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Nobuyuki Hamajima

Publications and source records attributed to Nobuyuki Hamajima.

At least 55 records · Page 3Linked to original sources

[Stage progression of dental patients following brief interventions for smoking cessation].

PURPOSE: Potential effects of brief intervention for smoking cessation were evaluated by examination of stage progression with respect to quitting the habit in dental patients. METHODS: Stage progression was retrospectively evaluated in 25 patients undergoing brief interventions since April 2001 at a university dental hospital. Stage of cessation was requested prior to and following interventions (June to December 2003) according to the modification method of Prochaska's model. Brief interventions were conducted by indication of effects of smoking in the mouth and on dental treatment at each visit. Cessation techniques were explained in instances where subjects displayed an interest in smoking cessation. RESULTS: The intervals between dental visits varied (1-6 months). Prior to intervention, numbers of patients in the pre-contemplation, contemplation and preparation stages were 15, 5 and 5, respectively; this changed to 6, 2 and 1, respectively, following intervention, with 16 participants attempting smoking cessation, and 9 reporting continued abstinence. Stage progression was noted in 18 subjects. In the remaining 7 patients, 6 in the pre-contemplation and 1 in the contemplation stage, no change was registered. More than half of the patients (11/20) who had not prepared for cessation prior to intervention and all patients (5/5) in the preparation period reported smoking cessation following the brief interventions. CONCLUSION: Brief interventions in dental practice can induce smoking cessation in patients.

Aged↗

A randomized trial of adjuvant chemotherapy with uracil-tegafur for adenocarcinoma of the lung.

BACKGROUND: In a previous phase 3 trial of adjuvant chemotherapy after resection of non-small-cell lung cancer, a combination of uracil and tegafur (often referred to as UFT) taken orally was shown to prolong survival. A subgroup analysis disclosed that most patients who benefited had pathological stage I adenocarcinoma. METHODS: We randomly assigned patients with completely resected pathological stage I adenocarcinoma of the lung to receive either oral uracil-tegafur (250 mg of tegafur per square meter of body-surface area per day) for two years or no treatment. Randomization was performed with stratification according to the pathological tumor category (T1 vs. T2), sex, and age. The primary end point was overall survival. RESULTS: From January 1994 through March 1997, 999 patients were enrolled. Twenty patients were found to be ineligible and were excluded from the analysis after randomization; 491 patients were assigned to receive uracil-tegafur and 488 were assigned to observation. The median duration of follow-up for surviving patients was 73 months. The difference in overall survival between the two groups was statistically significant in favor of the uracil-tegafur group (P=0.04 by a stratified log-rank test). Grade 3 toxic effects occurred in 10 of the 482 patients (2 percent) who actually received uracil-tegafur. CONCLUSIONS: Adjuvant chemotherapy with uracil-tegafur improves survival among patients with completely resected pathological stage I adenocarcinoma of the lung.

Adenocarcinoma↗

Gene-environment interactions between the smoking habit and polymorphisms in the DNA repair genes, APE1 Asp148Glu and XRCC1 Arg399Gln, in Japanese lung cancer risk.

APE1 (apurinic/apyrimidinic endonuclease 1) and XRCC1 (X-ray cross-complementing group 1) are DNA repair proteins that play important roles in the base excision repair (BER) pathway. Polymorphisms in their encoding genes are associated with altered DNA repair capacity and thus may impact on cancer risk. In the present case-control study with 178 Japanese incident lung cancer cases and 449 age- and sex-matched controls, we investigated the gene-environment interaction among APE1 Asp148Glu, XRCC1 Arg399Gln and smoking habit in lung cancer risk. The results were analyzed by using conditional logistic regression models, adjusted for age, sex and smoking status. The adjusted odds ratio for the current smokers with APE1 148Asp/Asp, Asp/Glu and Glu/Glu genotype as compared with the never smokers with the Asp/Asp genotype were 3.01 (95% CI 1.39-6.51, P = 0.005), 2.73 (95% CI 1.29-5.77, P = 0.008) and 7.33 (95% CI 2.93-18.3, P < 0.001), respectively. The gene-environment interaction between current smoking and APE1 148Glu/Glu genotype was statistically significant (OR 3.59, 95% CI 1.28-10.1, P = 0.015). When APE1 Asp148Glu and XRCC1 Arg399Gln polymorphisms were evaluated together, the adjusted odds ratios for the current smokers with 0-1, 2 and 3-4 of APE1 148Glu or XRCC1 399Gln alleles as compared with never smokers with the 0 of these alleles were 2.96 (95% CI 1.57-5.58, P = 0.001), 3.86 (95% CI 1.85-8.05, P < 0.001) and 6.01 (95% CI 2.25-16.1, P < 0.001), respectively. The gene-environment interaction between current smoking and three or more APE1 148Glu or XRCC1 399Gln alleles was statistically significant (OR 2.44, 95% CI 1.00-9.22, P = 0.049). The OR for the gene-environment interaction of Glu/Glu genotype of APE1 codon 148 with heavy smoking was 1.04 (95% CI 0.38-2.90, P = 0.936) and that with light smoking was 2.67 (95% CI 1.00-7.68, P = 0.049). These results suggest that APE1 Asp148Glu and XRCC1 Arg399Gln polymorphisms might modify the risk of lung cancer attributable to cigarette smoking exposure.

