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Biomedical subjects

A Endo

Publications and source records attributed to A Endo.

At least 127 records · Page 7Linked to original sources
PubMed1995

The molecular mechanism of the induction of the low density lipoprotein receptor by chenodeoxycholic acid in cultured human cells.

In a cultured human hepatoblastoma cell line, Hep G2, chenodeoxycholic acid (CDCA) induced LDL receptor mRNA levels approximately 4 fold and mRNA levels for HMG-CoA reductase and HMG-CoA synthase two fold. In contrast, the mRNA levels for mevalonate kinase, farnesyl pyrophosphate synthase and squalene synthase were not changed significantly. The pattern of the induction of the sterol-sensitive genes was similar to the induction by N-acetyl-leucyl-leucyl-norleucinal (ALLN), an SREBP degradation inhibitor, suggesting that CDCA may increase mature SREBPs. CDCA could inhibit the 25-hydroxycholesterol mediated inactivation of SREBP without affecting mRNA levels of SREBPs. These results suggest that CDCA can affect sterol metabolism by a novel mechanism involving the inhibition of the oxysterol-mediated inactivation of SREBP.

Alkyl and Aryl Transferases↗
PubMed1995

Combined effects of maternal age and delayed fertilization on the frequency of chromosome anomalies in mice.

Animal experiments indicate that both maternal age and delayed fertilization increase the incidence of chromosome errors in the offspring. In the present study, therefore, we examined how both factors act in combination. We set up normal (0 h delay) and delayed fertilization (6 h delay) subgroups in three different age groups (young, 3-4 months; middle-aged, 9-11 months; and old, 13-15 months), and compared the incidence of chromosome anomalies and other reproductive effects among them. Although the present study confirmed two previous findings that aneuploidies increase with advancing maternal age, and that polyploidies increase with delayed fertilization in mice, it was not clear whether maternal age and delayed fertilization affected the occurrence of aneuploidies either additively or multiplicatively.

Animals↗
PubMed1995

Characteristics of the chemical forms of 11C, 13N, and 15O induced in air by the operation of a 100 MeV electron linear accelerator.

To characterize airborne radioactivity induced by the operation of high-energy accelerators, the fractions of aerosol and gaseous components, and the chemical forms of 11C, 13N, and 15O produced in the air of a target room of a 100 MeV electron linear accelerator were studied. Measurements of radioactivity using a particulate air sampling filter and a gas flow-through ionization chamber showed that more than 98% of 11C, 13N, and 15O were present as gaseous forms. Their chemical forms, detected by means of radio-gas chromatography, were 11C as CO2; 13N as N2 and NO; and 15O as O2 and NO. Machine operating conditions, which affect the compositions of the induced radionuclides and of their chemical forms, and the resulting effect on the estimation of internal doses are discussed.

Aerosols↗
PubMed1995

Viability, development and incidence of chromosome anomalies of preimplantation embryos from XO mice.

We examined the viability and developmental status of XO embryos at preimplantation stage (day 3 of gestation) by assessing blastocyst formation and counting cell number using our XO mouse colony. We also examined the incidence of chromosome anomalies. Embryos from XO mice (XY, XX and XO) developed more slowly (in cell numbers and blastocoele formation) than those from XX mice (XY and XX). XO embryos also tended to develop more slowly than XX embryos in the XO group. Although litter size at the preimplantation stage of gestation was almost twice as large (12.7) as those at mid-gestation (7.6) and near-term (7.2) in this colony, the adjusted XY:XX:XO ratio (2.8:2.0:1.0) did not differ greatly. This indicates that almost half of the embryos must have been eliminated during the first half of gestation in the XO group, probably regardless of sex chromosome complements. Thus, we consider that maternal XO sex chromosome constitution is disadvantageous for the intrauterine development of the embryo during the early period of gestation. This may be related to precocious aging of XO mice. Further, we confirmed that a high incidence of abnormal karyotypes occurs in embryos from our XO mouse colony.

Animals↗
PubMed1995

Development of hypercalcemic crisis in a Graves' hyperthyroid patient associated with central diabetes insipidus.

A 26-year-old man with Graves' hyperthyroidism associated with central diabetes insipidus (DI), initially showed hypercalcemic crisis. Initially, very low serum levels of intact parathyroid hormone (PTH) and 1,25-dihydroxy vitamin D3 and a moderate rise of serum C-terminal PTH related protein (C-PTHrP) were observed which strongly suggested a humoral hypercalcemia of malignancy due to PTHrP. However, the serum C-PTHrP level later became normal. Mild hyperprolactinemia, no responses of growth hormone (GH) to insulin-induced hypoglycemia despite a normal growth hormone releasing hormone (GRH) test and mild thickening of the pituitary stalk on magnetic resonance imaging were observed. Thus, an autoimmune nature of his central DI is considered; it is noteworthy that the serum C-PTHrP level may be elevated by renal failure in patients with hypercalcemia due to causes other than PTHrP.

