Lehman Nance (hyenawinter64)

A large number of computer-based training programs have been developed as an intervention to help individuals with autism spectrum disorders (ASD) improve their facial emotion recognition ability, as well as social skills. However, it is unclear to what extent these facial emotion training programs can produce beneficial, long-lasting, and generalizable results. Using standard meta-analytic techniques, we investigated the effects of facial emotion training including generalization and maintenance restricted to randomized control trial studies comprising a total of 595 individuals with ASD. Our findings revealed that the intervention resulted in a robust improvement in emotion recognition for individuals receiving training compared with controls. However, while there was also some evidence for generalization of training effects, the small number of studies which conducted follow-ups and assessed social skills reported that improvements were not maintained and there was no evidence for general improvement in social skills. Overall, the analysis revealed a medium effect size in training improvement indicating that facial emotion training may be an effective method for enhancing emotion recognition skills in ASD although more studies are required to assess maintenance of effects and possible general improvements in social skills. LAY SUMMARY Facial emotion training as an intervention may be a potential way to help improve emotion recognition in autism spectrum disorder (ASD), however robust empirical support for its efficacy has not been sufficiently established. Here, we conducted a meta-analysis of previous studies to summarize the effects of facial emotion training on ASD. Our results show that the training produces a robust improvement in subsequent emotion recognition, while maintenance and generalization effects still need further investigation. To date, no experimentally verified improvements in social skills have been reported.The breakdown of the blood-brain barrier (BBB) is related to the occurrence and deterioration of neurological dysfunction in ischemic stroke, which leads to the extravasation of blood-borne substances, resulting in vasogenic edema and increased mortality. However, a limited understanding of the molecular mechanisms that control the restrictive properties of the BBB hinders the manipulation of the BBB in disease and treatment. Here, we found that the glycocalyx (GCX) is a critical factor in the regulation of brain endothelial barrier integrity. First, endothelial GCX displayed a biphasic change pattern, of which the timescale matched well with the biphasic evolution of BBB permeability to tracers within the first week after t-MCAO. Moreover, GCX destruction with hyaluronidase increased BBB permeability in healthy mice and aggravated BBB leakage in transient middle cerebral artery occlusion (t-MCAO) mice. Surprisingly, ultrastructural observation showed that GCX destruction was accompanied by increased endothelial transcytosis at the ischemic BBB, while the tight junctions remained morphologically and functionally intact. Knockdown of caveolin1 (Cav1) suppressed endothelial transcytosis, leading to reduced BBB permeability, and brain edema. Lastly, a coimmunoprecipitation assay showed that GCX degradation enhanced the interaction between syndecan1 and Src by promoting the binding of phosphorylated syndecan1 to the Src SH2 domain, which led to rapid modulation of cytoskeletal proteins to promote caveolae-mediated endocytosis. Overall, these findings demonstrate that the dynamic degradation and reconstruction of GCX may account for the biphasic changes in BBB permeability in ischemic stroke, and reveal an essential role of GCX in suppressing transcellular transport in brain endothelial cells to maintain BBB integrity. Targeting GCX may provide a novel strategy for managing BBB dysfunction and central nervous system drug delivery.The front cover artwork is provided by Prof. Sang-Hyun Oh's group at the U