Adult↗

Genetic polymorphisms of p73 G4C14-to-A4T14 at exon 2 and p53 Arg72Pro and the risk of cervical cancer in Japanese.

To examine the possible association between cervical cancer and p73 G4C14-to-A4T14 in exon 2 and p53 Arg72Pro polymorphisms, an incident case-control study was conducted in Japanese. The cases were 112 cervical cancer patients. Controls were 320 healthy women and 122 non-cancer female outpatients. Risk estimation for each genotype by an unconditional logistic model demonstrated a possible association between the p73 A4T14 variant and the risk of cervical cancer in our Japanese population (OR = 1.57; 95%CI, 0.99-2.48, P = 0.053). There was no significant difference in the p53 Arg72Pro genotype frequency between the controls and cases.

Adult↗

Methylenetetrahydrofolate reductase gene (MTHFR) polymorphisms and reduced risk of malignant lymphoma.

Folate and methionine are important nutrients in the "one-carbon" metabolism that is closely associated with DNA synthesis and DNA methylation. Genetic variation in these pathways may change susceptibility to cancer development. We have previously reported associations between lymphoma risk and germline polymorphisms in genes of methylenetetrahydrofolate reductase (MTHFR C677T and A1298C) and methionine synthase (MTR A2756G), finding the genotype other than the MTHFR 677CC/1298AA to confer a half-risk compared to the MTHFR 677CC/1298AA and a 3-fold higher risk with the MTR GG genotype than the AA/AG genotypes. To confirm the association and explore the histological difference, we extended the previous case series. A case-control study was conducted in Japan with a total of 372 lymphoma cases and 500 noncancer controls examined for genotypes. The relative risks were estimated by unconditional logistic regression analysis. In overall analyses, the age-sex adjusted odds ratio (OR) for the subjects harboring MTHFR 677T or 1298C alleles relative to 677CC/1298AA genotype was 0.58 (95% confidence interval: 0.41-0.83, P = 0.002). The MTR GG genotype showed an OR of 1.75 (0.87-3.52, P = 0.114). These findings were validated in separate analyses of the 273 new incident cases. Subgroup analyses according to histological subtype [diffuse large B-cell lymphoma (DLB), follicular lymphoma (FL), low-grade lymphoma of mucosa associated lymphoid tissue (MALT), and others] illustrated similar associations with certain exceptions for FL and MALT. Our data showed an association between the MTHFR polymorphisms and malignant lymphoma risk for all histological subtypes, although the extent of contribution of these polymorphisms may differ somewhat with histological subtype. Lack of association with MTR polymorphism was also confirmed.

5-Methyltetrahydrofolate-Homocysteine S-Methyltran↗

Association of Lewis and Secretor gene polymorphisms and Helicobacter pylori seropositivity among Japanese-Brazilians.

