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Biomedical subjects

A Endo

Publications and source records attributed to A Endo.

At least 199 records · Page 11Linked to original sources
PubMed1990

[Tissue culture course of a human hepatoma cell line].

A cell line, HuH-33 was cultured in vitro from a patient with hepatocellular carcinoma. This cell line has been in continuous culture over 12 month period with slow growth potential. HuH-33 was composed spindle-or polygonal-shaped cells as a major population. Chromosome number of the cells were widely distributed even in the primary culture. HuH-33 was transplantable into nude mice and secreted alpha-fetoprotein, albumin, beta 2 microglobulin, ferritin and tissue polypeptide antigen.

Aged↗
PubMed1989

Effects of non-24-hour days on reproductive efficacy and embryonic development in mice.

ICR female mice were exposed to either 22 (L11, D11) or 26 hour day (L13, D13) light/dark cycles for at least 2 weeks before mating and/or during pregnancy. The mating rates of these animals decreased considerably. When pregnant females were examined at gestation days 12.0 or 17.5, resorption rates were increased, the embryos weighed less, and development was retarded in the experimental groups with preconceptional exposure to non-24-hour days. We speculate that in mice maternal and paternal pre- and periconceptional environment of daily light/dark cycles is important for normal reproductive efficacy and normal embryonic development during pregnancy.

Animals↗
PubMed1989

Sex difference in digit and palate formation of mouse embryos at midgestation.

We investigated whether there is a difference in timing between the sexes of mouse embryos with regard to digit and palatal formation at midgestation by using a simple method of sex chromatin analysis for rodent embryos. At day 14.4 of gestation, although the mean body weight of male embryos was greater than that of female embryos, digit and palatal formation of female embryos was found to be more advanced than in males when compared according to their body weight. This was contrary to our previous finding of digit formation at the earlier stage (day 12.0 of gestation): namely, that digit development was more advanced in male embryos than in female embryos even when two sexes were compared according to their body weight. Thus, the development of female embryos catches up with that of male embryos at the later stages of midgestation. The period for digit development must be longer in male embryos than in female embryos. If mothers are exposed to some teratogens, a sex difference in incidence of digital defects might be produced.

Animals↗
PubMed1989

Teratogen susceptibility of XO mothers and XO embryos in mice.

We examined whether the chromosomal imbalance inherent in an XO constitution in mice is more susceptible to teratogenic influence of biotin deficiency using a newly established mouse colony with pure X monosomy. We hypothesized that XO mothers or XO embryos might be more susceptible to certain teratogens. Contrary to our expectation, the incidence of external malformations induced by biotin deficiency did not differ either between XX dams and XO dams or between XX fetuses and XO fetuses.

Animals↗
PubMed1989

Biochemical aspect of HMG CoA reductase inhibitors.

Subsequent to the discovery of compactin (ML-236B) as a specific inhibitor of HMG CoA reductase, a series of compactin analogs have been either isolated or synthesized. Several of these compounds, which include compactin, mevinolin (monacolin K) and CS-514, have been extensively studied. The inhibition of HMG CoA reductase by these compounds is reversible and competitive (Ki = approximately 1 nM). The 3', 5'-dihydroxypentanoic acid portion of the acid form of compactin analogs, which resembles the HMG portion of HMG CoA, plays a crucial role in inhibitory activity. These inhibitors block sterol synthesis both in cultured mammalian cells and in animals. Strong inhibition of sterol synthesis results in a marked increase in HMG CoA reductase activity both in vitro and in vivo. These compounds strongly lower plasma LDL-cholesterol levels in animals and humans. The lowering of LDL-cholesterol levels occurs by an inhibition of LDL synthesis and/or by an elevation of the receptor-mediated LDL catabolism in the liver.

Animals↗
PubMed1989

Species and strain differences in teratogenic effects of biotin deficiency in rodents.

