sodium was given weekly from the time of biopsy. Adriamycin was given at a dose of 0.8 mg/kg/day for 3 days after histological examination revealed sarcoma. Just prior to the adriamycin infusion, compound of 18,000 units of urokinase and 600 mg of dextran sulfate sodium was infused by bolous method. Course of therapy were repeated at every 3 to 4 weeks intervals. Surgical procedures were performed following completion of one to three courses of therapy. Total of 24 courses of therapy performed to 13 patients. Twelve patients had 20 courses preoperatively had three patients had 4 courses postoperatively. The overall objective clinical response rate (complete or partial response) by a combination of computed tomography and physical examination was 7/12 (58.3%). The overall histological response rate (greater than 75% tumor cell necrosis) was 4/9 (44.4%). During the period of follow up, with ranged from 2 to 60 months, none had local recurrence in the group performed radical operation (6 limb salvage procedures and 4 primary amputation). In this group one patient had lung metastases. The overall disease free survival rate was 8/10 (80.0%). In pharmacologic data from our series, adriamycin levels in venous blood adjacent to the arterially infused area were always higher than those from simultaneously sampled peripheral venous blood. Furthermore, peripheral blood levels of adriamycin following administration by the intraarterial route were not different from those obtained when the same dose is given intravenously. Our results of intraarterial high-dose adriamycin lend support and rationale to the use of regional intraarterial therapy even in patients with pulmonary metastasis. The latter will be exposed to a drug concentration expected from intravenous administration while the patient may also benefit from the augmented local effect.

Adolescent↗