BACKGROUND: Secretor ( Se) and Lewis ( Le) genes are involved in the synthesis of Lewis b (Le(b)) and type I antigens throughout the body, especially in the epithelial cells of gastric mucosa. Helicobacter pylori can attach to the gastric epithelial cells with the blood group antigen-binding adhesin, which binds to Le(b) or H type I carbohydrate structures. In a previous study, a marked association between H. pylori seropositivity and polymorphism of the Se and Le genes was observed among Japanese outpatients of a gastroenterology clinic. The present work aims to investigate the associations between Se and Le gene polymorphisms and H. pylori infection among Japanese-Brazilians. METHODS: The subjects consisted of 942 healthy volunteer Japanese-Brazilians, who were tested for the presence of anti- H. pylori IgG antibodies and genotyped for Se and Le polymorphisms. RESULTS: The sex-age-adjusted odds ratios (aORs) for H. pylori seropositivity were 0.99 for the Sese genotype relative to the SeSe genotype (95% confidence interval [CI], 0.73-1.33), and 1.03 for sese relative to SeSe (95% CI, 0.71-1.48). On the other hand, the aOR for the subjects with the le allele ( Lele or lele) relative to the LeLe genotype was 1.48 (95% CI, 1.07-1.79). When the Se and Le genotypes were analyzed in combination according to risk group, no statistically significant association was observed. CONCLUSIONS: These results are inconsistent with previous work and may have been modulated by an external factor or some other unidentified factor. Japanese-Brazilians are genotypically the same as Japanese, but their lifestyle is adapted to that of Brazil. Further investigations are necessary to clarify this influence on susceptibility to H. pylori infection.

Adult↗

Lack of association between DNA base excision repair gene XRCC1 Gln399Arg polymorphism and risk of malignant lymphoma in Japan.

Growing evidence suggests that the polymorphism of DNA base excision repair gene XRCC1 Arg399Gln is associated with altered DNA repair proficiency and subsequent cancer susceptibility; however, no evidence is available for malignant lymphoma. We therefore conducted a case-control study (372 cases, 500 controls) to evaluate links with malignant lymphoma risk in Japan. The risk was evaluated in terms of odds ratio (OR) and 95% confidence interval (CI) adjusted for age and sex in an unconditional logistic regression model. There was no statistical risk change with the Arg/Gln (adjusted OR 0.89; 0.65-1.23, P = 0.492) or the Gln/Gln (0.57; 0.27-1.17, P = 0.127) compared with the Arg/Arg of the XRCC1 Arg399Gln polymorphism. The results were unchanged in analyses according to histological subtype (diffuse large lymphoma, follicular lymphoma, low-grade lymphoma of mucosa-associated lymphoid tissue, and others). These data suggest that XRCC1 Gln399Arg polymorphism plays a limited role in lymphomagenesis. Further study on the interaction between the polymorphism and environmental exposure is required.

Adolescent↗

Polymorphisms of p53 Arg72Pro, p73 G4C14-to-A4T14 at exon 2 and p21 Ser31Arg and the risk of non-Hodgkin's lymphoma in Japanese.

We hypothesized that the polymorphisms in the two p53 family genes (p53 Arg72Pro and p73 G4C14-to-A4T14 at exon 2 (G4A)) and p21 Ser31Arg polymorphism might modulate the risk of non-Hodgkin's lymphoma, and conducted a hospital-based prevalent case control study at Aichi Cancer Center Hospital to clarify the association. Risk estimation for each genotype by the unconditional logistic model demonstrated the possible association between the p53 Pro72 allele and the risk of non-Hodgkin's lymphoma in Japanese population (OR = 1.59; 95% CI, 0.99-2.57, P = 0.057), although no other significant association was observed. The analyses of statistical interactions between these three polymorphisms (p73 G4A, p53 Arg72Pro and p21 Ser31Arg polymorphisms) revealed the marginally significant OR for interaction between p53 Arg72Pro and p73 G4A polymorphisms (OR = 2.54; 95% CI, 0.97 6.62, P = 0.057). When those without p53 Pro72 and p73 A4T14 alleles were defined as a reference, those with p53 Pro72 and p73 A4T14 alleles demonstrated a significantly higher OR (2.08; 95% CI, 1.11-3.90, P = 0.023). Further examination with a sufficiently larger population and other ethnicities are required to confirm our findings.

Adult↗

The association between tumour necrosis factor-alpha gene polymorphism and the susceptibility to rugal hyperplastic gastritis and gastric carcinoma.