The teratogenicity of maternal biotin deficiency of mice, rats and Syrian hamsters was compared. Biotin deficiency during pregnancy caused severe malformations and growth retardation in mouse fetuses. The malformations were mainly cleft palate, micrognathia, micromelia and open eyelid. The ICR and C57BL strains of mice were more susceptible than the A/Jax strain to biotin deficiency. In rats, no malformations were seen in the fetuses from biotin-deficient dams. In hamsters, embryonic lethality was very high in biotin-deficient dams, and teratogenicity of biotin deficiency was rather equivocal. The results of measurements of the maternal and fetal biotin content suggest that a possible underlying mechanism is a difference in the efficiency of the mother-to-fetus transport of biotin among these species.

Animals↗
PubMed1989

A case of X-trisomy in the mouse.

An X-trisomy individual, which was found in the phenotypically normal female offspring of an XO mouse, is described. This mouse was infertile, and the ovaries were small and contained only primordial and primary follicles.

Animals↗
PubMed1989

Alkaline phosphatase expression in human cell lines derived from primary hepatomas.

Isozyme patterns of alkaline phosphatase (ALP) were electrophoretically examined in human cell lines derived from one hepatoblastoma, five hepatocellular carcinomas (HCCs) and two cholangiocellular carcinomas. Most of the cell lines tested had a liver-type ALP isozyme. In addition, an abnormal ALP isozyme, which was similar to variant ALP, was detected in one hepatoblastoma and two HCC cell lines. One HCC cell line of these variant-like ALP-positive cell lines was alpha-fetoprotein (AFP)-negative. These findings suggest that variant-like ALP may be useful for the identification of human hepatoma cell lines, especially in AFP or albumin-negative cell lines.

Alkaline Phosphatase↗
PubMed1989

The effect of complexing phosphoproteins to decalcified collagen on in vitro calcification.

Decalcified samples of chicken bone containing phosphoproteins of varying concentrations were used to assess the effect of phosphoproteins and of protein-bound Ser(P) and Thr(P) in the in vitro nucleation of a Ca-P solid phase from metastable solutions of Ca and P. Phosphoproteins of bone as well as the phosphoproteins from egg yolk (phosvitin) were used. Increasing concentrations of phosphoprotein [as measured by the amount of protein bound Ser(P) and Thr(P)] in the decalcified bone particles significantly reduced the time required for nucleation to occur after exposure to metastable solutions of Ca and P (decreased operational lag times). Treatment with wheat germ acid phosphatase markedly reduced the concentration of Ser(P) and Thr(P) in the decalcified bone samples and in the decalcified bone collagen samples complexed with phosphoproteins (almost to zero). The loss of the organic phosphate groups significantly increased the operational lag time, but did not abolish nucleation of apatite crystals by the bone collagen fibrils essentially devoid of Ser(P) and Thr(P). Bone phosphoproteins were not specific; substitution of phosvitin for bone phosphoproteins as complexes with bone collagen also proved to be effective facilitators of nucleation, which was interesting since both types of phosphoproteins have certain common chemical and structural characteristics. Noncollagenous components other than phosphoproteins were present in the decalcified bone samples. However, the marked dependence of the lag time on the Ser(P) and Thr(P) concentrations and the very marked diminution in the efficacy of the nucleation phenomenon as a result of treatment with wheat germ acid phosphatase, clearly suggests that the organic phosphate residues of the phosphoproteins play a direct and significant role in the process of in vitro nucleation of a solid phase of Ca and P (apatite) by bone collagen, and by implication, possibly in in vivo mineralization as well.

Acid Phosphatase↗
PubMed1989

Biosynthesis of monacolins: conversion of monacolin L to monacolin J by a monooxygenase of Monascus ruber.

