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In order to compete with steel, a fibre-reinforced composite exhaust wall with a general-purpose resin system requires an effective but lightweight insulation layer. However a lack of experimental methods for heat transfer from turbulent gas flow to pipe walls lined with a porous insulation layer was discovered in literature. Such a test method is crucial to assess the influence of the permeability of such an insulation layer on the heat transfer rate, such that the lightest configuration can be selected. A new test method was developed and tested on samples representative for a composite exhaust. The accuracy of the method was assessed and the results for samples with different wall roughness were obtained. The behaviour of the samples under consideration proved to be more complicated than predicted by theories for impermeable pipe walls.

Lung cancer arises in a context of tumour-induced immune suppression. Dendritic cells (DCs) are central players in the induction of anti-tumoural immunity, providing critical signals that drive the induction of cytotoxic T-cell responses. Meanwhile, microRNAs are associated with tumour development as well as immune regulation. We postulated that lung tumours escape immune control by reprogramming DC immunogenicity at the microRNA level. Using an orthotopic model of lung cancer, we first identified the DC population responsible for transport and cross-presentation of lung tumour-derived antigens to naive T cells in the draining mediastinal lymph nodes (LNs). Profiling the full microRNA repertoire of these DCs revealed a restricted set of microRNAs that was consistently dysregulated in the presence of lung tumours, with miR-301a as one of the top upregulated transcripts. Overexpression of miR-301a in DCs suppressed IL-12 secretion, decreased IFN-gamma release from antigen-specific cytotoxic T cells, and shifted antigen-specific T helper cytokine profile away from IFN-gamma towards IL-13 and IL-17A-secreting T cells. Strikingly, DC-selective Dicer1 gene deletion resulted in delayed lung tumour growth and a survival benefit. Taken together, our data reveal that lung tumours induce an immunosuppressive microRNA signature in pulmonary DCs. Interfering with the DC-intrinsic capacity to remodel microRNA repertoires affects lung tumour outcome.