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Biomedical subjects

K Aihara

Publications and source records attributed to K Aihara.

At least 91 records · Page 5Linked to original sources
PubMed1988

Ultrastructural observation in clinical and experimental myocardial infarction, with reference to pathogenesis.

Electron microscopic investigation was carried out to confirm our hypothesis, derived from a large number of macroscopic and light-microscopic observations, that impairment of the peripheral circulation of the myocardium, and not the presence of coronary thrombi, plays the fundamental role in the development of acute myocardial infarction. The peripheral coronary vessels of 5 human hearts obtained at autopsy showed severe histolytic impairment of the endothelial cells and of the tunica media muscle cells, even though no myocardial necrosis was observed either macroscopically or microscopically. An additional experimental study using 12 rabbits was performed to ascertain the induction of myocardial necrosis without coronary occlusion, by intravenous administration of either epinephrine or endotoxin alone or a combination of both. One-third of the epinephrine group and all of the combined treatment group developed myocardial necrosis. The intramyocardial vessels of these rabbits showed similar hystolytic changes to those observed in human cases. These findings support our concept that derangement of the peripheral circulation precedes the development of a coronary thrombus in cases of acute myocardial infarction.

Animals↗
PubMed1988

Characterization and clinical study on the acellular pertussis vaccine produced by a combination of column purified pertussis toxin and filamentous hemagglutinin.

Bordetella Pertussis Tohama phase I was cultured in a 300-liter fermentor using a medium containing 0.1% heptakis (2,5-0-dimethyl) beta-cyclodextrin (MeCD). Pertussis toxin (PT) and filamentous hamagglutinin (FHA) were purified using affinity and ion exchange gel column chromatographies. Endotoxin contents of these antigens (10 micrograms PN/ml) were less than 10 ngLPS/ml. PT and FHA were independently treated with formalin in the presence of amino acid and were mixed at a protein concentration ratio of 1:4, the same ratio of our commercialized acellular pertussis vaccine. PDT vaccine containing 2 micrograms PN of PT and 8 micrograms PN of FHA per milliliter was prepared. This PDT vaccine satisfied all the items of the Japanese Minimum Requirements including potency and toxicity tests. Even after this vaccine was incubated for 4 weeks at 37 degrees C, no deaths of the inoculated mice were observed after challenge with 4 mg of histamine on the 4th and 12th day of the inoculation. Compared with the conventional vaccine, this new vaccine caused less swelling in the mouse footpad test. A field trial of our two vaccines, one manufactured by the conventional method (lot No. 21A) and the other produced by the new method (lot No. KC8702), revealed that children receiving KC8702 showed almost the same anti-PT and anti-FHA antibody levels as those given 21A. Those who received KC8702 suffered from less local side effects such as redness, swelling or induration than those given 21A. Our new method for the production of acellular pertussis vaccine permits us the economical manufacturing of the vaccine with uniform quality in a closed system.

Animals↗
PubMed1988

Chronic toxicity of muroctasin in mice.

The chronic toxicity of N2-[(N-acetylmuramoyl)-L-alanyl-D-isoglutaminyl]-N6-stearoyl-L-lysine (MDP-Lys(L-18), muroctasin), a synthetic muramyl dipeptide, was investigated in mice. Leukocytosis and immunologically activated appearances of splenic white pulp and lung were seen in mice, when treated with MDP-Lys(L18) for 26 weeks. Furthermore, inflammation around the injection site and synovial epithelium hyperplasia of the tarsal joint occurred in higher incidence in the high dose group. These changes were similar to those seen in the subacute toxicity study with mice.

Acetylmuramyl-Alanyl-Isoglutamine↗
PubMed1987

Effect of ONO-3144, a free radical scavenger, on reoxygenation injury in anoxic myocardium.

Thus, ONO-3144 treatment affords great protection against reoxygenation injury in the anoxic myocardium through the scavenging mechanism that includes .OH or closely related species of free radicals and also may inhibit thromboxane synthetase in the anoxic myocardium. We would hypothesize that free radical formation generated through the conversion of PGG2 to PGH2 should play an important role in the reoxygenation injury of the anoxic myocardium.