The microbial metabolites monacolins J and L are specific inhibitors of 3-hydroxy-3-methylglutaryl CoA reductase, the rate-limiting enzyme in cholesterol synthesis. The producing strain Monascus ruber M 4681 was found to convert exogenously added monacolin L to J. In this hydroxylation reaction 18O2 was incorporated into monacolin L, giving [18O]-monacolin J. The cell-free extracts of M. ruber quantitatively hydroxylated monacolin L to J, and molecular oxygen was required for the hydroxylation. The enzyme was located in the microsomal fraction and specific for NADPH. The enzyme activity was inhibited by metyrapone, carbon monoxide, sulfhydryl reagents and cytochrome c. The results indicate that monacolin L is the precursor of monacolin J, and that a monooxygenase is involved in this reaction.

Ascomycota↗
PubMed1989

[Studies on AFP-producing capacity and some other properties of human hepatoma cells treated with various anticancer drugs].

The effect of various anticancer drugs on alpha-fetoprotein (AFP) secretion and some other properties of human hepatoma cells was investigated in vitro with the following results. (1) There was a high correlation between AFP secretion and cell number after treatment of human hepatoma cells with anticancer drugs and the amounts of AFP secreted per 10(4) cells per 72 hours (AFP-secreting capacity) were not affected within therapeutically achievable concentrations (TAC). (2) The AFP-secreting capacity was affected with some exceptions in the cells treated with higher concentration of drugs than TAC. Furthermore, chromosomal and morphological aberrations in the similarly treated cells, were also observed, suggesting the relationship between the change of AFP-producing capacity and that of some other properties.

Antineoplastic Agents↗
PubMed1989

[A case of apnea during spinal anesthesia after intravenous injection of sedatives].

During spinal anesthesia for appendectomy (sensory level: -Th7), apnea occurred for about 20 minutes by intravenous administration of diazepam. Since the patient showed hyperventilation sign before the incident, this apnea might be caused by low PaCO2 and stopping respiratory stimulation from psychological unrest when diazepam, pentazocine and droperidol were administered. In the postoperative period, this patient showed normal neurologic and psychosomatic functions. In such a case as this, long duration of apnea might damage brain by severe hypoxia. Apnea after hyperventilation during spinal anesthesia as observed in this case could lead to a serious accident.

Adult↗
PubMed1989

[A case of WPW syndrome with slow Kent documented by ATP injection].

A 46-year-old woman with chest tightness and palpitation at exercise was admitted to Sapporo Medical College Hospital for the evaluation of the ST-T changes on stress electrocardiogram. In this patient, PQ time was 0.14 second and pre-exitation was not clearly documented on electrocardiogram at rest. Bolus injection of 10 mg of adenosine-5'-triphosphate (ATP) demonstrated deltawave through the elongation of antegrade conduction of atrio-ventricular (AV) node. Electrophysiological study also showed left lateral accessory pathway with slow antegrade conduction, slow Kent. Stress 201-T1 myocardial scintigraphy using bicycle ergometer did not show the existence of ischemic region in spite of the ST-T changes on electrocardiogram. In this case, it seemed that a false positive ST-T changes might be caused by ventricular pre-exitation through slow Kent fiber. From these findings, it was suggested that the transient interruption on conduction through AV node by ATP bolus injection may be a useful diagnostic method in borderline pre-exitation syndrome.

Adenosine Triphosphate↗
PubMed1988

Chemistry, biochemistry, and pharmacology of HMG-CoA reductase inhibitors.

