Establishing a Euro-Asia Network in Design and Manufacture Through Eu Projects

In an era of rapid economic growth and industrial development in developing countries in Asia, engineering education systems in these countries are under increasing pressure to meet the demands of the local labour markets. At the same time there is a lack of interest from students in engineering in Europe. With support from the Asia-Link Programme of European Commission, three projects on engineering design and manufacture, led by the University of Strathclyde, have been undertaken by eleven Institutions in nine countries in both Europe and Asia. These projects aim at establishing a European and Asian (EUROASIA) network in engineering design and manufacture, contributing to the demands of today’s multinational engineering industries, and promoting local development through engineering education for both Asia and Europe. One project has been successfully completed, and the other two projects are still ongoing. Overall, this network in engineering design and manufacture has been successfully built up; the proposed deliverables and achievements have been made; and the impact in the engineering sectors of Asian partner countries is positive and remarkable

Boundary Conditions for Elastohydrodynamics of Circular Point Contacts

The paper presents the solution of an elastohydrodynamic point contact condition using inlet and outlet lubricant entrainment with partial counter-flow. The inlet and outlet boundaries are determined using potential flow analysis for the pure rolling of contiguous surfaces. This shows that Swift–Stieber boundary conditions best conform to the observed partial counter-flow at the inlet conjunction, satisfying the compatibility condition. For the outlet region, the same is true when Prandtl–Hopkins boundary conditions are employed. Using these boundary conditions, the predictions conform closely to the measured pressure distribution using a deposited pressure-sensitive micro-transducer in a ball-to-flat race contact. Furthermore, the predicted conjunctional shape closely conforms to the often observed characteristic keyhole conjunction through optical interferometry. The combined numerical–experimental analysis with realistic boundary conditions described here has not hitherto been reported in the literature

Evaluation of Friction in Upsetting

Distributions of contact stresses at the neutral point in metal forming are very hard to be properly predicted due to the complex interface situation and lack of suitable friction models. In this paper, the dynamic friction model in which the friction depends on both time rate of strain and normal pressure has been applied to predict contact stresses in cylinder upsetting. Case studies have shown that the predicted results agreed with the experimental data chosen from literature. By comparing with two other friction models, the dynamic friction model seemed to give a better solution

Serum Amyloid a Promotes Visfatin Expression in Macrophages

Visfatin has been reported to exert an important role in the development of atherosclerosis. However, the mechanism that regulated the expression of Visfatin has not been elucidated yet. This study aimed to investigate the effect of SAA on the regulation of Visfatin, as well as the potential pathway. After RAW264.7 macrophages and primary monocytes were stimulated with SAA, the mRNA and protein expression of Visfatin was detected with real-time PCR and western blot, respectively. The concentration of Visfatin in the supernatant was measured with ELISA. Formyl peptide receptor 2 (FPR2) agonist (WKYMVm) and inhibitor (WRW4), extracellular signal-regulated kinase 1/2 (ERK1/2) inhibitor (PD98059), and peroxisome proliferator-activated receptor-γ (PPAR-γ) agonist (Rosiglitazone) and inhibitor (GW9662) were used to investigate the mechanism of regulation of Visfatin. The results demonstrated that SAA upregulated Visfatin expression in cultured RAW264.7 macrophages and in the primary monocytes. WRW4 decreased SAA-induced Visfatin production, while WKYMVm could induce Visfatin expression. PD98059 reduced SAA-induced Visfatin production. What is more, GW9662 inhibited SAA-induced Visfatin production, while Rosiglitazone promoted Visfatin expression. These results demonstrate that SAA upregulates Visfatin expression via a FPR2/ERK1/2/PPAR-γ signaling pathway