Additional file 1: of MiRNA-17 encoded by the miR-17-92 cluster increases the potential for steatosis in hepatoma cells by targeting CYP7A1

Figure S1. Expression of miR-17 increases in transgenic mice compared with wild-type mice. (JPG 599 kb

Additional file 5: of MiRNA-17 encoded by the miR-17-92 cluster increases the potential for steatosis in hepatoma cells by targeting CYP7A1

Figure S3. Luciferase activity changed in mouse psiCHECK-CYP7A1 and miR-17 co-transfection but not for psiCHECK-CYP7A1 mutant. (JPG 120 kb

Additional file 2: of MiRNA-17 encoded by the miR-17-92 cluster increases the potential for steatosis in hepatoma cells by targeting CYP7A1

Figure S4. miR-17 expression level was stable in miR-17 transgenic mice. (JPG 829 kb

Additional file 5: of MiRNA-17 encoded by the miR-17-92 cluster increases the potential for steatosis in hepatoma cells by targeting CYP7A1

Figure S3. Luciferase activity changed in mouse psiCHECK-CYP7A1 and miR-17 co-transfection but not for psiCHECK-CYP7A1 mutant. (JPG 120 kb

Additional file 3: of MiRNA-17 encoded by the miR-17-92 cluster increases the potential for steatosis in hepatoma cells by targeting CYP7A1

Figure S2. A – CYP7A1 is predicted to be a target of miR-17 in humans. B – CYP7A1 is predicted to be a target of miR-17 in mice. (JPG 87 kb

Dietary n-3 Polyunsaturated Fatty Acid Intakes Modify the Effect of Genetic Variation in <i>Fatty Acid Desaturase 1</i> on Coronary Artery Disease

<div><p>Background</p><p>Previous studies suggested that dietary fatty acids could affect blood lipids by interacting with genetic variations in <i>fatty acid desaturase 1 (FADS1)</i>. However, little is known about their direct effects on coronary artery disease (CAD). The aim of this study was to evaluate whether dietary n-3 long-chain polyunsaturated fatty acids (LCPUFAs) -eicosapentaenoic acid (EPA) and docosahexaenoic acid (DHA) could modulate the effect of <i>FADS1</i> rs174547 polymorphism on CAD.</p><p>Methods</p><p><i>FADS1</i> single-nucleotide polymorphisms rs174547 genotypes were measured in 440 CAD patients and 838 healthy controls. Dietary EPA and DHA intakes were assessed with a validated quantitative frequency food questionnaire. The association between <i>FADS1</i> rs174547 and CAD was estimated using logistic regression under both dominant and additive genetic models. The interactions between rs174547 polymorphism and LCPUFAs were analyzed by using multiple logistic regression and the “genotype × n-3 LCPUFAs” interaction term was included into the model.</p><p>Results</p><p>We found that the minor <i>T</i> allele of <i>FADS1</i> rs174547 increased CAD risk (OR = 1.36, 95%CIs 1.03-1.80), and observed significant interaction between rs174547 and dietary EPA intakes on CAD (<i>P</i>-interaction = 0.028). The <i>T</i>-allele was only associated with higher CAD risk among individuals with lower dietary EPA intakes, but not in those with higher EPA intakes. Similarly, significant interaction was also observed between rs174547 and dietary DHA intakes on CAD (<i>P</i>-interaction = 0.020).</p><p>Conclusions</p><p>Dietary n-3 LCPUFA intakes could modulate the association between <i>FADS1</i> rs174547 polymorphism and CAD. High dietary n-3 LCPUFA intakes could negate the unfavorable effect of genetic variation in <i>FADS1</i> on CAD in middle-aged and elderly Chinese population.</p></div

Nutrigenetic interaction of EPA and DHA with <i>FADS1</i> rs174547 on risk of CAD under a dominant genetic model^a.

<p>^a Adjusted for age, sex, body mass index, smoking, total cholesterol, triglyceride, diastolic blood pressure, education and energy intakes, the history of using statins.</p><p>Abbreviations:; HAenergy intakes. EPA, eicosapentaenoic acid; CAD, coronary artery disease; DHA, docosahexaenoic acid.</p><p>Nutrigenetic interaction of EPA and DHA with <i>FADS1</i> rs174547 on risk of CAD under a dominant genetic model<a href="http://www.plosone.org/article/info:doi/10.1371/journal.pone.0121255#t003fn001" target="_blank">^a</a>.</p

The n-3 and n-6 PUFAs metabolism pathways.

<p>AA, arachidonic acid; EPA, eicosapentaenoic acid; FADS: fatty acid desaturase.</p

General characteristics of the case-control study population.

<p>Abbreviations: HDL, high density lipoprotein; LDL, low density lipoprotein; LCPUFA, long-chain polyunsaturated fatty acid; EPA, eicosapentaenoic acid; DHA, docosahexaenoic acid.</p><p>General characteristics of the case-control study population.</p

Table_1_The role of rare earth elements and dietary intake in tongue cancer: a mediation analysis in southeast China.DOCX

ObjectiveThe current research aimed to examine how dietary intake and rare earth elements may affect the development of tongue cancer.MethodsThe serum levels of 10 rare earth elements (REEs) in 171 cases and 171 healthy matched controls were measured by inductively coupled plasma mass spectrometry (ICP-MS). The conditional logistic regression was used to examine the relationship between dietary intake, serum levels of 10 REEs, and tongue cancer. Mediation effect and multiplicative interaction analysis were then performed to estimate the potential contribution of REEs in dietary intake associated with tongue cancer.ResultsCompared with the control group, patients with tongue cancer consumed significantly less fish, seafood, fruit, green leafy vegetables, and non-green leafy vegetables, with higher serum praseodymium (Pr), dysprosium (Dy), and lanthanum (La) levels, and lower serum cerium (Ce) and scandium (Sc) levels. The interaction effect was observed between some REEs and food categories. Green vegetables' impact on the risk of tongue cancer is partially attributed to the La and Thorium (Th) elements (P ConclusionThe correlation between REEs and dietary intakes for tongue cancer is compact but intricate. Some REEs interact with food intake to influence tongue cancer, while others act as a mediator.</p