7 results on '"Egashira M"'
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2. LOCAL MICRO-DEFORMATION ANALYSIS BY MEANS OF MICROGRID AND ELECTRON BEAM MOIRÉ FRINGE METHOD
- Author
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Kishimoto, S., primary, Egashira, M., additional, Shinya, N., additional, and Carolan, R.A., additional
- Published
- 1992
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3. A longer body length and larger head circumference at term significantly influences a better subsequent psychomotor development in very-low-birth-weight infants.
- Author
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Egashira T, Hashimoto M, Shiraishi TA, Shichijo A, Egashira M, Mizukami T, and Takayanagi T
- Subjects
- Biomarkers, Birth Weight physiology, Body Height, Body Weight, Body Weights and Measures methods, Female, Head growth & development, Humans, Infant, Infant, Newborn, Japan, Longitudinal Studies, Male, Psychomotor Disorders, Retrospective Studies, Child Development physiology, Infant, Very Low Birth Weight growth & development, Infant, Very Low Birth Weight physiology
- Abstract
Aim: To clarify the influence of intra- and extra-uterine growth on subsequent psychomotor development in very-low-birth-weight (VLBW) infants., Methods: Two hundred and eighty VLBW infants (28.4 ± 2.6 weeks, 1000 ± 294 g) were enrolled. Psychomotor development was determined at 37.1 ± 2.1 months after birth using the Kyoto Scale of Psychological Development (KSPD), which includes Postural-Motor (P-M), Cognitive-Adaptive (C-A) and Language-Social (L-S) subscales. Subjects were divided into two groups based on whether each developmental quotient (DQ) was ≥85, and the perinatal variables that contributed to a DQ of ≥85 (for each DQ) were determined. The twelve variables that were evaluated included the z scores for body weight (zBW), body length (zBL), head circumference (zHC), which were obtained at birth and at term., Results: The median P-M, C-A, L-S values and total DQ were 92, 83, 81 and 83, respectively, and the percentage of patients with a DQ of ≥85 were 53%, 44%, 35% and 39%, respectively. A multivariate analysis revealed significant associations between the following variables and the DQs: P-M ≥ 85, GA [odds ratio; OR = 1.11] and zBL at term [OR = 1.26]; C-A ≥ 85, male gender [OR = 0.30], GA [OR = 1.14] and zHC at term [OR = 1.84]; L-S ≥ 85, male gender [OR = 0.55], GA [ OR = 1.20] and zHC at term [OR = 1.45]; total DQ ≥ 85, male gender [OR = 0.39], GA [OR = 1.19] and zBL at term [OR = 1.69]., Conclusion: In addition to less prematurity and female gender, a longer body length and larger head circumference at term were important indicators that influenced better psychomotor development in VLBW infants at three years of chronological age., (Copyright © 2018 The Japanese Society of Child Neurology. Published by Elsevier B.V. All rights reserved.)
- Published
- 2019
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- View/download PDF
4. Identification of regions responsible for heparin-induced amyloidogenesis of human serum amyloid A using its fragment peptides.
- Author
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Egashira M, Takase H, Yamamoto I, Tanaka M, and Saito H
- Subjects
- Amino Acid Sequence, Amino Acid Substitution, Amyloid chemistry, Amyloid genetics, Amyloid metabolism, Amyloid ultrastructure, Circular Dichroism, Heparin pharmacology, Humans, Microscopy, Electron, Transmission, Molecular Sequence Data, Peptide Fragments chemistry, Peptide Fragments genetics, Peptide Fragments metabolism, Peptide Fragments ultrastructure, Proline chemistry, Protein Conformation, Serum Amyloid A Protein genetics, Serum Amyloid A Protein ultrastructure, Spectrometry, Fluorescence, Heparin metabolism, Serum Amyloid A Protein chemistry, Serum Amyloid A Protein metabolism
- Abstract
Human serum amyloid A (SAA) is a precursor protein of amyloid fibrils. Although several studies have been performed, a detailed understanding of the molecular mechanism for SAA fibrillation remains elusive. Glycosaminoglycans such as heparin are suggested to serve as scaffolds in amyloid fibril formation in some cases. In the present study, amyloidogenic properties of synthetic fragment peptides corresponding to the N-terminal (residues 1-27), central (residues 43-63), and C-terminal (residues 77-104) regions of SAA molecule induced by heparin were examined using fluorescence, circular dichroism (CD), and electron microscopy. Fluorescence and CD measurements demonstrated that SAA (1-27) peptide is evidently involved in heparin-induced amyloidogenesis. Correspondingly, relatively minor changes in fluorescence and a quite different pattern in the CD spectrum were observed in SAA (43-63) peptide. In contrast, SAA (77-104) peptide did not show any changes induced by heparin. Transmission electron microscopy indicated that SAA (1-27) peptide forms short and straight fibrils, whereas SAA (43-63) peptide forms much longer and seemingly elastic fibrils. These results suggest that the N-terminal region plays a crucial role as a rigid core and the central region facilitates the elongation of fibrils in heparin-induced amyloidogenesis of SAA molecule., (Copyright © 2011 Elsevier Inc. All rights reserved.)
