Sleep Hygiene and Problem Behaviors in Snoring and Non- Snoring School-Age Children

Objectives—The effects of sleep-disordered breathing, sleep restriction, dyssomnias, and parasomnias on daytime behavior in children have been previously assessed. However, the potential relationship(s) between sleep hygiene and children’s daytime behavior remain to be explored. The primary goal of this study was to investigate the relationship between sleep hygiene and problematic behaviors in non-snoring and habitually snoring children. Methods—Parents of 100 5- to 8-year-old children who were reported to snore “frequently” to “almost always,” and of 71 age-, gender-, and ethnicity-matched children who were reported to never snore participated in this study. As part of a larger, ongoing study, children underwent nocturnal polysomnography and parents were asked to complete the Children’s Sleep Hygiene Scale (CSHS) and the Conners’ Parent Rating Scales-Revised (CPRS-R:L). Results—In the snoring group, strong negative correlations (r = −.39, p Conclusions—Parental reports of behavioral patterns in snoring children indicate that poorer sleep hygiene is more likely to be associated with behavior problems, including hyperactivity, impulsivity, and oppositional behavior. In contrast, no significant relationships between slee

Sclerostin neutralization unleashes the osteoanabolic effects of Dkk1 inhibition

The WNT pathway has become an attractive target for skeletal therapies. High-bone-mass phenotypes in patients with loss-of-function mutations in the LRP5/6 inhibitor Sost (sclerosteosis), or in its downstream enhancer region (van Buchem disease), highlight the utility of targeting Sost/sclerostin to improve bone properties. Sclerostin-neutralizing antibody is highly osteoanabolic in animal models and in human clinical trials, but antibody-based inhibition of another potent LRP5/6 antagonist, Dkk1, is largely inefficacious for building bone in the unperturbed adult skeleton. Here, we show that conditional deletion of Dkk1 from bone also has negligible effects on bone mass. Dkk1 inhibition increases Sost expression, suggesting a potential compensatory mechanism that might explain why Dkk1 suppression lacks anabolic action. To test this concept, we deleted Sost from osteocytes in, or administered sclerostin neutralizing antibody to, mice with a Dkk1-deficient skeleton. A robust anabolic response to Dkk1 deletion was manifest only when Sost/sclerostin was impaired. Whole-body DXA scans, μCT measurements of the femur and spine, histomorphometric measures of femoral bone formation rates, and biomechanical properties of whole bones confirmed the anabolic potential of Dkk1 inhibition in the absence of sclerostin. Further, combined administration of sclerostin and Dkk1 antibody in WT mice produced a synergistic effect on bone gain that greatly exceeded individual or additive effects of the therapies, confirming the therapeutic potential of inhibiting multiple WNT antagonists for skeletal health. In conclusion, the osteoanabolic effects of Dkk1 inhibition can be realized if sclerostin upregulation is prevented. Anabolic therapies for patients with low bone mass might benefit from a strategy that accounts for the compensatory milieu of WNT inhibitors in bone tissue

Communication Research

Contains reports on seven research projects.Rockefeller FoundationCarnegie Foundatio

Communication Research

Contains reports on nine research projects.Bell Telephone Laboratories, Incorporate

Communication Research

Contains reports on eight research projects

Communication Research

Contains reports on eight research projects.Bell Telephone Laboratories, IncorporatedCarnegie FoundationRockefeller FoundationOffice of Naval Researc

Microbicide excipients can greatly increase susceptibility to genital herpes transmission in the mouse

<p>Abstract</p> <p>Background</p> <p>Several active ingredients proposed as vaginal microbicides have been shown paradoxically to <it>increase </it>susceptibility to infection in mouse genital herpes (HSV-2) vaginal susceptibility models and in clinical trials. In addition, "inactive ingredients" (or excipients) used in topical products to formulate and deliver the active ingredient might also cause epithelial toxicities that increase viral susceptibility. However, excipients have not previously been tested in susceptibility models.</p> <p>Methods</p> <p>Excipients commonly used in topical products were formulated in a non-toxic vehicle (the "HEC universal placebo"), or other formulations as specified. Twelve hours after exposure to the excipient or a control treatment, mice were challenged with a vaginal dose of HSV-2, and three days later were assessed for infection by vaginal lavage culture to assess susceptibility.</p> <p>Results</p> <p>The following excipients markedly increased susceptibility to HSV-2 after a single exposure: 5% glycerol monolaurate (GML) formulated in K-Y^®Warming Jelly, 5% GML as a colloidal suspension in phosphate buffered saline, K-Y Warming Jelly alone, and both of its humectant/solvent ingredients (neat propylene glycol and neat PEG-8). For excipients formulated in the HEC vehicle, 30% glycerin significantly increased susceptibility, and a trend toward increased HSV-2 susceptibility was observed after 10% glycerin, and 0.1% disodium EDTA, but not after 0.0186% disodium EDTA. The following excipients did not increase susceptibility: 10% propylene glycol, 0.18%, methylparaben plus 0.02% propylparaben, and 1% benzyl alcohol.</p> <p>Conclusions</p> <p>As reported with other surfactants, the surfactant/emulsifier GML markedly increased susceptibility to HSV-2. Glycerin at 30% significantly increased susceptibility, and, undiluted propylene glycol and PEG-8 greatly increased susceptibility.</p

Analysis of the modes of energy consumption of the complex of an incoherent scattering of the institute of ionosphere of national academy of sciences and the ministry of education and science of Ukraine

