Friction Investigation of Closed-Cell Aluminium Foam during Radial-Constrained Test.

The energy-absorbing capacity and friction phenomena of different closed-cell aluminium foam-filled Al tube types are investigated through experimental compression tests. Concerning the kind of investigation, free, radial-constrained and friction tests occurred. The radial-constrained compression test results confirm that the process requires significantly more compression energy than without the constrain. Pushing away different pre-compressed foams inside the aluminium tube, the static and kinematic frictional resistances can be determined and the energy required to move them can be calculated. Knowing the value of the energy required for the frictional resistance, we can obtain how much of the energy surplus in radially inhibited compression is caused by the friction phenomena. The main goal present study is to reveal the magnitude of friction between the foam and the wall of the tube during the radially constrained test. The investigation used 0.4 and 0.7 g/cm3 density closed-cell aluminium foam whilst a compressive test was applied where the force-displacement data were recorded to calculate the absorbed energy due to friction. Considering the results of the test, it can be stated that 18% of the invested energy was used to overcome friction in the case of lighter foam and almost 23% with 0.7 g/cm3 foam during the radial-constrained test.

EGR2 is an epigenomic regulator of phagocytosis and antifungal immunity in alveolar macrophages.

Alveolar macrophages (AMs) act as gatekeepers of the lung's immune responses, serving essential roles in recognizing and eliminating pathogens. The transcription factor (TF) Early Growth Response 2 (EGR2) has been recently described as required for mature AMs in mice; however, its mechanisms of action have not been explored. Here, we identified EGR2 as an epigenomic regulator and likely direct proximal transcriptional activator in AMs using epigenomic approaches (RNA-sequencing, ATAC-sequencing, and CUT&RUN). The predicted direct proximal targets of EGR2 included a subset of AM identity genes, and ones related to pathogen recognition, phagosome maturation, and adhesion, such as Clec7a, Atp6v0d2, Itgb2, Rhoc, and Tmsb10. We provided evidence that EGR2 deficiency led to impaired zymosan internalization and reduced the capacity to respond to Aspergillus fumigatus. Mechanistically, the lack of EGR2 altered the transcriptional response, secreted cytokines (i.e., CXCL11), and inflammation-resolving lipid mediators (i.e., RvE1) of AMs during in vivo zymosan-induced inflammation, which manifested in impaired resolution. Our findings demonstrated that EGR2 is a key proximal transcriptional activator and epigenomic bookmarker in AMs responsible for select, distinct components of cell identity and a protective transcriptional and epigenomic program against fungi.