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Biomedical subjects

T Ono

Publications and source records attributed to T Ono.

At least 541 records · Page 30Linked to original sources
PubMed1996

Effect of a prenylamine analog (MG8926) on spontaneous action potentials in isolated rabbit sinoatrial node.

Effects of verapamil, prenylamine and a prenylamine analog, MG8926 on the intracellular spontaneous action potentials recorded from the isolated rabbit sinoatrial (SA) node were studied. Verapamil (1 microM), a selective inhibitor for slow Ca2+ channels, prolonged the cycle length, decreased the rate of diastolic depolarization, the rate of rise of action potential, the amplitude of action potential and the maximal diastolic potential, and usually arrested showing subthreshold fluctuation of the membrane potential within several ten min. Prenylamine (10 microM), a nonselective inhibitor for slow Ca2+ channels, tended to prolong the cycle length to decrease the diastolic depolarization, the rate of rise of action potential, the amplitude of action potential. However, these changes were statistically insignificant. Prenylamine at the concentration of 10 microM had no effect on the maximal diastolic potential. MG8926 (10 microM) prolonged the cycle length, decreased the rate of diastolic depolarization, the rate of rise of action potential and tended to decrease the amplitude of action potential. MG8926 at the concentration of 10 microM had almost no effect on the maximal diastolic potential. The present findings may indicate that replacement of phenyl residue of prenylamine by cyclohexyl residue increases the inhibitory action on the slow Ca2+ channels in rabbit SA node.

Action Potentials↗
PubMed1995

Tissue-specific regulation of the expression of rat intestinal bile acid-binding protein.

A lipid-binding protein identical to the rat intestinal bile acid-binding protein, termed I-15P, was expressed in steroid hormone-producing tissues such as ovary and adrenal gland, but not testis. In immature rats, I-15P was expressed in intestine but not in ovaries. The expression of I-15P in the ovaries of immature rats was induced to the level in immature rats by gonadotropin treatment. This suggests that the expression of I-15P in the ovaries is controlled by the ovarian cycle. The present results indicate that the expression of I-15P is developmentally and hormonally controlled in a tissue-specific manner.

Adrenal Glands↗
PubMed1995

Molecular cloning, expression, and characterization of a human intestinal 15-kDa protein.

We have isolated a cDNA encoding a human intestinal 15-kDa protein (I-15P) from a human ileal lambda gt 11 cDNA library, using a full-length rat I-15P cDNA. One clone encompassed 571 nucleotides and encoded a 128-amino-acid protein with a calculated molecular mass of 14355 Da. The deduced amino acid sequence of human I-15P showed high similarity to the rat counterpart (78%), mouse ileal lipid-binding protein (80%) and porcine gastrotropin (75%). It also exhibited 36% similarity to human liver fatty-acid-binding protein (L-FABP). Northern blot analysis of human I-15P revealed a single transcript only in ileum, however, the reverse-transcription/PCR demonstrated expression in ovary and placenta, but it was much lower than in ileum. Transformation of Escherichia coli with the I-15P cDNA resulted in the efficient expression of a protein that was identical to the ileal cytosolic I-15P. In vitro binding studies revealed that the bacterially expressed recombinant I-15P showed much lower affinities for palmitate and oleate than L-FABP. However, it showed similar affinity for taurocholate, compared with a control, BSA. Comparison of the structural features of human I-15P and human L-FABP suggested that loss of a long alpha-helix region and hydrophobic profile of I-15P may be attributable to a unique ligand-binding specificity of I-15P.

Aged↗
PubMed1995

Specific degradation of the D1 protein of photosystem II by treatment with hydrogen peroxide in darkness: implications for the mechanism of degradation of the D1 protein under illumination.

