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Biomedical subjects

Y Fukuda

Publications and source records attributed to Y Fukuda.

At least 487 records · Page 27Linked to original sources
PubMed1995

Serum anti-Helicobacter pylori antibodies and gastritis.

We investigated the relationship between the severity of Helicobacter pylori-associated gastritis and serum anti-H. pylori antibodies. A total of 158 consecutive patients underwent upper gastroduodenal endoscopy. At the time of endoscopy, three biopsy specimens were taken from the antrum and the body of the stomach for culture of H. pylori, CLO test, and histology. Specimens with a negative rapid urease test and no organisms found by culture were judged to be H. pylori-negative. The GAP test used for the antibody measurement is a kit designed to measure serum IgG, IgA, and IgM antibodies. The severity of gastritis was classified according to the Sydney System. The sensitivity and specificity of the IgG antibody measurement kit was 98.3 and 71.4%, respectively. The sensitivity and specificity of the IgM antibody measurement kit was 14.3 and 60.8%, respectively. The sensitivity and specificity of the IgA antibody measurement kit was 45.1 and 100%, respectively. Serum anti-H. pylori IgG antibody titers were correlated significantly with the severity of inflammation in both the antrum and body. Significant associations were found between serum anti-H. pylori IgG and IgA antibody titers and the development of atrophic gastritis. These results suggest that measurement of serum anti-H. pylori antibody titers is useful in the diagnosis of H. pylori infection and severity of gastritis.

Antibodies, Anti-Idiotypic↗
PubMed1994

Amplification and overexpression of the cyclin D1 gene in aggressive human hepatocellular carcinoma.

We analyzed the genetic alterations of the cyclin D1 and INT-2 genes in hepatocellular carcinomas (HCCs) from 45 patients. Among these, expression of the cyclin D1 mRNA was also analyzed in 18 of them by Northern blotting. The cyclin D1 gene was amplified 3-16 fold in five HCCs (11%); among these, the INT-2 gene was also amplified 2-10 fold in four HCCs. We analyzed the mRNA of cyclin D1 in four HCCs with gene amplifications, and 6-10 fold overexpressions were detected in all of them. Because the cyclin D1 gene was amplified in patients at an advanced stage of HCC with rapid tumor growth, it appeared to be associated with the aggressive behavior of tumors. Studies on loss of heterozygosity on chromosome 13q, where the retinoblastoma (RB) gene is located, indicated that all HCCs with an amplified cyclin D1 gene retained heterozygosity on chromosome 13q. These results suggest that amplification and overexpression of the cyclin D1 gene result in the rapid growth of a subset of HCC, even though the function of the RB gene is retained.

Carcinoma, Hepatocellular↗
PubMed1994

Molecular cloning and expression of rat prostaglandin E receptor EP2 subtype.

A cDNA clone encoding the rat prostaglandin (PG) E receptor EP2 subtype was cloned from a rat lung cDNA library. It encodes 488 amino acid residues with putative seven-transmembrane domains. Specific binding of [3H]PGE2 was found in COS-7 cells transfected with the cDNA and was displaced with unlabeled prostaglandins in the order of PGE2 = PGE1 >> iloprost > or = PGF2 alpha > or = PGD2. The binding was also inhibited by misoprostol, an EP2 and EP3 agonist, but not by sulprostone, an EP1 and EP3 agonist. Northern blot analysis demonstrated that the EP2 mRNA is widely expressed in various tissues, the significant expression being observed in the thymus, lung, spleen, heart stomach, and pancreas.

Amino Acid Sequence↗
PubMed1994

Metastatic potential in nude mice of Chinese hamster ovary cells expressing human carcinoembryonic antigen.

The role of carcinoembryonic antigen (CEA) in metastasis was examined using Chinese hamster ovary (CHO) cells which had been transfected with cDNA encoding CEA. When 2 x 10(6) cells of a clone of CEA-expressing transfectants, designated CHO/CEA, were injected intrasplenically into athymic nude mice, 8 out of 8 mice developed liver metastases. In contrast, a vector-transfectant C5 did not at all form metastasis in the assay (0 of 8). There was no difference in growth rate between CHO/CEA and C5 in vivo as well as in vitro. MoAbs to N-domain of CEA markedly inhibited the liver metastasis of CHO/CEA cells, while a MoAb to domain III of the antigen did not. These findings suggest that CEA may play an important role in hepatic metastasis, and that the N-domain of CEA molecule contributes to the function of CEA in metastasis.

