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  Subjects -> NUTRITION AND DIETETICS (Total: 201 journals)
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Lifestyle Genomics
Journal Prestige (SJR): 0.614
Citation Impact (citeScore): 2
Number of Followers: 2  

  This is an Open Access Journal Open Access journal
ISSN (Print) 2504-3161 - ISSN (Online) 2504-3188
Published by Karger Homepage  [122 journals]
  • Mechanism of glycitein in the treatment of colon cancer based on network
           pharmacology and molecular docking

    • Abstract: Introduction: The prevalence of colon cancer remains high across the world. The early diagnosis of colon cancer is challenging. Moreover, patients with colon cancer frequently suffer from poor prognoses.Methods: Differentially expressed genes (DEGs) in colon cancer were acquired based on TCGA-COAD dataset screening. DEGs were input into the Connectivity Map (CMap) database to screen small molecule compounds with the potential to reverse colon cancer pathological function. Glycitein ranked first among the screened small molecule compounds. We downloaded the main targets of glycitein from the Traditional Chinese Medicine Systems Pharmacology Database and Analysis Platform database and constructed protein-protein interaction (PPI) networks of those which were closely related to targets by Search Tool for the Retrieval of Interaction Gene/Proteins (STRING). Five potential targets of glycitein for treating colon cancer were identified (CCNA2, ESR1, ESR2, MAPK14, and PTGS2). These targets were used as seeds for random walk with restart (RWR) analysis of PPI networks. Then, the interaction network of glycitein-colon cancer-related genes was constructed based on the top 50 genes in affinity coefficients. Gene ontology (GO) and Kyoto Encyclopedia of Genes and Genomes (KEGG) enrichment analyses were conducted on the potential genes targeted by glycitein in colon cancer treatment and those were closely bound up with targets. Results: GO analysis demonstrated that the enrichment of these genes was primarily discovered in biological functions including regulation of fibroblast proliferation, response to oxygen levels, and epithelial cell proliferation. KEGG analysis results illustrated that the signaling pathways where these genes were mostly involved consisted of the mitogen-activated protein kinases signaling pathway, the phosphatidylinositol-3-kinase-Akt signaling pathway, and the p53 signaling pathway. Finally, stable binding of glycitein to five potential targets in colon cancer was verified by molecular docking. Conclusion: This study elucidated the key targets and main pathways of glycitein on the basis of network pharmacology and preliminarily analyzed molecular mechanisms in the treatment of colon cancer. A scientific basis is provided for glycitein application in treating colon cancer.

      PubDate: Fri, 30 Sep 2022 11:38:11 +020
       
  • Quantile-specific heritability of mean platelet volume, leukocyte count,
           and other blood cell phenotypes

    • Abstract: Introduction: “Quantile-dependent expressivity” occurs when the effect size of a genetic variant depends upon whether the phenotype (e.g. mean platelet volume, MPV) is high or low relative to its distribution. Methods: Offspring-parent (βOP) regression slopes were estimated by quantile regression, from which quantile-specific heritabilities (h2) were calculated (h2=2βOP/(1+rspouse)) for blood cell phenotypes in 3929 parent-offspring pairs from the Framingham Heart Study. Linear trends in βOP vs. percentiles of the phenotype distribution were tested using orthogonal polynomials.Results: Quantile-specific h2 (±SE) increased with increasing percentiles of the offspring’s age- and sex-adjusted MPV distribution (Plinear=0.0001): 0.48±0.09 at the 10th, 0.53±0.04 at the 25th, 0.70±0.06 at the 50th, 0.74±0.06 at the 75th, and 0.90±0.12 at the 90th percentile. Quantile-specific h2 also increased with increasing percentiles of the offspring’s white blood cell (WBC), monocyte, and eosinophil distributions (Plinear=0.002, Plinear=0.01, and Plinear=0.0005, respectively). In contrast, heritibilities of red blood cell count (RBC), hematocrit (HCT), and hemoglobin (HGB) showed little evidence for quantile-dependence. Discussion/Conclusion" Quantile-dependent expressivity may explain several purported gene-environment interactions, including: 1) greater increases in WBC and PLT concentrations in subjects who are glutathione-S-transferase Mu1 (GSTM1) null homozygotes than GSTM1 sufficient when exposed to endotoxin; 2) significantly higher WBC count in AA homozygotes than carriers of the G-allele of the glutathione S-transferase P1 (GSTP1) rs1695 polymorphism at low but not high benzene exposure in shoe factory workers; 3) higher WBC counts in TT homozygotes than C-allele carriers of the interleukin-1β (IL1B) c.315C>T polymorphism after undergoing surgery for infective endocarditis but not before surgery.