Acute Disease↗
PubMed1995

Inhibition of acyl-CoA: cholesterol acyltransferase by isohalobacillin, a complex of novel cyclic acylpeptides produced by Bacillus sp. A1238.

A complex of metabolites consisting of two isomeric cyclic acylpeptides was isolated from a culture of Bacillus sp. A1238 by successive chromatographies on Amberlite XAD-7, silica gel and silica ODS columns. By a combination of spectroscopic and chemical analyses, the two subcomponents were identified as isomers of halobacillin, and the complex was designated isohalobacillin. Each molecule of isohalobacillin subcomponents contains either a 3-hydroxy-1-oxo-13-methyltetradecyl or a 3-hydroxy-1-oxo-12 methyltetradecyl moiety in place of a 3-hydroxy-1-oxopentadecyl moiety that is found in the halobacillin molecule. In a cell-free assay, isohalobacillin inhibited acyl-CoA: cholesterol acyltransferase by 50% at a concentration of 50 microM. When added to a culture of macrophage J774, the agent inhibited oxidized low density lipoprotein-induced synthesis of cholesteryl ester from [14C]oleate without affecting surface binding, internalization and degradation of the lipoprotein in the cells.

Amino Acid Sequence↗
PubMed1995

Inhibition of the binding of oxidized low density lipoprotein to the macrophages by iturin C-related compounds.

Binding of modified lipoproteins including oxidized low density lipoprotein (oxidized LDL) to cell surface receptors is an initial step of conversion of monocyte-derived macrophages into lipid-laden foam cells, a key cellular component in the early lesions of atherosclerosis. We have searched for microbial metabolites that inhibit oxidized LDL-induced lipid accumulation in macrophages and isolated three compounds from a strain of Bacillus sp. as inhibitors of oxidized LDL binding. By chemical and spectroscopic analyses, these metabolites were shown to be related to the cyclic lipopeptide iturin C. Two of these compounds were novel metabolites having long chain beta-amino acid moieties of different length. These agents, at concentrations ranging from 5 to 20 microM, inhibited cell surface binding of oxidized 125I-LDL, resulting in reduced intracellular accumulation and degradation of the lipoprotein as well as in reduced cholesteryl ester formation from [14C]oleate in macrophages J774.

Amino Acid Sequence↗
PubMed1995

Isolation, characterization and biological activities of novel triprenyl phenols as pancreatic cholesterol esterase inhibitors produced by Stachybotrys sp. F-1839.

Ten triprenyl phenol metabolites were isolated as inhibitors of pancreatic cholesterol esterase from cultures of Stachybotrys sp. F-1839 by solvent extraction and column chromatographies. Combination of spectroscopic analyses revealed that two of these compounds are K-76 (1) and stachybotrydial (2), and that the remaining eight are new congeners (designated F1839-A (3), -B (4), -C (5), -D (6), -E (7), -F (8), -I (9) and -J (10). These compounds inhibited pancreatic cholesterol esterase by 50% at 6 x 10(-5) to 1.1 x 10(-1) M. Inhibition of the enzyme by compound 2, the most potent one among these compounds, was time-dependent and irreversible. When administered to normal rats, 2, at a single oral dose of 100 mg/kg, reduced [14C]cholesterol absorption by 50-60%. In cholesterol-fed mice, dietary supplementation of 2 (0.1%) for 14 days resulted in a 20% reduction in serum total cholesterol level without causing significant change in the high density lipoprotein cholesterol level.

Animals↗
PubMed1994

Sterol mediated regulation of SREBP-1a,1b,1c and SREBP-2 in cultured human cells.

Under conditions of cholesterol depletion and SREBP-1 accumulation, changes in the levels of sterol regulatory element binding protein(s) (SREBPs) and sterol regulated gene mRNA were studied in Hep G2 cells by RNase protection assay. Cholesterol depletion increased the expression of mRNAs for cholesterol biosynthetic enzymes and low density lipoprotein (LDL) receptor. mRNAs levels for SREBP-1c and SREBP-2 were also increased by the cholesterol depletion. In contrast, levels for SREBP-1a and 1b (1a/b) mRNA increased transiently and then decreased. To examine the effect of SREBP-1 accumulation, Hep G2 cells were incubated with a SREBP-1 degradation inhibitor, N-acetyl-leucyl-leucyl-norleucinal (ALLN). The ALLN treatment increased the LDL receptor mRNA significantly, and also increased mRNA levels for HMG-CoA reductase, SREBP-1a/b and SREBP-2. The mRNA level for squalene synthase was not changed, and for SREBP-1c was decreased by the treatment. In conclusion, the regulation of differential expression of SREBP mRNA may be involved in sterol mediated regulation of gene expression. Moreover, the regulation of the SREBP-1 level may be a critical step in the regulation of sterol mediated LDL receptor expression.