Animals↗
PubMed1994

Suppression of cytochrome P450IA1 by interleukin-6 in human HepG2 hepatoma cells.

The effects of interleukin-6 (IL-6), the major inducer of the acute-phase reaction, on the expression of cytochrome P450IA1 (CYPIA1) were examined using human HepG2 hepatoma cells. Treatment of cells with IL-6 decreased the level of 3-methylcholanthrene-induced CYPIA1 protein and its mRNA. Nuclear runoff analysis revealed that the effect of IL-6 was largely transcriptional. IL-6 treatment of HepG2 cells increased mRNA for microsomal heme oxygenase, the rate-limiting enzyme in heme catabolism, suggesting that the suppressive effect of IL-6 on CYPIA1 mRNA may be due to a loss of heme. Consistent with this hypothesis, simultaneous treatment of cells with Sn-mesoporphyrin, an inhibitor of heme oxygenase, prevented the IL-6-mediated suppression of CYPIA1. These findings suggest that the suppression of P450IA1 mRNA by IL-6 appears to occur, at least in part, from the decline in free heme content as a result of the induction of heme oxygenase. Our results raise the possibility that other physiological as well as environmental stimuli which affect cellular heme concentrations may also modulate the expression of P450s.

Carcinoma, Hepatocellular↗
PubMed1994

Regulation of beta-globin mRNA accumulation by heme in dimethyl sulfoxide (DMSO)-sensitive and DMSO-resistant murine erythroleukemia cells.

The level of mRNA encoding beta-globin was examined in dimethyl sulfoxide (DMSO)-sensitive (DS), and DMSO-resistant (DR) murine erythroleukemia (MEL) cells. DR cells lack erythroid-specific delta-aminolevulinate (ALA) synthase (AL-AS-E), and fail to undergo erythroid differentiation following treatment with DMSO. Treatment of cells with DMSO markedly increased ALAS-E mRNA in DS cells, while the same treatment downregulated the nonspecific ALA synthase (ALAS-N) mRNA levels in both DS and DR cells. The levels of beta-globin mRNA, heme content, and hemoglobin in DS cells increased, while those in DR cells decreased following treatment with DMSO. Treatment of DR cells with hemin caused an increase in beta-globin mRNA and hemoglobin, and partially restored the DMSO-mediated suppression of beta-globin mRNA and hemoglobin synthesis. DMSO treatment decreased heme oxygenase (HO) mRNA in hemin-treated DS cells, but not in hemin-treated DR cells. These findings indicate that heme is necessary for accumulation of the beta-globin transcript during erythroid differentiation, and that hemin-mediated HO induction becomes markedly downregulated in differentiated erythroid cells, presumably because less free heme is available for HO induction by a greater demand for the synthesis of hemoglobin.

5-Aminolevulinate Synthetase↗
PubMed1994

Transforming growth factor beta abrogates the effects of hematopoietins on eosinophils and induces their apoptosis.

Hematopoietins, interleukin (IL)-3, IL-5, and granulocyte/macrophage colony-stimulating factor (GM-CSF) have previously been shown to prolong eosinophil survival and abrogate apoptosis. The objective of this study was to investigate the effect of transforming growth factor beta (TGF-beta) on eosinophil survival and apoptosis. Eosinophils from peripheral blood of mildly eosinophilic donors were isolated to > 97% purity using discontinuous Percoll density gradient. Eosinophils were cultured with hematopoietins with or without TGF-beta for 4 d and their viability was assessed. We confirmed previous observations that hematopoietins prolonged eosinophil survival and inhibited apoptosis. TGF-beta at concentrations > or = 10(-12) M abrogated the survival-prolonging effects of hematopoietins in a dose-dependent manner and induced apoptosis as determined by DNA fragmentation in agarose gels. The effect of TGF-beta was blocked by an anti-TGF-beta antibody. The anti-TGF-beta antibody also prolonged eosinophil survival on its own. The culture of eosinophils with IL-3 and GM-CSF stimulated the synthesis of GM-CSF and IL-5, respectively, suggesting an autocrine mechanism of growth factor production. TGF-beta inhibited the synthesis of GM-CSF and IL-5 by eosinophils. TGF-beta did not have any effect on the expression of GM-CSF receptors on eosinophils. We also studied the effect of TGF-beta on eosinophil function and found that TGF-beta inhibited the release of eosinophil peroxidase. Thus, TGF-beta seems to inhibit eosinophil survival and function. The inhibition of endogenous synthesis of hematopoietins may be one mechanism by which TGF-beta blocks eosinophil survival and induces apoptosis.

