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Dental caries is one of the most prevalent chronic oral diseases. Dietary habits, oral hygiene, and accessibility to preventive interventions, notably fluoridated water, are critical elements of the causative pie in the multifactorial onset of dental caries. This paper investigates if the total sugar consumption in grams or percentage of total daily energy intake changes the likelihood of developing dental caries after adjusting for the water source, gender, family income, and race. The prevalence of dental caries experience, the mean incidence of tooth decay experience, and the proportion of energy consumed from sweets were all calculated using data from the National Health and Nutrition Examination Surveys (NHANES) for the years 2011-2012 and 2015-2016, along with the corresponding weights. Logistic regressions with many variables and levels were employed for the analysis. Odds ratios with 95% confidence intervals were presented. In 2011-2012, 69.03% and 2015-16, 69.93% of the US population had at least one caries experience. When stratified by age, dental caries experience was most prevalent amongst adolescents at 70.64% at 11-20 years in 2011-12 and 70.28% at 2-5 years 2015-16. The mean daily sugar consumption was 115.34 grams and 103.32 grams in 2011-12, respectively; 23.96% and 22.08% of mean daily energy consumption from sugar were observed in both years. In 2011-2012, Americans consumed 23.3% of their daily energy from sugars on average and 21.02% in 2015-16. The Chi-square test was not significant for categories of sugar consumption and caries experience. The overall amount of sugar consumed in grammes and the amount consumed as a proportion of total daily calorie intake changed in neither year, and neither did the likelihood of developing dental caries. The findings mentioned above confirm earlier research that net sugar consumption does not affect experience with caries; rather, the dietary aspect of the causative pie of caries experience has to be thoroughly researched in light of contemporary developments in dental public health. [ABSTRACT FROM AUTHOR]

Background: Long‐term breast cancer survivors are at risk for cardiotoxicity after treatment, but there is insufficient evidence to provide long‐term (~10 years) cardiovascular disease (CVD) screening recommendations. We sought to evaluate a tri‐modality CVD screening approach. Methods: This single‐arm, feasibility study enrolled 201 breast cancer patients treated ≥6 years prior without CVD at diagnosis. Patients were sub‐grouped: cardiotoxic (left‐sided) radiation (RT), cardiotoxic (anthracycline‐based) chemotherapy, both cardiotoxic chemotherapy and RT, and neither cardiotoxic treatment. Patients underwent electrocardiogram (EKG), transthoracic echocardiogram with strain (TTE with GLS), and coronary artery calcium computed tomography (CAC CT). The primary endpoint was preclinical or clinical CVD. Results: Median age was 50 (29–65) at diagnosis and 63 (37–77) at imaging; median interval was 11.5 years (6.7–14.5). Among sub‐groups, 44% had no cardiotoxic treatment, 31.5% had cardiotoxic RT, 16% had cardiotoxic chemotherapy, and 8.5% had both. Overall, 77.6% showed preclinical and/or clinical CVD and 51.5% showed clinical CVD. Per modality, rates of any CVD and clinical CVD were, respectively: 27.1%/10.0% on EKG, 50.0%/25.3% on TTE with GLS, and 50.8%/45.8% on CAC CT. No statistical difference was seen among the treatment subgroups (NS, χ2 test, p = 0.58/p = 0.15). Conclusion: This study identified a high incidence of CVD in heterogenous long‐term breast cancer survivors, most >10 years post‐treatment. Over half had clinical CVD findings warranting follow‐up and/or intervention. Each imaging test independently contributed to the detection rate. This provides early evidence that long‐term cardiac screening may be of value to a wider group of breast cancer survivors than previously recognized. [ABSTRACT FROM AUTHOR]

Chromatin remodeling is a key requirement for transcriptional control of cellular differentiation. However, the factors that alter chromatin architecture in mammary stem cells (MaSCs) are poorly understood. Here, we show that BPTF, the largest subunit of the NURF chromatin remodeling complex, is essential for MaSC self-renewal and differentiation of mammary epithelial cells (MECs). BPTF depletion arrests cells at a previously undefined stage of epithelial differentiation that is associated with an incapacity to achieve the luminal cell fate. Moreover, genome-wide analysis of DNA accessibility following genetic or chemical inhibition, suggests a role for BPTF in maintaining the open chromatin landscape at enhancers regions in MECs. Collectively, our study implicates BPTF in maintaining the unique epigenetic state of MaSCs., (Copyright © 2017 The Author(s). Published by Elsevier Inc. All rights reserved.)

DNA damaging agents cause rapid shrinkage of tumors and form the basis of chemotherapy for sarcomas despite significant toxicities. Drugs having superior efficacy and wider therapeutic windows are needed to improve patient outcomes. We used cell proliferation and apoptosis assays in sarcoma cell lines and benign cells; γ-H2AX expression, comet assay, immunoblot analyses and drug combination studies in vitro and in patient derived xenograft (PDX) models. BO-1055 caused apoptosis and cell death in a concentration and time dependent manner in sarcoma cell lines. BO-1055 had potent activity (submicromolar IC50) against Ewing sarcoma and rhabdomyosarcoma, intermediate activity in DSRCT (IC50 = 2-3μM) and very weak activity in osteosarcoma (IC50 >10μM) cell lines. BO-1055 exhibited a wide therapeutic window compared to other DNA damaging drugs. BO-1055 induced more DNA double strand breaks and γH2AX expression in cancer cells compared to benign cells. BO-1055 showed inhibition of tumor growth in A673 xenografts and caused tumor regression in cyclophosphamide resistant patient-derived Ewing sarcoma xenografts and A204 xenografts. Combination of BO-1055 and irinotecan demonstrated synergism in Ewing sarcoma PDX models. Potent activity on sarcoma cells and its relative lack of toxicity presents a strong rationale for further development of BO-1055 as a therapeutic agent., Competing Interests: none.