The D1 protein of the photosystem II (PSII) reaction center has a rapid turnover and is specifically degraded under illumination in vivo. When isolated PSII membranes were treated in darkness with 10 mM hydrogen peroxide (H2O2), an active form of oxygen that is generated at the acceptor side of PSII under illumination, proteins of the PSII reaction center were specifically damaged in almost the same way as observed under illumination with strong light. The D1 protein and, to a lesser extent, the D2 protein were degraded to specific fragments, and cross-linked products (the covalently linked adduct of the D1 protein and the alpha subunit of cytochrome b559 and the heterodimer of the D1 and D2 proteins) were generated concomitantly. The site of cleavage of the D1 protein that gave rise to a major fragment of 22 kDa was located in the loop that connects membrane-spanning helixes IV and V. Treatment with H2O2 caused the same damage to proteins in isolated thylakoids and in core complexes that contained the non-heme iron at the acceptor side, but not in isolated reaction centers depleted of the iron. From these observations and the effects of reagents that are known to interact with the non-heme iron, it is suggested that the damage to proteins is caused by oxygen radicals generated by the non-heme iron in the Fe(II) state in a reaction with H2O2. It is proposed, moreover, that a similar mechanism is operative during the selective and specific degradation of the D1 protein under illumination.

Chloroplasts↗
PubMed1995

Loss of heterozygosity at 11p15 in malignant glioma.

Deletions of loci on chromosome 11p have been found frequently in several malignant tumors including gliomas, suggesting the presence of tumor suppressor genes. We analyzed 38 gliomas [26 malignant gliomas (grades III and IV) and 12 less malignant gliomas (grade I and II)] for loss of heterozygosity using microsatellite sequences on 11p as polymorphic markers. Loss of heterozygosity was found in 8 of 26 malignant gliomas (31%) but not in the less malignant gliomas. In the region with loss of heterozygosity, loci on 11p15.5-pter were commonly deleted. Our results suggest that a putative tumor suppressor gene involved in malignant progression of gliomas is located in an approximately 21-cM region on 11p15.5-pter.

Base Sequence↗
PubMed1995

Association between sialyl Lewis(a) expression and tumor progression in melanoma.

Twenty-three primary and 27 metastatic melanoma lesions and 17 pigmented nevi lesions were tested utilizing the immunoperoxidase reaction with anti-sialyl Lewis(a) (sLea) and anti-sLex mAbs.sLea was expressed in 9, 25, and 5 and sLex was expressed in 6, 11, and 2 of these lesions, respectively. Expression of sLea in melanocytic tumors is associated with tumor progression. Serum levels of sLea and sLex were analyzed by a sandwich assay using mAbs in 25 melanoma patients. Only 2 patients at stage 4 showed higher levels of sLea and sLex than did normal control subjects. Moreover, sLea and sLex were expressed in 1 and 2 of 5 human melanoma cell lines, respectively, and expression of sLex and sLex was not modulated by cytokines. These findings suggest that the expression of sLea in melanocytic tumors is correlated with disease progression.

Antigens, Tumor-Associated, Carbohydrate↗
PubMed1995

Tissue-specific suppression of aortic fatty-acid-binding protein in streptozotocin-induced diabetic rats.

Fatty-acid-binding protein (FABP) expressed in rat aorta has been shown to be homologous to heart FABP (H-FABP) but its precise primary structure, cellular localization and function are not known. To establish the nucleotide identity between heart and aorta FABP, we performed an RNase protection assay with antisense RNA of rat H-FABP. The results demonstrate that the primary nucleotide sequence of aortic FABP is identical to that of rat H-FABP. In situ hybridization analysis revealed that aortic H-FABP mRNA is present in both smooth muscle cells and endothelial cells. In order to explore the function of aortic H-FABP, we examined whether a quantitative change in aortic H-FABP occurred in diabetes mellitus, since this pathological state has been shown to cause abnormalities in fatty acid metabolism. Northern blot analysis revealed that the level of aortic H-FABP mRNA was markedly decreased in rats made diabetic by streptozotocin treatment. The suppression of the mRNA level paralleled that of the protein level, as assessed by Western blot analysis. In distinct contrast, no major changes in the H-FABP mRNA level were observed in any other tissues examined, including heart, kidney and skeletal muscle, suggesting that this decrease is highly tissue-specific. The suppression of the aortic H-FABP in streptozotocin-diabetic rats was abolished by insulin supplementation. Taken together, these results suggest that the expression of the H-FABP gene in aorta may be specifically and dramatically suppressed in streptozotocin-diabetic rats, and that this suppression appears to be regulated by insulin.