OBJECTIVES: Some subjects infected by Helicobacter pylori have enlarged folds in the gastric body, the precise mechanism of which remains obscure. The aim of this study was to clarify the association of tumour necrosis factor-alpha (TNFA) gene polymorphism with susceptibility to hyper-rugosity. We also examined the association of TNFA polymorphism with gastric carcinoma. SUBJECTS AND METHODS: Four hundred and seventy-two subjects (male/female = 351/121, aged 26-81 years) without gastric carcinoma (control group), and 300 patients (male/female = 218/82, aged 32-91 years) with gastric carcinoma. Barium meal roentgenograms were performed in 396 subjects in the control group and fold width was measured at the greater curvature of the middle portion of the gastric body. Fasting plasma anti-H. pylori IgG titres, pepsinogens (PGs) I and II were analysed, and TNFA -857 promoter polymorphism was distinguished by the 5' nuclease polymerase chain reaction assay and polymerase chain reaction restriction fragment length polymorphism using HincII in both groups. RESULTS: Adjusted odds ratios of TNFA -857 T/T genotype and H. pylori seropositivity for hyper-rugosity (fold width = 6.0 mm) were 6.7 (95% confidence interval (CI) 1.5-28, P < 0.01) and 18.2 (95% CI 4.2-78, P < 0.0001), respectively. There were no significant differences in any genotype or allele frequencies between the control and total gastric carcinoma group. In a subgroup of gastric carcinoma patients who were negative for the PG assay, however, the odds ratio of the T allele was 1.4 (95% CI 1.0-2.0, P < 0.05). CONCLUSION: The TNFA -857 T/T genotype and H. pylori infection were strongly associated with rugal hyperplastic gastritis. The TNFA -857 T allele may promote gastric carcinoma without severe atrophy.

Adult↗

Clinical relevance of a newly identified HLA-A24-restricted minor histocompatibility antigen epitope derived from BCL2A1, ACC-1, in patients receiving HLA genotypically matched unrelated bone marrow transplant.

Minor histocompatibility antigens (mHAs) are major histocompatibility complex (MHC)-associated peptides, which trigger T-cell responses that mediate graft versus host disease (GVHD) and graft versus leukaemia effects. We recently identified a new mHA epitope, termed ACC-1, which is presented by HLA-A*2402 and encoded by BCL2A1, whose expression is restricted to haematopoietic cells including leukaemic cells. HLA-A24/ACC-1 tetramer detected the presence of ACC-1-specific CD8+ cells in the peripheral blood of a patient up to 7 months following transplantation, and these tetramer-positive cells were expandable in vitro by ACC-1 peptide stimulation. A retrospective analysis of 320 patients with HLA-A*2402 who had received a human leucocyte antigen (HLA) genotypically matched unrelated donor through the Japan Marrow Donor Programme was conducted to determine whether ACC-1 disparity is associated with adverse clinical outcomes such as GVHD. Among these patients, ACC-1 disparity was detected in 55 (17.2%) donor/recipient pairs. After adjusting for known risk factors, the hazard ratios or odds ratios of acute and chronic GVHD, relapse and disease-free survival were not statistically different between patients receiving ACC-1 compatible and incompatible transplantation. These data suggest that disparity of haematopoietic cell-specific mHA, ACC-1, is unlikely at least to augment GVHD, and that T cells specific for ACC-1 may also be used for immunotherapy of recurring leukaemia without GVHD.

Adolescent↗

Foods and beverages in relation to urothelial cancer: case-control study in Japan.

BACKGROUND: The roles of several foods and beverages in the development of bladder cancer remain unclear. METHODS: We undertook a hospital-based case-control study at Aichi Cancer Center Hospital, Japan. Subjects included 124 men and women (bladder cancer cases) with newly diagnosed cancers of the renal pelvis (n = 5), ureter (n = 6) or bladder (n = 113) and 620 age- and sex-matched, cancer-free outpatients (controls) presenting at the hospital in the period from 1994 to 2000. Smoking-adjusted odds ratios (OR) were estimated to assess the strength of associations between self-reported intake of foods or drinks and bladder cancer risk, using conditional logistic models. RESULTS: We found a decreased risk in relation to frequent intake of green-yellow vegetables; the OR for the highest intake score compared with the lowest was 0.54 (95% confidence interval [CI] 0.29-0.99). The OR for carrot intake of >/=5 times/week compared with </=1-3 times/month was 0.41 (95% CI 0.16-1.01) and a decreasing risk with increasing consumption of green vegetables was also detected (P for trend = 0.063). Inverse associations between black tea, eggs and meat and risk were also suggested, whereas moderate drinkers of green tea (5-9 cups/day) showed an elevated risk. Coffee and milk consumption did not appear to exert any influence. CONCLUSIONS: Those with an increased risk of bladder cancer, such as smokers, may benefit from increasing their consumption of green-yellow vegetables.

Adult↗

Association between smoking habits and tryptophan hydroxylase gene C218A polymorphism among the Japanese population.

