Online Gaming Behavior And Psychosocial Well-Being in Greek Adolescents

Online gaming is an appealing and popular activity among adolescents. However, several studies have shown that excessive engagement is related to psychosocial problems. The present study is based on data from the EU NET ADB project and examined the association between problematic online gaming and psychosocial wellbeing in a Greek school-student’s sample. Problematic online gaming is classified in the DSM-5 as Internet Gaming Disorder (IGD) and was measured with the Assessment of Internet and Computer game Addiction Scale — Gaming Module (AICA-S-gaming). Negative aspects of psychosocial well-being were operationally defined as a combination of behavioral, affective and cognitive problems and were assessed through the Youth Self-Report (YSR) scale. The results indicate that IGD has a significant impact on the externalizing and internalizing dimensions of the YSR scale and particularly in the subscales anxious depressed, withdrawn-depressed, social problems, thought problems, somatic complaints, rule-breaking behavior and aggressive behavior. Limitations and applications of the study are discussed

The COVID-19 Data Portal: Accelerating SARS-CoV-2 and COVID-19 research through rapid open access data sharing

The severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) pandemic will be remembered as one of the defining events of the 21st century. The rapid global outbreak has had significant impacts on human society and is already responsible for millions of deaths. Understanding and tackling the impact of the virus has required a worldwide mobilisation and coordination of scientific research. The COVID-19 Data Portal (https://www.covid19dataportal.org/) was first released as part of the European COVID-19 Data Platform, on April 20th 2020 to facilitate rapid and open data sharing and analysis, to accelerate global SARS-CoV-2 and COVID-19 research. The COVID-19 Data Portal has fortnightly feature releases to continue to add new data types, search options, visualisations and improvements based on user feedback and research. The open datasets and intuitive suite of search, identification and download services, represent a truly FAIR (Findable, Accessible, Interoperable and Reusable) resource that enables researchers to easily identify and quickly obtain the key datasets needed for their COVID-19 research

Active site variants in STT3A cause a dominant type I congenital disorder of glycosylation with neuromusculoskeletal findings

Congenital disorders of glycosylation (CDGs) form a group of rare diseases characterized by hypoglycosylation. We here report the identification of 16 individuals from nine families who have either inherited or de novo heterozygous missense variants in STT3A, leading to an autosomal-dominant CDG. STT3A encodes the catalytic subunit of the STT3A-containing oligosaccharyltransferase (OST) complex, essential for protein N-glycosylation. Affected individuals presented with variable skeletal anomalies, short stature, macrocephaly, and dysmorphic features; half had intellectual disability. Additional features included increased muscle tone and muscle cramps. Modeling of the variants in the 3D structure of the OST complex indicated that all variants are located in the catalytic site of STT3A, suggesting a direct mechanistic link to the transfer of oligosaccharides onto nascent glycoproteins. Indeed, expression of STT3A at mRNA and steady-state protein level in fibroblasts was normal, while glycosylation was abnormal. In S. cerevisiae, expression of STT3 containing variants homologous to those in affected individuals induced defective glycosylation of carboxypeptidase Y in a wild-type yeast strain and expression of the same mutants in the STT3 hypomorphic stt3-7 yeast strain worsened the already observed glycosylation defect. These data support a dominant pathomechanism underlying the glycosylation defect. Recessive mutations in STT3A have previously been described to lead to a CDG. We present here a dominant form of STT3A-CDG that, because of the presence of abnormal transferrin glycoforms, is unusual among dominant type I CDGs