An Analysis of Abusive Language Data Collected through a Game with a Purpose

In this work we present an analysis of abusive language annotations collected through a 3D video game. With this approach, we are able to involve in the annotation teenagers, i.e. typical targets of cyberbullying, whose data are usually not available for research purposes. Using the game in the framework of educational activities to empower teenagers against online abuse we are able to obtain insights into how teenagers communicate, and what kind of messages they consider more offensive. While players produced interesting annotations and the distributions of classes between players and experts are similar, we obtained a significant number of mismatching judgements between experts and players

A 3D Role-Playing Game for Abusive Language Annotation

Gamification has been applied to many linguistic annotation tasks, as an alternative to crowdsourcing platforms to collect annotated data in an inexpensive way. However, we think that still much has to be explored. Games with a Purpose (GWAPs) tend to lack important elements that we commonly see in commercial games, such as 2D and 3D worlds or a story. Making GWAPs more similar to full-fledged video games in order to involve users more easily and increase dissemination is a demanding yet interesting ground to explore. In this paper we present a 3D role-playing game for abusive language annotation that is currently under development

Influence of genetic factors in newly diagnosed type 2 diabeticpatients: the TCF7L2 and GENETIC LOAD studies.

Introduzione. Negli ultimi anni sono stati individuati molti nuovi polimorfismi (SNP, Single Nucleotide Polymorphisms) associati allo sviluppo di diabete di tipo 2 (T2DM), soprattutto grazie all\u2019avvento di nuove tecniche di genotipizzazione su larga scala, GWAS (Genome Wide Association Scan). Ogni SNP per\uf2 contribuisce da solo in modo marginale al rischio di sviluppare la malattia e spesso \ue8 poco chiara la funzione biologica di queste varianti geniche nella regolazione dell\u2019omeostasi del glucosio. Tra questi polimorfismi, la variante intronica rs7903146 del gene TCF7L2 (Transcription Factor 7 Like 2) \ue8 al momento il pi\uf9 forte fattore di rischio per il diabete di tipo 2 (O.R.= 1.37). Scopo dello studio. Chiarire l\u2019effetto di diversi loci associati allo sviluppo di T2DM su fenotipi clinici e patofisiologici (funzione beta-cellulare e sensibilit\ue0 insulinica) in pazienti con T2DM neo-diagnosticato. Metodi. Abbiamo analizzato 464 pazienti di discendenza italiana con T2DM neodiagnosticato, anti-GAD negativi. La caratterizzazione clinica standard \ue8 stata effettuata mediante metodi classici. La funzione beta-cellulare \ue8 stata valutata applicando un modello matematico alle curve di glucosio e di C-peptide derivanti da prelievi eseguiti durante OGTT, ed \ue8 differenziabile in due componenti: prima fase di secrezione insulinica o controllo derivativo, rappresentato dalla quantit\ue0 di insulina secreta in risposta all\u2019incremento unitario della concentrazione di glucosio, e la seconda fase di secrezione o controllo proporzionale, rappresentato come la velocit\ue0 di secrezione insulinica a concentrazioni crescenti di glucosio (5.5, 8.0, 11.0, 15.0 and 20.0 mM). La misura della sensibilit\ue0 insulinica deriva dalla quantit\ue0 di glucosio infuso che viene metabolizzato negli ultimi 60 minuti del clamp euglicemica, tale valore \ue8 detto M. Sono stati genotipizzati i seguenti SNP, gi\ue0 visti essere associati allo sviluppo di T2DM: rs7901695 (TCF7L2), rs7903146 (TCF7L2), rs11196205 (TCF7L2), rs12255372 (TCF7L2), rs679931 (CACNA1E), rs1801282 (PPARG), rs1044498 (ENPP1), rs10946398 (CDKAL1), rs1111875 (HHEX/IDE) rs10010131 (WFS1), rs4430796 (TCF2), rs4402960 (IGF2BP2). Risultati. TCF7L2. Gli alleli di rischio di 3 su 4 polimorfismi di TCF7L2 (rs7901695, rs7903146, rs11196205) sono associati a pi\uf9 alti valori plasmatici di glucosio a digiuno (p<0.001, p<0.03 e p<0.01 rispettivamente). Gli allele di rischio dei primi due SNP (rs7901695 e rs7903146) sono associati ad un aumento del controllo proporzionale della funzione beta cellulare (p<0.02 e p<0.03 rispettivamente). Tramite l\u2019analisi degli aplotipi sono stati individuati 4 aplotipi rappresentati nella popolazione in esame e due di questi (haplo4, frequenza: 0.038 e haplo9, frequenza: 0.086) hanno un forte impatto sulla funzione beta-cellulare. Altre varianti geniche. Nessuno dei rimanenti 8 polimorfismi (rs679931, rs1801282, rs1044498, rs10946398, rs1111875, rs10010131, rs4430796, rs4402960) ha mostrato associazione indipendente con alterazioni della funzione beta-cellulare o della sensibilit\ue0 insulinica. Abbiamo calcolato uno score genetico di queste varianti sommando il numero di alleli di rischio presenti