BACKGROUND: Genetic polymorphisms have proposed a new insight in smoking behavior. Genes in serotonin system are one of the candidates because of serotonin's role in mood regulation. A polymorphism C218A in intron 7 of the tryptophan hydroxylase (TPH) gene has been hypothesized in relation to smoking predisposition. METHODS: We examined the association on two Japanese populations: one was from the first-visit outpatients of Aichi Cancer Center Hospital during 3-month period between April and June, 2001 (N=591), and the second was from the examinees who attended a health checkup program supported by the Nagoya municipal government in 2000 (N=446). Written documents on informed consent were obtained and lifestyle questionnaires were recorded. TPH C218A genotypes were determined by the polymerase chain reaction with confronting two-pair primers (PCR-CTPP) method. RESULTS: The frequencies of the C- and A-allele were 52% and 48%, respectively, which was in Hardy-Weinberg equilibrium. As for current smoking status, no associations were statistically observed. It was, however, indicated that smokers with A/A genotype started smoking earlier in their life. Among male health examinees, mean ages at starting smoking were 18.7 (A/A), 19.9 (C/A), and 22.4 years (C/C), (P<0.01). Also, on the Aichi Cancer Center Hospital subjects aged 60 and older, mean ages were 19.0 (A/A), 20.2 (C/A), and 20.3 years (C/C) for males and 22.3 (A/A), 31.0 (C/A), and 33.0 years (C/C) for females (P<0.05). CONCLUSIONS: The present study demonstrated that the TPH C218A polymorphism in intron 7 had no association with current smoking status in Japanese population. The hypothesis of early smoking initiation of A/A genotype was partially in agreement.

Adolescent↗

[Genetic polymorphisms and cancer risk].

While hereditary disease genes have a high lifelong cumulative incidence rate (penetrance), the penetrance for polymorphism genotypes is not high. Polymorphisms relating to cancer incidence are classified into 1. carcinogen metabolizing enzymes (CYPs, GSTs, NQO1, etc.), 2. DNA repair enzymes (OGG1, XRCC1, XPD, etc.), 3. DNA synthesis and methylation (MTHFR, MS, etc.), 4. cytokines and inflammation-related enzymes (IL-1B, TNF-A, MPO, etc.), and 5. sex hormone metabolizing enzymes and the receptors (CYP19, SRD5A2, ER, etc.). Since genotypes cannot be manipulated, they are not the factors subject to prevention. However, the finding that the strength of association between lifestyle and disease occurrence is influenced by genotypes (gene-environment interaction), opens the door to genotype applications for disease prevention practice.

Cytochrome P-450 CYP1A1↗

Genotype announcement in a genetic polymorphism study for health checkup examinees at Nagoya University Hospital.

On June 9, 2003, we started free genetic tests of eight polymorphisms for health checkup examinees who attended a basic course at Nagoya University Hospital. They were informed of their genotypes within four weeks after blood donation for research purposes. The genotypes were those of alcohol dehydrogenase 2 (ADH2) Arg47His, aldehyde dehydrogenase 2 (ALDH2) Glu487Lys, NAD(P)H: quinone oxidoreductase (NQO1) C609T, glutathione S transferase M1 (GSTM1), glutathione S-transferase T1 (GSTT1), interleukin-1B (IL-1B) C-31T, and tumor necrosis factor A (TNF-A) T-1031C, angiotensin-converting enzyme (ACE) Ins/Del. In the first three months, 227 (89.4%) out of 254 examinees participated in the free tests, having been informed of the research aims, after which they consented to our use of research data. To date, there have been no complaints from the participants, indicating that the announcement of polymorphism genotypes may be accepted differently from that of hereditary disease genotypes.

Alcohol Dehydrogenase↗

Associations between disease risk and eight polymorphisms adopted for genotype announcements at Nagoya University Hospital.

