Evaluation of strain and stress states in the single point incremental forming process

Single point incremental forming (SPIF) is a promising manufacturing process suitable for small batch production. Furthermore, the material formability is enhanced in comparison with the conventional sheet metal forming processes, resulting from the small plastic zone and the incremental nature. Nevertheless, the further development of the SPIF process requires the full understanding of the material deformation mechanism, which is of great importance for the effective process optimization. In this study, a comprehensive finite element model has been developed to analyse the state of strain and stress in the vicinity of the contact area, where the plastic deformation increases by means of the forming tool action. The numerical model is firstly validated with experimental results from a simple truncated cone of AA7075-O aluminium alloy, namely, the forming force evolution, the final thickness and the plastic strain distributions. In order to evaluate accurately the through-thickness gradients, the blank is modelled with solid finite elements. The small contact area between the forming tool and the sheet produces a negative mean stress under the tool, postponing the ductile fracture occurrence. On the other hand, the residual stresses in both circumferential and meridional directions are positive in the inner skin of the cone and negative in the outer skin. They arise predominantly along the circumferential direction due to the geometrical restrictions in this direction.The authors would like to gratefully acknowledge the financial support from the Portuguese Foundation for Science and Technology (FCT) under project PTDC/EMS-TEC/1805/2012. The first author is also grateful to the FCT for the postdoctoral grant SFRH/BPD/101334/2014.info:eu-repo/semantics/publishedVersio

Inhibition of TGF-β Signaling and Decreased Apoptosis in IUGR-Associated Lung Disease in Rats

Intrauterine growth restriction is associated with impaired lung function in adulthood. It is unknown whether such impairment of lung function is linked to the transforming growth factor (TGF)-β system in the lung. Therefore, we investigated the effects of IUGR on lung function, expression of extracellular matrix (ECM) components and TGF-β signaling in rats. IUGR was induced in rats by isocaloric protein restriction during gestation. Lung function was assessed with direct plethysmography at postnatal day (P) 70. Pulmonary activity of the TGF-β system was determined at P1 and P70. TGF-β signaling was blocked in vitro using adenovirus-delivered Smad7. At P70, respiratory airway compliance was significantly impaired after IUGR. These changes were accompanied by decreased expression of TGF-β1 at P1 and P70 and a consistently dampened phosphorylation of Smad2 and Smad3. Furthermore, the mRNA expression levels of inhibitors of TGF-β signaling (Smad7 and Smurf2) were reduced, and the expression of TGF-β-regulated ECM components (e.g. collagen I) was decreased in the lungs of IUGR animals at P1; whereas elastin and tenascin N expression was significantly upregulated. In vitro inhibition of TGF-β signaling in NIH/3T3, MLE 12 and endothelial cells by adenovirus-delivered Smad7 demonstrated a direct effect on the expression of ECM components. Taken together, these data demonstrate a significant impact of IUGR on lung development and function and suggest that attenuated TGF-β signaling may contribute to the pathological processes of IUGR-associated lung disease