SUMMARYThe goal of this research is to develop a low-cost face robot which has a lower degree-of-freedom facial expression mechanism. Many designs of facial robots have been announced and published in the past. Face robots can be classified into two major types based on their respective degrees of freedom. The first type has various facial expressions with higher degrees of freedom, and the second has finite facial expressions with fewer degrees of freedom. Due to the high cost of the higher-degree-of-freedom face robot, most commercial face robot products are designed in the lower-degrees-of-freedom form with finite facial expressions. Therefore, a face robot with a simplified facial expression mechanism is proposed in this research. The main purpose of this research is to develop a device with a lower degree-of-freedom mechanism that is able to generate many facial expressions while keeping one basic mouth shape variation. Our research provides a new face robot example and development direction to reduce costs and conserve energy.
Aberrant neutrophil extracellular trap (NET) formation and the loss of barrier integrity in inflamed intestinal tissues have long been associated with inflammatory bowel disease (IBD). However, whether NETs alter intestinal epithelium permeability during colitis remains elusive. Here, we demonstrated that NETs promote the breakdown in intestinal barrier function for the pathogenesis of intestinal inflammation in mouse models of colitis. NETs were abundant in the colon of mice with colitis experimentally induced by dextran sulfate sodium (DSS) or 2,4,6-trinitrobenzene sulfonic acid (TNBS). Analysis of the intestinal barrier integrity revealed that NETs impaired gut permeability, enabling the initiation of luminal bacterial translocation and inflammation. Furthermore, NETs induced the apoptosis of epithelial cells and disrupted the integrity of tight junctions and adherens junctions. Intravenous administration of DNase I, an enzyme that dissolves the web-like DNA filaments of NETs, during colitis restored the mucosal barrier integrity which reduced the dissemination of luminal bacteria, and attenuated intestinal inflammation in both DSS and TNBS models. We conclude that NETs serve a detrimental factor in the gut epithelial barrier function leading to the pathogenesis of mucosal inflammation during acute colitis.
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