Adenosine Triphosphate↗
PubMed1986

Antithyroid effects of propylthiouracil and sulfamonomethoxine in rats and monkeys.

Experiments were performed to investigate the species difference in antithyroid effects of propylthiouracil (PTU) and sulfamonomethoxine (SMM). Sprague-Dawley rats were administered 30 mg/kg of PTU, or 30 or 270 mg/kg of SMM orally for 5 weeks, while squirrel monkeys received 30 mg/kg of PTU or 270 mg/kg of SMM. In rats receiving 30 mg/kg of PTU, a decrease of both serum 3,5,3'-triiodothyronine and thyroxine concentrations and of 131I incorporation into the thyroid hormone precursors was observed, together with elevation of serum thyroid-stimulating hormone concentration, an increase in thyroid weight, and hyperplasia of the follicular epithelium of the thyroid gland. Similar changes were seen in rats receiving 270 mg/kg of SMM; however, the antithyroid effects of SMM were less severe than those of PTU. No change was produced in monkey thyroids by 5-week treatments with 30 mg/kg of PTU or with 270 mg/kg of SMM. The molar concentration of PTU required for the in vitro inhibition of thyroid peroxidase was markedly lower in rats than in monkeys. SMM showed a similar species difference in the inhibition of thyroid peroxidase in vitro, but the enzyme inhibition of SMM was weaker than that of PTU. These findings suggest that rats were more sensitive to the antithyroid effects of PTU and SMM than monkeys, and that inhibition of thyroid peroxidase may play an important role in species difference in the antithyroid effects of the two drugs.

Animals↗
PubMed1986

HO-323, a human B-lymphoblastoid cell line useful for making human-human hybridomas.

A 6-thioguanine-resistant human B-lymphoblastoid cell line, HO-323, was isolated for making human-human hybridomas with high efficiency. Fusions with peripheral blood lymphocytes of systemic lupus erythematosus (SLE) patients and lymphocytes isolated from lymph nodes of lung and breast cancer patients yield constantly more than one hybridoma clones per 10(5) HO-323 cells plated. HO323 cells also fused with lymphocytes from normal peripheral blood to give hybridomas in the same efficiency. The HO-323 cells were diploid with 46 chromosomes and non-secretors of immunoglobulins. This parent cells doubled every 15 hr and could proliferate in serum-containing medium, even if they were plated at low cell density of less than 10(3) cells/ml. The cells could grow in serum-free medium as well as in serum-containing medium, and the resultant human-human hybridomas could also grow in the same media.

B-Lymphocytes↗
PubMed1986

Immunohistochemical localization of CA 125 antigen in formalin-fixed paraffin sections of ovarian tumors with the use of Pronase.

The OC 125 monoclonal antibody was used to localize CA 125 antigen in routine paraffin sections of ovarian tumors with the use of a modified avidin-biotin-peroxidase complex (ABC) technic. Pretreatment of the paraffin sections with Pronase allowed subsequent detection of CA 125 antigen. OC 125 stained 4 (80%) of 5 benign and borderline serous ovarian tumors, 12 (86%) of 14 serous adenocarcinomas, and 3 (23%) of 13 benign and malignant mucinous ovarian tumors. The pattern of distribution of CA 125 antigen was mostly at the intraluminal and peripheral cell surfaces, while intracytoplasmic staining also was seen. Overall, CA 125 antigen detectability rate in paraffin sections was found to be compatible with those reported in frozen sections. The method allows retrospective immunohistochemical examination of a large number of cases with ovarian tumors.

Antibodies, Monoclonal↗
PubMed1985

Trace elements (copper, zinc, manganese, and selenium) in plasma and erythrocytes in relation to dietary intake during infancy.

