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Biomedical subjects

H Kishi

Publications and source records attributed to H Kishi.

At least 235 records · Page 13Linked to original sources
PubMed1979

Thiamin and pyridoxine requirements during intravenous hyperalimentation.

Studies were undertaken to determine rational dosages of vitamin B1 and B6 during long-term intravenous hyperalimentation, using more sensitive techniques than formerly used to evaluate B1 and B6 status. A standard vitamin combination, type A, (usually commercially available products) has been used up to now because of convenience, disregarding the effects of long-term administration. This combination lacks biotin, folic acid, and vitamin E and contains from 10 to 100 times the dietary allowances of such vitamins as B1, B2, B6, B12, and C. In response to the possibility of vitamin overdose, two new vitamin combinations, type B (from commercial products) and type C (a convenient and easily administered combination produced at the hospital) were developed in order to provide the normal dietary allowances and at the same time eliminate any harmful side-effects. From the results obtained, 5 mg/day for thiamin HCl and 3 mg/day for pyridoxine HCl in type B and type C were found to be a sufficient and safe level as opposed to 55 mg/day for thiamin HCl and 102 mg/day for pyridoxine HCl in type A.

Adult↗
PubMed1978

Levels of the glutamic oxaloacetic transaminase of erythrocytes of pregnant women and of cord bloods of newborn infants.

The mean basal specific activity (S.A.) of the glutamic oxaloacetic transaminase of erythrocytes (EGOT) for a group of 64 pregnant women was lower (p less than 0.001) than the value for the cord bloods of newborn infants, and lower (p less than 0.001) than the value for adults who had a top limit of S.A. of EGOT. In establishing the top limit of the S.A., it is important that the mean basal S.A. of the cord bloods from 49 newborn infants was identical to the mean basal S.A. of adults who had an adequate supplement of pyridoxine. There were no differences in the mean basal S.A.'s of the cord bloods between asymptomatic mothers and mothers who had anemia, edema, hypertension, proteinuria and glucosuria. An infant may be born with a top limit of S.A. which is non-deficient in pyridoxal 5'-phosphate, but a mother can have a low level of the transaminase, and which is deficient in the coenzyme.

Aspartate Aminotransferases↗
PubMed1977

Deficiency of vitamin B6 in women taking contraceptive formulations.

The specific activities (S.A.) of the glutamic oxaloacetic transaminase from erythrocytes (EGOT) of 75 women taking 16 diversified contraceptive formulations were determined by the principle (CAS) of unsaturation and saturation of receptors of the Coenzyme-Apoenzyme-System with the coenzyme, pyridoxal 5'-phosphate. 52 women were not taking pyridoxine; 20 were taking 1-5 mg; 3 were taking 25-100 mg. The mean basal S.A. of the 52 women without pyridoxine was lower (p less than 0.01) than for the 20 on 1-5 mg. The mean basal S.A. for the women on 25-100 mg was higher (p less than 0.01) than for the women without pyridoxine. The mean % deficiency for the women on 25-100 mg was negligible and lower (p less than 0.01) than 18+/-8 for the 52 women, and 14+/-6 for the 20 women. These data indicate that 1-5 mg of pyridoxine is inadequate for women on contraceptives. The requisite daily dosage is projected at 50-100 mg. Other data indicate that 5-12 weeks of supplementation with pyridoxine can be required to reach a stable "ceiling" of S.A. of EGOT. This period indicates some regulatory mechanism by diminished levels of the apoenzyme upon gene expression to bring about normal levels of the transaminase.

Adolescent↗
PubMed1976

Improved and effective assays of the glutamic oxaloacetic transaminase by the coenzyme-apoenzyme system (CAS) principle.

Standardized and reliable methods have been devised to assay preparations of the glutamic oxaloacetic transaminase from human erythrocytes by the CAS principle, i.e., the unsaturation and saturation of the coenzyme (pyridoxal 5'-phosphate) of a Coenzyme-Apoenzyme System. This dual enzymic assay is effective to detect and measure human deficiencies of vitamin B6. A preferred procedure has been developed, particularly for individuals and for limited groups, but is also applicable to large groups. A simplified procedure, which emphasizes the statistical significance of difference between large groups was also developed. Lyophilized erythrocyte hemolysates appear stable for up to 7 days for simplified transportation.

Apoenzymes↗
PubMed1976

Bioenergetics in clinical medicine. XI. Studies on coenzyme Q and diabetes mellitus.