After an extensive searching for a microbial product that inhibits cholesterol synthesis, compactin and a series of related metabolites like monacolin K (mevinolin) have been isolated from molds as active agents. These compounds, which were structurally related to hydroxymethylglutaryl coenzyme A, were potent competitive inhibitors of hydroxymethylglutaryl coenzyme A reductase, the rate-limiting enzyme in cholesterol synthesis. The inhibition was reversible and the inhibitor constant Ki for compactin was around 10(-9) M. Compactin inhibited cholesterol synthesis in mammalian cells at 10(-9) M. Sterol synthesis in vivo was also reduced when compactin was given orally to rats at a dose of 50 mg/kg. Hydroxymethylglutaryl coenzyme A reductase activity of both cultured cells and rat liver was elevated when sterol synthesis was strongly inhibited by compactin. Both the growth inhibition and reductase induction could be overcome by the presence of mevalonate. A compactin-resistant cell line of mouse FM3A cells, called CR200, was developed by stepwise selection. CR200-cells had an abnormally high level of reductase activity and amplified reductase gene. Compactin was not able to lower plasma cholesterol levels in mice, rats, and hamsters. However, it was highly effective in rabbits, dogs, and monkeys; plasma cholesterol of dogs was reduced by 30%-40% at a dose of 20-50 mg/kg. The low-density lipoprotein cholesterol, which is responsible for atherosclerosis, was preferentially lowered. Compactin was also highly effective in hypercholesterolemic patients at a small dose. The results of the current studies have proved that compactin and related compounds are far more effective in lowering plasma cholesterol than any other drugs available.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1988

Inactivation of rabbit muscle glyceraldehyde-3-phosphate dehydrogenase by koningic acid.

Koningic acid, a sesquiterpene antibiotic, is a specific inhibitor of the enzyme glyceraldehyde-3-phosphate dehydrogenase (D-glyceraldehyde-3-phosphate:NAD+ oxidoreductase (phosphorylating), EC 1.2.1.12). In the presence of 3 mM of NAD+, koningic acid irreversibly inactivated the enzyme in a time-dependent manner. The pseudo-first-order rate constant for inactivation (kapp) was dependent on koningic acid concentration in saturate manner, indicating koningic acid and enzyme formed a reversible complex prior to the formation of an inactive, irreversible complex; the inactivation rate (k 3) was 5.5.10(-2) s-1, with a dissociation constant for inactivation (Kinact) of 1.6 microM. The inhibition was competitive against glyceraldehyde 3-phosphate with a Ki of 1.1 microM, where the Km for glyceraldehyde 3-phosphate was 90 microM. Koningic acid inhibition was uncompetitive with respect to NAD+. The presence of NAD+ accelerated the inactivation. In its absence, the charcoal-treated NAD+-free enzyme showed a 220-fold decrease in apparent rate constant for inactivation, indicating that koningic acid sequentially binds to the enzyme next to NAD+. The enzyme, a tetramer, was inactivated when maximum two sulfhydryl groups, possibly cysteine residues at the active sites of the enzyme, were modified by the binding of koningic acid. These observations demonstrate that koningic acid is an active-site-directed inhibitor which reacts predominantly with the NAD+-enzyme complex.

Animals↗
PubMed1988

Individual and strain differences in patterns of long-term persistence of urethane-induced sister chromatid exchanges (SCEs) in mouse lymphocytes and their relation to carcinogen susceptibility.

Using an improved microculture method, we investigated how the patterns of persistence of urethane-induced SCEs in lymphocytes differ among individuals and strains of mice (the ddY and C57BL strains), and we attempted to speculate on their relationship to carcinogen susceptibility. After a single intraperitoneal (i.p.) injection of 900 mg/kg of body weight of urethane into ten female mice each for the two strains, blood samples for the SCE analysis were collected from the tail vein at ten times during the 180 posttreatment days for each individual. Immediately after the treatment, SCE values increased to about three to four times the spontaneous values in all of the animals tested and then fell gradually. (The difference from spontaneous values was statistically significant until 120 days after the treatment.) Even after 180 days, however, some "outlier" cells with exceptionally high SCEs (greater than 20) persisted. Although there was some difference in average SCEs between the ddY and C57BL strains, the magnitude of the difference was too small to account for the difference between the strains in the incidence of urethane-induced malignancy. Also, when autopsy data at the 200th posttreatment day were matched individually with the data of SCE values within each strain, it was difficult to predict the individual risk of the occurrence of lung adenoma or other tumors from the relative difference in SCE values.

Adenoma↗