Identifying SARS-CoV-2 infected cells with scVDN.

Introduction: Single-cell RNA sequencing (scRNA-seq) is a powerful tool for understanding cellular heterogeneity and identifying cell types in virus-related research. However, direct identification of SARS-CoV-2-infected cells at the single-cell level remains challenging, hindering the understanding of viral pathogenesis and the development of effective treatments.

Methods: In this study, we propose a deep learning framework, the single-cell virus detection network (scVDN), to predict the infection status of single cells.

Functional consequences of postnatal interventions in a mouse model of Fragile X syndrome.

Background: Fragile X syndrome (FXS) is a leading genetic cause of autism and intellectual disability with cortical hyperexcitability and sensory hypersensitivity attributed to loss and hypofunction of inhibitory parvalbumin-expressing (PV) cells. Our studies provide novel insights into the role of excitatory neurons in abnormal development of PV cells during a postnatal period of inhibitory circuit refinement.

Methods: To achieve Fragile X mental retardation gene (Fmr1) deletion and re-expression in excitatory neurons during the postnatal day (P)14-P21 period, we generated Cre/Fmr1 (cOFF) and Cre/Fmr1 (cON) mice, respectively.

Deletion of Fmr1 from Forebrain Excitatory Neurons Triggers Abnormal Cellular, EEG, and Behavioral Phenotypes in the Auditory Cortex of a Mouse Model of Fragile X Syndrome.

Fragile X syndrome (FXS) is a leading genetic cause of autism with symptoms that include sensory processing deficits. In both humans with FXS and a mouse model [Fmr1 knockout (KO) mouse], electroencephalographic (EEG) recordings show enhanced resting state gamma power and reduced sound-evoked gamma synchrony. We previously showed that elevated levels of matrix metalloproteinase-9 (MMP-9) may contribute to these phenotypes by affecting perineuronal nets (PNNs) around parvalbumin (PV) interneurons in the auditory cortex of Fmr1 KO mice.