Objective To investigate the relationship between white matter lesions (WML) within the cholinergic pathway and vascular cognitive impairment.Method Middle-aged and elderly stroke patients underwent brain MRI examination and Montreal Cognitive Assessment (MoCA).Cholinergic Pathways Hyperintensities Scale (CHIPS) scores and the overall WML burden by Schelten on fluidattenuated inversion recovery MRI images were determined and compared with MoCA scores.Spearman partial rank correlation coefficients and standardized regression coefficients were calculated.Results Thirty four patients were included ( mean age ( 62.2 ± 8.8 ) years, 45-82 years).MoCA scores negatively correlated with WML burdens by Schelten scores ( β = - 0.357, P = 0.042) and CHIPS scores ( β =-0.382,P=0.026).CHIPS scores were negatively associated with visuospatial and executive function (r = - 0.290, P = 0.048 ), naming function ( r = - 0.486, P = 0.002 ), attention ( r = - 0.311, P =0.037) and abstraction ( r = - 0.344, P = 0.023).Schelten scores were negatively associated with naming function (r = - 0.492, P = 0.002), attention ( r = - 0.364, P = 0.017) and abstraction ( r = - 0.390,P=0.011).Conclusion WML lesions within the cholinergic pathyway play a possible role in vascular cognitive impairment especially in visuospatial and executive function.

The secondary structures of hepatitis C virus (HCV) RNA and the cellular proteins that bind to them are important for modulating both translation and RNA replication. However, the sets of RNA-binding proteins involved in the regulation of HCV translation, replication and encapsidation remain unknown. Here, we identified RNA binding motif protein 24 (RBM24) as a host factor participated in HCV translation and replication. Knockdown of RBM24 reduced HCV propagation in Huh7.5.1 cells. An enhanced translation and delayed RNA synthesis during the early phase of infection was observed in RBM24 silencing cells. However, both overexpression of RBM24 and recombinant human RBM24 protein suppressed HCV IRES-mediated translation. Further analysis revealed that the assembly of the 80S ribosome on the HCV IRES was interrupted by RBM24 protein through binding to the 5'-UTR. RBM24 could also interact with HCV Core and enhance the interaction of Core and 5'-UTR, which suppresses the expression of HCV. Moreover, RBM24 enhanced the interaction between the 5'- and 3'-UTRs in the HCV genome, which probably explained its requirement in HCV genome replication. Therefore, RBM24 is a novel host factor involved in HCV replication and may function at the switch from translation to replication.
Cells, Cultured ; Hepacivirus ; genetics ; growth & development ; metabolism ; Humans ; Protein Biosynthesis ; RNA-Binding Proteins ; metabolism ; Virus Replication ; genetics