Antibodies, Monoclonal↗
PubMed1994

Demonstration of retinal cells expressing messenger RNAs of the c-kit receptor and its ligand.

We found cells expressing c-kit receptor and its ligand (Sl factor, SLF) in the retina of rats and mice. c-kit messenger RNA (mRNA) was detected in a limited number of cells in the inner nuclear layer of rats and mice by in situ hybridization. The c-kit-expressing cells were assumed to be a subpopulation of the amacrine cells on the basis of their size and distribution pattern. c-kit protein-containing cells were demonstrated in the mouse retina by using ACK2 monoclonal antibody against the extracellular domain of the mouse c-kit receptor. The c-kit protein was detected in cell bodies and processes of the presumed amacrine cells. Hybridization signals for SLF mRNA were observed in the retinal ganglion cells. The results suggest that the c-kit receptor and its ligand may play some roles in the formation of junctions between the amacrine and retinal ganglion cells.

Animals↗
PubMed1994

Muscarinic acetylcholine responses in the early embryonic chick retina.

The action of acetylcholine on cytoplasmic Ca2+ concentration ([Ca2+]i) was studied in early embryonic chick retinae. Whole neural retinae were isolated from embryonic day 3 (E3) chicks and loaded with a Ca(2+)-sensitive fluorescent dye (Fura-2). Increases in [Ca2+]i were evoked by the puff application of acetylcholine at concentrations higher than 0.1 microM. The Ca2+ response became larger in a dose-dependent manner up to 10 microM of acetylcholine applied. The rise in [Ca2+]i was not due to the influx of Ca2+ through calcium channels, but to the release of Ca2+ from internal stores. A calcium channel antagonist, nifedipine, which completely blocks the Ca2+ rise caused by depolarization with 100 mM K+, had no effects on the acetylcholine response and the Ca2+ response to acetylcholine occurred even in a Ca(2+)-free medium. The Ca2+ response to acetylcholine was mediated by muscarinic receptors. Atropine of 1 microM abolished the response to 10 microM acetylcholine, whereas d-tubocurarine of 100 microM had no effects. Two muscarinic agonists, muscarine and carbamylcholine (100 microM each), evoked comparable responses with that to 10 microM acetylcholine. The developmental change of the muscarinic response was examined from E3 to E13. The Ca2+ response to 100 microM carbamylcholine was intense at E3-E5, then rapidly declined until E8. The muscarinic Ca2+ mobilization we found in the early embryonic chick retina may be regarded as a part of the "embryonic muscarinic system" proposed by Drew's group, which appears transiently and ubiquitously at early embryonic stages in relation to organogenesis.

Acetylcholine↗
PubMed1994

Characterization of a novel cis-acting element that is responsive to a fungal elicitor in the promoter of a tobacco class I chitinase gene.

The expression of tobacco class I chitinase gene is effectively induced by a fungal elicitor in suspension-cultured tobacco cells. To identify cis-acting DNA elements that respond to the elicitor, a series of promoter constructs of the chitinase gene CHN50 fused to beta-glucuronidase gene was introduced into tobacco cultured cells. Promoter deletion analysis of the chitinase gene CHN50 in transgenic tobacco calli indicated that the DNA region between positions -788 and -345 from the start site of transcription is required for inducibility by the elicitor. A gel mobility shift assay revealed that nuclear factor(s) specifically interacted with the DNA region between positions -574 and -476. Moreover, this novel DNA-binding activity was present in nuclear extracts prepared from elicitor-treated cultured cells but not in extracts from untreated cells. Competitive binding assays and methylation interference experiments showed that the nuclear factor(s) bound specifically to a sequence of 22 bp that extended from positions -539 to -518 and contained a direct repeat of GTCAG spaced by three nucleotides. This motif is a candidate for a cis-acting elicitor-responsive element (ElRE) that is involved in the transcription of the class I chitinase gene.

Base Sequence↗