      PubDate: Thu, 22 Sep 2022 07:46:21 +020
       
  • The rs9939609 variant in FTO increases the risk of hypercholesterolemia in
           metabolically healthy subjects with excess weight

    • Abstract: Introduction: The fat mass and obesity-associated gene (FTO) is largely/primarely expressed in the hypothalamus. It plays a role in energy balance, regulation of food intake, and adipogenesis. According to metabolic phenotypes, studies have associated the FTO rs9939609 variant with body mass index (BMI), body fat mass, and dietary intake, but not with serum lipids. This study aimed to analyze the association of the FTO rs9939609 variant with serum lipids in Mexican adults with different metabolic phenotypes. Methods: We included 306 subjects aged 18-65 years, classified as normal weight (NW) or excess weight (EW) according to their BMI. EW included BMI from 25 to 39.9 kg/m2. Participants were classified into two metabolic phenotypes: metabolically healthy/metabolically unhealthy (MH/MUH). We use the homeostatic model assessment of insulin resistance and NCEP-ATP III cut-offs for glucose, triglycerides, high-density lipoprotein, and blood pressure. Subjects with ≥2 altered parameters were classified as MUH. The variant was determined by allelic discrimination with TaqMan® probes. Results: In subjects with the A-allele, significantly higher total cholesterol and low-density lipoprotein cholesterol were found (p
      PubDate: Wed, 21 Sep 2022 12:13:19 +020
       
  • Influences of the interactions of genetic variations of seven core
           circadian clock genes with lifestyle factors on metabolic parameters

    • Abstract: Introduction: In mammals, circadian rhythms regulate many behavioral and physiological processes. Genetic and epidemiological studies have shown that dysregulation of the circadian rhythm induces chronic metabolic diseases, such as obesity, diabetes, and dyslipidemia. We aimed to know the interactions of genetic variations of seven core circadian clock genes with lifestyle factors on the determination of metabolic parameters. Methods: We have analyzed the impacts of genotype of seven core circadian clock genes (i.e., CLOCK, BMAL1, PER1, PER2, PER3, CRY1 and CRY2) and lifestyle factors (i.e., physical activity and sleep duration) in 575 Japanese males on the determination of metabolic parameters (i.e., BMI, glucose, HbA1c, LDL-C and HDL-C). Results: We have detected the associations between genotypes of PER3 and serum HbA1c level, and genotypes of CRY1 and serum LDL-C level. Additionally, the interactions of the genotypes of PER1 and PER3 with physical activity for determining BMI, the genotypes of CLOCK with physical activity for determining serum HbA1c levels, was observed. Furthermore, for determining of serum HDL-C levels, the interactions of the genotypes of CRY2 with physical activity or sleep duration was observed. Discussion/Conclusion: Our findings indicate that the interactions of genotypes for core circadian clock genes and lifestyle factors (i.e., physical activity and sleep duration) are important for determining of metabolic parameters.

      PubDate: Tue, 13 Sep 2022 08:28:29 +020
       
  • Investigation of the association between high arachidonic acid synthesis
           and colorectal polyp incidence within a generally healthy UK population: a
           Mendelian randomisation approach

    • Abstract: Background: Arachidonic acid (ARA) is associated with colorectal cancer (CRC), a major public health concern. However, it is uncertain if ARA contributes to the development of colorectal polyps which are pre-malignant precursors of CRC.Objective: To investigate the association between lifelong exposure to elevated ARA and colorectal polyp incidence. Methods: Summary level GWAS data from European, Singaporean, and Chinese cohorts (n=10,171) identified 4 single nucleotide polymorphisms (SNPs) associated with blood ARA levels (p
      PubDate: Thu, 11 Aug 2022 11:31:11 +020
       
  • Smoking-interaction loci affect obesity traits: a gene-smoking stratified
           meta-analysis of 545,131 Europeans