У даній статті представлені результати аналізу режимів енергоспоживання комплексу некогерентного розсіяння Інституту іоносфери НАН і МОН України з метою вирішення проблеми підвищення енергоефективності науково-дослідного комплексу та створення енергоефективної системи електропостачання, яка забезпечить стійку роботу наукового обладнання для виконання дослідницьких програм НАН України. Описана система електроживлення комплексу та режими енергоспоживання комплексу. Описано пристрої радарної системи, а також найбільш потужні споживачі електроенергії, які споживають електроенергію на експериментальні і господарські потреби. Проаналізовано енергоспоживання комплексу некогерентного розсіяння за 2013 р. Отримано і представлено графіки середньої споживаної потужності (середньодобовий показник) і середньої споживаної потужності в режимі вимірювань. Описана доцільність проведення робіт з оптимізації енергопостачання науково-дослідного комплексу Інституту іоносфери. Запропоновано можливі заходи для зниження економічної вартості проведення експериментів з дослідження іоносфери науково-дослідного комплексу некогерентного розсіяння. Проведено аналіз робіт сучасних авторів з метою показати, що підвищення ефективності функціонування систем електропостачання є актуальною проблемою сучасних досліджень.This article presents the results of the analysis of the energy consumption modes of the incoherent scattering complex of the Institute of Ionosphere of the National Academy of Sciences and the Ministry of Education and Science of Ukraine to solve the problem of increasing the energy efficiency of a research complex and creating an energy efficient power supply system that will ensure the sustainability of scientific equipment for research programs of the National Academy of Sciences of Ukraine. The system of power supply of the complex and modes of power consumption of the complex are described. The devices of the radar system are described, as well as the most powerful consumers of electricity, which consume electricity for experimental and economic needs. The energy consumption of the incoherent scattering complex in 2013 is analyzed. Graphs of the average power consumption (daily average) and average power consumption in measurement modes were obtained and presented. The feasibility of work to optimize the energy supply of the research complex of the institute of the ionosphere is described. Possible measures are proposed to reduce the economic cost of conducting experiments on the study of the ionosphere of an incoherent scattering research complex. The analysis of the works of modern authors i s carried out in order to show that increasing the efficiency of the power supply systems is an actual problem of modern research

RIG-I Is Required for the Inhibition of Measles Virus by Retinoids

Vitamin A can significantly decrease measles-associated morbidity and mortality. Vitamin A can inhibit the replication of measles virus (MeV) in vitro through an RARα- and type I interferon (IFN)-dependent mechanism. Retinoid-induced gene I (RIG-I) expression is induced by retinoids, activated by MeV RNA and is important for IFN signaling. We hypothesized that RIG-I is central to retinoid-mediated inhibition of MeV in vitro. We demonstrate that RIG-I expression is increased in cells treated with retinoids and infected with MeV. The central role of RIG-I in the retinoid-anti-MeV effect was demonstrated in the Huh-7/7.5 model; the latter cells having non-functional RIG-I. RAR-dependent retinoid signaling was required for the induction of RIG-I by retinoids and MeV. Retinoid signaling was also found to act in combination with IFN to induce high levels of RIG-I expression. RIG-I promoter activation required both retinoids and MeV, as indicated by markers of active chromatin. IRF-1 is known to be regulated by retinoids and MeV, but we found recruitment of IRF-1 to the RIG-I promoter by retinoids alone. Using luciferase expression constructs, we further demonstrated that the IRF-1 response element of RIG-I was required for RIG-I activation by retinoids or IFN. These results reveal that retinoid treatment and MeV infection induces significant RIG-I. RIG-I is required for the retinoid-MeV antiviral response. The induction is dependent on IFN, retinoids and IRF-1

Genomic distance entrained clustering and regression modelling highlights interacting genomic regions contributing to proliferation in breast cancer

<p>Abstract</p> <p>Background</p> <p>Genomic copy number changes and regional alterations in epigenetic states have been linked to grade in breast cancer. However, the relative contribution of specific alterations to the pathology of different breast cancer subtypes remains unclear. The heterogeneity and interplay of genomic and epigenetic variations means that large datasets and statistical data mining methods are required to uncover recurrent patterns that are likely to be important in cancer progression.</p> <p>Results</p> <p>We employed ridge regression to model the relationship between regional changes in gene expression and proliferation. Regional features were extracted from tumour gene expression data using a novel clustering method, called genomic distance entrained agglomerative (GDEC) clustering. Using gene expression data in this way provides a simple means of integrating the phenotypic effects of both copy number aberrations and alterations in chromatin state. We show that regional metagenes derived from GDEC clustering are representative of recurrent regions of epigenetic regulation or copy number aberrations in breast cancer. Furthermore, detected patterns of genomic alterations are conserved across independent oestrogen receptor positive breast cancer datasets. Sequential competitive metagene selection was used to reveal the relative importance of genomic regions in predicting proliferation rate. The predictive model suggested additive interactions between the most informative regions such as 8p22-12 and 8q13-22.</p> <p>Conclusions</p> <p>Data-mining of large-scale microarray gene expression datasets can reveal regional clusters of co-ordinate gene expression, independent of cause. By correlating these clusters with tumour proliferation we have identified a number of genomic regions that act together to promote proliferation in ER+ breast cancer. Identification of such regions should enable prioritisation of genomic regions for combinatorial functional studies to pinpoint the key genes and interactions contributing to tumourigenicity.</p