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One of the great strengths of X-ray computed tomography over conventional inspection methods (ultrasound, thermography, radiography) is that it can image damage in 3D. However for curved ordeformed composite panels it can be difficult to automatically ascribe the damage to specific plies or inter-ply interfaces. An X-ray computed tomography (CT) data processing methodology is developed to extract the through-thickness distribution of damage in curved or deformed composite panels. The method is applied to [(0°/90°)2]s carbon fibre reinforced polymer (CFRP) panels subjected low velocity impact damage (5 J up to 20 J) providing 3D ply-by-ply damage visualisation and analysis. Our distance transform approach allows slices to be taken that approximately follow the composite curvature allowing the impact damage to be separated, visualised and quantified in 3D on a ply-by-ply basis. In this way the interply delaminations have been mapped, showing characteristic peanut shaped delaminations with the major axis oriented with the fibres in the ply below the interface. This registry to the profile of the panel constitutes a significant improvement in our ability to characterise impact damage in composite laminates and extract relevant measurements from X-ray CT datasets.
T cells need to adapt their cellular metabolism for effector cell differentiation. This relies on alterations in mitochondrial physiology. Which signals and molecules regulate those alterations remains unclear. We recently reported, that the mitochondrial protein TCAIM inhibits activation-induced changes in mitochondrial morphology and function and thus, CD effector T cell formation. Using conditional TCAIM knock-in (KI) and knockout (KO) mice, w now show that it also applies to CD8+ T cells and more importantly, delineate the molecular processes in mitochondria by which TCAIM controls effector cell differentiation. TCAIM KI resulted in reduced activation-induced HIF1α protein expression. Metabolomics and transcriptional data in combination with mathematical flux modeling revealed an impaired induction of anabolic pathways, especially of the mevalonate pathway and cholesterol biosynthesis in TCAIM KI CD8+ T cells. Addition of cholesterol completely rescued HIF1α protein expression, activation and proliferation of TCAIM KI CD8+ T cells. At the molecular level, TCAIM delayed activation-induced mitochondria-ER contact (MERC) formation by binding to MERC promoting proteins such as RMD3 and VDAC2. In summary, we demonstrate that TCAIM suppresses effector cell differentiation by inhibiting MERC formation, which induce HIF1α-mediated increase in cellular metabolism and cholesterol biosynthesis.