    • Abstract: Introduction: Although many studies have investigated the association between smoking and obesity, very few have analyzed how obesity traits are affected by interactions between genetic factors and smoking. Here, we aimed to identify the loci that affect obesity traits via smoking status-related interactions in European samples. Methods: We performed stratified analysis based on the smoking status using both the UK Biobank (UKB) data (N = 334,808) and the Genetic Investigation of ANthropometric Traits (GIANT) data (N = 210,323) to identify gene-smoking interaction for obesity traits. We divided the UKB subjects into two groups, current smokers and nonsmokers, based on the smoking status, and performed genome-wide association study (GWAS) for body mass index (BMI), waist circumference adjusted for BMI (WCadjBMI), and waist-hip ratio adjusted for BMI (WHRadjBMI) in each group. And then we carried out the meta-analysis using both GWAS summary statistics of UKB and GIANT for BMI, WCadjBMI, and WHRadjBMI, and computed the stratified P-values (Pstratified) based on the differences between meta-analyzed estimated beta coefficients with standard errors in each group. Results: We identified four genome-wide significant loci in interactions with the smoking status (Pstratified < 5×10–8); rs336396 (INPP4B) and rs12899135 (near CHRNB4) for BMI, and rs998584 (near VEGFA) and rs6916318 (near RSPO3) for WHRadjBMI. Moreover, we annotated the biological functions of the SNPs using expression quantitative trait loci (eQTL) and GWAS databases, along with publications, which revealed possible mechanisms underlying the association between the smoking status-related genetic variants and obesity. Conclusions: Our findings suggest that obesity traits can be modified by the smoking status via interactions with genetic variants through various biological pathways.

      PubDate: Wed, 06 Jul 2022 10:39:17 +020
       
  • Upregulated miR-146a expression in peripheral blood relates to Th17 and
           Treg imbalance in elder rheumatoid arthritis patients

    • Abstract: Background: The expression level of microRNA-146a (miR-146a) increased in peripheral blood and synovialis tissue of rheumatoid arthritis (RA) patient, it may play an important role in the pathological process of RA. We investigated its possibility as a diagnostic marker and the correlation with Th17 and Treg cells in elder RA patients. Methods: Blood samples were collected from 38 active RA patients, 38 inactive RA patients, and 40 healthy controls. RNA expression levels of miR-146a were detected from the peripheral blood samples. The proportion of Th17 and Treg cells were analyzed, as well as their cell-specific transcription factor retinoic acid-related orphan receptor variant 2 (RORc) and forkhead box protein 3 (FOXP3). Furthermore, secretion of pre-inflammatory and anti-inflammatory factors were detected. Correlations between miR-146a and these factors were also analyzed.Results: Compared with healthy control, expression levels of miR-146a in inactive and active groups were significant higher, with the highest level in active group. The expression of miR-146a and the RA severity, T helper 17 (Th17) cell ratio, RORc expression, IL-17 level showed a significant positive correlation, while it showed a significantly negative correlation with Treg cell ration, FOXP3 expression, and TGF-β1 secretion. Conclusions: These results suggested that miR-146a may be used as a disease progression marker in the peripheral blood of elder RA patients.

      PubDate: Fri, 10 Jun 2022 10:04:14 +020
       
  • Understanding gene-lifestyle interaction in obesity: the role of mediation
           versus moderation

    • Abstract: Background: Obesity results from complex interactions between genetic susceptibility to weight gain and poor eating and lifestyle behaviors. The approach that has been traditionally used in genetics to investigate gene-environment/lifestyle interaction in obesity is based on the concept of moderation, or effect modification. Another approach called mediation analysis can be used to investigate gene-environment interaction in obesity. The objective of this review article is to explain the differences between the concepts of moderation and mediation and summarize the studies that have used mediation analysis to support the role of eating or lifestyle behaviors as putative mediators of genetic susceptibility to obesity.Summary: Moderation is used to determine whether the effect of an exposure (genes associated with obesity) on an outcome (obesity phenotype) differs in magnitude and/or direction across the spectrum of environmental exposure. Mediation analysis is used to assess the extent to which the effect of the exposure on the outcome is explained by a given set of hypothesized mediators with the aim of understanding how the exposure could lead to the outcome. In comparison with moderation, relatively few studies used mediation analyses to investigate gene-environment in obesity. Most studies found evidence that traits related to appetite or eating behaviors partly mediated genetic susceptibility to obesity in either children or adults. Key messages: Moderation and mediation represent two complementary approaches to investigate gene-environment interaction in obesity and address different research questions pertaining to the cause-effect relationship between genetic susceptibility to obesity and various obesity outcomes. More studies relying on mediation are needed to better understand the role eating and lifestyle habits in mediating genetic susceptibility to obesity.