- Published
- 2011
- Full Text
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5. Novel nonsynonymous polymorphisms of the CYP1A1 gene in Japanese.
- Author
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Saito T, Egashira M, Kiyotani K, Fujieda M, Yamazaki H, Kiyohara C, Kunitoh H, and Kamataki T
- Abstract
We found five novel nonsynonymous polymorphisms of the human CYP1A1 gene from Japanese individuals. The five single nucleotide polymorphisms (SNP) in exon 7 (2346_2347 ins T, 2414T>A, 2461C>T, 2500C>T and 2546C>G causing premature stop codon, Ile(448)Asn, Arg(464)Cys, and Arg(477)Trp and Pro(492)Arg, respectively) were as follows:SNP, 030212Saito001; GENE NAME, CYP1A1; ACCESSION NUMBER, X02612; LENGTH, 25 base; 5'-GTCAACCCATCT-/TGAGTTCCTACCT-3'.SNP, 030212Saito002; GENE NAME, CYP1A1; ACCESSION NUMBER, X02612; LENGTH, 25 base; 5'-GTGAGAAGGTGAT/ATATCTTTGGCAT-3'.SNP, 030212Saito003; GENE NAME, CYP1A1; ACCESSION NUMBER, X02612; LENGTH, 25 base; 5'-GAGACCGTTGCCC/TGCTGGGAGGTCT-3'.SNP, 030212Saito004; GENE NAME, CYP1A1; ACCESSION NUMBER, X02612; LENGTH, 25 base; 5'-ATCCTGCTGCAAC/TGGGTGGAATTCA-3'.SNP, 030212Saito005; GENE NAME, CYP1A1; ACCESSION NUMBER, X02612; LENGTH, 25 base; 5'-TGGACATGACCCC/GCATCTATGGGCT-3'.
- Published
- 2003
- Full Text
- View/download PDF
6. P-glycoprotein expression on normal and abnormally expanded natural killer cells and inhibition of P-glycoprotein function by cyclosporin A and its analogue, PSC833.
- Author
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Egashira M, Kawamata N, Sugimoto K, Kaneko T, and Oshimi K
- Subjects
- ATP Binding Cassette Transporter, Subfamily B, Member 1 antagonists & inhibitors, ATP Binding Cassette Transporter, Subfamily B, Member 1 physiology, Adult, Aged, CD56 Antigen analysis, Cell Line, Child, Female, Gene Expression, Genes, MDR genetics, Humans, Killer Cells, Natural immunology, Leukemia, Lymphocytic, Chronic, B-Cell metabolism, Leukemia, Lymphoid metabolism, Lymphoproliferative Disorders metabolism, Male, Middle Aged, Receptors, IgG analysis, Reverse Transcriptase Polymerase Chain Reaction, ATP Binding Cassette Transporter, Subfamily B, Member 1 analysis, Cyclosporine pharmacology, Cyclosporins pharmacology, Immunosuppressive Agents, Killer Cells, Natural chemistry
- Abstract
P-glycoprotein (P-gp), a transmembrane efflux pump encoded by the MDR1 gene, has been found to be expressed in many normal bone marrow and peripheral blood cells. Among normal leukocytes, CD3(-)CD16(+) or CD3(-)CD56(+) lymphocytes, ie, natural killer (NK) cells, express relatively high levels of P-gp, but little is known about P-gp in abnormally expanded NK cells. In this study, we examined the expression and activity of P-gp on NK cells derived from three normal donors, six patients with indolent NK cell-lineage granular lymphocyte-proliferative disorder (NK-GLPD), three patients with aggressive NK cell tumors (one NK cell leukemia and two nasal NK cell lymphoma), and two NK cell lines. By flow cytometric analysis using the monoclonal antibody (MoAb) MRK16 and rhodamine 123 dye (Rh123), P-gp expression and the efflux of Rh123 were found in all NK samples except one NK cell line. The Rh123 efflux of NK cells was inhibited by cyclosporin A (CsA) and its analogue PSC 833, but the aggressive NK tumor cells were less inhibited than were the other NK cells. The percent inhibition of efflux in the normal NK cells, indolent NK-GLPD cells and aggressive NK cell tumors was 81.8% +/- 0. 