Does television viewing predict dietary intake five years later in high school students and young adults?

<p>Abstract</p> <p>Background</p> <p>Prior research has found that television viewing is associated with poor diet quality, though little is known about its long-term impact on diet, particularly during adolescence. This study examined the associations between television viewing behavior with dietary intake five years later.</p> <p>Methods</p> <p>Survey data, which included television viewing time and food frequency questionnaires, were analyzed for 564 middle school students (younger cohort) and 1366 high school students (older cohort) who had complete data available at Time 1 (1998–1999) and five years later at Time 2 (mean age at Time 2, 17.2 ± 0.6 and 20.5 ± 0.8 years, respectively). Regression models examined longitudinal associations between Time 1 television viewing behavior and Time 2 dietary intake adjusting for sociodemographic characteristics, Time 1 dietary intake, and Time 2 total daily energy intake.</p> <p>Results</p> <p>Respondents were categorized as limited television users (<it><</it>2 hours/daily), moderately high television viewers (2–5 hours/daily), and heavy television viewers (≥5 hours/daily). Among the younger cohort, Time 1 heavy television viewers reported lower fruit intake and higher sugar-sweetened beverage consumption than the other two groups. Among the older cohort, watching five or more hours of television per day at Time 1, predicted lower intakes of fruits, vegetables, whole grain and calcium-rich foods, and higher intakes of trans fat, fried foods, fast food menu items, snack products, and sugar-sweetened beverages (products commonly advertised on television) five years later.</p> <p>Conclusion</p> <p>Television viewing in middle and high school predicted poorer dietary intake five years later. Adolescents are primary targets of advertising for fast food restaurants, snack foods, and sugar-sweetened beverages, which may influence their food choices. Television viewing, especially during high school, may have long-term effects on eating choices and contribute to poor eating habits in young adulthood.</p

Methylation of Leukocyte DNA and Ovarian Cancer: Relationships with Disease Status and Outcome

Genome-wide interrogation of DNA methylation (DNAm) in blood-derived leukocytes has become feasible with the advent of CpG genotyping arrays. In epithelial ovarian cancer (EOC), one report found substantial DNAm differences between cases and controls; however, many of these disease-associated CpGs were attributed to differences in white blood cell type distributions. We examined blood-based DNAm in 336 EOC cases and 398 controls; we included only high-quality CpG loci that did not show evidence of association with white blood cell type distributions to evaluate association with case status and overall survival

Investigating Wastewater Reuse at MnDOT Truck Stations

The University of Minnesota (UMN) and the Minnesota Department of Transportation (MnDOT) conducted a study to determine whether implementing a wastewater reuse program would be a feasible option for MnDOT-owned truck washing stations. MnDOT has 137 truck stations in the state, where trucks are frequently washed to remove road salt build-up. MnDOT recognized an opportunity to potentially reuse the wastewater for appropriate greywater uses and recapture the salt for road use. Sampling was done to assess the wastewater contaminants in truck wash water at 11 truck-washing stations in Minnesota. Then technologies suited to removing organics and total suspended solids (TSS) but not chlorides were reviewed. The recommendation is that either a recirculating sand filter (RSF) or a membrane bioreactor (MBR) would be feasible technologies to use for this purpose. Using the MnDOT truck station in Arden Hills, Minnesota, an economic evaluation was done. Both systems could be used to effectively treat wastewater and produce brine for reuse, but the most economical solution for MnDOT would be to invest in a MBR. Compared with a RSF, an MBR is one-third less expensive over time, primarily due to low material and installation cost as well as a lower annual maintenance costs

Prospectus, March 2, 1994

https://spark.parkland.edu/prospectus_1994/1003/thumbnail.jp

Risk of Ovarian Cancer and Inherited Variants in Relapse-Associated Genes

Background: We previously identified a panel of genes associated with outcome of ovarian cancer. The purpose of the current study was to assess whether variants in these genes correlated with ovarian cancer risk. Methods and Findings: Women with and without invasive ovarian cancer (749 cases, 1,041 controls) were genotyped at 136 single nucleotide polymorphisms (SNPs) within 13 candidate genes. Risk was estimated for each SNP and for overall variation within each gene. At the gene-level, variation within MSL1 (male-specific lethal-1 homolog) was associated with risk of serous cancer (p = 0.03); haplotypes within PRPF31 (PRP31 pre-mRNA processing factor 31 homolog) were associated with risk of invasive disease (p = 0.03). MSL1 rs7211770 was associated with decreased risk of serous disease (OR 0.81, 95 % CI 0.66–0.98; p = 0.03). SNPs in MFSD7, BTN3A3, ZNF200, PTPRS, and CCND1A were inversely associated with risk (p,0.05), and there was increased risk at HEXIM1 rs1053578 (p = 0.04, OR 1.40, 95 % CI 1.02–1.91). Conclusions: Tumor studies can reveal novel genes worthy of follow-up for cancer susceptibility. Here, we found that inherited markers in the gene encoding MSL1, part of a complex that modifies the histone H4, may decrease risk of invasiv

Pan-cancer Alterations of the MYC Oncogene and Its Proximal Network across the Cancer Genome Atlas

Although theMYConcogene has been implicated incancer, a systematic assessment of alterations ofMYC, related transcription factors, and co-regulatoryproteins, forming the proximal MYC network (PMN),across human cancers is lacking. Using computa-tional approaches, we define genomic and proteo-mic features associated with MYC and the PMNacross the 33 cancers of The Cancer Genome Atlas.Pan-cancer, 28% of all samples had at least one ofthe MYC paralogs amplified. In contrast, the MYCantagonists MGA and MNT were the most frequentlymutated or deleted members, proposing a roleas tumor suppressors.MYCalterations were mutu-ally exclusive withPIK3CA,PTEN,APC,orBRAFalterations, suggesting that MYC is a distinct onco-genic driver. Expression analysis revealed MYC-associated pathways in tumor subtypes, such asimmune response and growth factor signaling; chro-matin, translation, and DNA replication/repair wereconserved pan-cancer. This analysis reveals insightsinto MYC biology and is a reference for biomarkersand therapeutics for cancers with alterations ofMYC or the PMN

Pan-Cancer Analysis of lncRNA Regulation Supports Their Targeting of Cancer Genes in Each Tumor Context

Long noncoding RNAs (lncRNAs) are commonly dys-regulated in tumors, but only a handful are known toplay pathophysiological roles in cancer. We inferredlncRNAs that dysregulate cancer pathways, onco-genes, and tumor suppressors (cancer genes) bymodeling their effects on the activity of transcriptionfactors, RNA-binding proteins, and microRNAs in5,185 TCGA tumors and 1,019 ENCODE assays.Our predictions included hundreds of candidateonco- and tumor-suppressor lncRNAs (cancerlncRNAs) whose somatic alterations account for thedysregulation of dozens of cancer genes and path-ways in each of 14 tumor contexts. To demonstrateproof of concept, we showed that perturbations tar-geting OIP5-AS1 (an inferred tumor suppressor) andTUG1 and WT1-AS (inferred onco-lncRNAs) dysre-gulated cancer genes and altered proliferation ofbreast and gynecologic cancer cells. Our analysis in-dicates that, although most lncRNAs are dysregu-lated in a tumor-specific manner, some, includingOIP5-AS1, TUG1, NEAT1, MEG3, and TSIX, synergis-tically dysregulate cancer pathways in multiple tumorcontexts