Promoting dental care to children using traditional and interactive media following threat appeals

In recent years, computer games have become an important part of children’s lives. Gaming is not only one of their favorite pastime activities, but games are also increasingly used by marketers in an attempt to influence children’s purchase behavior. Today, almost every food and beverage brand targeting children has an advergame on its website. Advergames are “computer games specifically created to function as advertisements to promote brands”, containing brand identifiers such as logos and brand characters (Kretchmer, 2005: 7). Games can also be powerful learning tools. Several authors (e.g., Gee, 2003; Prensky, 2001) argue that computer games can be more enjoyable, more interesting and thus more effective than traditional learning modes to increase children’s knowledge. Empirical studies that evaluated the impact of the use of games within disciplines such as mathematics, science, language, geography and computer science show positive outcomes in terms of learning effectiveness in relation to curricular objectives (e.g., Papastergiou, 2009; Rosas et al., 2003). However, these authors mainly focus on the learning ability of games rather than their persuasive impact for social marketing purposes. In the area of health education, playing computer games has often been seen with skepticism (e.g., Bale, 1994; Funk and Buchman, 1995)

Correction: Differential Adaptation of Candida albicans In Vivo Modulates Immune Recognition by Dectin-1

The b -glucan receptor Dectin-1 is a member of the C-type lectin family and functions as an innate pattern recognition receptor in antifungal immunity. In both mouse and man, Dectin-1 has been found to play an essential role in controlling infections with Candida albicans , a normally commensal fungus in man which can cause superficial mucocutaneous infections as well as life-threatening invasive diseases. Here, using in vivo models of infection, we show that the requirement for Dectin-1 in the control of systemic Candida albicans infections is fungal strain-specific; a phenotype that only becomes apparent during infection and cannot be recapitulated in vitro . Transcript analysis revealed that this differential requirement for Dectin-1 is due to variable adaptation of C. albicans strains in vivo , and that this results in substantial differences in the composition and nature of their cell walls. In particular, we established that differences in the levels of cell-wall chitin influence the role of Dectin-1, and that these effects can be modulated by antifungal drug treatment. Our results therefore provide substantial new insights into the interaction between C. albicans and the immune system and have significant implications for our understanding of susceptibility and treatment of human infections with this pathogen

The Vehicle, Spring 1993

1993 Commemorative Edition: Celebrating 35 Years Table of Contents The Vehicle Editors\u27 Lineagepage 5 Milestonespage 6 THE SIXTIES Coverspage 7 Editors\u27 Notespage 8 Sureness is Never - excerptDon Shepardsonpage 9 SophisticationBenjamin Polkpage 10 A SonnetMignon Stricklandpage 11 The Twenty-Third ChannelBen Polkpage 11 Opposite AttractionsC.E.M. (Christine McColl)page 12 John F. KennedyJoel E. Hendrickspage 13 The Girl on the White PonyLarry Gatespage 14 The TimesW.D.M. (William Moser)page 16 Home ThoughtsJane Careypage 17 1966Roger Zulaufpage 18 Nagging ThoughtJanet Andrewspage 18 THE SEVENTIES Coverspage 19 Editors\u27 Notespage 20 RevolutionsSteve Siegelpage 21 UntitledKristine Kirkhampage 23 The Arithmetic ProblemJanice Forbuspage 23 Willie Seeverson Threw a Worm at MeMary Pipekpage 24 a love poem (by approximation)Ted Baldwinpage 25 Night and Summer in Two WorldsBarry Smithpage 26 Story of a Teenage PickleTerry Louis Schultzpage 27 Danny Lonely, Danny WildDevin Brownpage 28 Always TomorrowMary McDanielpage 29 THE EIGHTIES Coverspage 31 Having ChildrenDevon Flesorpage 33 What is Unnatural Is Sometimes MagicAngelique Jenningspage 34 If My Father Were A Writer, He Would Still BuildAngelique Jenningspage 35 Photo AlbumPatrick Peterspage 36 Poet Born in Pearl HarborAngelique Jenningspage 37 The History of High School BasketballPatrick Peterspage 38 Banana BreadGail Bowerpage 39 Cover LetterBob Zordanipage 40 Home MoviesBob Zordanipage 41 MigrationPatrick Peterspage 42 THE NINETIES Ba, Ba, Black SheepVictoria Bennettpage 45 Daily LessonsJennifer Moropage 49 Folding My OwnLaurie Ann Malispage 51 About the Authorspage 53 Editors\u27 Notespage 56https://thekeep.eiu.edu/vehicle/1062/thumbnail.jp

