OBJECTIVES. To analyze the prevalence of bullying victims among children and adolescents aged 8 to 18 years in 11 European countries and to investigate the associated sociodemographic, physical, and psychosocial factors. METHODS. Being a bullying victim was measured by using the social acceptance (bullying) scale from the Kidscreen-52, a health-related quality-of-life questionnaire administered to 16 210 children and adolescents aged 8 to 18 and their parents in postal or school-based surveys in 11 European countries. Standardized mean differences (effect size) were computed to measure the percentage of children/adolescents scoring 1 SD below the mean on the Kidscreen bullying scale. Logistic regression models were used to determine which sociodemographic, physical, and psychosocial factors were associated with being bullied. RESULTS. The percentage of children being bullied was 20.6% for the entire sample, ranging from 10.5% in Hungary to 29.6% in the United Kingdom. In almost all countries the factors most strongly associated with being bullied were younger age, having probable mental health problems, having a low score on the Kidscreen-52 moods and emotions dimensions, and poor social support. Using the grand mean for all countries as the reference category, there was an above-average likelihood of children or adolescents reporting that they had been victims of bullying in 5 countries (Austria, Netherlands, Spain, Switzerland, and the United Kingdom), and a below-average likelihood in 3 countries (France, Greece, Hungary). CONCLUSIONS. This study indicated considerable variation between countries in the prevalence of those perceiving themselves to be victims of bullying but also revealed a clear profile of those likely to be bullied. The study also suggests that the Kidscreen bullying scale could be useful in identifying potential bullying victims.

Background: The objective of the present study was to compare three different sampling and questionnaire administration methods used in the international KIDSCREEN study in terms of participation, response rates, and external validity. Methods: Children and adolescents aged 8–18 years were surveyed in 13 European countries using either telephone sampling and mail administration, random sampling of school listings followed by classroom or mail administration, or multistage random sampling of communities and households with self-administration of the survey materials at home. Cooperation, completion, and response rates were compared across countries and survey methods. Data on non-respondents was collected in 8 countries. The population fraction (PF, respondents in each sex-age, or educational level category, divided by the population in the same category from Eurostat census data) and population fraction ratio (PFR, ratio of PF) and their corresponding 95% confidence intervals were used to analyze differences by country between the KIDSCREEN samples and a reference Eurostat population. Results: Response rates by country ranged from 18.9% to 91.2%. Response rates were highest in the school-based surveys (69.0%–91.2%). Sample proportions by age and gender were similar to the reference Eurostat population in most countries, although boys and adolescents were slightly underrepresented (PFR <1). Parents in lower educational categories were less likely to participate (PFR <1 in 5 countries). Parents in higher educational categories were overrepresented when the school and household sampling strategies were used (PFR = 1.78–2.97). Conclusion: School-based sampling achieved the highest overall response rates but also produced slightly more biased samples than the other methods. The results suggest that the samples were sufficiently representative to provide reference population values for the KIDSCREEN instrument.

The aim was to develop a tool for the critical appraisal of epidemiological cross-sectional studies. Several recommendations or guidelines for assessing the strength of scientific evidence provided by observational studies were reviewed, like those from the Agency for Healthcare Research and Quality, the Scottish Intercollegiate Guidelines Group, the Osteba (Basque Office for Health Technology Assessment), and the STROBE Initiative. The tool has 27 items to assess: study question or objective, participants, comparability between groups, definition and measure of main variables; analysis and confusion, results, conclusions, external validity and applicability, and conflict of interest. This tool can be used to critically appraise research papers or to rate evidence during the elaboration of systematic reviews.

The aim of this work was to identify risk genes related to the development and progression of squamous cell carcinoma head and neck (SCCHN) and do a meta-analysis of available estimates. Eligible gene/polymorphism studies were identified by electronic searches. Individual participant data of 8540 patients with HNC and 9844 controls from 19 genetic studies were analyzed, yielding adjusted (tobacco, gender, age and alcohol) odds ratios (OR) and 95% confidence intervals (CIs) comparing cases with controls. A meta-analysis was done on the studies that applied fixed and random models. People have an increase of polymorphism expression related to inflammation (NFKB1-294-ATTG, TNFα308-A2A2/A2A1, and TNFβ252- B2B2/B2B1) or carcinogenic metabolism (GSTM1 null, and CYP1A1 m1/m1), representative of malignancy development. Furthermore, the increased expression of genes associated with the stabilization and repair of the cellular (OGG1-Asp267Asn, Ser279Gly Ile253Phe, 1578A>T, 1582C>T Ala399Glu (1542C>A) 1582insG 1543_1544delCT), and genes associated with the regulation of proliferation, apoptosis or tumor survival (miRNA499-CT/CC, CRYABC802G-CG/GG) are considered as risk factors. In this scheme, only the polymorphisms of ADH7A92G-GG and DEC1606-T/C genes are protective against malignancy transformation. The TP53, GSTM1 and CYPA1genes have been evaluated in more than one study and analyzed for homogeneity in each genotype. The meta-analysis showed no significant association between different allelic variants of Arg72Pro rs1042522 and SCCHN risk. In a model of tumorigenesis, an increased risk of SCCHN is associated with DNA repair and DNA stabilization genes. In addition, the polymorphisms involved in inflammation and carcinogenic metabolism processes represent an increased risk of SCCHN.