9%, 93.4% +/- 3.1% and 36.9% +/- 11.7%, respectively, by 1 micromol/L CsA, and 80.2% +/- 3.6%, 91.7% +/- 2.6% and 32.7% +/- 10. 1%, respectively, by 1 micromol/L PSC833. In reverse transcription-polymerase chain reaction (RT-PCR) analysis, the low inhibitory effect of P-gp modulators in aggressive NK cell tumors did not correlate to the expression level of MDR1 gene, multidrug resistance-associated protein gene, or human canalicular multispecific organic anion transporter gene. This phenomenon could be related to the presence of other transporters or to unknown cellular or membrane changes. Some patients with NK cell tumors have been reported to show a highly aggressive clinical course and to be refractory to chemotherapy, and this could be related to the expression of P-gp on NK cells. Our results suggest that, although the inhibitors for P-gp have been used in combination with chemotherapy in some hematologic tumors, these inhibitors may be less effective against aggressive NK cell tumors.
- Published
- 1999
7. Temporal and spatial distribution of DNA topoisomerase II alters during proliferation, differentiation, and apoptosis in HL-60 cells.
- Author
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Sugimoto K, Yamada K, Egashira M, Yazaki Y, Hirai H, Kikuchi A, and Oshimi K
- Subjects
- Cell Differentiation, Cell Division, Flow Cytometry, HL-60 Cells, Humans, Apoptosis, DNA Topoisomerases, Type II metabolism
- Abstract
We related cellular content of DNA topoisomerase (topo) IIalpha and IIbeta with the cell cycle position in proliferating, differentiated, and apoptotic HL-60 cells using two-dimensional flow cytometry. In logarithmically growing HL-60 cells, topo IIalpha increased especially in late S to G2/M phases, although the topo IIbeta level was almost constant throughout the cell cycle. Induction of differentiation by all-trans retinoic acid dramatically reduced the topo IIalpha but not the topo IIbeta level. A new G2/M population containing virtually no topo IIalpha appeared during differentiation and was supposed to be alive and noncycling. Two-dimensional flow cytometry of topo IIalpha or IIbeta staining and terminal deoxynucleotidyl transferase-mediated dUTP-biotin nick end-labeling assay showed that one topo IIbeta epitope situated at the C-terminal end decreased specifically in apoptotic HL-60 cells treated with Ara-C, etoposide, and vincristine. The amounts of a topo IIalpha epitope and another topo IIbeta epitope located at a more central portion were almost equal between apoptotic and nonapoptotic cells. Western blot analysis confirmed that topo IIbeta protein was completely degraded into smaller fragments and lost its C-terminal end during apoptosis. On the contrary, a large portion of topo IIalpha remained of its original size, although both topo IIalpha and IIbeta left from the nuclear fraction in apoptotic cells. Confocal laser microscopy showed nuclear localization of topo IIalpha and IIbeta in growing HL-60 cells. Although topo IIalpha and IIbeta were distributed throughout the cell during mitosis, only topo IIalpha was densely concentrated in the mitotic chromosomes. Both enzymes were dissociated from the genomic DNA even at an early phase of apoptosis and completely separated from the propidium iodide signal of DNA in the advanced stage. Chromatin condensation process in apoptosis is therefore completely topo II-independent and obviously differs from the mitotic one.
- Published
- 1998
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