Amino Acid Sequence↗
PubMed1994

Increased incidence of unpartnered single chromatids in metaphase II oocytes in 39,X(XO) mice.

Since rare cases of sex chromosome anomalies such as XXX and XXY were observed in the offspring of our XO breeder mice, we performed a cytogenetic analysis of metaphase II oocytes of XO mice to determine whether any changes in chromosomal configurations occur. We found a significantly increased incidence of unpartnered single chromatids in metaphase II oocytes of XO mice. Such single chromatids may contribute to embryonic aneuploidy. In addition, the tendency of the X-chromosome to segregate non-randomly to the oocyte rather than to the polar body was confirmed.

Animals↗
PubMed1994

Expression level of Rps4 mRNA in 39,X mice and 40,XX mice.

Contrary to the effects of X-chromosome monosomy in humans (Turner syndrome), XO mice are fertile and anatomically normal. The human RPS4X gene encodes ribosomal protein S4 and escapes X-chromosome inactivation, and its haplo-insufficiency has been suspected to contribute to Turner syndrome. Therefore, we compared the expression level of mRNA of Rps4 (the mouse homolog of RPS4X) between XX and XO mice using Northern blot analysis. The XO/XX ratio of Rps4 mRNA obtained from Northern blot analysis was 0.9. There was no difference in the expression level of Rps4 mRNA between XX and XO mice. The difference in the RPS4/Rps4 transcription pattern between humans and mice may contribute, at least in part, to the phenotypic difference in monosomy X between humans and mice.

Aneuploidy↗
PubMed1994

Chronic administration of citalopram inhibited El mouse convulsions and decreased monoamine oxidase-A activity.

Serotonin (5-HT) is thought to play an important role in the seizures of El mice because the seizure threshold of El mice correlates with the 5-HT concentration in the central nervous system. In this study, the anticonvulsant effect of a 5-HT reuptake blocker, citalopram, was evaluated behaviorally and biochemically. El mouse convulsions were inhibited by chronic administration of citalopram (80 mg/kg/day, p.o. for 2 weeks), but were not inhibited by acute administration of citalopram (80 mg/kg, i.p., 2 h after single injection). Both chronic and acute administration of citalopram decreased the concentration of 5-hydroxyindolacetic acid in the brain, whereas the concentration of 5-HT was not changed by treatment with citalopram. Tryptophan hydroxylase activity was not different between the citalopram and control groups, although the monoamine oxydase-A activity was lowered by chronic administration of citalopram. These findings suggest that both acute and chronic administration of citalopram depresses the 5-HT turnover rate, however chronic administration is necessary to inhibit El mouse convulsions.

Administration, Oral↗
PubMed1994

Gypsetin, a new inhibitor of acyl-CoA:cholesterol acyltransferase produced by Nannizzia gypsea var. incurvata IFO 9228. I. Fermentation, isolation, physico-chemical properties and biological activity.

A novel inhibitor of acyl-CoA:cholesterol acyltransferase (ACAT), designated gypsetin, was isolated from the cultured broth of Nannizzia gypsea var. incurvata IFO 9228 by solvent extraction, silica gel chromatography and crystallization. Gypsetin inhibited rat liver microsomal ACAT activity competitively with respect to the substrate oleoyl-CoA with an apparent Ki value of 5.5 microM. In cultured macrophage J774 cells incubated with oxidized low density lipoprotein, gypsetin inhibited cholesteryl ester formation from [14C]oleate by 50% at a concentration of 0.65 microM without affecting cell surface binding, uptake and degradation of the lipoprotein.

Animals↗
PubMed1994

Gypsetin, a new inhibitor of acyl-CoA: cholesterol acyltransferase produced by Nannizzia gypsea var. incurvata IFO 9228. II. Structure determination.

The elucidation of the structure of gypsetin, a new inhibitor of acyl-CoA: cholesterol acyltransferase, is described in this paper. By spectroscopic and X-ray crystallographic analyses, the structure of gypsetin has been determined to be 8a,16a-dihydroxy-5a,13a-bis[1,1-dimethylallyl]-[1]benzazolidine [3''' 2''':4'',5'']azolidino[1'',2'':4',5'][1,4]perhydrodiazin[1', 2':1, 5]azolidino[2,3-b]-[1]benzazolidine-7,15-dione.

Crystallography, X-Ray↗