      PubDate: Tue, 01 Mar 2022 09:53:52 +010
       
  • Dairy product intake modifies microRNAs expression among individuals with
           hyperinsulinemia – A post-intervention cross-sectional study

    • Abstract: Introduction: microRNA (miRNA) profiles have been shown to change after intake of dairy products. Dysregulation of miRNA is associated with the changes in the level of glycemic parameters. The objectives are 1- to investigate miRNAs expression after consumption of dairy products; and 2- to study the association between miRNAs and glycemic profile among individuals with hyperinsulinemia. Methods: In crossover design, 24 participants were randomized into 2 phases: high-dairy (HD) (≥4 servings / day according to the Canadian Food Guide (2007)) and adequate-dairy (AD) (≤2 servings / day) over 6-week. First, miRNAs were extracted from a pooled plasma sample of 10 subjects after HD and AD intervention which analyzed in duplicate by array hybridization (Affymetrix Gene Chip miRNA Array v. 4.0). Secondly, 6 miRNAs related to type 2 diabetes (T2D) were validated by qRT-PCR from plasma of 24 participants. Results: Microarray analysis indicated that 237 miRNAs expressed differentially (FC ≥ ±1.2; p value < 0.05)) between AD and HD. Among pooled miRNAs, the level of selected miRNAs, including miR-652-3p, miR-106b-5p, miR-93-5p, and miR-107 were down-regulated; conversely, miR-223-3p and miR-122-5p were up-regulated. After qRT-PCR validation, only the expression level of miR-106-5p increased after HD compared to AD (p = 0.02). After AD intervention, the level of fasting plasma glucose (FPG) and insulin, HOMA-IR were negatively correlated with miR-122-5p. Similarly, negative correlation was found between miR-106-5p and FPG. Conclusion: The miRNAs profile was modified after HD compared to AD and this may have role in modifying the risk of T2D (Registration number: NCT02961179)

      PubDate: Fri, 25 Feb 2022 11:50:53 +010
       
  • Efficacy of Probiotic, Chlorhexidine, and Sodium Fluoride Mouthrinses on
           Mutans Streptococci in 8- to 12-Year-Old Children: A Crossover Randomized
           Trial

    • Abstract: Introduction: The oral cavity is home to a diverse and distinct microbiome. While the role of oral bacteria in cariogenic and other dental diseases is irrefutable, their beneficial effects in the form of probiotics (PB) has been less studied, especially pertaining to oral diseases in children. This study compares the efficacy of a PB mouthrinse with 0.12% chlorhexidine (CHX) and 0.05% sodium fluoride (NaF) mouthrinse on the colony counts of mutans streptococci (MS) in children. Methods: A triple-blind crossover randomized trial between interventional groups was planned. Fifty-one children between 8 to 12 years of age were divided into three groups (I, II, and III) and were exposed to all three mouthrinses (A, B, and C) by randomized allocation for a period of two weeks with an inter-phase washout period of four weeks. Pre- and post-interventional MS counts (CFU/mL) were assessed, and the mean change was analysed using the t test (intragroup) and ANOVA (intergroup and crossover). Results: The mean changes in the colony counts obtained with the use of PB, CHX, and NaF mouthrinses were −1.0223 (−1.2201 to −0.8246), −0.9564 (−1.1503 to −0.7626), and −0.9511 (−1.1554 to −0.7467), respectively, which were statistically significant (p #x3c; 0.0001). However, the intergroup comparison for the mean change in colony counts revealed no statistically significant differences (p #x3e; 0.05). Conclusion: The study concluded that the PB mouthrinse was equally efficacious as compared to CHX and NaF mouthrinses against MS in 8- to 12-year-old children. However, further studies are recommended to strengthen the evidence.
      Lifestyle Genomics
      PubDate: Wed, 12 Jan 2022 07:56:21 +010
       
 
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