in ogni paziente (escludendo TCF7L2). I pazienti sono stati divisi in tre gruppi: portatori di un numero di alleli di rischio 64 6 (gruppo A, n=76), pazienti con un numero di alleli di rischio compresa tra 7 e 9 (gruppo B, n=226) e soggetti con un numero di alleli di rischio 65 10 (gruppo C, n=69). Il controllo proporzionale della funzione beta cellulare risultava alterato in modo statisticamente significativo (p=0.05) nel gruppo C rispetto agli altri due gruppi. Maggiore \ue8 il numero di alleli di rischio associato a T2DM, peggiore \ue8 la funzione beta-cellulare. Conclusioni. Questi dati mostrano come diverse varianti geniche giocano un ruolo significativo nel determinare il fenotipo patofisiologico dei pazienti con T2DM neo-diagnosticato, influenzando soprattutto la funzione beta-cellulare. Perci\uf2, la valutazione dei genotipi di rischio per il T2DM potrebbe tornare utile per scopi diagnostici, prognostici e terapeutici in pazienti con T2DM neodiagnosticato.Background. Genome wide association studies (GWAS) have played a primary role in demonstrating that genetic variation in a number of loci, as assessed by single nucleotide polymorphisms (SNPs), affects the risk of type 2 diabetes mellitus (T2DM). Among these, rs7903146, an intronic variant of the TCF7L2 (Transcription Factor 7 Like 2) gene, is possibly the strongest known genetic risk factor for T2DM (O.R.=1.37). Each risk variant, however, per se contributes quantitatively little to the overall risk and is often of questionable biological significance in affecting the determinants of glucose regulation. Aim(s). To elucidate the effects of several T2DM risk genetic loci on clinical and pathophysiological (beta-cell function and insulin sensitivity) phenotypes of patients with newly diagnosed T2DM. Methods. We studied 464 patients of Italian ancestry with newly diagnosed, GAD-antibody negative, type 2 diabetes mellitus. Standard clinical phenotyping was carried out by classical methods. Beta-cell function and insulin sensitivity were assessed by mathematical modeling of glucose and C-peptide curves during a 240\u2019 frequently sampled OGTT and by euglycemic insulin clamp, respectively. Beta-cell function is described as the sum of two components: i. first phase of insulin secretion or derivative control (DC), presented as the pulse secretory response to a unit rate of change in glucose concentration; ii. second phase of insulin secretion or proportional control (PC), presented as the insulin secretion rate at glucose concentrations of 5.5, 8.0, 11.0, 15.0 and 20.0 mM, respectively. Insulin sensitivity is presented as the amount of glucose infused which is metabolized in the last 60\u2019 of the euglycemic clamp (M value). The following SNPs (related gene in brackets), already known to be risk loci of T2DM, were genotyped: rs7901695 (TCF7L2), rs7903146 (TCF7L2), rs11196205 (TCF7L2), rs12255372 (TCF7L2), rs679931 (CACNA1E), rs1801282 (PPARG), rs1044498 (ENPP1), rs10946398 (CDKAL1), rs1111875 (HHEX/IDE) rs10010131 (WFS1), rs4430796 (TCF2), rs4402960 (IGF2BP2). Results. TCF7L2. The risk alleles of 3 (rs7901695, rs7903146, rs11196205) out of 4 TCF7L2 SNPs were associated with higher fasting plasma glucose (p<0.01, p<0.03 and p<0.01 respectively). The risk alleles of the first two SNPs (rs7901695, rs7903146) were associated to a decrease in the proportional control of beta-cell function (p<0.02 and p<0.03 respectively). Four TCF7L2 haplotypes were detected, two of which (haplo4, frequency: 0.038; and haplo9, frequency: 0.086) had a strong impact on beta-cell function. Haplo4 was associated with the lowest proportional control of beta-cell function while haplo9 showed the highest. Other genetic variants. None of the 8 remaining SNPs (rs679931, rs1801282, rs1044498, rs10946398, rs1111875, rs10010131, rs4430796, rs4402960) showed any significant independent association with insulin sensitivity or beta-cell function. We computed a genetic risk score of this variants, by summing the number of the T2DM risk alleles present in each patient (excluding TCF7L2). The patients were divided into three groups: 6 or less risk alleles (group A, n=76), 7-9 risk alleles (group B, n=226), 10 or more risk alleles (group C, n=69). The porportional control of beta-cell function was significantly impaired (P=0.05) in group C than in the other two groups, i.e. the higher the number of T2DM risk variants the lower beta cell function. Conclusions. These data show that several genetic variants play a significant role in determining the pathophysiological phenotype of patients with newly diagnosed type 2 diabetes, with most of the influence exerted on beta-cell function. Thus, assessment of T2DM risk genotype may turn to be useful for diagnostic, prognostic and therapeutic purposes in patients with newly diagnosed T2DM