All determinations of copper, zinc, manganese, and selenium were performed with a flameless atomic absorption spectrophotometer. Seventy-three full-term infants aged 1 to 52 weeks were divided into three age groups. Each age group contained two subgroups, breast-fed and formula-fed. No statistically significant differences between formula-fed and breast-fed subgroups were found in regard to the levels of copper and zinc in plasma and erythrocytes. At 1 to 5 weeks of age, the manganese concentration of erythrocytes was higher in formula-fed than in breast-fed infants (p less than 0.001). This might be due to the high dietary intake of this element in the formula-fed subgroup. On the other hand, plasma selenium concentrations were significantly higher in breast-fed than in formula-fed infants of all ages (p less than 0.01 at 1 to 5 weeks and p less than 0.05 at 6 to 52 weeks). This suggests that selenium compounds are biologically more available for infant nutrition in breast milk than in formula.

Copper↗
PubMed1985

Zinc, copper, manganese, and selenium metabolism in patients with human growth hormone deficiency or acromegaly.

This study was designed to evaluate trace metal metabolism in patients with known abnormalities of human growth hormone (hGH). The mean concentration of zinc in plasma and urine decreased in patients with hGH deficiency after hGH injection, whereas, after adenomectomy, in patients with acromegaly, zinc increased in plasma, remained the same in erythrocytes, and decreased in urine. There was a negative correlation between plasma zinc and serum hGH levels and a positive correlation between urinary zinc excretion and serum hGH levels in acromegaly. In hGH deficiency, the copper content remained unchanged in plasma and erythrocytes and rose in urine after treatment; however, in acromegaly, the copper content increased in plasma and remained unchanged in erythrocytes and urine after surgery. The mean concentration of erythrocyte manganese did not change significantly after treatment in patients with hGH deficiency or acromegaly, but the pre-hGH treatment level of erythrocyte manganese in hGH deficiency was lower than in the controls. Plasma selenium concentrations were decreased in hGH deficiency and increased in acromegaly patients after therapy. These results suggest that hGH affects the metabolism of zinc, copper, manganese, and selenium.

Acromegaly↗
PubMed1984

Periodic and non-periodic responses of a periodically forced Hodgkin-Huxley oscillator.

Membrane potential responses of a Hodgkin-Huxley oscillator to an externally-applied sinusoidal current were numerically calculated with relation to bifurcation parameters of the amplitude and the frequency of the stimulating current. The Hodgkin-Huxley oscillator, or the Hodgkin-Huxley axon in the state of self-sustained oscillation of action potentials, was realized by immersing the axon in calcium-deficient sea water. The forced oscillations were analysed by the stroboscopic plots and/or the Lorenz plots. The results show that the periodically forced Hodgkin-Huxley oscillator exhibits not only periodic motions (harmonic or sub-harmonic synchronization) but also non-periodic motions (quasi-periodic or chaotic oscillation), that the motions were determined by the amplitude and the frequency of the stimulating current, and that the characteristic motions obtained in the present study were in reasonable agreement with those of our previous results, found experimentally in squid giant axons. Also, two kinds of routes to the chaotic oscillations were found; successive period-doubling bifurcations and formation of the intermittently chaotic oscillation from sub-harmonic synchronization.

Action Potentials↗
PubMed1984

Isolated growth hormone deficiency type 1A in a Japanese family.

A Japanese family is described in which a 7-year-old child had isolated growth hormone deficiency type 1A, as described by Illig et al. He was shown to be homozygous for a deletion of the structural gene for hGH (hGH-N gene). Initially his growth rate responded well to hGH administration, but rapidly he developed high titers of hGH antibodies, and growth ceased. At that time, a somatomedin-C generation test gave negative results, suggesting that the growth arrest was related to the inability of hGH to generate somatomedin. Both parents were heterozygous for the hGH-N gene deletion and had a low hGH response to arginine and L-dopa tolerance tests, but had normal basal somatomedin-C levels and normal somatomedin-C generation tests. This family is the fourth to be reported with IGHD type 1A caused by deletion of the hGH-N gene. This cause of growth hormone deficiency can be distinguished from other severe autosomal recessive types of hGH deficiency by the demonstration of the deletion of hGH-N gene using restriction endonuclease analysis.

Adult↗