Search

BackgroundDevelopmental disabilities are a set of heterogeneous delays or difficulties in one or more areas of neuropsychological development. Considering that childhood is an essential stage of brain development and developmental delays lead to personal or social burdens, the early detection of childhood developmental disabilities is important. However, early screening for developmental disabilities has been a challenge because of the fear of positive results, expensive tests, differences in diagnosis depending on examiners’ abilities, and difficulty in diagnosis arising from the need for long-term follow-up observation. ObjectiveThis study aimed to assess the feasibility of using a serious game–derived index to identify heterogeneous developmental disabilities. This study also examines the correlation between the game-derived index and existing neuropsychological test results. MethodsThe randomized controlled trial involved 48 children with either normal development or developmental disabilities. In this clinical trial, we used 19 features (6 from the Korean-Wechsler Preschool and Primary Scale of Intelligence, 8 from the Psychoeducational Profile Revised, 2 from the Bruininks-Oseretsky Test of Motor Proficiency, Second Edition, and 3 from the Pediatric Evaluation of Disability Inventory) from neuropsychological tests and 9 (7 game scores, path accuracy, and completion rate) from the serious game, DoBrain. The following analysis was conducted based on participants’ baseline information and neuropsychological test and game-derived index data for one week: (1) we compared the baseline information between the normal development and developmental disabilities groups; (2) then we measured the correlation between the game-derived index and the neuropsychological test scores for each group; and (3) we built a classifier based on the game-derived index with a Gaussian process method and then compared the area under the curve (AUC) with a model based on neuropsychological test results. ResultsA total of 16 children (normal development=9; developmental disabilities=7) were analyzed after selection. Their developmental abilities were assessed before they started to play the serious games, and statistically significant differences were found in both groups. Specifically, the normal development group was more developed than the developmental disabilities group in terms of social function, gross motor function, full-scale IQ, and visual motor imitation, in that order. Similarly, the normal development group obtained a higher score on the game-derived index than the developmental disabilities group. In the correlation analysis between the game-derived index and the neuropsychological tests, the normal development group showed greater correlation with more variables than the developmental disabilities group. The game-derived index–based model had an AUC=0.9, a similar detection value as the neuropsychological test–based model’s AUC=0.86. ConclusionsA game-derived index based on serious games can detect children with heterogenous developmental disabilities. This suggests that serious games can be used as a potential screening tool for developmental disabilities. Trial RegistrationClinical Research Information Service KCT0003247; https://cris.nih.go.kr/cris/en/search/search_result_st01 .jsp?seq=12365

SARS-CoV-2, like other RNA viruses, has a propensity for genetic evolution owing to the low fidelity of its viral polymerase. Several recent reports have described a series of novel SARS-CoV-2 variants. Some of these have been identified as variants of concern (VOCs), including alpha (B.1.1.7, Clade GRY), beta (B.1.351, Clade GH), gamma (P.1, Clade GR), and delta (B.1.617.2, Clade G). VOCs are likely to have some effect on transmissibility, antibody evasion, and changes in therapeutic or vaccine effectiveness. However, the physiological and virological understanding of these variants remains poor. We demonstrated that these four VOCs exhibited differences in plaque size, thermal stability at physiological temperature, and replication rates. The mean plaque size of beta was the largest, followed by those of gamma, delta, and alpha. Thermal stability, evaluated by measuring infectivity and half-life after prolonged incubation at physiological temperature, was correlated with plaque size in all variants except alpha. However, despite its relatively high thermal stability, alpha's small plaque size resulted in lower replication rates and fewer progeny viruses. Our findings may inform further virological studies of SARS-CoV-2 variant characteristics, VOCs, and variants of interest. These studies are important for the effective management of the COVID-19 pandemic. [ABSTRACT FROM AUTHOR]

N6-methyladenosine (m6A) RNA methylation has recently emerged as a significant co-transcriptional modification involved in regulating various RNA functions. It plays a vital function in numerous biological processes. Enzymes referred to as m6A methyltransferases, such as the methyltransferaselike (METTL) 3-METTL14-Wilms tumor 1 (WT1)-associated protein (WTAP) complex, are responsible for adding m6A modifications, while m6A demethylases, including fat mass and obesity-associated protein (FTO) and alkB homolog 5 (ALKBH5), can remove m6A methylation. The functions of m6A-methylated RNA are regulated through the recognition and interaction of m6A reader proteins. Recent research has shown that m6A methylation takes place at multiple sites within hepatitis B virus (HBV) RNAs, and the location of these modifications can differentially impact the HBV infection. The addition of m6A modifications to HBV RNA can influence its stability and translation, thereby affecting viral replication and pathogenesis. Furthermore, HBV infection can also alter the m6A modification pattern of host RNA, indicating the virus's ability to manipulate host cellular processes, including m6A modification. This manipulation aids in establishing chronic infection, promoting liver disease, and contributing to pathogenesis. A comprehensive understanding of the functional roles of m6A modification during HBV infection is crucial for developing innovative approaches to combat HBV-mediated liver disease. In this review, we explore the functions of m6A modification in HBV replication and its impact on the development of liver disease.