The Vehicle, Spring 1993

1993 Commemorative Edition: Celebrating 35 Years Table of Contents The Vehicle Editors\u27 Lineagepage 5 Milestonespage 6 THE SIXTIES Coverspage 7 Editors\u27 Notespage 8 Sureness is Never - excerptDon Shepardsonpage 9 SophisticationBenjamin Polkpage 10 A SonnetMignon Stricklandpage 11 The Twenty-Third ChannelBen Polkpage 11 Opposite AttractionsC.E.M. (Christine McColl)page 12 John F. KennedyJoel E. Hendrickspage 13 The Girl on the White PonyLarry Gatespage 14 The TimesW.D.M. (William Moser)page 16 Home ThoughtsJane Careypage 17 1966Roger Zulaufpage 18 Nagging ThoughtJanet Andrewspage 18 THE SEVENTIES Coverspage 19 Editors\u27 Notespage 20 RevolutionsSteve Siegelpage 21 UntitledKristine Kirkhampage 23 The Arithmetic ProblemJanice Forbuspage 23 Willie Seeverson Threw a Worm at MeMary Pipekpage 24 a love poem (by approximation)Ted Baldwinpage 25 Night and Summer in Two WorldsBarry Smithpage 26 Story of a Teenage PickleTerry Louis Schultzpage 27 Danny Lonely, Danny WildDevin Brownpage 28 Always TomorrowMary McDanielpage 29 THE EIGHTIES Coverspage 31 Having ChildrenDevon Flesorpage 33 What is Unnatural Is Sometimes MagicAngelique Jenningspage 34 If My Father Were A Writer, He Would Still BuildAngelique Jenningspage 35 Photo AlbumPatrick Peterspage 36 Poet Born in Pearl HarborAngelique Jenningspage 37 The History of High School BasketballPatrick Peterspage 38 Banana BreadGail Bowerpage 39 Cover LetterBob Zordanipage 40 Home MoviesBob Zordanipage 41 MigrationPatrick Peterspage 42 THE NINETIES Ba, Ba, Black SheepVictoria Bennettpage 45 Daily LessonsJennifer Moropage 49 Folding My OwnLaurie Ann Malispage 51 About the Authorspage 53 Editors\u27 Notespage 56https://thekeep.eiu.edu/vehicle/1062/thumbnail.jp

Amyloid Plaques Beyond Aβ: A Survey of the Diverse Modulators of Amyloid Aggregation

Aggregation of the amyloid-β (Aβ) peptide is strongly correlated with Alzheimer’s disease (AD). Recent research has improved our understanding of the kinetics of amyloid fibril assembly and revealed new details regarding different stages in plaque formation. Presently, interest is turning toward studying this process in a holistic context, focusing on cellular components which interact with the Aβ peptide at various junctures during aggregation, from monomer to cross-β amyloid fibrils. However, even in isolation, a multitude of factors including protein purity, pH, salt content, and agitation affect Aβ fibril formation and deposition, often producing complicated and conflicting results. The failure of numerous inhibitors in clinical trials for AD suggests that a detailed examination of the complex interactions that occur during plaque formation, including binding of carbohydrates, lipids, nucleic acids, and metal ions, is important for understanding the diversity of manifestations of the disease. Unraveling how a variety of key macromolecular modulators interact with the Aβ peptide and change its aggregation properties may provide opportunities for developing therapies. Since no protein acts in isolation, the interplay of these diverse molecules may differentiate disease onset, progression, and severity, and thus are worth careful consideration

Whole-genome sequencing reveals host factors underlying critical COVID-19

Critical COVID-19 is caused by immune-mediated inflammatory lung injury. Host genetic variation influences the development of illness requiring critical care1 or hospitalization2–4 after infection with SARS-CoV-2. The GenOMICC (Genetics of Mortality in Critical Care) study enables the comparison of genomes from individuals who are critically ill with those of population controls to find underlying disease mechanisms. Here we use whole-genome sequencing in 7,491 critically ill individuals compared with 48,400 controls to discover and replicate 23 independent variants that significantly predispose to critical COVID-19. We identify 16 new independent associations, including variants within genes that are involved in interferon signalling (IL10RB and PLSCR1), leucocyte differentiation (BCL11A) and blood-type antigen secretor status (FUT2). Using transcriptome-wide association and colocalization to infer the effect of gene expression on disease severity, we find evidence that implicates multiple genes—including reduced expression of a membrane flippase (ATP11A), and increased expression of a mucin (MUC1)—in critical disease. Mendelian randomization provides evidence in support of causal roles for myeloid cell adhesion molecules (SELE, ICAM5 and CD209) and the coagulation factor F8, all of which are potentially druggable targets. Our results are broadly consistent with a multi-component model of COVID-19 pathophysiology, in which at least two distinct mechanisms can predispose to life-threatening disease: failure to control viral replication; or an enhanced tendency towards pulmonary inflammation and intravascular coagulation. We show that comparison between cases of critical illness and population controls is highly efficient for the detection of therapeutically relevant mechanisms of disease

Genetic mechanisms of critical illness in COVID-19.

Host-mediated lung inflammation is present1, and drives mortality2, in the critical illness caused by coronavirus disease 2019 (COVID-19). Host genetic variants associated with critical illness may identify mechanistic targets for therapeutic development3. Here we report the results of the GenOMICC (Genetics Of Mortality In Critical Care) genome-wide association study in 2,244 critically ill patients with COVID-19 from 208 UK intensive care units. We have identified and replicated the following new genome-wide significant associations: on chromosome 12q24.13 (rs10735079, P = 1.65 × 10-8) in a gene cluster that encodes antiviral restriction enzyme activators (OAS1, OAS2 and OAS3); on chromosome 19p13.2 (rs74956615, P = 2.3 × 10-8) near the gene that encodes tyrosine kinase 2 (TYK2); on chromosome 19p13.3 (rs2109069, P = 3.98 ×  10-12) within the gene that encodes dipeptidyl peptidase 9 (DPP9); and on chromosome 21q22.1 (rs2236757, P = 4.99 × 10-8) in the interferon receptor gene IFNAR2. We identified potential targets for repurposing of licensed medications: using Mendelian randomization, we found evidence that low expression of IFNAR2, or high expression of TYK2, are associated with life-threatening disease; and transcriptome-wide association in lung tissue revealed that high expression of the monocyte-macrophage chemotactic receptor CCR2 is associated with severe COVID-19. Our results identify robust genetic signals relating to key host antiviral defence mechanisms and mediators of inflammatory organ damage in COVID-19. Both mechanisms may be amenable to targeted treatment with existing drugs. However, large-scale randomized clinical trials will be essential before any change to clinical practice