Genetic polymorphisms have the potential to predict disease susceptibility. This may be especially useful among individuals with a high-risk lifestyle, so that the genotyping could be adopted for disease prevention through modifications toward a lower-risk lifestyle. We started a program of free genotype announcements in a polymorphism study among health checkup examinees at the Nagoya University Hospital on June 9, 2003. Since such announcements remain controversial for fear of unexpected harmful effects and counseling system, the accumulated evidence on the association between disease risk and genotypes announcements in our study was reviewed in this article. The genotypes used were those of alcohol dehydrogenase 2 (ADH2) Arg47His, aldelhyde dehydlrogenase 2 (ALDH2) Glu487Lys, NAD(P)H: quinone oxidoreductase (NQO1) C609T, glutathlione S transferase M1 (GSTM1), glutathione S-transferase T1 (GSTT1), interleukin-1B (IL-1B) C-31T, and tumor necrosis factor A (TNF-A) T-1031C, angiotensin converting enzyme (ACE) Ins/Del. Since showed a potential for widespread use in health checkups, the information on the above polymorphisms seems worth documenting. Although there have been no complaints from the participants to date, careful treatments are requested.

Alcohol Dehydrogenase↗

Possible association of interleukin 1B C-31T polymorphism among Helicobacter pylori seropositive Japanese Brazilians with susceptibility to atrophic gastritis.

Associations between anti-Helicobacter pylori seropositivity (HP+) and interleukin 1B (IL-1B) C-31T polymorphism have been reported and little is known about the host factors involved in the development of atrophic gastritis (AG) among infected individuals. This study aimed to examine the IL-1B C-31T polymorphism among anti-HP antibody seropositive Japanese descendants with AG in Brazil and to investigate the interactions with lifestyle factors. Subjects were 455 seropositive from four cities in Brazil, aged 33-69 years. Sex-age-adjusted odds ratio (OR) of AG for 61 current smokers was 1.29, 95% confidence interval (CI): 0.18-9.26 for T/T, while that for 325 never smokers was 0.52, 95% CI: 0.27-0.98. A negative association for AG and never alcohol drinking, every day fruit consumption and milk drinking, and less frequently coffee drinking in individuals with C/T or T/T genotype was observed. This study suggested that host genetic constitution and lifestyle factors may influence the protective effect for AG development.

Adult↗

The CYP19 gene codon 39 Trp/Arg polymorphism increases breast cancer risk in subsets of premenopausal Japanese.

The production of estrogen from androgen via the estrogen biosynthesis pathway is catalyzed by aromatase P450 (CYP19). To assess the association between breast cancer risk and a polymorphism at codon 39 Trp/Arg of the encoding gene, a case-control study was conducted at Aichi Cancer Center Hospital in Japan. Subjects were 248 histologically confirmed breast cancer patients and 603 hospital controls without cancer. Odds ratios (OR) and 95% confidence intervals (95% CI) were determined by logistic regression analysis. The allele frequency among controls was 3.8% for the C allele, and the OR (95% CI) of the polymorphism relative to TT genotype was 1.21 (0.69-2.14) for TC/CC genotypes combined. There was no association between CYP19 gene polymorphism and breast cancer risk in the study group as a whole, but homozygous and heterozygous carriers of the variant Arg allele showed a significantly increased risk of breast cancer among premenopausal women with a late age at first full-term pregnancy (OR 7.31, 95% CI 1.88-28.5) or a high body mass index (OR 2.77, 95% CI 1.12-6.87). Additional larger studies should be done to confirm that the rare CYP19 variant increases the risk of breast cancer among premenopausal Japanese women.

Adult↗

Contribution of specific foods to fat, fatty acids, and cholesterol in the development of a food frequency questionnaire in Koreans.

The present study identified dietary sources of fat, fatty acids, and cholesterol in Koreans residing in and near Seoul. The study also identified foods to be included in a food frequency questionnaire (FFQ) by both contribution analysis (CA) and multiple regression analysis (MRA). Three-day dietary records were collected from 224 subjects (107 men and 117 women) aged 30 to 85 years. Pork was the main source of total fat and the largest contributor to saturated fatty acids (SFA) was beef. MRA identified animal food as the primary source of between-person variance for SFA. Arachidonic acid, eicosapentaenoic acid, and docosahexaenoic acid originated primarily from marine products. About a fourth of the total cholesterol intake was derived from chickens' eggs by CA, while chickens' eggs accounted for 46% of the cholesterol intake for between-person variance by MRA. With 10 food items, the FFQ could explain more than half of total intakes except for total fat and n-3 polyunsaturated fatty acids (PUFA), and at least 65% of between-person variances. The percentage coverage in the FFQ ranged from 61% for n-6 PUFA and linoleic acid and to 90% for arachidonic acid. The value of this FFQ is that it can estimate usual dietary food patterns and nutrient intake in Koreans for epidemiological studies. It can also potentially be used to study the relationship between specific diseases and nutrient intakes of interest.

Adult↗