Animals↗
PubMed1995

Nucleotide sequence of a cDNA for mouse squalene epoxidase.

A full-length cDNA encoding mouse squalene epoxidase was isolated by screening a mouse liver cDNA library with the rat squalene epoxidase gene as a probe. The cDNA had an open reading frame for a 572 amino acid polypeptide with a calculated molecular mass of 63.8 kDa. The predicted amino acid sequence of the mouse enzyme contained an FAD-binding motif, and was 93% identical to that of the rat enzyme. The former is one amino acid shorter than the latter. Blotting analyses showed that the mRNA is 2.8 kb in size and that a single copy of the gene is present in the mouse genome.

Amino Acid Sequence↗
PubMed1995

Human high molecular weight-melanoma associated antigen mimicry by mouse anti-idiotypic MAb MK2-23. Immunohistochemical analysis of the reactivity of anti-anti-idiotypic MAb with surgically removed melanoma lesions.

The mouse anti-id MAb MK2-23 bears the internal image of the antigenic determinant defined by anti-HMW-MAA MAb 763.74. Active specific immunotherapy with anti-id MAb MK2-23 is associated with a statistically significant prolongation of survival in patients with malignant melanoma. Characterization of the immune response elicited by anti-id MAb MK2-23 may contribute to our understanding of the mechanisms underlying the apparent beneficial clinical effects of active specific immunotherapy with anti-id MAb MK2-23. Therefore, 8 HMW-MAA binding anti-anti-id MAbs elicited with MAb MK2-23 were characterized in their reactivity with a large panel of surgically removed benign and malignant tumors and of normal tissues. The 8 anti-anti-id MAbs displayed subtle differences in their immunoperoxidase staining of both benign and malignant lesions and of normal tissues. The diversity in the fine specificity of the 8 anti-anti-id MAbs is likely to reflect the few somatic mutations which occur in the amino-acid sequence of the variable regions of their heavy and light chains in the course of the immune response to MAb MK2-23. The reactivity patterns of the 8 anti-anti-id MAbs with the tissue substrates are similar, although not superimposable upon that of anti-HMW-MAA MAb 763.74 elicited with melanoma cells. This difference may reflect the imperfect mimicry by anti-id MAb MK2-23 of the antigenic determinant defined by anti-HMW-MAA MAb 763.74.

Animals↗
PubMed1995

Cloning and sequencing of the gene encoding the mouse vitamin D receptor.

The mouse vitamin D receptor (VDR)-encoding cDNA was cloned and the coding regions were sequenced. Comparison of the amino-acid sequence to that of humans and rats revealed high homology in the DNA- and ligand-binding domains. Divergence appeared in the internal region between the two domains.

Amino Acid Sequence↗
PubMed1995

Reciprocal IL-1 beta gene expression in medial and lateral hypothalamic areas in SART-stressed mice.

Specific alteration of rhythm of temperature (SART) stress has been found to induce thymic atrophy via activation of the hypothalamus-pituitary-adrenal (HPA) axis. We demonstrate here that SART stress induces increment of IL-1 beta mRNA levels in the medial hypothalamic area (MHA) and decrement of IL-1 beta mRNA levels in the lateral hypothalamic area (LHA). The altered levels of IL-1 beta expression in these loci return to those of non-stressed mice upon cessation of the stress. These data imply that the reciprocal wave of SART stress-induced IL-1 beta gene expression in MHA and LHA may contribute to activation of the HPA axis and the resulting immunological dysfunction.

Animals↗