Recovery from disability after stroke as a target for a behavioural intervention: Results of a randomised controlled trial

Purpose: Disability following stroke is highly prevalent and is predicted by psychological variables such as control cognitions and emotions, in addition to clinical variables. This study evaluated the effectiveness of a workbook-based intervention, designed to change cognitions about control, in improving outcomes for patients and their carers. Method: At discharge, stroke patients were randomly allocated (with their carers) to a 5-week intervention (n = 103) or control (normal care: n = 100). The main outcome (at 6 months) was recovery from disability using a performance measure, with distress and satisfaction as additional outcomes. Results: The intervention group showed significantly better disability recovery, allowing for initial levels of disability, than those in the control group, F(1,201) = 5.61, p = 0.019. Groups did not differ in distress or satisfaction with care for patients or carers. The only psychological process variable improved by the intervention was Confidence in Recovery but this did not mediate the effects on recovery. Conclusions: A large proportion of intervention participants did not complete the workbook tasks. This was perhaps associated with the fairly low level of personal contact with workbook providers. The modest success of this intervention suggests that it may be possible to develop effective behavioural interventions to enhance recovery from disability in stroke patients

Effects of Exercise in Children and Adolescent with Type 1 Diabetes Mellitus

Exercise is one of the most important components, together with insulin therapy and diet, in the clinical management of type 1 diabetes mellitus (T1DM). Physical activity has multiple health benefits, like blood pressure reduction, improvement of cardiovascular fitness and lipoprotein profile. The benefits for children with diabetes may also include positive effects on glycemic metabolism. The following review examines the main studies about the effects of exercise on diabetes. Additional longitudinal studies are needed to verify the hypothetical positive relationship between sport and T1DM and between sport and diabetic complications. However, aerobic and moderate intensity physical activity in children and adolescents with T1DM should be encouraged also for its beneficial psychological effects