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3 results on '"Akemi Kameta"'

1. Validity and Reliability of the Child and Adolescent Version of the Iron Intake Scale (CIIS) as an Educational Tool

Author

Satoko Okabe, Shinya Ito, Akemi Kameta, and Aya Goto

Subjects
Computer applications to medicine. Medical informatics, R858-859.7, Public aspects of medicine, RA1-1270
Abstract

Introduction/Objective: In Asia, 42% of young children suffer from iron deficiency anemia. Children have an increased requirement for iron intake because of growth and physical activity. Education plays an important role in anemia prevention and in ensuring children are aware of appropriate iron intake and the iron content of different foods. As a tool for this purpose, we adapted the adult version of the Revised Iron Intake Scale (RIIS) to create the Child and Adolescent Version of the Iron Intake Scale (CIIS), using illustrations to help children recognize the foods listed in the CIIS. We aimed to evaluate the validity and reliability of this new scale. Methods: We conducted a cross-sectional study using a self-administered questionnaire to examine the criterion-related validity of the CIIS. We used Spearman’s rank correlation coefficient to compare iron intake estimated by the CIIS with that calculated by the Brief-type Diet History Questionnaire (BDHQ-15y), which assesses respondents’ dietary habits over the past month and is standardized among Japanese children. The survey was repeated twice to examine reliability. Results: We found a moderate positive correlation for iron intake between the CIIS and BDHQ-15y, with a correlation coefficient of .52 (n = 258, P

Published
2024
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2. Increased expression of IgE-dependent histamine-releasing factor in endometriotic implants

Author

Masahiko Kuroda, Tetsuya Ohbayashi, Yoshinori Kosugi, Akemi Kameta, Masaomi Takayama, Kiyoshi Mukai, Kosuke Oikawa, and Keiichi Isaka

Subjects
medicine.medical_specialty, T cell, Endometriosis, Inflammation, Biology, Pathology and Forensic Medicine, Peritoneal cavity, Endometrium, Mice, Internal medicine, medicine, Biomarkers, Tumor, Cytochrome P-450 CYP1A1, Macrophage, Animals, Humans, Northern blot, Peritoneal Cavity, Mice, Inbred BALB C, Monocyte, Tumor Protein, Translationally-Controlled 1, 3T3 Cells, Immunoglobulin E, medicine.disease, Endocrinology, medicine.anatomical_structure, Gene Expression Regulation, Cancer research, Immunohistochemistry, Female, medicine.symptom
Abstract

A complex network of cytokines mediates the immunoregulatory responses leading to endometriosis. Recent intensive studies suggest that monocyte and T cell chemoattractants contribute to the inflammatory environment of endometriotic implants. The relationship between the inflammation present during endometriosis and the development of endometriotic implants in the peritoneal cavity remains unclear. On the other hand, the association between endometriosis and 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD; dioxin) exposure has been discussed in recent years, and our previous results revealed that IgE-dependent histamine-releasing factor (HRF) is inducible by TCDD. The present study aimed to clarify the expression, localization, and function of HRF in endometriosis. Northern blot analysis demonstrated that HRF is overexpressed in endometriotic implants. RT-PCR with Southern blot analysis, however, showed that HRF overexpression was not always accompanied by CYP1A1 induction in endometriotic implants, suggesting that HRF is inducible in endometriosis without exposure to TCDD. HRF is also inducible by macrophage colony-stimulating factor (M-CSF). Immunohistochemistry showed CD68-positive macrophages in the stroma of endometriotic implants, adjacent to regions with prominent HRF accumulation. HRF-overexpressing cells exhibited high implantation efficiency in comparison to control cells when the cells were injected into the peritoneal cavities of nude mice. These results suggest that the accumulation of macrophages in endometriotic implants induces HRF; the overexpression of HRF accelerates the growth of endometriotic implants.

Published
2003

3. Dioxin induces a novel nuclear factor, DIF-3, that is implicated in spermatogenesis

Author

Ryoko Iwata, Akemi Kameta, Kazumi Evine, Yoshiaki Fujii-Kuriyama, Kiyoshi Mukai, Masahiko Kuroda, Taku Isobe, Tetsuya Ohbayashi, Yoichi Matsuda, Junsei Mimura, and Kosuke Oikawa

Subjects
Male, Polychlorinated Dibenzodioxins, Mrna expression, Biochemistry, Dioxin inducible factor-3, Mice, Structural Biology, Testis, heterocyclic compounds, Fluorescent Antibody Technique, Indirect, Aryl hydrocarbon receptor, Oligonucleotide Array Sequence Analysis, Zinc finger, Expressed Sequence Tags, biology, Reverse Transcriptase Polymerase Chain Reaction, Stem Cells, Gene Expression Regulation, Developmental, Nuclear Proteins, Zinc Fingers, humanities, Cell biology, Zinc-finger protein, Reproductive toxicity, medicine.medical_specialty, DNA, Complementary, Blotting, Western, Molecular Sequence Data, Biophysics, behavioral disciplines and activities, Cell Line, Complementary DNA, Internal medicine, Genetics, medicine, Animals, Northern blot, RNA, Messenger, 2,3,7,8-Tetrachlorodibenzo-p-dioxin, Spermatogenesis, Molecular Biology, Gene Expression Profiling, fungi, Cell Biology, Blotting, Northern, body regions, Molecular Weight, Endocrinology, Animals, Newborn, biology.protein, Representational difference analysis
Abstract

2,3,7,8-Tetrachlorodibenzo-p-dioxin (TCDD; dioxin), a member of a class of environmental pollutants represented by polychlorinated dibenzo-p-dioxins and dibenzofurans, is one of the most toxic artificial compounds ever developed. In this study, we identified a novel TCDD target gene, DIF-3 (dioxin inducible factor-3), by cDNA representational difference analysis. DIF-3 protein is a nuclear factor and possesses a zinc-finger motif at its N-terminus. High DIF-3 mRNA expression in the testes was demonstrated by Northern blot analysis and abundant DIF-3 protein was detected during spermatogenesis. Thus, these results suggest that DIF-3 may be a target gene mediating the reproductive toxicity induced by TCDD.

Published
2001

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