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1.
J Prim Care Community Health ; 15: 21501319241259410, 2024.
Article in English | MEDLINE | ID: mdl-38864205

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 < .001). Cronbach's alpha coefficient was .718. The CIIS reproducibility test yielded a correlation coefficient of .67. CONCLUSION: Our results indicated that the CIIS was valid, reliable, and reproducible. We therefore believe that the scale can be used to improve education about iron deficiency anemia and thereby reduce anemia rates among children and adolescents.


Subject(s)
Anemia, Iron-Deficiency , Humans , Cross-Sectional Studies , Child , Female , Male , Reproducibility of Results , Adolescent , Anemia, Iron-Deficiency/prevention & control , Surveys and Questionnaires , Iron, Dietary/administration & dosage , Child, Preschool , Japan , Feeding Behavior
2.
J Pathol ; 199(3): 318-23, 2003 Mar.
Article in English | MEDLINE | ID: mdl-12579533

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.


Subject(s)
Biomarkers, Tumor/metabolism , Endometriosis/metabolism , Immunoglobulin E/physiology , 3T3 Cells/transplantation , Animals , Biomarkers, Tumor/genetics , Cytochrome P-450 CYP1A1/genetics , Endometriosis/genetics , Endometrium/metabolism , Female , Gene Expression Regulation , Humans , Mice , Mice, Inbred BALB C , Peritoneal Cavity/pathology , Tumor Protein, Translationally-Controlled 1
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