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In the present study, an innovative approach to produce hybrid thermoset‐thermoplastic structure by means of co‐curing technique together with injection overmolding technique is proposed. To make thermoset composite bondable, a thermoplastic film was firstly co‐cured on the surface of thermoset composite. Five different types of thermoplastic film were chosen to co‐cure with thermoset composite. The bonding strength between thermoplastic film and thermoset composite was evaluated with lap shear strength. The results show that plasma treatment on thermoplastic film can promote polar groups at interface, which has positive effect on increasing wettability and can increase bonding strength by up to 69.7% of co‐cured structure. Meanwhile, increasing the surface roughness of thermoplastic film can also increase bonding strength by 162.9% because of mechanical interlock. Especially, because of low melting temperature of metallocene polypropylene, some fiber bundles in the interface zone were impregnated with molten metallocene polypropylene, resulting in strong bonding strength increased by 266.2% of the resultant co‐cured structure. Based on these results, polyamide 6 film was selected as the best thermoplastic boundary for co‐cured structure. Finally, hybrid thermoset‐thermoplastic was fabricated by injection overmolding of molten polyamide 6 on co‐cured structure, which has high average lap shear strength of around 14.9 MPa. [ABSTRACT FROM AUTHOR]

Overmolded hybrid fiber reinforced thermoplastic composites (hybrid thermoplastic composites) composed of continuous fiber and short fiber reinforcement benefit from high mechanical performance, geometric complexity as well as low production cycle times. The effective bonding of continuous fiber reinforced part and injection molding compounds plays a vital role in controlling the mechanical performance of hybrid composites. In this present work, plasma treatment was applied on continuous fiber reinforced polypropylene composites laminate for increasing interface strength of hybrid composites. The effect of the plasma treatment was studied through experiments and molecular dynamics (MD) simulation. The results show that plasma treatment increases the interface strength of hybrid composites because of the generation of polar groups of OH, COOH, and NH2. The contribution of each aspect to the improved interface strength was quantified by MD simulation. It is found that these active functional groups can promote the diffusion coefficient at interface. Moreover, the introduction of NH2 is more likely to enhance the bonding strength from the perspective of generated interaction energy at the interface. [ABSTRACT FROM AUTHOR]

Adaptive immunity and innate immunity have been implicated in the pathogenesis of abdominal aortic aneurysm (AAA), and damage and remodelling in the tunica media are a focus of the aneurysm development. Thus, identification of key immune cells or molecules that might be targets for the treatment of AAA is critical. We characterized the innate immune cells in human AAA tissue specimens by flow cytometry and found that apart from other lymphocytes, many invariant natural killer T (iNKT) cells marked as CD3 and Va24Ja18 had invaded the aortic tissues and were numerous, especially in the tunica media. These infiltrating iNKT cells have a high expression of CD69, indicating a highly active function. We were interested in whether iNKT cells could be the drivers of media damage in AAA. To answer this question, we used an AAA mouse model induced by angiotensin II (Ang II) infusion, which can reproduce the inflammatory response of AAA in mouse, which was confirmed by RNAseq. The results showed that the incidence of AAA was significantly higher after administration of α‐galactosylceramide (α‐GalCer), a synthetic glycolipid that activates iNKT cells via CD1d, compared with the Ang II‐induced AAA alone (61·54% vs 31·82%) in mice. Histopathological and immunofluorescent staining results showed significantly more severe inflammatory infiltration and pathological lesions in the Ang II+α‐GalCer treatment group. These results are highly suggestive that activated iNKT cells greatly contribute to AAA development and that the control of the activation state in iNKT cells may represent an important therapeutic strategy for AAA. [ABSTRACT FROM AUTHOR]

ABSTRACT Oral lichen planus (OLP) is a chronic inflammatory disorder of oral mucosa of unknown cause. Microbial infection and dysimmunity appear to play important roles in its pathogenesis. In this study, differences in genetic profiling of salivary microbial communities in two subtypes of OLP and healthy controls were evaluated by means of PCR-denaturing gradient gel electrophoresis (DGGE). Additionally, ELISA was used to investigate the possible role of Th17 in lesion formation by detecting two related cytokines IL-17 and IL-23 in the saliva of OLP patients. When the DGGE profiles were analyzed, the bacterial populations were found to be significantly less rich in subjects with reticular and erosive OLP than in healthy controls. There was significantly less microbial diversity, as denoted by the Shannon index, in saliva samples from subjects with erosive OLP than in those from healthy controls. Cluster analysis and principal component analysis showed that the DGGE profiles formed distinctly group-specific clusters. Salivary concentrations of IL-17 in subjects with erosive OLP group were significantly higher than in those with reticular OLP and healthy controls. What's more, significantly positive correlations were observed between salivary IL-17 concentrations and disease clinical scores. Microbial richness and diversity was negatively correlated with salivary IL-17 concentrations. These results suggest there is significantly less salivary bacterial diversity and complexity in subjects with OLP han in healthy controls and that the shifted community composition is closely related to an immune cytokine, IL-17. [ABSTRACT FROM AUTHOR]