The activity of the succinate dehydrogenase-coenzyme Q10 reductase from 120 diabetic patients was significantly lower (P less than 0.001) and the per cent deficiency was significantly higher (P less than 0.001) than that of the controls. The diabetes of 37 patients was controlled by diet; the enzyme activity was lower (P less than 0.001) and the deficiency was higher (P less than 0.02) than for controls. In decreasing effectiveness, Dymelor, Glyburide, Phenformin and Tolazamide inhibited the COQ10-enzyme, NADH-oxidase. Tolbutamide, Glypizide, and Chlorpropamide were noninhibitory to succinoxidase and NADH-oxidase. Patients receiving Tolazamide and Phenformin showed a higher incidence (P less than 0.001 to P less than 0.05) of COQ10-deficiency than patients controlled by diet or normal controls. Certain diabetic patients controlled by diet may have a deficiency of COQ10 which may be enhanced by the inhibition by certain commonly used antidiabetic drugs of COQ10-enzymes. A deficiency of COQ10 in the pancreas could impair bioenergetics, the generation of ATP, and the biosynthesis of insulin.

Adult↗
PubMed1975

Integration of R plasmid Rts1 to the gal region of the Escherichia coli chromosome.

An R plasmid Rts1 was integrated into the gal region of the chromosome of Escherichia coli XA-7012 (galE) strain by the directed transposition technique. The integration of the Rts1 genome was confirmed mainly by conjugation studies and also by transduction experiments using phage P1. As a result, it was found that the integrated genome contained genes responsible for kanamycin resistance, conjugal transferability, and for autonomous replication. As reported previously, Rts1 is temperature sensitive in replication and inhibits the growth of the host at nonpermissive temperature. However, although a plasmid derived from the integrated Rts1 genome still demonstrates temperature sensitivity upon transfer and high level of kanamycin resistance, this plasmid no longer displays temperature sensitivity in replication and the inhibitory effect on the host. These results indicate that the temperature sensitivity of replication of Rts1 and its inhibitory effect on the host cell are due to the presence of a gene or gene cluster on the Rts1 genome and that the gene(s) is clearly discriminated from the one responsible for the temperature sensitivity of transfer.

Centrifugation, Density Gradient↗
PubMed1975

Bioenergetics in clinical medicine. II. Adjunctive treatment with coenzyme Q in periodontal therapy.

Eight patients under routine care for periodontitis received oral treatment with a form of coenzyme Q (7 / CoQ10 and 1 / hexahydrocoenzyme Q4). An unchanged plaque score showed the patients cooperated and were under plaque control. The periodontal score decreased (p less than 0.01) on CoQ treatment. Unexpectedly, the periodontal pocket depth decreased (P less than 0.05) on CoQ treatment since all patients were considered candidates for surgical intervention. Healing was so excellent 5-7 days post-biopsy that the biopsy sites were difficult to locate. The healing was viewed as extraordinarily effective. The mean value of the specific activities of the succinate dehydrogenase-coenzyme Q10 reductase of gingival biopsies increased (P less than 0.05) during treatment which could correlate with the extraordinarily healing. Treatment of periodontitis with coenzyme Q should be considered as adjunctive treatment with current dental practice.

Adult↗
PubMed1975

Bioenergetics in clinical medicine. III. Inhibition of coenzyme Q10-enzymes by clinically used anti-hypertensive drugs.

Background data revealed that some American and Japanese patients with essential hypertension, including many who were not being treated with any anti-hypertensive drug, had a deficiency of coenzyme Q10. Eight clinically used anti-hypertensive drugs have now been tested for inhibition of two mitochondrial coenzyme Q10-enzymes of heart tissue, succinoxidase and NADH-oxidase. Diazoxide and propranolol significantly inhibited the CoQ10-succinoxidase and CoQ10-NADH-oxidase, respectively. Metoprolol did not inhibit succinoxidase, and was one-fourth as active as propranolol for inhibition of NADH-oxidase. Hydrochlorothiazide, hydralazine, ans clonidine also inhibited CoQ10-NADH-oxidase. Reserpine did not inhibit either CoQ10-enzyme, and methyldopa was a very eak inhibitor of succinoxidase. The internationally recognized clinical side-effects of propranolol may be due, in part, to inhibition of CoQ10-enzymes which are indispensable in the bioenergetics of cardiac function. A pre-existing deficiency of coenzyme Q10 in the myocardium of hypertensive patients could be augmented by subsequent treatment with propranolol, possibly to the "life-threatening" state described by others.

Animals↗